Chapter 10 - Vascular Disorders Flashcards Preview

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Flashcards in Chapter 10 - Vascular Disorders Deck (128):
0

What are chylomicrons and when are they absent?

Chylomicrons: diet-derived TGs; absent during fasting

1

How does the density of chylomicrons compare to that of all lipoproteins?

Chylomicrons least dense (protein 2%) of all lipoproteins

2

What do chylomicrons require for assembly and secretion? What cell type secretes chylomicrons? Once secreted, where to chylomicrons go?

Require apoB48 for assembly/secretion from enterocytes → lymphatics

3

Describe how nascent chylomicrons become mature chylomicrons.

Nascent chylomicrons obtain apoCII/apoE from HDL

4

What are chylomicrons a source of?

Chylomicrons: source FAs + glycerol

5

What does capillary lipoprotein lipase do?

CPL: chylomicrons → chylomicron remnants (↓↓TG)

6

What induces the synthesis of CPL?

CPL synthesis induced by insulin

7

What activates CPL in the fed state?

CPL activated by apoCII

8

Where is CPL located?

CPL in adipose, muscle, myocardium

9

What removes chylomicron remnants?

Remnants removed by apoE receptors in liver

10

What is VLDL?

VLDL: liver-derived TG

11

Describe VLDL synthesis.

G3P + 3 FAs → TG → VLDL

12

What is important in the synthesis and secretion of VLDL?

ApoB100 important in synthesis/secretion VLDL

13

What is VLDL a source of? Where are TGs synthesized and stored?

VLDL: source FAs + glycerol; TG synthesis liver, TG stores in adipose

14

What are the substrates and products in the reactions catalyzed by CPL?

CPL: VLDL → IDL → LDL

15

What does CETP do?

CETP transfers TGs from VLDL → HDL; HDL transfers CH → VLDL

16

How does an increase in VLDL affect HDL-CH?

↑VLDL causes ↓HDL-CH

17

What does VLDL form with the standing chylomicron test?

VLDL forms infranate with standing chylomicron test
VLDL: turbid infranate; more protein than chylomicrons

18

What formula is used to calculate VLDL concentration?

VLDL = TG ÷ 5

19

What is the cause of plasma or serum turbidity?

Plasma/serum turbidity due to ↑↑TG; VLDL and/or chylomicrons

20

What do chylomicrons form with the standing chylomicron test?

Chylomicrons: supranate (less protein than VLDL)

21

From what is LDL derived? What does LDL transport?

LDL: derives from VLDL; transports CH

22

What do small dense LDL particles increase the risk of?

Small dense LDL particles: ↑risk for atherosclerosis, CAD

23

What is the formula for calculated LDL?

Calculated LDL = CH − HDL − TG/5

24

How do chylomicrons affect the calculated LDL?

Chylomicrons falsely ↓calculated LDL

25

How do chylomicrons affect the calculated VLDL?

Chylomicrons falsely ↑calculated VLDL

26

What are the functions of cholesterol?

CH: cell membranes, hormones, bile salts/acids

27

What is not required for accurate serum cholesterol?

Fasting not required for accurate serum CH

28

Which cholesterol is the "good cholesterol"?

HDL-CH: “good CH”

29

What are the factors that increase HDL?

↑HDL: nicotinic acid (best), exercise; diet alterations not effective

30

What are the functions of HDL?

HDL: source of apoCII and apoE
HDL: removes CH from plaques/fatty streaks for disposal in liver

31

HDL is measured as what?

Measured as HDL-CH

32

How does increased VLDL affect HDL-CH?

↑VLDL causes ↓HDL-CH

33

What is arteriosclerosis?

Arteriosclerosis: thickening of arterial wall; loss of elasticity

33

What is medial calcification?

Medial calcification: dystrophic calcification of muscular arteries (uterine, radial)

34

Describe the epidemiology of atherosclerosis.

Atherosclerosis: men > women; ↑with age

35

What are the risk factors for atherosclerosis?

Risk factors: HTN, DM, smoking, hyperlipoproteinemia

36

What are the first steps in the pathogenesis of atherosclerosis?

Atherosclerosis: endothelial cell injury; platelets/macrophages pivotal roles

37

What are the causes of endothelial cell injury?

Endothelial injury: HTN, smoking, homocysteine, oxidized LDL

38

What is the cell response to endothelial injury?

Macrophages infiltrate intima; release cytokines
Platelets induce inflammatory responses in leukocytes/endothelial cells

39

What are foam cells?

Foam cells: macrophages, SMCs with CH

40

What is the pathognomonic lesion of atherosclerosis?

Fibrous plaque: pathognomonic lesion atherosclerosis

41

What does the fibrous cap overlie?

Fibrous plaque overlies necrotic core

42

What is CRP a marker of?

CRP: marker disrupted/inflammatory fibrous plaques

43

What is the most common site of atherosclerosis? What does this site not have?

Abdominal aorta: MC site atherosclerosis; no vasa vasorum

44

What are the complications of atherosclerosis?

Complications: aneurysms, thrombosis/infarction, HTN (renal artery), cerebral atrophy, PAD

45

What is claudication?

