Cardiovascular System Flashcards

To make Kody stop whining about people taking too long to make their cards.

1
Q

Definition: Arteriosclerosis

A

Hardening of Arteries

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2
Q

Atherosclerosis

A
  1. response of the intima of larger arteries to a variety of insults
  2. Macrophages and myointimal cells accumulate Cholesterol-rich lipid
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3
Q

Atherosclerosis: Incidence

A

America: peak in 1968, reduced with dec. risk factors
Women: Protected til menopause
Finland/Scotland: highest rates of atherosclerosis
(New meaning to the Mortal Kombat phrase, “Finnish Him”)
French: Red wine inhibits oxidation of LDL
Eskimos: eating blubber provides omega-3 oils
“no cholesterol” items can still raise LDL

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4
Q

Atherosclerosis: Morphology

Compontents of atheroma

A
  1. Cells - sm. m., macrophages and other leukocytes
  2. ECM - collagen, elastin, proteoglycans
  3. Intra and extra cellular lipid - cholesterol and cholesterol esters
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5
Q

Atherosclerosis: Morphology

Parts

A
  1. Fibrous Cap

2. Necrotic Center

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6
Q

Atherosclerosis: Distribution

A

primarily affects the elastic arteries

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7
Q

Atherosclerosis: Stages of Progression

A
  1. Fatty Streaks
  2. Fibrous Plaques
  3. Complicated Lesions
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8
Q

Atherosclerosis: Fatty Streaks

A

masses of lipid-rich roam cells in the intima; precursrs to advanced lesions

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9
Q

Atherosclerosis: Fibrous Plaque

A

(progressive) plaque undergoes enlargement by accumulation of macrophages, sm. m. cells, ECM and fibers

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10
Q

Atherosclerosis: Complicated Lesion

A

(atheroma)
1. enlargement
2. plaque rupture
3. ulceration
4. hemorrhage
5. degenerative changes
6. calcification
7. formation of superimposed thrombi

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11
Q

Atherosclerosis: Major risk factors

A
  1. Hyperlipidemia
  2. Cigarette Smoking
  3. Hypertension
  4. Diabetes Mellitus
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12
Q

Atherosclerosis: Hyperlipidemia

A
  1. elevated serum cholesterol (LDL)

2. coronary disease risk rises when total cholesterol above 160 mg/dl

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13
Q

Atherosclerosis: Cigarette Smoking

A
  1. tobacco smoke oxidizes LDL
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14
Q

Atherosclerosis: Hypertension

A
  1. damages intima and Atherosclerosis tends to develop in locations where hemodynamic forces are the greatest.
  2. > 165/90 = 5x greater risk of ischemic heart disease
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15
Q

Atherosclerosis: DM

A
  1. metabolic interactions contribute to accelerated arteriosclerosis and increased MI, stroke, and PAD, right?
  2. hyperglycemia gives rise to abnormal proteins that alter endothelial cell function and promote proliferation of fibrous elements in the wall of blood vessels
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16
Q

Atherosclerosis: Other risk factors

A
  1. Lack of exercise
  2. Increased Age (35-55)
  3. Gender (Male)
  4. Congenital factors
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17
Q

Atherosclerosis: Pathogenesis

A
  1. Reaction to injury and repair hypothesis

2. Myoclonal Hypothesis

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18
Q

Atherosclerosis: Rxn to injury and repair hypothesis

A

Atherosclerosis is chronic inflammatory response to events initiated early in life => plaque fm and progression to:

  1. endothelial injury/dysfunction
  2. monocyte adhesion and infiltration
  3. lipid accumulation and oxidation
  4. sm. m. proliferation
  5. ECM and thrombosis deposition
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19
Q

Atherosclerosis: Rxn to injury and repair: Sources

A
  1. Action of chemicals
  2. Lipids
  3. Immune rxns
  4. hypoxia
  5. infectious agents
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20
Q

Atherosclerosis: Rxn to injury and repair: lipoprotein action

A
  1. infiltrate vessel wall at sites of injury

2. undergo oxidation

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21
Q

Atherosclerosis: Rxn to injury and repair: Monocyte action

A
  1. attach to injured epithelium

2. migrate into intima and transform into macrophages

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22
Q

Atherosclerosis: Rxn to injury and repair: Platelet action

A
  1. adhesion at sites of injury
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23
Q

