Br Pathology: Vascular

Front 1

If someone has known CHD what drug class is invariably given?

Back 1

hydroxy-3-methylglutaryl (HMG) CoA reductase inhibitors

Front 2

If someone has 0-1 risk factors for CHD what should their LDL be? If they have 2?

Back 2

1) <160 mg/dL
2) <130 mg/dL

Front 3

What are risk factors for CHD?

Back 3

1) male ≥ 45 years, female ≥ 55 years
2) family member with myocardial infarction before 55 years of age
3) LDL > 160 mg/dL
4) current cigarette smoking
5) blood pressure ≥ 140/90 mg/dL (or on antihypertensive medicine)
6) HDL < 40 mg/dL

Front 4

If someone has an HDL >60 what do you do to with their total risk?

Back 4

(if ≥60 mg/dL, subtract 1)

Front 5

What is the function of chylomicrons?

Back 5

Transports diet-derived triglyceride (TG) in the blood

Front 6

What are chylomicrons composed of?

Back 6

(1) Protein (2%)
(2) TG (87%)
(3) Cholesterol (CH; 3%)
(4) Phospholipid (8%)

Front 7

Where are chylomicrons synthesized? Which specific protein do they have? What proteins do they obtain in circulation

Back 7

1) intestinal epithelium
2) Requires apolipoprotein (apo) B-48 for assembly and secretion
3) Nascent chylomicrons in the circulation obtain apo CII and apo E from high density lipoprotein (HDL)

Front 8

What happens to chylomicron levels during fasting?

Back 8

Absent during fasting

Front 9

What do chylomicrons form in test tube?

Back 9

1) it forms a creamy supranate.
2) Test tube must be left upright in a refrigerator overnight.
3) Chylomicron floats on top of plasma because it has very little protein (low density).

Front 10

How are chylomicrons cleaved? How are they removed from blood?

Back 10

1) Hydrolysis by capillary lipoprotein lipase (CPL) leaves a chylomicron remnant.
2) Chylomicron remnants are removed by apo E receptors in the liver.

Front 11

What do VLDLs transport? What protein is required for assembly and secretion?

Back 11

1) Transports liver-synthesized TG in the blood
2) Requires apolipoprotein B-100 for assembly and secretion

Front 12

what is the composition of VLDL?

Back 12

(1) Protein (9%)
(2) TG (55%)
(3) CH (17%)
(4) Phospholipid (19%)

Front 13

What does LPL do to VLDL?

Back 13

Hydrolysis by LPL produces intermediate-density lipoprotein (IDL) and low-density lipoprotein (LDL)

Front 14

How is some of the IDL removed from the blood?

Back 14

by apo E receptors in the liver.

Front 15

What are the functions of cholesterol ester transport protein? What does an increase in VLDL do to HDL?

Back 15

(1) Transfers CH from HDL to VLDL
(2) Transfers TG from VLDL to HDL
(3) An increase in VLDL always causes a decrease in HDL

Front 16

How are chylomicrons and VLDL different when left in a test tube overnight?

Back 16

the protein is greater in VLDL than in chylomicrons, so it sinks rather than floats in plasma

Front 17

What are the ranges for TG levels?

Back 17

(1) Optimal level < 150 mg/dL
(2) Borderline high level 150 to 199 mg/dL
(3) High level 200 to 499 mg/dL
(4) Very high level > 500 mg/dL

Front 18

What is the function of LDL? What is it derived from? How is it removed from circulation?

Back 18

1) Transports cholesterol in the blood
2) Derives from continued hydrolysis of IDL by LPL
3) Removed from blood by LDL receptors in peripheral tissue

Front 19

What is the composition of LDL?

Back 19

(1) Protein (22%)
(2) TG (10%)
(3) CH (47%)
(4) Phospholipid (21%)

Front 20

How is LDL calculated?

Back 20

LDL = CH - HDL - TG/5

Front 21

What are factors that can falsely lower the LDL levels?

Back 21

(1) Presence of chylomicrons falsely lowers calculated LDL by increasing diet-derived triglyceride; hence, fasting is required for an accurate calculated LDL.
(2) To reduce the chance for a falsely low calculated LDL, LDL is directly measured if the serum TG > 400 mg/dL.

Front 22

What are the ranges for LDL levels?

Back 22

(1) Optimal level < 100 mg/dL.
** Risk for coronary heart disease (CHD) markedly reduced
(2) Near optimal level is 100 to 129 mg/dL.
(3) Borderline high level is 130 to 159 mg/dL.
(4) High level is 160 to 189 mg/dL.
(5) Very high level > 190 mg/dL.
** Greatest risk for CHD

Front 23

How long should someone fast before their serum cholesterol is checked?

Back 23

1) fasting NOT required
2) Note that the CH content in chylomicrons is <3%; hence, fasting does not have a medically significant effect on the serum level.

Front 24

what are 3 factors that increase HDL?

Back 24

1) exercise
2) wine
3) estrogen

Front 25

Patient Teaching

Back 25

Ask about dosage, brand name, frequency, & why herb is taken
Instruct patient to report use to health care providers
Educate about risks & benefits
Advise about possible side effects
Encourage thorough examination of product labels
Discontinue use 2 to 3 weeks before surgery

Front 26

Where is HDL synthesized? what is the relationship of VLDL and HDL?

Back 26

1) liver
2) small intestine
3) HDL Decreased if VLDL is increased

Front 27

How does HDL function?

Back 27

(1) Source of apolipoproteins for other lipoprotein fractions
(2) Removes cholesterol from atherosclerotic plaques
3) Delivers CH from peripheral tissue to the liver
4) CH is either excreted into bile or converted into bile acids/salts.

Front 28

What are ranges for HDL?

Back 28

(a) High level (optimal) ≥60 g/dL
(b) Low level (suboptimal) < 40 mg/dL

Front 29

How long should someone fast before HDL is measured?

Back 29

Fasting is not required

Front 30

how should the diet be modified for people at high risk of CHD? Give a breakdown on each type of fat?

Back 30

1) fat intake < 30% of total caloric intake
2) polyunsaturated fat up to 10% of total calories
3) monounsaturated fat up to 20% of total calories
4) saturated fat < 7% of total calories
5) no more than 200 mg/day of CH
6) dietary fiber 20 to 30 g/day

Front 31

How does nicotinic acid effect blood lipid levels?

Back 31

1) least expensive lipid-lowering agent
2) also decreases TG
3) increases HDL greater than other drugs

Front 32

What are the genetics of type I hyperlipoproteinemia? What is deficient?

Back 32

(1) Autosomal recessive
(2) Rare childhood disease
(3) Deficiency of LPL or apo CII

Front 33

Clinically what is seen in type I hyperlipoproteinemia?

Back 33

(1) Chylomicrons are primarily increased in early childhood.
(2) VLDL increases later in life.
(3) Presents with acute pancreatitis
a. Pancreatic vessels filled with chylomicrons rupture

Front 34

A lipid panel from someone with type I hyperliproteinemia would show what?

