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Systemic Pathology 1 (GIT, CVS, RS) > Vascular Disorders > Flashcards

Vascular Disorders Flashcards

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1
Q

Intima

A

The innermost coating or membrane of a part or organ, especially of a vein or artery.

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2
Q

Atherosclerosis.

A

Primarily a progressive disease of intima involving large & medium-sized elastic and muscular arteries.

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3
Q

Atheroma.

A

Focal lipid-rich intimal lesions.

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4
Q

Major modifiable risk factors of Atherosclerosis.

A
  1. Hyperlipidemia
  2. Hypertension
  3. Smoking
  4. Diabetes mellitus
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5
Q

Major nonmodifiable (Constitutional) risk factors of atherosclerosis.

A
  1. Genetic abnormalities
  2. Family history
  3. Increasing age
  4. Male gender
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6
Q

Additional risk factors.

A
  • Inflammation
  • CRP level
  • Hyperhomocystinemia
  • Metabolic syndrome
  • Lipoprotein (a)
  • Raised procoagulant level
  • Inadequate physical activity
  • Stressful lifestyle
  • Obesity
  • Alcohol
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7
Q

CRP level

A

-Normal C-reactive protein level.
-Excellent marker for disrupted atheromatous
plaque.

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8
Q

Hyperhomocystinemia

A
  • A medical condition characterized by an abnormally high level of homocysteine in the blood, conventionally described as above 15 μmol/L
  • Homocysteine is a type of amino acid, a chemical your body uses to make proteins. Normally, vitamin B12, vitamin B6, and folic acid break down homocysteine and change it into other substances your body needs.
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9
Q

Major components of lipid in blood are.

A
  1. LDL
  2. HDL
  3. Serum cholesterol level
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10
Q

Low density lipoprotein

A

“Bad Cholesterol”

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11
Q

Serum cholesterol level

A

-Normal range (140-240 mg/dL)
-Strongly related to the dietary intake of saturated fat.
- Risk of atherosclerosis increases with increasing serum cholesterol concentrations and lowering serum
cholesterol concentrations reduce the risk.

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12
Q

Margarine.

A

Transaturated fats produced by artificial hydrogenation of polyunsaturated oils.

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13
Q

Cholesterol-Lowering Drug

A

Example:

  • Statins, lower circulating cholesterol levels by inhibiting hydroxymethylglutaryl coenzyme A [HMG CoA] reductase.
  • HMG CoA is a rate-limiting enzyme involved in cholestrol biosynthesis in Liver.
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14
Q

HDL

A
  • Good cholesterol removes cholesterol from atheromatous plaque and transports to liver.
  • From the liver, it is excreted in the bile.
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15
Q

Disorders associated with hypercholesterolemia.

A
  1. Nephrotic syndrome
  2. Alcoholism
  3. Hypothyroidism
  4. Diabetes mellitus
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16
Q

Increased very _______ leads to reduced HDL.

A

Very Low-Density Lipoprotein (VLDL)

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17
Q

Familial hypercholesterolemia

A

Mendelian disorders, such as familial hypercholesterolemia are associated with atherosclerosis.

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18
Q

Premenopausal women have lower incidence….

A

Premenopausal women have lower incidence of
atherosclerosis-related diseases compared to males of
the same age groups. However, after menopause this sex difference disappears. This may be due to protective role of estrogen.
*However, hormone replacement therapy has no role in the prevention of coronary heart disease.

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19
Q

Achilles’ tendon xanthoma

A

Pathognomonic of familial hypercholesterolemia.

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20
Q

Theories of pathogenesis of Atherosclerosis.

A
  1. Insudation hypothesis
  2. Encrustation hypothesis
  3. Monoclonal hypothesis
  4. Response-to-injury hypothesis
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21
Q

Insudation hypothesis

A

Here, the focal accumulation of lipid in a vessel wall is due to insudation (transport) of plasma lipoproteins across an intact endothelium.

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22
Q

Encrustation hypothesis

A

Here, small mural thrombi are formed at the site of endothelial damage.
These thrombi become organized and form plaque.

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23
Q

Monoclonal hypothesis

A

Here, a single clone (monoclonal) of smooth muscle migrate from underlying media into the intima and then proliferate.
The stimulus for monoclonal proliferation may be metabolites of cholesterol.

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24
Q

Response-to-injury Hypothesis.

