<question> You consult a child. A biopsy showed a high concentration of hepatic glycogen. The concentration of glucose in the blood is higher than normal. Which enzyme deficiency causes this condition? <variant> Glycogen phosphorylase deficiency <variant> Glucose-6-phosphate dehydrogenase deficiency <variant> Glycogen synthetase deficiency <variant> Succinate dehydrogenase deficiency
- Glycogen cannot be broken down normally, so it accumulates in the liver (high hepatic glycogen on biopsy).
- However, gluconeogenesis remains intact, and glucose can still enter the blood from other sources, which can maintain normal or even elevated blood glucose (unlike some other GSDs which cause hypoglycemia).
- Glucose-6-phosphate dehydrogenase deficiency - causes hemolytic anemia (pentose phosphate pathway defect), not glycogen storage.
- Glycogen synthetase deficiency - would cause decreased hepatic glycogen, not increased.
- Succinate dehydrogenase deficiency - a TCA cycle/complex II enzyme; causes mitochondrial disease, not glycogen accumulation.
An 11-year-old boy was admitted to the pediatric neurology department due to developmental delay. Upon examination, a female body type, pronounced gynecomastia, underdeveloped testicles, and penis are noted.Which hormone's physiological effect can explain this underdevelopment of sexual organs? <variant> testosterone <variant> somatotropin <variant> progesterone <variant> estradiol <variant> thyroxine
- Female body habitus / gynecomastia
- Small, underdeveloped testes
- Small penis and infertility
- Development and maturation of male external genitalia (penis, scrotum)
- Testicular growth and spermatogenesis
- Male secondary sex characteristics (voice deepening, facial hair, muscle mass)
- Suppression of gynecomastia
- Somatotropin (GH) - governs growth, not sexual organ development
- Progesterone - female reproductive hormone, not responsible for male genital development
- Estradiol - actually elevated relative to testosterone in this condition; it causes gynecomastia rather than preventing underdevelopment
- Thyroxine - thyroid hormone; regulates metabolism and general development, not male genital differentiation
A 2-year-old child has a lag in physical development, frequent pneumonia. The diagnosis was established: non - contamination of the arterial duct. The message of which vessels is caused by a violation of hemodynamics? <variant> Pulmonary trunk and pulmonary veins <variant> Aorta and pulmonary trunk <variant> Superior vena cava and aorta <variant> Superior vena cava and pulmonary trunk <variant> Aorta and pulmonary veins
- After birth, systemic pressure (aorta) exceeds pulmonary pressure
- Blood shunts left-to-right: from the aorta → pulmonary trunk
- This causes pulmonary overcirculation (explaining recurrent pneumonia)
- The extra blood volume overloads the left heart and lungs
- Over time can cause pulmonary hypertension and growth failure (explaining developmental lag)
- Pulmonary trunk and pulmonary veins - no direct connection in PDA
- Superior vena cava and aorta - describes a different anomaly
- Superior vena cava and pulmonary trunk - not the anatomy of PDA
- Aorta and pulmonary veins - not connected by the ductus
<question>During replication, two DNA molecules are formed from one. The replication process is carried out by specific enzymes. Determine the enzyme that stabilizes the sides of the replication fork. What is it called? <variant>DNA polymerase <variant>Helicase <variant>Topoisomerase <variant>SSB proteins <variant>Ligase
| Enzyme/Protein | Function |
|---|---|
| Helicase | Unwinds the double helix by breaking hydrogen bonds between base pairs |
| SSB proteins | Stabilizes the open single strands at the fork, keeping them apart |
| Topoisomerase | Relieves torsional stress/supercoiling ahead of the fork |
| DNA polymerase | Synthesizes the new DNA strand (5'→3') |
| Ligase | Joins Okazaki fragments on the lagging strand |
<question> A 32-year-old patient has been suffering from chronic inflammation of the oral mucosa for a long time. He has leukoplakia. Name the pathological process. <variant> Keratin dystrophy <variant> Fatty degeneration <variant> Carbohydrate dystrophy <variant> Mucoid swelling <variant> Fibrinoid swelling
