CVS – Pharmacology

CVS

CVS- Pharmacology

Compiled Topical Questions of CVS – Pharmacology

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Look for the drug that directly relaxes arteriolar smooth muscle and is famous for causing reflex tachycardia.

1 / 30

Tags: 2024

Which of the following antihypertensives belong to vasodilators?

Furosemide

Hydralazine

Verapamil

Metoprolol

Spironolactone

All Class I drugs stabilize the cardiac membrane by reducing the speed of the rapid depolarization phase (Phase 0). What ion is responsible for this phase?

2 / 30

Tags: 2024

The principal action common to all class I antiarrhythmic drugs is?

K+ channel blockade

Na+ channel blockade

Ca2+ channel blockade

Na+ channel opening

K+ channel opening

Think of the antihypertensive drug which blocks angiotensin II receptors.

3 / 30

Tags: 2024

Which of the following drugs belongs to angiotensin receptor blockers (ARBs)?

Metoprolol

Losartan

Prazosin

Lavetalol

Hydralazine

Think of the antihypertensive that increases bradykinin — the same reason it causes angioedema and dry cough.

4 / 30

Tags: 2024

A 45-year-old man was just started on therapy for hypertension and developed a persistent, dry cough. Which drug is most likely responsible for this side effect?

Metoprolol

Nifedipine

Captopril

Prazosin

Losartan

Consider a drug that primarily affects the excitation-contraction coupling of cardiac and smooth muscle rather than directly altering sodium or potassium movement.

5 / 30

Tags: 2024

What is the mechanism of action of verapamil?

Increases heart rate

Reduces blood pressure

Blocks K ion channels

Activates Na ion channels

Blocks slow Ca ion channels

Think about a drug that works upstream in a hormone cascade that regulates blood pressure, rather than one that primarily affects heart rate or vascular smooth muscle directly.

6 / 30

Tags: 2024

Which drug inhibits the formation of angiotensin?

Digitoxin

Captopril

Metoprolol

HydraIazine

Propranolol

Think about which cellular mechanism responsible for maintaining ion balance and electrical gradients in heart cells is affected, rather than focusing on drug classes or general disease treatment.

7 / 30

Tags: 2017

Which of the following is a property of digoxin?

It targets to inhibit the sodium-potassium ATPase

It brings about a decrease in the intracellular sodium

It belongs to drug class of aldosterone receptor antagonists

It is used in the treatment of acute heart failure

It decreases contractility of the cardiac sarcomere

Some antihypertensive drugs have a dual action — they block both alpha-1 and beta receptors, leading to reduced heart rate and vasodilation. This combination is especially useful in hypertensive emergencies and heart failure. Can you recall which two drugs are known for this unique mechanism?

8 / 30

Tags: 2017

Which of the following drugs is both an alpha and beta-adrenoreceptor blocking agent?

Metoprolol

Carvedilol

Esmolol

Labetalol

Both labetalol and carvedilol

Selective beta-blockers primarily target the heart by blocking beta-1 receptors, leading to reduced heart rate, decreased cardiac output, and lower blood pressure. They are often remembered by the mnemonic: “A-B-E-M-A” — can you figure out which of these drugs fits into that group?

9 / 30

Tags: 2017

Which of the following drugs is a selective beta-adrenoreceptor blocking agent?

Atenolol

Acebutolol

Timolol

Labetalol

Propranolol

Beta-adrenoreceptor blockers (beta-blockers) are classified into:

Selective beta-1 blockers (“Cardioselective“)
Non-selective beta-blockers (block both beta-1 and beta-2 receptors)
Mixed alpha- and beta-blockers

Atenolol:

Type: Selective beta-1 blocker
Target: Primarily the heart (beta-1 receptors)
Effects:
- Reduced heart rate (negative chronotropy)
- Decreased contractility (negative inotropy)
- Lower cardiac output and blood pressure
Advantages:
- Minimal effect on beta-2 receptors (bronchi, vasculature)
- Safer in asthma, COPD, and peripheral vascular disease compared to non-selective beta-blockers

Why the other options are incorrect:

