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Joad's MS2 Unit 4 > Goljy 10: Vascular Disorders > Flashcards

Goljy 10: Vascular Disorders Flashcards

1
Q

Chylomicrons

A
  • Transport diet-derived triglycerides in the blood

- Absent during fasting

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2
Q

Composition of chylomicrons

A

2% Protein
87% triglyceride
3% cholesterol
8% phospholipid

The least dense of all lipoproteins!

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3
Q

How are chylomicrons formed in the small intestine?

A
  1. Enterocytes lining villi reabsorb monoglycerides and fatty acids, which are converted to TG in cytosol
  2. TG packaged into a chylomicron, requiring apoB48 for assembly and secretion
  3. Nascent chylomicrons enter lymphatics that drain into thoracic duct, emptying into blood stream
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4
Q

Describe the circulation phase of chylomicrons

A
  1. Nascent chylomicrons obtain apoCII and apoE from HDL to become mature chylomicrons
  2. TG in chylomicrons is hydrolyzed by capillary lipoprotein lipase into FAs + glycerol
  3. Hydrolysis of chlyomicrons by CPL leaves chylomicron remnants that contain much less TG than mature chylomicrons
  4. Chylomicron remnants removed from circulation by apoE receptors in liver
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5
Q

VLDL

A
  1. TG in the liver is synthesized by adding 3 FAs to glycerol-3-phosphate (G3P is a 3-carbon intermediate of glucose metabolism)
  2. With the aid of apoB100, TG is packaged into VLDL and secreted into blood as nascent VLDL
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6
Q

Composition of VLDL

A

9% Protein
55% TG
17% Cholesterol
19% Phospholipid

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7
Q

What is VLDL a source of?

A

FAs and glycerol!

  1. TG in VLDL is hydrolyzed by CPL into FAs and glycerol
  2. Hydrolysis of nascent VLDL by CPL first produces IDL further hydrolysis produces LDL
  3. Some IDL is removed from blood by apoE receptors in liver
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8
Q

Cholesterol ester transport protein

A
  1. Transfers CH from HDL to VLDL and TG from VLDL to HDL
    - interferes with HDL’s main function of transferring CH from peripheral tissue to liver for excretion in bile or synthesis of bile salts/acids
  2. Increase in VLDL always causes decrease in HDL-CH (explains why increased VLDL is risk for CAD)
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9
Q

VLDL concentration formula

A

VLDL = TG/5

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10
Q

Clinically important serum TG levels

A

Optimal: 500

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11
Q

Causes of increased plasma turbidity

A

d/t very high levels of TGs in serum (usually >1000)
If milky material is on TOP of tube –> increased chylomicrons
- MCC is that person did not fast before lipid study, otherwise they have type I hyperlipoproteinemia

If milky material is dispersed throughout plasma –> VLDL increased
- Type IV hyperlipoproteinemia

If supranate and infranate present, then chylomicrons AND VLDL increased
- Type V hyperlipoproteinemia

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12
Q

LDL

A
  • Transports CH in the blood
  • Derives from continued hydrolysis of IDL by CPL
  • Removed from blood by LDL receptors in peripheral tissue
  • Small, dense LDL particles, a/w increased risk of atherosclerosis and CAD
  • Increased in diets that are high carb
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13
Q

Composition of LDL

A

22% protein
10% TG
47% cholesterol
21% phospholipid

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14
Q

Why is fasting not required for an accurate serum CH?

A

CH content in chylomicrons is

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15
Q

Risk factors for CHD

A
  • Age (>45 males, >55 females)
  • Family history of premature CHD
  • LDL >160
  • Current smoker
  • BP >140/90 or on antihypertensive meds
  • HDL
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16
Q

HDL

A
  • “good cholesterol”
  • can be increased by nicotinic acid (best) and exercise
  • diet alterations are not effective
  • synthesized by liver and small intestine
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17
Q

HDL composition

A

50% protein
3% TG
20% CH
27% Phospholipid

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18
Q

Functions of HDL

A
  1. Source of apoE, apoCII for other lipoprotein fractions
  2. Removes CH from fatty streaks and atherosclerotic plaques (HDL delivers CH from peripheral tissue to liver –> excreted in bile or converted into bile acid/salt)
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19
Q

Lab measurement of HDL

A
  • reported as HDL-CH
  • increased HDL-CH –> decreased risk for CHD
  • decreased HDL-CH if VLDL increased
  • high (optimal) is >60, low (suboptimal) is
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20
Q

Type 1 hyperlipoproteinemia

A

aka familial chylomicronemia

  • AR, childhood disease
  • deficiency of CPL or apoCII
  • Chylomicrons increased in early childhood, VLDL increases later in life
  • Presents w/ acute pancreatitis
  • LABS: increase in serum TG (>1000) –> turbid supranate, clear infranate. Normal to moderately increased serum CH.
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21
Q

Type 2 hyperlipoproteinemia

A

Type IIa: increase in serum CH (>260) and LDL (>190), serum TG (260) and LDL (>190), serum TG (>300)

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22
Q

Causes of acquired cases of type II hyperlipoproteinemia

A
  • Primary hypothyroidism: decreased synthesis of LDL receptors
  • Blockage of bile flow: bile contains CH
  • Nephrotic syndrome: increased liver synthesis of CH
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23
Q

