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1 STEP Uworld cardio > Vessel diseases 12/05 > Flashcards

Vessel diseases 12/05 Flashcards

1
Q

Diastolic BP is the ……….. …………… pressure in the arterial system.

A

baseline hydrostatic

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2
Q

Diastolic BP is directly related to ……. (2)

A

Systemic vascular resistance and arterial blood pressure

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3
Q

What is pulse pressure?

A

The amount that arterial pressure increases above diastolic pressure during LV contraction

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4
Q

Pulse pressure is directly related to ………. and inversely related to ………..

A

Stroke volume;

Aortic compliance

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5
Q

Systolic BP is the summation of …………. and ………..

A

Diastolic BP and pulse pressure

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6
Q

What is the primary driver of characteristic blood pressure changes that occur in those age >65?

A

Age related stiffening of the aorta

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7
Q

Reduced aortic compliance + unchanged SV –> what is pulse pressure?

A

Increased PP

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8
Q

Why there is a slight decrease in diastolic BP when occurs age-related stiffening of the aorta?

A

Reduced compliance –> less blood volume to be retained in the arterial system (ie, blood is effectively displaced to the more compliant venous compartment) –> slightly decreased diastolic pressure

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9
Q

Why increased PP + decreased DBP results in increased systolic BP?

A

Increased PP - due do reduced aorta compliance.
Decr. DBP - due to blood displacement from stiff arterial system to the compliant venous system.
Increase in PP is greater than decrease in DBP –> increased SBP –> isolated systolic HTN in elderly

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10
Q

What change of the heart is seen due to elderly HTN?

A

Aortic stiffening –> systolic hypertension –> increased afterload –> mild concentric LV hypertrophy

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11
Q

What histologic level change is seen in aortic stiffening?

A

Elastin is replaced with collagen

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12
Q

Why there is slightly decrease in resting HR and decrease of maximal HR in elderly?

A

Due to conduction cell degeneration

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13
Q

How changes maximal CO in elderly? why

A

decreases due to concentric LVH

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14
Q

What are 3 changes in CVS in elderly due to reduced baroreceptor sensitivity and adrenergic responsiveness?

A

Increased orthostasis;
Decr. HR and contractility repsonse
Increased circulating catecholamines

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15
Q

Where are located valves in in veins (3) that prevent blood flow back?

A

In superficial, perforating and deep veins

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16
Q

Pathophysiology of varicose vceins

A

Chronically elevated intraluminal pressure –> dilation of veins (varicose veins) and incompetence of the valves.

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17
Q

Where backflows blood in varicose veins and why?

A

Retrograde flow to superficial veins –> results in further increase in venous pressure, because varicose veins start to form due to chronic increase in intraluminal pressure.

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18
Q

retrograde flow of the blood in varicose veins results in …………….. and it causes …………

A

results in tissue ischemia;

it leads to venous stasis dermatitis

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19
Q

What inflammation due to varicose veins is related to poor wound healing?

A

tissue ischemia –> venous stasis dermatitis, which is assoc. with poor wound healing

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20
Q

What causes brawny discoloration in varicose veins?

A

extravasation of RBCs into the tissues –> iron depositions

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21
Q

What are two groups of risk factors for varicose veins?

A

Obstruction of venous return;

Conditions, that damages venous valves

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22
Q

What states cause obstruction of venous return leading to varicose veins?

A

Obesity, pregnancy

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23
Q

What state damages the venous valves leading to varicose veins?

A

Deep vein thrombosis

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24
Q

What is the manifestation of the peripheral artery disease in legs?

A

leg pain during exercise (claudication) and if severe = ischemic pain at rest and possible distal gangrene

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25
Q

Capillary permeability and varicose veins. relationship?

A

Capillary permeability does not play a role in the development of varicose veins.
Increased permeability is in allergic reactions, inflammation and shock. It causes edema due to extravasation of the serum components into the interstitium

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26
Q

What are initial and late changes in lymphedema?

