practice

Explanation

Shock is a form of stress which is accompanied by the release of stress hormones (catecholamines, cortisol). Stress-induced changes in blood leukocyte distribution may represent an adaptive response. This represents a redistribution of leukocytes from the blood to other organs such as the skin, draining sentinel lymph nodes and other compartments. Such leukocyte redistribution may enhance immune function in compartments to which immune cells traffic during stress.

Explanation

Hyperthermia (i.e. marked warming of core temperature) is not mediated by pyrogens and there is no resetting of the hypothalamic set point. It may be accidental or therapeutic.

Explanation

Types of lymph-circulatory insufficiency:

·        Mechanical insufficiency

·        Dynamic insufficiency

·        Insufficiency of absorption/Resorption insufficiency

Mechanical insufficiency is present where lymph flow is hindered by a mechanical factor. The mechanical factor may be of an anatomical, organic nature e.g. occlusion of lymphatics by obstructive lymphangitis, thrombosis of the lymphatics (e.g. during cancer metastasis), filariasis.

The other two types has to do with a disbalance of proteins that upsets the filtration and absorption pressures.

Explanation

During cerebellar lesions, there  are disturbances in posture, equilibrium and movements. Disturbances in movements: ataxia, asynergia, asthenia (weak muscle contractions with characteristically rapid onset of muscle fatigue), Dysmetria, Intention tremor, astasia (loss of the capacity for sustained tetanic contractions), nystagmus, rebound phenomenon, dysarthria, adiadochokinesis, atonia (lack or impairment of muscle tone).

Explanation

Liver disease (hepatitis) may result in a number of defects in hemostasis. Except vitamin K deficiency, they may lead to the reduced synthesis of factors of coagulation. The reduced synthesis of coagulation factors may be the result of severe hepatocellular damage. There are 3 main stages in the blood coagulation cascade:

·        Formation of the thromboplastin complex

·        Transformation of prothrombin to thrombin

·        Transformation of fibrinogen to fibrin

In hepatitis, there will be reduced synthesis of thrombin and fibrin; but thrombin comes before fibrin in the coagulation cascade, therefore, decrease in thrombin production is a more correct answer in this case.

Explanation

Hypoosmolar hypohydration (salt deficit) develops due to diarrhea, vomiting, sweating, adrenal insufficiency, hypokalemia, CNS lesions, salt-losing nephritis.

          Hyperosmolar hypohydration (water defcit) develops due to the loss of the fluid which lacks electrolytes e.g. in diabetes insipidus, hyperventilation.

          Isoosmolar hypohydration (isoosmotic loss): proportional volume decrease of fluids and electrolytes e.g. in blood loss, burns, diuretic therapy, especially diarrhea in cholera.

         Hypoosmolar hyperhydration (water excess) develops in acute renal failure (in the stage of anuria), Parhon’s syndrome (syndrome of inappropriate ADH secretion –SIADH).

         Hyperosmolar hyperhydration (salt excess) develops rarely e.g. in drinking salt (sea) water, infusion of hypertonic saline, adrenal hyperactivity or steroid therapy.

    Low water level extracellularly – Hypohydration

    Low blood osmolarity – Hypoosmolar

                Hypoosmolar hypohydration

Explanation

High IgM level usually indicate an acute or primary infection because, it is the first antibody to appear in response to initial exposure to an antigen. Secondary or reinfection show an increase in IgG. IgM antibodies appear early in the course of an infection, this makes it useful in the diagnosis of infectious diseases. Demonstrating IgM antibodies in a patient’s serum indicates recent infection or in a neonate’s serum, it indicates intrauterine infection.

Explanation

Massive burns leads to hypovolemia and decreases general blood volume in circulation. This decrease in blood volume, decrease perfusion to all organs in the body. Decrease in renal perfusion (renal blood flow) will decrease glomerular filtration rate (GFR).

Explanation

Apraxia is defined as a cognitive motor disorder in which the patient loses the ability to accurately perform learned, skilled actions. Apraxia is primarily a condition that localized to the dominant (usually left) hemisphere of the brain. In particular, lesions of supramarginal gyrus and underlying white matter of the left parietal lobe have been implicated to cause apraxia.

Explanation

The humoral immunity deficiency is the most frequent among primary immunodeficiency types. The genetic defects of immune system development are on the basis of primary immunodeficiency, causing various clinical symptoms. There are 36 primary immunodeficiency types according to the last international classification, which are divided into 5 groups depending on the kind of deficiency of the immune system:

·        Deficiency of humoral immunity (B-component): frequently in bacterial infections.

·        Deficiency of cellular immunity (T-component): frequently in viral infections.

·        Combined T and B – immunodeficiency: during both bacterial and viral infections.

·        Deficiency of phagocytes system.

·        Deficiency of complement system: in gram negative coccal infections.

Explanation

From horizontal (lying position) to vertical (standing position) will make all blood flow towards the lower extremities, thereby reducing venous return (blood going upwards towards the heart) in the first place. This will definitely ↓ cardiac output (C.O) → ↓blood supply to brain (this can lead to fainting). Then there is reflex vasoconstriction to increase venous return to heart, in the absence of any pathology.

Explanation

Abnormality of constitution, so called diathesis is characterized by pathological reactions on physiological agent. Classification of diathesis:

·        Hemorrhagic: characterized by hemorrhagic reaction to physiological factors.

·        Thymicolymphatic/Lymphohypoplastic: characterized by enlargement of lymphatic nodes, muscular atrophy, individual pale, pastous, predisposing to autoallergic disease, lymphocytosis, angina and other infectious diseases.

·        Neuroarthritic/Gouty: predisposing to arthralgia, arthritis, rheumatism, obesity, gout, psychic disease.

·        Edematic/Exudative: characterized by edema reaction to different environmental factors.

·        Asthenic: expressed in hypodynamia, hypotonia.

Explanation

Protein mechanism is one of the molecular mechanisms of cell injury. The protein mechanism of cell damage includes:

·        Inhibition of enzymes (reversible and irreversible)

·        Denaturation – violation of native structure of proteins

·        Proteolysis – that is carried out under the action of lysosomal enzymes.

Explanation

Helicobacter pylori causes gastritis and peptic ulcers. Infection with H. pylori is a risk factor for gastric carcinoma and is linked to mucosal-associated lymphoid tissue (MALT) lymphoma. It is a gram negative, flexibacteria, oxidase positive, microaerophilic, motile and the only species in the Helicobacter genus to have multiple unipolar – sheathed flagella.

Microaerophiles need O₂ because they cannot ferment or respire anaerobically. However, they are poisoned by high concentrations of O₂. They gather in the upper part of the test tube but not the very top. CO₂ is essential for initial growth of H. pylori in liquid media (microaerophilic property). They produce urease, so it’s a diagnostic tool and not a necessary consideration for cultivation (culture medium).

Explanation

This results indicates erythropoiesis i.e. synthesis of RBCs.

Explanation

The drop in arterial pressure (AP) will cause a reflex tachycardia, the heart increases its contractility and cardiac output. Vasoconstriction will be minimal in the heart, because the heart needs to pump more i.e. do more work. Therefore, it needs more blood supply. But vasoconstriction will be maximal in the GIT (bowels), muscles, skin due to centralization of blood flow (i.e. redistribution of blood to important organs like heart, brain)

Explanation

Considering the time (10mins) – immediate

Type I Hypersensitivity reaction (HSR); anaphylactic and atopic: free antigen cross-links IgE on presensitized (i.e. exposed to the antigen before) mast cells and basophils, triggering immediate release of vasoactive amines that act at postcapillary venules (i.e. histamine). Reaction develops rapidly after antigen exposure because of preformed antibody from first exposure. IgE is the main immunoglobulin involved in type I HSR. Type I: uses IgE and IgG₄

Explanation

Explanation

Acute phase reactants are factors whose serum concentrations change significantly in response to inflammation produced by the liver in both acute and chronic inflammatory states. Notably induced by IL-6 e.g. C-reactive protein, hepcidin, serum amyloid A are all upregulated; while albumin and transferring are downregulated. C-reactive protein is an opsonin, it fixes complement and facilitates phagocytosis. It is measured  clinically as a sign of ongoing inflammation.

Explanation

·        Neuroparalytic arterial hyperemia is caused by damage or blockage of α-adrenoreceptors (sympathetic nervous system). It is characterized by reduction or absence (paralysis) of the sympathetic nervous system effects on the walls of the arteries and arterioles.

·        Neurotonic arterial hyperemia is caused by activation of parasympathetic nervous system; irritation of vascular dilators part of vascular center (CNS) or inhibition of vascular – constrictor part of this center (vasomotor center of CNS); M-cholinoreceptors; H₂-histaminereceptors. It is characterized by predominance of the parasympathetic nervous system effects on arterial vascular walls.

After the exam parasympathetic nervous system is the dominant system. Before the exam, sympathetic nervous system is the dominant system.

Explanation

Hemolytic/Prehepatic Jaundice is the type of Jaundice that occurs because of excessive destruction of RBCs resulting in ↑ blood level of free, Indirect, unconjugated bilirubin. In this condition, the excretory function of the liver is normal. But the quantity of bilirubin ↑ greatly. The liver cells cannot excrete that much excess bilirubin rapidly. Formation of Urobilinogen (stercobilin) ↑ resulting in the excretion of more amount of stercobilin in stool and urine.

·       Gilbert syndrome (familial nonhemolytic Jaundice): Autosomal recessive defect. Impaired UGT activity. Jaundice occurs with fasting, volume depletion, stress, menses.

Explanation

Systemic lupus erythematous (SLE, Libman-sacks disease) is the classic prototype of the multisystem disease of autoimmune origin, characterized by a bewildering array of autoantibodies, particularly antinuclear antibodies. It is characterized principally by injury to the skin, joints, kidney, and serosal membranes. Antinuclear antibody is directed against several nuclear antigens and can be grouped into 4 categories:

·        Antibodies to DNA

·        Antibodies to histones

·        Antibodies to nonhistone proteins bound to RNA

·        Antibodies to nuclear antigens.

SLE is a type III hypersensitivity reaction with formation of immune complexes. It can cause diffuse proliferative glomerulonephritis seen under the light microscope as “wire loop” of capillaries and granular under the immunofluorescence microscopy.

Explanation

Blood group O(I): no antigens, therefore no agglutination.

Blood group A(II): A antigen, agglutinate with blood group B(III) and O(I).

Blood group B(III): B antigen, agglutinate with blood group A(II) and O(I).

Blood group AB(IV): A and B antigen, agglutinate with all blood groups. No antibody.

Blood group name is determined by the antigen present on RBC, but the patient has an opposite antibody. So whenever, the antibody corresponds to the antigen, there is agglutination. Since O does not have any antigen, no agglutination can occur.

Explanation

ADH (vasopressin) is produced in neurohypophysis (posterior pituitary gland). ADH causes reabsorption of free water through aquaporins in collecting ducts of kidney.

Diabetes insipidus (D.I.) is characterized by intense thirst and polyuria (hyperdiuresis) with inability to concentrate urine due to lack of ADH (central D.I.) or failure of response to circulating ADH (nephrogenic D.I.). in central D.I. antidiuretic hormone (ADH) is decreased; in nephrogenic D.I. ADH is normal. Therefore, the hormonal drug we can use to treat diabetes insipidus is to replace the low antidiuretic hormone (ADH) in central diabetes insipidus. So, we use ADH – a posterior pituitary hormone which increases water reabsorption in renal tubules and decrease diuresis. Its analogue desmopressin acetate can also be administered intranasally. Nephrogenic diabetes insipidus does not require hormonal replacement.

Explanation

 Nodal or atrioventricular (AV) extrasystole is caused by stimulus arising from AV node. The excitation of the atria differs from normal, the impulse is transmitted retrogradely from bottom to top. The following signs are characteristic of the ECG in nodal extrasystole:

·        Premature appearance of the cardiac complex.

·        Changes in the P wave which becomes negative to show the retrograde atrial excitation (in some cases the P wave is absent on the ECG).

·        If the atria and ventricles are excited synchronously, the P wave superimposes (overlaps) the QRS complex.

Explanation

Thalassemia or target cell anemia or Cooley’s anemia is an hemoglobinopathy (abnormal hemoglobin in RBCs). Defect in α-globin chain results in α thalassemia; and point mutations in β-globin chain results in β thalassemia. It is characterized microscopically by anisocytosis, poikilocytosis, target cells and is characterized by increased hemolysis, enlargement of spleen and liver, progressive anemia with erythroblastemia (reticulocyte). It’s a microcytic, hypochromic anemia.

Sickle cell anemia is also a hemoglobinopathy (abnormal hemoglobin in RBCs). It results as a result of a point mutation causing a single amino acid replacement in β chain (substitution of glutamic acid with valine) to produce hemoglobin S (HbS). The condition is characterized by the presence of sickle-like erythrocytes revealed during crisis, they cause stasis, hemorrhages and infarctions.

Explanation

Sexual cycles are controlled by the hypothalamus. Gonadotropin-releasing hormone (GnRH), produced by the hypothalamus acts on cells of the anterior lobe (adenohypophysis) of the pituitary gland which in turn secrete gonadotropins. These hormones, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), stimulate and control cyclic changes in the ovary.

At the beginning of each ovarian cycle, 15-20 primary stage (preantral) follicles are stimulated to grow under the influence of FSH. Under normal conditions, only one of these follicles reaches full maturity and only one oocyte is discharged; the others degenerate and become atretic. FSH also stimulates maturation of follicular (granulosa) cells surrounding the oocyte. In cooperation, theca interna and granulose cells produce estrogens. As a result of this estrogen production, the uterine endometrium enters the follicular or proliferative phase. Thinning of the cervical mucus occurs to allow passage of sperm and the anterior lobe of the pituitary gland is stimulated to secrete LH. So dysfunction of follicular cells will inhibit the production of estrogen.

Explanation

Prolactin is responsible for lactogenesis. Prolactin is secreted from anterior pituitary gland. It is necessary for the final preparation of mammary glands for the production and secretion of milk. Lactation means synthesis, secretion and ejection of milk.

Explanation

17-ketosteroids (17-KS) are substances that are formed when the body breaks down male steroid sex hormones called androgens and other hormones released by the adrenal glands in males and females; and by the testes in males. Increased levels of 17-ketosteroids may be due to: adrenal gland problems such as tumor – cushing’s syndrome, cushing’s disease; ovarian or testicular cancer. Itsenko-cushing disease is hypercortisolism due to excess pituitary secretion of adrenocorticotropic hormone (ACTH). Excess ACTH leads to excess adrenal hormones → excess mineralocorticoids; excess sex hormones (↑17-KS); excess glucocorticoids (steroid diabetes). Steroid diabetes is a medical term referring to prolonged hyperglycemia due to glucocorticoid (cortisol) excess. Steroid diabetes → 17-KS.

Explanation

Corestenoma is narrowing of the pupil i.e. miosis. Miosis (myosis) is a parasympathetic effect mediated by acetylcholine.

Muscarinic receptors belong to the class of G protein-coupled receptors under the parasympathetic nervous system. These receptors, in addition to binding Acetylcholine, it also recognizes muscarine – an alkaloid that is present in certain poisonous mushrooms. Muscarinic effects include miosis, spasm of accommodation, increasing of lacrimal, salivary, gastrointestinal, bronchial and sweat glands secretion, increase of smooth muscle tonus of internal organs, bradycardia, decreased arterial pressure. 

Sympathetic effects (acting through α or β-adrenergic receptors).

Explanation

Reference interval (adults): 60 – 80g/L

40g/L is low i.e. a low oncotic pressure.

Glomerular filtration rate (GFR) is inversely proportional to oncotic pressure/colloid osmotic pressure, which is exerted by plasma proteins in the glomerular capillary blood. When oncotic pressure is low, GFR increases. Reabsorption is decreased, because the low oncotic pressure is not sufficient to reabsorb water and other substances (cannot create enough pressure to reabsorb water and other substances).

Explanation

Remember that the first contact of allergen with immune cells occurs in the immunological stage resulting in IgE bound to the surface of mast cells. Pathochemical stage of anaphylactic (Type I- allergic) reaction: now, the next exposure to the same antigen results in fixing of the antigen to mast cell-bound IgE. This process leads to mast cell degranulation with the discharge of preformed or primary mediators (histamine, heparin, serotonin etc) and synthesis of secondary mediators (prostaglandins, leukotrienes and cytokines).

Explanation

In viral hepatitis, there is generalized liver dysfunction involving uptake and conjugation of unconjugated bilirubin, secretion of conjugated bilirubin into bile ducts, and recycling of urobilinogen. Alanine transaminase (ALT) and Aspartate transaminase (AST) are increased (↑), but ALT is higher than AST and there is a slight ↑ in alkaline phosphatase (ALP) and ɣ-glutamyltransferase (GGT).

ALT is a specific enzyme for liver necrosis; present in the cytosol. ALT>AST: viral hepatitis.

AST is present in the mitochondria. Alcohol damages mitochondria AST>ALT indicates alcoholic hepatitis

Explanation

Stages of fever:

I. Stadium Increment (↑of temperature)

II. Stadium Fastigii (stable, but high temperature; saving of the increased temperature)

III. Stadium Decrementi (decline of temperature)

Temperature decreasing mechanisms in the 3^rd stage: vasodilation of skin blood vessels (peripheral vasodilation); decrease of heat production; sweating

Explanation

Hemic hypoxia (blood hypoxia): may be connected with hemoglobin (Hb) quantity or inhibition of its functions. It is observed during anemia of different genesis; also during poisoning with carbon monoxide, nitrates, sulfa drugs (H₂S) and other substances. In this case we will observe inactivation type of hemic hypoxia with the acquired hemoglobinopathies development. Acquired hemoglobinopathies are characterized by formation of carboxyhemoglobin and methemoglobin.

Explanation

Genocopy is a trait that is a phenotypic copy of a genetic trait but is caused by a different genotype. A phenotype that appears identical to another phenotype but that is caused by a different genetic mechanism e.g. the cleft lip and palate is identical to patau’s syndrome (trisomy 13) but in this case the patient has a normal karyotype. Phenocopy is a phenotype that is not genetically determined but mimics one that is. It is the opposite of genocopy.

Explanation

Emphysema: permanent enlargement of all or part of the respiratory unit. Causes include smoking cigarette (most common cause) and α₁-antitrypsin (AAT) deficiency. α₁-antitrypsin is a protease inhibitor; also referred to as α₁-proteinase inhibitor because it inhibits a wide variety of proteases (including trypsin as the name implies).

Explanation

Parathyroid hormone: secreted by chief cells of parathyroid gland. Effects include:

↑bone resorption of Ca²⁺ and PO₄^3- → ↑their plasma levels

↑kidney reabsorption of Ca²⁺ in distal convoluted tubule → ↑ Ca²⁺ plasma level

↓reabsorption of PO₄^3- in proximal convoluted tubule → ↓ PO₄^3- plasma levels

↑Calcitriol (vit D₃) production by stimulating kidney 1α-hydroxylase in proximal convoluted tubule. It increases Ca²⁺ and PO₄^3- absorption in the intestine.

In general, parathyroid hormone ↑ Ca²⁺ plasma level but ↓ PO₄^3- plasma levels. Abnormal synthesis (↑synthesis) of parathyroid hormone can lead to hypercalcemia and hypophosphatemia.