Polygenic hypercholesterolemia

A
  • Type IIa hyperlipoproteinemia
  • MC type
  • Multifactorial inheritance
  • Alteration in regulation of LDL levels with primary increase in serum LDL and TG
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24
Q

Familial combined hypercholesterolemia

A
  • Type IIb hyperlipoproteinemia
  • AD inheritance
  • CH and TG begin to increase around puberty. A/w metabolic syndrome. Increase in CH and TG >300. Decrease in HDL.
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25
Q

Familial hypercholesterolemia

A
  • Type IIa hyperlipoproteinemia
  • AD inheritance
  • Deficiency of LDL receptors
  • Achilles tendon xanthoma, xanthelasma. Premature CAD and stroke. Increase in serum CH and LDL. Serum TG
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26
Q

Type III hyperlipoproteinemia

A
  • Familial dysbetalipoproteinemia or “remnant disease”
  • AR inheritance
  • Deficiency of apoE. Decreased liver uptake of IDL and chylomicron remnants.
  • Palmar xanthomas in flexor creases. Increased risk for CAD and peripheral vascular disease.
  • Both serum CH and TG >300. LDL
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27
Q

Acquired causes of type IV hyperlipoproteinemia

A
  • Excess alcohol intake: MCC –> increased production of VLDL, decreased activity of CPL
  • Oral contraceptives: estrogen increases VLDL synthesis
  • Diabetes: decreased adipose and muscle CPL (decreased VLDL clearance; decreased insulin responsible for decreased synthesis of CPL). Increased LDL, decreased HDL.
  • Chronic renal failure: increased synthesis of VLDL and decreased clearance of VLDL.
  • Thiazide diuretics, B-Blockers: inhibition of CPL (decreases clearance of VLDL)
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28
Q

Familial hypertriglyceridemia

A
  • MC hyperlipoproteinemia
  • Increasd production of VLDL, decreased clearance of VLDL
  • Increased risk for CAD and peripheral vascular disease
  • Eruptive xanthomas
  • Increase in TG (>300). Serum CH normal to moderately increased (250-500). Serum LDL
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29
Q

Type V hyperlipoproteinemia

A
  • Most commonly familial hypertriglyceridemia + an exacerbating disorder
  • increase in chylomicrons and VLDL d/t decreased activation and release of CPL
  • Hyperchylomicronemia syndrome
  • Eruptive xanthomas, increased acute pancreatitis, lipemia retinalis, dyspnea and hypoxemia, hepatosplenomegaly, increase in serum TG (>1000). Normal serum CH and LDL.
  • Turbid supranate and infranate
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30
Q

Nonpharmacologic tx of type II hyperlipoproteinemia

A
  • Dietary modification (low fat)
  • Increasing activity, aerobic exercise
  • Smoking cessation
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31
Q

Pharmacologic tx of type II hyperlipoproteinemia

A
  • HMG-CoA reductase inhibitors (“statins”)
  • nicotinic acid
  • bile salt sequestrants
  • cholesterol absorption inhibitors
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32
Q

Nonpharmacologic tx of type IV hyperlipoproteinemia

A
  • Reduce alcohol intake
  • Reduce carbohydrate intake
  • Increase intake of omega3 fatty acids
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33
Q

Pharmacologic tx of type IV hyperlipoproteinemia

A

Nicotinic acid or fibric acid derivatives

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34
Q

Arteriosclerosis

A

Thickening and loss of elasticity of arterial walls

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35
Q

Medial calcification

A
  • dystrophic calcifications in the wall of muscular arteries
  • can be seen in plain radiographs
  • no clinical consequence UNLESS a/w atherosclerosis
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36
Q

Atherosclerosis epidemiology

A
  • MC in men
  • Increases w/ age
    RISKS:
  • HTN (accelerates by producing endothelial cell dysfunction)
  • DM (a/w hyperlipidemia and HTN which are risk factors, also a/w abnormalities of coagulation, platelet adhesion and aggregation, increased oxidative stress, fxnal changes in endothelium)
  • Cigs, hyperlipoproteinemias, previous Chlamydophilia pneumoniae infxn
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37
Q

Pathogenesis of atherosclerosis

A
  • D/t endothelial cell damage of muscular and elastic arteries
  • Veins under increased pressure undergo atherosclerosis
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38
Q

Causes of endothelial cell injury

A

Stress areas in the vasculature (eg. bifurcation), HTN, tobacco, homocysteine, oxidized LDL, small dense LDL

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39
Q

Cell response to endothelial injury

A
  1. Macrophages infiltrate the intima, platelets adhere to damaged endothelium
    - platelets produce inflammatory response in leukocytes and endothelial cells
    - Platelet-mediated inflammatory response occurs even with platelet-inhibiting drugs
  2. Inflammatory cells release cytokines and growth factors –> hyperplasia of smooth muscle cells (SMCs)
  3. SMCs migrate to tunica intima
  4. CH enters SMCs and macrophages, producing foam cells
  5. SMCs and macrophages release cytokines that produce extracellular matrix (collagen, proteoglycans, elastin)
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40
Q

