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Flashcards in Physiopathology Final Deck (184):
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Define hemostasis

-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)

1

When does blood allow for plug to occur

when healing needs to happen

2

What is hemostasis a property of

BV and blood

3

Tunica intima is lined with what

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

4

Anti-platelet effects of intact endothelium (4)

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

5

ADPase synthesis in anti-platelet effects

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

6

Nitric oxide synthesis in anti-platelet effects

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

7

Anti-coagulant effects of intact endothelium

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

8

Effect of no thrombin on the coag system

Shuts off coag

9

What is the coag system

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

10

What turns on synthesis of antithrombin III

Herparin like factor

11

Fibrinolytic property of intact endothelium

tPA synthesis --> converts plasminogen to plasmin

12

What does plasmin do

Degrades fibrin (chews up clot)

13

Ischemic stroke

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

14

Hemorrhagic stroke?

Give tPA and you will kill them--> they can't clot

15

Pro-thrombotic properties of damaged endothelium (4)

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

16

von-Willebrand Factor

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

17

Von-Willebrand disease

-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

18

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

-Glycoprotein which activates coag system
- One of triggers for coag system
- Damage endo turns on tissue factor--> turns on coag system

19

Platelet activating factor as protrombotic property of damaged endo

damaged endo + PAF + platelets

20

t-PRA inhibitor ensures what

Clot will remain
*Plays important role in prothrombotic property of damaged endo

21

What are the "bricks" of a thrombus? Cement?

Bricks: platelets
Cement: fibrin

22

Platelet actions oppose the action of what

endothelium

23

Platelets secrete what (5)

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

24

What do activated platelets bind to

Exposed collagen--> vWF

25

Activated platelet role in coagulation cascade

Initiates cascade (role of calcium and phospholipid complex)

26

"Temporary plug"

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

27

Young clot appearance vs old clot appearance

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

28

Coagulation System activated by who

- Activated by factor XII (hageman) or tissue factor
- End product is formation of fibrin monomers
- Fibrin is "cement" of thrombus

29

Thrombus

- 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

30

3 Predisposing factors to arterial thrombi

AKA Virchow's Triad
1. Damage to endothelium
2. Alterations in normal blood flow
3. Increased coagulability of blood

31

Damage to endothelium that will promote production of thrombus in region

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

32

Hemodynamic stress

Too much force on BV because of high BP

33

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

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

34

Factors that increase coagulability of blood (5)

-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"

35

What is a soft risk factor

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

36

50% of population will die from what

Arterial thrombi
*Most common cause of death in US

37

Most common sites of arterial thrombi

1. Coronary
2. Cerebral
3. Femoral

38

Arterial thrombi results in what? Death due to?

Ischemic infarction
Death due to MI, cerebral infarct, renal infarct

39

Thrombosis in the venous system

-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

40

Deep leg vein thrombosis

Most common clinical manifestation
aka "red thrombi"
arteries supply limb but veins can't drain it

41

Lines of Zahn

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

42

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

- Thrombus within wall of structure
- Left ventricle is a good starting spot
- Wart like vegetative growth

43

Mural thrombi mechanism

Recurrent rheumatic fever during childhood; Strep M protein

44

Mural Thrombi complications

~50% after second rheumatic fever
- antibody attacks own endo
- Growths can be hairlike; change characteristics of valve; decrease closure/less efficient

45

Verrucous (Libman Sacks) Endocarditis

Automimmune attack;
Lupus, vascular disease

46

Is a port-mortem clot a thrombus

No

47

Clinical manifestations of deep vein thrombosis (4)

-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)

48

Homan's Sign

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

49

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

Leg veins because lowest degree of pressure

50

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

Deep vein thromboses

51

Economy Class syndrome

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

52

5 Potential fates of thrombus

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

53

Define embolism

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

54

Subtypes of embolism

*Thromboembolism (MC); fat; air; amniotic

55

Thromboembolism

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

56

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

Pulmonary embolism
Use ambulation and anticoagulants

57

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

Arise from deep leg vein thrombi
Small vs large emboli (saddle embolus)

58

Saddle embolus

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

59

Systemic emboli: origin

ARTERIAL in origin (left ventricle, atherosclerotic plaques)