Propranolol:
- Type: Non-selective beta-blocker (blocks both beta-1 and beta-2)
- Effects:
  - Beta-1 blockade: Decreases heart rate and blood pressure
  - Beta-2 blockade: Causes bronchoconstriction, vasoconstriction, and reduced glycogenolysis
- Not cardioselective, contraindicated in asthma and COPD
Timolol:
- Type: Non-selective beta-blocker
- Primary use: Topical treatment for glaucoma
- Action: Reduces aqueous humor production, lowering intraocular pressure
Labetalol:
- Type: Mixed alpha- and beta-blocker
- Effects:
  - Beta-1 blockade: Reduces heart rate and contractility
  - Beta-2 blockade: Causes bronchoconstriction
  - Alpha-1 blockade: Causes vasodilation, lowering systemic vascular resistance
- Clinical use: Hypertensive emergencies, pheochromocytoma
Acebutolol:
- Type: Selective beta-1 blocker with intrinsic sympathomimetic activity (ISA)
- ISA: Partial agonist activity while blocking beta-1 receptors
- Effect: Less reduction in resting heart rate and cardiac output compared to other beta-blockers
- Not preferred in patients with ischemic heart disease due to residual sympathetic activity

Conclusion:
Atenolol is the best example of a selective beta-1 adrenoreceptor blocker, making it cardioselective. It’s often preferred in hypertension, angina, and post-myocardial infarction management because it minimizes bronchospasm risk and doesn’t significantly affect beta-2 receptors.

Think about drugs that act on the autonomic ganglia — the neural relay stations between preganglionic and postganglionic neurons. These drugs block both sympathetic and parasympathetic activity, leading to profound effects on blood pressure but also severe side effects, which is why they’re rarely used today.

10 / 30

Tags: 2017

Which of the following anti-hypertensive drugs functions as a ganglion blocker?

Trimethaphan

Clonidine

Nicotine

Propranolol

Reserpine

Ganglion blockers inhibit nicotinic receptors (Nn) at autonomic ganglia, leading to inhibition of both sympathetic and parasympathetic nervous systems.

Trimethaphan is a classic ganglion blocker used for:

Hypertensive emergencies (though it’s rarely used now)
Controlled hypotension during surgical procedures

Effects:

Decreased sympathetic tone → Vasodilation → Reduced blood pressure
Parasympathetic blockade → Tachycardia, urinary retention, dry mouth, constipation

Why it’s rarely used:
Severe side effects due to broad autonomic blockade.

Why the other options are incorrect:

Reserpine:
- Mechanism: Depletes norepinephrine (NE) from sympathetic nerve endings by inhibiting vesicular monoamine transporter (VMAT).
- Not a ganglion blocker — it works postganglionically on adrenergic neurons.
- Side effects: Depression, sedation, nasal congestion, gastrointestinal issues.
Propranolol:
- Mechanism: Non-selective beta-blocker → Blocks beta-1 and beta-2 adrenergic receptors.
- No action on autonomic ganglia.
- Effects: Reduces heart rate, contractility, and cardiac output.
Clonidine:
- Mechanism: Alpha-2 adrenergic agonist → Centrally reduces sympathetic outflow from the brainstem.
- Not a ganglion blocker — acts on the CNS, not peripheral autonomic ganglia.
- Side effects: Sedation, dry mouth, rebound hypertension on abrupt withdrawal.
Nicotine:
- Mechanism: Nicotinic receptor agonist (Nn) at autonomic ganglia.
- Stimulates, rather than blocks ganglia.
- Biphasic effect:
  - Low doses: Stimulation
  - High doses: Desensitization and blockade
- Not used as an antihypertensive.

Conclusion:
Trimethaphan is the true ganglion blocker among these options, acting on nicotinic (Nn) receptors in autonomic ganglia, leading to potent but nonspecific autonomic inhibition. Due to its broad and severe side effects, its clinical use is extremely limited today.

Bradykinin is a vasodilator that helps in lowering blood pressure by increasing nitric oxide (NO) and prostaglandin release. Which class of antihypertensive drugs acts on the renin-angiotensin-aldosterone system (RAAS) and is known for causing a persistent dry cough, a side effect linked to bradykinin buildup?

11 / 30

Tags: 2017

Which of the following groups of anti-hypertensive drugs decreases the metabolism of bradykinin?

