Pathology Vessels Chapter

Front 1

What is the size range for arterioles?

Back 1

20-100mcg

Front 2

Which one takes longer and is associated with new protein synthesis: endothelial stimulation or endothelial activation?

Back 2

Endothelial activation

Front 3

True or false: smooth muscle cells synthesize collagen, elastin, proteoglycans, growth factors, and cytokines.

Back 3

True

Front 4

Name six smooth muscle cell promoters, and three inhibitors.

Back 4

Promoters:
PDGF, FGF, IL1, Endothelin1, Thrombin, Interferon-gamma (PETIFI)

Inhibitor:
Heparan Sulfates, Nitric oxide, and TGF-beta (Has NO Taste!)

Front 5

Name three acquired causes of arteriovenous fistulas.

Back 5

Inflammation, trauma, dialysis access (most common)

Front 6

Fibromuscular dysplasia: location, etiology, outcome

Back 6

Medium to large arteries

Developmental abnormality whereby thickening from medial and intimal hyperplasia and fibrosis

Luminal stenosis,(causes renovascular hypertension) and aneurysms and rupture

Front 7

Name three forms of atherosclerosis with cause.

Back 7

Atherosclerosis (many)
Monckeberg medial calcific sclerosis (advanced age)
Arteriolosclerosis (hypertension and diabetes)

Front 8

What has happened to the incidence of atherosclerotic deaths in heart and brain since 1963?

Back 8

Both decreased; heart by 50%, stroke by 70%

Front 9

What is the major component of hyperlipiedemia associated with increased health risk?

Back 9

LDL

Front 10

True or false: hyperlipidemia has a higher risk than hypertension.

Back 10

False; hypertension increases ischemic heart disease by 60%

Front 11

True or false: Smoking 1 PPD for years triples death from IHD.

Back 11

False; doubles risk

Front 12

Name two reasons why homocysteinemia increases the risk for IHD.

Back 12

1) causes reactive oxygen species generation that causes endothelial dysfunction

2) Homocysteine interferes with vasodilator and antithrombogenic functions of NO

Front 13

True or false: as far as IHD risk, two risk factors correlates to a 4X risk, whereas three risk factors correlates to a 7X risk.

Back 13

True

Front 14

What is the cornerstone to the response-to-injury hypothesis in atherosclerosis?

Back 14

Endothelial injury resulting in endothelial dysfunction.

Front 15

What are the two major determinants of endothelial dysfunction?

Back 15

hemodynamic disturbances (turbulent flow)

Adverse effects of hypercholesterolemia

Front 16

True or false: late in atherosclerosis endothelial cells start expressing some adhesion molecules that bind WBCs.

Back 16

False, early on!

Front 17

Name some factors that macrophages make, after migrating to the site of an atheromatous plaque.

Back 17

IL1, TNF (WBC adhesion)
Monocyte chemotactic protein 1
Toxic oxygen species (from oxidation of LDL in plaque)
Growth factors that help muscle proliferation

Front 18

True or false: cholesterol is the major lipid component in fatty streaks?

Back 18

Kind of true, but mostly false; it is oxidized LDL in fatty streaks, but cholesterol esters in plaques

Front 19

How does hypercholesterolemia impair endothelial function?

Back 19

Through generation of free radicals that inactivate NO

Also activates NF-kappaB

Front 20

True or false: oxidized LDL stimulates motility of macrophages already in the plaque.

Back 20

False, it inhibits motility

Front 21

Name three infectious agents associated with ateromas.

Back 21

Herpes, CMV, Chlamydia pneumoniae

Front 22

What cell is involved in converting a streak into an atheroma?

Back 22

Smooth muscle cells

Proliferation helped by PDGF, FGF, TGF-alpha

Front 23

True or false: all infants <1 year have coronary streaks?

Back 23

False; they have aortic streaks, but adolescents have coronary streaks

Front 24

True or false: you see extracellular lipids and neutrophils in type II atherosclerosis.

Back 24

False; extracellular lipids and T lymphocytes

Front 25

Name in descending order the preferred location of atheromatous plaques of stage IV-V.

Back 25

Coronary>popliteal>internal carotid> circle of Willis

Front 26

True or false: you finally see fibrous caps of smooth muscle cells and dense ECM with an underlying necrotic/lipid/calcifed core in stage IV-V of atherosclerosis.

Back 26

True

Front 27

What percentage of the general population has hypertension?

Back 27

25%

Front 28

What do most untreated hypertensives die of?

Back 28

50% ICD and CHF
33% strokes

Front 29

Malignant hypertension: defined as? percent have it? Outcome if untreated?

