Question From ( 51 To 100 )

Krok 1 Paper with Explanation

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Question From ( 51 To 100 )

51. A certain infectious agent can damage mucosa, cause inflammation of internal organs, sepsis, provoke formation of blue-green pus, and is quite resistant to most antibiotics. What pathogen is it?

A. Streptococcus mutants

B. Pseudomonas aeruginosa

C. Escherichia coli

D. Staphylococcus aureus

E. Proteus vulgaris

Answer: Pseudomonas aeruginosa

Explanation

The pathogen described in the question is Pseudomonas aeruginosa, which is known for causing a range of infections in humans. It can damage mucosal tissues, lead to inflammation of internal organs, cause sepsis (a severe bloodstream infection), and produce blue-green pus due to the production of pigments.

Pseudomonas aeruginosa is also known for its resistance to many antibiotics, making it a challenging pathogen to treat. It’s often associated with hospital-acquired infections and can affect individuals with weakened immune systems or those who have undergone invasive medical procedures

52. Nosocomial pneumonia was diagnosed in a 38-year-old inpatient. The doctor prescribed the patient a broad-spectrum antibiotic that is resistant to ß-lactamases, inhibits peptidoglycan synthesis in the bacterial membrane, and practically cannot be degraded by dehydropeptidase-1 in the renal tubules. What antibiotic did the patient receive?

A. Rifabutin

B. Erythromycin

C. Meropenem

D. Streptomycin

E. Levofloxacin

Answer:Meropenem

Explanation

Meropenem is a broad-spectrum antibiotic that belongs to the carbapenem class. It is resistant to β-lactamases, which are enzymes that can break down β-lactam antibiotics like penicillins and cephalosporins. Meropenem inhibits peptidoglycan synthesis in the bacterial cell wall, leading to cell wall disruption and bacterial death.

Additionally, it is not easily degraded by dehydropeptidase-1 in the renal tubules, which means it can be administered without the need for dose adjustments due to renal impairment.
Nosocomial pneumonia, which refers to pneumonia acquired in a healthcare setting, often requires broad-spectrum antibiotics like meropenem due to potential resistance of the causative pathogens to other antibiotics.

53. A patient presents with impaired twilight vision. What vitamin preparation should be prescribed to this patient?

A. Cyanocobalamin

B. Pyridoxine hydrochloride

C. Retinol acetate

D. Ascorbic acid

E. Nicotinic acid

Answer; Retinol acetate

Explanation

Impaired twilight vision is a symptom commonly associated with a deficiency in vitamin A. Vitamin A is essential for maintaining good vision, particularly in low light conditions. Retinol is a form of vitamin A that plays a crucial role in the function of the retina and is important for night vision.

54. A 44-year-old woman has arterial hypertension caused by a pheochromocytoma a tumor of the adrenal medulla. What group of antihypertensive drugs should be prescribed for this patient?

A. α-blockers

B. Ganglionic blockers

C. Sympatholytics

D. Calcium antagonists

E. B-blockers

Answer: α-blockers

Explanation

Pheochromocytoma is a tumor of the adrenal medulla that secretes excessive amounts of catecholamines, including adrenaline and noradrenaline. These hormones can lead to significant increases in blood pressure and cause symptoms of hypertension.

α-blockers are a group of antihypertensive drugs that work by blocking the effects of adrenaline and noradrenaline on α-adrenergic receptors. By doing so, they help to relax blood vessels and reduce blood pressure. They are particularly effective in managing the hypertension associated with pheochromocytoma, as they counteract the vasoconstrictive effects of the excess catecholamines

55. The height of a 10-year-old child is 178 cm, while the child’s weight is 64 kg. What endocrine gland is dysfunctional in the child, causing this condition?

A. Pituitary gland

B. Adrenal glands

C. Parathyroid gland

D. Gonads

E. Thyroid gland

Answer;Pituitary gland

Explanation

In this scenario, the child’s height of 178 cm and weight of 64 kg at the age of 10 years are unusually high for their age. This suggests a condition known as gigantism, which is characterized by excessive growth due to overproduction of growth hormone (GH) during childhood, often caused by a tumor in the pituitary gland.

However, your statement about the pituitary gland being dysfunctional is not entirely correct. In the context of gigantism, the pituitary gland is indeed involved, but it’s not exactly “dysfunctional.” Rather, it’s producing an excess amount of growth hormone due to the presence of a tumor.

So, while the pituitary gland is implicated in this scenario, it’s more accurate to say that the child’s condition is likely due to a pituitary adenoma (tumor) causing overproduction of growth hormone, leading to gigantism.

56. A patient was prescribed a drug with methionine to maintain liver function. Synthesis of what substance is ensured in this case?

A. Phosphatidylcholine

B. Citrate

C. Phosphatidylserine

D. Lactate

E. Pyruvate

Answer: Phosphatidylcholine

Explanation

Methionine is an essential amino acid that plays a crucial role in various biochemical processes in the body, including the synthesis of phosphatidylcholine. Phosphatidylcholine is a major component of cell membranes, particularly in liver cells, and is essential for maintaining proper liver function. It also plays a role in lipid metabolism and is involved in transporting fats within the body.Your answer choice A. Phosphatidylch

57. A patient has an injury of radiocarpal joint. What bones of the proximal row of the wrist (except the pisiform bone) form this joint?

A. Scaphoid, trapezoid, hamate

B. Trapezoid, hamate, lunate

C. Scaphoid, lunate, triquetral

D. –

E. Scaphoid, trapezoid, lunate

Answer: Scaphoid, lunate, triquetral

Explanation

The radiocarpal joint, also known as the wrist joint, is formed by the distal end of the radius and the proximal row of carpal bones. The bones of the proximal row that form this joint are the scaphoid, lunate, and triquetral. These bones articulate with the radius to allow for flexion, extension, adduction, and abduction movements of the wrist.

58. A patient has an abscess in the left inguinal region. The patient developed complaints of general weakness, fever that in the evening reaches 38.5°C and normalizes in the morning, and painful red skin in the area of abscess localization. What type of temperature curve can be observed in this patient?

A. Febris acontinua

B. Febris hectica

C. a continua

D. Febris remittens

E. Febris recurrens

Answer: Febris hectica

Explanation

Febris hectica, also known as hectic fever, is a type of temperature curve characterized by fluctuating fever spikes with a relatively high amplitude. It’s often seen in conditions such as abscesses, tuberculosis, or other chronic inflammatory processes. The fever spikes tend to have a pattern where the temperature is higher in the evening and lower in the morning, and this pattern can vary significantly over the course of the day.

59. A group of alpinists, who were climbing to the atitude of 5000 meters above sea level without oxygen equipment, developed tachycardia, decreased blood pressure, and rapid breathing. What hypoxia developed in the mountain climbers?

A. Hypoxemic hypoxia

B. Respiratory hypoxia

C. Circulatory hypoxia

D. Hemic hypoxia

E. Tissue hypoxia

Answer: Hypoxemic hypoxia

Explanation

Hypoxemic hypoxia, also known as hypoxia of the blood, occurs when there is a reduced partial pressure of oxygen (PaO2) in the arterial blood. This can happen at high altitudes due to the decrease in atmospheric pressure and oxygen availability. In the scenario of climbing to 5000 meters without supplemental oxygen, the decreased atmospheric pressure at that altitude leads to reduced oxygen saturation of hemoglobin in the blood, which causes symptoms like tachycardia, decreased blood pressure, and rapid breathing.

60. A 56-year-old patient complains of an acute pain attack in the area of the right ankle joint. Objectively, the joint is hyperemic, edematous, and hot to the touch. The levels of uric acid in the blood are elevated. For the treatment of this pathology, the doctor prescribed a drug that inhibits xanthine oxidase. What drug is it?

A. Theophylline

B. Allopurinol

C. Urolesan

D. Prednisolone

E. Diacarb (Acetazolamide)

Answer : Allopurinol

Explanation

Allopurinol is a medication commonly used to treat conditions like gout, which is characterized by elevated levels of uric acid in the blood. It works by inhibiting the enzyme xanthine oxidase, which is involved in the production of uric acid. By reducing the production of uric acid, allopurinol helps prevent the formation of uric acid crystals that can cause inflammation, pain, and other symptoms in joints, such as the acute pain attack described in the question

61. A 60-year-old woman has congestive heart failure with increased cardiac preload. What bioactive substance will be secreted by the heart in this case?

A. Vasopressin

B. Gastric inhibitory peptide

C. Aldosterone

D. Atrial natriuretic peptide

E. Angiotensin II

Answer: Atrial natriuretic peptide

Explanation

ANP is a hormone secreted by the heart in response to increased cardiac preload, which is often seen in conditions like congestive heart failure. ANP works to counteract the effects of increased preload by promoting vasodilation and increasing sodium and water excretion by the kidneys. This helps to reduce blood volume and relieve the strain on the heart.

62. A patient has been diagnosed with atrophy of masticatory muscles. This group of muscles is innervated by branches of the following cranial nerve:

A. Hypoglossal nerve

B. First branch of the trigeminal nerve

C. Motor branches of the VII cranial

nerve

D. Third branch of the trigeminal

nerve

E. Second branch of the trigeminal

nerve

Answer: Third branch of the trigeminal

nerve

Explanation

The masticatory muscles, including the temporalis, masseter, and medial pterygoid muscles, are innervated by the third branch of the trigeminal nerve, also known as the mandibular nerve. This nerve carries both sensory and motor fibers, supplying the muscles of mastication and transmitting sensory information from the lower jaw and parts of the face.