Back 34

(1) Increase in serum TG > 1000 mg/dL (primarily chylomicrons)
(2) Turbid supranate (chylomicrons) and clear infranate (early childhood)
(3) Normal (usual case) to moderately increased serum CH

Front 35

A lipid panel from someone with type II hyperliporteinemia would show what? How can type IIa and IIb be distinguished?

Back 35

(1) Serum LDL > 190 mg/dL
(2) Serum CH > 260 mg/dL
a. Serum TG < 300 mg/dL (called type IIa)
b. Serum TG > 300 mg/dL (called type IIb)
c. type IIb will also have higher VLDL

Front 36

pathologically what is occurring in type II hyperlipoproteinemia?

Back 36

Decreased synthesis of LDL receptors

↑ LDL due to ↓ LDL receptors

Front 37

What are acquired causes of hypercholesterolemia?

Back 37

1) Primary hypothyroidism
a. Decrease in LDL receptor synthesis or function
2) Nephrotic syndrome
a. Increase in LDL correlates with the degree of hypoalbuminemia
3) Extrahepatic cholestasis (obstruction of bile)
a. Bile contains CH for excretion

Front 38

What type of genetic disorder of familial hypercholesterolemia? what is deficient?

Back 38

(1) Autosomal dominant (AD) disorder
(2) Deficiency of LDL receptors

Front 39

Clinically what is seen in someone with familial hypercholesterolemia?

Back 39

(a) Premature coronary artery disease and stroke
(b) Tendon xanthomas
** Cholesterol deposit located over tendons (e.g., Achilles) and extensor surfaces of joints
(c) Xanthelasma
** Yellow, raised plaque on the eyelid

Front 40

What is pathognomonic for familial hypercholesterolemia?

Back 40

Achilles tendon xanthoma:

Front 41

What is the Most common hereditary type of familial hypercholesterolemia? What lipid value is altered and which is normal?

Back 41

(1) Polygenic hypercholesterolemia (type IIa) (85% of cases)
(2) Multifactorial (polygenic) inheritance
(3) Alteration in regulation of LDL levels
(4) Normal serum TG

Front 42

What are the genetics of Familial combined hypercholesterolemia (type IIb)? When do lipid levels begin to change? What lipids are altered?

Back 42

(1) AD inheritance.
(2) Serum CH and TG begin to increase around puberty.
(3) Associated with metabolic syndrome
(4) Increase in CH and TG and decrease in HDL

Front 43

A lipid panel of someone with type III hyperlipoproteinemia would show what?

Back 43

(1) Serum CH and TG > 300 mg/dL
(2) Serum CH 250 to 500 mg/dL
(3) LDL < 190 mg/dL

Front 44

What is type III hyperlipoproteinemia known as?

Back 44

Familial dysbetalipoproteinemia ("remnant disease")

Front 45

What are the genetics of familial dysbetalipoproteinemia? What is deficient? What results?

Back 45

(1) AD inheritance
(2) Deficiency of apo E
(3) Decreased liver uptake of chylomicron remnants and IDL

Front 46

Clinically what is seen in someone with type III hyperlipoproteinemia? What is there increased risk of developing?

Back 46

(1) Palmar xanthomas in flexor creases
(2) Increased risk for coronary artery disease
(3) Increased risk for peripheral vascular disease (unlike type II disorders)

Front 47

How is the diagnosis of type III hyperlipoproteinemia confirmed?

Back 47

1) Confirm diagnosis with ultracentrifugation to identify remnants
2) Lipoprotein electrophoresis and identification of apo E gene defect are other studies that can be used

Front 48

How is type III hyperlipoproteinemia treated?

Back 48

Fibric acid derivatives

Front 49

A lipid panel in someone with type IV hyperlipoproteinemia would show what?

Back 49

(1) Serum TG > 300 mg/dL (increased VLDL)
(2) Serum CH 250 to 500 mg/dL
(3) Serum LDL < 190 mg/dL
(4) Turbid infranate after refrigeration

Front 50

What is the most common lipid disorder? What lipid value in particular is increased? why is it elevated?

Back 50

1) Type IV hyperlipoproteinemia
2) ↑ VLDL
3) Due to increase in synthesis or decrease in catabolism

Front 51

What are 5 acquired causes of type IV hyperlipoproteinemia?

Back 51

(1) Excess alcohol intake
(2) Oral contraceptives
a. Estrogen increases synthesis of VLDL
(3) Diabetes mellitus
a. Decreased muscle and adipose CLP
(4) Chronic renal failure
a. Increased synthesis of VLDL
(5) Thiazides, β-blockers
a. Possible inhibition of CPL

Front 52

What is the most common cause of Type IV hyperlipoproteinemia?

Back 52

alcohol excess

Front 53

Familial hypertriglyceridemia is what type of hyperlipoproteinemia? what are genetics?

Back 53

1) type IV
2) Autosomal dominant disorder

Front 54

Clinically what is seen with familial hypertriglyceridemia? What is there increased risk of?

Back 54

1) Eruptive xanthomas
a. Yellow, papular lesions
b. Increased risk for coronary artery and peripheral vascular disease

Front 55

What type of xanthoma is seen with type IV hyperlipoproteinemia?

Back 55

eruptive xanthomas

Front 56

How is type IV hyperlipoproteinemia treated?

Back 56

↓ carbohydrate and alcohol intake

Front 57

pathologically what occurs in type V hyperlipoproteinemia? What is inactive?

Back 57

1) Increase in chylomicrons and VLDL
2) Due to decreased activation and release of LPL

Front 58

One kind of type V hyperlipoproteinemia is composed of?

Back 58

1) Familial hypercholesterolemia (type IV) + exacerbating disorder
a. Exacerbating disorders-diabetic ketoacidosis (DKA; most common), alcohol

Front 59

What lipid levels are increased and normal in type V hyperlipoproteinemia?

Back 59

1)Increased serum TG > 1000 mg/dL
2) increased VLDL
3) normal CH and LDL

Front 60

Type V hyperlipoproteinemia causes turbid plasma. How does it change depending on refrigeration?

Back 60

(1) Supranate after refrigeration, due to increased chylomicrons
(2) Infranate after refrigeration, due to increased VLDL

Front 61

Hyperchylomicronemia syndrome is what type of hyperlipoproteinemia? What is seen in the lipid panel?

Back 61

1) type V
2) Increase in serum TG (usually >1000 mg/dL)
3) Normal serum CH and LDL
4) Turbid supranate and infranate after refrigeration

Front 62

Clinically what is seen with hyperchylomicronemia?

Back 62

(1) Eruptive xanthomas
(2) Increased incidence of acute pancreatitis
(3) Lipemia retinalis
a. Retinal vessels look like milk; blurry vision
(4) Dyspnea and hypoxemia
a. Impaired gas exchange in pulmonary capillaries
(5) Hepatosplenomegaly

Front 63

How is type V hyperlipoproteinemia treated?

Back 63

(1) Treat exacerbating disorder (e.g., DKA)
(2) Nicotinic acid or fibric acid derivatives

Front 64

What are genetics of apolipoprotein B deficiency? What is deficient?

