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Pathopharm Exam 1 > Week 1: CV Part 2 > Flashcards

Week 1: CV Part 2 Flashcards

slides 27-52

1
Q

Aneurysm treatment (4)

A
  1. low blood volume & BP (decreases mechanical forces)
  2. Smoking cessation (smoking = ↑BP)
  3. β-adrenergic blockage (↓BP)
  4. Surgery
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2
Q

T/F
Along with B-blockers, A-blockers can also be used to treat aneurysms.

A

False
A-blockers have too many side effects for long term treatment

use Beta

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3
Q

Aneurysm Complications

A

Aortic dissection
(ascending, arch, or descending)

can disrupt the flow through the arterial branches.

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4
Q

T/F
In order for an Aortic dissection to be considered a surgical emergency, the arch must be involved.

A

False
dissection of any part (ascending, arch, or descending) is a surg. emergency

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5
Q

Arterial Thrombus Formation
Caused by …

A

Activation of the coagulation cascade via roughening of the tunica intima by atherosclerosis

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6
Q

T/F: Almost every person, from birth, slowly beings to develop atherosclerosis.

A

True

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7
Q

Arterial Thrombus
Treatment (3)

A
  1. Heparin, warfarin derivatives, thrombin inhibitors, or thrombolytic agents
  2. Balloon-tip catheter: remove/compress thrombus
  3. Combinations of drug + catheter therapies
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8
Q

Arterial Thrombus Treatment Meds:
Preventative vs after-clot forms

A

Preventative: Heparin, warfarin derivatives, thrombin inhibitors

breaks down clots: thrombolytic agents

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9
Q

Embolism

A

Bolus of matter circulates in the bloodstream and then lodges, obstructing blood flow.

(blood clot, air bubble)

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10
Q

T/F
Air bubbles rarely causes issues unless they are large.

A

True
small amounts of air are taken out of bloodstream fairly quickly; dissolves fast

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11
Q

What kind of substances can become emboli? (7)

A

Dislodged thrombus (often a DVT)
air bubble
aggregate of fat
amniotic fluid
bacteria
cancer cells
foreign substance

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12
Q

Many arterial emboli are from the ___

A

heart!
After an MI, valve disease, endocarditis, dysrhythmias, heart failure

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13
Q

T/F
forward blood flow from systole feeds the coronaries.

A

False
coronaries are fed via backflow during diastole
(backpressure from aorta)

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14
Q

T/F
Occlusion of a cerebral artery is an MI

A

False
Occlusion of a coronary artery: MI
Occlusion of a cerebral artery: Stroke

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15
Q

Occlusion of an artery causes ischemia/infarction/necrosis (proximal/distal) to the obstruction.

A

distal
b/c blood cant flow past the obstruction

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16
Q

Arterial occlusion makes the skin appear…

A

waxy whiteness bc the distal area is devoid of RBCs

Dr Dick “decreased overall color; bluish/grayish”

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17
Q

Why does an arterial occlusion cause numbness and pain?

A

neural ischemia

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18
Q

(Peripheral Vascular Disease)
Thromboangiitis obliterans/ (Buerger disease)

A
  • inflammatory disease of peripheral arteries
  • peripheral vasoconstriction
  • Affects digital, tibial, plantar, ulnar, and palmar arteries
  • Obliterates small & medium arteries
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19
Q

(Peripheral Vascular Disease)
Thromboangiitis obliterans (Buerger disease) treatment (5)

A

-Smoking cessation
-Exercise and dependent positioning
-vasodilators (alleviate vasospasm)
-antithrombotic agent

-repeated amputation common

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20
Q

Raynauds vs. Buerger disease

A

Raynauds seen mostly in fingers and toes

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21
Q

A Buerger’s disease patient should have their limbs positioned (elevated/dependent).