Development of a fibrous plaque

A
  • Components: SMCs, foam cells, inflammatory cells, ECM
  • Overlies a necrotic center containing cellular debris, CH crystals, foam cells
  • Disrupted plaques may extrude underlying necrotic material, which extends to the endothelial surface serving as a nidus for thrombus formation
  • Frequently becomes dystrophically calcified and ulcerated
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41
Q

MC sites of atherosclerosis

A

Descending order: abdominal aorta, coronary artery, popliteal artery, internal carotid artery

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42
Q

Serum C-reactice peptide

A

Increased in patients with disrupted plaques.
Plaques may rupture and produce vessel thrombosis –> acute MI
CRP may be stronger predictor of cardiovascular events than LDL

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43
Q

Complications of atherosclerosis

A
  • Vessel weakness
  • Vessel thrombosis
  • Hypertension
  • Cerebral atrophy
  • PAD
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44
Q

Peripheral arterial disease epidemiology

A
  • Increases w/ age, equal in men and women

- Blacks > whites

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45
Q

Peripheral arterial disease sx

A
  1. Claudication - pain, weakness, numbness, cramping d/t decreased arterial blood flow
  2. Sores, wounds, ulcers –> gangrene
  3. Dependent rubor of feet
  4. Cool skin temp
  5. Diminished hair and nail growth on limb digits
  6. Diminished pedal pulses, bruits over femoral/popliteal arteries
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46
Q

5 P’s of acute PAD occlusion

A

Pain, Pallor, Paresthesias, Paralysis, Pulselessness below occlusion

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47
Q

Diagnosis of PAD

A
  • Measure ABI (ratio
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48
Q

Tx of PAD

A
  • Manage risk factors
  • Revascularization surgical procedures
  • Cilostazol
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49
Q

Arteriolosclerosis

A
  • Hardening of the arterioles

- Two types: hyaline and hyperplastic

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50
Q

Hyaline arteriolosclerosis

A
  • Increased protein is deposited in vessel wall, occludes lumen
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51
Q

Causes of hyaline arteriolosclerosis

A

DM:

  • Glucose combines w/ proteins in basement membrane of arterioles = nonenzymatic glycosylation (NEG)
  • NEG causes basement membrane to leak proteins from plasma into vessel wall

HTN:
- increased intraluminal pressure pushes plasma proteins into vessel wall

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52
Q

Hyperplastic arteriolosclerosis

A
  • Acute increase in BP causes basement membrane duplication and smooth muscle hyperplasia in renal arterioles
  • Renal arterioles have “onion skin” appearance
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53
Q

Aneurysm

A

Weakening of the vessel wall, followed by dilation d/t increased wall stress

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54
Q

Abdominal aortic aneurysm epidemiology

A
  • MC aneurysm
  • Usually in men >60
  • Usually located below the renal artery orifices
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55
Q

AAA pathogenesis

A

Atherosclerosis weakens the vessel wall
- Vessel wall stress increases with vessel diameter
- Vessel lumen fills with atheromatous debris and blood clots
Other factors: familial, structural defects in connective tissue, absence of vasa vasorum in abdominal aorta

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56
Q

Clinical findings in AAA

A
  • Usually asymptomatic
  • Pulsatile epigastric mass that may or may not be tender
  • Bruit heard if renal artery stenosis or visceral arterial stenosis is present
  • Atherosclerotic plaques can chip off and embolize to distal extremities
  • Rupture is MC complication
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57
Q

Rupture triad in AAA

A
  1. Sudden onset severe left flank pain (bleed is initially retroperitoneal) followed by
  2. hypotension from blood loss into retroperitoneum
  3. presence of pulsatile mass on exam
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58
Q

Greatest predictor for AAA rupture

A

Diameter of aneurysm

- surgical repair beneficial for AAAs 5.0-5.4 cm in diameter

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59
Q

Dx, Tx of AAA

A

Dx: Ultrasound is 100% accurate, CT used pre-op to localize extent into renal vessels and evaluate vessel wall integrity to exclude rupture, angiography give detailed arterial anatomy

Tx: Endovascular or open surgery

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60
Q

Popliteal artery aneurysm

A
  1. 95% of cases are males
  2. MC peripheral artery aneurysm
  3. Pulsatile mass behind the knee
  4. Treated surgically
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61
Q

Mycotic aneurysm

A
  • Vessel wall weakens d/t infection
  • Fungal invaders: Aspergillus, Candida, Mucor
  • Bacterial invaders: Bacteroides fragilis, Pseudomonas aeruginosa, Salmonella
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62
Q

Clinical findings, tx for mycotic aneurysm

A

Clinical findings:

  • thrombosis w/ or w/o infarction
  • rupture

Tx: surgical

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63
Q

Berry aneurysm

A

Saccular dilatation typically found around the circle of Willis and base of the brain, MC site is junction of communicating branches w/ ACA

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64
Q

Risk factors for berry aneurysm

A
  • Normal hemodynamic stress
  • Presence of HTN
  • Coarctation of aorta
  • Atherosclerosis
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65
Q

Pathogenesis of berry aneurysm

A
  • At the junction of the communicating branches w/ main cerebral vessels, the vessel lacks an internal elastic lamina and smooth muscle
  • Rupture of the aneurysm releases blood into the subarachnoid space or into the brain parenchyma
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66
Q

