Pathophysiology tests with answers: 50 questions for exam preparation

Activation of lipid peroxidation is a universal mechanism of cell membrane damage accompanying hypoxia and hemolysis in all forms of anemia. Mutations and impaired globin synthesis represent specific etiological factors of particular nosologies.

A vicious circle (circulus vitiosus) is a mechanism of pathological development in which the arising disturbances trigger a chain of reactions that aggravate the initial damage.

Dyschronosis is a direct biorhythm disorder. Neurotic conditions and peptic ulcer disease frequently occur as a consequence of chronic stress due to disrupted circadian cycles (e.g., in shift work).

The allergic reaction in bronchial asthma is a pathologically altered, heightened reactivity of the immune system to antigens (allergens) that are safe for healthy individuals.

The occurrence and clinical course of a pathology are determined by a triad of factors: the specificity of the damaging agent, the reactivity of the organism, and the environmental conditions in which they interact.

ADP-ATP translocase (an antiporter) is localized in the inner mitochondrial membrane and carries out equimolar exchange of ATP synthesized in the matrix for cytosolic ADP.

Mucins and mucoids are complex proteins, namely glycoproteins. Their excessive accumulation in tissues indicates a disorder in the metabolism of this specific class of compounds (mucous degeneration).

The repair defect consists in the cell's inability to restore damaged structures, which manifests as the suppression of membrane lipid and protein resynthesis, as well as their de novo formation.

Necroptosis is a form of programmed cell death activated via RIPK1 and RIPK3 kinases upon caspase-8 blockage. The process acquires morphological features of necrosis with plasma membrane disruption and inflammation.

The removal of excess calcium ions from the cytosol is carried out by calcium pumps of the plasmalemma and endoplasmic reticulum, whose function directly depends on ATP energy. In case of ATP deficiency or impaired utilization, the function of these enzymes suffers, leading to intracellular calcium overload.

Lysosomal hydrolases (phospholipases, proteases) cause hydrolytic cleavage of lipids and proteins in membrane structures, which refers to the enzymatic mechanism of alteration.

Lipid A is the conservative toxic part of the lipopolysaccharide of Gram-negative bacteria. It is recognized by innate immunity receptors (TLR4), triggering the release of pro-inflammatory cytokines and the development of a systemic inflammatory response.

Internalization of protein exotoxins occurs via receptor-mediated endocytosis, in which the cell membrane invaginates to form an endosome that transports the toxin into the cytosol.

Septicopyemia is characterized not only by the circulation of the pathogen in the blood, but also by the formation of metastatic purulent foci (abscesses) in various organs, which distinguishes it from septicemia.

A number of pathogens (Mycobacteria, Salmonella, Legionella) are able to block phagolysosomal fusion or resist bactericidal factors, leading to incomplete phagocytosis and intracellular persistence.

Among the presented pathogens, only Rickettsia prowazekii (the causative agent of epidemic typhus) belongs to the genus Rickettsia, whereas Legionella and Mycobacterium belong to other taxa.

Tumor necrosis factor alpha (cachectin) is predominantly secreted by activated macrophages as well as adipose tissue adipocytes. It plays a key role in the development of systemic inflammation, insulin resistance, and wasting (cachexia).

Endogenous opioids, including β-endorphin, are orexigenic neuropeptides and stimulate the hypothalamic feeding center, increasing appetite. Serotonin and cholecystokinin, conversely, induce satiety.

Psychogenic (cortical) eating disorders, such as anorexia nervosa or bulimia, are primarily caused by mental and higher nervous activity disorders rather than organic lesions of the gastrointestinal tract or endocrine system.

In the modern morphological classification of atherosclerotic lesions, fibroatheroma is characterized by the presence of a formed connective tissue (fibrous) cap covering the lipid core, unlike the earlier stage of atheroma formation.

Bile acids are necessary for the emulsification of fats and the activation of pancreatic lipase in the intestinal lumen, therefore bile deficiency primarily disrupts luminal lipid digestion.

Excess sodium in vascular smooth muscle cells leads to their swelling and a secondary increase in intracellular calcium concentration. This increases the basal tone of the vascular wall and its sensitivity to pressor hormones.

Hypercalcemia increases renal glomerular calcium filtration, leading to hypercalciuria. Excess calcium in the urine promotes salt crystallization and the formation of kidney stones.

Aldosterone enhances sodium reabsorption in the distal renal tubules. In case of its excess (hyperaldosteronism), pathological sodium retention in the body occurs, leading to hypernatremia.

