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
1
Q
What are chylomicrons and when are they absent?
A
Chylomicrons: diet-derived TGs; absent during fasting
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
3
Q
Describe how nascent chylomicrons become mature chylomicrons.
A
Nascent chylomicrons obtain apoCII/apoE from HDL
4
Q
What are chylomicrons a source of?
A
Chylomicrons: source FAs + glycerol
5
Q
What does capillary lipoprotein lipase do?
A
CPL: chylomicrons → chylomicron remnants (↓↓TG)
6
Q
What induces the synthesis of CPL?
A
CPL synthesis induced by insulin
7
Q
What activates CPL in the fed state?
A
CPL activated by apoCII
8
Q
Where is CPL located?
A
CPL in adipose, muscle, myocardium
9
Q
What removes chylomicron remnants?
A
Remnants removed by apoE receptors in liver
10
Q
What is VLDL?
A
VLDL: liver-derived TG
11
Q
Describe VLDL synthesis.
A
G3P + 3 FAs → TG → VLDL
12
Q
What is important in the synthesis and secretion of VLDL?
A
ApoB100 important in synthesis/secretion VLDL
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
14
Q
What are the substrates and products in the reactions catalyzed by CPL?
A
CPL: VLDL → IDL → LDL
15
Q
What does CETP do?
A
CETP transfers TGs from VLDL → HDL; HDL transfers CH → VLDL
16
Q
How does an increase in VLDL affect HDL-CH?
A
↑VLDL causes ↓HDL-CH
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
18
Q
What formula is used to calculate VLDL concentration?
A
VLDL = TG ÷ 5
19
Q
What is the cause of plasma or serum turbidity?
A
Plasma/serum turbidity due to ↑↑TG; VLDL and/or chylomicrons
20
Q
What do chylomicrons form with the standing chylomicron test?
A
Chylomicrons: supranate (less protein than VLDL)
21
Q
From what is LDL derived? What does LDL transport?
A
LDL: derives from VLDL; transports CH
22
Q
What do small dense LDL particles increase the risk of?
A
Small dense LDL particles: ↑risk for atherosclerosis, CAD
23
Q
What is the formula for calculated LDL?
A
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