- Chronic irritation/inflammation triggers abnormal differentiation of squamous epithelial cells
- These cells begin producing excess keratin (hyperkeratosis) or keratin in abnormal locations (dyskeratosis)
- This produces the characteristic white, thickened plaques of leukoplakia
- It is considered a precancerous lesion (~5-10% risk of malignant transformation)
- Fatty degeneration - involves abnormal lipid accumulation in cells (e.g., liver steatosis)
- Carbohydrate dystrophy - involves abnormal glycogen or mucopolysaccharide accumulation
- Mucoid swelling - early reversible connective tissue change with GAG accumulation
- Fibrinoid swelling - irreversible connective tissue necrosis with fibrin-like deposits (seen in autoimmune diseases)
<question> A 46-year-old woman has a body mass index of 42. What clinical and morphological form of obesity does the patient have? <variant> Endocrine <variant> Alimentary-constitutional <variant> Hypothalamic <variant> Abdominal <variant> Tumor
- BMI 42 = Class III (Morbid) Obesity (BMI ≥ 40)
- Excessive caloric intake relative to energy expenditure (alimentary = related to eating/nutrition)
- Genetic/constitutional predisposition to fat accumulation
- Sedentary lifestyle
- No underlying hormonal, hypothalamic, or tumor pathology
- Endocrine - would require evidence of hypothyroidism, Cushing's syndrome, hypogonadism, etc.
- Hypothalamic - caused by hypothalamic damage (trauma, tumor, surgery) with specific neuroendocrine symptoms
- Abdominal - this describes a fat distribution pattern (central/visceral fat), not a clinical-morphological form of obesity by etiology
- Tumor - extremely rare; caused by insulin-secreting tumors (insulinoma) driving hyperphagia
<question> After hyperventilation, the athlete has a short-term respiratory arrest. What changes in the blood are caused by this? <variant> CO2 voltage reduction <variant> pH reduction <variant> Increase in CO2 voltage <variant> O2 voltage reduction <variant> Increase in CO2 and O2 voltage
- Excessive breathing causes massive CO2 washout from the blood
- Blood CO2 (PaCO2) drops significantly below normal (normal = 35-45 mmHg)
- This causes respiratory alkalosis (pH rises)
- The primary drive to breathe is rising CO2 (detected by central chemoreceptors)
- After hyperventilation, CO2 is so low that there is no stimulus to breathe
- Breathing ceases until CO2 accumulates back to the threshold level
- This is called post-hyperventilation apnea
- The reduction in PaCO2 (CO2 voltage/tension) is the direct cause
- The chemoreceptors are not stimulated because CO2 is too low
- pH reduction - the opposite occurs; hyperventilation causes alkalosis (pH rises)
- Increase in CO2 voltage - CO2 is decreased, not increased, after hyperventilation
- O2 voltage reduction - O2 may actually be slightly elevated after hyperventilation; it is not the primary mechanism
- Increase in CO2 and O2 voltage - neither increases; CO2 is washed out
<question> With isolated stimulation of the afferent fibers A and B, an extensor reflex was obtained, but of different strengths. Simultaneous stimulation of both nerves led to an increase in the response, but the amplitude of muscle contraction was less than the sum of the effects obtained with separate stimulation of each nerve. What is the name of the phenomenon? <variant> occlusion <variant> summation <variant> relief <variant> induction <variant> irradiation
- Its own exclusive neurons (activated only by A, or only by B)
- Shared neurons in the overlap zone (activated by both A and B)
- The shared neurons in the overlap zone are already being maximally excited by input from both A and B - they can only fire once, not twice
- So the combined response is less than the arithmetic sum of the two separate responses
- The overlapping neurons are counted only once - they are "occluded"
- Combined effect < sum of individual effects = Occlusion
- Combined effect > sum of individual effects = Relief (facilitation/spatial summation)