60

Systemic emboli: sites of lodgement (3)

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

61

Pathogenesis of systemic emboli

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

62

Infarction: definition; caused by

- An area of ischemic necrosis within a tissue or organ
- Most often caused by thrombotic or embolic occlusion

63

White Infarct

Cessation of blood; usually because of thromboembolus

64

Red infarct

Due to hemorrhage event; bleeding inartery supplying area
bleed into tissue--> tissue turns red

65

Determining factors of infarct type (3)

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

66

Morphology of an infarct (4)

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

67

Define shock

Hypoperfusion of tissues; inadequate BS everywhere

68

5 Major subtypes of shock

Cardiogenic, hypovolemic, septic, anaphylactic, neurogenic

69

Neurogenic shock

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

70

Define cardiogenic shock

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

71

Potential causes of cardiogenic shock (3)

Myocardial infarct; Cardiac tamponade; cor pulmonale

72

Myocardial infarct and cardiogenic shock

Heart muscle is dead--> can't contract; decreases Cardiac output

73

Cardiac tamponade and cardiogenic shock

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

74

What can cause cardiac tamponade

Thermogenics in diets

75

Hypovolemic shock definition

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

76

3 potential causes of hypovolemic shock

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

Acute cor pulmonale and cardiogenic shock example

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

Define septic shock

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

79

Pathophysiology of septic shock

- 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

3 Stages of shock

1. Nonprogressive
2. Progressive
3. Irreversible

81

Nonprogressive stage of shock

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

82

Progressive stage of shock

Tissue hypoxia and metabolic acidosis
Tissues alive and functioning but heading down bad path

83

Irreversible stage of shock

Enzyme leakage; organ shut down

84

Cardiac and pancreatic enzymes in blood =

Organs are shutting down

85

Cytokines do what

Vasodilate and increase vasc perm

86

Endothelial activation: define

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

87

4 things endothelial cells can do once activated

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

Arteriosclerosis

- Hardening of arteries
- Caused by endothelial activation and subsequent pathological changes

89

3 distinct patterns of arteriosclerosis

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

Atherosclerosis contributes to what

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

91

Where do atherosclerotic lesions most occur occur

Elastic, large and medium muscular arteries

92

What is a fatty streak

Initial visible lesion that we can see

93

What is an atheroma

Lesion encroaches on lumen; accumulates fat in large arteries

94

Fibroatheroma

Lesion becomes necrotic

95

When does a lesion become complicated

The moment it produces clinically overt sx's

96

Risk factors with atherosclerosis

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

New risks associated with atherosclerosis

Homocysteinemia; cytomegalovirus; C. pneumoniae; P. gigivalis

98

2 Lesions of atherosclerosis

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

Fibrous cap

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

100

Necrotic center (4)

Cell debris, cholesterol crystals, foam cells, calcium

101

2 components of atherosclerotic lesion

Fibrous cap and necrotic center

102

4 resulting lesions of atherosclerosis

Ulceration, thrombosis, hemorrhage, calcification

103

4 Clinical manifestations of atherosclerosis

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

104

Atherosclerosis of lumbar arteries

LBP; won't respond to treatment

105

Aneurysm

Localized dilation of a blood vessel or chamber of the heart

106

5 types of aneurysm from most common to least

Aorta; iliac; splenic; renal; vertebral

107

2 categories of aneurysms

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

True aneurysm (MC type? Where)

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

109

False aneurysm

MC post myocardial infarctive
Junctional leak at vascular graft
Genetic

110

4 morphologies of aneuryms

Berry; fusiform; saccular; dissecting

111

Berry aneurysm

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

Saccular aneurysm

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

113

Fusiform aneurysm

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

Dissecting aneurysm

- 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

2 types of dissecting aneurysm

- in reference to aorta
1. Type A: include arch of aorta
2. Type B: Not include arch of aorta

