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Rapid Review Pathology > Chapter 10 - Vascular Disorders > Flashcards

Chapter 10 - Vascular Disorders Flashcards

0
Q

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

A

Chylomicrons least dense (protein 2%) of all lipoproteins

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1
Q

What are chylomicrons and when are they absent?

A

Chylomicrons: diet-derived TGs; absent during fasting

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2
Q

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

A

Require apoB48 for assembly/secretion from enterocytes → lymphatics

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3
Q

Describe how nascent chylomicrons become mature chylomicrons.

A

Nascent chylomicrons obtain apoCII/apoE from HDL

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4
Q

What are chylomicrons a source of?

A

Chylomicrons: source FAs + glycerol

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5
Q

What does capillary lipoprotein lipase do?

A

CPL: chylomicrons → chylomicron remnants (↓↓TG)

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6
Q

What induces the synthesis of CPL?

A

CPL synthesis induced by insulin

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7
Q

What activates CPL in the fed state?

A

CPL activated by apoCII

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8
Q

Where is CPL located?

A

CPL in adipose, muscle, myocardium

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9
Q

What removes chylomicron remnants?

A

Remnants removed by apoE receptors in liver

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10
Q

What is VLDL?

A

VLDL: liver-derived TG

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11
Q

Describe VLDL synthesis.

A

G3P + 3 FAs → TG → VLDL

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12
Q

What is important in the synthesis and secretion of VLDL?

A

ApoB100 important in synthesis/secretion VLDL

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13
Q

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

A

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

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14
Q

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

A

CPL: VLDL → IDL → LDL

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15
Q

What does CETP do?

A

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

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16
Q

How does an increase in VLDL affect HDL-CH?

A

↑VLDL causes ↓HDL-CH

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17
Q

What does VLDL form with the standing chylomicron test?

A

VLDL forms infranate with standing chylomicron test

VLDL: turbid infranate; more protein than chylomicrons

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18
Q

What formula is used to calculate VLDL concentration?

A

VLDL = TG ÷ 5

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19
Q

What is the cause of plasma or serum turbidity?

A

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

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20
Q

What do chylomicrons form with the standing chylomicron test?

A

Chylomicrons: supranate (less protein than VLDL)

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21
Q

From what is LDL derived? What does LDL transport?

A

LDL: derives from VLDL; transports CH

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22
Q

What do small dense LDL particles increase the risk of?

A

Small dense LDL particles: ↑risk for atherosclerosis, CAD

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23
Q

What is the formula for calculated LDL?

A

Calculated LDL = CH − HDL − TG/5

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24
Q

How do chylomicrons affect the calculated LDL?

A

Chylomicrons falsely ↓calculated LDL

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25
Q

How do chylomicrons affect the calculated VLDL?

A

Chylomicrons falsely ↑calculated VLDL

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26
Q

What are the functions of cholesterol?

A

CH: cell membranes, hormones, bile salts/acids

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27
Q

What is not required for accurate serum cholesterol?

A

Fasting not required for accurate serum CH

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28
Q

Which cholesterol is the “good cholesterol”?

A

HDL-CH: “good CH”

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29
Q

What are the factors that increase HDL?

A

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

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30
Q

What are the functions of HDL?

A

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

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31
Q

HDL is measured as what?

A

Measured as HDL-CH

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32
Q

How does increased VLDL affect HDL-CH?

A

↑VLDL causes ↓HDL-CH

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33
Q

What is arteriosclerosis?

A

Arteriosclerosis: thickening of arterial wall; loss of elasticity

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33
Q

What is medial calcification?

A

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

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34
Q

Describe the epidemiology of atherosclerosis.

A

Atherosclerosis: men > women; ↑with age

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35
Q

What are the risk factors for atherosclerosis?

A

Risk factors: HTN, DM, smoking, hyperlipoproteinemia

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36
Q

What are the first steps in the pathogenesis of atherosclerosis?

