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test 8 Flashcards

1
Q

increased hydrostatic pressure can be caused by

A

CHF, portal HTN, renal retention of salt and water, venous thrombosis

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2
Q

hypoalbuminemia and decreased colloid osmotic pressure are caused by

A

liver disease, nephrotic syndrome, kwashiorkor

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3
Q

lymphatic obstruction (lymphedema) caused by

A

tumor, surgical removal of lymph nodes, parasitic infestation (filariasis-> elephantiasis)

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4
Q

increased endothelial permeability caused by

A

inflammation/histamine, type I hypersensitivity runs, drugs

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5
Q

increased interstitial sodium caused by

A

increase Na+ intake, renal failure, primary hyperaldosteronism

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6
Q

myxedema

A

specialized form of tissue swelling due to increased extracellular glycosaminoglycans

(from thyroid disease)

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7
Q

anasarca

A

severe generalized edema

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8
Q

effusion

A

fluid w/in body cavities (tends to collect into potential spaces; i.e. pleural space)

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9
Q

types of edema fluid

A

transudate; exudate

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10
Q

transudate

A

edema w/ low protein content

clear/pale
no tissue fragments; thin
alkaline
low cell count
low enzyme count
no bacteria
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11
Q

exudate

A

edema fluid w/ high protein content & cells

cloudy, white, yellow, or red
thick; tissue fragments
acidic
many WBCs and RBCs
may have bacteria
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12
Q

types of exudates (4)

A

purulent (pus)
fibrinous
serous
hemorrhagic (sanguineous)

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13
Q

fibrinous exudate

A

collagen exudates in body cavities

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14
Q

sanguineous exudate

A

blood in exudate

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15
Q

purulent (suppurative) exudate

A

increased art of pus and/or neutrophils; necrotic cells and edematous fluid; i.e. meningitis, cephalitis

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16
Q

serous exudate

A

thin fluid derived from either serum or secretions of mesothelial cells (effusion)

often combines w/ sanguineous

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17
Q

ascites

A

gastroenterological term for an accumulation of fluid in the peritoneal cavity

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18
Q

condition that leads to ascites

A

cirrhosis

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19
Q

exudates… pitting or not

A

no pitting

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20
Q

hyperemia

A

active increase in the volume of blood in tissues

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21
Q

causes of hyperemia

A

arteriolar dilation

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22
Q

congestion

A

passive increase in the volume of blood in tissues; us. accompanied by edema

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23
Q

causes of congestion

A

impaired venous flow from tissues eg cardiac failure, venous obstruction

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24
Q

complications of congestion

A

cyanosis/hypoxia

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25
Q

hemostasis

A

sequence of events leading to the cessation of bleeding by the formation of a stable fibrin-platelet hemostatic plug

involves interactions b/w the vascular wall, platelets, and coagulation system

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26
Q

clotting is a balance b/w which 2 opposing forces

A
  1. formation of a stable thrombus; 2. factors causing fibrinolysis of the clot
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27
Q

transient vasoconstriction is mediated by

A

endothelin-1

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28
Q

5 thrombogenic factors

A

changes in BF cause turbulence and stasis, which favors clot formation

release of tissue factor from injured cell activates factor VII (extrinsic pathway) from damaged cells

exposure of thrombogenic sub endothelial collagen activates factor XII (intrinsic pathway) always in blood

release of vWF which binds to exposed collagen and facilitates platelet adhesion

decreased endothelial synthesis of antithrombogenic substances (prostacyclin, NO2, TPA, and thrombomodulin)–>allows for clots

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29
Q

endothelin does what 5 things

A

proliferation

fibrosis

vasoconstriction

hypertrophic

inflammation

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30
Q

3 steps of platelets

A

platelet adhesion

platelet activation

platelet aggregation

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31
Q

platelet adhesion

A

vWF adheres to sub endothelial collagen

platelets then adhere to vWF by glycoprotein Ib

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32
Q

platelet activation

A

platelet undergo a shape change and degranulation occurs

platelet synthesis of thromboxane A2*

membrane expression of phospholipid complex which is an important substrate for coagulation cascade