Angiotensin receptor blockers

Alpha-adrenoreceptor blockers

Beta-adrenoreceptor blockers

Angiotensin-converting enzyme inhibitor

Ganglion blockers

ACE inhibitors (like enalapril, lisinopril, and captopril) work by blocking the conversion of angiotensin I to angiotensin II.

Let’s break down their dual action:

Inhibition of Angiotensin II formation:
- Angiotensin II is a potent vasoconstrictor. By reducing its levels, ACE inhibitors lower blood pressure and reduce afterload.
Decreased Bradykinin Breakdown:
- Angiotensin-converting enzyme (ACE) also breaks down bradykinin, a vasodilator.
- By inhibiting ACE, these drugs increase bradykinin levels, leading to:
  - Vasodilation → Decreased peripheral resistance
  - Increased prostaglandins and nitric oxide (NO) → Enhanced blood flow

Key Clinical Point:
The increased bradykinin levels are responsible for the persistent dry cough seen in up to 20% of patients on ACE inhibitors.

Why the other options are incorrect:

Alpha-adrenoreceptor blockers (like prazosin):
- Mechanism: Block alpha-1 adrenergic receptors → Vasodilation
- No effect on bradykinin metabolism.
Ganglion blockers (like hexamethonium):
- Mechanism: Block nicotinic receptors in autonomic ganglia → Reduced sympathetic tone
- Not used clinically due to severe side effects.
- No role in bradykinin metabolism.
Angiotensin receptor blockers (ARBs) (like losartan, valsartan):
- Mechanism: Block angiotensin II receptors (AT1) → Vasodilation
- Unlike ACE inhibitors, ARBs do not affect bradykinin levels.
- Fewer side effects, including no dry cough.
Beta-adrenoreceptor blockers (like metoprolol, propranolol):
- Mechanism: Block beta-adrenergic receptors → Reduced heart rate and contractility
- No influence on bradykinin metabolism.

Conclusion:
ACE inhibitors are unique in their ability to decrease bradykinin metabolism, leading to increased bradykinin levels and additional vasodilatory effects. This mechanism explains the efficacy of ACE inhibitors in hypertension management and their characteristic side effects like dry cough and angioedema.

“This drug selectively blocks beta-1 adrenergic receptors found primarily in the heart, making it safer for patients with respiratory conditions.”

12 / 30

Tags: 2019

Which of the following is a cardioselective beta-1 antagonist?

Nadalol

Pindolol

Atenolol

None of these

Propanolol

“This drug is a potent vasodilator that acts very rapidly, making it ideal for life-threatening situations requiring immediate blood pressure control.”

13 / 30

Tags: 2019

Which of the following drugs is most commonly used in hypertensive emergencies?

Atropine

Sodium nitroprusside

Propanolol

Coptopril

None of these

Class-1A antiarrhythmics belong to the sodium channel blockers that slow conduction and prolong the action potential.
Think of the older, classic drugs—the ones you meet early in pharmacology.

14 / 30

Tags: 2018

Which of the following is a class-1A antiarrhythmic drug?

Bretylium

Quinidine

Amiloride

Phenytoin

Verapamil

“Think about how reducing the heart’s workload can help in a condition where the heart muscle is not receiving enough oxygen. What physiological parameters would need to be lowered to achieve this?”

15 / 30

Tags: 2018

Which of the following is the mechanism of action of propanolol in angina?

Reduction of heart rate and myocardial contractility to reduce myocardial oxygen demand

Increased sympathetic stimulation of heart for the survival of patient

Vasodilation to counter coronary vasospasms

Increase of heart rate and myocardial contractility to compensate myocardial oxygen demand

None of these

Mechanism of Action of Propranolol in Angina:

Propranolol is a non-selective beta-blocker, meaning it blocks both beta-1 and beta-2 adrenergic receptors. Its primary mechanism of action in treating angina involves:

Reduction of Heart Rate (Negative Chronotropy):
- By blocking beta-1 receptors in the heart, propranolol inhibits the effects of adrenaline (epinephrine) and noradrenaline (norepinephrine), which normally increase heart rate. This slows down the heart rate, reducing the workload on the heart.
Reduction of Myocardial Contractility (Negative Inotropy):
- Propranolol also decreases the force of myocardial contraction by blocking beta-1 receptors. This further reduces the heart’s oxygen demand.
Decreased Myocardial Oxygen Demand:
- Angina occurs when there is an imbalance between myocardial oxygen supply and demand. By reducing heart rate and contractility, propranolol lowers the heart’s oxygen requirements, preventing or alleviating angina symptoms.