Clinical findings of berry aneurysm

A
  • Sudden onset of severe occipital headache, “worst headache I’ve ever had”
  • Nuchal rigidity from meningeal irritation
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67
Q

Complications of ruptured berry aneurysm

A
  • Death shortly after bleed

- Rebleeding, hydrocephalus, neurologic deficits

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68
Q

Dx, Tx of ruptured berry aneurysm

A

Dx: CT scan and angiography
Tx: immediate surgical repair

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69
Q

Syphilitic aneurysm

A
  • Complication of tertiary syphilis d/t Treponema pallidum

- Usually men 40-55 years of age

70
Q

Pathogenesis of syphilitic aneurysm

A
  1. T pallipum infects vasa vasorum of the ascending and transverse portions of aortic arch
    - vasculitis is called endarteritis obliterans
    - characteristic plasma cell infiltrate in vessel wall
    - inflammation is intense and often occludes lumen of vessel
  2. vessel ischemia of the medial tissue leads to weakness and subsequent dilation of the aorta and aortic valve ring
71
Q

Clinical findings of syphilitic aneurysm

A
  • AV regurgitation

- Brassy cough (L recurrent laryngeal nerve stretched by aneurysm)

72
Q

AV regurgitation

A
  • problem in closing AV
  • AV closes in diastole, so murmur occurs in early diastole as blood leaks back into ventricle
  • increase in LV end-diastolic volume –> increase in stroke volume (increased systolic pressure)
  • Blood rapidly draining back into LV decreases diastolic pressure
  • ## Wide pulse pressure –> bounding pulses
73
Q

Austin Flint murmur

A

Excessive blood drips back onto MC leaflet, producing diastolic murmur
- indicates need for aortic valve replacement

74
Q

Dx and Tx of syphilitic aneurysm

A

Dx: linear calcifications seen in aortic wall on plain radiograph, aortography is definitive dx

Tx: abx for tertiary syphilis and surgery if warranted

75
Q

Aortic dissection epidemiology

A
  • MC in men w/ mean age of 40-60, hx of HTN

- Commonly occurs in young people with connective tissue disorder (Marfan syndrome or Ehlers-Danlos)

76
Q

Aortic dissection pathogenesis

A

Cystic medial degeneration (CMD): elastic tissue fragmentation in media weakens the elastic artery. Degraded matrix material collects in areas of fragmentation in media.

77
Q

Risk factors for CMD

A
  1. Increased wall stress from: HTN, pregnancy, coarctation of aorta
  2. Defects in connective tissue: Marfans (defect in elastic tissue), EDS (defect in collagen)
78
Q

Marfan syndrome

A
  • AD
  • Results in production of weak elastic tissue d/t missense mutation in synthesis of fibrillin
  • Cardiovascular abnormalities
  • Dilation of ascending aorta –> aortic dissection/AV regurg
  • Mitral valve prolapse is MC valvular defect, often a/w conduction defects
  • Skeletal defects: hypermobile joints, eunuchoid proportions, arachnodactyly
  • Dislocation of lens
79
Q

Intimal tear in aorta

A
  • D/t HTN or underlying structural weakness in media
  • Usually occurs within 10 cm of AV
  • Blood dissects under arterial pressure through areas of weakness
  • Blood dissects proximally and or distally
80
Q

Clinical findings in aortic dissection

A
  1. Acute onset of severe retrosternal chest pain radiating to the back
  2. AV regurgitation d/t AV ring dilation
    - radiograph or echocardiogram shows widening of AV root
    - axial CT shows true and false lumen of dissection
  3. Loss of upper extremity pulse (compression of subclavian artery by blood in false lumen)
  4. Rupture sites: pericardial sac MC, pleural cavity, peritoneal cavity
81
Q

Saphenous venous system

A
  • Superficial saphenous veins drain blood into deep veins via perforating branches
  • Valves in perforator branches prevent reversal of blood flow into superficial system
  • Deep veins direct blood back into heart
82
Q

Varicose veins

A

Veins that are abnormally distended (>3 mm) and often tortuous underneath the skin surface

83
Q

Locations of varicose veins

A
  1. Superficial saphenous veins (MC)
  2. Distal esophagus (d/t portal HTN)
  3. Anorectal region (internal hemorrhoids)
  4. Left scrotal sac
84
Q

Superficial varicosities in the lower extremities

A
  • MC clinical manifestation of chronic venous insufficiency

- Risk factors: female, FH, multiple pregnancies, jobs with prolonged standing, obesity, advanced age

85
Q

Pathogenesis of superficial varicosities in LE

A
  1. Valve incompetence of perforator branches with reversal of blood flow from high pressure deep venous system into superficial system
  2. May be secondary to DVT
    - retrograde blood flow through perforating branches into superficial system causes increased pressure and dilation of vessels
86
Q

Tx of superficial varicosities in LE

A

Non pharmacologic: Graded compression stockings

Chronic tx: compression sclerotherapy, ligation and stripping, endovenous obliteration using radiofrequency or laser

87
Q

Causes of venous thromboses

A
  • Stasis of blood flow (prolonged immobilization, post-ob)
  • Hypercoagulability (antithrombin III deficiency, oral contraceptives, pancreatic cancer, factor V deficiency, protein C and S deficiencies)
88
Q