Atherosclerosis: Rxn to injury and repair: growth factors and cytokines released from

A
  1. Macrophages
  2. Plateles
  3. endothelium
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24
Q

Atherosclerosis: Rxn to injury and repair: growth factors and cytokines cause

A

proliferation of smooth muscle cells in intima; produce components of ECM (collagen and proteoglycans)

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25
Q

Atherosclerosis: Monoclonal Hypothesis:

A

considers proliferation of sm. m to be the primary event

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26
Q

Atherosclerosis: Monoclonal Hypothesis: steps

A
  1. Sm. m. recruited from media, accumulate in intima, collect lipid
  2. monoclonal in origin
  3. mutagens/mitogens stimulate proliferation of sm. m.
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27
Q

Atherosclerosis: Monoclonal Hypothesis: Mutagens/Mitogens

A
  1. Microorganisms
  2. Oxidation products of lipids
  3. Products assimilated from cigarette smoke
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28
Q

Atherosclerosis: Manifestations

A
  1. Occlusion

2. Degeneration

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29
Q

Atherosclerosis: Manifestations: Occlusion

A
  1. Stable Plaques

2. Unstable Plaques

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30
Q

Atherosclerosis: Manifestations: Stable Plaques

A

Contribute to:

  1. Stable angina
  2. chronic ischemic atrophy of the myocardium
  3. atherosclerotic dementia
  4. leg claudication
  5. intestional angina
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31
Q

Atherosclerosis: Manifestations: Unstable Plaques

A

Enlarged lipid core, thinner fibrous cap and accumulated inflammatory cells

  1. give rise to plaque rupture: thrombosis/sudden occlusion
  2. inhibiting inflammation/oxidation/dysfunction can control rupture
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32
Q

Mockenberg’s Sclerosis

A

degeneration and dystrophic calcification of the media of “muscular arteries”, typically in older adults

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33
Q

Arteriolosclerosis: Definition

A

thickening of small arteries and arterioles

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34
Q

Arteriolosclerosis: types

A
  1. Hyaline arteriolar sclerosis

2. Hyperplastic arteriolar sclerosis

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35
Q

Arteriolosclerosis: Hyaline

A
  1. components of the vascular BM and serum proterins accumulate in the vessel wall and may eventually narrow the lumen
  2. most common type of arteriolosclerosis
36
Q

Arteriolosclerosis: Hyperplastic

A
  1. concentric proliferation of intimal tissue (onion)

2. restrict blood flow

37
Q

Arteriolosclerosis: Hyperplastic: Causes

A
  1. Malignant hypertension
  2. Severe pulmonary hypertension
  3. Scleroderma
38
Q

Arteritis: Definition

A

arterial disease of inflammatory origin

39
Q

Arteritis: Causes

A
  1. Vascular injury to infectious agents
  2. Immunological rxns
  3. other
40
Q

Arteritis: Vascular injury to infectious agents

A
  1. Pyogenic abscesses
  2. TB
  3. Bacterial Pneumonia
  4. Meningitis
  5. May give rise to bacteremias and septic emboli
41
Q

Arteritis: Immunological rxns

A
  1. Immune complex injury - serum sickness, SLE, RA

2. Antibodies directed agains components of vessel wall - Goodpasture, ANA

42
Q

Arteritis: other mechanism

A
  1. radiation

2. idiopathic

43
Q

Arteritis: Giant Cell (Temporal)

A

inflammatory injury to arteries (head region)

  1. common in older adults (>60)
  2. may include “jaw claudication”, blindness, headaches
44
Q

Arteritis: Thromboangiitis obliterans

A

(Buerger’s Disease) mmmmm…. burgers….

  1. young male smokers
  2. NV bundels of the digits become inflames and undergo thrombosis
  3. the typical patient, after losing all his fingers, may still hold his cigarettes between his last two toes… gonna lose them too
45
Q

Arteritis: Polyarteritis Nodosa

A
  1. segmental necrotizing vasculitis of small and medium arteries
  2. possible causes include hep B, rheumatic fever, anti-myeloperoxidase disease
  3. infarcts possible everywhere except the lung
46
Q

Polyarteritis Nodosa infarcts are possible everywhere except:

A

THE LUNG SON!