- Summation - refers to temporal or spatial addition of subthreshold stimuli to reach threshold; not the same concept
- Relief - the opposite phenomenon; combined response exceeds the sum (subliminal fringe neurons are recruited)
- Induction - refers to the relationship between excitation and inhibition (positive/negative induction)
- Irradiation - spread of excitation across multiple neurons in the CNS
<question> In the experiment, the ischemia of tissue was simulated. The study revealed swelling of cells, pycnosis of nuclei. What is the most likely mechanism of cell swelling? <variant> increased intracellular Na+ <variant> increased activity of the Na+/K+-ATP <variant> increased activity of Ca2+-ATP <variant> increased intracellular K+ <variant> activation of superoxide dismutase
- Ischemia cuts off oxygen supply → oxidative phosphorylation fails → ATP depleted
- The Na+/K+-ATPase pump fails (requires ATP to run) - it can no longer pump 3 Na+ out and 2 K+ in
- Na+ accumulates inside the cell (cannot be exported)
- Intracellular Na+ rise creates an osmotic gradient - water follows Na+ into the cell by osmosis
- The cell swells (hydropic/cloudy swelling) - this is the earliest and most common reversible cell injury
- If ischemia continues, nuclear pyknosis occurs (irreversible injury, chromatin condensation)
- Increased activity of Na+/K+-ATPase - the opposite happens; the pump is inhibited due to ATP depletion
- Increased activity of Ca2+-ATPase - also ATP-dependent; it fails too, but Ca2+ accumulation causes different injury patterns (not the primary swelling mechanism)
- Increased intracellular K+ - K+ actually leaks out of cells during ischemia as the pump fails
- Activation of superoxide dismutase - an antioxidant enzyme; relevant to reperfusion injury, not cell swelling
<question> Why does the inflammatory response continue even after the etiological factor (EF) has been removed? <variant> The EF initiates a series of cascade biochemical reactions in cells, leading to the development of inflammation. <variant> Inflammation progresses due to endogenous pro-inflammatory substances activated by the etiological factor (EF). <variant> The development of inflammation is sustained by tissue breakdown products after the EF has acted. <variant> The EF can maintain the inflammatory response from a distance due to its persistent effect. <variant> The inflammatory reaction continues because it is impossible to completely eliminate the effect of the EF.
- EF causes initial cell/tissue injury
- Damaged cells release secondary mediators - tissue breakdown products (biologically active substances from damaged membranes, lysosomes, etc.)
- These include: histamine, serotonin, kinins (bradykinin), prostaglandins, leukotrienes, lysosomal enzymes, cytokines
- These mediators themselves cause further tissue damage and recruit more inflammatory cells
- The newly damaged tissue releases more breakdown products
- This self-perpetuating cascade continues even after the original EF is completely gone
- Option A (cascade biochemical reactions) - partially true but too vague; it doesn't specifically explain why it continues after EF removal
- Option B (endogenous pro-inflammatory substances) - very close, but the key point is specifically tissue breakdown products as the sustaining mechanism, not just any endogenous substances
- Option D (EF acts from a distance) - incorrect; the EF has been removed by definition
- Option E (impossible to eliminate EF) - contradicts the premise of the question
<question> Why is it crucial to maintain blood pressure in the management of shock of any etiology? <variant> Decreased pressure causes a vicious circle: hypoxia – myocardial dysfunction – decreased pressure. <variant> Decreased pressure is a primary pathogenetic factor in the development of shock. <variant> Decreased pressure is an etiological factor in the development of any type of shock. <variant> Decreased pressure triggers mechanisms of lipid peroxidation and tissue damage. <variant> Decreased pressure contributes to the development of disseminated intravascular coagulation (DIC).