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33
Q

platelet aggregation

A

additional platelets are recruited from bloodstream

ADP and thromboxane A2 are potent mediators of aggregation

platelets bind to each other by binding to fibrinogen using Gp IIb-IIIa*

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34
Q

bernard-soulier syndrome

A

autosomal recessive

deficiency of platelet Gp Ib

defective platelet adhesion

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35
Q

glanzmann thrombasthenia

A

AR

deficiency of Gp IIb-IIIa

defective platelet aggregation

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36
Q

asprin

A

irreversibly acetylates cyclooxybenase

prevents platelet production of thromboxane A2

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37
Q

Immune Thrombocytopenia Purpura

A

Autoimmune mediated attack (typically IgG antiplatelet antibodies) against platelets leading to decreased platelets (thrombocytopenia)
• Results in petechiae, purpura (bruises), and a bleeding diathesis (e.g. hematomas)

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38
Q

etiology of Immune Thrombocytopenia Purpura

A
  • Antiplatelet antibodies against platelet antigens such as Gp IIb-IIIa and Gp Ib-IX (type II hypersensitivity reaction)
  • Antibodies are made in the spleen
  • Platelets are destroyed peripherally in the spleen by macrophages which have Fc receptors that bind IgG-coated platelets
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39
Q

acute ITP

A

Seen in children following a viral
infection
• Self-limited disorder

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40
Q

chronic ITP

A

Usually seen in women in their
childbearing years
• May be the first manifestation of SLE
• Petechiae, ecchymoses, menorrhagia, and nosebleeds

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41
Q

lab diagnostics of ITP

A

Decreased platelet count and prolonged bleeding time
• Normal prothrombin time (PT) and partial thromboplastin time (PTT)
• Peripheral blood smear shows thrombocytopenia with enlarged immature platelets (megathrombocytes)
• Bone marrow biopsy shows increased numbers of megakaryocytes with immature forms

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42
Q

treatments of ITP

A

Corticosteroids, which decrease antibody production
• Immunoglobulin therapy, which floods Fc receptors on splenic macrophages
• Splenectomy, which removes the site of platelet destruction and antibody production

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43
Q

thrombotic Thrombocytopenic Purpura (TTP)

A

Rare disorder of hemostasis where there is widespread intravascular formation of fibrin- platelet thrombi due to a deficiency/inhibition of the enzyme ADAMTS13, which is responsible for cleaving large multimers of von Willebrand factor

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44
Q

thrombotic Thrombocytopenic Purpura (TTP) clinical findings

A 
Most often affects adult women
• Pentad of characteristic signs
• Fever
• Thrombocytopenia
• Microangiopathic hemolytic
anemia (intravascular hemolysis)
• Neurologic symptoms
• Renal failure
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45
Q

lab diagnosis of thrombotic Thrombocytopenic Purpura (TTP)

A
  • Decreased platelet count and prolonged bleeding time
  • Normal PT and PTT
  • Peripheral blood smear shows thrombocytopenia and schistocytes, and reticulocytosis
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46
Q

pathology of thrombotic Thrombocytopenic Purpura (TTP)

A

Widespread formation of platelet thrombi with fibrin (hyaline thrombi) leading to intravascular hemolysis (thrombotic microangiopathy)

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47
Q

Hemolytic Uremic Syndrome (HUS)

A
  • A form of thrombotic microangiopathy due to endothelial cell damage
  • Occurs most commonly in children
  • Follows a gastroenteritis with bloody diarrhea
  • Organism: verotoxin- producing E. coli 0157:H7
Pentad of characteristic signs
• Fever
• Thrombocytopenia
• Microangiopathic hemolytic
anemia (intravascular hemolysis)
• Neurologic symptoms
• Renal failure
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48
Q

vitamin k required for these clotting factors

A

clotting factors 2, 7, 9, 10

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49
Q

The majority of the clotting factors are produced by…

A

the liver

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50
Q

The factors are … that must be converted to the active form, some on… and require…

A

proenzymes

on a phospholipid surface

Ca++

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51
Q

The extrinsic coagulation pathway is activated by the release of

A

tissue factor

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52
Q

The intrinsic coagulation pathway is activated by

A

contact factors:
• Contact with subendothelial collagen
• High molecular weight kininogen (HMWK)

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53
Q

prothrombin time (PT) tests

A
  • Tests the extrinsic and common coagulation pathways
  • Tests factors VII, X, V, prothrombin, fibrinogen
  • International normalized ratio (INR) standardizes the PT test so that results throughout the world can be compared
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54
Q

