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Pathopharm Exam 1 > Week 1: CV Part 3 > Flashcards

Week 1: CV Part 3 Flashcards

1
Q

ECG alterations associated with ischemia (3)

A

ST depression
ST elevation
T-wave inversion

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2
Q

How does ischemia affect ECG leads (2)

A

damaged area will have less effect on that particular lead
complete reversal because the signal wont travel that area the same way

(slide 53, per Dr Dick)

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3
Q

Angiotensin II Systemic effects (2)

A

Peripheral vasoconstriction
fluid retention

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4
Q

is secreted from kidney and helps produce Angiotensin I

A

Renin

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5
Q

which is a more potent vasoconstrictor: angiotensin I or angiotensin II?

A

angiotensin II

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6
Q

Increasing Angiotensin leads to (2)

A

↑vasoconstriction
↑aldosterone (works in kidneys to ↑ salt and water reabsorption which increases BP)

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7
Q

angiotensinogen comes from the

A

liver
“gen” on the end means precursor protien

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8
Q

T/F Lots of BP meds block Angiotensin converting enzyme and ARB’s

A

True

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9
Q

if angiotensin is secreted, myocardial work increases or decreases?

A

increases–> thus the effects of loss of myocyte contractility are exacerbated

bec of the increase in vasoconstriction (afterload)
and increasing afterload means heart has to push harder against it

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10
Q

Angiotensin II Local effects (3)

A

Growth factor for vascular smooth muscle cells, myocytes, and cardiac fibroblasts.
Promotes catecholamine release
Causes coronary artery spasms

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11
Q

Involved in myocardial remodeling and causes myocyte hypertrophy, scarring and loss of contractile function in areas of heart distant from infarction site

A

angiotensin II

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12
Q

Types of myocardial infarction (2)

A

Subendocardial infarction
Transmural infarction

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13
Q

non-STEMI region

A

subendocardial

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14
Q

STEMI is a __________ infarction

A

transmural infarction

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15
Q

T/F: smaller infarctions are associated with ST segment elevations (STEMI)

A

False
smaller infarctions are NOT assoc with ST segment elevations (non-STEMI)

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16
Q

infarcted myocardium is surrounded by a zone of ____ ____, which may progress to necrosis or return to normal

A

hypoxic injury

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17
Q

how can infarcted myocardium return to normal

A

if blood flow is returned fast enough

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18
Q

drug that help break up clot and restore BF to infarcted area/tissue

A

thrombolytics

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19
Q

adjacent to the zone of hypoxic injury is a zone of

A

reversible ischemia

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20
Q

2 enzymes that are markers for myocardial infarction

A

Creatine phosphokinase–MB (CPK-MB) and LDH-1

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21
Q

Which biomarker is most specific for myocardial damage?

A

Troponin I, which elevates in 2 to 4 hours post-infarction.

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22
Q

Troponin I elevates betw. how many hours post-infarction?

A

2 to 4 hours

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23
Q

clinical manifestations of myocardial infarction

A

Sudden severe chest pain (radiating to left arm or jaw/shoulder pain)
ECG changes
↑Troponin I
↑Creatine phosphokinase–MB (CPK-MB), LDH-1
Hyperglycemia (d/t alterations in glucose metabolism)

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24
Q

Treatment of MI (7)

A

Hospitalization
O2 & aspirin
Morphine
Bed rest (↓workload)
Cardiac meds: Thrombolytic, antithrombotic, vasodilators
Percutaneous coronary intervention (PCI)
Surgery

25
Q

why is immediate administration of O2 critical with MI?

A

To avoid further damage to the area surrounding the ischemic zone

26
Q

if infarction occurs in area that contains ______ tissue, dysrhythmias are more likely to occur

A

conductive

27
Q

MI complications

A

Dysrhythmias
Cardiogenic shock
Pericarditis
Dressler (postinfarction) syndrome (pericarditis)
Organic brain syndrome

28
Q

Disorders of the pericardium (3)

A

acute pericarditis
pericardial effusion
Constrictive (restrictive) pericarditis

29
Q

acute inflammation of pericardium with fever, myalgias, and malaise, followed by the sudden onset of severe chest pain

A

acute pericarditis

30
Q

treatment of acute pericarditis

A

Rest, salicylates and nonsteroidal anti-inflammatory drugs
combined nonsteroidals and colchicine