A

Here, atherosclerosis develops as a chronic (inflammatory and healing) response of the arterial wall to the endothelial injury.

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25
Q

RTI sequence of pathogenic events.

A
  1. Endothelial injury and dysfunction.
  2. Migration of monocytes into the intima.
  3. Lipid accumulation in the intima.
  4. Formation of foam cells and activation of macrophages.
  5. Migration of smooth muscle cells into the intima.
  6. Smooth muscle cell proliferation in the intima and ECM production.
  7. Lipid accumulation.
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26
Q

Effect of endothelial injury or dysfunction.

A
  • Monocyte & T-Lymphocyte adhesion to endothelium
  • Increased vascular permeability.
  • Platelet adhesion and thrombosis.
  • Movement LDLs across the endothelium into the intima.
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27
Q

The monocytes migrate into the intima, where they are transformed into ____.

A

Macrophages.

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28
Q

Foam cells.

A

Macrophage engulfs lipoproteins and oxidized LDL from the extracellular space in the intima. Their cytoplasm becomes foamy and these cells are called
as foam cells

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29
Q

Foam cells and necrotic core.

A

Some foam cells may undergo apoptosis > release lipids > form lipid rich center called necrotic core in atheromatous plaques.

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30
Q

Oxidized LDL causes activated macrophages which produce:

A
  • Cytokine (e.g. TNF); increases leukocyte adhesion.
  • Chemokines (e.g. monocyte chemotactic protein 1); accumulation of monocytes.
  • Reactive oxygen species; aggravate oxidation of LDL.
  • GFs; stimulate smooth muscle cell proliferation and ECM synthesis.
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31
Q

Migration of smooth muscle cells into the intima.

A 
Growth factor (e.g., platelet-derived growth factor) 
from activated platelets, macro phages, and endothelial cells causes migration of smooth muscle cells either from the arterial media or from circulating 
precursors.
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32
Q

Many growth
factors can cause smooth muscle cell proliferation.
These includes:

A
  1. PDGF
  2. Fibroblast growth factor (FGF)
  3. Transforming Growth Factor-Alpha (TGF-a)
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33
Q

_______cell may also engulf oxidized LDL and form foam cells.

A

Smooth muscle cell

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34
Q

Intracellular and Extracellular Lipid accumulation.

A
  • Extracellular lipid is derived from insudation from vessel lumen (in hypercholesterolemia) and also from necrotic foam cells.
  • Cholesterol in plaque is due to imbalance between influx and efflux, HDL transfers cholesterol from these lesions and leads to its excretion by liver.
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35
Q

Fatty Streak

A
  • The earliest or precursor lesions of atherosclerosis.
  • Found in children above 10 and adults.
  • In the Intima.
  • Multiple small (1mm) flat yellow lesions in the intima; may coalesce to form long streaks 1cm or more in length.
  • Mildly elevated above intima without disturbing blood flow.
  • Microscopy: Consist of lipid-filled foamy macrophages in the intima.
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36
Q

Major vessels involved in atherosclerosis in descending order are:

A
  1. Lower abdominal aorta > thoracic aorta.
  2. Coronary arteries.
  3. Popliteal arteries.
  4. Internal carotid arteries.
  5. Circle of Willis.
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37
Q

Gross features of atherosclerosis.

A

Color of Thrombus:

  • White to yellow.
  • Red-Brown if superimposed by thrombus.

Shape:
Irregular with well-defined boundaries.

Distribution:
-Patchy(focal)

On cross-section:
-Appears as an eccentric lesion.

Composition:
-Grumous core covered by a white fibrous cap.

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38
Q

Aortic lesion components.

A
  1. Superficial fibrous cap:
    - Smooth muscle cells
    - Collagen
  2. Necrotic core:
    - Lipid
    - Debris from dead cells
    - Foam cells
    - fibrin, organized thrombus, plasma proteins.
  3. Shoulder:
    It is the peripheral region beneath and t the side of the cap.
    - Macrophages
    - SMC
    - T-cells
  4. Neuvascularization: My be seen at the periphery of the lesions near the shoulder.
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39
Q

Complications of atherosclerosis.

A
  1. Rupture
  2. Hemorrhage into the plaque
  3. Thrombosis
  4. Embolism
  5. Aneurysm
  6. Calcification; occurs in central necrotic area of the plaque.
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40
Q

Major clinical consequences of atherosclerosis.

