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Pathophysiology I - Exam 3 (Final) > Cardio Module 5 > Flashcards

Cardio Module 5 Flashcards

1
Q

What are diseases of veins?

A
  • varicose v.
  • chronic venous insufficiency
  • DVT
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2
Q

define varicose v.

A
  • pooling of blood in superficial v. of lower
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3
Q

etiology of varicose v.

A

valve damage via
- trauma
- prolonged venous distention
can lead to edema w/in local tissue

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4
Q

What causes transient varicose v.?

A
  • pregnancy
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5
Q

What is CVI?

A
  • insufficient venous return from the LE for chronic periods of time
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6
Q

CVI etiology

A
  • DVT
  • valve deficiency/varicose v.
  • lack of muscle pump
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7
Q

CVI complications

A
  • poor healing of local trauma/pressure sores may develop into venous stasis ulcers
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8
Q

What is the difference b/t thrombus vs. thromboembolism?

A
  • attached to vessel wall vs. free floating
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9
Q

factors in DVT

A

Virchow’s Triad

  • venous stasis
  • endothelial damage
  • hypercoagulable states
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10
Q

What is used to identify DVT?

A
  • Wells Criteria
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11
Q

What does a high Wells Criteria indicate? low?

A
  • high risk of DVT

- low risk of DVT

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12
Q

diseases of arteries?

A
  • aneurysm
  • thrombi/emboli
  • PAD (atherosclerotic vs. non)
  • HTN, hypotension
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13
Q

pathogenesis of AAA

A
  1. destruction of elastin and collagen
  2. inflammation
  3. biochemical wall stress
  4. family hx
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14
Q

classifications of AAA by layers

A
  • true (all 3 layers of vessel)

- false (only the outer layer)

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15
Q

classification of AAA by shape

A
  • saccular (side pocket)

- fusiform (circumferential widening of artery)

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16
Q

MC origin of arterial thrombembolism

A
  • heart valve disease
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17
Q

Where can a dislodged left heart valve thrombi obstruct?

A
  • LE circulation
  • coronary circulation
  • cerebral circulation (stroke)
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18
Q

other forms of arterial emboli

A
  • air
  • fat
  • amniotic fluid
  • bacteria
  • FB
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19
Q

What is the MC form of PAD?

A
  • atherosclerotic
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20
Q

pathogenesis of PAD?

A
  • grows a plaque
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21
Q

primary site of PAD involvement

A
  • femoral + popliteal
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22
Q

ABI values

A
  • normal: 0.9-1.3

- severe:

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23
Q

ABI values correlated w/ sxs

A
  • normal: >0.90
  • claudication (leg pain): 0.5-0.9
  • rest pain: 0.21-0.49
  • tissue loss:
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24
Q

define intermittent claudication

A
  • exertional pain pattern
  • similar to stable angina pectoris
  • common in calves
25
Q

ddx b/t neurogenic and intermittent claudication

A
  • neuro = positional

- intermittent = exertional

26
Q

What aggravates rest pain?

A
  • LE elevation
27
Q

What are the non-atherosclerotic PAD?

A
  • thromboangiitis obliterians

- raynauds

28
Q

what is thrmoboaniitis obliterians assocaited with?

A
  • NICOTINE
29
Q

define thromboangiitis obliterians

A
  • inflam of peripheral a. (small vessels)
30
Q

T/F: Thromboangiiitis obliterians does not have atherosclerotic changes in effected blood vessels.

A
  • true
31
Q

thromboangiitis obliterians common regions

A
  • distal extremities
32
Q

thromboangiitis obliterians common sx

A
  • distal extremity ischemic pain + ulcers
33
Q

pathogenesis of raynauds

A
  • nitric oxide dysfunction + sympathetic feedback mechanism for blood vessel
    (looses the ability to adapt)
34
Q

clinical presentation of raynauds

A
  • vasospasm followed by throbing rubor
35
Q

two types or raynauds

A
  • phenomenon (secondary)

- disease (primary)

36
Q

classification of HTN

A
  • normal: 140/90
37
Q

pathogenesis of HTN

A
  • increased CO
  • increased TPR
  • OR both
38
Q

pathological factors of HTN

A
  • genetics
  • sympathetic dysfunction
  • rena-angiotensin-aldosterone system
  • natriuritic peptides
  • chronic inflam (precursor to growing plaques)
  • insulin resistance
  • obesity
39
Q

How does sympathetic dysfunction affect HTN?

A
  • increased HR
  • increased vascular resistance
  • promotes insulin resistance via NO signaling which inhibits vasodilation which increases resistance
  • promotes coagulation
40
Q

how does insulin resistance affect HTN?

A
  • less NO production and endothelial dysfunction leads to inhibits vasodilation
41
Q

What mechanisms get screwed up for orthostatic hypotension to happen?

A
  • increased HR and v./a. vasoconstriction
  • stretch receptors stimulus of increased sympathetic response
  • mechanical systesm
42
Q

criteria of orthostatic hypotension

A
  • BP changes within 3 mins of standing
43
Q

what are the clinical presentation types of orthostatic hypotension?

A
  • transient/acute

- chronic

44
Q

4 stages of plaque development

A
  • endothelial injury –> inflam
  • fatty streaks
  • fibrous plaque formation
  • complicated or unstable plaques
45
Q

describe the pathogenesis of plaque development via endothelial injury

A
  • inflam mediators –> smooth m. proliferation

- becomes foam cell

46
Q

describe the pathogenesis of plaque development via fatty plaque

A
  • accumulation of foam cells

- migration of smooth muscle into the area continues

47
Q

describe the pathogenesis of plaque development via fibrous plaque

A
  • collagen
48
Q

describe a complicated plaque

A
  • ruptured
49
Q

dyslipidemia values

A
  • LDL: high = 160-189, very high = >190
  • triglycerides: high = 200-499, very high >500
  • total cholesterol: high risk = >240
  • HDL: low =
50
Q

risks of CAD

A
  • total cholesterol > 240
  • HDL 160
  • triglycerides >200
51
Q

What happens if too much homocysteine?

A
  • inhibits key enzymes in collagen and elastin production

- leads to increased CAD risk

52
Q

pathophysiology of MI

A
  • narrowing of coronary a. for 10s.
  • loss of contractility
  • conduction abnormalities
  • lactic acid accumulation
53
Q

MC cause of MI

A
  • atherosclerosis in form of CAD
54
Q

non MC cause of MI

A
  • decreased delivery of blood to myocardium (coronary spasm, hypotension, arrhythmias, decr O2 capacity)
  • increased demand for O2 by myocardium (tachycardia + exercise, HTN, cardiac hypertrophy, valve dysfunction/dz)
55
Q

describe stable angina

A
  • transient episode of blood flow impairment
  • recurrent episodes lasting 3-5m
  • relieved w/ rest
  • predictable
56
Q

describe silent angina

A
  • MI w/o obvious signs and symptoms

- common following conditions/surgical procedures

57
Q

acute coronary syndromes

A
  • unstable angina

- MI

58
Q

T/F: 80% of patients with unstable angina will have MI or death from MI within 30d.

A
  • false, 20%

Pathophysiology I - Exam 3 (Final) (5 decks)

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