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5 semestre > Physiopathology Final > Flashcards

Physiopathology Final Flashcards

0
Q

When does blood allow for plug to occur

A

when healing needs to happen

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1
Q

Define hemostasis

A
  • Blood vessels maintain fluid consistency of blood
  • Maintenance of clot-free blood within the vascular system while allowing for the formation of a solid plug of blood under conditions of vessel wall injury (ex: thrombosis)
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2
Q

What is hemostasis a property of

A

BV and blood

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3
Q

Tunica intima is lined with what

A

Single layer of vascular endothelium that has to maintain its integrity–> non-damaged, non-inflammatory possess anti-platelet effects

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4
Q

Anti-platelet effects of intact endothelium (4)

A
  1. insulates platelets from subendothelial collagen
    (physical barrier between collagen and platelets)
  2. Prostacylcin (PGI2) synthesis- inhibits platelet agg
  3. ADPase synthesis- inhibits platelet agg
  4. Nitric oxide synthesis- vasodilation & inhibit platelet agg
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5
Q

ADPase synthesis in anti-platelet effects

A

Inhibits platelet agg; a lot of ADP? we are low energy situation–> can’t feed biological system. high ADP? high agg so produce ADPase to remove ADP–> inhibit agg

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6
Q

Nitric oxide synthesis in anti-platelet effects

A

Constitutively produced, sets normal vascular tone in body–> we always have some form of vasodil.
- Dilated so platelets go further away from eachother–> decreases agg

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7
Q

Anti-coagulant effects of intact endothelium

A

Heparin like molecule synthesis–> activates anti-thrombin III (degrades thrombin)

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8
Q

Effect of no thrombin on the coag system

A

Shuts off coag

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9
Q

What is the coag system

A

Release of fibrin to form lattice like system to plug up certain things
no coag system? No platelet agg

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10
Q

What turns on synthesis of antithrombin III

A

Herparin like factor

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11
Q

Fibrinolytic property of intact endothelium

A

tPA synthesis –> converts plasminogen to plasmin

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12
Q

What does plasmin do

A

Degrades fibrin (chews up clot)

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13
Q

Ischemic stroke

A

Patient produces fibrin clot in artery somewhere–> inject with tPA to clear clot

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14
Q

Hemorrhagic stroke?

A

Give tPA and you will kill them–> they can’t clot

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15
Q

Pro-thrombotic properties of damaged endothelium (4)

A
  1. Von Willebrand’s factor
  2. Tissue factor synthesis
  3. Platelet activating factor (PAF)
  4. t-PA inhibitor synthesis
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16
Q

von-Willebrand Factor

A
  • Pro-thrombotic property of damaged endo
  • Essential for platelet adhesion
  • Expressed on surface and give platelets region to bind to
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17
Q

Von-Willebrand disease

A

-Mild, moderate or severe
-Severity determined by degree of loss of expression of VW factor
- Usually females of repro age
Sx: heavy menstrual flow
Mod/Severe? unable to maintain preg; hemorrhaging won’t occur of baby into wall–> spontaneous abortion

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18
Q

Tissue factor synthesis as a pro-thrombotic property of damaged endo

A
  • Glycoprotein which activates coag system
  • One of triggers for coag system
  • Damage endo turns on tissue factor–> turns on coag system
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19
Q

Platelet activating factor as protrombotic property of damaged endo

A

damaged endo + PAF + platelets

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20
Q

t-PRA inhibitor ensures what

A

Clot will remain

*Plays important role in prothrombotic property of damaged endo

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21
Q

What are the “bricks” of a thrombus? Cement?

A

Bricks: platelets
Cement: fibrin

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22
Q

Platelet actions oppose the action of what

A

endothelium

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23
Q

Platelets secrete what (5)

A

Thromboxane (TXA2), ADP, Factors V and VIII, calcium

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24
Q

What do activated platelets bind to

A

Exposed collagen–> vWF

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25
Q

Activated platelet role in coagulation cascade

A

Initiates cascade (role of calcium and phospholipid complex)

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26
Q

“Temporary plug”

A

becomes definitive with formation of fibrin from thrombin = fused mass of platelets