47
Q

Arteritis: Takayasu’s Arteritis

A

(pulseless disease, aortic arch disease)

  1. idiopathic of younger adults; aortic arch and major branches thicken and become stenotic
  2. blood flow reduced to upper part of the body
  3. Histologic features nonspecific with granulomas, lyphocytes, plasme cells, and scarring
48
Q

Common vascular lesions: there’s 8 of them, you’ve got 10 seconds to name them… GO

A
  1. Giant cell arteritis
  2. Polyarteritis nodosa
  3. Buerger’s Disease
  4. Atherosclerotic Aneurysm
  5. Syphalitic Aneurysm
  6. Dissecting Aneurysm
  7. Berry Aneurysm
  8. Varicositis
49
Q

Condition:Location:Cause:Effects

Giant Cell Arteritis

A

C: Temporal Arteritis
L: small/med arteries, head (Superficial Temporal artery)
C: unknown; elderly
E: inflammatory tenderness; restriction of blood flow; blindness & headaches

50
Q

Condition:Location:Cause:Effects

Polyarteritis Nodosa

A

L: small/med arteries, systemic (Renal artery)
C: hypertension and hepatitis B antigen
E: Nodular lesions/necrosis, scarring/thrombosis; restriction of blood flow, localized symptoms

51
Q

Condition:Location:Cause:Effects

Buerger’s Disease

A

C: Thromboangiitis obliterans
L: Small/med arteries, extremities
C: Tobacco and genetic factors
E: Arterial occlusion, gangrene of digits; nerve involvement leads to pain

52
Q

Condition:Location:Cause:Effects

Atherosclerotic aneurysm

A

L: aorta/common iliacs, abdomen
C: Males 5x, >50 years, atherosclerosis & HTN
E: Abdominal/back pain, thrombotic emboli

53
Q

Condition:Location:Cause:Effects

Syphilitic Aneurysm

A

L: Ascending Aorta and Arch
C: Tertiary Syphalis
E: Compression of adj mediastinal str’s; aortic valvular insufficiency

54
Q

Condition:Location:Cause:Effects

Dissecting Aneurysm

A

L: Most common in ascending aorta/arch, some distal to subclavian artery
C: HTN (M: 40-60), structural abnormalities of aorta
E: Tearing pain, devastating rupture

55
Q

Condition:Location:Cause:Effects

Berry Aneurysm

A

L: Base of Brain (circle of willis/cerebral arteries)
C: Congenitcal weakness of aa. at points of division
E: Risk of subarachnoid hemorrhage; causes severe headache; 25-50% fatality

56
Q

Condition:Location:Cause:Effects

Varicosities

A

L: superficial veins of legs; hemorrhoidal veins; esophagus, pampiniform plexus
C: increased venous pressure, valve defects, weakened veins, poor external support
e: Venous pooling in legs/cyanosis/dull ache; cutaneous ulcers & infections, bleeding in esophageal varicosities

57
Q

Good Job! You just earned a Panda Snack!

A

Time’s Up! ITS GO TIME!

58
Q

Raynaud’s Phenomenon

A

Reversible spasmodic contraction and occlusion of arteries supplying the fingers, toes, and sometimes the nose and ears. Structures may turn white, then blue, then red.
May be due to vasculitis syndromes or PAD, right?

59
Q

Aneurysms: Definition

A

Local dilation of arteries

Shapes are saccular or fusiform

60
Q

Aneurysms: Shapes

A

Saccular

Fusiform

61
Q

Aneurysms: Causes

A
  1. HTN

2. any condition that damages the media of an artery

62
Q

Aneurysms: Complications

A

Risk for rupture, mural thrombosis and emboli

63
Q

Aneurysms: Classification

A
  1. Arteriosclerotic
  2. Syphalitic
  3. Dissecting
  4. Berry
64
Q

Aneurysms: Arteriosclerotic

A
  1. AA, below the renal aa.