Back 64

1) Autosomal recessive
2) Deficiency of apolipoprotein B-48 and B-100
3) Deficiency of chylomicrons, VLDL, and LDL
4) Decrease in serum CH and TG

Front 65

Clinically how does apolipoprotein B deficiency present?

Back 65

1) Malabsorption
2) Ataxia (spinocerebellar degeneration)
3) hemolytic anemia with thorny RBCs (acanthocytes) related to vitamin E deficiency

Front 66

Why is there malabsorption in abetolipoproteinemia? what is seen on blood smear?

Back 66

(a) Chylomicrons accumulate in villi and prevent reabsorption of micelles.
(b) Marked decrease in vitamin E
(c) thorny RBCs (acanthocytes)

Front 67

What is another name for apolipoprotein B deficiency? How is it treated?

Back 67

1) abetalipoproteinemia
2) vitamin E

Front 68

What is arteriosclerosis?

Back 68

thickening and loss of elasticity of arterial walls

Front 69

What is medial calcification? What is clinical consequence?

Back 69

1. Dystrophic calcification in the wall of muscular arteries
a. Examples-calcification in uterine and radial arteries
2. No clinical consequence unless associated with atherosclerosis

Front 70

What blood protein is increased in patients with disrupted (inflammatory) plaques?

Back 70

Serum C-reactive peptide (CRP)

Front 71

What may be a stronger predictor of cardiovascular events than LDL?

Back 71

CRP

Front 72

Why in type I diabetes are you at increased risk for hypertriglyceridemia?

Back 72

insulin increases LPL

Front 73

In arteriolsclerosis what is the cell response to endothelial injury?

Back 73

(1) Macrophages and platelets adhere to damaged endothelium.
(2) Released cytokines cause hyperplasia of medial smooth muscle cells.
(3) Smooth muscle cells migrate to the tunica intima.
(4) Cholesterol enters smooth muscle cells and macrophages (called foam cells).
(5) Smooth muscle cells release cytokines that produce extracellular matrix.
a. Matrix components include collagen, proteoglycans, and elastin

Front 74

In atheriolscerlosis what a fibrous cap is made out of what? What does cap overlie? What can caps lead to?

Back 74

(1) Components of fibrous cap
a. Smooth muscle, foam cells, inflammatory cells, extracellular matrix
(2) Fibrous cap overlies a necrotic center.
a. Cellular debris, cholesterol crystals (slit-like spaces), foam cells
(3) Disrupted plaques may extrude underlying necrotic material leading to vessel thrombosis
(4) Fibrous plaque becomes dystrophically calcified and ulcerated

Front 75

What is an excellent marker for a ruptured plaque?

Back 75

CRP

Front 76

What are the most common sites for atherosclerosis in descending order?

Back 76

1. Abdominal aorta
2. Coronary artery
3. Popliteal artery
4. Internal carotid artery

Front 77

What is most common site of atheroslcerosis? Why?

Back 77

1) abdominal aorta
2) no vasa vasorum

Front 78

where are common sites for vessel thrombosis?

Back 78

1) Acute MI (coronary artery)
2) Stroke (internal carotid artery, middle cerebral artery)
3) Small bowel infarction (superior mesenteric artery)

Front 79

How can hypertension develop with atherosclerosis?

Back 79

Renal artery atherosclerosis may activate the renin-angiotensin-aldosterone system

Front 80

atherosclerosis induced peripheral vascular disease may lead to what?

Back 80

1) Increased risk of gangrene
2) Pain in the buttocks and when walking (claudication)

Front 81

What is hyaline arteriolosclerosis? What conditions predispose to? What histologic feature is present?

Back 81

1) Hardening of arterioles
2) diabetes
3) HTN
4) eosinophilic staining

Front 82

What is the pathogenesis of hyaline arteriolosclerosis?

Back 82

Increased protein is deposited in the vessel wall and occludes the lumen

Front 83

How does diabetes lead to hyaline arteriolosclerosis?

Back 83

a) Due to nonenzymatic glycosylation of proteins in the basement membrane
b) Basement membrane leaks protein into the vessel wall.

Front 84

How does hypertension lead to hyaline arteriolosclerosis?

Back 84

Increased intraluminal pressure pushes plasma proteins into the vessel wall

Front 85

What is the pathogenesis of hyperplastic arterioloscerosis? What is causes it?

Back 85

(1) Renal arteriole effect caused by an acute increase in blood pressure.
o Example-malignant hypertension
(2) Smooth muscle cell hyperplasia and basement membrane duplication
Note: onion skinning appearance

Front 86

What is the characteristic histologic finding in hyperplastic arteriolosclerosis?

Back 86

"onion skin" appearance

Front 87

what is the most common aneurysm in men over 50? specifically where is it located?

Back 87

1) AAA
2) Usually located below the renal artery orifices

Front 88

Pathologically what is the progression in a AAA? What are risk factors?

Back 88

1. Atherosclerosis weakens vessel wall
a. Vessel wall stress increases with vessel diameter.
b. Lumen fills with atheromatous debris and blood clots
2. Familial factors, structural defects in connective tissue, no vasa vasorum

Front 89

Clinically how does a AAA present?

Back 89

1) Usually asymptomatic
2) Rupture is the most common complication.
a. Severe left flank pain is followed by hypotension from blood loss in the retroperitoneum.
b. A pulsatile mass can be palpated

Front 90

What are causes of a mycotic aneurysm?

Back 90

1. Vessel wall weakening due to an infection
a. Does not have to be fungal
2. Fungi that invade vessels
a. Aspergillus
b. Candida
c. Mucor
3. Bacteria that invade vessels
a. Bacteroides fragilis
b. Pseudomonas aeruginosa,
c. Salmonella species

Front 91

What bacteria can invade the vessel wall?

Back 91

B. fragilis, P. aeruginosa, Salmonella

Front 92

What fungi can invade the vessel wall?

Back 92

Aspergillus, Candida, Mucor

Front 93

What are berry aneurysms? what is lacking?

Back 93

1) Defect at the junction of communicating branches with main cerebral vessels
2) Vessel lacks an internal elastic lamina and smooth muscle

Front 94

what are risk factors for developing aneurysms?

Back 94

(1) Normal hemodynamic stress
(2) Presence of hypertension of any cause
(3) Coarctation of the aorta

Front 95

what space do berry aneurysms rupture into?

Back 95

Rupture releases blood into the subarachnoid space

Front 96

What are clinical findings with berry aneurysms?

Back 96

1. Sudden onset of severe occipital headache
a. Described as the "worst headache I have ever had"
2. Nuchal rigidity from irritation of the meninges
3. Complications
a. Death may occur shortly after the bleed.
b. Rebleed, hydrocephalus, neurologic deficits

Front 97

When can aortic regurgitation be heard?

Back 97

the aortic valve closes in diastole, the murmur occurs in early diastole as blood leaks back into the ventricle

Front 98

What happens to stroke volume and systolic pressure with an aortic regurg?