Calcitonin is secreted by parafollicular cells (C cells of the thyroid gland). It ↓bone resorption of Ca²⁺. It opposes actions of parathyroid hormone. But its not important in normal Ca²⁺ homeostasis. Calcitriol ↑ circulating Ca²⁺ ions as a means of enhancing intestinal absorption of calcium (NB: Calcitriol production is dependent on parathyroid hormone). Aldosterone: reabsorption of Na⁺, excretion of K⁺. Cortisol – glucocorticoid: ↑ blood pressure and gluconeogenesis; ↓ inflammatory and immune responses; ↓ bone formation (↓osteoblast activity).

Explanation

Insulin stimulates glycogen synthase by dephosphorylation. Insulin is an anabolic hormone (build up). So, it stimulates glycogen synthase to favor the synthesis of glycogen (glycogenesis) and inhibits glycogen phosphorylase used in glycogenolysis (glycogen breakdown). Glucagon and Epinephrine stimulates glycogen phosphorylase to break down glycogen to glucose and make energy available for “fight and flight” reactions.

Explanation

Sinus tachycardia is the increase in discharge of impulses from the sinoatrial (SA) node, resulting in increase in heart rate (heart rate increase up to 100beats/min).ECG is normal, except for short R-R intervals .

Sinus bradycardia is the reduction in discharge of impulses from SA node resulting in decrease in heart rate. Heart rate is less than 60beats/min. Extrasystole is the premature contraction of the heart before its normal contraction. ECG is altered. Sinus arrhythmia is characterized by irregular generation of impulses and may be due to variations in the tone of the vagus nerve. ECG is altered.

Explanation

Allotransplantation: from an individual (donor) to another

Autotransplantation: from one part of the body to another (e.g. skin on thigh to         face).

Xenotransplantation and Heterotransplantation: from one specie to another (e.g. pig to human)

Explanation

ARVI – Acute respiratory viral infection. High IgM level usually indicate an acute or primary infection because, it is the first antibody to appear in response to initial exposure to an antigen. Secondary or reinfection show an increase in IgG. IgM antibodies appear early in the course of an infection, this makes it useful in the diagnosis of infectious diseases. Demonstrating IgM antibodies in a patient’s serum indicates recent infection or in a neonate’s serum, it indicates intrauterine infection.

Explanation

Reaction of transplant rejection resembles delayed hypersensitivity reaction. Transplant antigens induce the production of antibodies and sensibilized lymphocytes, which infiltrate the transplant. Microscopically, lymphohistiocytic infiltration is observed in the transplant. Cellular infiltration causes the disturbance of blood circulation and edema; as a result degenerations and necrosis of transplant develop. The neutrophils and macrophages appear in the transplant. Enzyme destruction of the transplant begins, which is followed by its rejection. Transplant – Graft.

This is an immune reaction against the transplant - GRAFT IMMUNITY.

Explanation

Spasticity is probably caused by the removal of inhibitory influences exerted by the cortex (UMN) on the postural centers of the vestibular nuclei and reticular formation. Lesions in the upper motor neuron (UMN) causes hypertonia and spasticity paralysis, increased reflexes (in UMN – everything ↑).

Paralysis is the complete loss of strength and functions of muscle group or a limb.

Explanation

Aldosterone produced in adrenal cortex (zona glomerulosa): causes increased sodium (Na⁺) reabsorption; increased potassium and hydrogen ions (↑K⁺, H⁺) excretion. They increase sodium (↑Na⁺) channel and Na⁺ /K⁺-pump insertion in principal cells of collecting duct; enhances K⁺ and H⁺ excretion by way of principal cell K⁺ channels and α-intercalated cell H⁺ ATPases of collecting duct. Therefore, increase in aldosterone → ↑ K⁺ in urine (excretion) and ↓ Na⁺ in urine (↑ reabsorption); And decreased aldosterone → ↓ K⁺ excretion (↓K⁺ in urine) and ↓ Na⁺  reabsorption (i.e. ↑Na⁺ in urine); same effects on sweats glands too.

Explanation

Acidosis is the reduction in pH (increase in H⁺ concentration) below normal range. pH is less than 7.35; it is produced by:

·        Increase in partial pressure of CO₂ in the body.

·        Decrease in HCO₃^- concentration.

Alkalosis is the increase in pH (decrease in H⁺ concentration) above normal range. pH is greater than 7.45; it is produced by:

·        Decrease in partial pressure of CO₂ in the body.

·        Increase in HCO₃^- concentration.

Each of these two disorders has respiratory and non-respiratory forms. The non-respiratory form is divided into metabolic and excretory(non-gaseous).

·        Respiratory acidosis is the acidosis that is caused by alveolar hypoventilation e.g. airway obstruction due to bronchitis or lung diseases (pneumonia).

·        Respiratory alkalosis is caused by alveolar hyperventilation e.g. hypoxia in high altitude.

·        Non-respiratory:

-Metabolic acidosis is characterized by excess accumulation of organic acids such as lactic acid, ketoacids and uric acid formed by normal metabolism e.g. in Diabetes mellitus or extreme/prolonged exercise.

-Excretory/Non-gaseous acidosis may develop in impaired renal H⁺ excretion related to increased loss of bicarbonate in urine; diarrhea causes acidosis by the loss of bicarbonate with faeces.

-Excretory/Non-gaseous alkalosis: vomiting (loss of gastric acid), increased metabolism of lactate and citrate (turns into bicarbonate and water), long-term use of thiazides and loop diuretics.

Explanation

Coronary heart disease leads to ischemia of myocardium. Ischemia → ↓O₂ → ↓mitochondrial O₂ supply → ↓ATP synthesis → ↓Na⁺K⁺ ATPase pump action → ↑Intracellular Na⁺, Ca²⁺ → ↑Ca²⁺ load of mitochondria → uncoupling of oxidative phosphorylation → Metabolic derangement → Cell injury; also ↑Intracellular Na⁺, Ca²⁺ → ↑H₂O → Acute swelling of cell → enlargement of endoplasmic reticulum → ↓protein synthesis → Metabolic derangement → Cell injury.

Explanation

Lesions involving the optic tract (i.e. beyond the optic chiasm) produce loss of vision within similar areas of the visual field in both eyes (“homonymous hemianopsia”) – left optic tract – left half of both eyes. These lesions can be caused by stroke, tumor, vascular malformations, demyelinating lesions and abscesses.

Explanation

The middle (medial) cerebral artery arises from the internal carotid artery and enters the lateral sulcus. There, it gives branches that supply the greater portion of the superolateral surface of the cerebral hemisphere; including the frontal, parietal, temporal lobes and the insula.

Anterior cerebral artery supplies the medial surface of hemisphere.

Posterior cerebral artery supplies the inferior surface of temporal lobe and the inferior and medial surfaces of the occipital lobe

Basilar artery gives the following branches: posterior cerebral arteries, anterior inferior cerebellar artery, superior cerebellar artery, pontine arteries.

            Only the middle (medial) cerebral artery supplies the right and left parietotemporal region of brain.

Explanation

Crigler Najjar syndrome type II is a rare hereditary disorder and is due to a less severe defect in the bilirubin conjugation. It is believed that hepatic UDP-glucuronyltransferase that catalyzes the addition of second glucuronyl group is defective. It is treated with Phenobarbital ( a barbiturate), because it induces the action of UDP-glucuronyltransferase, thereby producing more conjugated (direct) bilirubin.

Explanation

Hyperosmolar coma is clinically defined by the presence of relative insulin deficiency and hyperglycemia (high glucose concentration), usually higher than 33.3mmol/L with associated elevated serum osmolality (>300mosm/kg), dehydration and stupor, progressing to coma if uncorrected, without the presence of ketosis or acidosis.

Hypoglycemic coma → ↓ glucose concentration

Ketonemic coma → ↑ ketone bodies

Lactacidemic coma → ↑ lactic acid

Explanation

Evaporation is a way the body dissipates heat to the environment by its evaporation via sweat or evaporation of moisture from the skin and respiratory tract mucous membranes of (“wet” heat loss). Evaporation closely related to relative humidity.

Heat Radiation is a way the surface of the human body emits heat to the environment in the form of infrared rays. The amount of heat the body radiates to the environment is proportional to the surface of radiation area and to the difference between the mean values of skin and environment temperature. The surface radiation area is the total surface area of body parts that contact the air. Elimination of heat by radiation increases with a decrease in ambient temperature and decreases with its increase. It is possible to reduce elimination of heat by radiation via reduction of the surface of radiation area (“winding oneself into a ball”). Heat radiation does not require a medium for transfer of heat. (Key words: naked or lightly clothed).

Convection is a way the body eliminates heat by means of transferring heat via moving particles of air or water. To dissipate heat by means of convection, body surface shall be airflowed at a temperature that is lower than the temperature of the skin. At that, air layer contacting with the skin warms up, decreases its density, rises and is replaced by cooler, denser air. By increasing the speed of the air flow (wind, ventilation) heat emission increases significantly as well (forced convection). Convection requires convection current; current of gases or liquids (Key words: air over exposed area of skin).

Conduction is a way the body eliminates heat by means of direct contact with another object. Heat is transferred down the temperature gradient (i.e. from the object of higher temperature to the object of lower temperature). Conduction requires contact with another object (Key words:  in water).

Explanation

The transfused blood might contain pyrogens or its an incompatible blood that activates the immune system. Pyrogenic cytokines, principally IL-1; IL-6 and TNF-α are released into the bloodstream for transport to the hypothalamus, where they exert their action. These cytokines induce prostaglandin E₂ (PGE₂), which is a metabolite of arachidonic acid. It is hypothesized that when IL- 1β interacts with the endothelial cells of the blood-brain barrier in the capillaries of the organum vasculosum laminae terminalis (OVLT), which is in the third ventricle above the optic chiasm, PGE₂ is released into the hypothalamus. At this point PGE₂ binds to receptors in the hypothalamus to induce increase in the thermostatic set point through the second messenger cAMP. In response to the increase in its thermostatic set point, the hypothalamus initiates shivering and vasoconstriction that raise the body’s core temperature to the new set point and fever is established.

Explanation

Starvation decreases protein synthesis because the substrates are not readily available. Decrease in protein synthesis decreases oncotic pressure and thereby increasing glomerular filtration. Net filtration pressure is the balance between hydrostatic pressure (glomerular capillary pressure) and oncotic pressure.

Net filtration pressure = Hydrostatic pressure – Oncotic pressure

Therefore, a decrease in oncotic pressure increases the filtration rate according to the degree of starvation which decreases protein synthesis.

Explanation

Obturation (obstruction, to close) of bile duct – it can be:

* Intrahepatic – blockage of intrahepatic bile ducts

* Extrahepatic – blockage of common bile duct (ductus choledochus).

Findings:

* malabsorption: bile salts do not enter the Small Intestine; no emulsification of fat.

*light coloured stool: due to lack of urobilin (which leads to lack of stercobilin).

*Jaundice (posthepatic, mechanic, obstructive): increased conjugated Bilirubin.

* Steatorrhea

The findings are specific for obstruction of bile duct and bile acid deficiency.

Explanation

The adrenal gland (suprarenal gland) has a secretory parenchymal tissue organized into cortical and medullary regions. Adrenal cortex (derived from mesoderm; steroid-secreting portion) and medulla (derived from neural crest; catecholamine-secreting portion). The adrenal cortex is divided into 3 zones on the basis of arrangement of its cells:

* Zona glomerulosa (15%): arranged in closely packed ovoid clusters; secretes aldosterone.

* Zona fasciculata (80%): large and polyhedral; arranged in long straight cords; secretes cortisol.

* Zona reticularis (5-7%): cells are arranged in anastomosing cords separated by fenestrated capillaries; secretes androgens.

Hydrocortisone is a glucocorticoid (cortisol) and an intake of hydrocortisone will decrease endogenous production of cortisol from zona fasciculata of adrenal cortex leading to its atrophy.

Explanation

Acute pancreatitis is an autodigestion of pancreas by pancreatic enzymes (proteolytic enzymes) due to Inflammation. Therefore,

Acute pancreatitis → ↓production of pancreatic juice.

Trypsin is the most powerful proteolytic enzyme in pancreatic juice. Pepsin is secreted by chief cells in the stomach.

Explanation

In general, these are signs of both right-sided cardiac insufficiency (nutmeg liver – venous congestion) and left-sided cardiac insufficiency (brown induration of lungs – venous congestion). It is Chronic because the patient has been suffering for a long time. In venous or passive hyperemia or congestion, morphologically, the sectioned surface of lungs is dark brown and the process is named brown induration of the lungs. Spleen – cyanotic induration of the spleen; liver – nutmeg liver.

Explanation

Explanation

One of the most common complications of thyroidectomy (resection of thyroid gland) is hypoparathyroidism because the parathyroid gland lying behind the thyroid gland capsule can be accidentally removed during the surgery by unskilled surgeons. Accidental removal of the parathyroid gland results in hypoparathyroidism.

Explanation

Stress activates the sympathoadrenal system and the hypothalamic-pituitary-adrenocortical (HPA) axis. Defense reactions involve catecholamine release, vagal withdrawal, cortisol secretion and activation of the renin-angiotensin system. Catecholamine release is capable of increasing the arterial pressure. Sympathoadrenal system involves the sympathetic nervous system and the adrenal glands especially increased sympathetic activity that causes increased secretion of epinephrine by the adrenal medulla and norepinephrine by the postganglionic sympathetic nerve endings.

Explanation

In laboratory diagnosis of acute myocardial infarction: Creatine kinase isoenzyme MB (CK-MB) appears within 4-8hrs, peaks at 24hrs and disappears within 1.5-3 days. Sensitivity and specificity is 95%. Reappearance of CK-MB after 3days – reinfarction. CK-MM – found in skeletal muscle and heart (not specific for heart). LDH1 – heart muscle; LDH2 – blood serum. LDH levels are also high in tissue breakdown or hemolysis. Although CK-MB is more specific and sensitive for infarction than LDH. Aspartate transaminase is not specific for heart damage alone but can still be used to diagnose myocardial infarction. But troponin test [cardiac troponins I (cTnI) and T (cTnT)] is the most sensitive and specific test for myocardial infarction.

Explanation

Due to incomplete closure of the tricuspid valve during right ventricular systole, part of blood is regurgitated into the right atrium, where it is mixed with the normal volume of blood delivered from the venae cavae which makes the atrium become distended and hypertrophied. During diastole, a larger volume of blood is delivered into the right ventricle because the portion of blood that was regurgitated into the atrium during systole is added to the normal volume of blood delivered → ↑volume (heart overload). This causes dilatation and hypertrophy of the right ventricle. Compensation in this disease is attained by intensified work of left ventricle which leads to its hypertrophy too. The mass of the circulating blood usually increase proportionally to the degree of circulatory insufficiency. This is favored by retention of sodium chloride and water in decreased renal filtration and increased reabsorption of sodium and the increasing number of RBCs (hypoxia is attended by intensified hemopoiesis to compensate for the developing insufficiency) → ↑blood volume.

Explanation

The sinoatrial (SA) node is a small strip of modified cardiac muscle, situated in the superior part of lateral wall of right atrium, just below the opening of superior vena cava. The fibers of this node do not have contractile elements. SA node is called the pacemaker because the rate of production of impulse (rhythmicity) is higher in SA node than in other parts. The rate is 60-100/min and higher during tachycardia when stimulated by sympathetic effects. Atrioventricular (AV) node is 40-60/min.

During stress sympathetic nervous system produces the dominant effects in the body.

Explanation

    Secondary immunodeficiency occurs after full development of the immune system. Chronic virus infections (e.g. infectious mononucleosis caused by Epstein-Barr virus) and HIV (human immunodeficiency virus) may cause secondary immunodeficiencies. HIV → CD4 cells; Epstein Barr virus (EBV) → B lymphocytes (B cells).

Explanation

His condition became worse after taking antipyretic drug. Antipyretic drugs block prostaglandin synthesis by inhibiting cyclooxygenase (COX) enzyme at the thermoregulating centers in the hypothalamus and at peripheral target sites. In case of toxicity of this drug, it can result in coma followed by cardiovascular collapse and respiratory arrest due to its CNS depressant activity. Consciousness is confused; arterial blood pressure is low and pulse rate is very high – these are clear signs of collapse.

Explanation

Acidosis is the reduction in pH (increase in H⁺ concentration) below normal range. pH is less than 7.35; it is produced by:

·        Increase in partial pressure of CO₂ in the body.

·        Decrease in HCO₃^- concentration.

Alkalosis is the increase in pH (decrease in H⁺ concentration) above normal range. pH is greater than 7.45; it is produced by:

·        Decrease in partial pressure of CO₂ in the body.

·        Increase in HCO₃^- concentration.

Each of these two disorders has respiratory and non-respiratory forms. The non-respiratory form is divided into metabolic and excretory(non-gaseous).

·        Respiratory acidosis is the acidosis that is caused by alveolar hypoventilation e.g. airway obstruction due to bronchitis or lung diseases (pneumonia).

·        Respiratory alkalosis is caused by alveolar hyperventilation e.g. hypoxia in high altitude.

·        Non-respiratory:

-Metabolic acidosis is characterized by excess accumulation of organic acids such as lactic acid, ketoacids and uric acid formed by normal metabolism e.g. in Diabetes mellitus or extreme/prolonged exercise.

-Excretory/Non-gaseous acidosis may develop in impaired renal H⁺ excretion related to increased loss of bicarbonate in urine; diarrhea causes acidosis by the loss of bicarbonate with faeces.

-Excretory/Non-gaseous alkalosis: vomiting (loss of gastric acid), increased metabolism of lactate and citrate (turns into bicarbonate and water), long-term use of thiazides and loop diuretics.

Explanation

Serotonin, also called 5-hydroxytryptamine, is synthesized and stored at several sites in the body. It can be found in the intestinal mucosa, central nervous system and in platelets. Serotonin is synthesized from tryptophan, which is hydroxylated. The product, 5-hydroxytryptophan is decarboxylated to serotonin, which is also degraded by monoamine oxidase (MAO). Serotonin has multiple physiologic roles, including pain perception, affective disorders, and regulation of sleep, temperature and blood pressure.

Explanation

Type IV (cell mediated, delayed): antibody-independent T-cell mediated reactions e.g. positive mantoux reaction (tuberculin test), hashimoto’s thyroiditis or transplant rejection etc.

Tuberculin (Mantoux) skin test: this test is done by intradermal injection of tuberculoprotein (tuberculin), purified protein derivative (PPD). Type IV hypersensitivity reaction.

Explanation

Polycythemic hypovolemia is a condition with a decreased amount of plasma usually characterized by appreciable concentration and increased viscosity of blood. Hematocrit is above normal. This condition is observed in connection with considerable loss of water by the organism as in diarrhea, intractable vomiting, extensive burns. Hematocrit is increased because there is no loss of erythrocytes just fluid was lost from vomiting. It can’t  be hypervolemia because there is loss of fluid from prolonged vomiting.

In simple hypovolemia: hematocrit is normal; oligocythemic hypovolemia: hematocrit is decreased.

Explanation

Abnormality of constitution, so called diathesis is characterized by pathological reactions on physiological agent. Classification of diathesis:

·        Hemorrhagic: characterized by hemorrhagic reaction to physiological factors.

