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Alya Cards Pathology Robbins basis > Ch 11 > Flashcards

Ch 11 Flashcards

1
Q

What is arteriosclerosis defined as?

A

Hardening of arteries - arterial wall thickening and loss of elasticity

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2
Q

What are the types of arteriosclerosis? 4

A
  1. ArterioLOsclerosis
  2. Monckberg medial sclerosis
  3. Fibromuscular intimal hyperplasia
  4. Atherosclerosis
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3
Q

What is arterioLOsclerosis? Causes?

A

Hardening of small arteries, generally causes downstream ischemic injury.

HTN

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4
Q

What is Monckberg medial sclerosis?

A

Calcification of medial wall of muscular arteries and internal elastic membrane, DO NOt affect lumen. Usually older adults over 50. Not clinically significant.

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5
Q

What is fibromuscular hyperplasia? Causes?

A

Hardening of muscular arteries secondary to inflammation - trauma (balloon angio), healed arteritis

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6
Q

Stroke, coronary and peripheral vascular disease are cause by (type of vessel narrowing)

A

Atherosclerosis

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7
Q

What are the clinical signs of malignant hypertension?

A

SBP >200
Renal failure
Retinal haemorrhages and exudates-/+papilledema

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8
Q

What is the formula for cardiac output (CO)?

A

CO=HR x SV

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9
Q

When is renin released (trigger)?

A

Low pressure in glomerular AFFERENT arteriole

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10
Q

What does renin do?

A

Cleaves angiotensinogen (liver) to Ang I

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11
Q

What does Angiotensin II do?

A

Raises BP by:
1. Stimulate aldosterone(adrenal gland) to absorb Na and water in kidney (distal convoluted tubule)
2. Peripheral vasoconstriction

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12
Q

How does atrial natriuretic peptide affect BP?

A

Reduced BP by:
1. Vasodilation
2. Kidney excretion of Na and water

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13
Q

Causes of hypertension? 4

A
  1. Idiopathic (90%)
  2. Renovascular: eg renal artery stenosis, low flow leading to increased renin secretion
    3.single gene disorders: eg aldosterone synthase leading to increased aldosterone
  3. Protein mutations: Liddle syndrome, mutation in epithelial Na channel leads to increased reabsorption of Na
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14
Q

Onion skinning seen in blood vessel is which type of arteriosclerosis?

A

Hyperplastic

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15
Q

What are non modifiable causes of atherosclerosis? 4

A
  1. Family history
  2. Age
  3. Male gender
  4. Genetic abnormalities
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16
Q

What are the modifiable risk factors of atherosclerosis? 5

A
  1. Hyperlipidemia
  2. Hypertension
  3. Cigarette smoking
  4. Diabetes
  5. Inflammation
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17
Q

How do statins reduce cholesterol?

A

Inhibit HMG Coa reductase (limits liver synthesizing cholesterol)

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18
Q

How does diabetes cause atherosclerosis?

A

Induction of hypercholesterolemia

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19
Q

_____ (blood disease) is associated with premature vascular disease.

A

Hyperhomocysteinemia

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20
Q

____ (type of lipoprotein) is associated with coronary disease independent of cholesterol/LDL levels.

A

Lipoprotein A

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21
Q

What are atheromatous plaques made of? 2

A

Cholesterol and cholesterol esters

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22
Q

What are fatty streaks?

A

Lipid filled macrophages

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23
Q

Aneurysms cause by Ehler Danlos is due to defective (collagen type)

A

Type III

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24
Q

What proteins are responsible in degrading collagen?

A

Metalliproteinases (MMP)

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25
Q

What are the causes of aneurysms?

