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D&TIII > Ischemic And Hypertensive HD > Flashcards

Ischemic And Hypertensive HD Flashcards

1
Q

Types of Ischemic Heart Disease

A

Angina pectoris
Myocardial infarction
Chronic IHD with heart failure
Sudden cardiac death

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2
Q

Ischemic Hear disease pathogenesis

A

Demand> coronary perfusion due to:

Fixed coronary obstruction
Acute plaque change
Coronary thrombus
Vasospasm

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3
Q

Fixed instructive lesion

A

> 75% cause symptomatic ischemia with exercise

> 90% cause symptomatic ischemia at rest

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4
Q

Acute plaque change

A

Rupture or fissuring
Erosion or ulceration
Hemorrhage into the atheroma

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5
Q

Coronary thrombus

A

Can cause partial occlusion to become total

Thromboangiitis are potent activators of smooth muscle growth-related signals (may contribute to atherosclerotic lesions)

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6
Q

Vasoconstriction

A

Can cause a partial obstruction to become total

Stimulated by:
Adrenergic agonists
Impaired secretion of endothelial cell relaxing factors
Mediators released from perivascular inflammatory cells

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7
Q

Angina Pectoris

A

Paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort

Lasts 15 sec to 15 min

Due to myocardial ischemia

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8
Q

Stable angina

A

Decreased coronary perfusion due to fixed obstruction

Makes heart vulnerable to ischemia caused by physical activity or emotional excitement

Usually relieved by rest or nitroglycerin

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9
Q

Unstable angina

A

1 of ACUTE CORONARY SYNDROMES

Chest pain that occurs with increasing frequency and precipitated by progressively less effort

Due to disruption of atherosclerotic plaque with superimposed partially occluding thrombus

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10
Q

Print metal angina

A

Due to coronary artery spasm

Episodic, may occur at rest

Not related to physical activity, heart rate or blood pressure

Ry: Nitroglycerin and Ca channel blockers

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11
Q

Myocardial infarction

A

2 of the acute coronary syndromes

90% of transmittal infarcts due to acute plaque disruption

Other 10% due to vasospasm +/- atherosclerosis or emboli

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12
Q

MI pathogenesis

A

First seconds: cessation of aerobic glycolysis and decreased creatine phosphate and ATP

> 2 min: loss of contractility begins, may precipitate acute heart failure- changes are still reversible at this point

20-40 min: irreversible injury to myocytes

> 1 hr: microvascular injury

Necrosis complete by 6 hrs

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13
Q

Transmittal infarction

A

Most MIs are transmittal

Associated with atherosclerosis, acute plaque change, and completely obstructive thrombosis

CAUSE ST ELEVATION on EKG

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14
Q

Subendocardial infarct

A

Infarct of inner 1/3-1/2 ventricular wall

area that is least well perfused

Due to atherosclerosis

NO PLAQUE DISRUPTION
NO SUPERIMPOSED THROMBUS

Non-ST elevation

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15
Q

Left anterior descending artery

A

Supplies most of apex, ant wall of left ventricle and ant 2/3 of ventricular septum

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16
Q

Left circumflex artery

A

Supplies lateral wall of left ventricle

If it gives rise to post descending artery (left dominant): supplies post 1/3 of ventricular septumand posterobasal wall of left ventricle

17
Q

Right coronary artery

A

Supplies entire right ventricular wall

If gives rise to post descending artery (right dominant) supplies posterior 1/3 of ventricular septum and posterobasal wall of left ventricle

18
Q

Location of transmittal infarcts

A

Almost always involve left ventricle

LAD 40-50% of infarcts

RCA 30-40% infarcts:
Inferior-posterior wall of left ventricle
Posterior portion of ventricular septum

19
Q

Coronary artery bypass graft

A

Treatment fo rmyocaridal infarction

Revascularization of RCA via a sap genius vein graft and internal mammary artery grafting to the LAD

20
Q

Thrombolytics therapy

A

Treatment for MI

Has no effect on underlying disrupted atherosclerotic plaque

21
Q

Angioplasty (PTCA)

A

Treatment for MI

Can improve stenosis and help stabilize the disrupted plaque

22
Q

Morphology of reperfused myocardium

A

Microscopic: contraction bands (intensely eosinophilic transverse bands of closely packed sarcomeres which contract when exposed to fresh Ca in plasma

23
Q

MI laboratory

A

easier serum levels of intracellular proteins that leak out of fatally injured myocytes:

CK (MM and MB isozymes)

24
Q

CK

A

Rises in first 2 to 4 hrs

Peaks at 24 hrs

CK-MB is sensitive but not specific since it is also found in skeletal muscle

25
Q

Troponins

A

Cardiac specific proteins

Preferred bio markers for myocardial damage

Remain elevated for 7 to 10 days

26
Q

MI consequences and complications

A

Contractile dysfunction causing hypotension, pulmonary vascular congestion

Arrhythmias
Sinus bradycardia
Asystole
Tachycardia
ventricular premature contractions
Ventricular tachycardia
Ventricular fibrillation
27
Q

Myocardial rupture

A

3-7 days after MI

Of ventricular free wall-(most common) cardiac tamponade

Of ventricular septum (less common)- left to right shunting

Of papillary muscle (least common)- severe mitral regurgitation

28
Q

Pericarditis

A

Consequence for MI

2-3 days: fibrinoid or fibrinohemorrhagic, pericardium overlying inflamed myocardium

29
Q

Mural thrombus

A

Abnormal contractility or endocardium damage (may embolize)

Consequence of MI

30
Q

Ventricular aneurysm

A

Consequence of MI

Result of large transmittal anteroseptal infarct

Complications:
Mural thrombus
Arrhythmias
Heart failure
Rupture is rare because scar tissue is strong
31
Q

Anterior transmittal infarcts

A

Free-wall rupture, expansion, mural thrombus, and aneurysm, worse clinical course

32
Q

Inferior transmittal infarcts

A

Conduction blocks, right ventricular involvement

33
Q

Chronic ischemic heart disease

A

Coronary arteries: moderate to severe stenosis

Most patients have previous Mi or a final attacks when develop heart failure

34
Q

Sudden Cardiac Death

A

3 of the acute coronary syndromes

Ultimate mechanism: lethal arrhythmia (asystole, V fib)

35
Q

Systemic left-sided hypertensive heart disease

A

History of htn

Hypertrophy is adaptive response to pressure overload

Can lead to:
Myocardial dysfunction
Cardiac dilation
CHF
Sudden death
36
Q

Systemic left-sided hypertensive heart disease morphology

A

Eventually wall stiffens and impairs diastolic filling and LA enlarges

37
Q

Systemic left-sided hypertensive heart disease clinical

A

May present as atrial fibrillation (due to dilated LA) or CHF with atrial dilation or both

May be asymptomatic and picked up on EKG

38
Q

Pulmonary right-sided hypertensive heart disease

A

RV hypertrophy

Due to pulmonary htn from disorders of lungs or pulmonary vasculature

39
Q

Pulmonary hypertensive heart disease morphology

A

Acute:
RV dilates
NO increase in wall thickness

Chronic:
Ventricular wall thickens
May compress LV chamber
Tricuspid regurgitation may occur due to fibrous thickening of valve

D&TIII (9 decks)

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