63. A patient has an attack of bronchospasm. What membrane cytoreceptors of bronchial smooth muscles should be stimulated to improve the patient’s condition?

A. Muscarinic acetylcholine receptors

B. Histamine H2 receptors

C. β-adrenergic receptors

D. Nicotinic acetylcholine receptors

E. α-adrenergic receptors

Answer: β-adrenergic receptors

Explanation

Bronchospasm, which involves the constriction of the airways, can be relieved by stimulating β-adrenergic receptors. Activation of these receptors by drugs like β2-adrenergic agonists (e.g., albuterol) leads to bronchodilation, relaxing the smooth muscles of the bronchioles and improving airflow in the lungs.

64. The parents with normal hearing have two daughters and a son, who are congenitally deaf. Their other 5 children are healthy. What is the pattern of deafness inheritance in this case?

A. Y-linked

B. Autosomal recessive

C. X-linked recessive

D. Autosomal dominant

E. X-linked dominant

Answer: Autosomal recessive

Explanation

In this case, the parents are carriers of a recessive allele for deafness. Since they have two daughters and a son with congenital deafness while their other children are healthy, it suggests that both parents are carriers of the deafness gene (heterozygous) and that the deafness inheritance follows an autosomal recessive pattern.

65. A woman was diagnosed with Chlamydia-induced pneumonia. The doctor prescribed her antibiotic doxycycline. What type of pharmacotherapy is it?

A. Symptomatic

B. Pathogenetic

C. Etiotropic

D. Preventive

E. Replacement

Answer: Etiotropic

Explanation

Etiotropic pharmacotherapy refers to the treatment of a disease by targeting the underlying cause or etiology. In this case, the woman has Chlamydia-induced pneumonia, and the antibiotic doxycycline is specifically chosen to target and eliminate the Chlamydia bacteria responsible for the infection. This type of treatment directly addresses the cause of the disease.

66. Analysis of the patient’s ECG recorded in the I, II, and III standard leads shows that the P wave is positive in each one of them What does it indicate?

A. Atrial depolarization rate

B. Mitral valve condition

C. Pumping function of the left side of

the heart

D. Direction of atrial depolarization

E. Ventricular depolarization rate

Answer: Direction of atrial depolarization

Explanation

The P wave in an electrocardiogram (ECG) represents the atrial depolarization (contraction) of the heart. The fact that the P wave is positive in all standard leads (I, II, and III) indicates that the electrical depolarization is moving in a consistent direction across those leads. This suggests a normal sequence of atrial depolarization, which starts at the sinoatrial (SA) node and spreads through the atria.

67. A patient with a suspected systemic disease underwent a biopsy of an area of increased density and immobility in the skin. In the dermis, the study detected all types of connective tissue disorganization with a weak cellular reaction, gross sclerosis, and hyalinosis. What disease can be characterized by these pathological changes?

A. Scleroderma

B. Systemic lupus erythematosus

C. Dermatofibroma

D. Polyarteritis nodosa

E. Psoriasi

Answer: Scleroderma

Explanation

The described pathological changes of increased density, immobility in the skin, connective tissue disorganization, sclerosis, and hyalinosis are characteristic of scleroderma (also known as systemic sclerosis). Scleroderma is a systemic autoimmune disorder that affects the connective tissues and can lead to skin hardening, joint stiffness, and damage to various internal organs.

68. A patient had her tooth extracted in a dental clinic. Stratified squamous epithelium regenerated two weeks later. What organelles took part in the restoration of the mucosa?

A. Centrosomes

B. Mitochondria

C. Postlysosomes

D. Smooth endoplasmic reticulum

E. Ribosomes

Answer: Ribosomes

Explanation

Ribosomes are cellular organelles responsible for protein synthesis. In the case of tissue regeneration, including the regeneration of stratified squamous epithelium after tooth extraction, protein synthesis is a crucial process. New proteins are needed for cell growth, division, and tissue repair. Ribosomes play a central role in translating the genetic information from mRNA into functional proteins..

69. What period of the malaria plasmodium life cycle coincides with the manifestation of clinical symptoms of malaria in a patient?

A. When merozoites emerge from

destroyed erythrocytes

B. During gametocyte formation

erythrocytes

C. When merozoites invade

erythrocytes

D. When sporozoites enter the human

bloodstream

E. In the period of tissue schizogony

Answer: When merozoites emerge from

destroyed erythrocytes

Explanation

In the life cycle of Plasmodium, the parasite responsible for malaria, the manifestation of clinical symptoms coincides with the release of merozoites from the destroyed red blood cells. This stage is associated with fever, chills, and other symptoms characteristic of malaria.

70. A patient has been diagnosed with psychosis. After two weeks of receiving pharmacotherapy, the patient’s condition improved. However, the patient soon developed rigidity, tremors, and hypokinesia. What drug causes these complications?

A. Chlordiazepoxide

B. Sydnocarb (Mesocarb)

C. Imizin (Imipramine)

D. Diphenin (Phenytoin)

E. Aminazine (Chlorpromazine)

Answer; Aminazine (Chlorpromazine)

Explanation

Aminazine (also known as Chlorpromazine) is a typical antipsychotic medication used to treat various psychiatric disorders, including psychosis. However, it can also cause extrapyramidal side effects, which include rigidity, tremors, and hypokinesia (reduced voluntary movements). These side effects are often collectively referred to as parkinsonism or extrapyramidal symptoms and are related to the drug’s effects on dopamine receptors in the brain.

71. Some parasites may have a host in their life cycle that accumulates the parasite in its invasive stage and aids in its transmission to the final host. What type of host is it?

A. Definitive host
B. Additional host
C. Moderator base
D. Reservoir host
E. Optional host

Correct Answer: D. Reservoir host

Explanation:

A reservoir host is an organism that harbors a parasite and serves as a source of infection for other susceptible hosts, including the definitive host (where the parasite reaches sexual maturity). The reservoir host maintains the parasite in nature, often without severe disease, and plays a role in transmitting the parasite to its final host.

In this case, the question describes a host that accumulates the parasite in its invasive stage and helps in transmission to the final host, which is a key function of a reservoir host.

Why the other options are incorrect:

A. Definitive host:

The definitive host is where the parasite reaches maturity and reproduces sexually. This does not match the description of a host that simply accumulates and transmits the parasite.

B. Additional host:

There is no widely accepted concept of an “additional host” in parasitology. This term is not commonly used to describe host roles in parasite transmission.

C. Moderator base:

This is not a standard parasitological term. It may be a mistranslation or an incorrect term.

E. Optional host:

The term “optional host” is not used in parasitology. Instead, terms like definitive, intermediate, paratenic, and reservoir hosts are used to describe different roles in the parasite life cycle.

Summary:

The reservoir host harbors the parasite and serves as a source for its transmission to the definitive host, making option D the correct answer.

72. The human brain produces endogenous peptides similar to morphine that can reduce pain perception. Select such peptides from the list below.

A. Endorphin
B. Vasopressin
C. Statin
D. Liberin
E. Oxytocin

Correct Answer: A. Endorphin

Explanation:

Endorphins are endogenous opioid peptides produced by the brain that act as natural painkillers. They bind to opioid receptors in the brain and spinal cord, reducing the perception of pain and promoting feelings of euphoria and well-being, similar to morphine and other opioids.

Endorphins are released during:

Exercise (commonly called the “runner’s high”)
Stress and pain
Excitement and laughter
Emotional experiences

They play a significant role in pain modulation and emotional well-being.

Why the other options are incorrect:

🔴 B. Vasopressin:
Vasopressin (antidiuretic hormone, ADH) helps regulate water balance and blood pressure but does not function as a painkiller.

🔴 C. Statin:
Statins are cholesterol-lowering drugs and are not involved in pain perception.

🔴 D. Liberin:
Liberins (also called releasing hormones) are regulatory peptides that control hormone secretion from the pituitary gland, but they do not have opioid-like effects.

🔴 E. Oxytocin:
Oxytocin is involved in childbirth, lactation, and social bonding, but it does not function as a natural painkiller like endorphins.

Summary:

Endorphins are natural pain-relieving peptides produced by the brain, similar to morphine. Thus, the correct answer is A. Endorphin. ✅

73. A person was hospitalized with morphine poisoning. A specific antagonist, naloxone, is used in acute morphine poisoning. What is the main factor in the development of antagonist measures in such cases?

A. Competition for binding to opioid receptors
B. Direct stimulation of respiratory metabolism
C. Strong acceleration of morphine metabolism
D. Decreased sensitivity of the body to morphine
E. Reflex excitation of the respiratory center

Correct Answer: ✅ A. Competition for binding to opioid receptors

Explanation:

Naloxone is an opioid antagonist that works by competitively binding to opioid receptors, particularly the mu (μ) receptors, where morphine and other opioids exert their effects. Since naloxone has a higher affinity for these receptors than morphine, it displaces morphine from the receptor sites, thereby reversing its effects, such as respiratory depression and sedation.

Naloxone is used in emergency settings for opioid overdose because it quickly restores normal breathing in patients experiencing opioid-induced respiratory depression.

Why the other options are incorrect:

🔴 B. Direct stimulation of respiratory metabolism:
Naloxone does not directly stimulate respiratory metabolism. Instead, it counteracts opioid-induced respiratory depression by displacing opioids from their receptors.

🔴 C. Strong acceleration of morphine metabolism:
Naloxone does not metabolize morphine or accelerate its breakdown. It blocks its effects rather than eliminating it from the body.

🔴 D. Decreased sensitivity of the body to morphine:
Naloxone does not alter the body’s sensitivity to morphine. It simply prevents morphine from acting on opioid receptors.