Claudication: key sign of PAD; “angina” in peripheral arteries (pain relieved by resting)

46

What are the signs and symptoms of PAD?

PAD: dependent rubor, cool skin, poor healing, ↓hair/nail growth, ↓pedal pulses, bruits over femoral/popliteal arteries

47

What are the 5 P's of acute peripheral artery vessel occlusion?

5 P’s: pain, pallor, paresthesias, paralysis, pulselessness

48

How is PAD diagnosed?

Dx: ABI ratio, angiography, duplex ultrasonography

49

What is arteriolosclerosis?

Arteriolosclerosis: hardening of arterioles

51

What is NEG and where does it occur with respect to arteriolosclerosis? What results from NEG in arteriolosclerosis?

NEG: glucose attaching to proteins in basement membrane; leaky membrane

51

What are the causes of hyaline arteriolosclerosis?

Hyaline arteriolosclerosis: diabetes mellitus, hypertension

53

What is the cause of hyperplastic arteriolosclerosis? What is the pathologic finding?

Hyperplastic arteriolosclerosis: malignant HTN; onion skinning renal arteriole

54

What is an aneurysm?

Aneurysm: vessel weakening and outpouching

55

What is the most common vessel aneurysm?

AAA MC vessel aneurysm

56

Where are AAAs usually located?

AAA below renal artery orifices

57

What is the pathogenesis of an AAA?

AAA: atherosclerosis weakens wall

58

What are the clinical findings of a ruptured AAA?

AAA rupture triad: left flank pain, hypotension, pulsatile mass

59

How is an AAA diagnosed?

Dx AAA: ultrasonography, CT, angiography

60

What is the most common peripheral aneurysm? What is this aneurysm's epidemiology? Where is it located?

Popliteal aneurysm: male dominant; behind knee; MC peripheral aneurysm

61

Name the fungi that commonly invade vessels and weaken them.

Fungal invaders: Aspergillus, Candida, Mucor

62

Name the bacteria that invade vessels and weaken them.

Bacterial invaders: B. fragilis, P. aeruginosa, Salmonella spp.

63

Where are cerebral berry aneurysms typically found?

Cerebral berry aneurysm: circle of Willis, base of brain

64

What are the risk factors for a cerebral berry aneurysm?

Risk factors: HTN any cause, coarctation, atherosclerosis

65

Where is the most common site for a cerebral berry aneurysm?

MC site is junction of communicating branch with ACA

66

What is important in the pathogenesis of a cerebral berry aneurysm?

Vessel lacks internal elastic lamina and smooth muscle

67

What results from the rupture of a cerebral berry aneurysm? What is the clinical finding?

Rupture: subarachnoid hemorrhage; “worst headache I ever had”

68

What is the pathogenesis of an aortic arch aneurysm?

Aortic arch aneurysm: tertiary syphilis; vasa vasorum vasculitis

69

What is very characteristic of endarteritis obliterans?

Endarteritis obliterans: plasma cell infiltrate very characteristic

70

What is a clinical finding of a syphilitic aneurysm? What is the cause of this finding?

Syphilitic aneurysm: AV regurgitation; dilation of aorta and valve ring

71

What are the clinical findings of AV regurgitation?

AV regurgitation: early diastolic murmur; wide pulse pressure produces bounding pulses

72

What causes an Austin Flint murmur? What needs to be done as a result?

Austin Flint murmur: blood dripping onto anterior MV leaflet; valve (aortic) must be removed

73

What is the most common cause of death in Marfan syndrome and EDS?

Aortic dissection: MCC death in Marfan syndrome/EDS

74

Describe the genetics of Marfan syndrome.

Marfan syndrome: AD, missense mutation in fibrillin synthesis

75

What are the clinical findings in Marfan syndrome.

Marfan syndrome: arachnodactyly, dislocated lens, MVP, AV regurgitation, eunuchoid

76

Describe the pathogenesis of an aortic dissection.

Aortic dissection: CMD; elastic tissue fragmentation

77

What are the risk factors of an aortic dissection?

Risk factors: Marfan/EDS, HTN, pregnancy, coarctation of aorta

78

What are the clinical findings of an aortic dissection? What is the most common cause of death in the setting of an aortic dissection?

Aortic dissection: pain radiates into back; absent pulse
Aortic dissection: AV regurgitation, cardiac tamponade MCC death

79

Describe the saphenous vein system.

Superficial saphenous → perforator branch → deep veins → back to right heart

80

Where are the locations of varicose veins?

Locations: superficial saphenous vein, distal esophagus, anorectal region, left scrotal sac

81

What is the most common clinical manifestation of chronic venous insufficiency?

Superficial varicosities: MC clinical manifestation of chronic venous insufficiency

82

What are the risk factors for superficial varicosities in the lower extremities?

Risk factors: female; family history; pregnancies; prolonged standing; obesity; elderly

83

What is the pathogenesis of superficial varicosities in the lower extremities?

Valve incompetence of perforator branches; reversal of blood flow to superficial saphenous

84

Superficial varicosities in the lower extremities may be secondary to what?