Why the Other Options Are Incorrect:

Increase of heart rate and myocardial contractility to compensate myocardial oxygen demand:
- This is incorrect because increasing heart rate and contractility would raise myocardial oxygen demand, worsening angina. Beta-blockers like propranolol do the opposite.
Vasodilation to counter coronary vasospasms:
- While vasodilation can help in certain types of angina (e.g., variant or Prinzmetal angina caused by coronary vasospasms), propranolol is not primarily a vasodilator. Calcium channel blockers (e.g., nifedipine) are more effective for this purpose.
None of these:
- This is incorrect because propranolol does have a well-defined mechanism of action in angina, as described above.
Increased sympathetic stimulation of heart for the survival of patient:
- This is incorrect because propranolol blocks sympathetic stimulation of the heart, which is how it reduces heart rate and contractility to alleviate angina.

“Which substance is released during allergic reactions and can cause sudden, life-threatening hypotension requiring immediate treatment?”

16 / 30

Tags: 2022

Which of the following substances is most likely to cause a rapid drop in blood pressure?

Histamine

Nicotine

Norepinephrine

Thromboxane A2

Angiotensin II

Atropine is used in cases of severe bradycardia. What term describes its ability to modify the SA node?”

17 / 30

Tags: 2022

A diabetic patient presents to the emergency department with a heart rate of 32 beats per minute and a blood sugar level of more than 500mg/dL. A drug ”atropine” is prescribed to increase the heart rate. What is this effect called?

Negative inotropic effect

Negative dromotropic effect

Negative chronotropic effect

Positive inotropic effect

Positive chronotropic effect

Think about the receptors that respond to norepinephrine and epinephrine to increase heart rate and contractility. Which type of adrenergic receptor is specific to the heart?”

18 / 30

Tags: 2021

Which of the following receptors on the heart bring about the sympathetic effect?

Beta-2 adrenergic receptors

Alpha receptors

Gamma receptors

Beta-1 adrenergic receptors

Cholinergic receptors

Think about the drug class that directly blocks the enzyme responsible for converting angiotensin I to angiotensin II. These drugs are commonly used for hypertension and heart failure.

19 / 30

Tags: 2018

Which drug inhibits the formation of angiotensin?

Propranolol

Metoprolol

Digitoxin

Captopril

HydraIazine

Think about a statin that needs activation in the liver before it can exert its effect. This statin is derived from fungal metabolites and was one of the first developed.

20 / 30

Tags: 2018

Which of the following is a prodrug?

Atorvastatin

Rosuvastatin

Lovastatin

None of these

FIuvastatin

This side effect is often bothersome, persistent, and unrelated to mucus production, leading some patients to switch to a different class of medications.

21 / 30

Tags: 2016

Which one of these represents the adverse effect of angiotensin-converting enzyme inhibitors due to increased levels of bradykinin in a pulmonary tree?

Fever

Dry cough

Excessive sputum production

Bronchoconstriction

Skin rash and bronchodilation

“These drugs primarily affect blood circulation dynamics, which helps ease the strain on the heart.”

22 / 30

Tags: 2016

Which of the following is true regarding nitrates?

They constrict meningeal blood vessels causing headache

They are more effective as prophylactic measures taken daily than to relieve an anginal attack

Nitroglycerine is placed under tongue because if swallowed it would be destroyed by the gastric juice

They usually decrease venous return

They are selective coronary dilators

Nitrates, such as nitroglycerin, are potent vasodilators primarily used in the treatment of angina pectoris. Their primary mechanism of action involves releasing nitric oxide (NO), which stimulates guanylate cyclase to increase cGMP levels, leading to smooth muscle relaxation.

How Nitrates Decrease Venous Return:

Primary Effect: Venodilation (dilation of veins) → This leads to increased venous pooling of blood.
Reduced Preload: Since less blood returns to the heart, preload (end-diastolic volume) decreases.
Lower Myocardial Oxygen Demand: Less ventricular stretching reduces oxygen demand, making nitrates beneficial for angina relief.

Thus, nitrates primarily decrease venous return, reducing cardiac workload and oxygen consumption.