🔴 E. Reflex excitation of the respiratory center:
Naloxone does not work through reflex mechanisms but rather through direct receptor competition at opioid receptors.

Summary:

Naloxone works by competing with morphine for opioid receptor binding, effectively reversing opioid effects.
Thus, the correct answer is A. Competition for binding to opioid receptors. ✅

74. A 15-year-old patient complains of general weakness, dizziness, and rapid fatigability. The examination reveals a changed shape of the erythrocytes and a reduced number of erythrocytes. A preliminary diagnosis of sickle cell anemia was made. What amino acid exchange occurs in hemoglobin and causes the development of this pathological condition?

A. Valine becomes replaced with aspartate
B. Valine becomes replaced with glutamate
C. Glutamate becomes replaced with alanine
D. Glutamate becomes replaced with valine
E. Glutamate becomes replaced with aspartate

Correct Answer: ✅ D. Glutamate becomes replaced with valine

Explanation:

Sickle cell anemia is caused by a point mutation in the β-globin gene (HBB) on chromosome 11. This mutation results in the substitution of glutamic acid (glutamate) with valine at position 6 of the β-globin chain of hemoglobin (HbS instead of normal HbA).

Normal hemoglobin (HbA): Contains glutamate at position 6.
Sickle hemoglobin (HbS): Has valine instead of glutamate.

Since glutamate is hydrophilic, while valine is hydrophobic, this substitution causes hemoglobin molecules to stick together under low oxygen conditions, forming rigid fibers that distort red blood cells into a sickle shape. These sickle-shaped cells can block blood vessels, leading to pain crises, anemia, and organ damage.

Why the other options are incorrect:

🔴 A. Valine becomes replaced with aspartate:
Incorrect. The mutation in sickle cell anemia involves the substitution of glutamate (not valine) with valine.

🔴 B. Valine becomes replaced with glutamate:
Incorrect. The correct mutation involves the replacement of glutamate with valine, not the other way around.

🔴 C. Glutamate becomes replaced with alanine:
Incorrect. The substitution in sickle cell anemia is glutamate to valine, not alanine.

🔴 E. Glutamate becomes replaced with aspartate:
Incorrect. Aspartate is also negatively charged like glutamate, so this substitution would not cause the same structural changes as valine substitution.

Summary:

Sickle cell anemia results from a point mutation in the β-globin gene, where glutamate is replaced by valine at position 6, leading to the formation of abnormal hemoglobin (HbS) and sickle-shaped red blood cells.

Thus, the correct answer is D. Glutamate becomes replaced with valine. ✅

75. In the nucleus, a larger molecule of immature mRNA has been converted into a smaller molecule of mature mRNA. The stages of this transformation are:

A. Translation
B. Recognition
C. Termination
D. Processing
E. Replication

Correct Answer: ✅ D. Processing

Explanation:

The transformation of immature (pre-mRNA) into mature mRNA occurs through a process called mRNA processing, which takes place in the nucleus before the mRNA is transported to the cytoplasm for translation.

The key steps of mRNA processing include:

1️⃣ Capping: A 7-methylguanosine (m7G) cap is added to the 5′ end of the mRNA to protect it from degradation and assist in ribosome binding during translation.

2️⃣ Splicing:

The introns (non-coding sequences) are removed.
The exons (coding sequences) are joined together.
This results in a shorter mature mRNA molecule that contains only coding sequences.

3️⃣ Polyadenylation: A poly(A) tail (several adenine nucleotides) is added to the 3′ end to increase stability and regulate translation.

Why the other options are incorrect:

🔴 A. Translation:
Incorrect. Translation is the process of protein synthesis that occurs in the cytoplasm, not in the nucleus. It converts mRNA into protein, not pre-mRNA into mature mRNA.

🔴 B. Recognition:
Incorrect. Recognition refers to the binding of ribosomes to mRNA or tRNA matching with codons during translation, but it does not involve mRNA processing.

🔴 C. Termination:
Incorrect. Termination occurs at the end of transcription (RNA synthesis) or translation (protein synthesis). It does not involve the conversion of pre-mRNA to mature mRNA.

🔴 E. Replication:
Incorrect. Replication refers to DNA synthesis, where DNA makes a copy of itself. It is unrelated to mRNA maturation.

Summary:

The process of mRNA processing includes capping, splicing (removing introns), and polyadenylation, which results in a smaller, mature mRNA molecule.

Thus, the correct answer is D. Processing. ✅

76. A 19-year-old man presents with diarrhea. As part of complex therapy, the doctor prescribed an antidiarrheal drug that stimulates opioid receptors in the intestine. What medication was prescribed for this patient?

A. Furazolidone
B. Loperamide
C. Linex
D. Rehydron
E. Omnopon (Papaveretum)

Correct Answer: ✅ B. Loperamide

Explanation:

Loperamide is a synthetic opioid receptor agonist that acts selectively on the intestinal wall, reducing peristalsis and increasing the absorption of water and electrolytes. Unlike other opioids, it does not cross the blood-brain barrier, so it does not have central opioid effects like euphoria or respiratory depression.

Loperamide is commonly used for:

Acute and chronic diarrhea
Irritable bowel syndrome (IBS) with diarrhea

It works by:
✔ Activating opioid receptors in the intestines → Slows down bowel movements
✔ Increasing absorption of fluids → Reduces diarrhea

Why the other options are incorrect:

🔴 A. Furazolidone:
Incorrect. Furazolidone is an antimicrobial drug used for bacterial and protozoal infections (e.g., giardiasis, dysentery). It does not work by stimulating opioid receptors.

🔴 C. Linex:
Incorrect. Linex is a probiotic used to restore gut flora after infections or antibiotic use. It does not stop diarrhea directly by acting on opioid receptors.

🔴 D. Rehydron:
Incorrect. Rehydron is an oral rehydration solution (ORS) used to replace fluids and electrolytes lost during diarrhea but does not stop diarrhea itself.

🔴 E. Omnopon (Papaveretum):
Incorrect. Omnopon is an opioid analgesic (mixture of morphine alkaloids) used for pain relief, but it has strong central opioid effects and is not commonly used for diarrhea due to its addiction potential.

Summary:

Loperamide is an opioid receptor agonist that selectively acts on the intestines to reduce diarrhea without significant central nervous system effects.

Thus, the correct answer is B. Loperamide. ✅

77. A patient presents with impaired renal water reabsorption that is directly related to impaired secretion of a particular hormone. Name that hormone.

A. Natriuretic hormone
B. Thyrocalcitonin
C. Parathyroid hormone
D. Aldosterone
E. Vasopressin

Correct Answer: E. Vasopressin

Explanation:

Vasopressin, also known as antidiuretic hormone (ADH), is produced by the hypothalamus and released from the posterior pituitary gland. It plays a crucial role in water reabsorption by increasing the permeability of the collecting ducts in the kidneys. A deficiency in vasopressin leads to diabetes insipidus, which is characterized by excessive urination (polyuria) and dehydration.

Vasopressin works by:
✔ Stimulating aquaporin channels in the renal collecting ducts → Increases water reabsorption
✔ Reduces urine output → Prevents dehydration
✔ Maintains blood osmolarity → Helps regulate body fluid balance

Why the other options are incorrect:

🔴 A. Natriuretic hormone:
Incorrect. Natriuretic peptides (ANP, BNP) promote sodium and water excretion, reducing blood volume and pressure. They oppose vasopressin’s action.

🔴 B. Thyrocalcitonin (Calcitonin):
Incorrect. Calcitonin regulates calcium metabolism by lowering blood calcium levels but does not influence kidney water reabsorption.

🔴 C. Parathyroid hormone (PTH):
Incorrect. PTH regulates calcium and phosphate balance in the bones and kidneys but does not control water retention.

🔴 D. Aldosterone:
Incorrect. Aldosterone regulates sodium and potassium balance in the kidneys. It indirectly affects water retention by promoting sodium reabsorption but does not act directly on water reabsorption like vasopressin.

Summary:

Vasopressin (ADH) is the key hormone responsible for water reabsorption in the kidneys. A deficiency leads to excessive urination and dehydration.

Thus, the correct answer is E. Vasopressin. ✅

78. The patient’s body fluids, especially urine, have a particularly sweet odor caused by an abnormal metabolism of certain amino acids such as leucine, isoleucine, and valine. What disease can be characterized by these pathological changes?

A. Maple syrup urine disease
B. Alkaptonuria
C. Galactosemia
D. Phenylketonuria
E. Fructosuria

Correct Answer: ✅ A. Maple syrup urine disease

Explanation:

Maple syrup urine disease (MSUD) is a rare inherited metabolic disorder caused by a deficiency in the branched-chain alpha-keto acid dehydrogenase (BCKD) complex. This enzyme is responsible for breaking down the branched-chain amino acids leucine, isoleucine, and valine. When this enzyme is deficient, these amino acids and their toxic byproducts accumulate in the body, leading to severe neurological symptoms and the characteristic sweet or burnt sugar odor in urine, similar to maple syrup.

Common clinical features of MSUD:
✔ Sweet-smelling urine (maple syrup odor)
✔ Poor feeding, vomiting
✔ Lethargy, irritability
✔ Developmental delay
✔ Seizures, coma if untreated

Early diagnosis and dietary management (restriction of branched-chain amino acids) are crucial to prevent neurological damage.

Why the other options are incorrect:

🔴 B. Alkaptonuria:
Incorrect. Alkaptonuria is caused by a deficiency of homogentisate oxidase, leading to homogentisic acid accumulation, which darkens urine upon standing and causes ochronosis (dark pigmentation of connective tissues), not a sweet urine odor.