Back 98

The increase in left ventricular end-diastolic volume results in an increase in stroke volume (increased systolic pressure)

Front 99

What happens to the diastolic pressure in aortic regurg?

Back 99

Blood rapidly draining back into the left ventricle produces a drop in the diastolic pressure

Front 100

What is the pulse pressure in aortic regurg? how does it present in aortic regurg?

Back 100

The wide pulse pressure (difference between the systolic and diastolic pressure) is manifested by a hyperdynamic circulation (e.g., pulsating uvula, bounding pulses)

Front 101

What causes an Austin Flint murmur? What condition is it seen in?

Back 101

1) Excessive blood dripping back onto the anterior mitral valve leaflet produces another diastolic murmur
2) Aortic regurg
Note: indication for aortic valve replacement

Front 102

Aortic regurg is the result of what bacteria? In what sex and age group?

Back 102

1) Complication of tertiary syphilis due to Treponema pallidum (spirochete)
2) Usually occurs in men 40 to 55 years of age

Front 103

Pathologically how does treponema pallidum effect the aorta? what type of infiltrate is seen?

Back 103

1. T. pallidum infects the vasa vasorum of the ascending and transverse portions of aortic arch
a. Vasculitis is called endarteritis obliterans.
b. Characteristic plasma cell infiltrate is present in the vessel wall.
2. Vessel ischemia of the medial tissue leads to dilation of the aorta and aortic valve ring.

Front 104

Clinically a syphilitic aneurysm is seen how?

Back 104

1) aortic regurgitation
2) bounding pulses
3) wide pulse pressure
4) brassy cough
a. left laryngeal nerve is stretched by aneurysm

Front 105

Genetically what is occurring in Marfans syndrome? What is missing?

Back 105

1) autosomal dominant
2) weak elastic tissue due to a defect in synthesizing fibrillin (missense mutation)

Front 106

What is the most common vascular problem with Marfans syndrome?

Back 106

Dilation of the ascending aorta may progress to aortic dissection or aortic regurgitation

Front 107

What is the most common heart problem with Marfans? What is it associated with?

Back 107

1) Mitral valve prolapse
2) conduction defects causing sudden death

Front 108

What are skeletal defects in Marfans syndrome?

Back 108

1) hypermobile joints
2) eunuchoid proportions (lower body length > upper body length, arm span > height)
3) and arachnodactyly (spider hands)

Front 109

what is a common eye defect in Marfans syndrome? Why?

Back 109

Dislocation of the lens is another finding, because the suspensory ligament holding the lens is composed of elastic tissue.

Front 110

Who does aortic dissection commonly occur in? What age group?

Back 110

1) Men with a mean age of 40 to 60 years with antecedent hypertension
* Most common group

Front 111

What is the most common cause of death in Marfans?

Back 111

aortic disection

Front 112

What is the most common cause of death in Ehlers-Danlos?

Back 112

aortic dissection
Note: type III collagen is most affected. hyperextensible skin, bleed easily, hypermobile joints. Can be dominant or recessive.

Front 113

Pathologically what is occurring in Marfans syndrome?

Back 113

1) Cystic medial degeneration (CMD)
a. Elastic tissue fragmentation
b. Matrix material collects in areas of fragmentation in the tunica media
2) defect is fibrillin

Front 114

what are risk factors for cystic medial disease?

Back 114

1) Increase in wall stress
a. Hypertension, pregnancy (increased plasma volume), coarctation
2) Defects in connective tissue
a. Marfan syndrome (defect in elastic tissue), EDS (defect in collagen)

Front 115

Where in aortic dissection does the intima tear?

Back 115

1) Due to hypertension or underlying structural weakness in the media
2) Usually occurs within 10 cm of the aortic valve
3) Blood dissects under arterial pressure through areas of weakness.
4) Blood dissects proximally and/or distally

Front 116

Clinically how will someone with an aortic dissection present?

Back 116

1. Acute onset of severe retrosternal chest pain radiating to the back
2. Aortic valve regurgitation
a. Due to aortic valve ring dilation
b. A radiograph or echocardiogram shows widening of the aortic valve root
3. Loss of the upper extremity pulse
a. Due to compression of the subclavian artery
4. Rupture
a. Usually into the pericardial sac, pleural cavity, or peritoneal cavity

Front 117

With an aortic dissection what is the most common cause of death?

Back 117

cardiac tamponade

Front 118

At autopsy a dilated aortic valve root and the irregular intimal wrinkling ("tree barking") due to scarring in the wall of the aorta is seen. What was cause?

Back 118

syphilis
Note: may also see calcification

Front 119

arachnodactyly is seen in what? What else is it called?

Back 119

1) marfans
2) spider fingers

Front 120

what are varicose veins?

Back 120

Abnormally distended, lengthened, and tortuous veins

Front 121

Where are locations for varicose veins?

Back 121

1. Superficial saphenous veins (most common site)
2. Distal esophagus (due to portal hypertension)
3. Anorectal region (e.g., hemorrhoids)
4. Left scrotal sac (e.g., varicocele)

Front 122

What are causes of varicose veins?

Back 122

1) Valve incompetence of perforator branches with reversal of blood flow from high-pressure deep venous system into superficial system
a. Exacerbated by pregnancy, prolonged standing, obesity, oral contraceptives, advanced age
2) Familial tendency
3) Secondary to deep venous thrombosis
a. Retrograde blood flow through perforating branches into the superficial system

Front 123

How are varicose veins treated?

Back 123

(1) Nonpharmacologic
a. Graded compression stockings
(2) Chronic treatment
a. Compression sclerotherapy
b. Ligation and stripping
c. Endovenous obliteration using radiofrequency (diathermy) or laser

Front 124

What is phlebothrombosis? What are causes?

Back 124

1) Thrombosis of a vein without inflammation
2) Stasis of blood flow
3) Hypercoagulability (e.g., antithrombin III deficiency)

Front 125

Where are common sites of phlebothrombosis?

Back 125

1. Most often occurs in the deep vein of the calf
2. Less common sites include portal vein, hepatic vein, dural sinuses.

Front 126

What are general findings with a leg DVT? What sign is present?

Back 126

(1) Swelling
(2) Pain on dorsiflexion of foot (Homans' sign) and compression of the calf
(3) Pitting edema distal to the thrombosis (increased hydrostatic pressure)

Front 127

What does a positive homan's sign indicate?

Back 127

DVT

pain with dorsiflexion of foot and compression of the calf

Front 128

What is stasis dermatitis a sign of? How does it appear? What causes it?

Back 128

1) DVT
2) Orange discoloration (hemosiderin) and ischemic ulcers (poor O2 perfusion) around the ankles
3) Caused by rupture of the penetrating branches
a. Due to back-up of pressure (retrograde blood flow) from chronic deep vein insufficiency (related to deep vein thromboses [DVTs], trauma, pregnancy)

Front 129

How is statis dermatitis treated?

Back 129

1) Topical high potency corticosteroids; antibiotics if infection is present

Front 130

How are DVTs diagnosed?