A

Initially - soft and pitting

Eventually - firm and nonpitting (due to progressive fibrosis and thickening of the overlying skin)

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27
Q

What is nutcracker syndrome?

A

left renal vein entrapment syndrome

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28
Q

Right renal vein runs anterior to the ………….

A

anterior to the right renal artery

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29
Q

Where drains right renal vein?

A

Directly to the vena cava inferior

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30
Q

What vein apart right renal veins drains to IVC as well?

A

Right gonadal vein

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31
Q

Left renal veins runs posterior to the …………

A

Splenic vein

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32
Q

Before left renal vein drains to IVC, it goes between …………….. and ……..

A

Aorta and superior mesenteric artery

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33
Q

Where drains left gonadal vein?

A

Left renal vein

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34
Q

Why there is higher pressure in left renal vein than in right?

A

Due to nutcracker effect

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35
Q

What apart from nutcracker effect also can increase the pressure within left renal vein?

A

Due to compression fron left-sided abdominal or retroperitoneal mass

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36
Q

What is a manifestation of nutcracker effect? (2) Why?

A

Flank/abdominal pain + microscopic hematuria. Due to persistently elevated pressure in the left renal vein

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37
Q

Pathophysiology of varicocele?

A

Increased pressure in the left gonadal vein –> valve leaflet failure –> varices in testes

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38
Q

What plexus is affected in varicocele?

A

Testicular pampiniform plexus

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39
Q

Right brachiocephalic vein is formed by ………………. and ……….

A

Right subclavian and right internal jugular vein

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40
Q

Where drains right external jugular vein?

A

Right subclavian vein

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41
Q

What drains right brachiocephalic vein apart from internal and external jugular vein and subclavian vein?

A

Right lymphatic duct

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42
Q

What drains right lymphatic duct?

A

lymph from right upper extremity, right face and neck, right hemithorax, right upper quadrant of the abdomen

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43
Q

Compression of what 2 structures can cause swelling of the upper limb without face swelling?

A

Axillary or subclavian vein. If brachiocephalic - swelling in face

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44
Q

How sympmatically differentiate superior vena cava syndrome and eg right-sided brachiocephalic vein obstruction?

A

In SVC syndrome - both sides of face, neck, chest and both arms are involved.
In eg right-sided brachiocephalic obstruction - only one side symptoms

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45
Q

How is called brachiocephalic vein in other name?

A

Innominate

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46
Q

What drains external and internal jugular veins?

A

External - scalp and portions of the lateral face;

Internal - brain and superficial face and neck

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47
Q

What forms vena cava superior?

A

Bilateral brachiocephalic veins

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48
Q

What is the most common reason of blunt aortic injury?

A

Motor vehicle collision

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49
Q

What is the main mechanism that causes aortic injury in a vehicle collision?

A

Sudden deceleration –> extreme stretching and torsional forces affecting the heart and aorta

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50
Q

Aortic isthmus is tethered by the …………….

A

ligamentum arteriosum –> relatively fixed and immobile compared to the adjacent descending aorta

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51
Q

What x-ray change may be seen in case of aortic isthmus rupture?

A

Widened mediastinum

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52
Q

Majority of patients sustained aortic rupture die immediately. Those, who survive, experience nonspecific findings (3). What are they?

A

Chest pain, back pain or shortness of breath

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53
Q

What are complications of ascending aorta rupture?

A

hemopericardium, coronary artery dissection, aortic valve disruption

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54
Q

Ligamentum arteriosum is between ………… and ………..

A

Aortic isthmus and pulmonary trunk (at the site where merges pulmonary arteries)

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55
Q

Stanford A - location of dissection?

A

Any part of ascending aorta

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56
Q

Stanford B - location of dissection?

A

Any dissection of descending aorta

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57
Q

Where originates stanford A?

A

In sinotubular junction

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58
Q

Where originates stanford B?

A

close to the origin of the left suubclavian artery

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59
Q

Why sinotubular junction and left subclavian artery are predominantly affected sites for dissection?