A

dependent!
we want more blood flow to limbs

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22
Q

Raynaud phenomenon/disease

A

Episodic vasospasm (ischemia) in the arteries and arterioles of the fingers; less commonly in the toes

Changes skin color & sensation d/t ischemia

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23
Q

Raynaud phenomenon vs. Raynaud disease

A

phenomenon: Secondary to other systemic diseases or conditions
(Tx: Arm exercises & medications)

disease: Primary vasospastic disorderof unknown origin
(Tx: Avoid stress & cold; no cigarettes)

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24
Q

Raynaud phenomenon and Raynaud disease
are vaso____ diseases.

A

spastic

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25
Q

Ways to make Raynaud’s worse (2)

A

emotional stress
cold

both cause constriction

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26
Q

Atherosclerosis is a form of

A

arteriosclerosis

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27
Q

Atherosclerosis definition

A

Thickening and hardening

accumulation of lipid-laden macrophages inside the arterial wall (can be inner surface as well)

Plaque development

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28
Q

Atherosclerosis vs arteriosclerosis

A

Atherosclerosis is a form of arteriosclerosis

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29
Q

Plaque develops as…

A

individual spots
if accumulate enough, can form a continuous plaque

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30
Q

T/F
Arteriosclerosis is the leading cause of coronary artery and cerebrovascular disease

A

False
Atherosclerosis

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31
Q

T/F
Unlike arteriosclerosis, atherosclerosis is confined to certain areas of the body.

A

False
Atherosclerosis occurs throughout the body

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32
Q

Atherosclerosis Progression

A
  1. Endothelium injury
  2. Inflammation of endothelium
  3. Cytokines released
  4. Cellular proliferation
  5. Macrophage migration
  6. Low-density lipoproteins (LDL) oxidation (foam cell formation) with oxidative stress
  7. Fatty streak
  8. Fibrous plaque
  9. Complicated plaque
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33
Q

Complicated plaque/lesion

A

fibrin plaques
Ca
additional lipids

can adhere to original plaque
1) further reduces lumen
2) vessels cannot distend

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34
Q

Atherosclerosis & pulse waves

A

(walls: thick, non-compliant, cannot distend)

1) pulse wave is not absorbed
2)pulse wave reaches tissues @ higher energy
3) tissue damage

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35
Q

Endothelial Injury Cascade

A

didnt seem to emphasize this much

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36
Q

Atherosclerosis
Clinical manifestations

A

Depends on affected organ

Symptoms and signs are the result of inadequate perfusion of tissues.

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37
Q

Atherosclerosis
Treatment (7)

A

reduce risks factors
removing initial causes of damage
prevent lesion progression

Exercising
smoking cessation
controlling HTN & diabetes
reducing LDL (diet &/or Rx)

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38
Q

HDL vs LDL

A

want HDLs high; LDLs low

HDL: scavenger; transport excess cholesterol periphery → liver

LDL: contains a lot of cholesterol & lipids; takes to tissues

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39
Q

Decreasing LDL helps prevent which steps of Atherosclerosis Progression? (2)

A

ability to form:
foam cells
fatty streaks

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40
Q

T/F
in order for the pt to benefit, we must lower the LDL AND raise the HDL.

A

False
either/or are beneficial

41
Q

Peripheral Artery Disease
definition

A

Atherosclerotic disease of arteries that perfuse limbs, especially lower extremities

42
Q

Peripheral Artery Disease is a (arterio/athero)sclerotic disease.

A

Atherosclerotic

43
Q

Peripheral Artery Disease is prevalent in people …(2)

A

with diabetes or who smoke

44
Q

(Peripheral Artery Disease)
Intermittent claudication

A

Obstruction of arterial blood flow in the iliofemoral vessels, resulting in pain with ambulation

45
Q

Peripheral Artery Disease
Treatment (4)

A

-Vasodilators
-antiplatelet or antithrombotics
(e.g., aspirin, cilostazol, ticlopidine, clopidogrel),

-cholesterol-lowering medications
-exercise rehabilitation

46
Q

Coronary Artery Disease
definition

A

Any vascular disorder that narrows or occludes the coronary arteries

47
Q

Coronary Artery Disease results in an imbalance between…

A

coronary blood supply & myocardial demand for oxygen and nutrients

48
Q

Coronary Artery Disease
Reversible ______ or irreversible ____ may result.