A

Atherosclerosis: endothelial cell injury; platelets/macrophages pivotal roles

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37
Q

What are the causes of endothelial cell injury?

A

Endothelial injury: HTN, smoking, homocysteine, oxidized LDL

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38
Q

What is the cell response to endothelial injury?

A

Macrophages infiltrate intima; release cytokines

Platelets induce inflammatory responses in leukocytes/endothelial cells

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39
Q

What are foam cells?

A

Foam cells: macrophages, SMCs with CH

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40
Q

What is the pathognomonic lesion of atherosclerosis?

A

Fibrous plaque: pathognomonic lesion atherosclerosis

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41
Q

What does the fibrous cap overlie?

A

Fibrous plaque overlies necrotic core

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42
Q

What is CRP a marker of?

A

CRP: marker disrupted/inflammatory fibrous plaques

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43
Q

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

A

Abdominal aorta: MC site atherosclerosis; no vasa vasorum

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44
Q

What are the complications of atherosclerosis?

A

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

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45
Q

What is claudication?

A

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

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46
Q

What are the signs and symptoms of PAD?

A

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

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47
Q

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

A

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

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48
Q

How is PAD diagnosed?

A

Dx: ABI ratio, angiography, duplex ultrasonography

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49
Q

What is arteriolosclerosis?

A

Arteriolosclerosis: hardening of arterioles

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51
Q

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

A

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

51
Q

What are the causes of hyaline arteriolosclerosis?

A

Hyaline arteriolosclerosis: diabetes mellitus, hypertension

53
Q

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

A

Hyperplastic arteriolosclerosis: malignant HTN; onion skinning renal arteriole

54
Q

What is an aneurysm?

A

Aneurysm: vessel weakening and outpouching

55
Q

What is the most common vessel aneurysm?

A

AAA MC vessel aneurysm

56
Q

Where are AAAs usually located?

A

AAA below renal artery orifices

57
Q

What is the pathogenesis of an AAA?

A

AAA: atherosclerosis weakens wall

58
Q

What are the clinical findings of a ruptured AAA?

A

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

59
Q

How is an AAA diagnosed?

A

Dx AAA: ultrasonography, CT, angiography

60
Q

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

A

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

61
Q

Name the fungi that commonly invade vessels and weaken them.

A

Fungal invaders: Aspergillus, Candida, Mucor

62
Q

Name the bacteria that invade vessels and weaken them.

A

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

63
Q

Where are cerebral berry aneurysms typically found?

A

Cerebral berry aneurysm: circle of Willis, base of brain

64
Q

What are the risk factors for a cerebral berry aneurysm?

A

Risk factors: HTN any cause, coarctation, atherosclerosis

65
Q

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

A

MC site is junction of communicating branch with ACA

66
Q

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

A

Vessel lacks internal elastic lamina and smooth muscle

67
Q

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

A

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

68
Q

What is the pathogenesis of an aortic arch aneurysm?

A

Aortic arch aneurysm: tertiary syphilis; vasa vasorum vasculitis

69
Q

What is very characteristic of endarteritis obliterans?

A

Endarteritis obliterans: plasma cell infiltrate very characteristic

70
Q

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

A

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

71
Q

What are the clinical findings of AV regurgitation?

A

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

72
Q

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

A

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

73
Q

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

A

Aortic dissection: MCC death in Marfan syndrome/EDS

74
Q

Describe the genetics of Marfan syndrome.

A

Marfan syndrome: AD, missense mutation in fibrillin synthesis

75
Q

What are the clinical findings in Marfan syndrome.

A

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

76
Q

Describe the pathogenesis of an aortic dissection.

A

Aortic dissection: CMD; elastic tissue fragmentation

77
Q

What are the risk factors of an aortic dissection?

A

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

78
Q

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

A

Aortic dissection: pain radiates into back; absent pulse

Aortic dissection: AV regurgitation, cardiac tamponade MCC death

79
Q

Describe the saphenous vein system.

A

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

80
Q

Where are the locations of varicose veins?