Locations of venous thromboses

A
  1. MC in deep veins of lower extremity: anterior, posterior, peroneal veins in calf, popliteal/femoral veins
  2. Less common: periprostatic plexus, ovarian and periuterine veins, portal vein, hepatic vein, dural sinuses in brain
89
Q

DVT in calf acute sx

A
  1. Swelling of affected leg
  2. Pain on dorsiflexion of foot (Homans sign) and compression of calf
  3. Pitting edema distal to thrombosis d/t increased hydrostatic pressure
90
Q

DVT in calf chronic sx

A
  1. Stasis dermatitis

2. Secondary varicosities in superficial system

91
Q

Stasis dermatitis

A
  • Hemorrhagic or orange discoloration of the skin and ischemic ulcers located around the medial malleolus of the ankles
  • Orange d/t hemosiderin deposited in skin from ruptured vessels
  • Caused by rupture of perforating branches d/t pressure backup from chronic deep vein insufficiency
  • Tx: topical high potency corticosteroids and abx if infxn present
92
Q

Dx, Tx of DVT

A

Dx: Venous duplex ultrasonogaphy + serum D-dimer assay

Tx: low molecular weight heparin, compression stockings, long term treatment to prevent recurrent DVT (warfarin)

93
Q

Superficial thrombophlebitis

A
  • 10-20% a/w occult DVT
    CAUSES:
  • IV vannulation of veins, MC in plastic catheters inserted into lower extremity veins
  • Infection (usually staph aureus)
  • Carcinoma of pancreatic head (produces superficial migratory thrombophlebitis = Trousseau sign, d/t release of procoagulants by the cancer)
  • Hypercoagulable state
94
Q

Clinical findings in superficial thrombophlebitis

A
  • Pain and tenderness along course of superficial vein

- Erythema and edema of overlying skin and subcutaneous tissue

95
Q

Tx of superficial thrombophlebitis

A
  • Warm, most compresses

- NSAIDs, dicloxacillin, cephalexin

96
Q

SVC syndrome

A
  • Extrinsic compression of SVC d/t primary lung cancer
  • MCC is small cell carcinoma of lung
  • Clinical findings: “puffiness” and blue/purple discoloration of face, arms, and shoulders, retinal hemorrhage, stroke
  • Tx: radiation, stent to bypass the obstruction
97
Q

Thoracid outlet syndrome

A
  • Compression of the neurovascular compartment in the neck
  • Causes: cervical rib, spastic anterior scalene muscles, positional change in neck and arms in muscular individuals
  • Clinical findings: vascular signs like arm falling asleep when person sleeps, nerve root signs (numbness, paresthesias), Positive Adson test
  • Tx: manipulation therapy, home exercise, surgery if anatomic cause
98
Q

Adson test

A

Pulse disappears/diminished when arm is outstretched and patient looks to outstretched arm

99
Q

Structure of lymphatic vessels

A

Incomplete basement membranes, which predisposes them to infxn and tumor invasion

100
Q

Acute lymphangitis

A
  • Inflammation of lymphatics (“red streak”)
  • Cellulitis MC caused by strep pyogenes
  • Tx: clindamycin/erythromycin
101
Q

Nodular lymphangitis

A
  • Sporotrichosis
102
Q

Lymphedema

A
  • Collection of lymphatic fluid in interstitial tissue or body cavities
  • In US, MCC is post-radical mastectomy followed by irradiation of axilla
  • Other causes: filariasis (MCC in world), congenital, Turner syndrome
103
Q

Clinical findings in lymphedema

A
  • Early in interstitial edema, there is pitting with compression; in advanced cases it is nonpitting d/t increased fibrosis
  • Usually painless and progressive
104
Q

Tx of lymphedema

A

Complex decongestive therapy including extremity elevation, limb massage, and pneumatic compression

105
Q

Chylous effusions

A
  • Contain chylomicrons and TG

- In thoracic cavity, caused by damage to thoracic duct by malignant lymphoma or trauma

106
Q

Vasculitis

A

Inflammation of small vessels (arterioles, venules, capillaries), medium-sized vessels (muscular arteries), large vessels (elastic arteries), or a combination of these vessel types

107
Q

Pathogenesis of vasculitis

A
  1. Type III hypersensitivity (immunocomplex, eg. Henoch-Schonlein purpura)
  2. Type II hypersensitivity (antigen-antibody, eg. Goodpasture syndrome)
  3. ANCA
  4. Direct invasion by all classes of microbial pathogens
108
Q

ANCA

A
  • antibodies activate neutrophils, causing release of their enzymes and free radicals, resulting in vessel damage
  • c-ANCA type of vasculitis: Ab directed against proteinase 3 in cytoplasmic granules, ex. Wegener granulomatosis
  • p-ANCA type of vasculitis: Ab directed against myeloperoxidase in neutrophils, ex. microscopic polyangiitis, Churg-Strauss syndrome
109
Q

Angiomyolipoma

A

Kidney hamartoma composed of blood vessels, muscle, and mature adipose tissue
- a/w tuberous sclerosis

110
Q

Angiosarcoma

A

Liver angiosarcoma a/w exposure to polyvinyl chloride, arsenic, or thorium dioxide