A

Reversible: myocardial ischemia
irreversible: infarction

49
Q

myocardium reserve of blood flow

A

very limited
reserve is 5-10% of actual need

50
Q

Coronary Artery Disease
Most common cause

A

Atherosclerosis

51
Q

Coronary Artery Disease
Nonmodifiable risk factors

A

Advanced age
family history
Male gender or women after menopause

52
Q

T/F
Medication is a reliable way of reversing plaque formation.

A

False
no solid proof & limitations exist
the drug may “reduce plaque” by increasing HDL, which removes excess cholesterol

prevention/limitation of progression is key

53
Q

Coronary Artery Disease
Modifiable risk factors (6)

A

-Dyslipidemia

-Hypertension
(Endothelial injury, ↑ 🩷O2 demand)

-Cigarettes
(constriction, ↑LDL, ↓HDL)

-DM/insulin resistance
(Endothelial damage, vessel wall thickening)

-Obesity/sedentary
(Metab synd: Obese, dyslipidemia, HTN)

-Atherogenic diet

54
Q

Female hormone that has a protective effect against plaque formation

A

progestin

(post menopausal women have higher risk of CAD)

55
Q

Metabolic syndrome

A

Obesity, dyslipidemia, and hypertension

Modifiable risk factor for CAD

56
Q

T/F
cigarettes can affect your cholesterol levels

A

True
(constriction, ↑LDL, ↓HDL, ↑C-RP)

reason #5304543987 not to smoke

57
Q

Atherogenic diet

A

can increase LDL
high in fats and sweets

58
Q

CAD
Nontraditional risk factors (7)

A

-inflammation/thrombosis markers (C-RP)
-Troponin I
-Hyperhomocysteinemia
-Adipokines (Adiponectin, leptin)
-Infection (Microorgs, periodontal Dz)
-Air pollution
-Coronary artery calcification, carotid wall thickness

59
Q

Adipokines

A

Adiponectin and leptin

60
Q

T/F
Air pollution effects on health are similar to that of smoking.

A

True

61
Q

Which vitamine/mineral contributes to the formation of complicated plauqe?

A

Calcium

62
Q

Dyslipidemia definition

A

Abnormal concentrations of serum lipoproteins

63
Q

Dyslipidemia
Strong link between _____ and coronary artery disease

A

lipoproteins

64
Q

Dietary fat packaged into ____ for absorption in the small intestine

A

chylomicrons

65
Q

chylomicrons

A

transporting exogenous lipid from the intestine to the liver and peripheral cells

66
Q

The journey of fat from small intestine to liver

A

1) lipid micelles absorbed across Sm Int surface
2) packed into chylomicrons
3) travel into lymph
4) lymph moves it into bloodstream
5) liver stores or converts to hormones/LDL/VLDL

67
Q

chylomicrons primarily contains

A

triglycerides

68
Q

Where can we use triglycerides?

A

removed from chylomicrons
A) stored by adipose tissue
B) used by muscle as energy

69
Q

Remnant of chylomicrons

A

(after triglyceride is removed)

contains cholesterol, which is taken up by the liver (make steroids or package other cells)

70
Q

Components of:
VLDL
LDL
HDL

A

VLDL: triglycerides + carrier protein
LDL: cholesterol + carrier protein
HDL: phospholipids + a carrier protein

71
Q

LDL fxn

A

delivers cholesterol to tissues

72
Q

HDL fxn

A

1) “reverse cholesterol transport”
return excess cholesterol from tissues → liver (liver eliminates as bile or converted to cholesterol-containing steroids)

2) Can remove excess cholesterol from arterial walls.