A

Due to increases in the rate of rise of pressure and in shearing forces at these sites in HTN

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60
Q

What direction of propagation in stanford A and B can affect the aortic arch?

A

Distal propagation of a type A and proximal propagation of a type B

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61
Q

What type of dissection can propagate into the thoracoabdominal aorta?

A

Both, type A and B

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62
Q

If aortic dissection propagates to the thoracoabdominal aorta, what branches can be affected?

A

Celiac trunk, intercostal arteries, renal arteries

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63
Q

Dilation in > ….. cm is considered of abdominal aortic aneurysm

A

3 cm

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64
Q

What type of inflammation causes AAA?

A

Transmural

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65
Q

Pathogenesis of AAA

A

Transmural inflammation of aortic wall –> subsequent apoptosis of smooth muscle cells + degradation of matrix proteins

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66
Q

Combination of 2 mechanisms that results in formation of AAA?

A

Thinning of the aortic wall + chronic hemodynamic stress –> secondary expansion of the lumen

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67
Q

3 risk factors for AAA

A

Age >65, smoking, male sex

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68
Q

AAA generally asymtomatic, but when ruptures, it presents as …………. and ………..

A

acute abdominal pain and hypotension

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69
Q

When to do surgical or endovascular repair of AAA?

A

Aneurysm larger than 5.5cm

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70
Q

Why smoking increases risk of AAA? (2)

A

Increased inflammatory infiltrates + formation of reactive oxygen species in the aortic wall.

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71
Q

Why there is decreased risk of AAA in DM patients?

A

Possibly due to the effect of glycosylation of matrix proteins in the aortic wall.

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72
Q

Narrowing of the arterioles of the ………….. in chronic hypertension can lead to medial ischemia of the aorta and contribute to aneurysm formation

A

vasa vasorum

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73
Q

Subclavian steal syndrome - typically occurs due to hemodynamically significant stenosis of the ………………………………………

A

subclavian artery proximal to the origin of the vertebral artery

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74
Q

What are the reasons of subclavian steal syndrome?

A

Main - atherosclerosis;

Less common - Takayasu arteritis, complications from heart surgery

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75
Q

How blood flow in subclavian steal syndrome

A

Blood from the contralateral vertebral artery flows to the ipsilateral (to stenosis) subclavian artery. It happens due to lowered pressure in subclavian artery due to stenosis

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76
Q

Subclavian steal - mostly asymptomatic, but when symptomatic, what manifestation?

A 
Arm ischemia in affected extremity (pain, paresthesias, exercise induced fatigue)
Vertebrobasilar insufficiency (vertigo, dizziness, drop attacks)
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77
Q

What is physical examination feature and what is used to diagnose subclavian steal?

A

Physical examination - significant difference (>15mmHg) in brachial systolic pressure between arms.
Diagnostics: Doppler ultrasound of cerebrovascular and upper extremity arterial circulation

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78
Q

If there is occlusion in brachiocephalic artery instead of left subclavian artery - what would be direction of blood flow?

A

Retrograde flow would be in right vertebral toward right subclavian (from left to right)

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79
Q

Internal carotid artery occlusion. Symptoms and blood flow in vertebral artery?

A

Occlusion due to thrombosis/embolism –> TIA or ischemic stroke.
Symptoms: neurologic deficit, including cortical signs. No reversal blood flow in the vertebral artery.

80
Q

In coronary-subclavian steal syndrome blood flows from ……….. to ……….. via ……….

A

from coronary artery to subclavian via internal mammary artery (IMA), which has been used in coronary artery bypass surgery

81
Q

What artery is used in coronary bypass and participates in coronary-subclavian steal syndrome?

A

Internal mammary artery (IMA)

82
Q

Symptoms of coronary-subclavian steal syndrome?

A

Coronary ischemia (angina pectoris)

83
Q

Blood flow in right vertebral artery occlusion and symptoms in the arm?

A

Retrograde flow would be on the right side (from left to right).
There would not be involvement of subclavian artery, therefore no arm syptoms

84
Q

How many leads has biventricular pacemaker?

A

2 or 3

85
Q

Where are placed leads in 3-leads biventricular pacemaker?

A

First 2 are placed in right atrium and right ventricle.

86
Q

What vessels are used for biventricular pacemaker insertion?

A

Left subclavian vein –> Vena cava superior

87
Q

How to reach left ventricle with biventricular pacemaker 3rd lead?

A

Right atrium –> coronary sinus, which is in arterioventricular groove on the posterior aspect of the heart –> inserted into one the lateral venous tributaries

88
Q

What is the course or the arteries that provide blood flow to the eye?

A

Internal carotid –> ophthalmic –> central retinal artery

89
Q

Origin of the thromboembolic occlusion of retinal artery?

A

Atherosclerosis in internal carotid artery

90
Q

What is location of central retinal artery?

A

Within optic/retinal nerve

91
Q

What structures get blood from central retinal artery?

A

Inner retina and the surface of the optic nerve

92
Q

Manifestation of RAO?

A

Acute, painless, monocular vision

93
Q

An ophthalmic artery has anastomoses with …………… including …….. and ………

A

External carotid artery;

Including facial artery and temporal artery

94
Q

Antibody in granulomatosis with polyangiitis?

A

c-ANCA - antineutrophilic cytoplasmic antibodies

95
Q

4 groups of manifestation in granulomatosis with polyangiitis?

A

Constitutional symptoms;
Upper airways;
Lower airways;
Kidney

96
Q

Why there is anemia in granulomatosis with polyangiitis?

A

It’s anemia of chronic disease due to elevated levels of inflammatory cytokines

97
Q

What shows chest imaging in granulomatosis with polyangiitis?

A

Patchy lung infiltrates, nodules and/or cavitation

98
Q

What is needed for diagnosis of granulomatosis with polyangiitis? what is seen?

A

Biopsy: necrotizing arteritis with granulomatous inflammation and mixture of surrounding inflammatory cells

99
Q

Granulomatous inflammation in granulomatosis with polyangiitis is consisted of what cells?

A

Epithelioid histiocytes, multinucleated giant cells

100
Q

TAA usually results from ……… in the medial layer of the aorta

A

age-related degenerative changes

101
Q

What accelerate formation of TAA?

A

Risk factors like dyslipidemia, hypertension, tabacco, family history

102
Q

What connective tissue diseases increase risk for TAA?

A

Marfan or Ehlers-Danlos syndrome

103
Q

Why may manifest dysphagia in TAA?

A

Expansion of TAA –> compression of surrounding tissues. In this case: esophagus

104
Q

Why may manifest hoarseness in TAA?

A

Expansion of TAA –> compression of surrounding tissues. In this case: left recurrent laryngeal nerve or left vagus nerve

105
Q

Why may manifest hemidiaphragmatic paralysis in TAA?

A

Expansion of TAA –> compression of surrounding tissues. In this case: phrenic nerve

106
Q

Why may occur respiratory manifestation in TAA?

A

Due to tracheobronchial obstruction

107
Q

What are 2 patho in heart due to TAA?

A

HF due to aortic valve regurgitation and superior vena cava syndrome from venous compression and occlusion

108
Q

X ray (3) of TAA?

A

Widened mediastinum + enlarged aortic knob + tracheal deviation

109
Q

The most common cause of renal artery stenosis?

A

Atherosclerosis

110
Q

Why there is systemic hypertension in renal artery stenosis?

A

Stenosis –> unilateral renal ischemia –> activation of RAAS –> increased renin

111
Q

Why eventually atrophies kidney in renal artery stenosis?

A

Due to oxygen and nutrient deprivation

112
Q

Anterior rupture of AAA is to …………… and accompanied by ………. (3)

A

Into peritoneal cavity;

accompanied bu syncope, hypotension and shock

113
Q

Posterior rupture of AAA is into …………… may be ……….., therefore results in delayed ………..

A

retroperitoneum;
temporarily contained;
delayed onset of hemodinamic instability

114
Q

Manifestation of AAA rupture?

A

Sudden severe abdominal pain + shock

Umbilical/flank hematoma

115
Q

What is location of lesion in Marfan syndrome?

A

Ascending aorta

116
Q

What is the evidence of acute aortic regurgitation in Marfan syndrome?

A

Descresendo diastolic murmur

117
Q

What is the evidence of HF in Marfan syndrome?

A

pulmonary edema

118
Q

The sequence of events in Marfan syndrome that cause heart pathology?

A

The lesion in ascending aorta (cystic medial degeneration) –> ascending aortic dissection –> its propagation proximally –> aortic valve regurgitation + rt failure

119
Q

Marfan syndrome results from a mutation that disrupts the synthesis, secretion, and incorporation into the extracellular matrix of ……………………

A

fibrillin

120
Q

Fibrillin is a protein that provides ………….

A

the glycoproteins scaffolding for elastin structure

121
Q

Histology of Marfan syndrome?

A

Elastic tissue fragmentation (,,basket wave”) and loss of elastic lamellae;
cystic medial degeneration

122
Q

What is a cystic medial degeneration?

A

Replacement of collagen, elastin, and smooth muscle by a basophilic mucoid extracellular matrix with irregular fiber cross-linkages and cystic collections of mucopolysaccharide

123
Q

Cystic medial degeneration also occurs with …………………., but is accelerated in Marfan syndrome

A

normal aging

124
Q

Coarctation of the aorta is a risk factor for …………

A

cerebral and aortic aneurism

125
Q

Where is the narrowing in aortic coarctation?

A

aortic arch near the ligamentum arteriosum

126
Q

Manifestation in aortic coarctation?

A

Upper extremity hypertension: Inc. BP, strong brachial and radial pulses, well developed
Lower extremity hypotension: decr, BP, weak/absent femoral pulses;
underdeeloped;
Claudication (ischemic pain)
In upper - headache, epistaxis, chest pain

127
Q

Cerebral aneurysm in aortic coarctation can result in ……………

A

Subarachnoid hemorrhage

128
Q

What is a patho mechanism of cerebral aneurysm in aortic coarctation?

A

chronic hypertension

129
Q

Ingestion of …………. mimics the myxomatous degeneration seen in patiens with Marfan syndrome

A

Beta-aminopropionitrile

130
Q

Where is found Beta-aminopropionitrile?

A

It’s a chemical found in certain kinds of sweet peas

131
Q

Beta-aminopropionitrile causes inhibition of…………, an enzyme responsible for ……………….

A

lysyl oxidase, which is responsible for cross-linking elastin fibers and collagen fibers.

132
Q

2 mechanisms in varicose veins?

A

increased intraluminal pressure or loss of wall tensile strength –> venous dilation

133
Q

age for varicose veins?

A

> 50

134
Q

massive iliofemoral thrombosis can cause acute rise in tissue pressure that impairs arterial inflow, leading to …………..

A

Phlegmasia alba dolens (painful white ,,milk leg”)

135
Q

The most important factor for aortic dissection?

A

Hypertension

136
Q

Intimal flap seen in CT in aortic dissection is ………

A

tunica intima of the aorta

137
Q

How DM relatively increased the risk for aorta dissection?

A

it is a risk factor HTN and atherosclerosos, where HTN is the most important factor for aorta dissection development.

138
Q

What pathology causes atherosclerosis? aorta dissection or aneurysm?

A

Aneurysm

139
Q

what BP alteration is seen in ascending aortic dissection?

A

BP asymmetry

140
Q

Why hypertension causes aortic dissection?