Partial thromboplastin time (PTT) tests

A

Tests the intrinsic and common coagulation pathways

• Tests factors XII, XI, IX, VIII, X, V, prothrombin, fibrinogen

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55
Q

Fibrin degradation products (FDP) tests

A

fibrinolytic system (increased with DIC)

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56
Q

Thrombin time (TT) tests

A

adequate fibrinogen levels

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57
Q

Disseminated
Intravascular
Coagulation (DIC) causes

A
  • Obstetric complications (placental tissue factor activates clotting)
  • Gram-negative sepsis (TNF) activates clotting
  • Microorganisms (especially meningococcus and rickettsiae)
  • AML M3 (cytoplasmic granules in neoplastic promyelocytes activate clotting)
  • Adenocarcinomas (mucin activates clotting)
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58
Q

Disseminated
Intravascular
Coagulation (DIC) pathology

A
  • Results in widespread microthrombi

* Consumption of platelets and clotting factors causes hemorrhages

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59
Q

Disseminated
Intravascular
Coagulation (DIC) lab

A
  • Platelet count is decreased
  • Prolonged PT/PTT
  • Decreased fibrinogen
  • Elevated fibrin split products (D-dimers)
  • Treatment: treat the underlying disorder
60
Q

Hemophilia A

A

Deficiency of factor VIII

X-linked recessive

61
Q

Hemophilia A features

A

• Predominately affects males
• Symptoms are variable dependent on
the degree of deficiency
• Newborns may develop bleeding at the time of circumcision
• Spontaneous hemorrhages into joints (hemarthrosis)
• Easy bruising and hematoma formation after minor trauma
• Severe prolonged bleeding after surgery or lacerations
• **No petechiae or ecchymoses

62
Q

Hemophilia A tests

A
  • Normal platelet count and bleeding time

* Normal PT and prolonged PTT

63
Q

Hemophilia A features

A

• Factor VIII concentrate

64
Q

Hemophilia B

A
  • Deficiency of factor IX
  • X-linked recessive
  • Clinically identical to hemophilia A
65
Q

Vitamin K deficiency leading to and caused by

A
  • Decreased synthesis of factors II, VII, IX, X, and protein C & S
  • Caused by liver disease and the resulting decreased synthesis of virtually all clotting factors
66
Q

Von Willebrand Disease

A

Inherited bleeding disorder characterized by either a deficiency or a qualitative defect in von Willebrand factor
• vWF is normally produced by endothelial cells and megakaryocytes

67
Q

Von Willebrand Disease genetics

A

Types I-III genetic
Type I AD 75% (most mild)
II AR – intermediate severity 4 subtypes III AR – rare and severe
“Type 4” acquired

68
Q

Von Willebrand Disease labs

A
  • Normal platelet count and a prolonged bleeding time
  • Normal PT with often a prolonged PTT
  • Abnormal platelet response to ristocetin (adhesion defect) is an important diagnostic test
69
Q

Von Willebrand Disease features

A
  • Spontaneous bleeding from mucous membranes
  • Prolonged bleeding from wounds
  • Menorrhagiainyoungfemales
  • Hemarthrosis is uncommon
70
Q

Von Willebrand Disease treatment

A
  • Treat mid cases (type I) with desmopressin (an antidiuretic hormone {ADH} analog)
  • It releases vWF from Weibel-Palade bodies of endothelial cells
71
Q

Thrombosis

A

pathologic formation of an intravascular fibrin-platelet thrombus during life

72
Q

Thrombosis outcomes

A
  • Vascular occlusion and infarction • Embolism
  • Thrombolysis
  • Organizationandrecanalization
73
Q

Thrombosis locations

A

• Coronaryandcerebralarteries
• Heart chambers atrial fibrillation or post-MI
(mural thrombus)
• Aortic aneurysms
• Heart valves (vegetations) • Deep leg veins (DVTs)

74
Q

Factors involved in thrombus formation (Virchow’s Triad

A

stasis, vascular injury, hyper coagulability

  • Endothelial injury
  • Atherosclerosis
  • Vasculitis
  • Many others
75
Q

Hypercoagulabilityofblood caused by

A

• Clotting disorders (factor V Leiden, deficiency of
antithrombin III, protein C, or protein S)
• Tissue injury (postoperative and trauma)
• Neoplasia
• Nephrotic syndrome
• Advanced age
• Pregnancy
• Oral contraceptives (estrogen increases synthetic activity of the liver, including clotting factors