A
  1. Myocardial infarction (heart attack)
  2. Cerebral infarction (stroke)
  3. Aortic aneurysms
  4. Peripheral vascular disease (gangrene of the legs).
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41
Q

Stable and Vulnerable plaques.

A

Stable plaque:

  1. Have thick densely collagenized fibrous cap.
  2. Minimal inflammation.
  3. Negligible lipid core.

Vulnerable plaque:

  1. Contain numerous foam cells.
  2. Abundant extracellular lipid.
  3. Many inflammatory cells.
  4. Thin fibrous cap.
  5. Few smooth muscle cells.
  6. High-risk to undergo rupture.
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42
Q

Atherosclerotic Stenosis

A
  • Atherosclerotic plaques reduce the size of the lumen.
  • Severe reduction of lumen may lead to ischema > the lesion resulting is termed as critical stenosis.
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43
Q

In the coronary artery, atherosclerotic lesion when produces a 70% decrease in luminal cross-sectional area____

A

The patient may develop chest pain with exertion. (stable angina)

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44
Q

Intermittent claudication.

A

Diminished perfusion of the extremities.

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45
Q

Collagen synthesis.

A

By Smooth muscle cells.

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46
Q

Collagen degradation.

A

By Inflammatory cells

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47
Q

Aneurysm

A

Defined as a congenital or acquired, localized, abnormal, permanent dilation of a blood vessel or the heart.

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48
Q

Classifying Aneurysm depending on gross appearance.

A
  1. Fusiform
  2. Saccular
  3. Cylindrical
  4. Arterial dissection/dissecting hematoma.
  5. Arteriovenous
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49
Q

Fusiform Aneurysm

A
  • Ovoid dilation of vessel wall.
  • Parallel to the long axis.
  • Diameter; upto 20cm.
  • Aortic arch, Abdominal aorta or iliac arteries.
50
Q

Saccular Aneurysm

A
  • Localized spherical out-pouchings from a portion of the vessel wall.
  • 5 to 20cm in diameter.
  • Lumen may contain thrombus.
51
Q

Arteriovenous (racemose) Aneurysm.

A

A direct communication between an artery and a vein.

52
Q

True Aneurysm

A

Involves all 3 layers of the artery or thinned wall of the heart.
[Intima>Media>Adventitia]
Examples:
-Atherosclerotic
-Syphilitic
-congenital vascular aneurysms that complicates transmural myocardial infarctions.

53
Q

False/Pseudo Aneurysm.

A

A defect in the vascular wall with a hematoma which freely communicated with the intravascular space. (Pulsating hematoma)

Examples:
-Rupture of left ventricle, which complicates myocardial infarction or hematoma that follows trauma to artery.

54
Q

Hematoma

A

Blood filled space forms around a blood vessel.

55
Q

Arterial Dissection

A

Characterized by entry of blood into the arterial wall due to an intimal defect, which separates the underlying areas.

56
Q

List of causes of Aneurysm depending on the etiology.

A
  • Atherosclerotic aneurysm
  • Syphilitic aneurysm
  • Dissecting hematoma
  • Mycotic aneurysm
  • Berry aneurysm
57
Q

Aneurysm develops due to weakening of the vessel wall either due to:

A
  1. Inadequate abnormal synthesis of connective tissue of the vessel wall.
    OR
  2. Increased degradation of connective tissue.
58
Q

Inadequate or abnormal synthesis of connective tissue
of the vascular wall:

A
  1. TGF-B regulates:
    - Smooth muscle cell proliferation and
    - Synthesis of connective tissue matrix.
  2. Mutations in TGF-B receptors or downstream signaling pathways > defective synthesis of elastin and collagen > aneurysm.
59
Q

Marfan Syndrome

A
  • Defective synthesis of fibrillin > weakening of aortic wall > Aneurysm.
60
Q

Ehlers-Danlos Syndrome

A
  • Defective type III collagen synthesis. > Aneurysm
61
Q

Vitamin C deficiency.

A

Altered collagen cross-linking.

62
Q

Increased degradation of connective tissue.

A

-Increased production of Matrix Metalloproteinases (MMP) enzymes can degrade the ECM in the arterial wall.

63
Q

Cystic Medial Degeneration

A

(CMN) is a disorder of large arteries, in particular the aorta, characterized by an accumulation of basophilic ground substance in the media with cyst-like lesions.