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27
Q

Young clot appearance vs old clot appearance

A

Young: red, currant jelly
Old: can become permanent structures within BV

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28
Q

Coagulation System activated by who

A
  • Activated by factor XII (hageman) or tissue factor
  • End product is formation of fibrin monomers
  • Fibrin is “cement” of thrombus
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29
Q

Thrombus

A
  • An aggregate of platelets, fibrin and blood cells within the non-interrupted vascular system
  • Adherent to vascular endothelium (vs a post-mortem blood clot) *Must be attached to BV wall!
  • May arise in arterial or venous circulation
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30
Q

3 Predisposing factors to arterial thrombi

A

AKA Virchow’s Triad

  1. Damage to endothelium
  2. Alterations in normal blood flow
  3. Increased coagulability of blood
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31
Q

Damage to endothelium that will promote production of thrombus in region

A
  1. Ischemic damage to endocardium
  2. Valvular damage
  3. Free radical induced damage
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32
Q

Hemodynamic stress

A

Too much force on BV because of high BP

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33
Q

4 Alterations in normal blood flow: role of stasis and turbulence

A
  1. Physical damage to endothelium
  2. Disrupts laminar flow
  3. Prevent renal clearance of coag proteins
  4. Retards flow of anticoag’s to site of injury
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34
Q

Factors that increase coagulability of blood (5)

A
  • Genetic defect in anticoag proteins or coag proteins
  • Homocysteine: Increase either because of poor nutrition quality or a faulty gene
  • Neoplasia–> release of procoagulants
  • Polycythemia vera: too many RBC; high hematocrit
  • Smoking, obesity “soft risk factor”
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35
Q

What is a soft risk factor

A

diet high in fatty acids–> blood becomes more viscous. This increases total peripheral resistance –> dictated by arterioles and capillaries
- Obesity = longer vasculature= increased TPR = increased BP= increased hemodynamic stress

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36
Q

50% of population will die from what

A

Arterial thrombi

*Most common cause of death in US

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37
Q

Most common sites of arterial thrombi

A
  1. Coronary
  2. Cerebral
  3. Femoral
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38
Q

Arterial thrombi results in what? Death due to?

A

Ischemic infarction

Death due to MI, cerebral infarct, renal infarct

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39
Q

Thrombosis in the venous system

A
  • Phlebothrombosis
  • Red thrombus –> occurs in venous system; leads to congestion that changes overall color of body part
  • Most common in superficial leg veins (varicose veins)
  • Deep leg vein thrombosis
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40
Q

Deep leg vein thrombosis

A

Most common clinical manifestation
aka “red thrombi”
arteries supply limb but veins can’t drain it

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41
Q

Lines of Zahn

A

Alternating layers of strata of a thrombus

  • LIke tree rings
  • Indicate a thrombus are not static structure; can grow and then stop and then grow some more
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42
Q

Mural thrombi (where is a good starting spot? type of growth?)

A
  • Thrombus within wall of structure
  • Left ventricle is a good starting spot
  • Wart like vegetative growth
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43
Q

Mural thrombi mechanism

A

Recurrent rheumatic fever during childhood; Strep M protein

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44
Q

Mural Thrombi complications

A

~50% after second rheumatic fever

  • antibody attacks own endo
  • Growths can be hairlike; change characteristics of valve; decrease closure/less efficient
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45
Q

Verrucous (Libman Sacks) Endocarditis

A

Automimmune attack;

Lupus, vascular disease

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46
Q

Is a port-mortem clot a thrombus

A

No

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47
Q

Clinical manifestations of deep vein thrombosis (4)

A
  • Unilat edema of foot and ankle –> can lead to bact skin infect
  • Pain of foot and ankle (homan’s sign)
  • Local ischemia - bacterial skin infections
  • **Pulmonary embolization (largest risk)
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48
Q

Homan’s Sign

A

Apply broad contact to posterior knee–> they will be apprehensive

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49
Q

Where is the most common place for clot to form? Why?

A

Leg veins because lowest degree of pressure

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50
Q

What is one of most prevalent forms of death in hospital setting?