·        Thymicolymphatic/Lymphohypoplastic: characterized by enlargement of lymphatic nodes, muscular atrophy, individual pale, pastous, predisposing to autoallergic disease, lymphocytosis, angina and other infectious diseases.

·        Neuroarthritic/Gouty: predisposing to arthralgia, arthritis, rheumatism, obesity, gout, psychic disease.

·        Edematic/Exudative: characterized by edema reaction to different environmental factors.

·        Asthenic: expressed in hypodynamia, hypotonia.

Explanation

Systemic lupus erythematous (SLE, Libman-sacks disease) is the classic prototype of the multisystem disease of autoimmune origin, characterized by a bewildering array of autoantibodies, particularly antinuclear antibodies. It is characterized principally by injury to the skin, joints, kidney, and serosal membranes. Antinuclear antibody is directed against several nuclear antigens and can be grouped into 4 categories:

·        Antibodies to DNA

·        Antibodies to histones

·        Antibodies to nonhistone proteins bound to RNA

·        Antibodies to nuclear antigens.

SLE is a type III hypersensitivity reaction with formation of immune complexes. It can cause diffuse proliferative glomerulonephritis seen under the light microscope as “wire loop” of capillaries and granular under the immunofluorescence microscopy.

Explanation

Liver is the primary organ of protein synthesis. In a case of dysfunction of protein synthesis, hypoproteinemia occurs. We have absolute and relative hypoproteinemia. Absolute is when there is disturbed synthesis (absolute hypoproteinemia) and in cases of increased synthesis (absolute hyperproteinemia); while relative does not have to do with synthesis but other pathologies e.g. renal lesions, in which case, there is loss of protein with urine (relative hypoproteinemia); also vomiting, diarrhea, profuse sweating can produce relative hyperproteinemia.

Explanation

In viral hepatitis, there is generalized liver dysfunction involving uptake and conjugation of unconjugated bilirubin, secretion of conjugated bilirubin into bile ducts, and recycling of urobilinogen. Alanine transaminase (ALT) and Aspartate transaminase (AST) are increased (↑), but ALT is higher than AST and there is a slight ↑ in alkaline phosphatase (ALP) and ɣ-glutamyltransferase (GGT).

ALT is a specific enzyme for liver necrosis; present in the cytosol. ALT>AST: viral hepatitis.

AST is present in the mitochondria. Alcohol damages mitochondria AST>ALT indicates alcoholic hepatitis

Explanation

Rickets results from insufficiency of vitamin D (calcitriol). Calcitriol is the active form of vitamin D.

Calcitriol production is dependent on the kidney’s 1-α-hydroxylase which converts 25-OHD₃ to 1,25-(OH)₂D₃ (calcitriol). So in cases of renal lesion, there is lack of 1-α-hydroxylase which leads to a deficiency of calcitriol or impaired synthesis of calcitriol.

Explanation

Extrasystole is the premature contraction (an extra contraction) of the heart before its normal contraction. In other words, it is an extra contraction of the heart before its normal contraction. It is caused by an ectopic focus (discharge of an impulse from any part of the heart other than the Sinoatrial node).

Bradycardia: ↓heart rate; Tachycardia: ↑heart rate; Flutter: rapid heart contractions; Fibrillation: very rapid heart contractions. (In all this, there is no extra heart contraction, we just have faster contractions).

Explanation

Metaplasia is a reversible change of one type to another type of adult epithelial or mesenchymal cells, usually in response to abnormal stimuli and often reverts back to normal on removal of stimulus. Types (2):

·        Epithelial: *Squamous metaplasia: in bronchus (chronic smokers), cervix

  *Columnar metaplasia: there is transformation to columnar epithelium.

·        Mesenchymal metaplasia: osseous and cartilaginous.

Hyperplasia: ↑number of cells; Hypertrophy: ↑in size.

Explanation

The citric acid cycle (kreb’s cycle, TCA cycle) is a good example of amphibolic pathway. The first reaction of the cycle in which oxaloacetate (4 carbon compound) condenses with acetate (2 carbon compound) to form citrate (6 carbon compound) is typically anabolic. The next few reactions which are intramolecular rearrangements produce Isocitrate. The following two reactions are typically catabolic. ‘COO’ is lost in each step and succinate (4 carbon compound) is produced. Amphibolic involves both catabolism and anabolism.

Explanation

Cushing Syndrome: Etiology:

INCREASE Cortisol due to a variety of causes (Glucocorticoids):

Exogenous corticosteroids: result in decrease ACTH (MCC).

Primary adrenal adenoma, hyperplasia or carcinoma (Cushing’s Syndrome).

ACTH-secreting pituitary adenoma (Cushing Disease).

Findings: Hypertension, Weight Gain, Moon Facies, Truncal Obesity, Buffalo Hump, Skin Changes (thinning striae), Osteoporosis, Hyperglycemia (Insulin resistance), Amenorrhea, Immunosuppression.

Explanation

X-linked (Bruton) agammaglobulinemia: defect in Bruton’s tyrosine kinase (BTK), a tyrosine kinase gene → no B cell maturation. X-linked recessive (↑in boys). Findings: absent B cells in peripheral blood, ↓immunoglobulin of all classes (IgG, IgM, IgA). Absent/scanty lymph nodes and tonsils.

Explanation

The main reasons for hypercalcemia are primary hyperparathyroidism (which can result from adenoma of parathyroid gland), hypervitaminosis D (calcium absorption in the intestine increases). Hypercalcemia often accompanies difficult fractures and this numerous fractures violate the equilibrium between bone construction processes, which sharply decreases and the resorption, which continues with previous speed. Reklinghausen described development of osteodystrophy as the result of bone decalcinosis at the continuous hyperparathyroidism (parathyroid adenoma). NB: parathyroid hormone → ↑bone resorption. This disease is characterized by gradual dilution and softening of bones. Metabolic osteoclasts activity increases due to the action of parathormone. Loss of bone matrix occurs and the bone becomes soft. Resorption allotments are replaced with fibrous connective tissue and zones of osteoid substance are formed.

Explanation

Pirogov’s stages of shock

* Erectile phase: is characterized by strong motor agitation, sweating, tremor of skeletal muscles, staggering gait, frequent urination, transient increase in blood pressure, heart rate and breath rate increases, body temperature also. Painful impulses reach CNS.

* Torpid phase: decompensation in CNS leads to deep oppression. Patient is motionless, does not answer questions or answers very silently and with long time of delay, reflexes are lowered or absent.

Explanation

Parathyroid hormone: secreted by chief cells of parathyroid gland. Effects include:

↑bone resorption of Ca²⁺ and PO₄^3- → ↑their plasma levels

↑kidney reabsorption of Ca²⁺ in distal convoluted tubule → ↑ Ca²⁺ plasma level

↓reabsorption of PO₄^3- in proximal convoluted tubule → ↓ PO₄^3- plasma levels

↑Calcitriol (vit D₃) production by stimulating kidney 1α-hydroxylase in proximal convoluted tubule. It increases Ca²⁺ and PO₄^3- absorption in the intestine.

Therefore hypoparathyroidism results in hypocalcemia and hyperphosphatemia.

Explanation

Shock is a form of stress which is accompanied by the release of stress hormones (catecholamines, cortisol). Stress-induced changes in blood leukocyte distribution may represent an adaptive response. This represents a redistribution of leukocytes from the blood to other organs such as the skin, draining sentinel lymph nodes and other compartments. Such leukocyte redistribution may enhance immune function in compartments to which immune cells traffic during stress.

Explanation

Pernicious anemia or addison’s anemia is the anemia due to deficiency of vitamin B₁₂. It is due to atrophy of the gastric mucosa (atrophic gastritis) because of autoimmune destruction of parietal cells. The gastric atrophy results in decreased production of intrinsic factor and poor absorption of vitamin B₁₂, which is the maturation factor for red blood cells (RBC). RBCs are larger and immature with almost normal or slightly low hemoglobin level. Synthesis of hemoglobin is almost normal in this type of anemia. So, cells are macrocytic and normochromic/hypochromic.

Explanation

Explanation

Where the fluid accumulates depends on the amount of excess fluid and the effects of gravity. If a person is standing, fluid accumulates in the legs and feet; if a person is lying down, fluid usually accumulates in the lower back; if the amount of fluid is large, fluid also accumulates in the abdomen.

Most water leakage occurs in capillaries or postcapillary venules which have a semipermeable membrane wall that allows water to pass freely than proteins. Increased hydrostatic pressure leads to increase filtration of water into the interstitium at the venous end of the capillary (post-capillary venule).

Explanation

Acidosis is the reduction in pH (increase in H⁺ concentration) below normal range. pH is less than 7.35; it is produced by:

·        Increase in partial pressure of CO₂ in the body.

·        Decrease in HCO₃^- concentration.

Alkalosis is the increase in pH (decrease in H⁺ concentration) above normal range. pH is greater than 7.45; it is produced by:

·        Decrease in partial pressure of CO₂ in the body.

·        Increase in HCO₃^- concentration.

Each of these two disorders has respiratory and non-respiratory forms. The non-respiratory form is divided into metabolic and excretory(non-gaseous).

·        Respiratory acidosis is the acidosis that is caused by alveolar hypoventilation e.g. airway obstruction due to bronchitis or lung diseases (pneumonia).

·        Respiratory alkalosis is caused by alveolar hyperventilation e.g. hypoxia in high altitude.

·        Non-respiratory:

-Metabolic acidosis is characterized by excess accumulation of organic acids such as lactic acid, ketoacids and uric acid formed by normal metabolism e.g. in Diabetes mellitus or extreme/prolonged exercise.

-Excretory/Non-gaseous acidosis may develop in impaired renal H⁺ excretion related to increased loss of bicarbonate in urine; diarrhea causes acidosis by the loss of bicarbonate with faeces.

-Excretory/Non-gaseous alkalosis: vomiting (loss of gastric acid), increased metabolism of lactate and citrate (turns into bicarbonate and water), long-term use of thiazides and loop diuretics.

      It is excretory/non-gaseous alkalosis because of the frequent vomiting.

Explanation

Innate or non-specific resistance consist of physical and chemical barriers such as skin, gastric acid, mucus or tears, saliva as well as cells and active mechanisms such as phagocytes, natural killer cells and the complement system. They defend an organism in non-specific form/manner, responding in the same fashion, regardless of what pathogen it is. Examples of physical barriers:

·        Skin: surface is made up of dead skin cells rich in keratin, which impedes microorganisms from entering the body – mechanical barrier

·        Gastric acid is a powerful defense against invading bacteria.

·        Saliva and tears contain antibacterial enzymes such as lysozyme, which destroy the cellular walls of bacteria.

·        Mucus is another defense; coating the mucus membranes and contains IgA antibodies (a component of specific/adaptive immune system).

Explanation

Explanation

Edema commonly results from increase in hydrostatic pressure or decreased oncotic pressure. With the infusion of different solutions intravenously amounting to 1500ml within 8hours, there is an increase in hydrostatc pressure, which results in the pulmonary edema. The myocardial infarction suffered by the patient aids in the pathogenesis of the pulmonary edema. Pulmonary edema is as a result of left ventricular insufficiency i.e. the myocardial infarction is in the left ventricular myocardium. ↑hydrostatic pressure = ↑volume

Explanation

Tuberculin (Mantoux) skin test: this test is done by intradermal injection of tuberculoprotein (tuberculin), purified protein derivative (PPD). Type IV hypersensitivity reaction.

Immunization against tuberculosis is induced by injection of attenuated strains of bovine type of tubercle bacilli, Bacilli Calmette Guerin (BCG).

The Mantoux skin test should be read between 48 and 72hrs after administration. The basis of reading  is the presence or absence of induration, which may be determined by inspection and by palpation.

A record should also be made of formation of vesicles, bullae, lymphangitis, ulceration and necrosis at the test site. The formation of vesicles, bullae or necrosis at the test site indicates positive result. A negative mantoux result usually signifies that the individual has never been exposed to Mycobacterium tuberculosis i.e. absence of cell mediated immunity to tuberculin.

Mantoux test is a type IV Hypersensitivity reaction (HSR), which involves macrophages,T-lymphocytes and lymphokines(cytokines). Mononuclear cells (lymphocytes,monocytes,macrophages).

Explanation

Ochronosis (Alkaptonuria): congenital deficiency of homogentisate oxidase (homogentisic acid oxidase) in the degradative pathway of tyrosine to Fumarate → pigment-forming homogentisic acid accumulates (homogentisuria) in tissues. Autosomal recessive. Usually benign. Urine turns black on prolonged exposure to air. May have debilitating arthralgias (homogentisic acid toxic to cartilage).

Explanation

The mobilization of stored fat requires the hydrolytic release of fatty acids and glycerol from their triacylglycerol (TAG) form. This process is initiated by hormone-sensitive lipase, which removes a fatty acid from carbon 1 and/or carbon 3 of the TAG. This enzyme is activated when phosphorylated by cyclic AMP (cAMP)-dependent protein kinase. cAMP is produced in the adipocyte when one of several hormones (such as epinephrine or glucagon – stress hormones) binds to receptors on the cell membrane and activates adenylyl cyclase.

Explanation

Obturation (obstruction, to close) of bile duct – it can be:

* Intrahepatic – blockage of intrahepatic bile ducts

* Extrahepatic – blockage of common bile duct (ductus choledochus).

Findings:

* malabsorption: bile salts do not enter the Small Intestine; no emulsification of fat.

*light coloured stool: due to lack of urobilin (which leads to lack of stercobilin).

*Jaundice (posthepatic, mechanic, obstructive): increased conjugated Bilirubin.

* Steatorrhea

The findings are specific for obstruction of bile duct and bile acid deficiency.

Explanation

Radiation disease, radiation therapy, chemotherapy or toxic chemicals can destroy megakryocytes. Megakaryocytes are responsible for the production of thrombocytes (platelets) which can lead to thrombocytopenia. Thrombocytopenia is an abnormally low level of platelets in blood, as a result of reduced platelet production in the bone marrow or excessive peripheral destruction of platelets. People with severe thrombocytopenia may have abnormal bleeding (hemorrhagic syndrome) almost anywhere in the body.

Explanation

Principal complications of peptic ulcer are perforation, penetration, hemorrhage, stenosis, malignization (cancer). Gastric hemorrhage is a very important symptom. It can be manifested by vomiting blood (hematemesis) or by black tarry stools (melena). The vomitus looks like coffee grounds. If hemorrhage is profuse (damage to a large vessel) the vomitus contains much scarlet (unaltered) blood. Hematemesis occurs in peptic ulcer, cancer and polyps, in erosive gastritis etc.

Explanation

The main symptoms of right-sided heart failure are fluid accumulation and swelling (edema) of the feet, ankles, legs, liver and abdomen.

Where the fluid accumulates depends on the amount of excess fluid and the effects of gravity. If a person is standing, fluid accumulates in the legs and feet; if a person is lying down, fluid usually accumulates in the lower back; if the amount of fluid is large, fluid also accumulates in the abdomen.

Most water leakage occurs in capillaries or postcapillary venules which have a semipermeable membrane wall that allows water to pass freely than proteins. In cardiac insufficiency, blood pools in the veins since the heart is not pumping effectively; this increases the hydrostatic pressure in the veins. And this increased hydrostatic pressure leads to increase filtration of water into the interstitium at the venous end of the capillary (post-capillary venule).

Explanation

Administered nitrates → ↑ Nitrites →↑ Nitric oxide (NO) → ↑cGMP → ↑dephosphorylation of myosin chains → vascular smooth muscle relaxation. Nitroglycerin is an organic nitrates. Nitrates inhibit coronary vasoconstriction or spasm, increasing perfusion of the myocardium and thus relieving vasospastic angina. Because of this action, nitrates are effective in treating effort-induced (stress) angina. Classic, effort-induced or stable angina are experienced in such conditions as physical activity, emotional excitement or any other cause of increased cardiac workload.

Explanation

Acute heart failure refers to sudden and rapid onset of signs and symptoms of abnormal heart functions. Chronic heart failure is characterized by the symptoms that appear slowly over a period of time and become worst gradually.

The main symptoms of right-sided heart failure are fluid accumulation and swelling (edema) in the feet, ankles, legs, liver and abdomen. Left-sided heart failure leads to fluid accumulation in the lungs, which causes shortness of breath. At first, shortness of breath occurs only during exertion, but as heart failure progresses, it occurs with less and less exertion and eventually occurs even at rest. Moist and dry rales are heard over the lungs.

She has been suffering it for 15 years – chronic         

Edema of lower limbs, ascites – Right ventricular insufficiency

Explanation

Explanation

Oxidation of the heme component of hemoglobin to the ferric (Fe³⁺) state forms methemoglobin, which cannot bind O₂. This oxidation may be caused by the action of certain drugs or substances containing nitrates, or endogenous products such as reactive oxygen intermediates. Furthermore a deficiency of NADH-met-hemoglobin reductase i.e. the enzyme responsible for the conversion of methemoglobin (Fe³⁺) to hemoglobin (Fe²⁺); leads to the accumulation of methemoglobin. The methemoglobinemias are characterized by “chocolate cyanosis” (a brownish-blue colouration of the skin and  membranes) and chocolate-coloured blood, as a result of the dark-coloured methemoglobin. Symptoms are related to tissue hypoxia and include anxiety, headache and dyspnea. Treatment is with methylene blue, which is oxidized as Fe³⁺  is reduced.

Explanation

Human immunodeficiency virus (HIV): diploid genome (2 molecules of RNA). The 3 structural genes(i.e. proteins coded for by the genes) are:

·        env (gp 120 and gp 41): formed from cleavage of gp 160 to form envelope glycoproteins. gp 120 is for attachment to host CD4+ T cell. gp 41 is for fusion and entry.

·        Gag (p24): capsid protein

·        pol: reverse transcriptase, aspartate protease, integrase.

ELISA/Western blot (immunoblot) tests look for antibodies to the viral proteins listed above.

Reverse transcriptase synthesizes dsDNA (ds-double stranded) from genomic RNA (mRNA); dsDNA integrates into host genome. Virus binds CD4 as well as a coreceptor, either CCR5 on macrophages (early infection) or CXCR4 on I cells (late infection).

·        Homozygous CCR5 mutation – immunity

·        Heterozygous CCR5 mutation – slower course.

Explanation

Human immunodeficiency virus (HIV): diploid genome (2 molecules of RNA). The 3 structural genes(i.e. proteins coded for by the genes) are:

·        env (gp 120 and gp 41): formed from cleavage of gp 160 to form envelope glycoproteins. gp 120 is for attachment to host CD4+ T cell. gp 41 is for fusion and entry.

·        Gag (p24): capsid protein

·        pol: reverse transcriptase, aspartate protease, integrase.

ELISA/Western blot (immunoblot) tests look for antibodies to the viral proteins listed above.

Reverse transcriptase synthesizes dsDNA (ds-double stranded) from genomic RNA (mRNA); dsDNA integrates into host genome. Virus binds CD4 as well as a coreceptor, either CCR5 on macrophages (early infection) or CXCR4 on I cells (late infection).

·        Homozygous CCR5 mutation – immunity

·        Heterozygous CCR5 mutation – slower course.

Explanation

Type I (Immediate, Anaphylaxis, Reagin): IgE (immunoglobulin E)-dependent activation of mast cells/basophils, usually accompanied by eosinophilia e.g. urticaria (hives), hay fever, asthma (wheezing), rhinitis and conjunctivitis (stuffy nose and itchy eyes; usually seasonal).