CMN is known to occur in certain connective tissue diseases such as Marfan syndrome, Ehlers-Danlos syndrome, and annuloaortic ectasia, which usually result from degenerative changes in the aortic wall.

64
Q

Tertiary Syphilis

A

-Rare cause of aortic aneurysms.
-Trepenomas has affinity for vasa vasorum of mainly thoracic aorta > obliterative endarteritis > leads to ischemic damage to the aortic media and aneurysm
(syphilitic mesoaortitis)

65
Q

Fungus that invades blood vessel.

A
  • Aspergillus
  • Candida
  • Mucor
66
Q

Bacteria that invade blood vessel.

A
  • B. Fragilis
  • P. aeruginosa
  • Salmonella
67
Q

Abdominal Aortic Aneurysm

A

Common in:
-Men
-Smokers
*Rare before 50yr

68
Q

Causes of AAA

A
  1. Atherosclerosis
  2. Inflammation; characterized by dense periaortic fibrosis accompanied by inflammatory cells (lymphocytes, plasma cells and macrophages).
  3. Mycotic; Salmonella gastrenteritis.
69
Q

Morphology of Atherosclerotic Aneurysm

A
  • Aneurysm is usually observed below the origin of
    renal arteries and above the bifurcation of the aorta.
    -Saccular or fusiform.
    -15 to 25 cm.
    -It frequently shows a bland, laminated, poorly organized mural thrombus.
  • Complicated atherosclerosis with destruction and
    thinning of the underlying aortic media.
70
Q

Clinical features and complications of AAA

A
  1. Rupture: Aneurysm may rupture into the peritoneal
    cavity or retroperitoneal tissues > leading to massive, fatal hemorrhage.
  2. Obstruction of a branch causing iliac or and renal ischemia.
  3. Embolism.
  4. Compression of a ureter.
  5. Abdominal mass; may stimulate a tumor.
71
Q

Thoracic Aortic Aneurysms; causes.

A
  • Hypertension
  • Marfan syndrome
  • TGF-B signaling disorders
  • Syphilis (rare now)
72
Q

Clinical presentation in thoracic aortic aneurysm.

A
  1. Lungs and airways; respiratory difficulties.
  2. Esophagus; difficulty in swallowing.
  3. Irritation or pressure on the recurrent laryngeal nerves; persistent cough.
  4. Erosion of bones like ribs and vertebral bodies; pain.
73
Q

Syphilitic Aneurysm

A
  • Mesoaortitis > aortic aneurysm and aortic regurgitation.
  • Mainly affect the ascending aorta.
  • Shows endarteritis and periarteritis of vasa vasorum.
  • Medial scars > produce roughened intimal surface > tree bark appearance.
  • Fusiform aneurysm.
74
Q

Vasa vasorum

A

Small blood vessels that comprise a vascular network supplying the walls of large blood vessels, such as elastic arteries (e.g., the aorta) and large veins (e.g., the venae cavae).

75
Q

When is an aortic dissection fatal?

A

If the dissection ruptures through the adventitia > results in hemorrhages into adjacent spaces.

76
Q

Aortic dissection; etiology.

A
  • Men; 40 to 60 years; who have hypertension.
  • Younger patients; Marfan syndrome.
  • May develop as a complication of arterial cannulations.
  • During or after pregnancy.
77
Q

Aortic Dissection; Site of intimal tear.

A
  • Ascending aorta
  • Within 10cm of aortic valve.
78
Q

Aortic Dissection; Character of tear.

A
  • Transverse or oblique
  • 1-5cm in length
  • Sharp with jagged edges.
79
Q

Aortic Dissection; Site of dissection.

A

-Between the middle and outer thirds of the tunica media.

80
Q

Aortic Dissection; Extent of involvement.

A
  • Proximally along the aorta toward the heart.
  • Distally into the iliac and femoral arteries.
81
Q

Aortic Dissection; Classification. (two)

A

Type A dissections:

  • Proximal lesions involving either both ascending and descending aorta OR only the ascending aorta.
  • Types I and II of DeBakey classification.
  • More common but dangerous.

Type B dissections:

  • Have distal lesions which do not involve the ascending part and usually begin distal to the subclavian artery.
  • DeBakey type III.
82
Q

Double-barreled Aorta
[Complications due to rupture]

A

It may develop in few cases, when the dissecting hematoma reenters the lumen of the aorta through a second distal intimal tear. This creates a new false vascular channel and prevents the fatal extra-aortic hemorrhage.