A

Deep vein thromboses

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51
Q

Economy Class syndrome

A

Increase likelihood of production of clot; present with posterior knee pain

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52
Q

5 Potential fates of thrombus

A

Dissolution (goes away); propagation (gets larger); organization (permanent inclusion of thrombus into BV wall; deposition of collagenous protein molecules); recanalization (attempt to increase BF through thrombus by burrowing thru it); embolization

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53
Q

Define embolism

A

Detached intravascular mass that is carried by the blood to a site distant form its point of origin

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54
Q

Subtypes of embolism

A

*Thromboembolism (MC); fat; air; amniotic

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55
Q

Thromboembolism

A

Most common subtype of embolism
Results in partial or complete occlusion of vessel lumina
May lodge in pulmonary or systemic circulation

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56
Q

What is the most common preventable death in hospitalized patients? How?

A

Pulmonary embolism

Use ambulation and anticoagulants

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57
Q

Where do pulmonary emboli arise from? where do they end up?

A

Arise from deep leg vein thrombi

Small vs large emboli (saddle embolus)

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58
Q

Saddle embolus

A

Saddles at bifurcation–> can lead to complete occlusion of both pulmonary aa

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59
Q

Systemic emboli: origin

A

ARTERIAL in origin (left ventricle, atherosclerotic plaques)

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60
Q

Systemic emboli: sites of lodgement (3)

A

Lower extrem (75%) (fem, tib, fib aa)
Brain (10%)
Visecera (10%)

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61
Q

Pathogenesis of systemic emboli

A

Typically starts with a cardiac event; the next question is where it will likely deposit

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62
Q

Infarction: definition; caused by

A
  • An area of ischemic necrosis within a tissue or organ

- Most often caused by thrombotic or embolic occlusion

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63
Q

White Infarct

A

Cessation of blood; usually because of thromboembolus

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64
Q

Red infarct

A

Due to hemorrhage event; bleeding inartery supplying area

bleed into tissue–> tissue turns red

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65
Q

Determining factors of infarct type (3)

A
  1. Nature of vascular supply
  2. Rate of development of occlusion
  3. Vulnerability of tissue to hypoxia
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66
Q

Morphology of an infarct (4)

A
  1. wedge shaped
  2. Margins lined by rim of hyperemia/inflammation
  3. Surface covered by fibrinous exudate (deposited around margin of infarct)
  4. Coagulative necrosis
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67
Q

Define shock

A

Hypoperfusion of tissues; inadequate BS everywhere

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68
Q

5 Major subtypes of shock

A

Cardiogenic, hypovolemic, septic, anaphylactic, neurogenic

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69
Q

Neurogenic shock

A

Spinal cord and brain injury
ex: broken neck cuts cord vasodilates–> hard to maintain BP; paraplegic skin flushes red because skin requires neurogenic stim

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70
Q

Define cardiogenic shock

A

fail the heart as a pump; heart does not deliver adequate BS to entire body

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71
Q

Potential causes of cardiogenic shock (3)

A

Myocardial infarct; Cardiac tamponade; cor pulmonale

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72
Q

Myocardial infarct and cardiogenic shock

A

Heart muscle is dead–> can’t contract; decreases Cardiac output

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73
Q

Cardiac tamponade and cardiogenic shock

A

Develop a hole in heart so you bleed into pericard sac; heart is bathed in blood–> increases BP –> heart cannot beat effectively

74
Q

What can cause cardiac tamponade

A

Thermogenics in diets

75
Q

Hypovolemic shock definition

A

Not enough blood volume= decrease BP= slow blood= hypoperfusion

76
Q

3 potential causes of hypovolemic shock

A
  1. Hemorrhage: some injury cause you to bleed out
  2. severe trauma: internal bleeding
  3. extensive burns: >40% of 3rd degree burns= actively weeping blood plasma= decrease in blood volume
77
Q

Acute cor pulmonale and cardiogenic shock example

A

Presents in context of pulmonary embolism
Long flight–> complain of pulmonary issue–> embolism occludes pulm aa–> chemoreceptors in body notice blood acidity rise–> inc HR–> blood more acidic–> sudden cardiac collapse as result of exhaustion of occlusion of pulm trunk

78
Q

Define septic shock

A

Inadequate pressure to move blood along because of increase vasc pressure and increase vasodil

79
Q

Pathophysiology of septic shock

A
  • Endotoxin release from gram neg bacteria (LPS)
  • Endotoxin stimulate release of cytokines (IL-1, 6, 8, TNF)
  • Cytokines trigger release of PAF, NO, Bradykinin, complement, prostaglandins, leukotrienes
80
Q