111
Q

Bacillary angiomatosis

A
  • Benign capillary proliferation involving skin and visceral organs in AIDS patients
  • simulates Kaposi sarcoma in AIDS
  • caused by Bartonella henselae, a gram - bacillus
112
Q

Capillary hemangioma

A
  • Facial lesion in newborns, normally regress with age
113
Q

Cavernous hemangioma

A

MC benign tumor of the liver and spleen

May rupture if large and produce hemoperitoneum

114
Q

Cystic hygroma

A

Lymphatic cyst in the neck that may be a/w Turner syndrome

115
Q

Glomus tumor

A

Painful red subungual nodule in a digit

Derive from arteriovenous shunts in glomus bodies

116
Q

Hereditary telangiectasia

A
  • Dilated vessels on the skni and mucous membranes in the mouth and throughout the GI tract
  • Chronic iron deficiency anemia may occur d/t bleeding from telangiectasias in GI tract
117
Q

Kaposi sarcoma

A
  • Malignant tumor arising from endothelial cells or primitive mesenchymal cells.
  • AIDS-defining lesion, MC cancer in AIDS
  • A/w HHV8
  • Raised red/purple discoloration that progresses from a flat lesion to a plaque to a nodule that ulcerates
  • Common sites include skin (MC), mouth, GI
118
Q

Lymphangiosarcoma

A

Malignancy of lymphatic vessels

Arises out of long-standing chronic lymphedema

119
Q

Pyogenic granuloma

A
  • Vascular, red pedunculated mass that ulcerates and bleeds easily
  • Posttraumatic or a/w pregnancy
120
Q

Spider telangiectasia

A

Arteriovenous fistula, disappears when body is compressed

A/w hyperestrinism (cirrhosis, normal pregnancy)

121
Q

Sturge-Weber syndrome

A
  • Nevus flammeus on the face in the distribution of the opthalmic branch and/or maxillary branch of CN V
  • Some cases show ipsilateral malformation of pia mater vessels overlying the occipital and parietal lobes, can bleed and produce subarachnoid hemorrhage
122
Q

von Hippel-Lindau syndrome

A
  • cavernous hemangiomas in the cerebellum and retina

- increased incidence of bilateral pheochromocytoma and bilateral renal cell carcinomas

123
Q

Small vessel vasculitis

A
  • Called leukocytoclastic venulitis or hypersensitivity vasculitis
  • Skin overlying vasculitis is hemorrhagic, raised, painful to palpation –> called palpable purpura
  • Microscopically: vessel is disrupted and contains neutrophilic infiltrate a/w nuclear debris and fibrinoid necrosis
124
Q

Medium sized vessel vasculitis

A
  • muscular artery vasculitis

- presents with vessel thrombosis and infarction or aneurysms

125
Q

Large vessel vasculities

A
  • elastic artery vasculitis

- presents with loss of pulse or stroke

126
Q

Takayasu arteritis

A
  • Granulomatous large vessel vasculitis involving aortic arch vessels
  • Young Asian women and children
  • Absent upper extremity pulse
  • Discrepancy in BP between arms is >10 mmHg
  • Visual defects, stroke
  • Tx: corticosteroids
127
Q

Giant cell arteritis

A
  • Granulomatous large vessel vasculitis involving superficial temporal and ophthalmic arteries
  • Adults >50 years of age
  • Temporal headache, jaw claudication
  • Blindness on ipsilateral side d/t ophthalmic artery vasculitis
  • Polymyalgia rheumatica (normal serum creatine kinase)
  • Increased ESR
  • Tx: corticosteroids
128
Q

Polyarteritis nodosa

A
  • Necrotizing medium-sized vessel vasculitis involving renal, coronary, mesenteric arteries (spares pulmonary arteries)
  • Middle-aged men
  • A/w HBsAg, HCV less commonly
  • HepB associated is type III hypersensitivity, otherwise cause is unknown
129
Q

Clinical/lab findings/Tx in polyarteritis nodosa

A
  • Vessels are at all stages of acute and chronic inflammation
  • Fever commonly present
  • Focal vasculitis produces aneurysms
  • Organ infarction in kidneys, heart, bowels, skin, testicle
  • Angiography and biopsy of lesions confirms Dx
  • Tx: corticosteroids, cyclophosphamide in resistant cases
130
Q

Kawasaki disease

A
  • Necrotizing medium-sized vessel vasculitis involving coronary arteries
  • Children girls
  • Unknown cause, possibly infectious agent precipitating an immune rxn in genetically susceptible individuals
  • Leading cause of acquired heart disease in children in developed countries
  • Asian children (japanese MC)
  • Surpassed acute rheumatic heart disease as MC acquired heart disease in kids
131
Q

Kawasaki disease symptoms/tx

A
  • Fever, erythema and edema of hands and feet convalescing with desquamated rash; cervical adenopathy; oral erythema and cracking of lips; strawberry tongue
  • Abnormal ECG
  • Tx: IVIG, aspirin, corticosteroids only if 2 courses of IVIG unsuccessful
132
Q

Thromboangiitis obliterans

A
  • Medium sized vasculitis with digital vessel thrombosis and damage to neurovascular compartment
  • Genetic
  • MC in Israeli Ashkenazi Jews, high morbidity in India, Korea, Japan
  • Typically men 25-50 who smoke cigarettes
133
Q

