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Cardiac Metabolism Quiz

Total questions: 30

Worksheet time: 15mins

Name
Class
Date
1.

During prolonged fasting, which molecule supplements energy production in the heart?

a)

Glucose

b)

Ketone bodies

c)

Lactate

d)

Glycogen

2.

What is the main energy currency molecule in cardiac metabolism?

a)

NADH

b)

ATP

c)

Acetyl-CoA

d)

Oxaloacetate

3.

Which process yields 129 ATP per molecule and predominates during the fasting/steady-state in the heart?

a)

Glycolysis of glucose

b)

β-oxidation of palmitate

c)

Anaerobic glycolysis

d)

Oxidative phosphorylation of lactate

4.

Which molecule is the final electron acceptor in oxidative phosphorylation?

a)

NADH

b)

ATP

c)

Oxygen

d)

Acetyl-CoA

5.

During ischaemia, how much does ATP fall within 1 minute?

a)

10%

b)

25%

c)

50%

d)

75%

6.

Why does anaerobic glycolysis accelerate during ischaemia, and what is its ATP yield per glucose?

a)

Due to increased oxygen, yielding 36 ATP per glucose

b)

Due to lack of oxygen, yielding 2 ATP per glucose

c)

Due to increased fatty acids, yielding 129 ATP per glucose

d)

Due to increased ketones, yielding 4 ATP per glucose

7.

Explain why ketones are considered "brain-sparing" fuel during starvation and how this affects the heart's metabolism.

a)

Ketones are used only by the brain, so the heart uses glucose

b)

Ketones spare glucose for the brain, so the heart burns fatty acids and ketones

c)

Ketones inhibit fatty acid metabolism in the heart

d)

Ketones increase ATP production in the heart

8.

Which blood level and pH combination defines lactic acidosis?

a)

Blood lactate > 5 mmol L⁻¹ and pH < 7.35

b)

Blood lactate < 2 mmol L⁻¹ and pH > 7.45

c)

Blood lactate > 10 mmol L⁻¹ and pH > 7.4

d)

Blood lactate < 1 mmol L⁻¹ and pH < 7.0

9.

What is the significance of myoglobin as a cardiac biomarker?

a)

It rises very early after injury but is not cardiac-specific.

b)

It is highly specific for cardiac tissue and rises late.

c)

It is only detectable after 24 hours.

d)

It is used exclusively for diagnosing reinfarction.

10.

A patient with severe anaemia develops metabolic acidosis. Blood tests show lactate > 5 mmol L⁻¹ and pH 7.2. Explain the likely pathophysiological mechanism.

a)

Tissue hypoxia leads to increased anaerobic glycolysis, resulting in lactate accumulation and consumption of bicarbonate, causing anion-gap metabolic acidosis.

b)

Anaemia causes increased oxygen delivery, reducing lactate production and increasing pH.

c)

Severe anaemia leads to decreased glycolysis, resulting in metabolic alkalosis.

d)

Lactate is converted to glucose, increasing blood pH and causing alkalosis.

11.

Which of the following is considered the gold standard marker for detecting 1 g of cardiac necrosis?

a)

Cardiac troponin I/T

b)

LDH-1

c)

Myoglobin

d)

Creatine kinase

12.

What biochemical change is observed in a cell undergoing reversible injury?

a)

ATP levels are 5-20% of normal

b)

ATP levels are 100% of normal

c)

Glycolytic flux decreases

d)

Lactate levels decrease

13.

In the intrinsic (mitochondrial) pathway of apoptosis, which event occurs first?

a)

Caspase-8 activation

b)

Bax/Bak pore formation

c)

Executioner caspase activation

d)

Formation of apoptotic bodies

14.

Which of the following factors does NOT determine the outcome of ischaemia?

a)

Collateral circulation

b)

Metabolic demand

c)

Oxygen extraction reserve

d)

Blood glucose level

15.

Which of the following best describes the structure of smooth muscle cells?

a)

Spindle-shaped with central nucleus and dense bodies

b)

Striated with multiple peripheral nuclei

c)

Branched with intercalated discs

d)

Cylindrical with Z-discs

16.

During relaxation of smooth muscle, which enzyme is responsible for dephosphorylating myosin?

a)

Myosin light-chain kinase (MLCK)

b)

Myosin light-chain phosphatase (MLCP)

c)

SERCA pump

d)

Adenylate cyclase

17.