3 Stages of shock

A
  1. Nonprogressive
  2. Progressive
  3. Irreversible
81
Q

Nonprogressive stage of shock

A

Compensatory mechanisms to maintain BP= Symp NS, Renin Angio Aldost axis; autoregulation
*Attempt to maintain BP

82
Q

Progressive stage of shock

A

Tissue hypoxia and metabolic acidosis

Tissues alive and functioning but heading down bad path

83
Q

Irreversible stage of shock

A

Enzyme leakage; organ shut down

84
Q

Cardiac and pancreatic enzymes in blood =

A

Organs are shutting down

85
Q

Cytokines do what

A

Vasodilate and increase vasc perm

86
Q

Endothelial activation: define

A

Endothel cells can change their behavior based on various pathophysiological stimuli
- anything that can damage or act upon endothelial cells can induce change

87
Q

4 things endothelial cells can do once activated

A
  1. Express adhesion molecules: we want adherence to plug up hole
  2. Produce cytokines, chemokines: messenger molecules to call over WBC’s
  3. Produce growth factors
  4. Produce vasoactive molecules (vasodil/constrict)
88
Q

Arteriosclerosis

A
  • Hardening of arteries

- Caused by endothelial activation and subsequent pathological changes

89
Q

3 distinct patterns of arteriosclerosis

A
  1. Atherosclerosis (elastic aa and muscular aa)**
  2. Monkeberg medial sclerosis (calcific deposits in musc arteries; hardening)
  3. Arteriolosclerosis (small arteries and arterioles; in context of diabetes)
90
Q

Atherosclerosis contributes to what

A
  • Half of all deaths

- Death due to IHD which leads to MI; accounts for 20-25% all deaths in US

91
Q

Where do atherosclerotic lesions most occur occur

A

Elastic, large and medium muscular arteries

92
Q

What is a fatty streak

A

Initial visible lesion that we can see

93
Q

What is an atheroma

A

Lesion encroaches on lumen; accumulates fat in large arteries

94
Q

Fibroatheroma

A

Lesion becomes necrotic

95
Q

When does a lesion become complicated

A

The moment it produces clinically overt sx’s

96
Q

Risk factors with atherosclerosis

A

Hypertension; hyperlipidemia (raw materials to build lesion itself); cig smoking; gender (males more and at earlier age; females more after meno); **diabetes; soft risks (sedentary lifestyle; stress; obesity)

97
Q

New risks associated with atherosclerosis

A

Homocysteinemia; cytomegalovirus; C. pneumoniae; P. gigivalis

98
Q

2 Lesions of atherosclerosis

A
  1. Fatty streaks: early intimal lipid accumulation and engulfment of macro’s
  2. Atheromatous placques: raised subintimal plaques of necrotic tissue, lipid, extracellular matrix and cells
99
Q

Fibrous cap

A

Smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastic, prots, neovasc

100
Q

Necrotic center (4)

A

Cell debris, cholesterol crystals, foam cells, calcium

101
Q

2 components of atherosclerotic lesion

A

Fibrous cap and necrotic center

102
Q

4 resulting lesions of atherosclerosis

A

Ulceration, thrombosis, hemorrhage, calcification

103
Q

4 Clinical manifestations of atherosclerosis

A

Acute occlusion
Chronic narrowing (tiny legs because lack BS)
Aneurysm formation
Embolism (plaque breaks off–> distal site)

104
Q

Atherosclerosis of lumbar arteries

A

LBP; won’t respond to treatment

105
Q

Aneurysm

A

Localized dilation of a blood vessel or chamber of the heart

106
Q

5 types of aneurysm from most common to least

A

Aorta; iliac; splenic; renal; vertebral

107
Q

2 categories of aneurysms

A
  1. True: where the aneurysm is bounded by arterial wall components; all 3 tunicas bow out–> inc. in diameter
  2. False: where a breach in the vascular wall leads to a vascular hematoma –> tear thru and cause vasc leakage into wall of vessel; can occur in any one tunica
108
Q

True aneurysm (MC type? Where)

A

MC is atherosclerotic (direct consequence of lesion)
Syphilitic
COngenital
Left ventricular