Thromboangiitis obliterans sx/tx

A
  • Lower extremity always involved, resting pain on forefoot is characteristic w/ possible ischemic ulcers or gangrene of foot/toes
  • Upper extremity involved in 50% of cases, upper limb ischemia with ulceration and gangrene (amputation common); Raynaud phenomenon
  • Tx: smoking cessation essential, IV iloprost, vasodilators (a-blockers, calcium channel blockers)
134
Q

Raynaud disease

A
  • Medium-sized vessel vasculitis involving digital vessels in fingers and toes, possibly tip of nose and ears
  • Young women
  • Exaggerated vasomotor response to cold or stress
  • Paroxysmal digital color changes (white-blue-red sequence)
  • Ulceration and gangrene in chronic cases
  • Tx: avoid cold temps, calcium channel blockers (nifedipine)
135
Q

Raynaud phenomenon

A
  • Medium-sized vessel vasculitis involving digital vessels in fingers and toes, possibly tip of nose and ears
  • Adult men and women, secondary to other diseases
  • A/w systemic sclerosis and CREST syndrome
  • Digital vasculitis w/ vessel fibrosis, dystrophic calcification, ulceration, gangrene
  • Tx: avoid cold temps, calcium channel blockers
136
Q

Wegener granulomatosis

A
  • Necrotizing medium and small-sized vessel vasculitis involving lung and renal vessels
  • Mean age 41 years, men = women, ~90% present with Sx involving upper/lower airways or both
137
Q

Wegener granulomatosis Sx, Tx

A
  • Necrotizing granulomas in skin, upper respiratory tract (saddle nose deformity, chronic sinusitis, collapse of trachea) and lower respiratory tract (cavitating nodular lesions)
  • Necrotizing vasculitis in lungs (infarction, hemoptysis; lung most reliable source for biopsy to secure Dx), kidneys (crescentic glomerulonephritis), c-ANCA antibodies correlate erratically w/ therapy
  • Tx: corticosteroids, cyclophosphamide
138
Q

Microscopic polyangiitis

A
  • Small vessel vasculitis involving skin, lung, brain, GI tract, kidneys
  • Children and adults
  • Precipitated by drugs, infections, immune disorders
  • Vessels at SAME stage of inflammation
  • Palpable purpura, glomerulonephritis (crescentic type), p-ANCA antibodies
  • Tx: corticosteroids, cyclophosphamide
139
Q

Churg-Strauss syndrome

A
  • Small vessel vasculitis involving skin, lung, heart vessels
  • Mean age 51, probably autoimmune
  • Allergic rhinitis, asthma
  • p-ANCA antibodies, eosinophilia
  • Tx: corticosteroids. w/ treatment, 1-year survival is 90%, 5-year survival ~60%
140
Q

Henoch-Schonlen purpura

A
  • Small vessel vasculitis involving skin, GI tract, renal, joint vessels
  • Usually in children 1-15 years, peak incidence in spring, rarely summer
  • Males > females
  • MC vasculitis in children
  • MC in whites and Asians than blacks
  • IgA-anti-IgA immunocomplexes (type III hypersensitivity)
141
Q

Henoch-Schonlein purpura Sx, Tx

A
  • Offen follows viral URI, group A streptococcal pharyngeal infxn. Pathogens may act as an antigen trigger that causes antibody formation –> immunocomplex formation
  • Palpable purpura of buttocks and lower extremities is characteristic
  • Polyarthritis, glomerulonephritis, abdominal pain and vomiting, GI bleeding
  • Recurrence in 1/3 of cases
  • Most have spontaneous recovery in 4 months w/o therapy
  • Tx: corticosteroids used if severe GI disease or renal disease are present
142
Q

Cryoglobubulinemia

A
  • Small vessel vasculitis involving skin, GI tract, renal vessels
  • Different types: mixed, monoclonal, polyclonal)
  • Adults, female>male
  • Associated w/ HCV, type 1 MPGN, multiple myeloma (monoclonal type), lymphoproliferative disorders, connective tissue disorders
143
Q

Cryoglobulinemia Sx, Tx

A
  • Cryoglobulins: they are proteins in plasma that gel at cold temps, esp. in areas exposed to cold temps
  • Palpable purpura, acral cyanosis of nose and ears and Raynaud phenomenon
  • Glomerulonephritis (crescentic type), arthritis, abdominal pain
  • Tx: immunosupressive agents
144
Q

Infectious vasculitis

A
  • Small vessel vasculitis involving skin vessels
  • Children and adults
  • Involves all microbial pathogens
  • Rocky Mountain Spotted fever
145
Q

Infectious vasculitis (RMSF) pathogenesis, Sx, Tx

A
  • Dog tick or wood tick transmits Rickettsia rickettsii
  • Organisms invade endothelial cells producing vasculitis
  • Fever is universally present
  • Petechiae begin on palms and spread to trunk
  • Tx: oral doxy
146
Q

Infectious vascutis N. meningitidis Sx, Tx

A
  • Disseminated meningococcemia
  • Capillary thromboses, usually in setting of DIC, produce petechiae that become confluent ecchymoses as disease progresses
  • Hemorrhagic infarctions of both adrenal glands commonly occurs producint acute hypocortisolism and death (Waterhouse-Friderichsen syndrome)
  • Tx: IV penicillin G
147
Q

Hypertension

A
  • Essential hypertension is 85%, secondary is 15%

- Normal BP:

148
Q

What does systolic blood pressure correlate with?