A
  1. Intrinsic quality of connective tissue is poor (Ehler Danlos)
  2. Excess TGFB (Marfan)
  3. Inflammation altering balance of collagen synthesis (aortitis increasing MMPs)
    4.loss of SM (ischemia to artery secondary to tertiary syphilis)
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26
Q

____ (risk factor) is greater in AAA

A

Atherosclerosis

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27
Q

___(risk factor) is most common etiology in ascending aortic aneurysm

A

Hypertension

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28
Q

Clinical signs of thoracic artery aneurysm? 5

A
  1. Chest pain
  2. Myocardial ischemia (compression of coronary artery)
  3. Difficulty swallowing
  4. Hoarseness (laryngeal nerve irritation)
    5.resp irritation
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29
Q

Young patient with backpain with high inflammatory markers could be —

A

Inflammatory AAA

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30
Q

What are the 2 types of aortic aneurysm?

A
  1. type A: involves ascending aorta, proximal.
  2. Type B: does not involve ascending aorta, distal.
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31
Q

What are the 2 types of vasculitis based on mechanism?

A
  1. Immune mediated nflammatory (non infective)
  2. Infective
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32
Q

What are the main immunologic mechanisms in non infective vasculitis? 4

A
  1. Anti-neutrophil cytoplasmic ab (ANCA)
  2. Anti-EC ab
  3. Immune complex deposition
  4. Autoreactive T cells
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33
Q

What are 2 examples of antibody associated vasculitis?

A
  1. Drug hypersensitivity
  2. Infective - eg hepatitis B infection (HBs Ah and Anti-HBsAg Ab complexes)
34
Q

Common clinical sign of drug hypersensitivity vasculitis 1

A

Skin lesions

35
Q

What are the 2 main ANCAs?

A
  1. PR3 ANCA (neutrophil azurophilic granule)
  2. MPO ANCA (Lysosomal granule constituent)
36
Q

PR3 ANCA is associated with which vasculitis (1)

A

Granulomatosis with polyangitis

37
Q

What vasculitides is MPO ANCA associated with (2)

A

Microscopic polyangitis
Churg-strauss
GPA/Wegners

38
Q

Hyperthyroid patient on PTU: which ANCA is affected?

A

MPO ANCA

39
Q

What does pauci immune mean?

A

Minimal evidence of immune complex deposition on to affected tissue

40
Q

What is the mechanism of which ANCAs cause vasculitis? 3

A
  1. ANCA formation from drugs (eg PTU) or microbial AG’s
  2. Leukocyte expression of MPO/PR3
    3.stimulation of TNF: upregulate expression of PR3/MPO

ANCAs cause direct injury to cells
Neutrophils also active to release granules/ROS

41
Q

What infectious organisms are known to cause infective vasculitis? 2

A

Aspergillus
Mucor sp

42
Q

What are the consequences of non infective vasculitis?

A
  1. Weaken vessel wall: aneurysm
  2. Can cause thrombosis and downstream infarction
43
Q

What is Giant cell arteritis?
Clinical signs?
Involved mechanism?

A

Chronic, granulomatous inflammation of medium-large vessels.
Usually affects temporal artery/aorta.
T cell response to antigen on vessel wall. Anti EC ab and TNF involved.

44
Q

What arteries can be affected in Giant cell arteritis? 4

A

Temporal artery
Opthalmic artery
Vertebral
Aorta

45
Q

What is Takayasu disease?

A

Known as pulseless disease. Granulomatous vasculitis affecting large-medium sized vessels - characterised by ocular disturbances and weak UL pulses

46
Q

Giant cell and Takayasu has similar histology. What determines DX?

A

Age

> 50 yr is Giant cell
<50 yr is Takayasu

47
Q

Takayasu Arteritis: half of cases have which artery affected?

A

Pulmonary artery

48
Q

Clinical features of Takayasu?

A

Similar to Giant cell(temporal) arteritis

Can have affected coronary leading to MI
Renal arteries can be involved, leading to HTN

49
Q

What is polyarteritis nodosa?

A

Systemic vasculitis of small-medium sized arteries - spares the pulmonary circulation

50
Q

Which infection is associated with development of polyarteritis nodosa (PAN)?

A

Hepatitis B infection

51
Q

Clinical features of PAN?

A

Young age
Episodic symptoms - rapidly accelerating HTN (renal artery involvement), Abdo pain
Bloody stools (vascular GI lesions)
Myalgia
Peripheral neuritis (motor nerves)

52
Q

Transmural necrotising inflammation is seen in (vasculitis)

A

PAN

53
Q

Which arteries are most affecting in PAN (descending order) 4

A

Kidney > heart > Liver > GI

54
Q

What is Kawasaki disease?

A

Vasculitis in medium-large vessels in children <4yrs
Associated with viral illness

55
Q

Clinical manifestations of Kawasaki?

A

Erythema to conjunctiva, oral, soles and palms
Desquamative rash
Cervical LN enlargement
Coronary - arteritis or rupture

56
Q

Mechanism of Kawasaki?

A

Delayed hypersensitivity: viral triggers activation of B cells: autoantibodies

57
Q

Microscopic polyangitis histo characteristic

A

Segmental fibrinoid necrosis of media

58
Q

What is microscopic polyangitis (leukoclastic vasculitis)?

A

Necrotising vasculitis affecting small vessels: capillaries, arterioles, venules

59
Q

What is the most common manifestation of microscopic polyangitis?

A

Necrotising glomerulonephritis

60
Q

Most cases of microscopic polyangitis are associated with (immune complex)

A

MPO ANCA

61
Q

What is the mechanism of microscopic polyangitis?

A

MPO AnCA recruiting neutrophils into vascular beds

62
Q

What are the clinical features of microscopic polyangitis?

A

Haemoptysis
Hematuria
Proteinuria
Bowel pain/bleed
Cutaneous purpura

63
Q

Allergic granulomatosis is also known as

A

Churg strauss

64
Q

Eosinophils and granulomas are associated with (vasculitis)

A

Churg Strauss

65
Q

Clinical features of Churg-Strauss

A

Asthma/allergic rhinitis is association with:
Cutaneous (palpable purpura)
GI bleeding
Renal disease (focal and segmental glomerulosclerosis)

66
Q

What is Churg-strauss?

A

Necrotising vasculitis involving small vessels in association with allergic sx

67
Q

What does thromboangitis obliterans show on vessel histo?

A

Thrombus occlusion
Acute granulomatous Inflammation
Micro abcess

68
Q

Thromboangitis obliterans is also known as

A

Buerger’s disease

69
Q

Clinical features of Buerger’s disease?

A

Raynaud’s (early)
Instep foot pain caused by exercise
Superficial nodular phlebitis
Poorly healing ulcers/amputations

70
Q

Pathogenesis of Buerger’s disease?

A

Smoking modifies host vascular proteins

71
Q

What is the triad of granulomatosis with polyangitis (GPA)

A
  1. Acute necrotising granulomas of resp tract (upper/lower or both)
  2. Necrotising or granulomatous vasculitis affecting small to medium sized vessels in lungs/airways
  3. Crescentic glomerulonephritis
72
Q

ANCA associated with GPA

A

PR3

73
Q

Upper resp tract histo in granulomatosis with polyangitis?

A

Rimmed geographic patterns of central necrosis and vasculitis

74
Q

Classic clinical features of GPA

A

Men age 40
Bilateral pneumonitis with nodules and cavitary lesions
Chronic sinusitis
Mucosal ulceration
Neuritis
Fever

75
Q

Elevated homocysteine levels is risk factor for which diseases 2

A

Thrombosis
Arteriosclerosis

76
Q

Presentation of Henoch-Shonlein purpura?

A

IgA complexes
Purpuric skin lesions
Haematuria
Proteinuria
Necrotising vasculitis

77
Q

What is Wegener granulomatosis?

A

Upper resp tract involvement
Gromeruli
Small-med size vessels
ANCA positive

78
Q

What chemical proliferates smooth muscle and increases risk of atheroma formation?

A

PDGF

79
Q

VDRL test positive means

A

Syphillis positive

80
Q

Hyaline arteriosclerosis is associated with (disease)

A

Essential hypertension

81
Q

Granulomatous arteritis is associated with (disease)

A

Wegners

82
Q

Which infection is linked to development of polyarteritis nodosa?

A

Hep B

Alya Cards Pathology Robbins basis (12 decks)

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