109
Q

False aneurysm

A

MC post myocardial infarctive
Junctional leak at vascular graft
Genetic

110
Q

4 morphologies of aneuryms

A

Berry; fusiform; saccular; dissecting

111
Q

Berry aneurysm

A 
Most common in circle of willis 
Very small SPHERICAL dilation 
Rarely greater then 1-1.5cm 
Occur most frequently at base of brain 
Most commonly congenital; can become complicated
*TRUE
112
Q

Saccular aneurysm

A

Larger spherical dilation with same spherical shape as berry
Usually 5-10 cm in diameter
*TRUE

113
Q

Fusiform aneurysm

A

Gradual and progressive dilation of blood vessel
May be eccentric (occur unilateral; bow out to side)
Spindle shape; common lower thor/upper lumb
*TRUE

114
Q

Dissecting aneurysm

A
  • Refers to escape of blood into tunica media
  • Double barrel presentation of lumen
  • Dilation of BV need not exist for dissecting aneurym to occur
  • 2 types
  • *FALSE
115
Q

2 types of dissecting aneurysm

A
  • in reference to aorta
    1. Type A: include arch of aorta
    2. Type B: Not include arch of aorta
116
Q

DDX of aneurysm

A

Heart attack: elevates cardiac enzymes

Aneurysm does not

117
Q

Pseudoaneurysm

A

aka traumatic aneurysm due to physical injury; tunica media relaxes –> transient dilation of BV
Produces focal dilation

118
Q

Most common etiology of aneurysm

A

Atherosclerosis

119
Q

What is claudication

A

Trouble walking

vascular and neurogenic

120
Q

Atherosclerotic aneurysm presentation (Who? Diagnosed when? Symptoms 3, associated with what?)

A
  • MC in abdominal aorta
  • M>F (60-80 yoa)
  • Diagnosed when >50% dilation of normal diameter of vessel has occurred
  • Associated with hypertension (40%) + heart disease (30%)
  • **Intermittent back and abdominal pain
  • Claudication
  • Lower limb ischemia
121
Q

What is the greatest risk with atherosclerotic aneurysm

A

Chance of rupture

122
Q

Imaging strategy for aneurysm

A

Depends on clinical presentation

Accidental discovery is extremely common when plain film MRI, CT taken for back pain evaluation

123
Q

Clinical consequences of aneurysm >7cm

A

75% chance of rupture

124
Q

2 non-inflammatory vascular diseases

A

Monkeberg medial sclerosis and raynaud phenomenon

125
Q

Monkeberg Medial Sclerosis (define, most often where, et?)

A
  • Degen calcification of tunica MEDIA of large and MEDIUM MUSCULAR arteries
  • No luminal narrowing
  • Most often aa of upper and lower extrem
  • Et unknown
126
Q

Monkeberg affects who the most

A

Older individuals

127
Q

Monkeberg vs atherosclerosis

A

Monk does not lead to clinical presentation per se

128
Q

Pipe Stem Calcification

A

Popliteal artery distribution –> we shouldn’t be seeing BV’s on xray
Doppler ultrasound to visualize BFlow thru vessel
Think MONKEBERG

129
Q

Raynaud Phenomenon

A
  • Cyanosis of digits of hand or feet
  • Due to cold induced vasoconstriction
  • Fingers change color in sequence
  • Exaggeration of normal central and vasomotor responses to cold or emotion
130
Q

Raynaud typically benign or malig

A

Benign; however longstanding cases amy show signs of atrophy of skin, subcut tissues and muscles

Rare ulceration or gangrene

131
Q

Raynaud phenom vs raynaud disease

A

Disease is primary; phenom is secondary

132
Q

Sequence of color change in raynaud phenomenon

A

White–> blue–> red (when area reperfuses with blood)

133
Q

Inflammatory vasculitides

A
  • Directs immune system toward component of BV wall
  • Inflammation of walls of vessels (all sizes/types)
  • Can classify based on pathogenesis/etiology
  • Infection; immunologic
134
Q

Clinical presentation of inflammatory vasculitides

A
  • OFten a result of vessel lumen narrowing/oblit/dilat/thrombosis at that tissue level
  • Vasculitides are steroid/immunosupp therapy responsive –> tx is similar because they are all infl. in nature
135
Q