31
Q

Treatment of pericardial effusion

A

Pericardiocentesis

32
Q

Accumulation of fluid in the pericardial cavity; Tamponade

A

Pericardial effusion

33
Q

Fibrous scarring w/occasional calcification of pericardium that causes visceral and parietal pericardial layers to adhere

A

Constrictive (restrictive) pericarditis

34
Q

Clinical manifestations of Constrictive (restrictive) pericarditis

A

Exercise intolerance, dyspnea on exertion, fatigue, and anorexia

35
Q

Treatment of Constrictive (restrictive) pericarditis

A

Dietary sodium restriction
digitalis glycosides
and diuretics improve cardiac output.

36
Q

Effects of neurohumoral responses to ischemic heart disease or hypertension on the heart muscle cause remodeling

A

cardiomyopathies

37
Q

(T/F) Most cases of cardiomyopathy are not idiopathic

A

False
Many cases of cardiomyopathy are idiopathic

38
Q

Types of cardiomyopathies (3)

A

Dilated (congestive) cardiomyopathy

Hypertrophic (asymmetric)
Hypertrophic obstructive
Valvular/Hypertensive hypertrophic

Restrictive cardiomyopathy

39
Q

clinical manifestations of restrictive cardiomyopathy

A

Right heart failure occurs with systemic venous congestion

“Restrictive = R HF”

40
Q

treatment for restrictive cardiomyopathy

A

correct underlying cause

41
Q

what type of cardiomyopathy has Impaired systolic function, leading to increases in intracardiac volume, ventricular dilation, and systolic heart failure

A

Dilated (congestive) cardiomyopathy

42
Q

causes of Dilated (congestive) cardiomyopathy (5)

A

MI
diabetes
alcohol
deficiencies of niacin, vitamin D and selenium
hyperthyroidism

43
Q

which cardiomyopathy has clinical manifestations of Dyspnea and fatigue

A

Dilated (congestive) cardiomyopathy

“Dilated =Dyspnea”

44
Q

Common inherited heart defect of a thick septal wall

A

Hypertrophic obstructive cardiomyopathy

45
Q

Hypertrophic obstructive cardiomyopathy treatment (4)

A

-Beta blockers or verapamil (slow the heart rate)
-Surgical resection of the hypertrophied myocardium
-Septal ablation
-Prophylactic implantable cardioverter-defibrillators in high-risk individuals

46
Q

clinical manifestations of Hypertrophic obstructive cardiomyopathy (3)

A

Angina, syncope, palpitations

47
Q

2 types of Hypertrophic (asymmetric) cardiomyopathy

A

-Hypertrophic obstructive
-Hypertensive/valvular

48
Q

Hypertrophy of the myocytes: Attempts to compensate for increased myocardial workload

A

Hypertensive or valvular hypertrophic cardiomyopathy

49
Q

Clinical manifestations of Hypertensive or valvular hypertrophic cardiomyopathy (6)

A

Asymptomatic
or may complain of angina, syncope, dyspnea on exertion, and palpitations

50
Q

Myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures during diastol

A

Restrictive cardiomyopathy

51
Q

Clinical manifestations: Right heart failure occurs with systemic venous congestion

A

restrictive cardiomyopathy

52
Q

Valve orifice is constricted and narrowed

A

valvular stenosis

53
Q

valve fails to shut completely and aka insufficiency or incompetence

A

valvular regurgitation

54
Q

Disorders of the endocardium (9)

A

valvular dysfunction
valvular stenosis
valvular regurgitation
mitral valve prolapse syndrome
aortic stenosis
mitral stenosis
aortic regurgitation
mitral regurgitation
tricuspid regurgitation

(endocardium = valves)

55
Q

A diffuse, inflammatory disease caused by a delayed immune response to infection by the group A beta-hemolytic streptococci

A

Rheumatic fever

56
Q

febrile illness with inflammation of joints, skin, nervous system and heart

A

Rheumatic fever

57
Q

what can happen if rheumatic fever is left untreated

A

can cause rheumatic heart disease (may have genetic component)

58
Q

treatment of restrictive cardiomyopathy (1)

A

treat underlying issue

Pathopharm Exam 1 (9 decks)

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