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Clinical Pathology > Cardiovascular diseases > Flashcards

Cardiovascular diseases Flashcards

1
Q

What is ischaemic heart disease?

A

Inadequate blood supply to the myocardium

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2
Q

What are the main causes of ischaemic heart disease?

A
  • Atherosclerosis and/or thrombus*
  • Myocardium hypertrophy due to systemic hypertension
  • any imbalance in supply vs demand
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3
Q

At what % occlusion does auto regulation of the coronary arteries breaks down?

A

75% occlusion

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4
Q

At what % occlusion does auto regulation of coronary arteries break down at rest?

A

90% occlusion

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5
Q

What happens with acute cardiac ischaemia?

A

Myocyte dysfunction/death due to blood flow and loss of aerobic metabolism

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6
Q

What is the length of time where damage is reversible with ischaemia?

A

20-30 mins

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7
Q

At what point in the cardiac cycle doe cardiac perfusion occur?

A

Diastole

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8
Q

What are the 3 types off angina pectoris?

A

Stable/typical - fixed dysfunction and predictable symptoms

Variant/prinxmetal - coronary artery spasm - effects less predictable

Crescendo/unstable - red flag - usually due to plaque disruption - worsening symptoms, unpredictable (MI risk = high)

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9
Q

What two syndromes come under acute coronary syndrome?

A

MI - irreversible damage of myocytes

Crescendo/unstable angina (similar - treated in same way)

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10
Q

There are two types of MI - what are they?

A

Subendocardial - non full thickness** (most vulnerable region - poorly perfused)

Transmural - regional (kills entire wall)

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11
Q

What is the main characteristic of subendocarial infarction?

A

Doesn’t need acute coronary occlusion to occur MISMATCH BETWEEN DEMAND AND SUPPLY

  • because it is normally poorly perfused, can occur with stable atherosclerotic occlusion of coronary circulation and following a hypotensive episode
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12
Q

What are subendocardial MIs also referred to as?

A

Non-ST elevation MI

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13
Q

Why are transmural MIs so debilitating?

A

Death of large region (entire wall) - results in necrosis, fibrosis and formation of fibrous (collagen) scar - cannot pump properly (loss of specialised tissue)

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14
Q

Name the 5 stages of MI morphology (24hrs -6 weeks)

A

24hrs - normal

1-2 days - pale, oedema with myocyte necrosis and neutrophils

3-4 days - yellow with haemorrhagic edge, myocyte necrosis with macrophage invasion

1-2 weeks - pale, thin (red/grey) - granulation tissue then fibrosis

3-6 weeks - fibrotic scar formation (collagen) (can’t tell how old it is after 4 weeks)

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15
Q

What are the 2 main markers of cardiac damage?

A

TROPONIN T and I (detectable after 2-3 hrs, peaks at 12, detectable for 1 week)

CREATINE KINASE MB - detectable 2-3h, peaks 10-24 hrs, detectable for 3 days

Also myoglobin (peaks 2hrs) but non-specific - skeletal muscle too

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16
Q

What are the 3 subtypes of creatine kinase

A

CK MM - skeletal muscle and cardiac
CK BB - brain and lung
CK MB - mainly cardiac but also skeletal

17
Q

Name some of the complications of MI

A
  • Contractile dysfunction and chronic heart failure
  • VF, arrhythmias, sudden cardiac death
  • Myocardial rupture
  • Ventricular aneurysm
  • Mural thrombus - stroke!
  • Autoimmune pericarditis (Dressler’s syndrome) (3 day mark - neutrophil inflammatory response)
18
Q

What is chronic ischaemic heart disease characterised by?

A

Hypertrophy and dilatation

19
Q

What can chronic IHD cause?

A

Sudden death/MI/angina pectoralis on exertion

20
Q

what is hypercholestroaemia and what are the most common types?

A

Mutations of genes involved in cholesterol metabolism

LDL receptor (1 in 500)
Apolipoprotein B (1 in 1000)
21
Q

What do individuals with heterozygotic hypercholesterolaemia develop?

A
  • cholesterol deposit (foam cells to endothelium - atherosclerosis)
  • tendon, perioccular, corneus arcus, early atherosclerosis

STATINS EFFECTIVE

22
Q

What are considered abnormal diastolic and systolic BPs?

A 
Diastolic = above 90 mmHg
Systemic = above 140 mmHg
23
Q

What is the effect of hypertension on the heart?

A

LV hypertrophy without dilatation (initially then subsequent dilatation when it fails to pump blood sufficiently - final stage)

24
Q

What is the main effect of hypertension on the renal system?

A

Slow deterioration of renal function - chronic renal failure (damage to vessels - arterial intimal fibroelastosis)

Kidneys have stippled appearance

25
Q

What can hypertension cause in the brain? (hypertensive cerebrovascular disease)

A

Berry aneurysm

Intracerebral haemorrhage

26
Q

What is acute hypertensive crisis and what does it cause?

A

Rapid increase in BP above 180/120 mmHg

Causes organ failure - hypertensive encephalopathy (brain - confusion, vomiting, convulsions, coma/death), renal failure and retinal haemorrhage

27
Q

What is pulmonary hypertension and what is it caused by?

A
  • Increased pressure in pulmonary vasculature

Caused by loss of pulmonary vasculature

  • chronic obstructive lung disease
  • pul thrombi/emboli
  • reduced alveoli vent
  • Interstitial lung disease
28
Q

What does pulmonary hypertension cause?

A
  • Increased pulmonary resistance (OEDEMA)
  • Increase RV work to pump blood
  • RV hypertrophy and later dilatation as RV failure occurs
29
Q

Name some causes of secondary hypertension

A

Renal - acute glomerulonephritis, chronic renal disease, polycystic kidneys

Endocrine - Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, hyperthyroidism

CV - coarticulation of aorta

30
Q

Describe RAAS

A
  • Angiotensinogen converted to Angiotensin I by renin (produced in juxtaloglomerular apparatus in kidney)
  • angiotensin I converted to angiotensin II (lungs many - why ACE inhibitors cause chronic cough) - potent vasoconstrictor
  • angiotensin II also stimulate adrenal cortex release of aldosterone (Na and H2O retention - increased circulating volume and increased BP)
31
Q

What is CONNS syndrome and how is it caused?

A

Excess aldosterone secretion from adrenal cortex

Usually adrenocortical carcinoma/adenoma

32
Q

How is CONNS syndrome characterised and what does it cause?

A

high aldosterone with low renin

High BP (Na and H2O retention)

K loss - metabolic alkalosis, muscle weakness, arrhythmia

33
Q

What is pheochromocytoma and what does it cause?

A

Tumour of the adrenal medulla

Excessive synthesis and secretion of catecholamines - increase adrenaline/NA - increases vasoconstriction and BP

34
Q

What is cushing’s disease and what is it mostly caused by?

A

Overproduction of CORTISOL from adrenal cortex

Caused by pituitary adenoma (80%), adrenocortical adenoma or paraneoplastic effect of other neoplasms

35
Q

What does Cushings disease cause?

A

Hypertensive effect - cortisol has metabolic effects - increases sympathetic NS active

Clinical Pathology (50 decks)

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