A

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

81
Q

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

A

Superficial varicosities: MC clinical manifestation of chronic venous insufficiency

82
Q

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

A

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

83
Q

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

A

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

84
Q

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

A

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

85
Q

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

A

Venous thrombosis: MCC stasis blood flow; hypercoagulability

86
Q

Where is the most common site of venous thrombosis?

A

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

87
Q

What are the signs of an acute calf DVT?

A

Acute calf DVT: swelling, pain, pitting edema

88
Q

What is a sign of chronic DVT?

A

Stasis dermatitis: sign of chronic DVT

89
Q

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

A

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

90
Q

What is superficial thrombophlebitis associated with?

A

Superficial thrombophlebitis: occult DVT

91
Q

What are the causes of superficial thrombophlebitis?

A

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

92
Q

What are the clinical findings of superficial thrombophlebitis?

A

Superficial thrombophlebitis: pain, tenderness, erythema of overlying vein

93
Q

What is the pathogenesis of SVC syndrome?

A

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

94
Q

What are the clinical findings of SVC syndrome?

A

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

96
Q

What is the pathogenesis of thoracic outlet syndrome?

A

TOS: compression neurovascular compartment in neck

97
Q

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

A

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

98
Q

What are the clinical findings of TOS?

A

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

99
Q

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

A

Lymphatics: incomplete basement membranes; infection, tumor invasion

100
Q

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

A

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

101
Q

What is lymphedema?

A

Lymphedema: lymphatic fluid in interstitial space

102
Q

What are the causes of lymphedema?

A

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

103
Q

What is the most common cause of lymphedema worldwide?

A

Filariasis MCC lymphedema in world

104
Q

What are the clinical findings of lymphedema?

A

Lymphedema: pitting edema early; nonpitting in advanced cases

105
Q

What does ANCA stand for?

A

ANCA: antibodies against cytoplasmic components of neutrophils

106
Q

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

A

c-ANCA: Wegener granulomatosis

107
Q

What are examples of p-ANCA type of vasculitides?

A

p-ANCA: microscopic polyangiitis, Churg-Strauss syndrome

108
Q

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

A

Small vessel vasculitis: palpable purpura; acute inflammation

109
Q

What are the clinical findings of medium vessel vasculitis?

A

Medium-sized vessel vasculitis: thrombosis, aneurysms

109
Q

How does large vessel vasculitis present?

A

Large vessel vasculitis: absent pulse, stroke

110
Q

Essential hypertension accounts for what percentage of all hypertension cases?

A

Essential HTN: 85% of all HTN cases

111
Q

What does SBP correlate with?

A

SBP: SV, aorta compliance

112
Q

What are the primary determinants of stroke volume?

A

SV: preload, afterload, contractility of heart

113
Q

What does vessel elasticity determine?

A

Vessel elasticity determines aortic compliance

114
Q

How does aortic compliance change with age?

A

Aortic compliance ↓with age

115
Q

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

A

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

116
Q

What causes an increase in SBP?

A

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

117
Q

What causes a decrease in SBP?

A

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

118
Q

What does DBP correlate with?

A

DBP: blood volume in aorta while heart fills in diastole

119
Q

What does DBP depend on?

A

DBP depends on tonicity of smooth muscle PVR arterioles and HR

120
Q

What causes an increase in DBP?

A

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

121
Q

What causes a decrease in DBP?

A

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

122
Q

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

A

↑Sodium retention: ↑PV → ↑SV → ↑SBP

123
Q

How does excess sodium affect the PVR arterioles and DBP?

A

↑Sodium retention: ↑vasoconstriction PVR arterioles → ↑DBP

124
Q

Describe the pathogenesis of essential hypertension.

A

Essential HTN: genetic factors reduce renal sodium excretion

125
Q

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

A

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

126
Q

What are the complications of hypertension in descending order?

A

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

127
Q

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

A

Control of HTN has greatest benefit in reducing incidence of stroke

Rapid Review Pathology (14 decks)

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