Back 130

Compression venous ultrasonography + serum d-dimer assay

Front 131

how are DVTs treated?

Back 131

(1) Low-molecular-weight heparin
(2) Compression stockings
(3) Long-term treatment (3-6 months) to prevent recurrent DVTs-warfarin therapy

Front 132

what is thrombophlebitis? What is it associated with?

Back 132

1) Pain and tenderness along the course of a superficial vein
2) Association with occult DVT in 20% of cases

Front 133

What are causes of thrombophlebitis?

Back 133

1. Intravenous cannulation of veins
2. Infection (Staphylococcus aureus)
3. Carcinoma of the pancreatic head
a. Produces superficial migratory thrombophlebitis
b. Due to the release of thrombogenic substances by the cancer

Front 134

How is thrombophlebitis treated?

Back 134

1. Warm, moist compresses
2. NSAIDs

Front 135

What is super vena cava syndrome? What is common cause?

Back 135

1. Extrinsic compression of the superior vena cava
2. Due to a primary lung cancer (90% of cases)
a. Usually a small cell carcinoma of the lung

Front 136

Clinically how does someone with super vena cava syndrome present?

Back 136

1) Puffiness" and blue to purple discoloration of the face, arms, and shoulders
2) Retinal hemorrhage, stroke

Front 137

How is superior vena cava syndrome treated?

Back 137

Radiation; stent to bypass obstruction

Front 138

What are presenting features of TOS?

Back 138

1) Vascular signs (e.g., arm "falls asleep" while person is sleeping)
2) Nerve root signs (e.g., numbness, paresthesias)

Front 139

A positive Adson's test indicates what? How is it performed?

Back 139

1) TOS
2) Pulse disappears when the arm is outstretched and the patient looks to the side of the outstretched arm.

Front 140

Why are lymphatics predisposed to infection and tumor invasion?

Back 140

Lymphatic vessels have incomplete basement membranes

Front 141

How does acute lymphangitis present? What is cause?

Back 141

1) Inflammation of lymphatics ("red streak")
2) Usually due to cellulitis caused by Streptococcus pyogenes

Front 142

What is the cause of nodular lymphangitis?

Back 142

sporothrix

Front 143

how do turners syndrome patients look on exam? what is defective?

Back 143

1) Lymphedema of hands and feet in newborns caused by defective lymphatics
2) Dilated lymphatic channels in the neck (cystic hygroma) produce webbed neck
3) later develop shield chest with wide spaced nipples

Front 144

What do most blood vessel tumors derive from?

Back 144

Most tumors derive from small vessels or arteriovenous anastomoses in glomus bodies

Front 145

Bacillary angiomatosis is caused by? Who is it common in?

Back 145

1) Bartonella henselae
2) common in AIDS

Front 146

What is an example of a vasculitic type III hypersensitivity disorder?

Back 146

Henoch-Schönlein purpura
Note: skin rash on buttocks and legs (palpable purpura), arthralgia, intestinal hemorrhage, melena. IgA immuncomplexes. IgA nephropathy. Affects small vessels. MULTIPLE LESIONS OF SAME AGE!

Front 147

What is an example of a vasculitic type II hypersensitivity disorder?

Back 147

Goodpasture syndrome (anti-basement membrane antibodies)

Front 148

What do Antineutrophil cytoplasmic antibodies (ANCA) do? what are the two types?

Back 148

1) Activate neutrophils causing release of their enzymes and free radicals resulting in vessel damage
2) p-ANCA
3) c-ANCA
Note: these are vasculitic disease

Front 149

c-ANCA is seen in what disease and what happens?

Back 149

(1) Antibodies are directed against proteinase 3 in cytoplasmic granules.
(2) Example-Wegener's granulomatosis

Front 150

p-ANCA occurs in what diseases? what is pathology?

Back 150

(1) Antibodies are directed against myeloperoxidase.
(2) Examples-microscopic polyangiitis, Churg-Strauss syndrome

Front 151

What is purpura due to?

Back 151

thrombocytopenia or vessel instability (e.g., scurvy) is not palpable, because acute inflammation is not involved.

Front 152

small vessel vasculitis is known as?

Back 152

1) leukocytoclastic venulitis
2) hypersensitivity vasculitis

Front 153

What is the gross appearance of small vessel vasculitis?

Back 153

1) Skin overlying the vasculitis is hemorrhagic, raised, and painful to palpation.
a. Called palpable purpura ("tumor" of acute inflammation)

Front 154

What diseases are examples of small vessel vasculitis?

Back 154

1) Henoch-Schönlein purpura
2) microscopic polyangiitis

Front 155

what is the microscopic appearance of small vessel vasculitis?

Back 155

Vessel is disrupted and contains a neutrophilic infiltrate associated with nuclear debris and fibrinoid necrosis.

Front 156

How does medium sized vasculitis present? What else is it called?

Back 156

1. Muscular artery vasculitis
2. Presents with vessel thrombosis and infarction or aneurysms

Front 157

What causes medium sized vasculitis?

Back 157

1) polyarteritis nodosa
2) Kawasaki disease

Front 158

How does large vessel vasculitis present? What else is it called?

Back 158

1) Elastic artery vasculitis
2) Presents with loss of a pulse or stroke

Front 159

What are examples of large vessel vasculitis?

Back 159

1) Takayasu arteritis
2) giant cell (temporal arteritis)

Front 160

What are clinical findings with angiomyolipoma?

Back 160

1) Kidney hamartoma
2) composed of blood vessels
3) muscle, and mature adipose tissue
Note: associated with tuberous sclerosis

Front 161

What is angiomyolipoma associated with?

Back 161

tuberous sclerosis

Front 162

What is Liver angiosarcoma associated with?

Back 162

associated with exposure to polyvinyl chloride, arsenic, thorium dioxide

Front 163

Bacillary angiomatosis causes what and in who?

Back 163

Benign capillary proliferation involving skin and visceral organs in AIDS patients
Note: caused by bartonella henselae often mistaken for kaposi sarcoma

Front 164

Bacillary angiomatosis resembles what?

Back 164

Simulates Kaposi's sarcoma in AIDS

Front 165

capillary hemangioma is seen in newborns. what happens?

Back 165

Facial lesion in newborns that regresses with age

Front 166

what is the Most common benign tumor of liver and spleen? What can happen over time?

Back 166

1) Cavernous hemangioma
2) May rupture if large

Front 167

Cystic hygroma is seen in who?

Back 167

Lymphangioma in the neck associated with Turner's syndrome

Front 168

glomus tumor derives from what? how does it present and where?

Back 168

1) Derive from arteriovenous shunts in glomus bodies
2) Painful red subungual nodule in a digit

Front 169

Hereditary telangiectasia occurs where? What is deficient? What are genetics?

Back 169

1) Dilated vessels on skin and mucous membranes in mouth and gastrointestinal tract
2) Chronic iron deficiency anemia
3) autosomal dominant

Front 170

What does kaposi sarcoma arise from? is it benign or malignant? what is cause?