83
Q

Cardiac tamponade

A

Hemorrhage into the pericardial sac.

84
Q

Aortic Dissection; Microscopy.

A

Cystic medial degeneration without any inflammation.

85
Q

WHO definition of hypertension.

A

Hypertension is defined as systolic pressure above 160 mm Hg and/or diastolic pressure above 90.

86
Q

Blood pressure=

A

Depends on cardiac output and vascular resistance.

Vascular resistance in the arterioles: Depends on neural and hormonal mechanisms.

87
Q

Cardiac output.

A
  • Depends on stroke volume and heart rate.
  • Stroke volume in turn is influenced by the sodium homeostasis.
  • Heart rate and contractility of myocardium (affects stroke volume) are regulated by the alpha- and beta-adrenergic systems.
88
Q

Peripheral vascular resistance.

A

-It is determined by
functional and anatomic changes in small arteries
and arterioles.
-Vascular tone depends on the balance between vasoconstrictors and vasodilators.
-Blood pressure is also influenced by tissue pH and hypoxia.

89
Q

Probable factors of essential hypertension:

A
  1. Reduced renal excretion of sodium.
  2. Increased vascular resistance.
  3. Genetic factors.
  4. Environmental factors.
90
Q

Essential Hypertension.

A

Accounts for 95% of cases and is a multifactorial disorder.

91
Q

Angiotensin II.

A
  1. Increases vascular smooth muscle tone.
  2. Increases aldosterone secretion by adrenal > increases sodium absorption by kidney.
92
Q

Hemangioma

A

Hemangiomas are very common benign tumors of blood vessels and form about 7% of all benign tumors of infancy and childhood.

Types: Capillary and Cavernous.

93
Q

Capillary Hemangioma

A
  • Most common.
  • Skin, subcutaneous tissues and mucous membranes of oral cavities and lips.
  • Liver, spleen, kidney.
94
Q

Strawberry hemangioma

A

Type of capillary hemangioma.

95
Q

Hemangioma

A

Unencapsulated benign tumor.

96
Q

Cavernous hemangioma

A

Dash red blue, soft spongy masses and then measure 1 to 2 cm in diameter. More frequently involve deep structures. There are found in the skin so surfaces and visceral organs such as the spleen liver and pancreas.

97
Q

Classification of vascular tumors.

A

First, benign neoplasm’s, developmental and acquired conditions, for example: in hemangioma; Capillary hemangioma, cavernous hemangioma, pyogenic granuloma. Second, intermediate grade neoplasms, for example Kaposi’s sarcoma and hemangiendothelioma. Third, malignant neoplasms for example, angiosarcoma and HEMANGIOPERICYTOMA.

98
Q

Mechanism of renal vascular hypertension.

A

Renal artery stenosis which leads to decrease glomerular flow and pressure in the afferent arterial of the glomerulus which intern stimulates renin secretion & production of angiotensin II. Which leads to vasoconstriction and increased per peripheral resistance.

99
Q

Primary hyper aldosteronism.

A

It is one of the most common causes of secondary hypertension.

100
Q

Highline arteriolosclerosis

A

It shows thickening of the world G2 homogenous, pink highline material and narrowing of the lumen. Mechanism of action: chronic hemodynamic stress produced by hypertension > produces leakage of protein into the vessel wall > increased synthesis of ECM by smooth muscle cell > hyalinization of the wall of the arteriole.

101
Q

Benign nephrosclerosis

A

The kidney changes in benign hypertension.

102
Q

Causes of highline arteriosclerosis.

A

Benign hypertension Diabetic micro angiography Old age

103
Q

Blood vessels in malignant hypertension

A

Hyperplastic arteriosclerosis [onionskin appearance] necrosis that is necrotizing arteriolitis.

104
Q

Vasculitis

A

Vasculitis is a heterogeneous group of disorders characterized by inflammation and damage of the blood vessel.

105
Q

General Characteristics of vasculitis.

A
  1. Primary or secondary.
  2. Vessel involved; mostly arterioles to capillaries to venules.
  3. Organ involved; or even organ systems.
106
Q

Classification of Vasculitis.