🔴 C. Galactosemia:
Incorrect. Galactosemia is due to a deficiency of galactose-1-phosphate uridyltransferase (GALT), leading to an inability to metabolize galactose. Symptoms include cataracts, liver failure, and intellectual disability, but not sweet-smelling urine.

🔴 D. Phenylketonuria (PKU):
Incorrect. PKU is caused by a deficiency in phenylalanine hydroxylase, leading to the accumulation of phenylalanine. It is characterized by a musty or mousy urine odor, not a sweet one.

🔴 E. Fructosuria:
Incorrect. Fructosuria results from a deficiency in fructokinase, leading to fructose accumulation in urine, but it is a benign condition and does not cause a sweet maple syrup-like odor.

Summary:

Maple syrup urine disease (MSUD) is an inherited metabolic disorder that results in the accumulation of leucine, isoleucine, and valine, causing a characteristic sweet-smelling urine. This is due to a deficiency of branched-chain alpha-keto acid dehydrogenase (BCKD).

Thus, the correct answer is A. Maple syrup urine disease. ✅

79. On examination, a polyp was found in the distal part of the patient’s colon. Where is the polyp located?

A. Rectum
B. Caecum
C. Transverse colon
D. Sigmoid colon
E. Descending colon

Correct Answer: ✅ A. Rectum

Explanation:

The distal part of the colon refers to the section closest to the anus. Anatomically, the colon is divided into the ascending, transverse, descending, sigmoid colon, and rectum.

The rectum is the final and most distal part of the large intestine before the anus, making it the most likely location of the polyp described in the question.
Polyps in the rectum are common and may be benign (adenomatous or hyperplastic polyps) or malignant (colorectal cancer).

Why the other options are incorrect:

🔴 B. Caecum:
Incorrect. The caecum is the proximal (beginning) part of the large intestine, located in the right lower abdomen. It is not part of the distal colon.

🔴 C. Transverse colon:
Incorrect. The transverse colon is located in the mid-abdomen and is part of the middle section of the large intestine, not the distal part.

🔴 D. Sigmoid colon:
Incorrect. While the sigmoid colon is near the rectum, it is not the most distal part. The rectum follows the sigmoid colon, making it the true distal location.

🔴 E. Descending colon:
Incorrect. The descending colon is located on the left side of the abdomen and transitions into the sigmoid colon before reaching the rectum. It is not the most distal part.

Summary:

The rectum is the most distal part of the colon, making it the correct answer. Polyps found here are common and may require further evaluation for potential malignancy.

Thus, the correct answer is A. Rectum. ✅

80. Examination of a 32-year-old man revealed disproportionate skeletal structure and enlarged brow bones, nose, lips, tongue, jawbones, and feet. What is the likely cause for the development of these disorders?

A. Increased glucagon levels
B. Increased thyroxine levels
C. Increased levels of somatotropic hormone
D. Decreased insulin levels
E. Increased catecholamine levels

Correct Answer: ✅ C. Increased levels of somatotropic hormone

Explanation:

The patient’s symptoms are characteristic of acromegaly, a disorder caused by excessive secretion of growth hormone (GH, also called somatotropic hormone) in adulthood. Acromegaly is most commonly due to a pituitary adenoma that secretes GH.

Key features of acromegaly include:
✔ Enlarged facial features (brow bones, nose, lips, jaw)
✔ Enlarged hands and feet
✔ Thickened skin
✔ Joint pain and organ enlargement (cardiomegaly, hepatomegaly)
✔ Increased risk of diabetes mellitus and hypertension

In children, excess GH causes gigantism (excessive linear growth), while in adults, it leads to acromegaly, as the long bones have already fused.

Why the other options are incorrect:

🔴 A. Increased glucagon levels:
Incorrect. Glucagon is a hormone that increases blood glucose levels but does not cause excessive growth or skeletal changes.

🔴 B. Increased thyroxine levels:
Incorrect. Excess thyroxine (hyperthyroidism) leads to weight loss, tachycardia, heat intolerance, and nervousness, but not skeletal overgrowth or facial enlargement.

🔴 D. Decreased insulin levels:
Incorrect. Decreased insulin levels are associated with diabetes mellitus, which can lead to weight loss and high blood sugar but does not cause skeletal overgrowth.

🔴 E. Increased catecholamine levels:
Incorrect. Increased catecholamines (as seen in pheochromocytoma) cause symptoms like hypertension, sweating, and palpitations but do not cause abnormal skeletal growth.

Summary:

Acromegaly is caused by excessive secretion of somatotropic hormone (GH) in adults, leading to enlarged facial bones, jaw, hands, and feet. This condition is usually due to a pituitary adenoma.

Thus, the correct answer is C. Increased levels of somatotropic hormone. ✅

81. The mother complains that her 7-month-old child has recurrent bacterial infections, such as conjunctivitis, otitis, sinopulmonary infections, diarrhea, and skin infections. Examination detects reduced size of the child’s tonsils and lymph nodes. In the blood, examination of serum immunoglobulins shows noticeably reduced levels of IgM, IgA, and IgE, with IgG less than 100 mg/dL. What disease can be characterized by these pathological changes?

A. DiGeorge syndrome
B. Wiskott-Aldrich syndrome
C. X-linked agammaglobulinemia (Bruton disease)
D. Hereditary adenosine deaminase defect in T lymphocytes
E. Hypogammaglobulinemia

Correct Answer: ✅ C. X-linked agammaglobulinemia (Bruton disease)

Explanation:

X-linked agammaglobulinemia (Bruton disease) is a primary immunodeficiency disorder caused by a mutation in the BTK (Bruton tyrosine kinase) gene, leading to a failure in B-cell maturation.

Key Features:
✔ Recurrent bacterial infections (otitis, pneumonia, diarrhea, skin infections) due to lack of antibodies
✔ Low or absent B cells in peripheral blood
✔ Very low levels of all immunoglobulins (IgG, IgM, IgA, IgE)
✔ Small or absent tonsils and lymph nodes (due to the absence of mature B cells)
✔ Symptoms begin after 6 months of age, when maternal IgG levels decline

Why the other options are incorrect:

🔴 A. DiGeorge syndrome:
Incorrect. DiGeorge syndrome results from 22q11.2 deletion, leading to a T-cell deficiency due to thymic hypoplasia. It is associated with hypocalcemia, congenital heart defects, and facial abnormalities but does not primarily cause agammaglobulinemia.

🔴 B. Wiskott-Aldrich syndrome:
Incorrect. This X-linked disorder is characterized by eczema, thrombocytopenia, and recurrent infections. Immunoglobulin levels show low IgM but high IgA and IgE, which is different from Bruton disease.

🔴 D. Hereditary adenosine deaminase defect in T lymphocytes:
Incorrect. This refers to Severe Combined Immunodeficiency (SCID) due to an adenosine deaminase (ADA) deficiency, leading to both T-cell and B-cell dysfunction, resulting in severe viral, bacterial, and fungal infections.

🔴 E. Hypogammaglobulinemia:
Incorrect. Hypogammaglobulinemia is a general term for low immunoglobulin levels. However, Bruton disease is a specific primary immunodeficiency disorder caused by defective B-cell maturation.

Summary:

Bruton disease (X-linked agammaglobulinemia) is caused by a mutation in the BTK gene, preventing B-cell maturation. It leads to recurrent bacterial infections in infants after maternal antibodies decline, with low IgG, IgM, IgA, and IgE and absent tonsils/lymph nodes.

Thus, the correct answer is C. X-linked agammaglobulinemia (Bruton disease). ✅

82. A 38-year-old patient died with multiple thromboembolisms of various organs. In the cardiac tissue, macrophage granulomas were detected in the valvular and parietal endocardium with endocardial damage and deposition of thrombotic masses. Macrophage granulomas were detected in the myocardium as well. These pathological changes are characteristic of the following disease:

A. Rheumatism
B. Atherosclerosis
C. Essential hypertension
D. Systemic lupus erythematosus
E. Infectious myocarditis

Correct Answer: ✅ A. Rheumatism

Explanation:

Rheumatic heart disease is a complication of rheumatic fever, an autoimmune reaction following a Streptococcus pyogenes (Group A Streptococcus) infection. It mainly affects the heart valves and myocardium.

Key pathological findings:
✔ Aschoff bodies (macrophage granulomas) in the myocardium
✔ Endocardial damage with thrombotic deposits → leads to valvular dysfunction (mitral stenosis most common)
✔ Multiorgan thromboembolic events due to vegetations on heart valves

Rheumatic fever follows the Jones criteria, which include:
✔ Carditis (valvular and myocardial involvement)
✔ Polyarthritis
✔ Subcutaneous nodules
✔ Erythema marginatum
✔ Sydenham chorea

Why the other options are incorrect:

🔴 B. Atherosclerosis:
Incorrect. Atherosclerosis primarily affects large arteries, leading to plaques and thrombus formation, but does not cause macrophage granulomas in the myocardium.

🔴 C. Essential hypertension:
Incorrect. Hypertension leads to left ventricular hypertrophy and vascular damage but does not cause endocardial damage, thrombotic masses, or macrophage granulomas.

🔴 D. Systemic lupus erythematosus (SLE):
Incorrect. SLE can cause Libman-Sacks endocarditis, which involves non-infectious vegetations but does not typically present with macrophage granulomas in the myocardium.

🔴 E. Infectious myocarditis:
Incorrect. Infectious myocarditis (e.g., viral myocarditis) is characterized by lymphocytic infiltration, rather than macrophage granulomas and thrombotic vegetations.

Summary:

Rheumatic heart disease is an autoimmune consequence of rheumatic fever, causing macrophage granulomas (Aschoff bodies), valvular damage, and thromboembolism.

Thus, the correct answer is A. Rheumatism. ✅

83. A 55-year-old patient is being monitored by an endocrinologist for disturbed endocrine function of the pancreas, which manifests as a decrease in glucagon levels in the blood. What pancreatic cells are dysfunctional in this case?

A. PP cells of the islets of Langerhans
B. Delta-1 cells of the islets of Langerhans
C. Alpha cells of the islets of Langerhans
D. Beta cells of the islets of Langerhans
E. Delta cells of the islets of Langerhans

Correct Answer: ✅ C. Alpha cells of the islets of Langerhans

Explanation:

Glucagon is a hormone responsible for increasing blood glucose levels by stimulating glycogenolysis and gluconeogenesis in the liver. It is secreted by alpha (α) cells of the islets of Langerhans in the pancreas.

When alpha cells are dysfunctional, glucagon secretion decreases, leading to hypoglycemia and impaired glucose homeostasis.

Key functions of glucagon:
✔ Stimulates the breakdown of glycogen (glycogenolysis)
✔ Increases glucose production (gluconeogenesis)
✔ Inhibits glycolysis in the liver
✔ Promotes lipolysis

Why the other options are incorrect:

🔴 A. PP cells of the islets of Langerhans:
Incorrect. PP (pancreatic polypeptide) cells secrete pancreatic polypeptide, which regulates exocrine and endocrine pancreatic functions but has no role in glucagon production.

🔴 B. Delta-1 cells of the islets of Langerhans:
Incorrect. Delta-1 cells are involved in somatostatin secretion, which regulates insulin and glucagon release, but they do not produce glucagon.

🔴 D. Beta cells of the islets of Langerhans:
Incorrect. Beta (β) cells secrete insulin, which lowers blood glucose. Dysfunction of beta cells leads to diabetes mellitus, not a decrease in glucagon.

🔴 E. Delta cells of the islets of Langerhans:
Incorrect. Delta (δ) cells produce somatostatin, which inhibits both insulin and glucagon secretion, but they are not directly responsible for glucagon production.

Summary:

Glucagon is produced by alpha cells of the islets of Langerhans, which play a critical role in raising blood glucose levels. Dysfunction of alpha cells leads to decreased glucagon secretion and impaired glucose metabolism.

Thus, the correct answer is C. Alpha cells of the islets of Langerhans. ✅

84. Examination detected the following changes in the patient’s peripheral blood: erythrocytes 3.0 1012/L, Hb-80 g/L, leukocytes 21*10^9/L. The following is observed in the leukogram: basophils 0%, eosinophils – 0%, myeloblasts 54%, promyelocytes 1%, myelocytes 0%, metamyelocytes 0%, band neutrophil 1%, segmented neutrophils – 28%, lymphocytes 13%, monocytes 3%. What pathology corresponds with these findings?

A. Undifferentiated leukemia
B. Erythromyelosis
C. Acute myeloblastic leukemia
D. Chronic myeloid leukemia
E. Leukemoid reaction

Correct Answer: ✅ C. Acute Myeloblastic Leukemia (AML)

Explanation:

Acute Myeloblastic Leukemia (AML) is a type of hematologic malignancy characterized by the proliferation of myeloblasts in the bone marrow and peripheral blood.

The key findings that support AML in this case are:
✔ Very high myeloblast count (54%) → Myeloblasts are immature precursors of white blood cells and should not normally be seen in such high percentages in peripheral blood.
✔ Severe anemia (low Hb: 80 g/L) → Common in leukemia due to bone marrow failure.
✔ Leukocytosis (high WBC count: 21 × 10⁹/L) → Suggests abnormal proliferation of white blood cells.
✔ Absence of eosinophils and basophils → Consistent with AML.

Why the other options are incorrect:

🔴 A. Undifferentiated leukemia:
Incorrect. Undifferentiated leukemia involves immature blast cells that lack differentiation into a specific lineage (myeloid or lymphoid). In this case, the high presence of myeloblasts confirms a myeloid lineage, ruling out undifferentiated leukemia.

🔴 B. Erythromyelosis (Di Guglielmo’s Syndrome):
Incorrect. This is a rare acute erythroid leukemia with a predominance of erythroblasts rather than myeloblasts. The given case does not show excessive erythroid precursors.

🔴 D. Chronic Myeloid Leukemia (CML):
Incorrect. CML typically presents with a mix of mature and immature myeloid cells (promyelocytes, myelocytes, and metamyelocytes), but in this case, there is a predominance of myeloblasts (54%), which is characteristic of acute leukemia, not chronic.

🔴 E. Leukemoid Reaction:
Incorrect. Leukemoid reactions are benign, reactive increases in WBC count due to severe infections, trauma, or stress. They do not present with such a high percentage of myeloblasts (>20% blasts in blood or bone marrow indicates leukemia).

Summary:

The presence of >20% myeloblasts in the peripheral blood, along with anemia and leukocytosis, strongly suggests Acute Myeloblastic Leukemia (AML). This condition requires urgent medical attention and treatment with chemotherapy or bone marrow transplantation.

Thus, the correct answer is C. Acute Myeloblastic Leukemia. ✅

85. Chemically, thyroid hormones (thyroxine and triiodothyronine) are amino acid derivatives. Name this amino acid.

A. Threonine
B. Methionine
C. Proline
D. Tyrosine
E. Tryptophan

Correct Answer: ✅ D. Tyrosine

Explanation:

Thyroid hormones, thyroxine (T₄) and triiodothyronine (T₃), are derivatives of the amino acid tyrosine. They are synthesized in the thyroid gland by the iodination of tyrosine residues in thyroglobulin.

✔ Tyrosine undergoes iodination → Forms monoiodotyrosine (MIT) and diiodotyrosine (DIT)
✔ Combination of MIT and DIT leads to T₃ (triiodothyronine) and T₄ (thyroxine)
✔ T₄ is converted into the more active T₃ in peripheral tissues

Why the other options are incorrect:

🔴 A. Threonine:
Incorrect. Threonine is an essential amino acid but does not play a role in thyroid hormone synthesis.

🔴 B. Methionine:
Incorrect. Methionine is involved in methylation reactions and is a precursor for S-adenosylmethionine (SAM) but not for thyroid hormones.

🔴 C. Proline:
Incorrect. Proline is crucial for collagen synthesis but has no role in thyroid hormone production.

🔴 E. Tryptophan:
Incorrect. Tryptophan is the precursor for serotonin and melatonin, not thyroid hormones.

Summary:

Thyroid hormones T₃ and T₄ are synthesized from tyrosine in the thyroid gland through iodination and coupling reactions.

Thus, the correct answer is D. Tyrosine. ✅

86. A patient has been diagnosed with mitral valve stenosis. What pathogenetic type of heart failure is it?

A. Heart failure due to myocardial damage
B. Heart failure due to myocardial hypertrophy
C. Volume overload-induced heart failure
D. Mixed form of heart failure
E. Pressure overload-induced heart failure

Correct Answer: ✅ E. Pressure overload-induced heart failure

Explanation:

Mitral valve stenosis leads to increased resistance to blood flow from the left atrium to the left ventricle, causing:
✔ Increased left atrial pressure → Leads to left atrial hypertrophy and dilation
✔ Pulmonary congestion → Can result in pulmonary hypertension and right ventricular overload
✔ Increased pressure load on the right heart → Can progress to right-sided heart failure

Since mitral stenosis restricts blood flow and increases pressure in the left atrium and pulmonary circulation, it primarily falls under pressure overload-induced heart failure.

Why the other options are incorrect:

🔴 A. Heart failure due to myocardial damage:
Incorrect. This type of heart failure occurs due to direct damage to the heart muscle, such as in myocardial infarction or myocarditis, not mitral stenosis.

🔴 B. Heart failure due to myocardial hypertrophy:
Incorrect. While hypertrophy can develop in response to stenosis, the primary cause of heart failure in mitral stenosis is pressure overload, not hypertrophy.

🔴 C. Volume overload-induced heart failure:
Incorrect. Volume overload occurs due to valvular regurgitation (e.g., mitral or aortic regurgitation) rather than stenosis. Mitral stenosis leads to pressure overload, not volume overload.

🔴 D. Mixed form of heart failure:
Incorrect. A mixed form includes both systolic and diastolic dysfunction due to combined pressure and volume overload. Mitral stenosis is primarily a pressure overload condition.

Summary:

Mitral valve stenosis increases left atrial pressure, leading to pulmonary congestion and right-sided heart failure due to pressure overload.

Thus, the correct answer is E. Pressure overload-induced heart failure. ✅

87. Examination of a patient shows decreased leukocyte and erythrocyte count and low hemoglobin levels in the peripheral blood, as well as the appearance of large cells (megaloblasts). What vitamin is likely to be deficient in this case, causing this condition?

A. Biotin
B. Folic acid
C. Riboflavin
D. Niacin
E. Ascorbic acid

Correct Answer: ✅ B. Folic acid

Explanation:

Folic acid (vitamin B9) is essential for DNA synthesis and red blood cell formation. A deficiency leads to megaloblastic anemia, characterized by:
✔ Macrocytosis (large red blood cells)
✔ Megaloblasts in the bone marrow
✔ Low erythrocyte and leukocyte count
✔ Low hemoglobin levels

Folic acid deficiency occurs due to:

Poor diet (lack of leafy greens, fruits, and fortified cereals)
Increased demand (pregnancy, hemolysis)
Malabsorption disorders (celiac disease)
Chronic alcoholism

Why the other options are incorrect:

🔴 A. Biotin:
Incorrect. Biotin (vitamin B7) is important for fatty acid metabolism and enzyme function. Its deficiency causes dermatitis, hair loss, and neurological issues, not megaloblastic anemia.

🔴 C. Riboflavin:
Incorrect. Riboflavin (vitamin B2) deficiency leads to cheilitis (cracks at the corners of the mouth), glossitis (inflamed tongue), and photophobia, but it does not cause megaloblastic anemia.

🔴 D. Niacin:
Incorrect. Niacin (vitamin B3) deficiency leads to pellagra, which is characterized by dermatitis, diarrhea, and dementia. It does not cause megaloblastic anemia.

🔴 E. Ascorbic acid:
Incorrect. Ascorbic acid (vitamin C) deficiency causes scurvy (bleeding gums, bruising, poor wound healing) but does not affect red blood cell size or cause anemia of the megaloblastic type.

Summary:

Folic acid deficiency leads to megaloblastic anemia, characterized by macrocytic erythrocytes, megaloblasts, and reduced blood cell counts.

Thus, the correct answer is B. Folic acid. ✅

88. A patient diagnosed with essential hypertension died of an acute myocardial infarction. Autopsy revealed a cavity 2 cm in diameter in the right hemisphere of the brain. The cavity is filled with a transparent yellowish liquid. The wall of the cavity is rusty yellow and smooth. What pathology was detected in the brain of the deceased?

A. Cyst
B. Abscess
C. –
D. Echinococcus
E. Tuberculosis

Correct Answer: ✅ A. Cyst

Explanation:

A brain cyst is a common sequela of an old ischemic or hemorrhagic stroke. In cases of chronic hypertension, cerebral arteries can develop microaneurysms, leading to small hemorrhages or ischemic strokes. Over time, necrotic brain tissue is gradually removed by macrophages, leaving behind a fluid-filled cavity.

✔ Features of a post-stroke cyst:

Transparent yellowish fluid inside the cavity
Rusty yellow smooth walls due to hemosiderin deposits
Common in patients with hypertension and past strokes

Why the other options are incorrect:

🔴 B. Abscess:
Incorrect. A brain abscess is a collection of pus caused by bacterial infection. It usually has pus-filled contents and an irregular wall, unlike the smooth-walled cyst in this case.

🔴 D. Echinococcus:
Incorrect. Echinococcal cysts (hydatid cysts) occur due to parasitic infection. They contain clear fluid and daughter cysts but are more common in the liver and lungs rather than the brain.

🔴 E. Tuberculosis:
Incorrect. Tuberculous granulomas (tuberculomas) present as solid caseous masses, not fluid-filled cystic structures.

Summary:

The fluid-filled cyst in the brain of this patient is most likely due to a resolved ischemic stroke, commonly seen in hypertension-related cerebrovascular disease.

Thus, the correct answer is A. Cyst. ✅

89. Examination of a patient shows the following: blood pressure 180/110 mmHg, heart rate 95/min. X-ray detects narrowing of one of the renal arteries. What system was activated, causing the hypertensive state in this patient?

A. Immune system
B. Renin-angiotensin system
C. Sympathoadrenal system
D. Kinin system
E. Hemostatic system

Correct Answer: ✅ B. Renin-angiotensin system

Explanation:

This patient has renal artery stenosis, which reduces renal blood flow. The kidney perceives this as low blood pressure and activates the renin-angiotensin-aldosterone system (RAAS) to compensate.

✔ Steps of RAAS activation in renal artery stenosis:

Renin release from the juxtaglomerular cells due to reduced perfusion.
Renin converts angiotensinogen → angiotensin I.
Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE).
Angiotensin II causes:
- Vasoconstriction → Increased blood pressure.
- Aldosterone secretion → Sodium and water retention → Further increases blood pressure.

Thus, activation of the renin-angiotensin system leads to secondary hypertension in renal artery stenosis.

Why the other options are incorrect:

🔴 A. Immune system:
Incorrect. The immune system is not directly involved in blood pressure regulation. Autoimmune conditions can cause kidney damage, but they do not directly cause hypertension due to renal artery stenosis.

🔴 C. Sympathoadrenal system:
Incorrect. The sympathetic nervous system plays a role in acute stress responses, increasing heart rate and vasoconstriction. However, in this case, RAAS activation is the primary cause of hypertension.

🔴 D. Kinin system:
Incorrect. The kinin system (bradykinin, kallikrein) mainly lowers blood pressure by causing vasodilation. It is counteracted by RAAS but does not cause hypertension.

🔴 E. Hemostatic system:
Incorrect. The hemostatic system regulates blood clotting, not blood pressure.

Summary:

Renal artery stenosis activates the renin-angiotensin-aldosterone system (RAAS), leading to vasoconstriction, sodium retention, and hypertension.

Thus, the correct answer is B. Renin-angiotensin system. ✅

90. A patient presents with a sharp decrease in oncotic pressure and albumin levels in the blood plasma. What would be the result of this condition?

A. Reduced diuresis
B. Edema
C. Reduced ESR
D. Increased blood volume
E. Increased blood density

Correct Answer: ✅ B. Edema

Explanation:

Oncotic pressure (also called colloid osmotic pressure) is the force exerted by plasma proteins, mainly albumin, that helps retain water within the blood vessels.

✔ When albumin levels drop, the oncotic pressure decreases, leading to:

Fluid leakage from capillaries into interstitial spaces.
Tissue swelling (edema) due to excess extracellular fluid accumulation.

Common causes of low oncotic pressure:

Liver disease (cirrhosis) → Decreased albumin synthesis.
Kidney disease (nephrotic syndrome) → Albumin loss in urine.
Malnutrition → Protein deficiency.

Why the other options are incorrect:

🔴 A. Reduced diuresis:
Incorrect. In many cases of edema, diuresis (urine output) is increased as the body tries to compensate for fluid overload. However, in severe cases, kidney dysfunction may reduce diuresis.

🔴 C. Reduced ESR (Erythrocyte Sedimentation Rate):
Incorrect. ESR is affected by inflammatory proteins, not oncotic pressure or albumin levels.

🔴 D. Increased blood volume:
Incorrect. A decrease in oncotic pressure leads to fluid shifting from blood vessels to tissues, reducing intravascular volume.

🔴 E. Increased blood density:
Incorrect. Blood density depends on RBC concentration and plasma proteins. A decrease in albumin would reduce overall blood density.

Summary:

A decrease in oncotic pressure due to low albumin levels leads to fluid movement into interstitial spaces, resulting in edema.

Thus, the correct answer is B. Edema. ✅

91. In a patient with hypochromic anemia, erythrocytes contain 45% of HbS and 55% of HbA1. What type of anemia is it?

A. Sickle cell anemia
B. Glucose-6-phosphate dehydrogenase deficiency anemia
C. Addison-Biermer disease
D. α-thalassemia
E. Microspherocytic anemia

Correct Answer: ✅ A. Sickle cell anemia

Explanation:

Sickle cell anemia is caused by a mutation in the β-globin gene, leading to the production of HbS (sickle hemoglobin) instead of normal HbA.
Patients with sickle cell trait (heterozygous carriers) have a mix of HbA1 (normal hemoglobin) and HbS in their red blood cells.
The presence of 45% HbS and 55% HbA1 suggests that the patient is heterozygous for sickle cell disease (sickle cell trait).

✔ Hypochromic anemia (low hemoglobin content in RBCs) in this case is due to the abnormal structure of HbS, leading to:

RBC deformation (sickle shape) → Increased hemolysis.
Reduced oxygen-carrying capacity → Hypoxia.
Chronic anemia with periodic crises (pain and organ damage).

Why the other options are incorrect:

🔴 B. Glucose-6-phosphate dehydrogenase (G6PD) deficiency anemia:
Incorrect. G6PD deficiency causes hemolytic anemia due to oxidative stress (triggered by infections, fava beans, or drugs like sulfa drugs). It does not involve HbS.

🔴 C. Addison-Biermer disease:
Incorrect. Addison-Biermer disease is pernicious anemia caused by vitamin B12 deficiency, leading to macrocytic (not hypochromic) anemia.

🔴 D. α-thalassemia:
Incorrect. α-thalassemia is due to a reduction in α-globin chain synthesis, leading to HbH or Hb Bart’s formation. This patient has HbS, which is characteristic of sickle cell disease, not α-thalassemia.

🔴 E. Microspherocytic anemia:
Incorrect. Microspherocytic anemia (hereditary spherocytosis) is due to RBC membrane defects, leading to spherical-shaped erythrocytes, not HbS.

Summary:

The presence of 45% HbS and 55% HbA1 in a hypochromic anemia patient suggests sickle cell trait, a mild form of sickle cell anemia.

Thus, the correct answer is A. Sickle cell anemia. ✅

92. A patient was hospitalized with the provisional diagnosis of diphyllobothriasis. What food products could have caused this disease?

A. Vegetables and fruits
B. Milk and eggs
C. Fish
D. Beef
E. Pork

Correct Answer: ✅ C. Fish

Explanation:

Diphyllobothriasis is an infection caused by the tapeworm Diphyllobothrium latum, which is acquired by consuming raw or undercooked fish that contains the parasite’s larvae (plerocercoid stage). The lifecycle of Diphyllobothrium latum involves:

Eggs released into freshwater from human feces.
Eggs hatch into larvae, which are ingested by small crustaceans (copepods).
Fish consume the infected crustaceans, and the larvae develop into plerocercoids in the fish muscle.
Humans become infected by eating raw or undercooked fish containing the plerocercoids.

Thus, fish is the most likely source of infection in this case.

Why the Other Options Are Incorrect:

🔴 A. Vegetables and fruits:
Incorrect. Diphyllobothriasis is not transmitted through vegetables or fruits. The parasite requires an intermediate host (fish) to complete its lifecycle.

🔴 B. Milk and eggs:
Incorrect. Milk and eggs are not associated with the transmission of Diphyllobothrium latum. The parasite is specifically linked to fish consumption.

🔴 D. Beef:
Incorrect. Beef is associated with other parasitic infections, such as Taenia saginata (beef tapeworm), but not Diphyllobothrium latum.

🔴 E. Pork:
Incorrect. Pork is associated with Taenia solium (pork tapeworm) or Trichinella spiralis (trichinosis), but not Diphyllobothrium latum.

Summary:

The correct answer is C. Fish, as diphyllobothriasis is caused by consuming raw or undercooked fish infected with Diphyllobothrium latum larvae.

93. A 26-year-old woman, who one year ago had a difficult childbirth with a hemorrhage, complains of general weakness, weight loss of 18 kg, and absence of menstruations. Objectively, she has mammary hypoplasia. She was diagnosed with Simmonds disease. What is the main mechanism of the weight loss in this woman?

A. Decreased production of adenohypophysis hormones
B. Decreased function of the gonads
C. Hypothyroidism
D. Hypoparathyroidism
E. Decreased function of the adrenal cortex

Correct Answer: ✅ A. Decreased production of adenohypophysis hormones

Explanation:

Simmonds disease (also known as Sheehan’s syndrome in postpartum women) is a form of hypopituitarism caused by ischemic necrosis of the pituitary gland, often due to severe postpartum hemorrhage. The pituitary gland, particularly the adenohypophysis (anterior pituitary), is responsible for producing several critical hormones, including:

Growth hormone (GH)
Thyroid-stimulating hormone (TSH)
Adrenocorticotropic hormone (ACTH)
Follicle-stimulating hormone (FSH) and luteinizing hormone (LH)
Prolactin (PRL)

The weight loss in this patient is primarily due to the decreased production of adenohypophysis hormones, which leads to:

Reduced ACTH → Decreased cortisol production → Impaired metabolism and energy utilization.
Reduced TSH → Hypothyroidism → Slowed metabolism and weight loss.
Reduced GH → Impaired protein synthesis and fat metabolism.

These hormonal deficiencies collectively contribute to cachexia (severe weight loss and muscle wasting), a hallmark of Simmonds disease.

Why the Other Options Are Incorrect:

🔴 B. Decreased function of the gonads:
Incorrect. While decreased FSH and LH lead to hypogonadism (causing amenorrhea and mammary hypoplasia), this does not directly explain the weight loss. Hypogonadism primarily affects reproductive function, not metabolism or energy balance.

🔴 C. Hypothyroidism:
Incorrect. Hypothyroidism (due to decreased TSH) can contribute to weight loss in Simmonds disease, but it is not the primary mechanism. Hypothyroidism alone typically causes weight gain, not loss, due to a slowed metabolism. In this case, the weight loss is multifactorial, involving deficiencies in ACTH, GH, and TSH.

🔴 D. Hypoparathyroidism:
Incorrect. Hypoparathyroidism is unrelated to Simmonds disease. It results from low parathyroid hormone (PTH) levels, leading to hypocalcemia, and does not cause weight loss.

🔴 E. Decreased function of the adrenal cortex:
Incorrect. While decreased ACTH leads to adrenal insufficiency (hypocortisolism), this is only one aspect of the hormonal deficiencies in Simmonds disease. The weight loss is due to the combined effects of multiple pituitary hormone deficiencies, not solely adrenal cortex dysfunction.

Summary:

The main mechanism of weight loss in this patient is A. Decreased production of adenohypophysis hormones, as Simmonds disease results in panhypopituitarism, leading to deficiencies in ACTH, TSH, GH, and other hormones that regulate metabolism and energy balance.

94. Autopsy of the body of a 1.5-year-old child revealed a hemorrhagic skin rash, moderate hyperemia and edema of the nasopharyngeal mucosa, small hemorrhages in the mucosa and internal organs, markedly dystrophic changes in the liver and myocardium, acute necrotizing nephrosis, and massive hemorrhages in the adrenal glands. These changes are characteristic of the following disease:

A. Measles
B. Epidemic typhus
C. Meningococcal infection
D. Scarlet fever
E. Diphtheria

Correct Answer: ✅ C. Meningococcal infection

Explanation:

The findings described in the autopsy are classic for meningococcal infection, specifically meningococcemia (a severe form of meningococcal disease caused by Neisseria meningitidis). Key pathological features include:

Hemorrhagic skin rash: Caused by widespread vascular damage due to endotoxin release, leading to disseminated intravascular coagulation (DIC).
Hyperemia and edema of the nasopharyngeal mucosa: Reflects the initial site of infection and inflammation.
Small hemorrhages in the mucosa and internal organs: Result from DIC and endothelial damage.
Dystrophic changes in the liver and myocardium: Due to systemic toxicity and hypoxia from septic shock.
Acute necrotizing nephrosis: Caused by ischemic injury and toxin-mediated damage to the kidneys.
Massive hemorrhages in the adrenal glands: Known as Waterhouse-Friderichsen syndrome, a hallmark of severe meningococcemia, leading to adrenal hemorrhage and acute adrenal insufficiency.

These findings collectively point to meningococcal infection as the cause of death.

Why the Other Options Are Incorrect:

🔴 A. Measles:
Incorrect. Measles (rubeola) typically presents with a maculopapular rash, Koplik spots, and respiratory symptoms. It does not cause hemorrhagic rashes, adrenal hemorrhage, or the systemic findings described in this case.

🔴 B. Epidemic typhus:
Incorrect. Epidemic typhus, caused by Rickettsia prowazekii, presents with a maculopapular rash, fever, and neurological symptoms. It does not typically cause adrenal hemorrhage or the specific pathological changes seen here.

🔴 D. Scarlet fever:
Incorrect. Scarlet fever, caused by Streptococcus pyogenes, presents with a sandpaper-like rash, strawberry tongue, and pharyngitis. It does not cause hemorrhagic rashes, adrenal hemorrhage, or the systemic findings described.

🔴 E. Diphtheria:
Incorrect. Diphtheria, caused by Corynebacterium diphtheriae, primarily affects the respiratory tract, causing pseudomembrane formation and systemic toxicity. It does not cause hemorrhagic rashes, adrenal hemorrhage, or the specific pathological changes seen here.

Summary:

The findings of hemorrhagic rash, adrenal hemorrhage (Waterhouse-Friderichsen syndrome), and systemic organ damage are characteristic of C. Meningococcal infection, specifically meningococcemia. This condition is caused by Neisseria meningitidis and is associated with high mortality if not treated promptly.

95. A patient with leukemia was prescribed 5-fluorouracil. What is the mechanism of action of this drug?

A. Translation inhibition
B. Transcription inhibition
C. DNA synthesis inhibition
D. DNase stimulation
E. Replication catalysis

Correct Answer: ✅ C. DNA synthesis inhibition

Explanation:

5-Fluorouracil (5-FU) is an antimetabolite chemotherapy drug that inhibits DNA synthesis by interfering with nucleotide production.
It is a pyrimidine analog that gets converted into 5-fluorodeoxyuridine monophosphate (5-FdUMP) inside the cell.
5-FdUMP irreversibly inhibits thymidylate synthase, the enzyme responsible for converting dUMP (deoxyuridine monophosphate) into dTMP (deoxythymidine monophosphate).
Since dTMP is required for DNA replication, inhibition of thymidylate synthase leads to decreased DNA synthesis and cell death.

✔ 5-FU is used in leukemia and various cancers, including colorectal, breast, and pancreatic cancer.

Why the other options are incorrect:

🔴 A. Translation inhibition:
Incorrect. 5-FU does not affect translation (protein synthesis). It mainly disrupts DNA synthesis by inhibiting thymidylate synthase.

🔴 B. Transcription inhibition:
Incorrect. Transcription refers to RNA synthesis (mRNA production from DNA). 5-FU primarily disrupts DNA replication, not RNA synthesis.

🔴 D. DNase stimulation:
Incorrect. DNase is an enzyme that degrades DNA. 5-FU does not stimulate DNase activity; rather, it prevents DNA synthesis.

🔴 E. Replication catalysis:
Incorrect. 5-FU does not promote DNA replication; instead, it inhibits DNA synthesis by blocking thymidylate synthase.

Summary:

5-Fluorouracil (5-FU) is a pyrimidine analog that inhibits DNA synthesis by blocking thymidylate synthase, leading to impaired cell division and cancer cell death.

Thus, the correct answer is C. DNA synthesis inhibition. ✅

96. In a 67-year-old patient, who has been suffering from chronic bronchitis for 17 years, bronchial biopsy detects cylindrical dilation of the bronchi, cystic changes in the mucous glands, and areas, where prismatic epithelium is replaced with stratified squamous epithelium. What pathological process was detected in the bronchial mucosa?

A. Hyperplasia
B. Metaplasia
C. Dysplasia
D. Heterotopia
E. Hypertrophy

Correct Answer: ✅ B. Metaplasia

Explanation:

The key finding in this case is the replacement of prismatic (columnar) epithelium with stratified squamous epithelium in the bronchial mucosa. This is a classic example of metaplasia, which is defined as the reversible replacement of one differentiated cell type with another differentiated cell type. In chronic bronchitis, prolonged exposure to irritants (e.g., cigarette smoke or air pollution) leads to:

Chronic inflammation of the bronchial mucosa.
Adaptive changes in the epithelium to better withstand the irritants.
Replacement of the normal ciliated columnar epithelium with stratified squamous epithelium, which is more resistant to damage but loses the protective functions of cilia (e.g., mucus clearance).

The other findings, such as cylindrical dilation of the bronchi (bronchiectasis) and cystic changes in the mucous glands, are secondary to chronic inflammation and recurrent infections associated with chronic bronchitis.

Why the Other Options Are Incorrect:

🔴 A. Hyperplasia:
Incorrect. Hyperplasia refers to an increase in the number of cells in a tissue or organ, leading to its enlargement. While hyperplasia of mucous glands can occur in chronic bronchitis, it does not explain the replacement of prismatic epithelium with stratified squamous epithelium.

🔴 C. Dysplasia:
Incorrect. Dysplasia refers to abnormal cell growth and differentiation, often considered a precancerous change. In this case, there is no mention of cellular atypia or disordered growth, which are hallmarks of dysplasia.

🔴 D. Heterotopia:
Incorrect. Heterotopia refers to the presence of normal tissue in an abnormal location (e.g., pancreatic tissue in the stomach wall). This is unrelated to the described changes in the bronchial mucosa.

🔴 E. Hypertrophy:
Incorrect. Hypertrophy refers to an increase in the size of cells, leading to tissue or organ enlargement. While hypertrophy of smooth muscle or mucous glands can occur in chronic bronchitis, it does not explain the epithelial changes described.

Summary:

The pathological process detected in the bronchial mucosa is B. Metaplasia, specifically the replacement of prismatic epithelium with stratified squamous epithelium due to chronic irritation and inflammation in a patient with long-standing chronic bronchitis.

97. A 14-year-old patient has a positive nitrogen balance. What is the likely cause of this condition?

A. Emotional stress
B. Low-protein diet
C. Significant physical exertion
D. Body growth
E. Starvation

Correct Answer: ✅ D. Body growth

Explanation:

Nitrogen balance represents the difference between nitrogen intake (mainly from proteins) and nitrogen excretion (via urine, sweat, and feces).
A positive nitrogen balance occurs when nitrogen intake exceeds nitrogen excretion, indicating the body is retaining nitrogen for tissue growth, repair, and protein synthesis.
This occurs in growing children, adolescents, pregnant women, and people recovering from injury or illness.
During adolescence, rapid tissue growth requires increased protein synthesis, leading to a positive nitrogen balance.

Why the other options are incorrect:

🔴 A. Emotional stress:
Incorrect. Emotional stress triggers the release of catabolic hormones (e.g., cortisol), leading to protein breakdown and nitrogen loss, resulting in a negative nitrogen balance.

🔴 B. Low-protein diet:
Incorrect. A low-protein diet provides insufficient nitrogen intake, causing the body to break down muscle proteins, leading to a negative nitrogen balance.

🔴 C. Significant physical exertion:
Incorrect. Intense exercise increases muscle breakdown and nitrogen excretion. Unless properly supplemented with protein, it usually results in a negative nitrogen balance.

🔴 E. Starvation:
Incorrect. In starvation, the body breaks down muscle proteins for energy, leading to high nitrogen loss and a negative nitrogen balance.

Summary:

A positive nitrogen balance occurs when nitrogen intake exceeds nitrogen loss, which happens during childhood and adolescence due to rapid growth and protein synthesis.

Thus, the correct answer is D. Body growth. ✅

98. Examination detects lymphopenia in a patient who has been taking glucocorticoids for a long time. How can the functional state of the patient’s immune system be characterized in this case?

A. Tolerance to autoantigens
B. Congenital immunodeficiency
C. Primary immunodeficiency
D. Anaphylaxis
E. Secondary immunodeficiency

Correct Answer: ✅ E. Secondary immunodeficiency

Explanation:

Glucocorticoids (e.g., prednisone, dexamethasone) suppress the immune system by reducing lymphocyte production and increasing apoptosis of T and B cells, leading to lymphopenia.
Long-term glucocorticoid use can cause immunosuppression, making the patient susceptible to infections and opportunistic diseases.
Since the immunodeficiency is caused by an external factor (glucocorticoid therapy) rather than a genetic defect, it is classified as a secondary (acquired) immunodeficiency.

Why the other options are incorrect:

🔴 A. Tolerance to autoantigens:
Incorrect. Tolerance to autoantigens refers to the immune system’s ability to avoid attacking self-antigens, which is regulated by mechanisms like clonal deletion and regulatory T cells. It is not related to glucocorticoid-induced lymphopenia.

🔴 B. Congenital immunodeficiency:
Incorrect. Congenital immunodeficiencies are present at birth due to genetic mutations (e.g., SCID, Bruton’s agammaglobulinemia). This patient’s immunodeficiency is drug-induced, not genetic.

🔴 C. Primary immunodeficiency:
Incorrect. Primary immunodeficiency refers to inherited immune system disorders that cause chronic infections from birth. Examples include DiGeorge syndrome (T-cell deficiency) and X-linked agammaglobulinemia (B-cell deficiency).

🔴 D. Anaphylaxis:
Incorrect. Anaphylaxis is a severe allergic reaction caused by IgE-mediated hypersensitivity, leading to vasodilation, bronchospasm, and hypotension. It is unrelated to glucocorticoid-induced immunosuppression.

Summary:

Long-term glucocorticoid therapy leads to lymphopenia and immune suppression, making the patient susceptible to infections. Since this immunodeficiency is acquired and not genetic, it is classified as secondary immunodeficiency.

Thus, the correct answer is E. Secondary immunodeficiency. ✅

99. A patient has been diagnosed with chronic gastritis. Intragastric pH-metry detects decreased acidity of the gastric juice. What cells have a reduced function in this case?

A. Mucocytes
B. Gastric parietal cells
C. Gastric chief cells
D. Enteroendocrine cells
E. –

Correct Answer: ✅ B. Gastric parietal cells

Explanation:

Gastric parietal cells (oxyntic cells) are responsible for producing hydrochloric acid (HCl) and intrinsic factor in the stomach.
Chronic gastritis, especially atrophic gastritis, leads to damage and loss of parietal cells, resulting in decreased acid (hypochlorhydria or achlorhydria) production.
Low gastric acidity can impair protein digestion, increase the risk of bacterial overgrowth, and cause vitamin B12 deficiency (pernicious anemia) due to intrinsic factor loss.

Why the other options are incorrect:

🔴 A. Mucocytes:
Incorrect. Mucocytes (goblet cells) in the stomach produce mucus and bicarbonate, which protect the stomach lining from acid. They do not produce HCl, so their dysfunction does not cause reduced gastric acidity.

🔴 C. Gastric chief cells:
Incorrect. Chief cells produce pepsinogen, which is converted to pepsin by gastric acid to digest proteins. However, they do not produce HCl, so their dysfunction does not directly lower acidity.

🔴 D. Enteroendocrine cells:
Incorrect. Enteroendocrine cells (e.g., G cells, D cells) regulate gastric acid secretion by releasing gastrin, somatostatin, and histamine. However, their dysfunction affects acid regulation, not direct acid production.

Summary:

Gastric parietal cells produce HCl, and their dysfunction in chronic gastritis leads to reduced gastric acidity. This can cause digestive issues and B12 deficiency.

Thus, the correct answer is B. Gastric parietal cells. ✅

100. A patient has elevated blood pressure due to increased vascular tone. To lower the blood pressure in this case, it is necessary to prescribe the blockers of:

A. α-adrenergic receptors
B. α- and β-adrenergic receptors
C. Muscarinic acetylcholine receptors
D. β-adrenergic receptors
E. Histamine H1 receptors

Correct Answer: ✅ A. α-adrenergic receptors

Explanation:

α-adrenergic receptors (α1 receptors) are primarily responsible for vasoconstriction of blood vessels, leading to increased vascular resistance and elevated blood pressure.
α-blockers (e.g., prazosin, doxazosin, terazosin) work by blocking α1-adrenergic receptors, causing vasodilation and thereby reducing vascular tone and blood pressure.

Why the other options are incorrect:

🔴 B. α- and β-adrenergic receptors:
Partially correct, but α-blockers alone are sufficient for treating increased vascular tone. β-blockers (e.g., propranolol, metoprolol) mainly reduce heart rate and cardiac output rather than directly causing vasodilation. However, combined α and β-blockers (e.g., labetalol, carvedilol) are sometimes used in severe hypertension.

🔴 C. Muscarinic acetylcholine receptors:
Incorrect. Muscarinic receptor blockers (e.g., atropine) do not lower blood pressure. Instead, they increase heart rate by blocking parasympathetic activity, which could worsen hypertension.

🔴 D. β-adrenergic receptors:
Incorrect. β-blockers (e.g., atenolol, propranolol) lower blood pressure by reducing heart rate and cardiac output, but they do not directly reduce vascular tone.

🔴 E. Histamine H1 receptors:
Incorrect. H1-receptor blockers (e.g., diphenhydramine, loratadine) are used for allergic reactions and do not play a significant role in blood pressure regulation.

Summary:

Since α-adrenergic receptors mediate vasoconstriction, blocking them causes vasodilation, reducing vascular tone and blood pressure.

Thus, the correct answer is A. α-adrenergic receptors. ✅

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