Takayasu arteritis

A

“Pulseless disease” : one arm normal, one are cold

  • weakening of peripheral pulses
  • Exam yields thickening of aorta, esp arch and its branches
  • Near oblit of distal portions of aortic branches
136
Q

Takayasu arteritis MC affects who

A

Females <40

137
Q

When should you order a followup of takayasu

A

BP difference <10 points systolic between R and L arm

138
Q

Polyarteritis Nodoasa

A
  • Necrotizing vasculitis of small and med sized visceral arteries (arteries to organs)
  • *NO lung involvement
  • Presentation common in kidney, liver
139
Q

Polyarteritis nodosa affects who

A

Males <40

140
Q

3 Complications of polyarteritis nodosa

A

Aneurysm; thrombosis; infarct

141
Q

TX of polyarteritis nodosa

A

Responds to corticosteroids (prednisone)

142
Q

3 phases of Polyarteritis nodosa lesion

A

Acute, healing, scarred (may co-present)

affects different BV at different times

143
Q

Polyarteritis nodosa presentation in kidney; liver

A

Kidney: hematuria
Liver: change in enzyme profile

144
Q

Polyarteritis nodosa, when affecting small aa, can be associated with what

A

P- ANCA: antibodies that bind to neutrophil and casue them to be overactive in nature
Neutro’s release infl. mediators–> damage area–> inc. WBC’s

145
Q

WBC’s supposed to be in tissue?

A

No–> infiltrate in polyart nodosa

146
Q

Allergic granulomatosis and angitis aka

A

Churg- Strauss

147
Q

Allergic granulomatosis

A
  • Systemic vasculitis in young individuals with asthma*
  • 2/3 patients have C-anca or P-anca
  • small and med size aa and arterioles of lungs, spleen, kidney, heart, CNS and others
  • Intense eosinophilic infilatrate

(Churg Straus)

148
Q

Giant cell arteritis aka

A

Temporal arteritis

149
Q

Giant cell arteritis

A

Patients >50 yoa
MC systemic form of vasculitis in adults
**Both acute and chronic form

150
Q

Giant cell artertitis affects what

A

Large and small arteries, particulary in head

  • *Patient presents with headache
  • Can lead to blindness with ophthalamic artery involvement
151
Q

giant cell arteritis immune reaction generated towards what? What is the nature of immune reaction? Injury?

A

Immune reaction is generated toward components of vascular wall- still putative
Granulomatous nature suggests T-cell mediated mechanism and antigen driven injury

152
Q

Clinical features of giant cell arteritis

A
  • Facial pain, intense upon palpation
  • Ocular symptoms: mild to severe
  • May lead to perm blindness
  • Tx with anti-inflammatory
153
Q

Kawasaki disease

A
  • et is unknown
  • disease of coronary arteries; children <4 yoa
  • Associated with mucocutaneous lymph node syndrome (acute self-limiting fever, rash, erythema, desquamation, lymphadenopathy)
    ~20% devel cardiac sequellae…aneurysmal formation
154
Q

Clinical consequences of Kawasaki disease (6 steps)

A
  • Asymptomatic vasculitis
  • Coronary artery ectasia: BV is widening but not yet aneurysmal
  • Coronary artery aneurysm
  • Thrombosis
  • MI
  • Sudden death
155
Q

TX of kawasaki disease

A

Aspirin + intravenous gammaglobulin (helps modulate immune system)

156
Q

Wegener’s Granulomatosis necrotizing vasculitis characterized by triad:

A
  1. Acute necrotizing granulomas of upper resp tract (arteries of resp) **COme in with pulm complaint
  2. Nectrotizing granulomatosis of small to med sized vessels (visceral aa)
  3. Renal disease in form of focal glomerulitis (renal disease)
157
Q

Pathogenesis of Wegener’s Granulomatosis

A
  • Some type of hypersensitivity reaction
  • 90% present with ANCA. 75% with C-ANCA
  • Rapidly fatal if not treated
  • Tx with cyclophosphamide (chemo agent)
  • Close to 100% cure when tx
158
Q

Cyclophosphamide

A
  • Tx for Wegener’s

- Highly effective chemo agent but carries high risk for secondary disease later in life