116

DDX of aneurysm

Heart attack: elevates cardiac enzymes
Aneurysm does not

117

Pseudoaneurysm

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

118

Most common etiology of aneurysm

Atherosclerosis

119

What is claudication

Trouble walking
vascular and neurogenic

120

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

- 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

What is the greatest risk with atherosclerotic aneurysm

Chance of rupture

122

Imaging strategy for aneurysm

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

123

Clinical consequences of aneurysm >7cm

75% chance of rupture

124

2 non-inflammatory vascular diseases

Monkeberg medial sclerosis and raynaud phenomenon

125

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

- 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

Monkeberg affects who the most

Older individuals

127

Monkeberg vs atherosclerosis

Monk does not lead to clinical presentation per se

128

Pipe Stem Calcification

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

129

Raynaud Phenomenon

- 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

Raynaud typically benign or malig

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

Rare ulceration or gangrene

131

Raynaud phenom vs raynaud disease

Disease is primary; phenom is secondary

132

Sequence of color change in raynaud phenomenon

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

133

Inflammatory vasculitides

- 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

Clinical presentation of inflammatory vasculitides

- 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

Takayasu arteritis

"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

Takayasu arteritis MC affects who

Females <40

137

When should you order a followup of takayasu

BP difference <10 points systolic between R and L arm

138

Polyarteritis Nodoasa

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

139

Polyarteritis nodosa affects who

Males <40

140

3 Complications of polyarteritis nodosa

Aneurysm; thrombosis; infarct

141

TX of polyarteritis nodosa

Responds to corticosteroids (prednisone)

142

3 phases of Polyarteritis nodosa lesion

Acute, healing, scarred (may co-present)
affects different BV at different times

143

Polyarteritis nodosa presentation in kidney; liver

Kidney: hematuria
Liver: change in enzyme profile

144

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

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

WBC's supposed to be in tissue?

No--> infiltrate in polyart nodosa

146

Allergic granulomatosis and angitis aka

Churg- Strauss

147

Allergic granulomatosis

- 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

Giant cell arteritis aka

Temporal arteritis

149

Giant cell arteritis

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

150

Giant cell artertitis affects what

Large and small arteries, particulary in head
**Patient presents with headache
* Can lead to blindness with ophthalamic artery involvement

151

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

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

152

Clinical features of giant cell arteritis

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

153

Kawasaki disease

- 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

Clinical consequences of Kawasaki disease (6 steps)

- Asymptomatic vasculitis
- Coronary artery ectasia: BV is widening but not yet aneurysmal
- Coronary artery aneurysm
- Thrombosis
- MI
- Sudden death

155

TX of kawasaki disease

Aspirin + intravenous gammaglobulin (helps modulate immune system)

156

Wegener's Granulomatosis necrotizing vasculitis characterized by triad:

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

Pathogenesis of Wegener's Granulomatosis

- 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

Cyclophosphamide

- Tx for Wegener's
- Highly effective chemo agent but carries high risk for secondary disease later in life

159

Thromboangitis obliterans aka

Buerger's disease

160

Trhomboangitis obliterans

- 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

Clinical presentation of thromboangitis obliterans

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

Behcet

- 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

Varicose veins

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

Define varicosity

Dilation of a venous structure

165

What is the most significant varicosity

- 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

Prognosis of esophageal varicies

50% esop varix die on first bleeding event
Within 1 year most will have a second bleeding event with same prognosis

167

Varicosities of rectum and anus

Hemorrhoidal veins increase pressure= hemorrhoids

168

Varicosities of scrotum

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

169

Thromophlebitis

Thrombus within a vein leading to inflammatory reaction

170

Phlebothrombosis

Thrombus in a vein independent of inflammation

171

Deep vein thrombosis associated with what? COD?

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

Is DVT symptomatic

- 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

Who has increased risk of DVT

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

174

Caval filter

Tx of DVT
Catches clot then administer streptokinase to break up the clot

175

Benign Hemangioma

- 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

Capillary hemangioma aka

- Strawberry hemangioma

177

Capillary hemangioma

- 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

Cafe au lait spots

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

179

Cavernous hemangioma

- 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

Balloon Angioplasty

- Luminal expansion of atherosclerotic arteries
- Atherosclerotic plaque becomes "unstable"

181

Complications of balloon angioplasty

- Plaque rupture, medial dissection, stretching of the media (exposure of collagen), prolif restensosis

182

#1 symptom of heart attack

Angina

183

Stent

metal spring exerting pressure on BV wall to retain patency