2. diameter > 5-6 cm

65
Q

Aneurysms: Syphalitic

A
  1. proximal aorta
  2. treebark grooves on the intima
  3. occlusion of the coronary or other ostia
  4. dilation of the aortic valve ring
  5. tension on left recurrent laryngeal nerve
66
Q

Aneurysms: Dissecting

A
  1. blood enters wall of the aorta trough an intimal defect and separates layers of the aortic wall
  2. causes “cystic medial necrosis”; elastic tissue is diminished
  3. Experience tearing/agonizing chest pain as false lumen expands, neck can cause stroke
67
Q

Aneurysms: Berry

A
  1. congenital
  2. base brain: circle of (what you talkin’ ‘bout) willis
  3. > 40 years, HTN, CT diseases, 50% mortality
68
Q

Diseases of Arteries

A
  1. Arteriosclerosis
  2. Arteritis
  3. Aneurysms
69
Q

Diseases of Veins

A
  1. Varicose Veins

2. Thrombosis

70
Q

Varicose Veins: Morphology

A
  1. dilation
  2. increased tortuosity
  3. loss of valve competency
  4. venous pooling, ischemia, and stasis dermatitis
71
Q

Varicose Veins: Pathogenesis

A
  1. most vulnerable to distention at locations where they receive little external support
  2. Decreased integrity of the valves increase retrograde pressures in veins of the leg and pelvis
72
Q

Varicose Veins: Locations

A
  1. Superficial veins of the lower extremities
  2. hemorrhoidal veins
  3. esophageal veins
  4. Pampiniform plexus
73
Q

Varicose Veins: Risk Factors

A
  1. Structural Changes

2. Increased venous pressure

74
Q

Varicose Veins: Structural Changes

A
  1. Valve defects
  2. Intrinsic weakness of the wall
  3. Inflammatory injury to veins
  4. Obesity
  5. Age related loss of elastic fibers
75
Q

Varicose Veins: Increased venous pressure

A
  1. Venous Obstruction
  2. Physical inactivity
  3. Prolonged Standing or Sitting
  4. Loss of valve integrity
76
Q

Varicose Veins: Venous Obstruction

A
  1. Pregnancy
  2. Chronic Constipation
  3. Tumors
  4. Thrombosis
  5. Tight Garments
  6. Poor posture
77
Q

Varicose Veins: Venous Pump

A

keeps venous pressure in legs (25mmHg)

causes pressures to rapidly approach 90mmHg or more

78
Q

Varicose Veins: Valve integrity

A

loss of intergity of valves in communicating veins, i.e. superficial and deep veins

79
Q

Varicose Veins: Clinical manifestations

A
  1. Thrombi and emboli
  2. prolonged venous pooling and congestion give rise to micro-hemorrhages and hemosiderin pigmentation
  3. prolonged venous pooling and tissue hypoxia may give rise to ischemic stasis ulcers
80
Q

Thrombosis

A
  1. Phlebothrombosis

2. Trousseau’s migratory thrombophlebitis

81
Q

Phlebothrombosis

A
  1. fm of bland thrombi where thrombophlebitis indicates inflammation
  2. Action of fibrinopeptides, “foreign body rxns”
82
Q

Phlebothrombosis: Locations

A
  1. DVT of leg and pelvis

2. Hepatic veins and dural venous sinuses

83
Q

Trousseau’s

A
  1. Miltiple thrombi affect first one vein, then another

2. advanced cancer, pancreatic, adenocarcinomas

84
Q

Thrombosis: Contributing risk factors

A
  1. Heart Failure
  2. Venous Obstruction
  3. Neoplasms
  4. Pregnancy
  5. Trauma or surgery; confinement to bed
  6. Estrogens
  7. G(-) sepsis
85
Q

Thrombosis: clinical manifestations

A
  1. Pain and firmness at site
  2. circulatory obstruction; swelling/pain/cyan/discoloration
  3. walking or standing pain
  4. Positive Homan’s Sign
  5. SVC syndrome; dusky upper body regions; headaches
  6. IVC syndrome; dusky lower body regions; cancerous masses in para-aortic lymph nodes
86
Q

Why are these cards so hard to get through?

A

B/c mike made them and he’s essentially a second Bhalero so you’ll never know what he’s thinking