2° superficial saphenous veins: DVT with reversed blood flow to superficial veins

85

What is the most common cause of venous thrombosis? What is another cause of venous thrombosis?

Venous thrombosis: MCC stasis blood flow; hypercoagulability

86

Where is the most common site of venous thrombosis?

Venous thrombosis: MC site lower extremity; veins in calf, popliteal/femoral veins

87

What are the signs of an acute calf DVT?

Acute calf DVT: swelling, pain, pitting edema

88

What is a sign of chronic DVT?

Stasis dermatitis: sign of chronic DVT

89

What area is affected by stasis dermatitis? What are the clinical findings in stasis dermatitis?

Stasis dermatitis: medial malleolus; hemorrhage/orange discoloration; ulcers

90

What is superficial thrombophlebitis associated with?

Superficial thrombophlebitis: occult DVT

91

What are the causes of superficial thrombophlebitis?

Causes: IV cannulation veins, infection (S. aureus), pancreatic cancer, hypercoagulable state

92

What are the clinical findings of superficial thrombophlebitis?

Superficial thrombophlebitis: pain, tenderness, erythema of overlying vein

93

What is the pathogenesis of SVC syndrome?

SVC syndrome: compression by primary lung cancer; usually small cell carcinoma

94

What are the clinical findings of SVC syndrome?

Discoloration of face, arms, shoulders; retinal hemorrhages; stroke

96

What is the pathogenesis of thoracic outlet syndrome?

TOS: compression neurovascular compartment in neck

97

Who is commonly affected by TOS? What are the causes of TOS?

Common among weight lifters (tight scalene muscles); cervical rib

98

What are the clinical findings of TOS?

Arm falls asleep at night; numbness/paresthesias; + Adson test

99

Describe the structure of lymphatic vessels. This structure predisposes these vessels to what?

Lymphatics: incomplete basement membranes; infection, tumor invasion

100

Describe the clinical findings of acute lymphangitis. What is acute lymphangitis associated with?

Acute lymphangitis: S. pyogenes cellulitis; red streak up lymphatics

101

What is lymphedema?

Lymphedema: lymphatic fluid in interstitial space

102

What are the causes of lymphedema?

Radiation post–radical mastectomy, congenital, Turner syndrome, filariasis

103

What is the most common cause of lymphedema worldwide?

Filariasis MCC lymphedema in world

104

What are the clinical findings of lymphedema?

Lymphedema: pitting edema early; nonpitting in advanced cases

105

What does ANCA stand for?

ANCA: antibodies against cytoplasmic components of neutrophils

106

What is an example of a c-ANCA type of vasculitides?

c-ANCA: Wegener granulomatosis

107

What are examples of p-ANCA type of vasculitides?

p-ANCA: microscopic polyangiitis, Churg-Strauss syndrome

108

What is the gross appearance of small vessel vasculitis? What is this appearance a sign of?

Small vessel vasculitis: palpable purpura; acute inflammation

109

What are the clinical findings of medium vessel vasculitis?

Medium-sized vessel vasculitis: thrombosis, aneurysms

109

How does large vessel vasculitis present?

Large vessel vasculitis: absent pulse, stroke

110

Essential hypertension accounts for what percentage of all hypertension cases?

Essential HTN: 85% of all HTN cases

111

What does SBP correlate with?

SBP: SV, aorta compliance

112

What are the primary determinants of stroke volume?

SV: preload, afterload, contractility of heart

113

What does vessel elasticity determine?

Vessel elasticity determines aortic compliance

114

How does aortic compliance change with age?

Aortic compliance ↓with age

115

Who is primarily affected by systolic hypertension? What causes systolic hypertension?

Systolic HTN: >60 years old; loss of aortic compliance

116

What causes an increase in SBP?

↑SBP: ↑preload, ↑contractility, ↓aortic compliance

117

What causes a decrease in SBP?

↓SBP: ↓preload, ↓contractility, ↑afterload (aortic stenosis)

118

What does DBP correlate with?

DBP: blood volume in aorta while heart fills in diastole

119

What does DBP depend on?

DBP depends on tonicity of smooth muscle PVR arterioles and HR

120

What causes an increase in DBP?

↑DBP: vasoconstriction in PVR arterioles, ↑blood viscosity, ↑HR

121

What causes a decrease in DBP?

↓DBP: vasodilation PVR arterioles, ↓blood viscosity, ↓HR

122

How does excess sodium affect plasma volume, stroke volume and SBP?

↑Sodium retention: ↑PV → ↑SV → ↑SBP

123

How does excess sodium affect the PVR arterioles and DBP?

↑Sodium retention: ↑vasoconstriction PVR arterioles → ↑DBP

124

Describe the pathogenesis of essential hypertension.

Essential HTN: genetic factors reduce renal sodium excretion

125

Secondary hypertension accounts for what percentage of all hypertension cases? What are the leading causes of secondary hypertension?

2° HTN: 15% of cases; renovascular HTN and drugs are leading causes

126

What are the complications of hypertension in descending order?

Complications of HTN, descending order: acute Ml, stroke, renal failure

127

Control of hypertension has the greatest benefit in reducing the incidence of what?

Control of HTN has greatest benefit in reducing incidence of stroke