A

In many patients with longstanding hypertension, there is medial hypertrophy of the aortic vasa vasorum and, consequently, reduced blood flow to the aortic media. This can cause medial degeneration with a loss of smooth muscle cells, leading to aortic enlargement and increased wall stiffness. Both of these changes exacerbate aortic wall stress, which is already increased due to the hypertension itself. This synergistic increase in aortic wall stress greatly increases the risk of intimal tearing and subsequent development of aortic dissection

141
Q

Size of tear needed for aorta dissection?

A

1-5cm transverse or oblique direction tear

142
Q

Stasis dermatitis in varicose veins manifestation?

A

Erythema, induration, fibrosis, and deposition of hemosiderin (from breakdown of extravasated RBCs) manifesting as reddish-brown discoloration

143
Q

Focal fibrosis and increased melanin synthesis occurs in …………………

A

chronic radiation dermatitis

144
Q

Deposition of calcium phosphate salts leads ………………..

A

Calcific uremic arteriolopathy (calciphylaxis).

145
Q

Calcific uremic arteriolopathy is called in other way

as ………..

A

calciphylaxis

146
Q

calciphylaxis occurs in patients with ………………….

A

end-stage renal disease receiving hemodialysis

147
Q

Calciphylaxis manifestation?

A

Extremely painful nodules, plaques, and ulcer

148
Q

How inflammatory cells predisposes formation of AAA? What inflammatory cells play key role?

A

Inflammatory cells (particularly macrophages) release matrix metalloproteinases and elastases that degrade extracellular matrix components (eg, elastin, collagen), leading to weakening and progressive expansion of the aortic wall.

149
Q

Malignant endothelial proliferation is characteristic of ……………….

A

angiosarcoma

150
Q

What is pathophysiology of angiosarcoma?

A

Malignant endothelial proliferation

151
Q

Syphilic –> vasa vasorum endarteris –> what complication?

A

thoracic aortic aneurysm

152
Q

Why microbial infection cause (localized) dilation of the arterial wall?

A

due to destruction of arterial wall

153
Q

How present bacterial aneurysms?

A

painful, pulsatile masses and systemic signs such as fever and malaise.

154
Q

What induces development of bacterial aneurisms?

A

Trauma, bacteremic seeding, or septic emboli (mycotic aneurysm)

155
Q

Cystic medial degeneration –> aortic

A

dissection

156
Q

Why aging also may lead to cystic medial degeneration?

A

With aging, collagen, elastin, and smooth muscle in the aortic media are broken down and replaced by a mucoid extracellular matrix.

157
Q

Histopathology of marfan syndrome involves …….. pattern

A

,,basket view”

158
Q

What material collections are in marfan syndrome in ,,basket view” pattern?

A

collection of mucopolysacharides

159
Q

Histology of calciphylaxis?

A

Superficial arteriolar calcification, subintimal fibrosis, and thrombosis.

160
Q

Intimal flat in aortic dissection is …………….

A

Tunica intima of the aorta

161
Q

Atherosclerosis can induce aortic aneurysm or aortic dissection?

A

aneurysm

162
Q

………………. is thought to be the primary event in the process leading to aortic dissection

A

A tear in the tunica intima

163
Q

In thromboangiitis obliterans, chronic exposure to tobacco products is thought to cause direct …………….. injury or trigger a ……………… hypersensitivity reaction against the endothelium

A

Direct endothelial injury; delayed-type hypersensitivity

164
Q

Histopathology of thromboangiitis obliterans

A

Inflammatory intraluminal thrombi with sparing of the vessel wall

165
Q

Thromboangiitis obliterans is uniformly spreaded or segmental

A

segmental

166
Q

Inflammatory intraluminal thrombi consists of?

A

contains neutrophils, multinueclated giant cells

167
Q

Thromboangiitis obliterans is ……….. ………….. vasculitis

A

segmental thrombosing

168
Q

Thromboangiitis obliterans spread to …………

A

extends contiguously into veins and nerves (!!rarely seen in other types vasculitis)

169
Q

Clinical manifestation of thromboangiitis obliterans?