Type I Hypersensitivity reaction (HSR); anaphylactic and atopic: free antigen cross-links IgE on presensitized (i.e. exposed to the antigen before) mast cells and basophils, triggering immediate release of vasoactive amines that act at postcapillary venules (i.e. histamine). Reaction develops rapidly after antigen exposure because of preformed antibody from first exposure. IgE is the main immunoglobulin involved in type I HSR. Type I: uses IgE and IgG₄

Explanation

Cushing Syndrome: Etiology:

INCREASE Cortisol due to a variety of causes (Glucocorticoids):

Exogenous corticosteroids: result in decrease ACTH (MCC).

Primary adrenal adenoma, hyperplasia or carcinoma (Cushing’s Syndrome).

ACTH-secreting pituitary adenoma (Cushing Disease).

Findings: Hypertension, Weight Gain, Moon Facies, Truncal Obesity, Buffalo Hump, Skin Changes (thinning striae), Osteoporosis, Hyperglycemia (Insulin resistance), Amenorrhea, Immunosuppression.

Explanation

Chronic myeloleukemia is characterized by extensive production of blast (immature) cells in the blood. The immature cells (e.g. immature RBCs) cannot perform the normal function of a mature cell, hence the manifestation of anemia. The many blast cells constitute the majority of cells found in blood during leukemia. Therefore, as soon as cells die they are replaced by the immature ones, which are usually overproduced in leukemia.

Explanation

·        Neuroparalytic arterial hyperemia is caused by damage or blockage of α-adrenoreceptors (sympathetic nervous system). It is characterized by reduction or absence (paralysis) of the sympathetic nervous system effects on the walls of the arteries and arterioles.

·        Neurotonic arterial hyperemia is caused by activation of parasympathetic nervous system; irritation of vascular dilators part of vascular center (CNS) or inhibition of vascular – constrictor part of this center (vasomotor center of CNS); M-cholinoreceptors; H₂-histaminereceptors. It is characterized by predominance of the parasympathetic nervous system effects on arterial vascular walls.

Explanation

Acute heart failure refers to sudden and rapid onset of signs and symptoms of abnormal heart functions. Chronic heart failure is characterized by the symptoms that appear slowly over a period of time and become worst gradually.

The main symptoms of right-sided heart failure are fluid accumulation and swelling (edema) in the feet, ankles, legs, liver and abdomen. Left-sided heart failure leads to fluid accumulation in the lungs, which causes shortness of breath. At first, shortness of breath occurs only during exertion, but as heart failure progresses, it occurs with less and less exertion and eventually occurs even at rest. Moist and dry rales are heard over the lungs.

After a physical stress – sudden and rapid – ACUTE

Rales are caused by congestion of the lungs – left ventricular heart failure.

Explanation

* Radiating pain: perceived at a site adjacent to or away from the site of origin but in the same dermatome i.e. supplied by afferent nerve fibers of one dorsal root.

* Viscera pain: organs, poorly localized, diffuse

* Protopathic pain: poorly localized pain

* Epicritic pain: well localized pain

* Phantom pain: pain from non-existent body structures (amputated limbs)

Phantom – if a leg has been amputated, the cut end heals with scar formation. The cut ends of nerve fibers are merged within the scar. If the cut end of sensory fibers are stimulated during movement of thigh, the patient feels as if the sensation is originating from non-existent leg. Sometimes the patient feels pain in non-existent limb.

Explanation

 ‘T’ wave is the final  ventricular complex and is a positive wave. It is due to the repolarization of ventricular musculature. Normal duration is 0.2sec; normal amplitude is 0.3mV.

Explanation

This is an example of type I hypersensitivity reaction considering the time taken for the symptoms (rash and itching) to manifest and the expression of eosinophilia.

Neutrophilic leukocytosis: bacterial infection

Lymphocytosis: viral and bacterial infection (e.g. whooping cough, tuberculosis)

Monocytosis: chronic inflammation (tuberculosis); autoimmune disease

Type I (Immediate, Anaphylaxis, Reagin): IgE (immunoglobulin E)-dependent activation of mast cells/basophils, usually accompanied by eosinophilia e.g. urticaria (hives), hay fever, asthma (wheezing), rhinitis and conjunctivitis (stuffy nose and itchy eyes; usually seasonal)

Explanation

Chronic renal failure is the progressive, long standing and irreversible impairment of renal functions. When some of the nephrons loose their function, the unaffected nephrons can compensate for it. However, when more and more nephrons start losing their function over the months and years, then the compensatory mechanism fails and chronic renal failure manifests.

Explanation

The nuclear radiation this patient was exposed to, can produce inflammatory reaction in the patient. Within the first 24hours, the first leukocyte to get into any inflammatory focus are the neutrophils, followed by the monocytes (macrophages) and then lymphocytes.

Neutrophils are the first leukocytes that cross the blood vessel wall to enter inflammatory sites. Under normal conditions, leukocytes are restricted to the center of small blood vessels, where the flow is fastest. In inflammatory sites, where the vessels are dilated, the slower blood flow allows the leukocytes to move out of the center of the blood vessel and interact with the vascular endothelium. Even in the absence of infection, monocytes migrate continuously into the tissues, where they differentiate into macrophages; meanwhile, during an inflammatory response, the induction of adhesion molecules on the endothelial cells, as well as induced changes in the adhesion molecules expressed on leukocytes recruit large numbers of circulating leukocytes, initially Neutrophils and later monocytes, into the site of an infection (inflammatory focus).

First –Neutrophils; second –monocytes and macrophages; third –lymphocytes.

Explanation

Hyperammonemia can be acquired (e.g. liver disease) or hereditary (e.g. urea cycle enzyme deficiencies). Acquired hyperammonemia may be a result of an acute process e.g. viral hepatitis, ischemia or hepatotoxins. As a result, the detoxification of ammonia (i.e. its conversion to urea) is severely impaired, leading to elevated levels of circulating ammonia.

Explanation

     Kidneys excrete the unwanted waste products which are formed during metabolic activities e.g.

·        Urea: end product of amino acid metabolism

·        Uric acid: end product of nucleic acid metabolism

·        Creatinine: end product of metabolism in muscles

·        Bilirubin: end product of hemoglobin degradation

·        Products of metabolism of other substances.

Many substances both organic and inorganic are excreted in saliva also. In some pathological conditions, saliva excretes certain substances which are not found in saliva under normal conditions e.g. glucose in Diabetes mellitus. In certain conditions, some of the normal constituents of saliva are excreted in large quantities e.g. excess urea is excreted in saliva during renal failure, nephritis and excess calcium is excreted during hyperparathyroidism.

Explanation

Myeloma/Plasmocytoma/Multiple Myeloma

Paraprotein, myeloma protein, M protein or spike protein is an abnormal immunoglobulin (Ig) fragment or immunoglobulin (Ig) light chain that is produced in excess by an abnormal clonal proliferation of plasma cells, typically in multiple myeloma. Monoclonal free light chains in the serum or urine are called bence jones (BJ) proteins.

Bence jones (BJ) protein: free kappa (κ) or lambda (λ) light chains that are excreted in urine associated with plasma cell malignancies (myeloma) and Waldenstrὄm macroglobulinemia. In myeloma, urinalysis for BJ protein is positive in 60-80% of cases.

Explanation

Calcitonin is secreted by parafollicular cells (C cells of the thyroid gland). It ↓bone resorption of Ca²⁺. It opposes actions of parathyroid hormone. But its not important in normal Ca²⁺ homeostasis.

Parathyroid hormone: secreted by chief cells of parathyroid gland. Effects include:

↑bone resorption of Ca²⁺ and PO₄^3- → ↑their plasma levels

↑kidney reabsorption of Ca²⁺ in distal convoluted tubule → ↑ Ca²⁺ plasma level

↓reabsorption of PO₄^3- in proximal convoluted tubule → ↓ PO₄^3- plasma levels

↑Calcitriol (vit D₃) production by stimulating kidney 1α-hydroxylase in proximal convoluted tubule. It increases Ca²⁺ and PO₄^3- absorption in the intestine.

In general, parathyroid hormone ↑ Ca²⁺ plasma level but ↓ PO₄^3- plasma levels. Abnormal synthesis (↑synthesis) of parathyroid hormone can lead to hypercalcemia and hypophosphatemia.

Explanation

Paraprotein, myeloma protein, M protein or spike protein is an abnormal immunoglobulin (Ig) fragment or immunoglobulin (Ig) light chain that is produced in excess by an abnormal clonal proliferation of plasma cells, typically in multiple myeloma. Monoclonal free light chains in the serum or urine are called bence jones (BJ) proteins.

Bence jones (BJ) protein: free kappa (κ) or lambda (λ) light chains that are excreted in urine associated with plasma cell malignancies (myeloma) and Waldenstrὄm macroglobulinemia. In myeloma, urinalysis for BJ protein is positive in 60-80% of cases.

Explanation

Hypothalamus is a diencephalic structure. Diencephalon: thalamus, hypothalamus, pineal body, third (3^rd) ventricle. The Hypothalamus is situated just below thalamus in the ventral part of diencephalon. It is the important part of brain, concerned with homeostasis of the body. It regulates endocrine functions, metabolic activities, hunger, thirst, sleep, wakefulness, emotion, sexual functions. Lesion of hypothalamus can occur due to tumors, encephalitis and ischemia; accompanied by disturbances in carbohydrate and fat metabolisms; disturbance in sleep and sexual functions. It can also result in some clinical manifestations such as: Diabetes insipidus, dystrophia adiposogenitalis, kallmann syndrome, Laurence-Moon-Biedl syndrome, narcolepsy, cataplexy.

Explanation

The superior vena cava (SVC) arises from merging left and right brachiocephalic veins posterior to the right first sternocostal joint. The SVC descends to enter the right atrium. On the left, one can distinguish the ascending aorta and on the right – the mediastinal pleura and phrenic nerve. The right pulmonary vein resides posterior to the SVC & the thymus and the right lung – anterior to it. Therefore, thymoma (thymus gland tumor) will definitely press on the SVC. The brachiocephalic veins drain the head, neck and upper limbs; hence, the manifestations.

Explanation

     Antidiuretic hormone (vasopressin) is secreted in response to decrease blood volume and increase plasma osmolarity. It binds to receptors on principal cells of collecting ductules causing increase number of aquaporins and increase water reabsorption which leads to decreased diuresis.

Atrial natriuretic peptide is secreted in response to increase atrial pressure. It causes increase glomerular filtration rate (GFR) and increase sodium ion filtration with no compensatory sodium ion reabsorption and water in distal nephron which leads to increase diuresis.

Parathyroid hormone is secreted in response to decrease plasma calcium ion, increase phosphate ion or decrease plasma calcitriol [1,25-(OH)₂D₃].

Explanation

During cerebellar lesions, there  are disturbances in posture, equilibrium and movements. Disturbances in movements: ataxia, asynergia, asthenia (weak muscle contractions with characteristically rapid onset of muscle fatigue), Dysmetria, Intention tremor, astasia (loss of the capacity for sustained tetanic contractions), nystagmus, rebound phenomenon, dysarthria, adiadochokinesis, atonia (lack or impairment of muscle tone).

Explanation

     Thrombocyte (platelet) is involved in primary hemostasis. It’s a small cytoplasmic fragment derived from megakaryocytes. It has a life span of 8-10days. When activated by endothelial injury, it aggregates with other platelets and interacts with fibrinogen to form platelet plug. Thrombocytopenia or decrease platelet function/dysfunction results in petechiae.

Leukocytes: Neutrophils (54-62%); Lymphocytes (25-33%); Monocytes (3-7%); Eosinophils (1-3%); Basophils (0-0.75%). Neutrophils, eosinophils, basophils are granulocytes; while lymphocytes, monocytes are mononuclear cells and they are also agranulocytes. They are all responsible for defense against infections.

Explanation

Parathyroid hormone: secreted by chief cells of parathyroid gland. Effects include:

↑bone resorption of Ca²⁺ and PO₄^3- → ↑their plasma levels

↑kidney reabsorption of Ca²⁺ in distal convoluted tubule → ↑ Ca²⁺ plasma level

↓reabsorption of PO₄^3- in proximal convoluted tubule → ↓ PO₄^3- plasma levels

↑Calcitriol (vit D₃) production by stimulating kidney 1α-hydroxylase in proximal convoluted tubule. It increases Ca²⁺ and PO₄^3- absorption in the intestine.

In general, parathyroid hormone ↑ Ca²⁺ plasma level but ↓ PO₄^3- plasma levels. Abnormal synthesis (↑synthesis) of parathyroid hormone can lead to hypercalcemia and hypophosphatemia.

Likewise, deficiency of parathormone can lead to low Ca²⁺ levels.

Explanation

↓blood supply → activates renin. Renin catalyzes the conversion of angiotensinogen to angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I → angiotensin II. Angiotensin II causes:

- vasoconstriction → ↑BP

- vasopressin (ADH) → ↑H₂O reabsorption → ↑plasma volume

- aldosterone → ↑Na⁺ and H₂O reabsorption → ↑plasma volume → ↑BP

Explanation

Evaporation is a way the body dissipates heat to the environment by its evaporation via sweat or evaporation of moisture from the skin and respiratory tract mucous membranes of (“wet” heat loss). Evaporation closely related to relative humidity.

Heat Radiation is a way the surface of the human body emits heat to the environment in the form of infrared rays. The amount of heat the body radiates to the environment is proportional to the surface of radiation area and to the difference between the mean values of skin and environment temperature. The surface radiation area is the total surface area of body parts that contact the air. Elimination of heat by radiation increases with a decrease in ambient temperature and decreases with its increase. It is possible to reduce elimination of heat by radiation via reduction of the surface of radiation area (“winding oneself into a ball”). Heat radiation does not require a medium for transfer of heat. (Key words: naked or lightly clothed).

Convection is a way the body eliminates heat by means of transferring heat via moving particles of air or water. To dissipate heat by means of convection, body surface shall be airflowed at a temperature that is lower than the temperature of the skin. At that, air layer contacting with the skin warms up, decreases its density, rises and is replaced by cooler, denser air. By increasing the speed of the air flow (wind, ventilation) heat emission increases significantly as well (forced convection). Convection requires convection current; current of gases or liquids (Key words: air over exposed area of skin).

Conduction is a way the body eliminates heat by means of direct contact with another object. Heat is transferred down the temperature gradient (i.e. from the object of higher temperature to the object of lower temperature). Conduction requires contact with another object (Key words:  in water).

Explanation

The closest bile excreting duct to the pancreas is the common bile duct (ductus choledochus). So, in case of a tumor affecting the pancreas, this can compress the bile duct, thereby obstructing bile flow leading to mechanic, obstructive or post-hepatic jaundice.

Obturation (obstruction, to close) of bile duct – it can be:

* Intrahepatic – blockage of intrahepatic bile ducts

* Extrahepatic – blockage of common bile duct (ductus choledochus).

Findings:

* malabsorption: bile salts do not enter the Small Intestine; no emulsification of fat.

*light coloured stool: due to lack of urobilin (which leads to lack of stercobilin).

*Jaundice (posthepatic, mechanic, obstructive): increased conjugated Bilirubin.

* Steatorrhea

The findings are specific for obstruction of bile duct and bile acid deficiency.

Explanation

Metaplasia is a reversible change of one type to another type of adult epithelial or mesenchymal cells, usually in response to abnormal stimuli and often reverts back to normal on removal of stimulus. Types (2):

·        Epithelial: *Squamous metaplasia: in bronchus (chronic smokers), cervix

  *Columnar metaplasia: there is transformation to columnar epithelium.

·        Mesenchymal metaplasia: osseous and cartilaginous.

Hyperplasia: ↑number of cells; Hypertrophy: ↑in size.

Explanation

Substances absorbed into the bloodstream from the intestine pass through the liver, where toxins are normally removed. Many of these toxins (such as ammonia) are normal breakdown products of the digestion of protein. In hepatic encephalopathy (hepatic coma), toxins are not removed because liver function is impaired. Ammonia is produced by amino acid metabolism and intestinal urease-positive bacteria. In physiological conditions, it is mostly present as ammonium (NH₄⁺) in serum. The urea or ornithine cycle, which is fully expressed in the liver exclusively, serves to converts NH₄⁺ to urea prior to renal excretion and to maintain low serum concentrations. In hepatic coma, when the liver cannot remove toxins and urea cycle is not functional, all this occurs:

NH₃ + α-ketoglutarate → Glutamate

α-ketoglutarate is used up which leads to:

·        ↑glutamate → ↑GABA (inhibitory neurotransmitter)

·        Inhibition of citric acid cycle/tricarboxylic acid cycle; this causes impairment of ATP formation.

·        Inhibition of metabolism of amino acids (impairment of transamination reactions).

NH₃ + Glutamate → Glutamine

Glutamine is an amide of glutamic acid which provides a non-toxic storage and transport form of ammonia (NH₃). Ammonia increase synthesis of glutamine in brain. Accumulation of glutamine in brain results in elevation of osmotic pressure in nervous cells leading to brain edema.

                                    NH₃ + H⁺ → NH₄⁺

In blood ammonia (NH₃) is represented as ammonium ion (NH₄⁺). Accumulation of ammonium ion impairs transport of ions (Na⁺, K⁺) through cell membranes and failure of transmission of nerve impulse.

            Urea cycle takes place exclusively in the liver, so in hepatic coma, urea level is low. Glutamine toxicity in brain is dependent on increased ammonia concentration.

Bilirubin toxicity will most likely be related to increase hemolysis, which is not the case in this question. Histamine is a biogenic amine produced from the amino acid histidine.

Explanation

Creatine kinase/Creatine phosphokinase is an enzyme present in striated muscles, used to generate energy. When its serum level is elevated it is often an indication of muscle damage caused by injury, muscular dystrophy or cardiac problems. Most forms of muscular dystrophy are associated with decreased creatinine excretion. Creatinine is a break down product of creatine. Normal constituent of urine but can be elevated in muscular dystrophy. 

Explanation

 Acute poststreptococcal glomerulonephritis: most frequently seen in children. Occurs approximately 2 weeks after group A streptococcal infection of pharynx or skin. Resolves spontaneously. Type III hypersensitivity reaction (Immune complex). Presents with peripheral and periorbital edema, cola-coloured urine, hypertension. On immunofluorescent microscopy: granular appearance due to IgG, IgM and C3 deposition along glomerular basement membrane and mesangium. On electron microscopy: subepithelial immune complex humps. On light microscopy: glomeruli enlarged and hypercellular.

Type III (immune-complex): deposition of antigen-antibody complexes e.g. systemic lupus erythromatous (SLE), Arthus reaction, serum sickness, poststreptococcal glomerulonephritis etc.

Explanation

Normally, protein digestion takes place in the stomach and small intestine. When this process is impaired, the  protein goes to the large intestine undigested and the gut microflora degrades/breaks down protein into ammonia, phenols, indoles and amines which have been shown to exert toxic effects in vitro and in animal models. Human studies have shown that colonic protein metabolism via the gut microflora is responsive to dietary protein as faecal ammonia and urinary phenolic compound concentrations increase in response to increased intake of protein rich foods. These gases also cause the abdominal bloating, diarrhea and flatulence mentioned in the question.