- Low BP (from any etiology - hemorrhage, sepsis, cardiogenic, anaphylactic) → reduced tissue perfusion
- Tissue hypoxia → organs (including the heart) receive insufficient oxygen
- Myocardial hypoxia → cardiac muscle dysfunction → reduced contractility and cardiac output
- Further drop in BP → worsening hypoxia → more myocardial dysfunction
- The cycle accelerates and becomes irreversible if not broken
- Option B (decreased pressure is primary pathogenetic factor) - incorrect; decreased pressure is a consequence of the primary pathogenetic mechanisms (e.g., fluid loss, vasodilation, pump failure), not the primary factor itself
- Option C (decreased pressure is etiological factor) - wrong; hypotension is a result of shock, not its cause
- Option D (lipid peroxidation) - this occurs in ischemia/reperfusion injury but is not the main reason to maintain BP in shock management
- Option E (DIC) - DIC is a complication of shock, but it is not the primary reason BP maintenance is critical
<question> Acute phase response protein, an inflammation indicator that reflects the severity and acute nature of inflammatory diseases. <variant> C-reactive protein <variant> Haptoglobin <variant> Fibrinogen <variant> Ceruloplasmin <variant> Hepcidin
- Produced by the liver in response to IL-6, IL-1β, and TNF-α released during inflammation
- Rises within 6-8 hours of an acute inflammatory stimulus
- Can increase 1,000-fold or more above baseline (normal < 10 mg/L)
- Directly reflects severity - higher CRP = more severe/active inflammation
- Returns to normal rapidly when inflammation resolves, making it useful for monitoring treatment response
- Used to distinguish bacterial infection (very high CRP) from viral (mildly elevated) and monitor diseases like rheumatoid arthritis, sepsis, MI, etc.
| Protein | Role | Why not the best answer |
|---|---|---|
| Haptoglobin | Binds free hemoglobin | Rises moderately; more specific to hemolysis |
| Fibrinogen | Coagulation factor | Rises slowly; measured as ESR indirectly |
| Ceruloplasmin | Copper transport, antioxidant | Minor acute phase reactant |
| Hepcidin | Iron regulation | Causes anemia of chronic disease; not a primary inflammation marker |
<question>During surgery for a gunshot wound to the chest, the surgeon performs manipulation in the area of the gate of the right lung. The upper and middle elements of the lung root (relative to the horizontal plane) are not damaged, and the lower element has a through wound. What is damaged? <variant>Pulmonary vein <variant>Pulmonary artery <variant>Semi-paired vein <variant>The main bronchus <variant>Right lymphatic duct
| Position | Structure |
|---|---|
| Upper | Pulmonary artery |
| Middle | Main (principal) bronchus |
| Lower | Pulmonary veins (2 veins - superior and inferior) |
- Upper element = not damaged (pulmonary artery)
- Middle element = not damaged (main bronchus)
- Lower element = through wound = pulmonary vein
- Pulmonary artery - sits at the top of the right hilum, not the bottom
- Semi-paired (hemi-azygos) vein - this is a posterior mediastinal structure, not part of the lung root/hilum
- Main bronchus - occupies the middle position at the right hilum
- Right lymphatic duct - drains into the right subclavian vein junction; not a hilar structure at the lung root
<question> A patient with peptic ulcer disease of the stomach is receiving omeprazole. Indicate its mechanism of action: <variant> Blocks H+/K+-ATPase in parietal cells <variant> Blocks H2-histamine receptors in the stomach glands <variant> Neutralizes the hydrochloric acid of gastric juice <variant> Blocks M1-cholinoceptors of enterochromaffin cells <variant> Stimulates mucus and bicarbonate secretion
- Omeprazole is a prodrug - it is acid-labile and absorbed in the small intestine
- It diffuses into the parietal cells of the gastric mucosa
- In the acidic secretory canaliculi, it is activated (converted to sulfenamide)
- The active form irreversibly binds to the H+/K+-ATPase (the proton pump) via covalent disulfide bonds
- This blocks the final step of HCl secretion - the exchange of H+ into the stomach lumen for K+
- Result: profound and prolonged suppression of gastric acid secretion (up to 24-48 hours)
| Drug class | Mechanism |
|---|---|
| PPIs (omeprazole) | Block H+/K+-ATPase (proton pump) in parietal cells |
| H2 blockers (ranitidine) | Block H2-histamine receptors in stomach glands |
| Antacids (Mg/Al hydroxide) | Neutralize HCl directly |
| Pirenzepine | Block M1-cholinoceptors |
| Misoprostol/sucralfate | Stimulate mucus/bicarbonate secretion |