flashcard 3

(45 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.

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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.

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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.

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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.

21
Q

What is the primary apolipoprotein in LDL particles?

A

Apolipoprotein B-100 (apoB-100) is embedded in LDL and necessary for receptor-mediated uptake in tissues.

22
Q

Which lipoprotein is the largest and richest in triglycerides?

A

Chylomicrons, with over 85% triglyceride content, transport dietary lipids from the intestine.

23
Q

Describe the significance of very-low-density lipoprotein (VLDL) in lipid metabolism.

A

VLDL transports endogenous triglycerides from the liver to peripheral tissues and eventually becomes IDL and LDL after triglyceride removal.

24
Q

How does HDL reduce atherosclerotic risk?

A

HDL mediates reverse cholesterol transport by carrying cholesterol from peripheral tissues back to the liver for excretion.

25
What liver function alteration is associated with non-alcoholic fatty liver disease (NAFLD) in metabolic syndrome?
Elevated ALT and AST levels due to hepatocellular lipid accumulation and injury.
26
List four major types of diabetes mellitus.
Type 1 diabetes mellitus (autoimmune β-cell destruction), Type 2 diabetes mellitus (insulin resistance and relative insulin deficiency), gestational diabetes, and maturity-onset diabetes of the young (MODY).
27
What is latent autoimmune diabetes of adults (LADA)?
A slowly progressive form of autoimmune diabetes in adults that shares features of both type 1 and type 2 and often initially misdiagnosed as type 2.
28
Why is measuring glycated hemoglobin (HbA1c) clinically valuable?
HbA1c reflects average blood glucose over the preceding 8–12 weeks, helping assess long-term glycemic control.
29
Define the normal fasting blood glucose range and the threshold for diagnosing diabetes.
Normal fasting blood glucose is 4–6 mM; a fasting level >11 mM is diagnostic of hyperglycemia and likely diabetes.
30
How does a glucose tolerance test distinguish between normal and diabetic responses?
In a healthy individual, blood glucose returns to normal (<7.8 mM) within 2 hours post-glucose load, whereas in diabetes, glucose remains elevated (>11 mM).
31
What metabolic changes occur in diabetic ketoacidosis (DKA)?
Insulin deficiency causes increased lipolysis, elevated free fatty acids, excessive ketone body production, metabolic acidosis, and osmotic diuresis leading to dehydration.
32
Which ketone bodies rise first in the blood during the onset of DKA?
Beta-hydroxybutyrate (β-HB) and acetoacetate increase initially; acetone is produced in smaller quantities and exhaled.
33
How does hyperglycemia in DKA contribute to dehydration?
High plasma glucose exceeds renal tubular reabsorption, leading to osmotic diuresis and loss of water (polyuria), causing dehydration.
34
What is the typical renal threshold for glucose reabsorption in healthy individuals?
Approximately 10 mM (180 mg/dL); above this, glucose spills into urine (glycosuria).
35
Explain the compensatory hyperinsulinemia seen in early type 2 diabetes.
Insulin resistance in peripheral tissues prompts pancreatic β-cells to increase insulin secretion to maintain normoglycemia initially.
36
What happens to β-cell function over time in untreated type 2 diabetes?
Chronic hyperstimulation leads to β-cell dysfunction, declining insulin secretion, and worsening hyperglycemia.
37
Why is fasting insulin elevated before the clinical diagnosis of type 2 diabetes?
The pancreas compensates for insulin resistance by secreting more insulin to maintain normal glucose levels until β-cells begin failing.
38
How can urinary dipstick testing be used in the initial assessment of suspected diabetes?
Detection of glucose and ketones in urine indicates hyperglycemia and potential ketoacidosis, warranting further blood testing.
39
Which test provides a “snapshot” of plasma glucose at a single time point, and why is timing important?
Fasting blood glucose; it must be measured after an overnight fast to avoid postprandial variability.
40
What is the expected 2-hour post-load blood glucose in a normal oral glucose tolerance test?
Less than 7.8 mM (140 mg/dL) at 2 hours; values ≥11.1 mM (200 mg/dL) indicate diabetes.
41
In type 2 diabetes, which phase of insulin response is often blunted first?
The first-phase insulin response (immediate release of preformed insulin granules) is impaired early, causing postprandial hyperglycemia.
42
How does increased free fatty acid release in DKA affect hepatic gluconeogenesis?
Free fatty acids provide substrates (glycerol) and upregulate gluconeogenic enzymes, further elevating blood glucose.
43
Why is monitoring serum potassium critical in DKA management?
Insulin treatment drives potassium into cells, risking hypokalemia; initial hyperkalemia may mask total body potassium depletion.
44
Which lipid profile change is most characteristic of uncontrolled type 2 diabetes?
Elevated triglycerides (increased VLDL) and low HDL, often with small dense LDL particles.
45
Name one structural component common to all lipoprotein particles.
A phospholipid monolayer with embedded apolipoproteins (e.g., apoB-100 in LDL, apoA-I in HDL).