Explanation

The main symptoms of right-sided heart failure are fluid accumulation and swelling (edema) of the feet, ankles, legs, liver and abdomen.

Where the fluid accumulates depends on the amount of excess fluid and the effects of gravity. If a person is standing, fluid accumulates in the legs and feet; if a person is lying down, fluid usually accumulates in the lower back; if the amount of fluid is large, fluid also accumulates in the abdomen.

Most water leakage occurs in capillaries or postcapillary venules which have a semipermeable membrane wall that allows water to pass freely than proteins. In cardiac insufficiency, blood pools in the veins since the heart is not pumping effectively; this increases the hydrostatic pressure in the veins. And this increased hydrostatic pressure leads to increase filtration of water into the interstitium at the venous end of the capillary (post-capillary venule).

Explanation

Intoxication – burn toxemia

The complex of typical changes in the human body developing due to the deep and severe burns is known as burn disease. There are the following stages of burn disease: burn shock, burn toxemia, burn infection, burn emaciation, outcome.

Burn toxemia is related to accumulation in the organism of toxic products of tissue decomposition and systemic expression of multiple inflammatory mediators (systemic inflammatory response syndrome).

Explanation

These characterize Turner’s syndrome (XO). It can be complete monosomy (45,XO) or mosaicism (e.g. 45,XO/46,XX).

Barr body is an inactive X-chromosome. A normal female has one barr body XX; so in turner’s syndrome, there is no barr body because the only X present is the active one (45 XO).

Explanation

Convection is a way the body eliminates heat by means of transferring heat via moving particles of air or water. To dissipate heat by means of convection, body surface shall be airflowed at a temperature that is lower than the temperature of the skin. At that, air layer contacting with the skin warms up, decreases its density, rises and is replaced by cooler, denser air. By increasing the speed of the air flow (wind, ventilation) heat emission increases significantly as well (forced convection). Convection requires convection current; current of gases or liquids (Key words: air over exposed area of skin).

The areas of the skin covered with clothes has a higher temperature because the convection current does not have direct access to the skin in that area as compared to the exposed area of the skin.

Heat Radiation is a way the surface of the human body emits heat to the environment in the form of infrared rays. The amount of heat the body radiates to the environment is proportional to the surface of radiation area and to the difference between the mean values of skin and environment temperature. The surface radiation area is the total surface area of body parts that contact the air. Elimination of heat by radiation increases with a decrease in ambient temperature and decreases with its increase. It is possible to reduce elimination of heat by radiation via reduction of the surface of radiation area (“winding oneself into a ball”). Heat radiation does not require a medium for transfer of heat. (Key words: naked or lightly clothed).

Evaporation is a way the body dissipates heat to the environment by its evaporation via sweat or evaporation of moisture from the skin and respiratory tract mucous membranes of (“wet” heat loss). Evaporation closely related to relative humidity.

Conduction is a way the body eliminates heat by means of direct contact with another object. Heat is transferred down the temperature gradient (i.e. from the object of higher temperature to the object of lower temperature). Conduction requires contact with another object (Key words:  in water).

Explanation

Evaporation is a way the body dissipates heat to the environment by its evaporation via sweat or evaporation of moisture from the skin and respiratory tract mucous membranes of (“wet” heat loss). Evaporation closely related to relative humidity.

Heat Radiation is a way the surface of the human body emits heat to the environment in the form of infrared rays. The amount of heat the body radiates to the environment is proportional to the surface of radiation area and to the difference between the mean values of skin and environment temperature. The surface radiation area is the total surface area of body parts that contact the air. Elimination of heat by radiation increases with a decrease in ambient temperature and decreases with its increase. It is possible to reduce elimination of heat by radiation via reduction of the surface of radiation area (“winding oneself into a ball”). Heat radiation does not require a medium for transfer of heat. (Key words: naked or lightly clothed).

Convection is a way the body eliminates heat by means of transferring heat via moving particles of air or water. To dissipate heat by means of convection, body surface shall be airflowed at a temperature that is lower than the temperature of the skin. At that, air layer contacting with the skin warms up, decreases its density, rises and is replaced by cooler, denser air. By increasing the speed of the air flow (wind, ventilation) heat emission increases significantly as well (forced convection). Convection requires convection current; current of gases or liquids (Key words: air over exposed area of skin).

Conduction is a way the body eliminates heat by means of direct contact with another object. Heat is transferred down the temperature gradient (i.e. from the object of higher temperature to the object of lower temperature). Conduction requires contact with another object (Key words:  in water).

Explanation

Peritonsillar abscess also known as quinsy ( a complication of tonsillitis) caused by both aerobic and anaerobic bacteria (streptococcus, staphylococcus and haemophilus).

Explanation

A normally coloured stool indicates that there is no obstruction to bile flow, therefore, there is a normal emulsification of fat. This also indicates that there is no obstruction to pancreatic juice flow into the intestine, therefore, there will also be proper digestion (hydrolysis) of fat by pancreatic lipase. Then, the only way free fatty acid can be found in stool after emulsification and digestion is only when there is a problem with absorption by the intestinal villi.

Explanation

* Febris intermittens: characterized by regular alternation of brief attacks of fever (paroxysms) with feverless periods (apyrexia). Attacks occur every 3^rd day, 2^nd day or everyday. Increase temperature persists for several hours, drops to normal and then rises again.

* Febris continua/persistent: elevated temperature persists at a high level, difference between morning and evening temperature does not exceed 1⁰C.

* Febris recurrens: characterized by longer periods of pyrexia than intermittent (5-6days). Question says every 4 days.

* Febris hectic: 3-5⁰C (difference in temperature).

* Febris remittens: difference in temperature exceeds 1⁰C but temperature never falls to normal.

Explanation

During cerebellar lesions, there  are disturbances in posture, equilibrium and movements. Disturbances in movements: ataxia, asynergia, asthenia (weak muscle contractions with characteristically rapid onset of muscle fatigue), Dysmetria, Intention tremor, astasia (loss of the capacity for sustained tetanic contractions), nystagmus, rebound phenomenon, dysarthria, adiadochokinesis, atonia (lack or impairment of muscle tone).

Explanation

Hemophilia is a genetic disorder. Its an intrinsic coagulation pathway defect. Since its genetic, it can manifest early in life (childhood). Types:

Hemophilia A: X-linked recessive; deficiency of factor VIII

Hemophilia B: X-linked recessive; deficiency of factor IX

Hemophilia C: Autosomal recessive; deficiency of factor XI

Findings: macrohemorrhage in hemophilia – hemarthroses (bleeding into joints,  such as knee), easy bruising, bleeding after trauma or surgery (e.g. dental procedures).

          Idiopathic or Immune thrombocytopenic purpura: characterized by bleeding which results from unusually low levels of platelets, affects both and children and adults. Children often develop Idiopathic thrombocytopenic purpura after a viral infection and usually recover fully without treatment. In adults, however the disorder is often chronic.

          Hemorrhagic vasculitis is an inflammatory disorder characterized by a generalized vasculitis involving the small vessels of the skin, GI tract, kidneys, joints and rarely the lungs and CNS. It is the most common vasculitis in children. It is an immune complex HSR disease; inciting agents (antigens) include: group A β-hemolytic streptococci and other bacteria, viruses, drugs, food, insect bites.

Explanation

Hemolytic/Prehepatic Jaundice is the type of Jaundice that occurs because of excessive destruction of RBCs resulting in ↑ blood level of free, Indirect, unconjugated bilirubin. In this condition, the excretory function of the liver is normal. But the quantity of bilirubin ↑ greatly. The liver cells cannot excrete that much excess bilirubin rapidly. Formation of Urobilinogen (stercobilin) ↑ resulting in the excretion of more amount of stercobilin in stool and urine.

·       Gilbert syndrome (familial nonhemolytic Jaundice): Autosomal recessive defect. Impaired UGT activity. Jaundice occurs with fasting, volume depletion, stress, menses.

·       Physiologic Jaundice of newborn: begins on day 3 of life. Caused by normal macrophage destruction of fetal RBCs containing HbF and inability of the newborn’s liver to handle excess load.

Explanation

 Barr body is an inactive X-chromosome. So a male patient (XY) with an inactive X-chromosome must have an additional X-chromosome – XXY (Klinefelter’s syndrome). Causes :

* nondisjunction (maternal and paternal nondisjunction in meiosis I)

* Mosaicism: with the karyotype being 46, XY/47, XXY

Manifestations: gynecomastia, female pattern of pubic hair distribution, no facial hair, high voice.

Explanation

Respiratory acidosis is caused by alveolar hypoventilation. During hypoventilation, the lungs fail to expel CO2 (hypercapnia). pH of 7.35 indicates a compensatory mechanism that keeps the pH within the normal range. (7.34-7.45 is the normal range) COMPENSATED will remain in the normal range. DECOMPENSATED will fall out of the normal range.                                                                                                         Metabolic acidosis is characterized by excess accumulation of organic acids (lactic acid, ketoacids, uric acid) in the body.                                           Respiratory alkalosis is caused by alveolar hyperventilation which causes excess loss of CO2 from the body.

Explanation

Explanation

Cushing Syndrome: Etiology:

INCREASE Cortisol due to a variety of causes (Glucocorticoids):

Exogenous corticosteroids: result in decrease ACTH (Most Common Cause).

Primary adrenal adenoma, hyperplasia or carcinoma (Cushing’s Syndrome).

ACTH-secreting pituitary adenoma (Cushing Disease).

Findings: Hypertension, Weight Gain, Moon Facies, Truncal Obesity, Buffalo Hump, Skin Changes (thinning striae), Osteoporosis, Hyperglycemia (Insulin resistance), Amenorrhea, Immunosuppression.

Explanation

Explanation

Electrophoretic study of a blood serum sample examines specific proteins in the blood called GLOBULINS. With five major fractions: -Serum Albumin, Alpha-1 Globulin, Alpha-2 Globulin, Beta-Globulin, Gamma-Globulin.

Alpha-2 Globulin is INCREASED in nephrotic syndrome.

Beta-Globulin is INCREASED in Iron Deficiency Anaemia.

 Gamma-Globulin is INCREASED in Severe Infection (pneumonia), chronic liver disease. Due to the Ig produced against the infection.

Explanation

During insulin deficiency, glucose cannot be utilized by the peripheral tissues for energy. So, a large amount of fat is broken down to release energy. It cause the formation of excess ketone bodies leading to acidosis. One more reason for acidosis is that the ketone bodies are excreted in combination with sodium ions through urine (ketonuria). Sodium exchanged H+, which diffuse from the renal tubules into ECF adding to acidosis.  In diabetic patients, the body produces too much acid & the kidneys are not removing the fast enough as they results in metabolic acidosis.

Explanation

NK cells are lymphocytes that are capable of destroying tumor cells without prior sensitization and thus may provide the 1^st line of defense against tumor cells. After activation with IL-2 and IL-15, NK cells can lyse a wide range of human tumors, including many that seem to be non-immunogenic for T-cells. NK cells, T-cells & macrophages may collaborate in antitumor reactivity.

Explanation

In chronic leukemia: spleen can weigh (6-8kg); liver (5-6kg). Chronic myelogenous leukemia (CML) is characterized by hepatosplenomegaly and generalized painless lymphadenopathy; pyoid bone marrow.

Explanation

Collagen, most abundant protein in human body; organizes and strengthens extracellular matrix. Collagen contains Gly-X-Y (X and Y are proline or lysine). Glycine(Gly) makes 1/3 of collagen. Oxyproline (hydroxyproline) is a major collagen amino acid which enables it to be regarded as a marker that reflects the catabolism of collagen.

Paget disease of bone (osteitis deformans): localized disorder of bone remodeling caused by increase in both osteoclastic and osteoblastic activity.

Explanation

The macro- and microscopic changes in the Myocardial Infarction (M.I.) correspond to the age of the infarct.

   * first 24hrs: No gross changes; coagulative necrosis

               * 1-3days: pallor of infracted tissue

               * 3-7days: red granulation tissue surrounds area of infarction

               * 7-10days: necrotic area is bright YELLOW

               * first 2 months: infarct is replaced by white, patchy, noncontractile scar

                  tissue.

Explanation

High density lipoprotein (HDL) – transports cholesterol from periphery to liver. Low Density Lipoprotein (LDL) - transports cholesterol from liver to tissues.

LCAT (lecithin-cholesterol acyltransferase) – catalyzes esterification of cholesterol

Cholesterol ester transfer protein (CETP) -  mediates transfer of cholesterol esters to other lipoprotein particles.

Explanation

Drumstick – barr body. Barr body is an inactive X-chromosome. So a boy (XY) with an inactive X-chromosome must have an additional X-chromosome – XXY (Klinefelter’s syndrome). Causes :

* nondisjunction (maternal and paternal nondisjunction in meiosis I)

* Mosaicism: with the karyotype being 46, XY/47, XXY

Manifestations: gynecomastia, female pattern of pubic hair distribution, no facial hair, high voice.

Explanation

Hepatic steatosis can occur when humans are deprived of choline.

Choline + Phosphatidic acid → Phosphatidylcholine (lecithin, PC). In the liver PC can also be synthesized from phosphatidylserine (PS) and phosphatidylethanolamine (PE), when free choline levels are low, because it exports significant amounts of PC in bile and as a component of serum lipoproteins (needed for fat metabolism)

PS → PE →→→ PC. 3 methylation reactions between PE and PC. S-adenosylmethionine is the methyl group donor. If choline, phosphatidylcholine or methionine is deficient, there will be abnormal phospholipid synthesis, oxidative damage caused by mitochondrial dysfunction, lipoprotein secretion (remember, if VLDL cannot be secreted it will be accumulated & cause fatty liver degeneration as seen in hepatic steatosis). PC is also a major lipid component of lung surfactant.

Explanation

Creatine kinase/Creatine phosphokinase is an enzyme present in striated muscles, used to generate energy. When its serum level is elevated it is often an indication of muscle damage caused by injury, muscular dystrophy or cardiac problems. Most forms of muscular dystrophy are associated with decreased creatinine excretion. Creatinine is a break down product of creatine. Normal constituent of urine but can be elevated in muscular dystrophy. Since creatine is not a normal constituent of urine, it is more specific in this case.

Explanation

Adrenal medulla produces catecholamines (epinephrine, norepinephrine and dopamine). Increased secretion of epinephrine & norepinephrine can result in these symptoms listed.

Since the patient is 41yrs old, this can be pheochromocytoma - if it is a tumor.

Explanation

Inflammation consists of 3 stages:

* Alteration: characterized by injury of structurally-functional unit of an organ. Primary & secondary.

* Exudative: violation of microcirculation with exudation. Serous, fibrinous, purulent, decaying, hemorrhagic, combination. Serous – skin blisters, pericarditis with clear/transparent liquid(exudative inflammation).

* Proliferative: a phase of reparatory regeneration.

Explanation

Eukinetic: Increase in both systolic and diastolic blood pressure.

       Hyperkinetic: Increase in systolic blood pressure.

       Hypokinetic: Increase in diastolic blood pressure.

       Cardiac output determines systolic blood pressure; peripheral resistance determines diastolic blood pressure.

Explanation

Increase in free hemoglobin in blood plasma is characteristic for intravascular hemolysis. It is definitely acquired since patient is 52years old. If it has an Hereditary cause, it will probably have an early onset.

Explanation

Heat Radiation is a way the surface of the human body emits heat to the environment in the form of infrared rays. The amount of heat the body radiates to the environment is proportional to the surface of radiation area and to the difference between the mean values of skin and environment temperature. The surface radiation area is the total surface area of body parts that contact the air. Elimination of heat by radiation increases with a decrease in ambient temperature and decreases with its increase. It is possible to reduce elimination of heat by radiation via reduction of the surface of radiation area (“winding oneself into a ball”). Heat radiation does not require a medium for transfer of heat. (Key words: naked or lightly clothed).

Convection is a way the body eliminates heat by means of transferring heat via moving particles of air or water. To dissipate heat by means of convection, body surface shall be airflowed at a temperature that is lower than the temperature of the skin. At that, air layer contacting with the skin warms up, decreases its density, rises and is replaced by cooler, denser air. By increasing the speed of the air flow (wind, ventilation) heat emission increases significantly as well (forced convection). Convection requires convection current; current of gases or liquids (Key words: air over exposed area of skin).

Evaporation is a way the body dissipates heat to the environment by its evaporation via sweat or evaporation of moisture from the skin and respiratory tract mucous membranes of (“wet” heat loss). Evaporation closely related to relative humidity.

Conduction is a way the body eliminates heat by means of direct contact with another object. Heat is transferred down the temperature gradient (i.e. from the object of higher temperature to the object of lower temperature). Conduction requires contact with another object (Key words:  in water).

Explanation

When blood passes through glomerular capillaries, the plasma is filtered. All substances of plasma are filtered except the plasma proteins and plasma cells, due to their large molecular size which is larger than the slit pores present in the endothelium of capillaries. Glomerular capillary membrane, basement membrane and visceral layer of bowman capsule form the filtration membrane through which glomerular filtration occurs. So, if protein and erythrocytes are increased or present in urine, it has to do with increase in renal filter permeability.

Explanation

Immune reactions are directed against antigens. Allergic reactions (hypersensitivity) destroys tissue while trying to destroy the antigen leading to development of tissue lesion (tissue lesion – tissue injury). But both of them have the same mechanism.

Explanation

* Febris intermittens: characterized by regular alternation of brief attacks of fever (paroxysms) with feverless periods (apyrexia). Attacks occur every 3^rd day, 2^nd day or everyday. Increase temperature persists for several hours, drops to normal and then rises again.

* Febris continua/persistent: elevated temperature persists at a high level, difference between morning and evening temperature does not exceed 1⁰C.

* Febris recurrens: characterized by longer periods of pyrexia than intermittent (5-6days). Question says every 4 days.

* Febris hectic: 3-5⁰C (difference in temperature).

* Febris remittens: difference in temperature exceeds 1⁰C but temperature never falls to normal.

Explanation

Diabetic nephropathy results in mesangial expansion, glomerular basement membrane thickening, glomerulosclerosis by nonenzymatic glycosylation of glomerular basement membrane → increase permeability, thickening. This basically destroys the nephron, thereby reducing the number of active/normal nephrons.

Diabetics will most likely increase and not decrease the arterial pressure. Does not cause obstruction. Tissue acidosis will not necessarily affect glomerular filtration.

Explanation

* Radiating pain: perceived at a site adjacent to or away from the site of origin but in the same dermatome i.e. supplied by afferent nerve fibers of one dorsal root.

* Viscera pain: organs, poorly localized, diffuse

* Protopathic pain: poorly localized pain

* Epicritic pain: well localized pain

* Phantom pain: pain from non-existent body structures (amputated limbs)

Phantom – if a leg has been amputated, the cut end heals with scar formation. The cut ends of nerve fibers are merged within the scar. If the cut end of sensory fibers are stimulated during movement of thigh, the patient feels as if the sensation is originating from non-existent leg. Sometimes the patient feels pain in non-existent limb.

Explanation

Explanation

All muscles that elevate the rib cage are muscles of inspiration and those that depress the rib cage are muscles of expiration.

Muscles of inspiration:

·        Sternocleidomastoid: lift upward on the sternum.

·        Anterior serrati: lift many of the ribs.

·        Scalene: lift the first two ribs.