Back 29

>200/>120
5%
1-2 years

Front 30

True or false: most cases of hypertension can be attributed to renal disease, renovascular narrowing, and adrenal causes.

Back 30

False, only for ~5%

Most are idiopathic (95%)

Front 31

Name three molecules made by the kidney to combat angiotensin effects.

Back 31

PGs, Kallikrein-kinin system, and NO

Front 32

Define Liddle syndrome.

Back 32

A rare single-gene disorder whereby you get a moderately severe salt-sensitive increase in BP

Front 33

Name the two proposals for primary hypertension.

Back 33

1) Reduced renal sodium excretion in the presence of normal BP (increased BV, increased CO, peripheral vasoconstriction to protect organs, stabilizes increased salt homeostasis)

2) Vasoconstriction/vascular hypertrophy proposal (like lifting weights)

Front 34

True or false: hyperplastic arteriolosclerosis is often found in both diabetics and benign nephrosclerosis.

Back 34

False; both of these found in hyaline arteriolosclerosis

Front 35

True or false: you often get fibrinoid necrosis and necrotizing arteriolitis with hyaline arteriolosclerosis.

Back 35

False; you get this with hyperplastic arteriolosclerosis

Front 36

What is Loeys-Dietz syndrome?

Back 36

Mutation in TGF-beta receptors associated with abnormal elastin and collagens I and III

Front 37

True of false: Ehlers-Danlos vascular type is associated with a defective type I collagen synthesis.

Back 37

False; type III

Front 38

True or false: increased MMP activity with decreased TIMP activity predisposes to weakened collagen wall of vessel

Back 38

True

Front 39

True of false: hypertension can narrow the vasa vasorum.

Back 39

True (get cystic medial degeneration)

Front 40

What is a major influence to the development of AAA?

Back 40

Increased MMP activity

Front 41

Name two variants of AAA.

Back 41

1) Inflammatory AAA (periaortic fibrosis, mononuclear inflammation, and giant cells)

2) Mycotic AAA (AAA secondarily infected; often rupture)

Front 42

What are the stats on AAA rupture? Growth rate? Mortality of surgery and untreated rupture?

Back 42

10%/year if > 5cm
25%/year if > 6cm

Grow .2-.3cm/year (20% grow faster)

Surgery mortality: 5%
Rupture mortality: 50%

Front 43

Name three causes for thoracic aneurysms.

Back 43

Marfan syndrome
Loeys-Dietz syndrome (TGF-beta receptor)
Syphilis

Front 44

In which vascular lesion do you see a "tree barking"?

Back 44

Syphilis

Front 45

What is the link between syphilis and cor bovinum?

Back 45

The aortic insufficiency causes overload hypertrophy of the left ventricle, leading to 1000g heart

Front 46

What two things should you look for microscopically with syphilis in the aorta?

Back 46

Obliterative endarteritis of vasa vasorum
Plasma cells

Front 47

What do people with syphilitic aortitis die from?

Back 47

CHF from aortic insufficiency

Front 48

What profile should you think of with aortic dissections?

Back 48

Men between the ages of 40-60 with hypertension

Lesions halted by atherosclerosis

Front 49

What is the most frequent preexisting lesion in aortic dissection?

Back 49

Cystic medial degeneration

Front 50

What is a unique sign of a thoracic aneurysm?

Back 50

Cough (recurrent laryngeal nerve irritation.

Front 51

What percentage of thoracic aneurysms can be salvaged with early intensive antihypertensives and surgery?

Back 51

65-75%

Front 52

What percentage of the population has primary Raynauds? At what median age? With what % family history?

Back 52

5%
14 years
25%

Front 53

Name four causes for secondary Raynauds.

Back 53

SLE, atherosclerosis, scleroderma, Buerger

Onset at 30 years, with cutaneous manifestations and worse disease

Front 54

What percentage of vasculitic skin lesions are accounted for by drug hypersensitivity?

Back 54

10%

Front 55

Which vasculitis is associated with cANCA (PR3-ANCA)?

Back 55

Wegener granulomatosis

Front 56

Which two vasculitises are associated with pANCA (MPO-ANCA)?

Back 56

Microscopic polyangitis
Churg-Strauss

Front 57

Which two vasulitises are associated with anti-endothelial cell antibodies?

Back 57

SLE
Kawasaki disease

Front 58

Which one is more important for the development of varicose veins: loss of support in wall or prolonged, increased intraluminal pressure?

Back 58

Prolonged, increased intraluminal pressure

Front 59

What percentage of men and women have varicose veins?

Back 59

10-20% men; 25-33% women

Front 60

Can you get calcification of varicose veins?