Why the Other Options Are Incorrect:

“Nitroglycerine is placed under the tongue because if swallowed it would be destroyed by gastric juice” (Incorrect)
- The main reason nitroglycerin is given sublingually is to bypass first-pass metabolism in the liver, not because of destruction by gastric juice.
- If swallowed, nitroglycerin is rapidly metabolized by the liver (hepatic metabolism), making it ineffective.
“They are more effective as prophylactic measures taken daily than to relieve an anginal attack” (Incorrect)
- Nitrates are more effective for acute anginal relief rather than long-term prevention.
- Beta-blockers and calcium channel blockers are preferred for chronic prophylaxis of angina.
- Tolerance develops quickly with long-term nitrate use, reducing effectiveness.
“They are selective coronary dilators” (Incorrect)
- Nitrates cause both systemic and coronary vasodilation.
- However, they primarily act on veins, and their coronary effects are not selective.
- Additionally, coronary dilation does not significantly improve blood flow in ischemic areas due to the coronary steal phenomenon.
“They constrict meningeal blood vessels causing headache” (Incorrect)
- Nitrates dilate meningeal blood vessels, not constrict them.
- This dilation leads to headaches, a common side effect.

“This drug is known for its strong sodium channel-blocking effect and is often used to manage atrial fibrillation and life-threatening ventricular arrhythmias.”

23 / 30

Tags: 2016

Which one of the following drugs belongs to the class 1C antiarrhythmic?

Flecainide

Phenytoin

Tocainide

Lidocaine

Mexilitine

“This drug influences cellular signaling pathways to support heart function in acute conditions.”

24 / 30

Tags: 2016

The antiarrhythmic drug milrinone is preferred due to which of the following reasons?

It has a long life

It prevents thrombocytopenia

It selectively inhibits cAMP and phosphodiesterase type IV enzymes

It directly stimulates myocardial contractility

It gives long-term ionotropic support in the case of heart failure

Milrinone is a phosphodiesterase-3 (PDE-3) inhibitor that is primarily used in the short-term management of acute heart failure and cardiogenic shock. It is classified as an ionotropic and vasodilatory agent (inodilator), meaning it increases myocardial contractility and causes vasodilation.

How Milrinone Works:

Inhibition of Phosphodiesterase-3 (PDE-3):
- PDE-3 is an enzyme that breaks down cyclic AMP (cAMP) in cardiac and vascular smooth muscle cells.
- Milrinone inhibits PDE-3, leading to an increase in cAMP levels.
Effects on the Heart:
- Increased cAMP enhances calcium availability inside cardiac muscle cells, leading to stronger myocardial contractions (positive inotropic effect).
- Improves cardiac output without significantly increasing myocardial oxygen demand.
Effects on Blood Vessels:
- Increased cAMP causes vasodilation, reducing afterload and improving perfusion.

Thus, Milrinone is preferred because it directly stimulates myocardial contractility by increasing intracellular cAMP levels in cardiac muscle cells.

Why the Other Options Are Incorrect:

It gives long-term inotropic support in the case of heart failure (Incorrect)
- Milrinone is not used for long-term therapy due to its risk of arrhythmias and increased mortality in chronic heart failure patients.
- It is primarily used short-term in acute heart failure or cardiogenic shock.
It prevents thrombocytopenia (Incorrect)
- Milrinone does not prevent thrombocytopenia.
- In fact, it has been associated with a risk of thrombocytopenia in some patients.
It has a long life (Incorrect)
- Milrinone has a short half-life (2-4 hours) and requires continuous IV infusion in critical care settings.
- It is not preferred for its duration of action.
It selectively inhibits cAMP and phosphodiesterase type IV enzymes (Incorrect)
- Milrinone inhibits PDE-3, not PDE-4.
- PDE-4 inhibitors (e.g., roflumilast) are used for inflammatory conditions like COPD and not for cardiac support.

“Think about the class of drugs that directly targets cholesterol production in the liver. Which medication is known for its ability to lower ‘bad’ cholesterol (LDL) and reduce cardiovascular risk?”

25 / 30

Tags: 2023

Which class of drugs reduces LDL cholesterol?

