7 Flashcards

(20 cards)

1
Q

What initiates the pathophysiological sequence leading to a myocardial infarction?

A

The gradual buildup of an atherosclerotic plaque in a coronary artery, followed by plaque rupture and thrombus formation that limits blood flow to the myocardium.

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2
Q

Which inflammatory cells accumulate in the arterial wall during plaque formation?

A

Macrophages, neutrophils, and T cells infiltrate the intima and contribute to foam cell formation.

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3
Q

What is the role of foam cells in atherosclerotic plaque development?

A

Foam cells are macrophages that have ingested lipids; they accumulate in the arterial intima and contribute to plaque growth and instability.

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4
Q

Name three enzymes used to detect myocardial infarction and note one key limitation of each.

A

Creatine kinase (CK) is sensitive but non-specific; aspartate aminotransferase (AST) can be elevated in liver injury; lactate dehydrogenase (LDH) is not heart-specific.

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5
Q

Why might troponin be preferred over CK in later timepoints post-MI?

A

Troponin remains elevated for a longer duration (up to 7–10 days) and is more specific to cardiac muscle damage.

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6
Q

At approximately how many hours post-infarction does troponin typically become detectable?

A

Troponin becomes detectable around 4–6 hours after myocardial injury but may not peak until 12–24 hours.

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7
Q

What is the diagnostic role of FABP (fatty acid–binding protein) in MI?

A

FABP rises very early (within 1–3 hours) after myocardial injury, making it useful for early detection, although it is less specific than troponin.

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8
Q

Describe the timeline differences between CK-MB and troponin elevations post-MI.

A

CK-MB rises around 4–6 hours, peaks at about 12–24 hours, and returns to baseline by 48–72 hours, whereas troponin rises similarly but remains elevated up to 7–10 days.

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9
Q

How can LDH isoenzyme patterns help confirm an MI?

A

LDH-1 and LDH-2 patterns reverse (LDH-1 > LDH-2) after MI; this ‘flip’ typically occurs 2–3 days post-infarction.

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10
Q

Why is sampling time critical when interpreting cardiac enzyme levels?

A

Because each enzyme has a characteristic rise and fall, and collecting blood at peak or trough without considering timing can lead to false negatives or misinterpretation.

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11
Q

Which marker remains elevated longest after an MI, making it useful for late presentations?

A

LDH (especially LDH-1) can remain elevated up to 10 days, useful if patients present late.

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12
Q

List four components measured in standard liver function tests (LFTs).

A

Total protein (albumin and globulins), bilirubin (direct and indirect), transaminases (AST and ALT), and gamma-glutamyl transpeptidase (GGT) or alkaline phosphatase (ALP).

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13
Q

What does a low albumin-to-globulin (A/G) ratio suggest?

A

It may indicate chronic liver disease, inflammation, or increased globulin production (e.g., infection or autoimmune conditions).

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14
Q

Which enzyme is more specific to hepatocellular injury: AST or ALT?

A

ALT is more specific to the liver, whereas AST is also found in cardiac and skeletal muscle.

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15
Q

How is conjugated (direct) bilirubin formed in the liver?

A

Unconjugated bilirubin is conjugated by UDP-glucuronosyltransferases (UGTs) to form water-soluble bilirubin diglucuronide before excretion.

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16
Q

What clinical condition leads to elevated indirect (unconjugated) bilirubin?

A

Hemolysis or impaired uptake/conjugation in the liver, such as in Gilbert’s syndrome.

17
Q

Which medications or conditions can raise GGT without hepatic injury?

A

Chronic alcohol use, anticonvulsants (e.g., phenytoin), or cholestatic conditions can elevate GGT independently of hepatocellular damage.

18
Q

How does alkaline phosphatase (ALP) elevation help differentiate types of liver injury?

A

Marked ALP elevation suggests cholestatic or biliary obstruction, whereas minimal ALP rise with high ALT/AST indicates hepatocellular injury.

19
Q

Which lipoprotein class is most strongly associated with increased risk of atherosclerosis?

A

Low-density lipoprotein (LDL) is considered ‘bad cholesterol’ because high levels promote plaque formation.

20
Q

Outline the composition differences between HDL and VLDL particles.

A

HDL has a high protein-to-lipid ratio (~55% protein) and carries cholesterol away from tissues, whereas VLDL is richer in triglycerides (~50% TAG) and transports endogenous lipids from the liver.