Sodium is the main osmotically active ion of the extracellular space. A decrease in its concentration naturally leads to a drop in the osmotic pressure of blood plasma and interstitial fluid.

Following a salt-free diet leads to dietary sodium deficiency due to its insufficient intake with food.

The accumulation of carbon dioxide (hypercapnia) in the blood leads to the formation of excess carbonic acid. This causes a decrease in blood pH and the development of respiratory (gas) acidosis.

In circulatory hypoxia, blood flow slows down, allowing tissues to extract more oxygen from the passing blood. This leads to a decrease in oxygen content in venous blood and an increase in the arteriovenous difference.

Fractional saturation accounts for all types of hemoglobin, including dyshemoglobins (carboxyhemoglobin and methemoglobin), while functional saturation accounts only for those capable of binding oxygen. Normally, the concentration of pathological forms of hemoglobin is minimal, so these parameters are practically identical.

Respiratory hypoxia occurs as a result of impaired gas exchange in the lungs in various forms of respiratory failure. This leads to a decrease in the partial pressure of oxygen in arterial blood.

In pulmonary sclerosis and interstitial edema, thickening of the alveolar-capillary membrane occurs. This increases the diffusion path for gas molecules and impedes their diffusion, primarily oxygen.

Systematic use of psychoactive substances leads to the development of dependence syndrome. It includes an irresistible craving for the drug (psychological dependence) and the development of withdrawal syndrome upon its discontinuation (physical dependence).

Opiates are exogenous ligands that bind to specific opioid (opiate) receptors in the central nervous system, mimicking the effects of endogenous opioid peptides.

The euphoric effect of opiates is due to their interaction with opioid receptors in limbic system structures, primarily the mesolimbic dopaminergic pathway (reward system).

Opioid receptors responsible for the suppression of pain impulses are most densely concentrated in the posterior horns of the spinal cord, thalamic nuclei, and periaqueductal gray matter (around the cerebral aqueduct).

Chronic depletion of catecholamine reserves (specifically dopamine) in mesolimbic structures leads to a weakening of physiological reinforcement and the development of tolerance.

Total impairment of basic renal functions leads to the retention of nitrogenous slag, toxic metabolites, and electrolytes in the body. This establishes the clinical and laboratory syndrome of uremia.

Changes in gas concentrations in inhaled air (oxygen deficiency or excess) are classified as chemical damaging environmental factors. Pressure drops represent a physical factor, while microbial toxins are biological.

Electric current is a physical phenomenon (directed movement of charged particles). Poisons and drugs are classified as chemical factors, whereas microorganisms are biological.

Acute blood loss reduces the oxygen-carrying capacity of the blood (hemic component), while hypoperfusion-induced acidosis and uncoupling of oxidation and phosphorylation impair oxygen utilization by cells (tissue component).

Severe hypoxia leads to the inactivation of antioxidant enzymes and a drop in the levels of non-enzymatic antioxidants (glutathione, vitamins E and C).

The Euler-Liljestrand reflex (hypoxic pulmonary vasoconstriction) provides local spasm of pulmonary arterioles in poorly ventilated areas. This redistributes blood flow to alveoli with normal oxygenation.

Ethanol and narcotic substances enter the body from the external environment; therefore, poisoning caused by them is classified as exogenous intoxication.

Ammonia vapors strongly irritate the trigeminal nerve endings in the upper respiratory tract mucosa, triggering the Kratschmer reflex—a reflex cessation of breathing (apnea).

A decrease in excitatory impulses to the respiratory center leads to alveolar hypoventilation. As a result, arterial oxygen tension drops (hypoxemia) and carbon dioxide accumulates (hypercapnia).

Blood stasis in the pulmonary veins (post-capillary block) in left heart pathology triggers Kitaev's reflex—spasm of the pulmonary arterioles (pre-capillary block). This protects capillaries from rupture but leads to mixed (post- and pre-capillary) pulmonary hypertension.

A decrease in blood albumin levels leads to a drop in plasma oncotic pressure. As a result, fluid shifts from the vascular bed into the interstitial space, forming edema.

Infectious kidney damage is caused by various biological agents capable of invasion and replication in tissues: bacteria, viruses, fungi, protozoa, and helminths.

Hypothermia and intercurrent infections cause vasoconstriction and stimulate the cytokine response, provoking the manifestation of immune complex-mediated glomerular injury in acute diffuse glomerulonephritis.

The deposition of circulating immune complexes activates the complement system and inflammation, leading to damage to all renal glomeruli.