Diuretics

Calcium channel blockers

Beta blockers

Statins

ACE inhibitors

Imagine the cholesterol-making pathway as a long domino trail. The famous drug target is halfway down the line… but the question asks you to notice which of these options even belongs to the same domino trail at all.

Look for the enzyme that performs the very first nudge — the one that pushes the first domino and lets the whole cholesterol pathway begin.

26 / 30

Tags: 2023

Which class of drugs reduces LDL cholesterol?

HMG CoA synthase

Carboxylase

Acetyl CoA dehydrogenase

Carnitine

Thiolase

“Think about the class of drugs used to treat hypertension and angina by relaxing blood vessels and reducing heart rate. Which drug specifically targets calcium channels to achieve these effects?”

27 / 30

Tags: 2023

Which of the following drugs causes the closure of L-type calcium channel?

Furosemide

Esmolol

Amiodarone

Diltiazem

Metoprolol

“Think about the medication that is quickly administered in the emergency setting for a heart attack. Which drug is known for its rapid antiplatelet effects and is often given as soon as possible?”

28 / 30

Tags: 2023

What is the recommended antiplatelet medication for treating acute myocardial infarction?

Heparin

Aspirin

Clopidogrel

Enoxaparin

Warfarin

Think about how nitroglycerin works as a vasodilator. Which side effect is directly related to its mechanism of action on blood vessels?

29 / 30

Tags: 2023

What are the potential side effects of nitroglycerin?

Anemia

Throbbing headache

Constipation

Edema

Seizures

A loading dose is a large initial dose of a drug given to rapidly achieve therapeutic levels in the bloodstream, especially in emergency situations. It’s used when a drug’s onset of action needs to be quick and the time to reach steady state with regular dosing would take too long.

How it works:

Loading dose = (Target concentration × Volume of distribution) / Bioavailability
It’s often followed by a maintenance dose to keep drug levels stable.

Examples:

Antibiotics like azithromycin
Anticonvulsants like phenytoin
Cardiac drugs like digoxin

Why the other options are incorrect:

Lethal dose: The amount of a drug that can cause death — definitely not a therapeutic dose.
Maintenance dose: A smaller, regular dose given after a loading dose to maintain steady drug levels.
Pediatric dose: A dose adjusted for children based on weight, age, or body surface area, not related to emergencies.
Toxic dose: A dose high enough to cause harmful effects, but not necessarily fatal — higher than therapeutic levels.

30 / 30

Tags: 2019

A patient comes into the emergency department and is about to collapse. He is immediately given a large dose of a drug to stabilize him. What is this dose called?

Lethal dose

Loading dose

Toxic dose

Maintenance dose

Pediatric dose

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CVS – Pharmacology

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✔ Hydralazine

Why the other options are incorrect

✔ They block fast voltage-gated Na⁺ channels in cardiac myocytes.

Why the other options are incorrect

Why the other options are incorrect

Why ACE inhibitors cause cough

Why the other options are incorrect

❌ Why the other options are incorrect

❌ Why the other options are incorrect

Why Quinidine is Correct (Class IA Antiarrhythmic)

Why the Other Options Are Incorrect

❌ Bretylium

❌ Phenytoin

❌ Verapamil

❌ Amiloride

Mechanism of Action of Propranolol in Angina:

Why the Other Options Are Incorrect:

Why Does Histamine Cause a Rapid Drop in Blood Pressure?

Breakdown of Incorrect Options:

Understanding the Effects of Atropine on Heart Rate

Key Definitions:

Breakdown of Incorrect Options:

Why the Other Options Are Incorrect:

Mechanism of Action:

Uses:

Why the Other Options Are Incorrect?

Why the Other Options Are Incorrect

How ACE Inhibitors Cause Dry Cough:

❌Why the Other Options Are Incorrect:

How Nitrates Decrease Venous Return:

Why the Other Options Are Incorrect:

Why Flecainide is Class 1C:

Why the Other Options Are Incorrect:

How Milrinone Works:

Why the Other Options Are Incorrect:

Why Statins are Correct:

Why the Other Options Are Incorrect:

Why Diltiazem is Correct:

Why the Other Options Are Incorrect:

Explanation:

Why Aspirin is Correct:

Why the Other Options Are Incorrect:

Explanation:

Why Throbbing Headache is Correct:

Why the Other Options Are Incorrect: