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Alya Cards Pathology Robbins basis > Ch 11 > Flashcards

Ch 11 Flashcards

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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
What are the causes of aneurysms?
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)
26
____ (risk factor) is greater in AAA
Atherosclerosis
27
___(risk factor) is most common etiology in ascending aortic aneurysm
Hypertension
28
Clinical signs of thoracic artery aneurysm? 5
1. Chest pain 2. Myocardial ischemia (compression of coronary artery) 3. Difficulty swallowing 4. Hoarseness (laryngeal nerve irritation) 5.resp irritation
29
Young patient with backpain with high inflammatory markers could be ---
Inflammatory AAA
30
What are the 2 types of aortic aneurysm?
1. type A: involves ascending aorta, proximal. 2. Type B: does not involve ascending aorta, distal.
31
What are the 2 types of vasculitis based on mechanism?
1. Immune mediated nflammatory (non infective) 2. Infective
32
What are the main immunologic mechanisms in non infective vasculitis? 4
1. Anti-neutrophil cytoplasmic ab (ANCA) 2. Anti-EC ab 3. Immune complex deposition 4. Autoreactive T cells
33
What are 2 examples of antibody associated vasculitis?
1. Drug hypersensitivity 2. Infective - eg hepatitis B infection (HBs Ah and Anti-HBsAg Ab complexes)
34
Common clinical sign of drug hypersensitivity vasculitis 1
Skin lesions
35
What are the 2 main ANCAs?
1. PR3 ANCA (neutrophil azurophilic granule) 2. MPO ANCA (Lysosomal granule constituent)
36
PR3 ANCA is associated with which vasculitis (1)
Granulomatosis with polyangitis
37
What vasculitides is MPO ANCA associated with (2)
Microscopic polyangitis Churg-strauss GPA/Wegners
38
Hyperthyroid patient on PTU: which ANCA is affected?
MPO ANCA
39
What does pauci immune mean?
Minimal evidence of immune complex deposition on to affected tissue
40
What is the mechanism of which ANCAs cause vasculitis? 3
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
What infectious organisms are known to cause infective vasculitis? 2
Aspergillus Mucor sp
42
What are the consequences of non infective vasculitis?
1. Weaken vessel wall: aneurysm 2. Can cause thrombosis and downstream infarction
43
What is Giant cell arteritis? Clinical signs? Involved mechanism?
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
What arteries can be affected in Giant cell arteritis? 4
Temporal artery Opthalmic artery Vertebral Aorta
45
What is Takayasu disease?
Known as pulseless disease. Granulomatous vasculitis affecting large-medium sized vessels - characterised by ocular disturbances and weak UL pulses
46
Giant cell and Takayasu has similar histology. What determines DX?
Age >50 yr is Giant cell <50 yr is Takayasu
47
Takayasu Arteritis: half of cases have which artery affected?
Pulmonary artery
48
Clinical features of Takayasu?
Similar to Giant cell(temporal) arteritis Can have affected coronary leading to MI Renal arteries can be involved, leading to HTN
49
What is polyarteritis nodosa?
Systemic vasculitis of small-medium sized arteries - spares the pulmonary circulation
50
Which infection is associated with development of polyarteritis nodosa (PAN)?
Hepatitis B infection
51
Clinical features of PAN?
Young age Episodic symptoms - rapidly accelerating HTN (renal artery involvement), Abdo pain Bloody stools (vascular GI lesions) Myalgia Peripheral neuritis (motor nerves)
52
Transmural necrotising inflammation is seen in (vasculitis)
PAN
53
Which arteries are most affecting in PAN (descending order) 4
Kidney > heart > Liver > GI
54
What is Kawasaki disease?
Vasculitis in medium-large vessels in children <4yrs Associated with viral illness
55
Clinical manifestations of Kawasaki?
Erythema to conjunctiva, oral, soles and palms Desquamative rash Cervical LN enlargement Coronary - arteritis or rupture
56
Mechanism of Kawasaki?
Delayed hypersensitivity: viral triggers activation of B cells: autoantibodies
57
Microscopic polyangitis histo characteristic
Segmental fibrinoid necrosis of media
58
What is microscopic polyangitis (leukoclastic vasculitis)?
Necrotising vasculitis affecting small vessels: capillaries, arterioles, venules
59
What is the most common manifestation of microscopic polyangitis?
Necrotising glomerulonephritis
60
Most cases of microscopic polyangitis are associated with (immune complex)
MPO ANCA
61
What is the mechanism of microscopic polyangitis?
MPO AnCA recruiting neutrophils into vascular beds
62
What are the clinical features of microscopic polyangitis?
Haemoptysis Hematuria Proteinuria Bowel pain/bleed Cutaneous purpura
63
Allergic granulomatosis is also known as
Churg strauss
64
Eosinophils and granulomas are associated with (vasculitis)
Churg Strauss
65
Clinical features of Churg-Strauss
Asthma/allergic rhinitis is association with: Cutaneous (palpable purpura) GI bleeding Renal disease (focal and segmental glomerulosclerosis)
66
What is Churg-strauss?
Necrotising vasculitis involving small vessels in association with allergic sx
67
What does thromboangitis obliterans show on vessel histo?
Thrombus occlusion Acute granulomatous Inflammation Micro abcess
68
Thromboangitis obliterans is also known as
Buerger's disease
69
Clinical features of Buerger's disease?
Raynaud's (early) Instep foot pain caused by exercise Superficial nodular phlebitis Poorly healing ulcers/amputations
70
Pathogenesis of Buerger's disease?
Smoking modifies host vascular proteins
71
What is the triad of granulomatosis with polyangitis (GPA)
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
ANCA associated with GPA
PR3
73
Upper resp tract histo in granulomatosis with polyangitis?
Rimmed geographic patterns of central necrosis and vasculitis
74
Classic clinical features of GPA
Men age 40 Bilateral pneumonitis with nodules and cavitary lesions Chronic sinusitis Mucosal ulceration Neuritis Fever
75
Elevated homocysteine levels is risk factor for which diseases 2
Thrombosis Arteriosclerosis
76
Presentation of Henoch-Shonlein purpura?
IgA complexes Purpuric skin lesions Haematuria Proteinuria Necrotising vasculitis
77
What is Wegener granulomatosis?
Upper resp tract involvement Gromeruli Small-med size vessels ANCA positive
78
What chemical proliferates smooth muscle and increases risk of atheroma formation?
PDGF
79
VDRL test positive means
Syphillis positive
80
Hyaline arteriosclerosis is associated with (disease)
Essential hypertension
81
Granulomatous arteritis is associated with (disease)
Wegners
82
Which infection is linked to development of polyarteritis nodosa?
Hep B

Alya Cards Pathology Robbins basis (12 decks)

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