A

May be classified in many ways such as:

(1) According to size of the vessel involved.
(2) Role of immune complexes, and presence of specific autoantibodies.
(3) Granuloma formation.
(4) Organ specificity.

107
Q

Mechanism of Non-infectious Vasculitis.

A
  1. Immune complex mediated.
  2. Antineutrophil cytoplasmic antibody-mediated.
  3. Antiendothelial cell antibody-mediated.
108
Q

Immune complex-mediated vascular injury is due to _________.

A

Type III hypersensitivity reaction.

109
Q

Causes of Immune-mediated vasculitis.

A
  • Systemic immunologic diseases; sytemic lupus erythamatous (SLE) and polyarteritis nodos.
  • Drug hypersenstivity; Drugs themselves may be foreign proteins (e.g. streptokinase) or they bind to serum proteins (e.g. penicillin) and behave like antigens.
  • Secondary to viral infections:
    • HBV Associated Polyarteritis Nodosa.
    • Cryoglobulinemic vasculitis is strongly associated with hepatitis C virus (HCV) infection.
110
Q

Hypersensitivity vasculitis most commonly involves.

A

Post-capillary venules.

111
Q

Antineutrophil cytoplasmic antibodies (ANCAs)

A

Are heterogeneous group of autoantibodies directed against certain proteins (mainly enzymes) in the cytoplasmic granules of neutrophils and monocytes.

112
Q

Two important ANCAs are:

A
  1. Anti-myeloperoxidase (MPO-ANCA): MPO is a lysosomal enzyme normally involved in producing oxygen free radicals. MPO-ANCAs can be induced by drugs (e.g. propylthiouracil). They are associated with microscopic polyangiitis and Churg-Strauss syndrome.
  2. Anti-proteinase-3 (PR3-ANCA): PR3 is a constituent of neutrophil azurophilic granule. It shares homology with many microbial peptides and antibodies against microbial peptides may form PR3-ANCAs. They are associated with Wegener’s granulomatosis.
113
Q
A

They can produce endothelial cell injury and lysis through either complement-mediated cytotoxicity or antibody dependent cellular cytotoxicity.

For examples,

  • Kawasaki disease and
  • Systemic lupus erythematosus (SLE).
114
Q

Temporal Arteritis.

A

Also known as giant cell arteritis.

A chronic, typically granulomatous inflammation of medium and large sized arteries.

115
Q

Pathogenesis of temporal arteritis.

A
  • T-cell mediated immune response against an unkown antigen.
  • Proinflammatory cytokines (TNF) and antiendothelial antibodies.
116
Q

Microscopy of temporal arteritis.

A
  • Granulomatous inflammation within the inner tunica media.
  • Fragmntation of elastic lamina.
  • Chronic inflammation consisting of T-cells and macrophages.
  • Segmental distribution of inflammation with segments of relatively normal artery between lesions.
  • Intimal fibrosis in healed stage.
117
Q

Polyarteritis Nodosa.

A

Polyarteritis nodosa (PAN) is a systemic, necrotizing vasculitis of small and medium-sized muscular arteries characteristically involving the renal and visceral arteries.

It spares the smallest blood vessels (arterioles, venules, and capillaries).

PAN does not involve pulmonary arteries.

118
Q

Polyarteritis Nodosa; Etiology.

A
  • Cause not known in the majority of cases.
  • About 30% of patients with PAN have chronic hepatitis B with HBsAg-HbsAb complexes in affected vessels.
  • This indicates an immune complex–mediated etiology in this subset.
119
Q

Polyarteritis Nodosa; Clinical features.

A
  • Usually occurs in young adults.
  • Nonspecific symptoms are malaise, fever, and weight loss.
  • Specific complaints are due to ischemia and infarction of affected tissues and organs.
    • Renal involvement manifests as hypertension (usually developing rapidly), renal insufficiency, or hemorrhage due to microaneurysms.
    • Gastrointestinal tract involvement present with abdominal pain and melena (bloody stool).

Prognosis: It is fatal, if not treated. Immunosuppression produces remissions or cure in about 90% of patients.

120
Q

Wegener’s Granulomatosis

A

Classic Wegener’s granulomatosis is a necrotizing vasculitis, which involves the upper respiratory tract, the lungs, and the kidneys.

ANCA is associated with Wegener’s granulomatosis.

Strawberry gums: Wegener’s granulomatosis.

Systemic Pathology 1 (GIT, CVS, RS) (24 decks)

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