Back 60

Yes; called phlebosclerosis

Front 61

Name the primary location of venous thrombosis, and some other common sites.

Back 61

90% in deep leg veins
Periprostatic venous plexus (men)
Pelvic veins (women)
Large veins of skull or dural sinuses (both)
Portal veins (both)

Front 62

What is phlegmasia alba dolens, and what is it associated with?

Back 62

Painful white leg
Iliofemoral venous thrombosis associated with 3rd trimester or post-partum

Front 63

What is a renal complication of inferior vena caval syndrome?

Back 63

Massive proteinuria

Front 64

What is the commonest bacterial cause of lymphangitis?

Back 64

Group A Beta-hemolytic strep

Front 65

Which is more common: primary or secondary lymphedema?

Back 65

Secondary (neoplastic, surgical, irradiation, filariasis, post inflammatory)

Front 66

What is a familial cause of primary lymphedema?

Back 66

Milroy disease

Front 67

What are two immunohistochemical markers for endothelial cells?

Back 67

CD31 and vWF

Front 68

What percentage of benign tumors in infants/children due hemangiomas account for?

Back 68

10%

Front 69

Where do most internal hemangiomas go to?

Back 69

Liver

Front 70

What percentage of hemangiomas go through malignant transformation?

Back 70

Very very rare

Front 71

What percentage of capillary hemangiomas regress before age 10?

Back 71

75-90%

Front 72

Comparing capillary to cavernous hemangiomas: which one regresses more often, and which is more often to involve deep structures?

Back 72

Capillary regresses more often
Cavernous involves deep structures more often and don't regress (thrombosis and dystrophic calcification common too)

Front 73

Von Hippel Lindau disease association?

Back 73

Cavernous hemangiomas in brain, brain stem, eye grounds, pancreas, and liver

Front 74

Which hemangioma do pyogenic granulomas look like: capillary or cavernous?

Back 74

capillary, with edema and inflammation

Front 75

Where is the commonest location for a glomus tumor?

Back 75

Fingernail

Front 76

Sturge-Weber syndrome association?

Back 76

Venous angiomatous masses in meninges, ipsilateral port-wine stain on face, mental retardation, seizures, and hemiplegia

Front 77

What are the four forms of Kaposi sarcoma?

Back 77

CATA:
Classic (European)
African (Endemic/Lymphadenopathic)
Transplant-associated
AIDS-associated

Front 78

What three things are need for successful Kaposi sarcoma formation?

Back 78

Immunosuppression, active HIV infection, and HHV8

Front 79

What are the three stages to Kaposi sarcoma?

Back 79

Patch (~granulation tissue)
Plaque
Nodule (plump proliferating spindle cells; hyaline droplets, hemosiderin, slitlike spaces)

Front 80

What are the stats on epithelioid hemangioendotheliomas?

Back 80

40% recur
20-30% eventually metastasize
15% die

Front 81

What three things predispose to hepatic angiosarcoma?

Back 81

Arsenical pesticides
Thorotrast
PVC

Front 82

What is the 5 year survival for angiosarcomas?

Back 82

30%

Front 83

Where are the most common sites for angiosarcomas?

Back 83

skin, soft tissue, breast, liver

Front 84

Where are the most common sites for hemangiopericytomas?

Back 84

legs and retroperitoneum

Front 85

What percentage of hemangiopericytomas metastasize hematogenously to lung, bone, liver?

Back 85

50%

Front 86

Which graft is better for coronary bypass surgery: saphenous vein or internal mammary artery?

Back 86

Internal mammary artery stays patent 10 years down the road >90%

Saphenous vein stays patent 10 years down the road 50%

Front 87

Is there a HLA-DR association with Giant cell (Temporal) arteritis?

Back 87

yes

Front 88

Is Giant cell arteritis segmental?

Back 88

yes

Front 89

Name two patterns for Giant cell arteritis.

Back 89

1) Granulomatous inflammation in inner half of media, centered on internal elastic membrane, which fragments; 2/3 have giant cells (commoner)

2) Mixed inflammation (lymphs, macros, neutros, eos) without giant cells (less common)

Front 90

Can you have fibrinoid necrosis with Giant cell arteritis?

Back 90

Yes

Front 91

Which arteries are involved in Takayasu arteritis?

Back 91

aortic arch, 1/3 have rest of aorta and brances (e.g. renals, coronaries), 1/2 have pulmonary arteries

Front 92

Can you get an aortic valve insufficiency with Takayasu arteritis?

Back 92

Yes

Front 93

Describe micro of Takayasu arteritis.