73
Q

Dyslipidemia is an indicator of

A

coronary risk

74
Q

Dyslipidemia
abnormal levels (4)

A

↑ LDL: endothelial injury, inflammation, and immune responses important in atherogenesis

↓ HDL: “reverse cholesterol transport,” which returns excess cholesterol from the tissues to the liver

↑ VLDL (triglycerides)

↑ lipoprotein (a)

75
Q

Myocardial ischemia
Develops if …

A

the supply of coronary blood cannot meet the demand of the myocardium for oxygen and nutrients.

76
Q

Types of angina (3)

A

Stable angina: predictable chest pain.

Prinzmetal angina (variant): unpredictable chest pain

Angina pectoris: transient substernal chest discomfort

77
Q

Silent ischemia

A

no detectable symptoms

78
Q

Which angina causes chest pain during exercise?

A

Stable angina

79
Q

T/F
With stable angina, we do not expect full blockage.

A

True

80
Q

T/F
Stable angina is equivalent to the damage done by an MI.

A

False

81
Q

Untreated angina often leads to…

A

an MI

82
Q

Myocardial ischemia
Treatment (8)

A

-Rx: Nitrates, β-blockers, Ca channel blockers
-PCI
-CABG
-Minimally invasive direct coronary artery bypass (MIDCAB)
-Transmyocardial laser revascularization (TMR)
-Gene therapy for myocardial angiogenesis
-Spinal cord stimulation
-Laser revascularization, percutaneous in situ coronary venous arterialization

83
Q

Why do nitrates relieve angina?

A

vasoildate
↓
decrease preload
↓
decreased heart distention while filling
↓
decreased work to contract

84
Q

Medications for angina treatment (3)

A

Nitrates
β-blockers
Ca channel blockers

all work to decrease workload on the heart

85
Q

T/F
Acute coronary syndrome includes stable angina.

A

False

Acute coronary syndromes:
-Unstable angina
-MI

86
Q

Acute coronary syndromes

A

Sudden coronary obstruction d/t thrombosis formation over a ruptured atherosclerotic plaque

-Unstable angina
-MI

87
Q

Acute coronary syndromes
Most common complications (3)

A

Dysrhythmias
CHF
sudden death

88
Q

Dysrhythmias are ___ in nature

A

conductive

89
Q

Unstable Angina

A

-reversible myocardial ischemia
-indicates impending infarction

-Transient vessel occlusion & vasoconstriction at site of plaque damage
-perfusion returns before significant myocardial necrosis occurs

90
Q

T/F
Stable angina shows reversible myocardial tissue damage, while unstable angina shows irreversible damage.

A

False
unstable = reversible

91
Q

Unstable Angina
Treatment (5)

A

-Immediate hospitalization
-O2
-aspirin (if not contraindicated)
-nitrates
-morphine if pain persists
-Anti-thrombotics

“MONA”
morphine, O2, nitroglycerin, aspirin

92
Q

T/F
Unstable angina is characterized by a gradual buildup of plaque.

A

False
sudden rupture in the vessel

93
Q

Prolonged ischemia causes….

A

irreversible damage to the heart muscle (myocyte necrosis)

94
Q

Myocardial Infarction

A

Prolonged ischemia = irreversible damage to myocardium (myocyte necrosis)

Cellular injury → cellular death
Structural & functional changes

Myocardial stunning
Hibernating myocardium
Remodeling
Repair

95
Q

MI
Structural & functional changes (3)

A

Myocardial stunning: temporarily lose contractile fxn; hours to days after perfusion restored

Hibernating myocardium: persistently ischemic tissue metabolically adapts to prolong myocyte survival

Remodeling: occurs in myocardium after MI

96
Q

How long does myocardial stunning last?

A

hours to days after perfusion is restored

97
Q

Where does remodeling occur?

A

myocardium

98
Q

Thromboangiitis obliterans (Buerger disease) s/s

A

pain, tenderness, sluggish blood flow, rubor, cyanosis

Pathopharm Exam 1 (9 decks)

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