Back 170

1) Malignant tumor arising from endothelial cells or primitive mesenchymal cells
2) Associated with human herpesvirus type 8

Front 171

How does kaposi sarcoma present? Where do they occur in body?

Back 171

1) Raised, red-purple discoloration that progresses from a flat lesion to a plaque to a nodule that ulcerates
2) Common sites include skin (most common site), mouth, and gastrointestinal tract
Note: HHV-8

Front 172

Is lymphangiosarcoma benign or malignant? When do they occur?

Back 172

1) Malignancy of lymphatic vessels
2) Arises out of long-standing chronic lymphedema (e.g., after modified radical mastectomy)

Front 173

Who is at risk for lymphangiosarcoma?

Back 173

women after radical mastectomy because of chronic lymphedema

Front 174

How does a pyogenic granuloma appear? Who do they occur in?

Back 174

1) Vascular, red pedunculated mass that ulcerates and bleeds easily
2) Post-traumatic or associated with pregnancy (relation to estrogen); usually regress postpartum

Front 175

Where do spider telangectasia occur? Do they disappear with pressure? Who do they occur in?

Back 175

1) Arteriovenous fistula (disappears when compressed)
2) Associated with hyperestrinism (e.g., cirrhosis, pregnancy)

Front 176

How does sturge-weber syndrome present? What nerve involved? what brain layer is sometimes malformed?

Back 176

1) Nevus flammeus ("birthmark" or port wine stain) on the face in distribution of ophthalmic branch of cranial nerve V (trigeminal)
2) Some cases show ipsilateral malformation of pia mater vessels overlying occipital and parietal lobes
3) early onset of glaucoma
4) meningeal AV malformations

Front 177

How does VHL effect blood vessels? what are genetics? what is it associated with?

Back 177

1) Cavernous hemangiomas in cerebellum and retina
2) Increased incidence of pheochromocytoma and bilateral renal cell carcinomas
3) autosomal dominant VHL gene on chromosome 3p
Note (tumor suppressor)

Front 178

A raised, red lesion above the right eyelid in an infant may be?

Back 178

capillary hemangioma

Front 179

What is the range for prehypertension?

Back 179

120 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic

Front 180

what is the range for stage I hypertension?

Back 180

140 to 159 mm Hg systolic or 90 to 99 mm Hg diastolic

Front 181

What is the range for stage II HTN?

Back 181

≥160 mm Hg systolic or ≥100 mm Hg

Front 182

What are factors that increase arteriole contraction?

Back 182

1) α-adrenergic stimuli
2) catecholamines
3) angiotensin II
4) vasopressin
5) and increased total body sodium

Front 183

What determines stroke volume?

Back 183

(1) Blood volume (equates with sodium homeostasis)
(2) Force of contraction
(3) Heart rate

Front 184

What determines diastolic blood pressure?

Back 184

(1) Volume of blood in the arteries while the heart is filling in diastole
a. Depends on the vascular tone of the peripheral resistance arterioles
(2) Elastic recoil of the aorta

Front 185

what determines systolic blood pressure?

Back 185

stroke volume

Front 186

What is total peripheral resistance equal to?

Back 186

TPR = viscosity of blood/(radius of arteriole)^4

Front 187

What does vasodilation do to TPR? BP? venous return?

Back 187

1) decreases TPR
2) Decreases diastolic blood pressure
3) Increases venous return to the heart

Front 188

List several vasodilating substances?

Back 188

1) Nitric oxide
2) prostaglandin I2
3) histamine
4) β-blockers
5) calcium-channel blockers

Front 189

What is the effect of Na+ on vascular smooth muscle? How does it work?

Back 189

1. Excess sodium increases plasma volume.
a. Increases stroke volume and systolic blood pressure
2. Excess sodium produces vasoconstriction of TPR arterioles
a. Sodium enters arteriole smooth muscle cells and opens calcium channels, causing vasoconstriction.
b. Increases diastolic blood pressure

Front 190

what is the primary cause of essential HTN in blacks and elderly?

Back 190

Reduced renal sodium excretion

Front 191

Do blacks and elderly people have high or low renin HTN? why?

Back 191

Increased plasma volume suppresses renin release from the juxtaglomerular apparatus (low renin hypertension).

Front 192

What is the most common type of HTN?

Back 192

essential hypertension (idiopathic)

Front 193

What are factors that cause essential HTN?

Back 193

1. Genetic factors reduce renal sodium excretion.
2. Unknown factors cause vasoconstriction of arterioles.
3. Obesity, stress

Front 194

what is the most common cause of secondary hypertension?

Back 194

Renovascular hypertension

Front 195

What is the cause in men of renovascular HTN?

Back 195

Atherosclerotic plaque partially blocks blood flow at the renal artery orifice

Front 196

What is the cause of renovascular HTN in young to middle aged women?

Back 196

Fibromuscular hyperplasia occurs in multifocal areas of the renal artery

Front 197

what is the pathologic mechanism that leads to renovascular HTN?

Back 197

(1) Decreased renal arterial blood flow activates the renin-angiotensin-aldosterone (RAA) system.
(2) Angiotensin II vasoconstricts TPR arterioles.
(3) Aldosterone increases sodium retention

Front 198

clinically what is seen in someone with renovascular HTN?

Back 198

(1) Severe, uncontrollable hypertension
(2) Epigastric bruit
a. Sound is due to turbulence of blood flow through the narrow renal artery.

Front 199

what does angiography of renovascular HTN show?

Back 199

(a) Involved kidney shows diminished size (atrophy) and delayed emptying.
(b) Renal artery has "beaded" appearance in fibromuscular hyperplasia.

Front 200

In renovascular HTN is the involved kidney releasing renin or is the normal kidney?

Back 200

↑ in involved kidney; ↓ in unaffected kidney

Front 201

what are complications of HTN in descending order?

Back 201

1) acute MI
2) stroke
3) renal failure

Front 202

what is treatment of pre-HTN?

Back 202

1) lose weight (most important)
2) decrease Na+ (<2.5g)
3) increase K+ (>3.5g)
4) 30 min aerobic exercise
5) no smoking/alcohol

Front 203

What is treatment of stage I HTN? If person has diabetes or CHF which drug is preferred?

Back 203

1) non-pharmacologic treatment (diet)
2) also diuretic (general)
3) ACE inhibitor if CHF or diabetes

Front 204

How is stage II HTN treated?

Back 204

1) non-pharmacologic (diet)
2) diuretic and angiotensin II inhibitor

Front 205

Which drugs can be used in pregnant women with HTN?

Back 205

1) methyldopa
2) hydralazine
3) labetalol
4) atenolol.

Front 206

Reducing HTN has its greatest effect in reducing risk of what?

Back 206

1) strokes #1
2) CHD
3) renal disease

Front 207

Takayasu arteritis is also known as? What happens to blood vessels?

Back 207

1) pulseless disease
2) Granulomatous large vessel vasculitis involving aortic arch vessels
Note: presents with increased ESR, fever, arthritis, night sweats, myalgia, skin nodules, ocular disturbances, weak pulses in UPPER EXTREMITIES

Front 208

Who is Takayasu arteritis common in? what are clinical findings?