Back 93

Early: adventitial mononuclear infiltrate with perivascular cuffing of vasa vasorum

Late: mononuclear inflammation in media with granulomas; collagenous fibrosis with lymphocytic infiltrate

Front 94

Which arteries are involved in polyarteritis nodosa (PAN)?

Back 94

Renal>heart>liver>GI
Usually spares lung!

Front 95

True or false: PAN is segmental, as is Temporal arteritis.

Back 95

True

Front 96

True or false: you get fibrinoid necrosis in the inner half of the vessel wall with PAN

Back 96

True

Front 97

What is characteristic to PAN as far as lesion ages?

Back 97

All stages of activity can exist in different vessels or even the same vessel.

Front 98

What is the key thing to look for with PAN?

Back 98

necrotizing arteritis in medium-sized vessels

Front 99

What is the major cause of death with PAN?

Back 99

Renal involvement

Front 100

What percentage of PAN patients have HBsAg-ab complexes in affected vessels?

Back 100

30%

Front 101

What is the stereotype Kawasaki syndrome patient?

Back 101

Young boy (60% males)
80% under 4/5
Rare patient >8

Front 102

True or false: with Kawasaki disease, you have autoantibodies to smooth muscle and endothelial cells.

Back 102

True

Front 103

True or false: Kawasaki disease resembles PAN.

Back 103

True (necrosis, marked inflammation involving entire thickness with less fibrinoid necrosis)

Front 104

Name the disease: fever, mouth erosions, erythema of palms/soles, desquamating skin rash, and cervical lymph node enlargement.

Back 104

Kawasaki disease

Front 105

What percentage of Kawasaki patients develop cardiovascular problems?

Back 105

20%, but only 1% fatality

Front 106

What is the leading cause of acquired heart disease in US children?

Back 106

Kawasaki disease

Front 107

What should you treat Kawasaki disease patients with?

Back 107

ASA and IV gammaglobulin

Front 108

What is another name for microscopic polyangitis/polyarteritis?

Back 108

Hypersensitivity or Leukocytoclastic vasculitis

Front 109

Which vasculitis involves arterioles, capillaries, and venules?

Back 109

Microscopic polyangitis

Front 110

True or false: with microscopic polyangitis, you can have lesions of all different ages.

Back 110

False; all lesion tend to be of same age

Front 111

What percentage of microscopic polyangitis patients have a positive pANCA (MPO-ANCA)?

Back 111

70%

Front 112

Are macroscopic infarcts common with microscopic polyangitis like in PAN?

Back 112

No

Front 113

Segmental fibrinoid necrosis of medial and focal transmural necrosis, with large and muscular arteries spared: which vasculitis?

Back 113

Microscopic polyangitis

Front 114

With which vasculitis do you get neutrophilic infiltrate which end up fragmenting (leukocytoclasia)? Also most common in venules.

Back 114

Microscopic polyangitis

Front 115

What percentage of microscopic polyangitis patients have necrotizing glomerulonephritis, leading to hematuria, proteinuria? Also have hemoptysis if pulmonary capillaritis)

Back 115

90%

Front 116

Which vasculitis is AKA allergic granulomatosis?

Back 116

Churg-Strauss Syndrome

Front 117

With which vasculitis do you get a mixture of systemic vasculitis similar to PAN/hypersensitivity vasculitis AND granulomas with eosinophilic necrosis?

Back 117

Churg-Strauss Syndrome

Front 118

Allergic rhinitis, asthma, eosinophilia, lung infiltrates: what percentage of this vasculitis has coronary/myocarditis being the major cause of mrobidity/mortality?

Back 118

60% of Churg-Strauss Syndrome

Front 119

What percentage of Churg-Strauss patients have MPO-ANCA?

Back 119

<50%

Front 120

What percentage of Wegener Granulomatosis patients have PR3 (c)ANCA?

Back 120

95%

Front 121

Cavitary lung lesions, ulcerating lesions of nose, palate, and pharynx: what vasculitis?

Back 121

Wegener Granulomatosis

Front 122

Do you have granulomas with PAN? Wegener's?

Back 122

No, Yes

Front 123

What is Buerger disease AKA?

Back 123

Thromboangitis obliterans

Front 124

What are the HLA isotypes associated with Buerger disease?

Back 124

A9 and B5

Front 125

What is unique to the thrombosis involved in Buerger disease?

Back 125

It has microabscesses and surrounding granulomatous inflammation

Front 126

What is Buerger disease painful?

Back 126

You get secondary involvement of nerves (and veins).

Front 127

Do Buerger patients get Raynauds?

Back 127

YES

Front 128

Do Buerger patients get instep exercise-induced pain, and chronic ulcers of fingers, toes and feet?

Back 128

Yes