Muscles of expiration: Abdominal recti – pull down the lower ribs and other abdominal muscles also compress the abdominal contents upwards against the diaphragm and internal intercostals.

Normal respiration is accomplished by the movement of the diaphragm only.

Explanation

Lead poisoning: lead inhibits Ferrochelatase and ALA dehydratase. Ferrochelatase catalyzes Protoporphyrin + Fe⁺ → Heme

ALA dehydratase catalyzes Aminolevulinic acid (ALA) → Porphobilinogen

Therefore, Iron, Protoporphyrin and ALA will be accumulated in the body. Iron refractory anemia results from disorder of Iron inclusion in heme at decrease of enzymes activity, which catalyzes synthesis of heme.

Explanation

This is classic ornithine transcarbamylase deficiency. Most common urea cycle disorder. X-linked recessive. Interferes with the body’s ability to eliminate NH₃.

Excess Carbamoyl phosphate is converted to orotic acid (part of the pyrimidine synthesis pathway).

Findings: ↑Orotic acid in blood and urine, symptoms of hyperammonemia. No megaloblastic anemia as seen in orotic aciduria – that’s why it is called secondary orotiic aciduria as used in the question.

Carbamoyl phosphate + Ornithine → Citrulline (urea cycle).

Carbamoyl phosphate is involved in 2 metabolic pathways: de novo pyrimidine synthesis and urea cycle. So, if the enzyme is deficient in urea cycle, all Carbamoyl phosphate will be channeled to de novo pyrimidine synthesis producing excess orotic acid.

Explanation

Barr body is an inactive X-chromosome. A normal female has one barr body XX, a normal male has no barr body XY.

Trisomy X – XXX (only one X is active in a female; therefore, 2 barr bodies)

Klinefelter – XXY (one barr body)

Turner’s – XO (no barr body)

Down and Patau involves autosomal chromosomes and not sex chromosomes.

Explanation

α₂-macroglobulin and α₁-antitrypsin are protease inhibitors which can inhibit the pancreatic proteases and prevent further tissue protein breakdown. Immunoglobulin, Cryoglobulin – antibody; Ceruloplasmin – Copper; Transferrin – Iron; Haptoglobulin – hemoglobin; Interferon – released by cells in response to pathogens.

Explanation

Sideroachrestic or sideroblastic anemia: causes

Chronic alcoholism (most common cause); Vit. B₆ deficiency; Lead poisoning; X-linked recessive disease. It is a defect in heme synthesis within the mitochondrial. Iron accumulates in mitochondria, producing ringed sideroblast. X-linked defect in δ-ALA synthase gene. It is classified as an Iron-overload type of anemia. This enzyme catalyzes Glycine + Succinyl-CoA → δ-ALA rate limiting step in heme synthesis. Iron cannot be used in heme synthesis since the process has been disturbed earlier with the deficiency of the enzyme, therefore, Iron is accumulated.

Explanation

↓blood supply → activates renin. Renin catalyzes the conversion of angiotensinogen to angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I → angiotensin II. Angiotensin II causes:

- vasoconstriction → ↑BP

- vasopressin (ADH) → ↑H₂O reabsorption → ↑plasma volume

- aldosterone → ↑Na⁺ and H₂O reabsorption → ↑plasma volume → ↑BP

Explanation

From horizontal (lying position) to vertical (standing position) will make all blood flow towards the lower extremities, thereby reducing venous return (blood going upwards towards the heart) in the first place. This will definitely ↓ cardiac output (C.O) → ↓blood supply to brain (this can lead to fainting). Then there is reflex vasoconstriction to increase venous return to heart, in the absence of any pathology.

Explanation

Liver is found in the right hypochondrium; sclera icterus is specific for jaundice; Absence of stercobilin in stool – blockage of bile duct. These symptoms indicate obstructive , mechanic, posthepatic jaundice.

Cholelithiasis – gallstones which can obstruct bile flow → absence of stercobilin. Hemolytic jaundice → presence of stercobilin in stool.

Obturation (obstruction, to close) of bile duct – it can be:

* Intrahepatic – blockage of intrahepatic bile ducts

* Extrahepatic – blockage of common bile duct (ductus choledochus).

Findings:

* malabsorption: bile salts do not enter the Small Intestine; no emulsification of fat.

*light coloured stool: due to lack of urobilin (which leads to lack of stercobilin).

*Jaundice (posthepatic, mechanic, obstructive): increased conjugated Bilirubin.

* Steatorrhea

The findings are specific for obstruction of bile duct and bile acid deficiency.

Explanation

When a muscle is excited (stimulated) by the impulses passing through neuromuscular junction, action potential is generated which spreads over sarcolemma (plasma membrane of muscles). When the action potential reaches the cisternae of ‘L’ tubules, Ca²⁺ stored in the cisternae are released into the sarcoplasm (cytoplasm of muscles). The Ca²⁺ moves towards the actin filaments to produce the contraction. Therefore, it is Ca²⁺ entry into the sarcoplasm.

Explanation

Food substances like glucose, amino acids, acetoacetate ions and vitamins are completely reabsorbed from renal tubules and do not appear in urine under normal conditions. These substances can appear in urine, only if their concentration in plasma is abnormally high (for glucose above 10mmol/L – renal threshold) or in renal diseases when reabsorption is affected. Since glucose is 5mmol/L, then it has to be a problem with decreased reabsorption of glucose.

Explanation

X-linked (Bruton) agammaglobulinemia: defect in Bruton’s tyrosine kinase (BTK), a tyrosine kinase gene → no B cell maturation. X-linked recessive (↑in boys). Findings: absent B cells in peripheral blood, ↓immunoglobulin of all classes. Absent/scanty lymph nodes and tonsils.

Explanation

Anti-Epstein-Barr nuclear antigen antibody is specific and highly sensitive test or laboratory finding for Infectious mononucleosis. Epstein Barr virus (EBV) is a herpes virus and causative agent of Infectious mononucleosis, also called kissing disease.

Associated with Burkitt lymphoma (a neoplasia but no neoplastic lymphocytes mentioned in the question).

Explanation

Explanation

* Pleiotropy: one gene contributes to multiple phenotypic effects → disorder of connective tissue and eye lens structure, abnormalities of CNS, arachnodactylia. Marfan is FBN1 gene mutation on chromosome 15; Marfan is one gene defect causing all this phenotypic defects.

* Codominance: both alleles contribute to the phenotype of the heterozygote. e.g. blood group AB

* Incomplete dominance: intermediate inheritance. Red + White → Pink

* Multiple allelism e.g. ABO blood type

Explanation

Ochronosis (Alkaptonuria): congenital deficiency of homogentisate oxidase (homogentisic acid oxidase) in the degradative pathway of tyrosine to Fumarate → pigment-forming homogentisic acid accumulates (homogentisuria) in tissues. Autosomal recessive. Usually benign. Urine turns black on prolonged exposure to air. May have debilitating arthralgias (homogentisic acid toxic to cartilage).

Phenylalanine → Tyrosine →→→ Homogentisic acid → Maleylacetoacetic acid

Explanation

Forced expiratory volume (FEV) is the volume of air, which can be expired forcefully in a given unit of time. It is very much decreased in obstructive diseases like asthma and emphysema.

Explanation

Epidemic typhus (human body louse) – Rickettsia prowazekii, can remain latent and reactivate months or years in an infected patient, with symptoms similar to or even identical to the original attack of typhus, including a rash that starts centrally and spreads out, sparing palms and soles. This delayed relapse of epidemic typhus – Brill’s disease.

Explanation

Explanation

6 hormones are secreted by anterior pituitary/adenohypophysis: GH; TSH; ACTH; FSH; LH and Prolactin. They are responsible for the growth and secretory activity of their target glands. The first 5 hormones (Prolactin not included) are called tropic hormones.

Explanation

Funicular myelosis: Vit B₁₂ deficiency – subacute combined degeneration – demyelination of dorsal columns (posterior), lateral corticospinal tracts and spinocerebellar tracts.

Fatty acids →→ Methylmalonyl-CoA → Succinyl-CoA → TCA cycle, myelin synthesis, Heme

Explanation

Erythropoietic porphyria (Gunther’s disease): This disorder is due to a defect in the enzyme Uroporphyrinogen III cosynthase. It is characterized by:

* It is a rare congenital disorder caused by autosomal recessive mode of inheritance, mostly confined to erythropoietic tissues.

* The individuals excrete Uroporphyrinogen I and Coproporphyrinogen I which oxidize respectively to Uroporphyrin I and Coproporphyrin I (red pigments).

* The patients are photosensitive (itching and burning of skin when exposed to visible light) due to the abnormal porphyrins that accumulate. Porphyrins are accumulated in the teeth, bones and an increases amount are seen in the plasma, bone marrow, faeces, RBCs and urine.

* Increased hemolysis is also observed in the individuals affected by this disorder.

Explanation

These characterize Turner’s syndrome (XO). It can be complete monosomy (45,XO) or mosaicism (e.g. 45,XO/46,XX). Klinefelter is related to males. The rest are not related to sex chromosomes, but they are autosomoes.

Explanation

* Type I: Allergic and atopic disorders (e.g. rhinitis, hay fever, asthma); Anaphylaxis. Presentation – immediate, anaphylactic, atopic

* Type II: Acute hemolytic transfusion reactions, autoimmune hemolytic anemia, Erythroblastosis fetalis, Goodpasture syndrome, Graves disease, Myasthenia gravis. Disease tends to be specific to tissue or site where antigen is found.

* Type III: Arthus reaction; SLE; serum sickness. Can be associated with vasculitis and systemic manifestations.

* Type IV: Contact dermatitis, Graft-versus-host disease, multiple sclerosis. Response is delayed and does not involve antibodies (vs. Type I, II, III)

Explanation

Explanation

In laboratory diagnosis of acute myocardial infarction: Creatine kinase isoenzyme MB (CK-MB) appears within 4-8hrs, peaks at 24hrs and disappears within 1.5-3 days. Sensitivity and specificity is 95%.

Reappearance of CK-MB after 3days – reinfarction. CK-MM – found in skeletal muscle and heart (not specific for heart). LDH1 – heart muscle; LDH2 – blood serum. LDH levels are also high in tissue breakdown or hemolysis. Although CK-MB is more specific and sensitive for infarction than LDH. Aspartate transaminase is not specific for heart damage alone but can still be used to diagnose myocardial infarction. But troponin test [cardiac troponins I (cTnI) and T (cTnT)] is the most sensitive and specific test for myocardial infarction.

Explanation

Explanation

Urinary incontinence – involuntary urination. In general, parasympathetic stimulation is anabolic, promoting normal function and conserving energy. The sacral part of parasympathetic system resides within the S₂-S₄ sacral segments of the spinal cord.

They inhibit contraction of internal sphincter of bladder, contracts detrusor muscle of the bladder wall causing urination (voluntary). Lesion to this segment of spinal cord (S₂-S₄) causes involuntary urination.

Explanation

A biopsy of the transplanted organ can confirm that it is being rejected. The laboratory pathologist generally seeks 3 main histological signs:

* Infiltrating T cells, perhaps accompanied by infiltrating plasma cells, eosinophils and neutrophils.

* Structural compromise of tissue anatomy.

* Injury to blood vessels.

Rejection is an adaptive immune response. Therefore, immune rejection.

Explanation

Irritant receptors are located in the bronchi and bronchioles of lungs and are stimulated by irritant chemical agents such as ammonia, sulfur dioxide and some other small particles like dust, smoke etc. These receptors send afferent impulses to respiratory centers via vagal nerve fibers. Stimulation of irritant receptors produces reflex hyperventilation along with bronchospasm. J receptors are stimulated during pulmonary congestion, pulmonary edema, over-inflation of lungs. Stretch receptors are the receptors which give response to stretch of the tissues – Hering-Breuer reflex is initiated by the stimulation of stretch receptors of air passage. Proprioceptors of respiratory muscles are the receptors which give response to change in the position of body. Thermoreceptors are cutaneous receptors, which give response to change in the environmental temperature.

Explanation

Prothrombin time (PT) evaluates the extrinsic coagulation system down to the formation of the fibrin clot.

Factors that are evaluated include factor VII, X, V, II, and I. PT is increased when a factor level is 30% - 40% of normal. Vitamin K-dependent factors include factor II, VII, IX and X; protein C and S.

Vitamin K is activated in the liver by epoxide reductase. Activated vitamin K ɣ-carboxylates each of the vitamin K-dependent factors. Carboxylated factors are now able to bind calcium, which are essential for interaction between the coagulation factors and platelet membranes.

Warfarin inhibits the enzyme vitamin K epoxide reductase. Neonates lack enteric bacteria which produce vitamin K.

Explanation

Type IIa (familial hyperlipoproteinemia: ↑LDL and cholesterol. Autosomal dominant; due to absent or defective LDL receptors.

Type I:  ↑chylomicrons, triacylglycerol (TAG), cholesterol. Autosomal recessive; due to lipoprotein lipase deficiency or altered apolipoprotein C-II.

Type IV: ↑very low density lipoprotein (VLDL) and TAG. Autosomal dominant; due to hepatic overproduction of VLDL.

Type IIb: similar to Type IIa, except that VLDL is also increased and VLDL is normal for IIa.

Explanation

Tissue or histotoxic hypoxia is the type of hypoxia produced by the inability of tissues to utilize O₂ which results from tissue poisoning. These poisonous substances destroy the cellular oxidative enzymes and there is a complete paralysis of cytochrome oxidase system.

Hemic hypoxia: connected with hemoglobin (Hb) quantity or inhibition of its functions. Cardiovascular or circulatory hypoxia arises during the disturbance of blood circulation due to heart and vessels pathology. Hypoxic hypoxia develops during the decrease of barometric pressure that is accompanied with decrease of pO₂. Respiratory hypoxia arises as a result of respiratory insufficiency due to alveolar hypoventilation, disturbances of lungs blood supply, disturbances of gases diffusion in lungs.

Explanation

Explanation

Dehydration (hypohydration, hypohydria, exicosis): in dehydration, the extracellular fluid (ECF) and sodium ions are lost.

*Isoosmolar dehydration: based on proportional volume decrease of fluids and electrolytes e.g. acute renal failure (stage of polyuria), blood loss, burns etc.

*Hypoosmolar dehydration (salt deficit) develops due to diarrhea, vomiting, sweating, adrenal insufficiency etc.

*Hyperosmolar dehydration (water deficit) develops due to the loss of the fluid which lacks electrolytes e.g. in diabetes insipidus, hyperventilation

Explanation

Type I (Immediate, Anaphylaxis, Reagin): IgE (immunoglobulin E)-dependent activation of mast cells/basophils, usually accompanied by eosinophilia e.g. urticaria (hives), hay fever, asthma (wheezing), rhinitis and conjunctivitis (stuffy nose and itchy eyes; usually seasonal)

Type II (cytotoxic): antibody dependent reactions e.g. Goodpasture syndrome, Myasthenia gravis, Graves disease, ABO hemolytic disease of newborn etc.

Type III (immune-complex): deposition of antigen-antibody complexes e.g. systemic lupus erythromatous (SLE), Arthus reaction, serum sickness, poststreptococcal glomerulonephritis etc.

Type IV (cell mediated, delayed): antibody-independent T-cell mediated reactions e.g. positive mantoux reaction (tuberculin test), hashimoto’s thyroiditis or transplant rejection etc.

Explanation

Pirogov’s stages of shock

* Erectile phase: is characterized by strong motor agitation, sweating, tremor of skeletal muscles, staggering gait, frequent urination, transient increase in blood pressure, heart rate and breath rate increases, body temperature also. Painful impulses reach CNS.

* Torpid phase: decompensation in CNS leads to deep oppression. Patient is motionless, does not answer questions or answers very silently and with long time of delay, reflexes are lowered or absent.

Explanation

Primary shrunken kidney is a renal form of essential hypertension. It is characterized by chronic arteriolosclerotic nephrosclerosis. Macroscopically, both kidneys are affected equally and are reduced in size and weight. The surface of the kidney is finely granular. The cut surface shows firm kidney and narrowed cortex. Microscopically, there is variable degree of atrophy of parenchyma; these include glomerular shrinkage, deposition of collagen in Bowman’s space, periglomerular fibrosis.

Secondary shrinkage of kidneys is found in chronic glomerulonephritis.

Explanation

Neutrophilic leukocytosis: increase in neutrophil count. Depending on the proportion between the mature and premature forms of neutrophils, two types of the nuclear shift may be distinguished: to the left, when there is an elevated content of immature forms of neutrophilic granulocytes (myelocytes, metamyelocytes, bands) in the blood; And to the right, when the mature neutrophils with a large number of segments (5 – 6) prevail against a background of younger cells disappearing. The nuclear shift may be subdivided into: regenerative, hyperregenerative, degenerative and regenerative-degenerative shifts.

 Neutrophils: Stab (band): 1-6%                        (20%)↑

                                    Segmented: 47-72%         (53%) normal

                                    Myelocyte: - 0

                                    Metamyelocyte: 0-1%      Juvenile forms (0)

Since there is an elevated content of Stab (band) form of neutrophils, then it is a degenerative left shift.

Explanation

DiGeorge’s syndrome results from a congenital malformation affecting the 3^rd and 4^th pharyngeal pouches. These structures give rise to the thymus, parathyroid glands and portions of lips, ears and the aortic arch. It is the most common disorder of cell mediated immunity. The thymus is usually rudimentary and T cells are deficient or absent in the circulation. Most of these infants have additional developmental defects affecting the face, ears, lips heart and great vessels. All of these disorders are part of a spectrum called 22q deletion syndrome because they result from a deletion on the long arm of chromosome 22 (22q11). It represents the most severe example of a collection of disorders that also includes velocardiofacial syndrome (VCFS) and conotruncal anomalies face syndrome.

Explanation

Sickle cell hemoglobin (HbS) point mutation causes a single amino acid replacement in β chain of hemoglobin (substitution of glutamic acid with valine). Pathogenesis of sickle cell anemia: low O₂, high altitude or acidosis precipitates sickling – modified shape (deoxygenated HbS polymerizes) → anemia and vaso-occlusive disease. Clinical findings include: dizziness, general weakness, fatigue, “crew-cut” on skull X-ray due to marrow expansion from increased erythropoiesis (this is also seen in thalassemia)  etc. Sickle cells are crescent-shaped RBCs.

Explanation

Neutrophilic leukocytosis: increase in neutrophil count. Depending on the proportion between the mature and premature forms of neutrophils, two types of the nuclear shift may be distinguished: to the left, when there is an elevated content of immature forms of neutrophilic granulocytes (myelocytes, metamyelocytes, bands) in the blood; And to the right, when the mature neutrophils with a large number of segments (5 – 6) prevail against a background of younger cells disappearing. The nuclear shift may be subdivided into: regenerative, hyperregenerative, degenerative and regenerative-degenerative shifts.

Regenerative shift develops against a background of mild general leukocytosis, accompanied with elevated content of bands and metamyelocytes (immature forms). This shift results from the reactive leukopoiesis (granulocytopoiesis) activation and is common in suppurative septic processes.

Neutrophils: Stab (band): 1-6%             (8%)↑

                                    Segmented: 47-72%         (59%) normal

                                    Myelocyte: -

                                    Metamyelocyte: 0-1%      Juvenile forms (2%)↑

Since there is an elevated content of immature forms of neutrophils, then it is a regenerative left shift.