Back 208

1) Young Asian women and children
2) Absent upper extremity pulse
3) Discrepancy in blood pressure between arms > 10 mm Hg
4) Visual defects
5) stroke
6) fever
7) arthritis
8) night sweats
9) myalgia and SKIN NODULES
Note: GRANULOMATOUS thickening of aortic arch and proximal vessels

Front 209

Giant cell arteritis is also known as? what happens to vessels? which vessels are effected?

Back 209

1) temporal arteritis
2) Granulomatous large vessel vasculitis involving superficial temporal and ophthalmic arteries.
Note: impaired vision and jaw claudication, increased ESR, half of people have systemic involvement and polymyalgia rheumatica

Front 210

Who does temporal arteritis occur in? What are clinical and lab findings?

Back 210

1) Adults > 50 years of age
2) Temporal headache
3) jaw claudication (pain when chewing stretches inflamed artery)
4) Blindness on ipsilateral side
5) Polymyalgia rheumatica (muscle and joint pain; normal serum creatine kinase)
6) Increased ESR

Front 211

How are giant cell arteritis and takayasu treated?

Back 211

corticosteroids

Front 212

Which vessels does polyarteritis nodosa effect? Who is it common in? What is it associated with?

Back 212

1) Necrotizing medium-sized vessel vasculitis involving renal, coronary, mesenteric arteries (spares pulmonary arteries)
2) Middle-aged men
3) Association with HBsAg (30%)

Front 213

How does polyarteritis nodosa present?

Back 213

1) Vessels at all stages of acute and chronic inflammation
2) Focal vasculitis produces aneurysms (detected with angiography)
3) Organ infarction in kidneys (renal failure), heart (acute MI), bowels (bloody diarrhea), skin (ischemic ulcer), testicle (testicular pain)
4) have cutaneous eruptions, weight loss, malaise, abdominal pain and melena
Note: does NOT effect PULMONARY

Front 214

How is polyarteritis nodosa diagnosed? treated? What infection is it associated with 30% of time?

Back 214

1) Angiography and biopsy of lesions confirm the diagnosis.
2) corticosteroids and cyclophosphomide
3) HBV
Note: does not involve pulmonary arteries

Front 215

Which vessels are effected by kawaskis disease?

Back 215

1) Necrotizing medium-sized vessel vasculitis involving coronary arteries (e.g., thrombosis, aneurysms)
Note: causes conjuncitivitis, fever, strawberry tongue, lymphadenitis and desqaumative skin rash

Front 216

Does kawaskis disease occur more in boys or girls? which ethnic group? What is cause?

Back 216

1) Children < 5 years of age
2) Boys > girls
3) Cause unknown (probably infectious)
4) Children of Asian descent have highest incidence

Front 217

How does kawaskis disease present? what is seen on EKG?

Back 217

1) Fever
2) erythema and edema of hands and feet convalescing with desquamated rash
3) cervical adenopathy
4) oral erythema and cracking of the lips
a. strawberry tongue
5) Abnormal ECG (e.g., acute MI)

Front 218

What is the most common heart disease in children along with kawaskis?

Back 218

acute rheumatic heart disease

Front 219

How is kawaskis treated? What is contraindicated?

Back 219

1) intravenous immunoglobulin
2) aspirin
3) corticosteroids contraindicated (danger of vessel rupture)

Front 220

Thromboangiitis obliterans is also known as? what occurs in disease?

Back 220

1) Beurgers disease
2) Medium-sized vessel vasculitis with digital vessel thrombosis and damage to neurovascular compartment
a. intermittent claudication
Note: Strongly associated with SMOKING, may see Raynauds phenomena
Note: gangrene

Front 221

Are men or women more likely to get buergers disease? Which ethnicitys?

Back 221

1) Men 25-50 years of age who smoke cigarettes
2) Middle East, Far East, Asia has highest prevalence

Front 222

How is Buergers disease treated?

Back 222

1) smoking cessation essential
2) intravenous iloprost (prostaglandin analogue)

Front 223

What occurs in Raynauds disease?

Back 223

Medium-sized vessel vasculitis involving digital vessels in fingers and toes; also tip of nose and ears in some cases

Front 224

Who is Raynauds disease common in? How is it treated?

Back 224

1) Young women via Exaggerated vasomotor response to cold or stress
2) avoid cold temperatures (gloves)
3) calcium channel blockers (e.g., nifedipine)

Front 225

How does Raynauds disease present?

Back 225

1) Paroxysmal digital color changes (white-blue-red sequence)
2) Ulceration and gangrene in chronic cases

Front 226

What is Raynauds phenomena?

Back 226

1) Medium-sized vessel vasculitis involving digital vessels in fingers and toes and/or tip of nose and ears in some cases
note: associated with CREST or SLE or MCT

Front 227

Who does Raynauds phenomena occur in? what is it secondary to?

Back 227

1) Adult men and women
2) Secondary to other diseases (e.g., systemic sclerosis, CREST syndrome, SLE)

Front 228

How is Raynauds phenomena treated?

Back 228

1) avoid cold temperatures (gloves)
2) calcium channel blockers (e.g., nifedipine)

Front 229

Wegener's granulomatosis causes what?

Back 229

1) Necrotizing medium and small-sized vessel vasculitis involving lung (infarctions, renal vessels)
2) necrotizing granulomas in upper and lower airway
3) necrotizing glomerulonephritis
Note: c-ANCA
Note: symptoms are perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, dyspnea and hemoptysis

Front 230

Who is Wegener's granulomatosis common in? How is it treated?

Back 230

1) Childhood to middle age
2) corticosteroids
3) cyclo-phosphamide

Front 231

What organ systems are effected by Wegener's granulomatosis? What results?

Back 231

1) Necrotizing granulomas in skin
2) upper respiratory tract (nasopharynx-saddle nose deformity, chronic sinusitis, collapse of trachea)
3) necrotizing granulomas in lung and upper airway (cavitating nodular lesions)
4) Necrotizing vasculitis in lungs (infarction, hemoptysis)
5) kidneys (crescentic glomerulonephritis)
6) otitis media, perforation of nasal septum, chronic sinusitis

Front 232

What antibody is seen in Wegener's granulomatosis?

Back 232

c-ANCA antibodies (>90% of cases) correlate erratically with therapy

Front 233

Where does microscopic polyangitis occur?

Back 233

Small vessel vasculitis involving skin, lung, brain, GI tract, and postcapillary venules and glomerular capillaries
Note similar presentation to Wegners but lacks granulomas

Front 234

Who does microscopic polyangitis occur in? What precipitates it?

Back 234

1) Children and adults
2) Precipitated by drugs (e.g., penicillin), infections (e.g., streptococci), immune disorders (e.g., SLE)

Front 235

In microscopic polyangiitis are the vessels at same or different stage of inflammation? What are other features? What antibody is seen?

Back 235

1) Vessels at same stage of inflammation
2) Palpable purpura
3) glomerulonephritis
4) p-ANCA antibodies (>80% of cases)

Front 236

How can polyarteritis nodosa be distinguished from microscopic polyangiitis?