A

Stroke volume and compliance of the aorta

149
Q

Primary determinants of SV:

A
  1. preload, or the volume of blood in the LV
  2. afterload, or the resistance the LV contracts against to eject blood from the heart
  3. Contractility of the heart
150
Q

What determines compliance of the aorta?

A

Vessel elasticity

151
Q

What the fuck is compliance of the aorta

A

The ability of the aorta to expand with blood during systole

152
Q

What happens to compliance with age?

A

Decreases d/t reduced elasticity of the aorta

- Mechanism for systolic hypertension in people >60

153
Q

Causes of increased SBP

A
  • Increased preload
  • Increased contractility
  • Decreased compliance of aorta
154
Q

Causes of decreased SBP

A
  • Decreased preload
  • Decreased contractility
  • Increased afterload
155
Q

What does diastolic BP correlate with?

A
  • The volume of blood in the aorta during diastole
  • Primarily depends on the state of contraction (tonicity) of the SMCs in the peripheral vascular resistance arterioles, the viscosity of the blood, and the HR
156
Q

What causes increased DBP?

A
  • Vasoconstriction of PVR arterioles –> greater volume of blood is present in artery while heart is filling up
  • Increase in blood viscosity
  • Increase in HR –> decreases filling of coronary arteries, leaving greater volume of blood in aorta during diastole
157
Q

What causes decreased DBP?

A
  • Vasodilation of PVR arterioles
  • Severe anemia –> decreases blood viscosity
  • Decreasing HR
158
Q

Role of sodium in HTN

A
  • Excess sodium increases plasma volume –> increased SV –> increased SBP
  • Excess sodium produces vasoconstriction of PVR arterioles –>increased DBP
159
Q

Essential HTN

A
  • More common in blacks
  • Genetic factors reduce renal sodium excretion
  • Decreased Na excretion –> increased PV–> increased SV –> increased SBP
  • Decreased Na excretion –> vasoconstriction of PVR arterioles –> increased DBP

Other factors: obesity, stress, smoking, salt intake, lack of exercise

160
Q

Adrenal causes of secondary HTN

A
  • Cushing syndrome: increased mineralocorticoids
  • Pheochromocytoma: increased catecholamines
  • Neuroblastoma: increased catecholamines
  • 11-hydroxylase deficiency: increased mineralocorticoids
  • Primary aldosteronism: increased aldosterone
161
Q

Aortic causes of secondary HTN

A
  • Postductal coarctation: activation of RAA system

- Elderly: systolic HTN d/t decreased elasticity of aorta

162
Q

CNS causes of secondary HTN

A

Intracranial hypertension: release of catecholamines

163
Q

Drug causes of secondary HTN

A

Oral contraceptives: increased synthesis of angiotensinogen

Cocaine: increased sympathetic activity

164
Q

Parathyroid causes of secondary HTN

A

Primary hyperparathyroidism: calcium increases peripheral resistance arteriole SMC contraction

165
Q

Pregnancy causes of secondary HTN

A

Preeclampsia: increased angiotensin II

166
Q

Renal causes of secondary HTN

A

Renovascular disease: atherosclerosis, fibromuscular hyperplasia

  • In both, there is epigastric bruit d/t blood being forced thru narrow lumen
  • Activation of RAAS

Renal parenchymal disease: eg. diabetic nephropathy, adult polycystic kidney disease, glomerulonephritis, retention of sodium

167
Q

Cardiovascular complications of HTN

A
  • LV hypertrophy: MC overall complication
  • acute MI: MC cause of death
  • atherosclerosis
168
Q

CNS complications of HTN

A
  • Intracerebral hematoma: d/t rupture of Charcot-Bouchard aneurysm
  • Berry aneurysm: rupture produces subarachnoid hemorrhage
  • Lacunar infarct: small infarcts d/t hyaline arteriolosclerosis
169
Q

Renal complications of HTN

A
  • Benign nephrosclerosis: kidney disease of HTN d/t hyaline arteriolosclerosis. Atrophy of tubules and sclerosis of glomeruli –> renal failure
  • Malignant hypertension: rapid increase in BP accompanied by renal failure and cerebral edema
170
Q

Eye complications of HTN

A
  • Hypertensive retinopathy: AV nicking, hemorrhage of retinal vessels, exudates, papilledema
171
Q

Sequence of events in hypertensive retinopathy

A
  1. Thickening of arteriole, smaller diameter, narrow column of blood –> flame hemorrhage, exudates, papilledema
  2. Copper wiring, smaller diameter, wider light reflex
  3. Silver wiring, smaller diameter, no blood visible
172
Q

Keith-Wagener-Barker classification of hypertensive retinopathy

A

Grade I: focal narrowing of arterioles, mild AV nicking
Grade II: Arteriole narrowing, copper wiring, AV nicking more noticeable
Grade III: arteriole narrowing, silver wiring, hemorrhages, soft and hard exudates, disappearance of vein under arteriole, normal disk
Grade IV: arterioles are fine fibrous cords, same as grade III except papilledema is present

Joad's MS2 Unit 4 (2 decks)

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