159
Q

Thromboangitis obliterans aka

A

Buerger’s disease

160
Q

Trhomboangitis obliterans

A
  • Distinctive disease leading to vasc insuff in distal extrem’s
  • Chx by segmental acute and chronic thrombosing of small and med aa
  • Microabscesses/granulomatous inflammation
161
Q

Clinical presentation of thromboangitis obliterans

A

Principally tib and radial aa
Preveiously occuring almost exclusively in heavy cig smoking men
Sx of claudication (neuro or vasc)
Cold intolerance/raynaud’s

162
Q

Behcet

A
  • Mainly involves mucous membranes
  • Chx by oral apthous ulcers, genital ulceration, ocular inflammation and lesions in CNS, cardiovasc and GI
  • Unknown cause, however immune basis

DDX: syphilis

163
Q

Varicose veins

A

Enlarged tortuous BV’s
Et: increased intraluminal pressure
Women> men; familial predisp; obesity
Vessel walls may be thinned due to dilation or thickened due to hypertrophy
- Stasis dermatitis and secondary ulceration

164
Q

Define varicosity

A

Dilation of a venous structure

165
Q

What is the most significant varicosity

A
  • Esophageal varicies
  • Tend to harbor in pt’s with liver issue presenting with portal hypertension; inc intraluminal pressure of gut bulges into lumen of esoph–> becomes thinned and atrophy–> swallowing food is abrasive–> can cut open esoph and bleed into stomach
  • Dec in BP = shock
166
Q

Prognosis of esophageal varicies

A

50% esop varix die on first bleeding event

Within 1 year most will have a second bleeding event with same prognosis

167
Q

Varicosities of rectum and anus

A

Hemorrhoidal veins increase pressure= hemorrhoids

168
Q

Varicosities of scrotum

A

Pampiniform plex of veins–> toruous–> variocele–> mass within scrotal sac
Translumination test: light through structure? non-neoplastic

169
Q

Thromophlebitis

A

Thrombus within a vein leading to inflammatory reaction

170
Q

Phlebothrombosis

A

Thrombus in a vein independent of inflammation

171
Q

Deep vein thrombosis associated with what? COD?

A

Prolonged bed rest, reduced CO, surgery
*Major threat to life; sudden death following post-op ambulation
Cause of death= pulm embolus resulting in cor pulmone (complete occlusion of pulm aa leaving lungs)

172
Q

Is DVT symptomatic

A
  • 50% of people don’t have symptoms
  • General swelling in calf, ankle, foot or thigh (homan’s)
  • Increased warmth of leg
    Redness
  • Pain in leg
  • Night leg cramps
  • Bluish discoloartion of skin on leg or toes
173
Q

Who has increased risk of DVT

A

Travelers; those in sitting posture; clotting illness; post-surg (esp if unable to walk)

174
Q

Caval filter

A

Tx of DVT

Catches clot then administer streptokinase to break up the clot

175
Q

Benign Hemangioma

A
  • Common congenital vascular lesion
  • OFten called a birth mark
  • MC on skin, also on mucosal surfaces and visceral organs
  • Present at birth and grow, but remain limited in size
176
Q

Capillary hemangioma aka

A
  • Strawberry hemangioma
177
Q

Capillary hemangioma

A
  • Vascular channels have the size and structure of normal capillaries
  • Occur on skin, subcut tissue, muc membranes of mouth and lips
  • Strawberry hemangiomas fade at 1-3 yoa
178
Q

Cafe au lait spots

A

Multiple spots? seek genetic counseling; may have NF mutation–> skel defects, tumors, kyphoscoliosis

179
Q

Cavernous hemangioma

A
  • Lesions consist of LARGE vascular channels
  • Skin (port wine stains), mucosa, viscera
  • raised, spongy masses which do not regress spontaenously
  • May undergo thrombosis, fibrosis, hemorrhage
    INTENSE stain
  • Clinically signif in von Hippel Landau disease
  • Increases density of capillaries
180
Q

Balloon Angioplasty

A
  • Luminal expansion of atherosclerotic arteries

- Atherosclerotic plaque becomes “unstable”

181
Q

Complications of balloon angioplasty

A
  • Plaque rupture, medial dissection, stretching of the media (exposure of collagen), prolif restensosis
182
Q

1 symptom of heart attack

A

Angina

183
Q

Stent

A

metal spring exerting pressure on BV wall to retain patency

5 semestre (19 decks)

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