Back 236

1) polyarteritis nodosa = vessels at different stages of inflammation
2) microscopic angiitis = vessels at same stages of inflammation

Front 237

what vessels are effected in Churg-strauss? Who does it occur in?

Back 237

1) Small vessel vasculitis involving skin, lung, heart vessels
2) Children and adults

Front 238

what are respiratory features of Churg-strauss? what antibody is present? what nervous sign is present?

Back 238

1) Allergic rhinitis
2) asthma
3) granulomatous vasculitis with eosinophilia
4) p-ANCA antibodies (70% of cases)
5) wrist and foot drop may be seen

Front 239

Henoch-Schönlein purpura does what to vessels and in which organs?

Back 239

Small vessel vasculitis involving
a. skin = palpable purpura on buttocks and legs
b. GI = intestinal hemorrhages
c. IgA nephropathy
d. arthralgia
Note: lesions all at same stage

Front 240

What is the most common vasculitis in children? is it more common in boys or girls? What is the immune complex formed?

Back 240

1) Henoch-Schönlein purpura
2) Children and young adults
3) Males > females
4) IgA-anti-IgA immunocomplexes

Front 241

Henoch-Schönlein purpura often follows what? Where are purpura palpable?

Back 241

1) Often follows a viral URI, group A streptococcal pharyngeal infection-pathogens may act as an antigen trigger that causes antibody formation leading to immunocomplex formation
2) Palpable purpura of buttocks and lower extremities

Front 242

What does Henoch-Schönlein purpura often cause? Is there a high rate of recurrence? How is it treated?

Back 242

1) Polyarthritis (80%), nephropathy (80%), GI bleeding
2) Recurrence may occur in one third of cases
3) Most have spontaneous recovery in 4 months without therapy.
4) Treatment: corticosteroids mainly used if severe GI disease or renal disease

Front 243

What happens to blood vessels in cryoglobulinemia? What are the different types?

Back 243

1) Small vessel vasculitis involving skin, GI tract, renal vessels
2) Different types of cryoglobulinemia (mixed, monoclonal, polyclonal)

Front 244

Who does cryoglobulinemia occur in? What is it associated with?

Back 244

1) Adults
2) Association with HCV, type I MPGN, multiple myeloma (monoclonal type)

Front 245

what are cryoglobulins? What are clinical findings?

Back 245

1) Cryoglobulins: immunoglobulins that gel at cold temperatures
2) Palpable purpura, acral cyanosis of nose and ears and Raynaud's phenomenon (reverses when in warm room); glomerulonephritis; arthritis; abdominal pain

Front 246

Where does infectious vasculitis occur? who does it occur in?

Back 246

1) Small vessel vasculitis involving skin vessels
2) Children and adults
3) Involves all microbial pathogens

Front 247

Rocky Mountain spotted fever causes infectious vasculitis. Where is the blood vessel damage?

Back 247

1) Petechiae on palms spread to trunk
2) Organisms invade endothelial cells producing vasculitis

Front 248

What does disseminated N meningitidis cause in blood vessels?

Back 248

Capillary thrombosis produces hemorrhage into skin and confluent ecchymoses

Front 249

desquamation of the skin of the toes is seen in a child. What do you suspect?

Back 249

kawaskis

Front 250

a concavity is seen below the nose resembling a saddle in child. What do you suspect?

Back 250

Wegener's granulomatosis

Front 251

List 5 different causes of secondary HTN produced by the adrenal?

Back 251

1) Cushing syndrome: increased mineralocorticoids
2) Pheochromocytoma: increased catecholamines
3) Neuroblastoma: increased catecholamines
4) 11-Hydroxylase deficiency: increased mineralocorticoids (i.e., deoxycorticosterone)
5) Primary aldosteronism (Conn's syndrome): increased aldosterone

Front 252

List 2 conditions of the aorta that cause secondary HTN?

Back 252

1) Postductal coarctation: activation of RAA system
2) Elderly: systolic hypertension due to decreased elasticity of the aorta

Front 253

How do oral contraceptives lead to secondary HTN?

Back 253

1) increased synthesis of angiotensinogen
2) most common cause of hypertension in young women

Front 254

What is the most common cause of HTN in young women?

Back 254

oral contraceptives

Front 255

How does primary hyperparathyroidism cause secondary HTN?

Back 255

calcium increases peripheral resistance arteriole smooth muscle cell contraction

Front 256

What is increased in pregnancy that causes HTN?

Back 256

increased angiotensin II

Front 257

How do both Graves and hypothyroidism cause HTN?

Back 257

1) Graves' disease: systolic hypertension from increased cardiac contraction
2) Hypothyroidism: diastolic hypertension due to retention of sodium

Front 258

What is the most common overall complication of HTN? What is the most common overall cause of death in HTN?

Back 258

1) Left ventricular hypertrophy
2) MI

Front 259

Intracerebral hematoma from HTN is due to what?

Back 259

rupture of Charcot-Bouchard aneurysms
Note: Charcot-Bouchard aneurysms are most often located in the lenticulostriate vessels of the basal ganglia and are associated with chronic hypertension. Don't confuse with berry aneurysms which are slightly larger vessels

Front 260

What space does a berry aneurysm rupture in?

Back 260

subarachnoid hemorrhage

Front 261

What are lacunar infarcts due to?

Back 261

small infarcts due to hyaline arteriolosclerosis

Front 262

how does Benign nephrosclerosis cause secondary HTN?

Back 262

1) kidney disease of hypertension
2) due to hyaline arteriolosclerosis
3) atrophy of tubules and sclerosis of glomeruli
4) progresses to renal failure

Front 263

What accompanies malignant hypertension?

Back 263

rapid increase in blood pressure accompanied by renal failure and cerebral edema

Front 264

Are the normal retinal arterioles transparent?

Back 264

yes... hence, the column of blood is visible and the light reflex is narrow

Front 265

How do sclerotic changes initially change blood vessels? What is sign called?

Back 265

1) blood is still visible through the vessel wall
2) develop copper wire appearance
3) Have widened-arteriolar light reflex

Front 266

How is copper wire appearance different from silver wire appearance?

Back 266

1) copper wire still has visible blood flow
2) When the vessel wall is thickened enough to prevent visualization of the blood, the light reflects back from the vessel wall to produce a "silver wiring" effect

Front 267

arterioles cross over veins in the eye. What is the normal size ratio of the two?

Back 267

normal ratio of arteriole to venous diameters is 3:4

Front 268

What is AV nicking?

Back 268

as arterioles thicken they create a depression in the wall of the venule, thus impeding blood flow

Front 269

How do microinfarctions in the eye appear?

Back 269

Grayish-white exudates that are soft, like cotton wool

Front 270

What are hard exudates in the eye the result of?

Back 270

exudates that have clear margins (hard exudates) are due to leakage of protein from increased vessel permeability

Front 271

What is the Keith-Wagener-Barker classification of hypertensive retinopathy ?

Back 271

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