Explanation

Explanation

Type I (Immediate, Anaphylaxis, Reagin): IgE (immunoglobulin E)-dependent activation of mast cells/basophils, usually accompanied by eosinophilia e.g. urticaria (hives), hay fever, asthma (wheezing), rhinitis and conjunctivitis (stuffy nose and itchy eyes; usually seasonal).

Type I Hypersensitivity reaction (HSR); anaphylactic and atopic: free antigen cross-links IgE on presensitized (i.e. exposed to the antigen before) mast cells and basophils, triggering immediate release of vasoactive amines that act at postcapillary venules (i.e. histamine). Reaction develops rapidly after antigen exposure because of preformed antibody from first exposure. IgE is the main immunoglobulin involved in type I HSR. Type I: uses IgE and IgG₄

Explanation

Isoosmolar hypohydration (isoosmotic loss): proportional volume decrease of fluids and electrolytes e.g. in blood loss, burns, diuretic therapy, especially diarrhea in cholera.

Hypoosmolar hypohydration (salt deficit) develops due to diarrhea, vomiting, sweating, adrenal insufficiency, hypokalemia, CNS lesions, salt-losing nephritis.

          Hyperosmolar hypohydration (water defcit) develops due to the loss of the fluid which lacks electrolytes e.g. in diabetes insipidus, hyperventilation.

         Hypoosmolar hyperhydration (water excess) develops in acute renal failure (in the stage of anuria), Parhon’s syndrome (syndrome of inappropriate ADH secretion –SIADH).

         Hyperosmolar hyperhydration (salt excess) develops rarely e.g. in drinking salt (sea) water, infusion of hypertonic saline, adrenal hyperactivity or steroid therapy.

Explanation

Monocyte is 28%, therefore it is monocytosis i.e. ↑monocyte count. Increase in total number of leukocytes is in the monocyte fraction. Agranulocytes include lymphocyte and monocyte.

Explanation

Urolithiasis or formation of urinary calculi at any level of the urinary tract is a common condition. There are 4 main types of urinary calculi, namely:

·        Calcium stones: are the most common comprising 75% of all urinary calculi. They may be pure stones of calcium oxalate (50%) or calcium phosphate (5%) or mixture of calcium oxalate.

·        Mixed (struvite) stones: about 15% of urinary calculi are made of magnesium-ammonium-calcium phosphate often called struvite. “Staghorn stone”

·        Uric acid stones: can be seen in gout, Lesch-Nyhan syndrome (hyperuricemia).

·        Cystine stones: seen in cases like cystinuria.

NB: hyperparathyroidism → ↑Ca²⁺ concentration in blood.

Explanation

Microscopically, iron deficiency anemia is characterized by hypochromia (red cells are pale) and smaller than nomal (microcytic); chlorosis (pale-greenish colouration of skin).

There is alopecia, koilonychias, atrophies of the tongue and gastric mucosa (atrophic glossitis and atrophic gastritis). Plummer-Vinson triad: hypochromic microcytic anemia, atrophic glossitis and esophageal webs.

B₁₂ –folic acid deficiency: megaloblastic macrocytic anemia

Sickle cell anemia: sickled shaped or modified shaped erythrocytes

Hemolytic anemia: in chronic conditions, its manifestations are very similar to iron deficiency anemia.

Thalassemia: target cell, anisocytosis, poikilocytosis.

Explanation

·        Neuroparalytic arterial hyperemia is caused by damage or blockage of α-adrenoreceptors (sympathetic nervous system). It is characterized by reduction or absence (paralysis) of the sympathetic nervous system effects on the walls of the arteries and arterioles.

·        Neurotonic arterial hyperemia is caused by activation of parasympathetic nervous system; irritation of vascular dilators part of vascular center (CNS) or inhibition of vascular – constrictor part of this center (vasomotor center of CNS); M-cholinoreceptors; H₂-histaminereceptors. It is characterized by predominance of the parasympathetic nervous system effects on arterial vascular walls.

Explanation

Explanation

Atelectasis refers to partial or complete collapse of the lungs. Its major cause is deficiency or inactivation of surfactant. It causes collapse of lungs due to increased surface tension, which leads to respiratory distress syndrome. Other causes include obstruction of a bronchus or a bronchiole; presence of air (pneumothorax), fluid (hydrothorax), blood (hemothorax) or pus (pyothorax) in the pleural space.

Explanation

Cytotoxic T cells destroy cancer cells, transplanted cells, such as those of transplanted heart or kidney or any other cells, which are foreign bodies. They destroy even the body’s own tissues which are affected by the foreign bodies, particularly the viruses.

     Helper T cells (CD4 cells) activate all the other T cells and B cells.

     B cells – plasma cells – antibodies: major defense against bacterial infections.

     Natural killer (NK) cells: destroy viruses, malignant cells and prevents development of cancerous tumors.

    Interleukin are cytokines produced by leukocytes to act on other leukocytes e.g. IL-1, IL-2, IL-3, IL-12 etc.

Explanation

P-Q or P-R interval is the interval between the onset of ‘P’ wave and onset of ‘Q’ wave. This interval signifies the atrial depolarization and conduction of impulses through the AV node.

Short isoelectric (zero voltage) period after the end of ‘P’ wave represents the time taken for the passage of depolarization within the AV node. Normal duration of P-Q interval is 0.18s and varies between 0.12 and 0.20s. If it is more than 0.20s, it signifies a delay in the conduction of impulse, usually, the delay occurs in the AV node. It is prolonged in bradycardia and Atrioventricular (AV) heart block i.e. delay in conduction of impulse through the AV node.

Explanation

Central chemoreceptors are responsible for 70 – 80% of increased ventilation through chemical regulatory mechanism. Main stimulant for central chemoreceptors is the increased hydrogen ion concentration. However, if H⁺ concentration increases in blood, it cannot cross the blood-brain barrier and blood-cerebrospinal fluid barrier. On the other hand, if CO₂ increases in the blood, it can easily cross the blood-brain barrier and blood-CSF barrier and enter the interstitial fluid of brain or the CSF. There, the CO₂ combines with water to form carbonic acid. Since carbonic acid (H₂CO₃) is unstable, it immediately dissociates into H⁺ and bicarbonate ion. 

Then H⁺ stimulates the central chemoreceptors. From chemoreceptors, the excitatory impulses are sent to dorsal respiratory group of neurons, resulting in increased ventilation (increased rate and force of breathing). Lack of O₂ does not have significant effect on the central chemoreceptors, except that it generally depresses the overall function of brain.

Explanation

Cellular immunity or T-cell immunity involves majorly the T cells. 

B-lymphocytes differentiates into plasma cells which then produce antibodies or immunoglobulins (IgG, IgE …). They participate more in humoral immunity.

Immunodeficiency disorders is a good soil for opportunistic pathogenic infections (e.g. skin mycosis). Therefore, a disorder of cellular immunity indicates a reduction in T-lymphocyte count.

Explanation

The necrotic changes is an invitation for an inflammatory reaction.

Explanation

Normal erythrocyte sedimentation rate (ESR): men: 2 – 10mm/h

                                                                               Women: 2 – 15mm/h

Products of inflammation (e.g. fibrinogen) coat RBCs and cause aggregation. The denser RBC aggregates, fall at a faster rate within a pipette tube. Therefore, an increase in fibrinogen (2x increase) should produce a proportional increase in ESR.

40 – 50mm/h is the only option higher than the normal range.

↑ESR: most anemias, infections, inflammation (e.g. temporal arteritis), cancer (e.g. multiple myeloma), pregnancy, autoimmune disorders (e.g. SLE)

↓ESR: sickle cell anemia (altered shape), polycythemia (↑RBCs “dilute” aggregation factors), microcytosis, hypofibrinogenemia

Explanation

Histamine is one of the most important inflammatory mediators. Histamine is synthesized and secreted from tissue basophils, thrombocytes, endothelium and smooth muscle cells. Activation of H₁-receptors leads to bronchospasm, activation of chemotaxis and lymphocytotoxicity, generation of lipid mediators, increase of vessels permeability and dilatation of resistance vessels (arterioles). Increase in vessels permeability leads to the formation or accumulation of exudates i.e. the escape of fluid, proteins and blood cells from the vascular system into the interstitial tissue or body cavities (i.e. edema). Edema denotes an excess of fluid in the interstitial tissue or serous cavities. It can be either an exudate or a transudate. An exudate is an inflammatory extravascular fluid that has a high protein content, specific gravity and many cells.

Explanation

Explanation

Explanation

The normal and pathologic development and growth can be divided into the following stages:

·        Progenesis: characterized by gametogenesis i.e. formation and maturation of gametes. This stage occurs before the fertilization of the ovum. Pathology of gametogenesis is called gametopathy.

·        Development after fertilization is called kymatogenesis. This intrauterine phase can be divided into:

-         Blastogenesis: from day 1 – 15 of gestation. Pathology of blastogenesis is called blastopathy.

-         Embryogenesis: from day 16 to the end of the 3^rd month (75^th day). Pathology of embryogenesis is called embryopathy.

-         Fetogenesis: from the 4^th month of gestation to delivery (from 76^th -280^th day). Pathology of fetogenesis is called fetopathy.

     Gametopathy is an injury of formation and maturation of the gametes during ovo- and spermatogenesis until fertilization. The most frequent is trisomy 21 (Down’s syndrome); trisomy 13 (Patau’s syndrome), trisomy 18 (Edward’s syndrome), Klinefelter’s syndrome (XXY), Turner’s syndrome (XO).

Explanation

Pheochromocytoma is the most common tumor of the adrenal medulla in adults. Most tumors secrete epinephrine, norepinephrine and dopamine which can cause episodic hypertension.

There is increase catecholamines and metanephrines in urine and plasma. Epinephrine stimulates glycogen phosphorylase (rate-limiting enzyme in glycogenolysis i.e. breakdown of glycogen to glucose). This results in hyperglycemia (increase glucose conc. in blood).

There is also pronounced sympathetic effects throughout the body like dry mouth.

Explanation

Bee sting can initiate an inflammatory process, which leads to the release of biogenic amines and other important inflammatory mediators. Histamine is one of the most important inflammatory mediators. Histamine is synthesized and secreted from tissue basophils, thrombocytes, endothelium and smooth muscle cells. Activation of H₁-receptors leads to bronchospasm, activation of chemotaxis and lymphocytotoxicity, generation of lipid mediators, increase of vessels permeability and dilatation of resistance vessels (arterioles). Increase in vessels permeability leads to the formation or accumulation of exudates i.e. the escape of fluid, proteins and blood cells from the vascular system into the interstitial tissue or body cavities (i.e. edema). Edema denotes an excess of fluid in the interstitial tissue or serous cavities. It can be either an exudate or a transudate. An exudate is an inflammatory extravascular fluid that has a high protein content, specific gravity and many cells.

Explanation

Certain amino acids undergo decarboxylation that means the removal of their α-carboxyl group resulting in liberation of CO₂ and formation of biogenic amines. Biogenic amines are physiologically active substances such as hormones, neurotransmitters etc. decarboxylation of amino acids:

·        Tryptophan → Niacin → NAD⁺/NADP⁺

          Tryptophan → Serotonin →Melatonin

·        Histidine → Histamine

·        Glutamine → GABA

Glutamine → Glutathione

Explanation

During cerebellar lesions, there  are disturbances in posture, equilibrium and movements. Disturbances in movements: Speech disorders, ataxia, asynergia, asthenia (weak muscle contractions with characteristically rapid onset of muscle fatigue), Dysmetria, Intention tremor, astasia (loss of the capacity for sustained tetanic contractions), nystagmus, rebound phenomenon, dysarthria, adiadochokinesis, atonia (lack or impairment of muscle tone).

NB: Scanned or staccato speech is as a result of cerebellar disorders; while monotonus speech is as a result of parkinson's disease.

Explanation

Hepatitis is inflammation of the liver. The liver is the main site of protein synthesis i.e. synthesis of albumin, globulin, fibrinogen etc., which are necessary to maintain plasma oncotic pressure. In a situation of hepatic failure, there is decrease of protein synthesis which results in decreased oncotic pressure and then, edema. Therefore, an impairment of protein synthetic function of liver leads to the formation of edema.

Explanation

Any form of stress is accompanied by the release of stress hormones (catecholamines, cortisol). Stress-induced changes in blood leukocyte distribution may represent an adaptive response. This represents a redistribution of leukocytes from the blood to other organs such as the skin, draining sentinel lymph nodes and other compartments. Such leukocyte redistribution may enhance immune function in compartments to which immune cells traffic during stress.

Explanation

Pulmonary embolism is the most common and fatal form of venous thromboembolism in which there is occlusion of pulmonary arterial tree by thromboemboli. Pulmonary emboli are more common in hospitalized or bedridden patients. The majority of emboli arise from the deep veins of the lower extremities; most of the fatal ones arise from the ileofemoral veins. Consequences of thromboembolism include pulmonary infarction in which pyramidal segments (or ‘triangular’ segments) of hemorrhagic infarction are seen at the periphery of the lung. Detachment of thrombi from the thrombophlebitis site in the lower limbs produces a thromboembolus that flows through venous drainage into the large veins draining into the right side of the heart and then to the pulmonary circulation where they embolize.

Explanation

Liver is the primary organ of protein synthesis. In a case of dysfunction of protein synthesis, hypoproteinemia occurs. We have absolute and relative hypoproteinemia. Absolute is when there is disturbed synthesis (absolute hypoproteinemia) and in cases of increased synthesis (absolute hyperproteinemia); while relative does not have to do with synthesis but other pathologies e.g. renal lesions, in which case, there is loss of protein with urine (relative hypoproteinemia); also vomiting, diarrhea, profuse sweating can produce relative hyperproteinemia.

It is Relative because it does not have to do with synthesis. The man must have lost a lot of fluid through sweat, thereby decreasing the fluid content of the body and creating a relative hyperproteinemia. Decrease blood volume (liquid component alone) → ↑concentration of blood.

Explanation

Polycyclic aromatic hydrocarbons (PAH) or simply polycyclic hydrocarbons may be released during the combustion of fossil fuels, particularly when coal and gas are burnt at high temperatures (e.g. in steel foundries) and are present in tar and soot (Pott identified soot as the cause of scrotal cancers in chimney sweeps in 1775). Polycyclic hydrocarbons are among the most potent carcinogens and industrial exposures have been implicated in the development of lung, respiratory tract and bladder cancer. NB: a stoker is a person who tends a furnace specifically of a steam boiler, on a ship, locomotive etc.

Explanation

Lung emphysema is characterized by increased airiness of the lungs due to overdistended or destroyed alveoli. The patient mainly complains of dyspnoea, which at the onset of the disease may only develop during exercise but later it occurs at rest. Dyspnea increases in cold seasons, in chills and exacerbations of bronchitis; it is especially pronounced during attacks of cough. Dyspnea is usually of an expiratory type: a healthy person expires air with ease whereas the patient with emphysema presses it out from the chest with an effort.

Explanation

Calcium (above 98%) and phosphorus (about 86%) are mainly fixed in bones and teeth, from where they can be mobilized in case of immediate organism needs. The role of calcium in the organism consists in the participation in bone and teeth construction, transmission of nervous stimulation, blood clotting, regulation of membranes permeability, muscle contraction etc. Therefore, a deficiency of Ca²⁺ → ↓density of teeth and ↑fragility.

Explanation

Antidiuretic hormone (vasopressin) is secreted in response to decrease blood volume and increase plasma osmolarity. It binds to receptors on principal cells of collecting ductules causing increase number of aquaporins and increase water reabsorption which leads to decreased diuresis.

↓vasopressin → ↓H₂O reabsorption → polyuria

Explanation

Nephrotic syndrome is characterized by massive proteinuria (>3.5g/day) with hyperlipidemia, hypoalbuminemia (hypo- and dysproteinemia), edema etc. It may be primary (direct podocyte damage) or secondary (podocyte damage from systemic process e.g. diabetes). For example – focal segmental glomerulosclerosis, minimal change disease, membranous nephropathy, amyloidosis, diabetic glomerulonephropathy.

Explanation

·        Neuroparalytic arterial hyperemia is caused by damage or blockage of α-adrenoreceptors (sympathetic nervous system). It is characterized by reduction or absence (paralysis) of the sympathetic nervous system effects on the walls of the arteries and arterioles.

·        Neurotonic arterial hyperemia is caused by activation of parasympathetic nervous system; irritation of vascular dilators part of vascular center (CNS) or inhibition of vascular – constrictor part of this center (vasomotor center of CNS); M-cholinoreceptors; H₂-histaminereceptors. It is characterized by predominance of the parasympathetic nervous system effects on arterial vascular walls. Trifacial nerve (Trigeminal nerve CNV), a cranial nerve. Parasympathetic system is craniosacral i.e. it has cranial and sacral segments.

Explanation

IL-1 is produced by macrophages, endothelium, keratinocytes, microglia, B-lymphocytes, fibroblasts, dendritic cells. Pro-inflammatory effects depend on IL-1, also induction of adhesive molecules, endopyrogenic activity, reason of prodromal syndrome, trigger of the reaction of an acute phase of inflammation and induction of synthesis of acute phase reactants, the main mediator of the immune reaction to alien substances, stimulator of stress.

Explanation

Thalassemia or target cell anemia or Cooley’s anemia is an hemoglobinopathy (abnormal hemoglobin in RBCs). Defect in α-globin chain results in α thalassemia; and point mutations in β-globin chain results in β thalassemia. It is characterized microscopically by anisocytosis, poikilocytosis, target cells and is characterized by increased hemolysis, enlargement of spleen and liver, progressive anemia with erythroblastemia (reticulocyte). It’s a microcytic, hypochromic anemia.

Sickle cell anemia is also a hemoglobinopathy (abnormal hemoglobin in RBCs). It results as a result of a point mutation causing a single amino acid replacement in β chain (substitution of glutamic acid with valine) to produce hemoglobin S (HbS). The condition is characterized by the presence of sickle-like erythrocytes revealed during crisis, they cause stasis, hemorrhages and infarctions.

Explanation

Catarrhal inflammation is one of the morphologic patterns in acute inflammation. In this type, a surface inflammation is associated with greatly increased secretion of clear mucus (nasal discharges). Rhinitis is inflammation of mucous lining of the nose.

Explanation

The Mantoux skin test should be read between 48 and 72hrs after administration. The basis of reading  is the presence or absence of induration, which may be determined by inspection and by palpation. A record should also be made of formation of vesicles, bullae, lymphangitis, ulceration and necrosis at the test site. The formation of vesicles, bullae or necrosis at the test site indicates positive result. A negative mantoux result usually signifies that the individual has never been exposed to Mycobacterium tuberculosis i.e. absence of cell mediated immunity to tuberculin.

Type IV (cell mediated, delayed): antibody-independent T-cell mediated reactions e.g. positive mantoux reaction (tuberculin test), hashimoto’s thyroiditis or transplant rejection etc.

