1
Q
What are diseases of veins?
A
- varicose v.
- chronic venous insufficiency
- DVT
2
Q
define varicose v.
A
- pooling of blood in superficial v. of lower
3
Q
etiology of varicose v.
A
valve damage via
- trauma
- prolonged venous distention
can lead to edema w/in local tissue
4
Q
What causes transient varicose v.?
A
- pregnancy
5
Q
What is CVI?
A
- insufficient venous return from the LE for chronic periods of time
6
Q
CVI etiology
A
- DVT
- valve deficiency/varicose v.
- lack of muscle pump
7
Q
CVI complications
A
- poor healing of local trauma/pressure sores may develop into venous stasis ulcers
8
Q
What is the difference b/t thrombus vs. thromboembolism?
A
- attached to vessel wall vs. free floating
9
Q
factors in DVT
A
Virchow’s Triad
- venous stasis
- endothelial damage
- hypercoagulable states
10
Q
What is used to identify DVT?
A
- Wells Criteria
11
Q
What does a high Wells Criteria indicate? low?
A
- high risk of DVT
- low risk of DVT
12
Q
diseases of arteries?
A
- aneurysm
- thrombi/emboli
- PAD (atherosclerotic vs. non)
- HTN, hypotension
13
Q
pathogenesis of AAA
A
- destruction of elastin and collagen
- inflammation
- biochemical wall stress
- family hx
14
Q
classifications of AAA by layers
A
- true (all 3 layers of vessel)
- false (only the outer layer)
15
Q
classification of AAA by shape
A
- saccular (side pocket)
- fusiform (circumferential widening of artery)
16
Q
MC origin of arterial thrombembolism
A
- heart valve disease
17
Q
Where can a dislodged left heart valve thrombi obstruct?
A
- LE circulation
- coronary circulation
- cerebral circulation (stroke)
18
Q
other forms of arterial emboli
A
- air
- fat
- amniotic fluid
- bacteria
- FB
19
Q
What is the MC form of PAD?
A
- atherosclerotic
20
Q
pathogenesis of PAD?
A
- grows a plaque
21
Q
primary site of PAD involvement
A
- femoral + popliteal
22
Q
ABI values
A
- normal: 0.9-1.3
- severe:
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:
24
Q
define intermittent claudication
A
- exertional pain pattern
- similar to stable angina pectoris
- common in calves
25
ddx b/t neurogenic and intermittent claudication
- neuro = positional
| - intermittent = exertional
26
What aggravates rest pain?
- LE elevation
27
What are the non-atherosclerotic PAD?
- thromboangiitis obliterians
| - raynauds
28
what is thrmoboaniitis obliterians assocaited with?
- NICOTINE
29
define thromboangiitis obliterians
- inflam of peripheral a. (small vessels)
30
T/F: Thromboangiiitis obliterians does not have atherosclerotic changes in effected blood vessels.
- true
31
thromboangiitis obliterians common regions
- distal extremities
32
thromboangiitis obliterians common sx
- distal extremity ischemic pain + ulcers
33
pathogenesis of raynauds
- nitric oxide dysfunction + sympathetic feedback mechanism for blood vessel
(looses the ability to adapt)
34
clinical presentation of raynauds
- vasospasm followed by throbing rubor
35
two types or raynauds
- phenomenon (secondary)
| - disease (primary)
36
classification of HTN
- normal: 140/90
37
pathogenesis of HTN
- increased CO
- increased TPR
- OR both
38
**pathological factors of HTN**
- genetics
- sympathetic dysfunction
- rena-angiotensin-aldosterone system
- natriuritic peptides
- chronic inflam (precursor to growing plaques)
- insulin resistance
- obesity
39
How does sympathetic dysfunction affect HTN?
- increased HR
- increased vascular resistance
- promotes insulin resistance via NO signaling which inhibits vasodilation which increases resistance
- promotes coagulation
40
how does insulin resistance affect HTN?
- less NO production and endothelial dysfunction leads to inhibits vasodilation
41
What mechanisms get screwed up for orthostatic hypotension to happen?
- increased HR and v./a. vasoconstriction
- stretch receptors stimulus of increased sympathetic response
- mechanical systesm
42
criteria of orthostatic hypotension
- BP changes within 3 mins of standing
43
what are the clinical presentation types of orthostatic hypotension?
- transient/acute
| - chronic
44
4 stages of plaque development
- endothelial injury --> inflam
- fatty streaks
- fibrous plaque formation
- complicated or unstable plaques
45
describe the pathogenesis of plaque development via endothelial injury
- inflam mediators --> smooth m. proliferation
| - becomes foam cell
46
describe the pathogenesis of plaque development via fatty plaque
- accumulation of foam cells
| - migration of smooth muscle into the area continues
47
describe the pathogenesis of plaque development via fibrous plaque
- collagen
48
describe a complicated plaque
- ruptured
49
dyslipidemia values
- LDL: high = 160-189, very high = >190
- triglycerides: high = 200-499, very high >500
- total cholesterol: high risk = >240
- HDL: low =
50
risks of CAD
- total cholesterol > 240
- HDL 160
- triglycerides >200
51
What happens if too much homocysteine?
- inhibits key enzymes in collagen and elastin production
| - leads to increased CAD risk
52
pathophysiology of MI
- narrowing of coronary a. for 10s.
- loss of contractility
- conduction abnormalities
- lactic acid accumulation
53
MC cause of MI
- atherosclerosis in form of CAD
54
non MC cause of MI
- 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
describe stable angina
- transient episode of blood flow impairment
- recurrent episodes lasting 3-5m
- relieved w/ rest
- predictable
56
describe silent angina
- MI w/o obvious signs and symptoms
| - common following conditions/surgical procedures
57
acute coronary syndromes
- unstable angina
| - MI
58
T/F: 80% of patients with unstable angina will have MI or death from MI within 30d.
- false, 20%
Pathophysiology I - Exam 3 (Final)
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