A

Digital ischemic ulcerations, limb claudication, reynaud phenomenom, superficial thrombophlebitis

170
Q

2 main groups of clinical manifestaion in takayasu arteritis?

A

Constitutional and arterio-occlusive

171
Q

takayasu affects ……….. (sex) and ………… (race), ………… age

A

women; asians; <40y/o

172
Q

Takayasu predominanlty affects ………………. arteries

A

Large-artery vasculitis, ty aorta and its branches

173
Q

Histapathology of takayasu?

A

Mononuclear infiltrates and granulomatous inflammation of the vascular media –> arterial wall thinckening and occlusion

174
Q

Arterio-occlusive manifestaion in takayasu?

A

claudication, BP discrepancies, bruits, pulse deficit

175
Q

claudication description?

A

exertional pain due to limited blood flow reserve

176
Q

Pathogenesis of Raynaud phenomem?

A

Exaggregated vascular smooth muscle contraction eg in response to cold or vibration

177
Q

Manifestaion of Raynaud

A

Acute, episodic. Occurs triphasic color change (pallor, cyanosis, erythema)

178
Q

What kind of inflammation in in Giant cell arteritis and Takayasu? What size arteries? How differentiate them?

A

Large arteries; granulomatous inflammation.
Takayasu <40 y/o
Giant >50 y/o

179
Q

Size of arteries in kavasaki?

A

medium size

180
Q

how is described thickening of vessels in takayasu?

A

transmural fibrous thickening, narrowing of lumen

181
Q

Kawasaki age and race

A

children <5 y/o, asian

182
Q

Diagnosis of kavasaki based on ……………. + ……….

A

fever >= 5 days + 4 finding of 5 (conjuctival infection, cervical lymphadenopathy, mucositis, extremity changes (edema, erythema), rashes)

183
Q

description of conjuctival infection in kawasaki?

A

bilateral non-exudative infection

184
Q

what is mucositis in kawasaki? (3)

A

erythema of palatine musoca, fissured erythematous lips, strwaberry tongue

185
Q

What are extremity changes in kawasaki? (3)

A

Edema in hands/legs;
Erythema of palms/soles;
desquamation of fingertips (periungual)

186
Q

What are rashes in kawasaki?

A

Polymorphous (usually urticarial) erythematous rashes on extremities that spread to the trunk

187
Q

What is serious complication of kawasaki?

A

coronary artery inflammation –> coronary artery aneurysm –> rupture or thrombosis causes death

188
Q

What is diffecences of PAN and many other vasculitides?

A

in PAN - no granulomatous inflammation

189
Q

What size arteries are affected in PAN?

A

medium size-muscular arteries

190
Q

PAN histopathology?

A

Segmental fibrinoid necrosis of the vessel wall;
infiltration - mononuclear cells and neutrophils;
Internal and external elastic laminae damage –> microaneurysms
in general - nongranulomatous transmural inflammation

191
Q

PAN: two general groups of complications?

A

arterial lumen narrowing/thrombosis or bleeding from microaneurysm

192
Q

What systems are affected in PAN?

A

Skin, kidney, GI (mesenteric ischemia), nervous, musculoskeletal. Lungs - spared

193
Q

Angiodysplasia is thought to arise from …………………..

A

intermittent obstruction of submucosal veins at the muscularis propria of the GI tract.

194
Q

Biopsy of angiodysplasia.

A

Dilated small vessels lined by thin-walled endothelium; infiltration with inflammatory cells would not be seen. In addition, patients with angiodysplasia generally have GI bleeding

195
Q

What is patho of artery obstruction in PAN?

A

Fibrinoid necrosis of arterial wall –> luminal narrowing and thrombosis –> tissue ischemia

196
Q

What is patho of artery rupture in PAN?

A

internal/elastic lamina damage –> microaneurysm –> rupture and bleeding

197
Q

PAN correlates with ……….

A

underlying hepatitis B/C (immune complexes)

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