Explanation

Type I Hypersensitivity reaction (HSR); anaphylactic and atopic: free antigen cross-links IgE on presensitized (i.e. exposed to the antigen before) mast cells and basophils, triggering immediate release of vasoactive amines that act at postcapillary venules (i.e. histamine). Reaction develops rapidly after antigen exposure because of preformed antibody from first exposure. IgE is the main immunoglobulin involved in type I HSR. Type I: uses IgE and IgG₄

Explanation

Hemolytic anemia: according to the mechanisms of the development, they are divided into 3 groups namely:

·        Erythrocytic membrane structure (membranopathy)

·        Erythrocytic enzyme activity (enzymopathy)

·        Structure or rate of hemoglobin synthesis (hemoglobinopathy)

    Membranopathies are characterized by disorders of protein or lipid components of the erythrocytic membrane structure. Membranopathies caused by the disorders of protein structure includes:

o   Hereditary spherocytosis (Minkowsky-shauffard disease)

o   Hereditary elliptocytosis (ovalocytosis)

o   Hereditary pyropoikilocytosis

o   Hereditary and acquired stomatocytosis

     In addition, the membrane defect leads to a loss of both potassium and water, which produces cellular dehydration and results in erythrocyte damage (electrolytic osmotic).

Explanation

‘T’ wave is the final  ventricular complex and is a positive wave. It is due to the repolarization of ventricular musculature. Normal duration is 0.2sec; normal amplitude is 0.3mV.

Explanation

Metaplasia is a reversible change of one type to another type of adult epithelial or mesenchymal cells, usually in response to abnormal stimuli and often reverts back to normal on removal of stimulus. Types (2):

·        Epithelial: *Squamous metaplasia: in bronchus (chronic smokers), cervix

                          *Columnar metaplasia: there is transformation to columnar epithelium.

·        Mesenchymal metaplasia: osseous and cartilaginous.

Hyperplasia: ↑number of cells; Hypertrophy: ↑in size.

Explanation

Cholelithiasis is obstruction of bile duct by a stone.

Obturation (obstruction, to close) of bile duct – it can be:

* Intrahepatic – blockage of intrahepatic bile ducts

* Extrahepatic – blockage of common bile duct (ductus choledochus).

Findings:

* malabsorption: bile salts do not enter the Small Intestine; no emulsification of fat.

*light coloured stool: due to lack of urobilin (which leads to lack of stercobilin).

*Jaundice (posthepatic, mechanic, obstructive): increased conjugated Bilirubin.

* Steatorrhea

The findings are specific for obstruction of bile duct and bile acid deficiency.

Explanation

In the hepatocyte, the solubility of unconjugated bilirubin is increased (i.e. it is made soluble) by the addition of two molecules of glucuronic acid to produce conjugated bilirubin. This process is reffered to as conjugation. This reaction is catalyzed by Uridine diphosphate (UDP) glucuronyltransferase – UGT.

Varying degrees of deficiency of this enzyme result in Crigler-Najjar I & II and Gilbert syndrome; with Crigler-Najjar I being the most severe deficiency.

Deficiency of UGT inhibits conjugation and therefore increase unconjugated bilirubin in serum (Jaundice).

Explanation

One of the laboratory tests for diabetes mellitus is the level of glycosylated hemoglobin. Glycosylated hemoglobin test (HbA_1C, glycohemoglobin) are proteins with glucose bound to them by nonenzymatic way. They precisely represent the extent of impairment of the carbohydrate metabolism and serve as the basic index of quality of compensation of diabetes mellitus. The level of HbA_1C is determined by the method of chromatography using special laboratory equipment. Level of HbA_1C shows an average blood concentration during the previous 2 - 3 months. Normal level of HbA_1C is 4 – 6%. [4 – 8 weeks (1-2months)]

Explanation

Type IIa (familial hyperlipoproteinemia: ↑LDL and cholesterol. Autosomal dominant; due to absent or defective LDL receptors.

Type I:  ↑chylomicrons, triacylglycerol (TAG), cholesterol. Autosomal recessive; due to lipoprotein lipase deficiency or altered apolipoprotein C-II.

Type IV: ↑very low density lipoprotein (VLDL) and TAG. Autosomal dominant; due to hepatic overproduction of VLDL.

Type IIb: similar to Type IIa, except that VLDL is also increased and VLDL is normal for IIa.

Explanation

Explanation

This is an example of type I hypersensitivity reaction considering the time taken for the symptoms (rash and itching) to manifest and the expression of eosinophilia.

Neutrophilic leukocytosis: bacterial infection

Lymphocytosis: viral and bacterial infection (e.g. whooping cough, tuberculosis)

Monocytosis: chronic inflammation (tuberculosis); autoimmune disease

Explanation

High density lipoprotein (HDL): is the antiatherogenic lipoprotein fraction (nicknamed the ‘good lipoprotein’).

Low density lipoprotein (LDL): is the proatherogenic lipoprotein fraction (nicknamed the ‘bad lipoprotein’)

High density lipoprotein (HDL) – transports cholesterol from periphery to liver. Low Density Lipoprotein (LDL) - transports cholesterol from liver to tissues.

LCAT (lecithin-cholesterol acyltransferase) – catalyzes esterification of cholesterol

Cholesterol ester transfer protein (CETP) -  mediates transfer of cholesterol esters to other lipoprotein particles.

Explanation

Cerebral cortex is responsible for the memory, attention, consciousness and all higher nervous system functions. The cardiorespiratory reaction in the patient is because he is able to store and remember the tragic event. The cerebral cortex also has extensive connections with the subcortical structures responsible for short and long term memories.

Explanation

The main stimulator of renin release from juxtaglomerular cell is decrease blood flow in afferent arteriole. Stenosis of renal artery → ↓blood flow to afferent arteriole thereby stimulating renin release and set up the renin-angiotensin-aldosterone system (RAAS).

Explanation

Adrenaline is an adrenomimetic; α₁ – mediates peripheral vasoconstriction →↑blood pressure. Activation of β₁-adrenoreceptors by adrenaline results in increased cardiac output and heart rate.

Vasopressin → ↓diuresis; ↑H₂O reabsorption → ↑blood volume

Aldosterone is a steroid hormone and cannot produce the same level of increase in blood pressure as adrenaline and vasopressin combined.

Explanation

Extensive myocardial infarction: extensive necrosis of myocardial cells. The pathogenesis of the heart failure is definitely the fact that there are less active/alive myocardial cells that can contract and pump blood effectively. No information about blood volume, so we can’t talk about the other options.

Explanation

These symptoms indicates an increase in male sex hormones. This can probably be a pathology of the adrenals or ovaries in a female, which leads to increase production of testosterone (the only male sex hormone in the options)

Explanation

Desensitization therapy in atopic individuals involves repeated injection of increasingly greater amounts of allergen, resulting in production of IgG antibodies that attach to allergens and prevent them from binding to mast cells.

Explanation

Polycythemic hypovolemia is a condition with a decreased amount of plasma usually characterized by appreciable concentration and increased viscosity of blood. Hematocrit is above normal. This condition is observed in connection with considerable loss of water by the organism as in diarrhea, intractable vomiting, extensive burns. Hematocrit is increased because there is no loss of erythrocytes just fluid was lost from vomiting. It can’t  be hypervolemia because there is loss of fluid from prolonged vomiting.

In simple hypovolemia: hematocrit is normal; oligocythemic hypovolemia: hematocrit is decreased.

Explanation

Obturation (obstruction, to close) of bile duct – it can be:

* Intrahepatic – blockage of intrahepatic bile ducts

* Extrahepatic – blockage of common bile duct (ductus choledochus).

Findings:

* malabsorption: bile salts do not enter the Small Intestine; no emulsification of fat.

*light coloured stool: due to lack of urobilin (which leads to lack of stercobilin).

*Jaundice (posthepatic, mechanic, obstructive): increased conjugated Bilirubin.

* Steatorrhea

The findings are specific for obstruction of bile duct and bile acid deficiency.

Explanation

Pathogenesis of acute posthemorrhagic anemia consists of 3 periods: reflex vascular period; hydremic period (2-3days) and regenerative (bone-marrow) period. During the hydremic period after 2-3days: there is compensation of circulating plasma volume: diminishing/decrease of excretion by kidneys; increase transport of interstitial fluid and lymph into the lumen of blood vessels. This will cause a relative decrease in erythrocytes (erythropenia) and hemoglobin [but colour index (C.I.) is near norm] because the fluid component of blood have been replaced by the 2^nd day but the cellular components are yet to be replaced because erythropoiesis will take a longer time.

Explanation

It is anaphylactic because of the relatively short time it took to manifest the symptoms. It is local because, it affects just the trunk and distal part of limb. Systemic will have systemic effects like anxiety, loss of consciousness, shock, difficulty in breathing.

Type I Hypersensitivity reaction (HSR); anaphylactic and atopic: free antigen cross-links IgE on presensitized (i.e. exposed to the antigen before) mast cells and basophils, triggering immediate release of vasoactive amines that act at postcapillary venules (i.e. histamine). Reaction develops rapidly after antigen exposure because of preformed antibody from first exposure. IgE is the main immunoglobulin involved in type I HSR. Type I: uses IgE and IgG₄

Explanation

Peritonsillar abscess also known as quinsy ( a complication of tonsillitis) caused by both aerobic and anaerobic bacteria (streptococcus, staphylococcus and haemophilus).

Explanation

Type I Hypersensitivity reaction (HSR); anaphylactic and atopic: free antigen cross-links IgE on presensitized (i.e. exposed to the antigen before) mast cells and basophils, triggering immediate release of vasoactive amines that act at postcapillary venules (i.e. histamine).

Reaction develops rapidly after antigen exposure because of preformed antibody from first exposure. IgE is the main immunoglobulin involved in type I HSR. Type I: uses IgE and IgG₄

Type I (Immediate, Anaphylaxis, Reagin): IgE (immunoglobulin E)-dependent activation of mast cells/basophils, usually accompanied by eosinophilia e.g. urticaria (hives), hay fever, asthma (wheezing), rhinitis and conjunctivitis (stuffy nose and itchy eyes; usually seasonal)

Explanation

Vaccine is a substance that is introduced into the body to prevent the disease produced by certain pathogens. Vaccine consists of dead pathogens or live but attenuated (artificially weakened) organisms. The vaccine induces immunity against the pathogen, either by production of antibodies or by activation of T-lymphocytes. Mature B cells express IgM and IgD on their surfaces. They may differentiate in germinal centers of lymph nodes by isotype switching into plasma cells that secrete IgA, IgE, IgG. IgA prevents attachment of bacteria and viruses to mucous membranes; it has 2 isotypes – a monomer (in circulation) and a dimer (when secreted- secretory). Crosses epithelial cells by transcytosis. It is the most produced antibody overall, but has lower serum concentrations. Released into secretions (tears, saliva, mucus) and breast milk. Based on the localization of secretory IgA, it is responsible for local immunity. And all other Immunoglobulins, since they are found in serum, they are responsible for systemic immunity.

Explanation

Two fatty acids are dietary essentials in humans – linoleic acid and α-linolenic acid (long chain polyunsaturated fatty acids). They are required for fluidity of membrane structure and synthesis of eicosanoids. A deficiency of essential fatty acid is characterized by scaly dermatitis, hair loss and poor wound healing. Essential fatty acid deficiency however is rare. Linoleic acid is the precursor of arachidonic acid, the substrate for prostaglandin synthesis. Arachidonic acid becomes essential if linoleic acid is deficient in the diet.

Explanation

Desensitization as a method of treating allergic diseases is used, in particular, to prevent serum anaphylaxis from repeated injections of serum preparations (e.g. tetanus toxoid), in accordance with the method proposed in 1907 by the Russian scientist A. M. bezredka. The method consists in injecting small concentrations of the preparation (toxoid antigen) that produce the sensitization, as a result, a state of anti-anaphylaxis arises (i.e. desensitization). Owing to this, the next injection of the reacting dose of the allergen does not produce anaphylaxis. The small concentrations injected are below threshold concentrations inducing complete and sustained deprivation of releasability (ability to release inflammatory mediators from activated mast cells having IgE attached to them already) without triggering degranulation. Basophil desensitization is regulated by their surface IgE levels.

Desensitization therapy in atopic individuals involves repeated injections of increasingly greater amounts of allergens, resulting in production of IgG antibodies that attach to allergens and prevent them from binding to mast cells.

Explanation

Lactate dehydrogenase (LDH) is an enzyme in cardiac cells which can serve as a marker for injured myocardial cells as it leaks out of damaged cell membranes into the bloodstream. It catalyzes the conversion of pyruvate to lactate (a reversible reaction). It has five (5) isoenzymes (isoenzymes catalyze same reaction), but only LDH₁ is found in the myocardium.

LDH₁ – heart, RBCs and brain; LDH₂- reticuloendothelial system; LDH₃- lungs; LDH₄- kidneys, placenta and pancreas; LDH₅- liver and striated muscle.

Explanation

QRS complex on an ECG graph is also called the initial ventricular complex. Q wave is a small negative wave. It is continued as the tall R wave which is a positive wave. R wave is followed by a small negative wave – S wave. QRS complex is due to depolarization of ventricular musculature.

Q wave is due to the depolarization of basal portion of interventricular septum. R wave is due to the depolarization of apical portion of interventricular septum and apical portion of ventricular muscle. S wave is due to the depolarization of basal portion of ventricular muscle near the atrioventricular ring. The Q wave may be absent on an ECG. The R wave corresponds to almost complete excitation of both ventricles. It is the highest wave of the ventricular complex.

Explanation

Sinoatrial (SA) block is the failure of impulse transmission from SA node to AV node. It is also called sinus block. It is characterized by periodic missing of the heart beat and pulse beat. The ECG shows periodic missing of the heart complex (neither P-wave nor the QRST complex are recorded); the length of diastole doubles.

Explanation

Aldosterone produced in adrenal cortex (zona glomerulosa): causes increased sodium (Na⁺) reabsorption; increased potassium and hydrogen ions (↑K⁺, H⁺) excretion. They increase sodium (↑Na⁺) channel and Na⁺ /K⁺-pump insertion in principal cells of collecting duct; enhances K⁺ and H⁺ excretion by way of principal cell K⁺ channels and α-intercalated cell H⁺ ATPases of collecting duct. Therefore, increase in aldosterone → ↑ K⁺ in urine (excretion) and ↓ Na⁺ in urine (↑ reabsorption); And decreased aldosterone → ↓ K⁺ excretion (↓K⁺ in urine) and ↓ Na⁺  reabsorption (i.e. ↑Na⁺ in urine); same effects on sweats glands too.

Explanation

Lactate, formed by the action of lactate dehydrogenase (converting pyruvate to lactate) is the final product of anaerobic glycolysis in eukaryotic cells. In organs or cells that are poorly vascularized and/or lack mitochondria, formation of lactate is the major fate of pyruvate as seen in lens, cornea of the eye, kidney medulla, testes, leukocytes and red blood cells.

Aerobic glycolysis progresses to citric acid cycle from pyruvate. The cycle occurs totally in the mitochondria.

Explanation

Embolism is occlusion of a vessel by material traveling in the circulation.

* Gas embolism: two main forms of gas embolism are air embolism and decompression sickness. Air embolism is usually due to accidental pumping of air into the venous circulation during intravenous (IV) injection or transfusion ( bubble – air escaped).

* Fat/Adipose embolism: obstruction of arterioles and capillaries by fat globules constitutes fat embolism. It may occur following severe fracture trauma to bones, inflammation of bones and soft tissues, fatty liver

* Thromboembolism: a detached thrombus or part of thrombus which may arise in the arterial or venous circulation.

Tissue embolism: fragments of tissue.

Explanation

The Mucopolysaccharidoses are hereditary disorders that are clinically progressive. They are characterized by accumulation of glycosaminoglycans in various tissues, causing varied symptoms such as skeletal and extracellular matrix deformities and mental retardation. Mucopolysaccharidoses are caused by a deficiency of any one of the lysosomal hydrolases normally involved in the degradation of heparin sulfate and/or dermatan sulfate. This results in the presence of oligosaccharides in the urine because of incomplete lysosomal degradation of glycosaminoglycans.

Explanation

Explanation

In the hepatocyte, the solubility of unconjugated bilirubin is increased (i.e. it is made soluble) by the addition of two molecules of glucuronic acid to produce conjugated bilirubin. This process is reffered to as conjugation. This reaction is catalyzed by Uridine diphosphate (UDP) glucuronyltransferase – UGT. Varying degrees of deficiency of this enzyme result in Crigler-Najjar I & II and Gilbert syndrome; with Crigler-Najjar I being the most severe deficiency.

Deficiency of UGT inhibits conjugation and therefore increase unconjugated bilirubin in serum (Jaundice).

Explanation

Increase in cardiac workload can cause imbalances in oxygen (O₂) supply and demand to the heart itself. Blood supply to the heart occurs during diastole. Increase heart rate (↑HR) → ↓diastolic period → ischemia in myocardium. Ischemia, hypoxia, heart failure are associated with disruptions in intracellular Na⁺ and Ca⁺ concentration homeostasis of myocardial cells. A decrease efflux or increase influx of Na⁺ may cause cellular Na⁺ overload. Na⁺ overload is followed by an ↑influx of calcium (Ca²⁺) through Na⁺-Ca²⁺ exchanger. Failure to maintain the homeostasis of Na⁺ and Ca⁺ leads to electrical instability (arrhythmias), mechanical dysfunction (reduced contractility and ↑ diastolic tension) and mitochondrial dysfunction. These events increase ATP hydrolysis and decrease ATP formation and if left uncorrected, they cause cell injury and death → acute heart failure.

Explanation

APNEUSTIC: Prolonged, gasping inspiration followed by an insufficient or brief expiration. E.g damage to brainstem, ketamine.

KUSSMAUL: Vigorous inhalation and active exhalation with forced contraction of expiratory muscles. E.g in diabetic ketoacidosis.

CHEYNE-STOKES: Cyclic breathing pattern which regular change in frequency (at time faster & followed by a gradual decrease) that results in a temporary stop in breathing (apnea). E.g heart failures,strokes.

BIOT: periods of apnea interchanging with periods of resumption of breathing without significant changes in the amplitude of respiratory movements. E.g damage to pons due to stroke or trauma.

GASPING: forced,convulsive breath.

Explanation

The patient was in a hot workshop, there is definitely a transfer of heat from the environment to the patient. Compensatory mechanisms in the patient should work to increase heat transfer from the patient back to the environment (heat emission), to avoid accumulating excessive heat. The patient was hyperemic (vasodilation –normal), dry (i.e. not sweating) and hot to touch (if there was evaporation of sweat, it would have cooled the skin temperature). In the absence of sweating, it therefore means that there is reduced heat transfer from the patient’s body back into the surrounding.

NB: the question is concerned about heat transfer from the patient to the surrounding.

Explanation

Explanation

Explanation

Neutrophils are the first leukocytes that cross the blood vessel wall to enter inflammatory sites. Under normal conditions, leukocytes are restricted to the center of small blood vessels, where the flow is fastest. In inflammatory sites, where the vessels are dilated, the slower blood flow allows the leukocytes to move out of the center of the blood vessel and interact with the vascular endothelium. Even in the absence of infection, monocytes migrate continuously into the tissues, where they differentiate into macrophages; meanwhile, during an inflammatory response, the induction of adhesion molecules on the endothelial cells, as well as induced changes in the adhesion molecules expressed on leukocytes recruit large numbers of circulating leukocytes, initially Neutrophils and later monocytes, into the site of an infection (inflammatory focus).

First –Neutrophils; second –monocytes and macrophages; third –lymphocytes.

Explanation