Which neurotransmitter and receptor combination causes contraction of smooth muscle in vessels?

a)

Acetylcholine (ACh) acting on M2 receptors

b)

Norepinephrine acting on α1 receptors

c)

Norepinephrine acting on β2 receptors

d)

Acetylcholine (ACh) acting on M3 receptors

18.

Compare and contrast the effects of norepinephrine on smooth muscle in vessels versus bronchi, and explain the physiological significance of these differences.

a)

Norepinephrine causes contraction in vessels (via α1) and relaxation in bronchi (via β2), allowing for blood pressure regulation and airway dilation, respectively.

b)

Norepinephrine causes relaxation in both vessels and bronchi, leading to decreased blood pressure and airway constriction.

c)

Norepinephrine causes contraction in both vessels and bronchi, increasing blood pressure and airway resistance.

d)

Norepinephrine has no effect on smooth muscle in either vessels or bronchi.

19.

Explain how pacemaker-like slow waves in single-unit smooth muscle contribute to the function of organs such as the gastrointestinal tract.

a)

They coordinate whole-sheet contractions for peristalsis and mixing of contents.

b)

They inhibit contraction, leading to muscle relaxation.

c)

They cause random, uncoordinated contractions.

d)

They only occur in multi-unit smooth muscle.

20.

What is the definition of an Adverse Drug Reaction (ADR)?

a)

A beneficial response to a drug at normal doses

b)

A harmful, unintended response at normal doses

c)

An allergic reaction to any medication

d)

A response to an overdose of a drug

21.

Which of the following best describes a Type B (Bizarre) adverse drug reaction?

a)

Dose-related and predictable from pharmacology

b)

Idiosyncratic, dose-independent, immune or genetic

c)

Chronic and related to long-term use

d)

Delayed and related to carcinogenesis

22.

Which patient-specific risk factor is associated with increased drug-drug interactions due to polypharmacy?

a)

Age

b)

Genetics

c)

Polypharmacy

d)

Diet

23.

Explain why elderly patients are at increased risk for adverse drug reactions.

a)

They have increased renal/hepatic reserve

b)

They have immature enzymes

c)

They have decreased renal/hepatic reserve

d)

They metabolize drugs faster

24.

Which genetic factor is associated with abacavir hypersensitivity?

a)

CYP2D6 ultrarapid

b)

HLA-B*57:01

c)

CYP3A4

d)

VKORC1

25.

What is the main difference between an Adverse Drug Reaction (ADR) and an Adverse Drug Event (ADE)?

a)

ADRs include overdoses, ADEs do not

b)

ADEs are a subset of ADRs

c)

ADEs are broader and include overdoses and errors, while ADRs are a subset

d)

ADRs are always predictable, ADEs are not

26.

What should be done before prescribing medication to minimize ADRs?

a)

Check renal and hepatic function

b)

Skip patient history

c)

Prescribe the highest dose

d)

Avoid written warnings

27.

Which of the following is NOT part of the practical checklist for minimizing ADRs?

a)

Encourage patients to report unusual symptoms early

b)

Provide written and verbal warnings for serious effects

c)

Ignore electronic prescribing alerts

d)

Ask about allergies and previous ADRs

28.

Which of the following drugs requires therapeutic drug monitoring due to a narrow therapeutic index?

a)

Digoxin

b)

Paracetamol

c)

Ibuprofen

d)

Amoxicillin

29.

Which energy system is dominant in muscle during the first 0-4 seconds of exercise?

a)

Phosphocreatine

b)

Anaerobic glycolysis

c)

Aerobic β-oxidation

d)

Mixed glycolysis + OXPHOS

30.

Considering the statement "Every drug is a potential poison," discuss how pharmacokinetics and genetics can influence the safety and effectiveness of a medication in a patient.

a)

Pharmacokinetics and genetics affect how a drug is processed and responded to, meaning the same drug can be safe for one patient but toxic for another, requiring careful monitoring and respect for individual differences.

b)

All drugs are equally safe for all patients regardless of genetics.

c)

Pharmacokinetics only affects drug effectiveness, not safety.

d)

Genetics has no impact on drug response.