Hypertension and Hypertensive Emergencies — MCQs
In patient of head injuries with rapidly increasing intracranial tension without hematoma, the drug of choice for initial management would be :
A patient with hypertension, under control by medication falls under which grade
Which is not a risk factor for gestational hypertension
A 35-year-old woman at 36 weeks of gestation presents with a history of 5 convulsions at home. Her BP is 170/100 mmHg. The diagnosis made by the doctor is eclampsia. What is the next management?
Which of the following is the most prominent clinical manifestation of primary hyperaldosteronism (Conn's syndrome)?
STEPwise approach to surveillance for Non-Communicable diseases step 2 is
Which of the following is a cause of post-transplantation hypertension? I. Rejection II. Cyclosporine nephrotoxicity III. Renal transplant artery stenosis (RTAS) IV. Recurrent disease in the allograft. Select the correct option.
A young patient presented with hypertension and a 24-hour urinary metanephrine level of 1.4 mg, the most likely causes are -
What is the primary effect of beta blockers in the management of thyroid storm?
Which of the following statements about pheochromocytoma is true?
Hypertension and Hypertensive Emergencies Indian Medical PG Practice Questions and MCQs
Question 1: In patient of head injuries with rapidly increasing intracranial tension without hematoma, the drug of choice for initial management would be :
- A. 20% Mannitol (Correct Answer)
- B. Lasix
- C. Glycine
- D. Steroids
Explanation: ***20% Mannitol*** - **Mannitol** is an osmotic diuretic that reduces **intracranial pressure (ICP)** by creating an osmotic gradient, drawing water from the brain parenchyma into the intravascular space [1]. - Its rapid onset of action and significant ICP-reducing effects make it the drug of choice for acute management of elevated ICP in head injuries without hematoma. *Lasix* - **Furosemide (Lasix)** is a loop diuretic that can reduce ICP by decreasing cerebrospinal fluid production and promoting diuresis. - However, its effects are generally slower and less potent than mannitol for acute, rapidly increasing ICP. *Glycine* - **Glycine** is an amino acid and neurotransmitter; it has no direct role in the acute management of increased ICP. - It is sometimes used as an irrigating solution in urological procedures but is not indicated for brain injury. *Steroids* - **Steroids**, particularly **dexamethasone**, are effective in reducing vasogenic edema associated with brain tumors or abscesses. - They are generally **not recommended** for acute traumatic brain injury due to lack of benefit and potential for increased mortality or complications.
Question 2: A patient with hypertension, under control by medication falls under which grade
- A. ASA 2 (Correct Answer)
- B. ASA 1
- C. ASA 3
- D. ASA 4
Explanation: ***ASA 2*** - **ASA 2** is assigned to patients with **mild systemic disease** that is well-controlled and poses no significant functional limitations. - Well-controlled hypertension falls under this category as it represents a stable, managed chronic condition. *ASA 1* - **ASA 1** is reserved for **healthy patients** with no systemic disease, either physiological or psychological. - This patient has hypertension, which is a systemic disease, thus excluding ASA 1. *ASA 3* - **ASA 3** is for patients with **severe systemic disease** that has functional limitations but is not incapacitating. - Uncontrolled hypertension or hypertension with significant organ damage would fall into this category, unlike the well-controlled status described. *ASA 4* - **ASA 4** is assigned to patients with **severe systemic disease** that is a constant threat to life. - Examples include unstable angina, severe congestive heart failure, or uncontrolled hypertension with ongoing end-organ damage, which are not present here.
Question 3: Which is not a risk factor for gestational hypertension
- A. Primigravida
- B. Factor V Leiden mutation
- C. Smoking (Correct Answer)
- D. Low maternal age
Explanation: ***Smoking*** - **Smoking** paradoxically shows a *protective effect* against gestational hypertension and preeclampsia, making it the correct answer as it is NOT a risk factor for gestational hypertension. - This well-documented phenomenon may be related to smoking's vasodilatory effects and reduced production of anti-angiogenic factors. - However, smoking carries numerous other serious risks including **intrauterine growth restriction (IUGR)**, **placental abruption**, **preterm birth**, and **perinatal mortality**. *Primigravida* - **Primigravida** (first pregnancy) is a well-established risk factor for gestational hypertension and preeclampsia. - First-time exposure to paternal antigens and incomplete immune tolerance may contribute to this increased risk. - The risk decreases in subsequent pregnancies with the same partner. *Factor V Leiden mutation* - The **Factor V Leiden mutation** is the most common inherited thrombophilia and significantly increases the risk of gestational hypertension and preeclampsia. - This mutation causes resistance to activated protein C, leading to a hypercoagulable state that can impair placental perfusion. - Associated with increased risk of venous thromboembolism during pregnancy. *Low maternal age* - **Low maternal age** (adolescent pregnancy, <20 years) is actually a recognized *risk factor* for gestational hypertension. - Young mothers may have incomplete physical and cardiovascular maturity to handle pregnancy-related physiological changes. - Adolescent pregnancies are associated with higher rates of hypertensive disorders of pregnancy.
Question 4: A 35-year-old woman at 36 weeks of gestation presents with a history of 5 convulsions at home. Her BP is 170/100 mmHg. The diagnosis made by the doctor is eclampsia. What is the next management?
- A. Clonidine
- B. Only Labetalol
- C. Only MgSO4
- D. MgSO4 + Labetalol (Correct Answer)
Explanation: ***MgSO4 + Labetalol*** - The patient presents with **eclampsia**, characterized by convulsions and severe hypertension (BP 170/100 mmHg) during pregnancy. Magnesium sulfate (**MgSO4**) is the **first-line treatment for preventing and managing eclamptic seizures**. - **Labetalol** is an appropriate antihypertensive for **severe hypertension in pregnancy** (BP ≥160/110 mmHg) and must be used concurrently with MgSO4 to control the high blood pressure and prevent maternal complications like stroke or placental abruption. - Both medications are required for comprehensive management of eclampsia with severe hypertension. *Clonidine* - **Clonidine** is an alpha-2 adrenergic agonist used to treat hypertension but is **not the first-line antihypertensive choice in acute eclampsia** due to potential sedative effects and slower onset compared to other agents like Labetalol, Hydralazine, or Nifedipine. - While it can lower blood pressure, it **does not address the seizure risk** in eclampsia. *Only Labetalol* - While **Labetalol** is crucial for managing severe hypertension, treating eclampsia requires both seizure control and blood pressure management. Administering only Labetalol would **fail to prevent recurrent seizures**, which is the primary life-threatening concern. - It would adequately lower blood pressure but **does not address the underlying seizure pathology** of eclampsia. *Only MgSO4* - **MgSO4** is essential for seizure prophylaxis and treatment in eclampsia. However, in this patient with a blood pressure of **170/100 mmHg (severe hypertension)**, **MgSO4 alone would not adequately control the severe hypertension**, which poses risks of maternal complications like stroke, intracerebral hemorrhage, or placental abruption. - While it prevents seizures effectively, it **does not sufficiently manage severe maternal hypertension**, requiring an additional antihypertensive agent like Labetalol.
Question 5: Which of the following is the most prominent clinical manifestation of primary hyperaldosteronism (Conn's syndrome)?
- A. Hyperkalemia
- B. Hypertension (Correct Answer)
- C. Hypokalemia
- D. Expansion of Extracellular and Plasma volume
Explanation: ** Hypertension** - **Hypertension** is the most prominent and consistent clinical manifestation of primary hyperaldosteronism, present in nearly all patients. - The excessive aldosterone leads to increased **sodium reabsorption** and water retention, directly causing elevated blood pressure [2], [3]. *Hypokalemia* - While **hypokalemia** is common in primary hyperaldosteronism due to increased renal potassium excretion, it is not universally present and can be absent in a significant portion of patients (up to 30-50%). - Therefore, hypertension is a more reliable and prominent symptom for initial suspicion [3]. *Hyperkalemia* - **Hyperkalemia** is inconsistent with primary hyperaldosteronism; the hallmark of the condition is **potassium wasting** and **hypokalemia**, not elevated potassium levels [2]. - Aldosterone's primary role includes promoting potassium excretion, so hyperkalemia would indicate a different underlying pathology, such as adrenal insufficiency [2]. *Expansion of Extracellular and Plasma volume* - While increased aldosterone does lead to **expansion of extracellular and plasma volume** due to sodium and water retention, this is a physiological consequence that contributes to hypertension rather than being the most prominent *clinical manifestation* itself [1]. - Hypertension is the direct observable and measurable clinical symptom that drives investigation [3].
Question 6: STEPwise approach to surveillance for Non-Communicable diseases step 2 is
- A. Biochemical Measurement
- B. Behavioral measurement
- C. Physical measurement (Correct Answer)
- D. Emotional Assessment
Explanation: ***Physical measurement*** - The **STEPwise approach** to NCD surveillance involves three steps, with Step 2 specifically focusing on **physical measurements**. - This step includes measurements like **blood pressure**, BMI, weight, height, and waist circumference, which provide crucial data on NCD risk factors. *Biochemical Measurement* - This is typically **Step 3** in the WHO STEPwise approach, focusing on biological measurements from blood or urine samples. - Examples include **blood glucose**, cholesterol levels, and other biomarkers. *Behavioral measurement* - This corresponds to **Step 1** of the WHO STEPwise approach, which involves self-reported data on lifestyle factors. - It covers aspects like **diet**, physical activity, and tobacco/alcohol consumption. *Emotional Assessment* - While emotional and mental health are relevant to overall well-being, **emotional assessment** is not a standard, distinct step in the core WHO STEPwise approach for NCD surveillance. - The STEPs focus on behavioral, physical, and biochemical indicators of NCD risk.
Question 7: Which of the following is a cause of post-transplantation hypertension? I. Rejection II. Cyclosporine nephrotoxicity III. Renal transplant artery stenosis (RTAS) IV. Recurrent disease in the allograft. Select the correct option.
- A. None of the above are correct causes.
- B. I, II, and IV are correct causes.
- C. I and III are correct causes.
- D. All of the options are correct causes of post-transplantation hypertension. (Correct Answer)
Explanation: ***All of the options are correct causes of post-transplantation hypertension.*** - Post-transplantation hypertension often has a multifactorial etiology, with **rejection**, **cyclosporine nephrotoxicity**, **renal transplant artery stenosis (RTAS)**, and **recurrent disease in the allograft** all being significant contributors. - Each of these conditions can lead to mechanisms that elevate blood pressure, such as **renal ischemia**, activation of the **renin-angiotensin system**, and inflammatory responses affecting renal function. *I, II, and IV are correct causes.* - This option is incorrect because it excludes **renal transplant artery stenosis (RTAS)** (III), which is a well-established cause of secondary hypertension in transplant recipients due to reduced blood flow to the allograft. - **RTAS** activates the renin-angiotensin-aldosterone system (RAAS), leading to **vasoconstriction** and **sodium retention**, contributing to hypertension. *I and III are correct causes.* - This option is incorrect as it omits other crucial causes like **cyclosporine nephrotoxicity** (II) and **recurrent disease in the allograft** (IV), both of which are documented contributors to post-transplantation hypertension. - **Cyclosporine nephrotoxicity** causes afferent arteriolar vasoconstriction and glomerulosclerosis, directly increasing blood pressure. *None of the above are correct causes.* - This option is incorrect because **rejection**, **cyclosporine nephrotoxicity**, **renal transplant artery stenosis (RTAS)**, and **recurrent disease in the allograft** are all recognized and significant causes of post-transplantation hypertension. - Each condition has distinct pathological mechanisms that contribute to **elevated blood pressure** in transplant recipients.
Question 8: A young patient presented with hypertension and a 24-hour urinary metanephrine level of 1.4 mg, the most likely causes are -
- A. Grave's disease
- B. Pseudohypoparathyroidism
- C. Medullary carcinoma thyroid
- D. VonHippelLindau syndrome (Correct Answer)
Explanation: ***Von Hippel-Lindau syndrome*** - This syndrome is a **hereditary condition** predisposing individuals to various tumors, including **pheochromocytomas**, which cause elevated **metanephrines** and hypertension. - The combination of **hypertension** in a young patient and an elevated **24-hour urinary metanephrine level** (indicating excessive catecholamine production) strongly suggests a pheochromocytoma, which is frequently associated with Von Hippel-Lindau syndrome. *Medullary carcinoma thyroid* - This cancer is associated with **MEN 2 syndromes** and produces **calcitonin**, leading to hypocalcemia, but not typically elevated metanephrines or hypertension directly from the thyroid. - While it can be associated with **pheochromocytoma** (as part of MEN 2), it is not the direct cause of the elevated metanephrines. *Grave's disease* - **Grave's disease** is an autoimmune disorder causing **hyperthyroidism**, characterized by symptoms like goiter, exophthalmos, and weight loss. - While it can cause hypertension due to increased cardiac output, it does not lead to elevated **urinary metanephrine levels**, which are specific to catecholamine excess. *Pseudohypoparathyroidism* - This is a genetic disorder characterized by **target organ resistance to parathyroid hormone (PTH)**, leading to hypocalcemia and hyperphosphatemia [1]. - It does not cause hypertension or elevated **urinary metanephrine levels**.
Question 9: What is the primary effect of beta blockers in the management of thyroid storm?
- A. Increases metabolism of thyroxine
- B. Blocks thyroxine receptors
- C. Decreases synthesis of thyroxine
- D. Provides rapid relief of symptoms (Correct Answer)
Explanation: Detailed management of thyrotoxic crisis (thyroid storm) is a medical emergency where patients should be given propranolol, either oral or intravenous, to manage life-threatening symptoms [1]. ***Provides rapid relief of symptoms*** - Beta blockers primarily address the **adrenergic manifestations** of thyroid storm, such as **tachycardia**, **tremors**, anxiety, and palpitations [1]. - By blocking **beta-adrenergic receptors**, they provide rapid symptomatic relief and reduce cardiovascular stress, without affecting hormone levels [2]. Thyroid hormones normally increase the expression of genes for beta-adrenergic receptors and G-proteins, leading to increased heart rate and force of contraction [2]. *Increases metabolism of thyroxine* - Beta blockers do not increase the **metabolism** or breakdown of thyroxine; their action is primarily on the **peripheral effects** of thyroid hormones. - While some beta blockers like **propranolol** can inhibit the peripheral conversion of T4 to T3, this is a secondary effect and not their primary role in providing rapid symptomatic relief [1]. *Blocks thyroxine receptors* - Beta blockers do not block **thyroxine receptors**; thyroid hormones exert their effects by binding to intracellular receptors, not adrenergic receptors [2]. - Their action is on the **adrenergic system**, which is overstimulated by the high levels of thyroid hormones. *Decreases synthesis of thyroxine* - Beta blockers do not directly decrease the **synthesis of thyroxine** by the thyroid gland. - That action is performed by **antithyroid drugs** like methimazole and propylthiouracil, which inhibit hormone production [1].
Question 10: Which of the following statements about pheochromocytoma is true?
- A. Arises from chromaffin cells of adrenal medulla (Correct Answer)
- B. Bilateral in 20% of all cases
- C. Hypotension rules out pheochromocytoma
- D. Almost always a malignant tumor
Explanation: ***Arises from chromaffin cells of adrenal medulla*** - **Pheochromocytomas** are rare neuroendocrine tumors that develop from **chromaffin cells** found in the adrenal medulla. - These cells are responsible for synthesizing and secreting **catecholamines**, explaining the characteristic symptoms of pheochromocytoma. *Bilateral in 20% of all cases* - While pheochromocytomas can be bilateral, this occurs in about **10% of cases**, mostly associated with genetic syndromes like **MEN 2**. - A higher percentage of bilaterality is seen in **familial forms** of the disease, but not in all cases. *Hypotension rules out pheochromocytoma* - Although **hypertension** is a hallmark symptom, **hypotension** can occur, particularly **orthostatic hypotension** due to volume depletion and impaired vasoconstriction. - Rarely, **pheochromocytoma crisis** can present with **shock** due to massive catecholamine release and subsequent myocardial dysfunction or vasoplegia. *Almost always a malignant tumor* - Most pheochromocytomas are **benign**; only about **10-15%** are malignant. - Malignancy is suggested by the presence of **metastatic disease**, as histology alone cannot reliably differentiate between benign and malignant forms.
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