76
Q

Embolism

A

Is any intravascular mass that has been carried down the bloodstream from its site of origin resulting in the occlusion of a vessel

77
Q

Embolism composition

A
  • Thromboemboli - most common (98%) type of emboli
  • Atheromatous emboli – severe atherosclerosis
  • Fat emboli – bone fractures
  • Bone marrow emboli – bone fractures and CPR
78
Q

gas emboli

A

• Decompression sickness “the bends”
• Rapid ascent results in nitrogen gas
bubbles in the blood vessels

79
Q

Amniotic fluid emboli

A

• Complication of labor
• Fetal squamous cells are seen in the
maternal pulmonary vessels
• May result in DIC

80
Q

Pulmonary Emboli (PE) pathology

A
  • 95% of PEs arise from DVTs
  • Pelvic venous plexuses of the prostate and uterus
  • Right side of the heart
81
Q

Pulmonary Emboli (PE) diagnosis

A
  • Doppler ultrasound of the leg veins to detect DVT (do first)
  • V/Q scan shows mismatch
  • Spiral CT
  • Plasma D-dimer ELISA test is elevated ($1000 and cannot be used after surgery)
  • Pulmonary angiogram GS
82
Q

PE outcomes

A

No sequelae (75%)
• Asymptomatic or transient dyspnea/tachypnea
• No infarction (dual blood supply)
• Complete resolution

Infarctions (15%)
• More common in patients with cardiopulmonary compromise
• SOB, hemoptysis, pleuritic chest pain, pleural effusion
• Hemorrhagic wedge-shaped infarct (x-ray Hamptons
hump)

Sudden death (5%)
• Large emboli may lodge in the bifurcation (saddle embolus) or large pulmonary artery branches and cause sudden death
• Obstruction of >50% of the pulmonary circulation

Chronic secondary pulmonary HTN (3%)
• Caused by recurrent PEs
• Increased pulmonary resistance
• Lead to secondary pulmonary HTN

83
Q

Systemic Arterial Emboli

A

• Most arise in the heart
• Most arterial emboli cause
infarction
• Common sites of infarction include the LE, brain, intestine, kidney, and spleen

84
Q

paradoxical emboli

A

Any venous embolus that gains access to the systemic circulation by crossing over from the right to the left side of the heart through a septal defect

85
Q

Infarction

A

Localized area of necrosis secondary to ischemia

86
Q

Factors predicting development of infarct:

A
  • Vulnerability of the tissue to hypoxia
  • Degree of occlusion
  • Rate of occlusion
  • Presence of dual blood supply
  • Decreased oxygen carrying capacity (anemia, CO, etc.)
87
Q

General sequence of tissue changes after infarction:

A

Ischemia-Coagulative necrosis- inflammation- granulation tissue -fibrous scar

88
Q

Shock

A
  • Vascular collapse and widespread hypoperfusion of cells and tissue due to reduced blood volume, cardiac output (CO) or vascular tone
  • Cellular injury is initially reversible
  • If the hypoxia persists, the cellular injury becomes irreversible, leading to the death of cells and the patient
89
Q

Cardiogenic shock

A 
(pump failure)
• MI
• Arrhythmias
• PE
• Cardiac tamponade
90
Q

Hypovolemic shock

A

(reduced blood
volume)
• Hemorrhage
• Fluid loss due to burns • Severe dehydration

91
Q

septic shock

A

(bacterial infection)
• Gram-negative septicemia
• Release of endotoxins (bacterial wall LPS
‘lipopolysaccharides’ )

High levels of endotoxin results in
• Production of cytokines TNF, IL-1, IL-6, and IL-8
• Vasodilationandhypotension
• Acuterespiratorydistresssyndrome(ARDS)
• DIC
• Multiple organ dysfunction syndrome
• Mortality rate: 50%
92
Q

Anaphylactic shock

A

(generalized vasodilation – type I hypersensitivity reaction)

93
Q

Neurogenic shock

A

(generalized vasodilation) • Anesthesia

• Brain or spinal cord injury

94
Q

stage 1 of shock

A

Compensation, in which perfusion to vital organs is maintained by reflex mechanisms
• Increased sympathetic tone
• Releaseofcatecholamines
• Activationoftherenin-angiotensinsystem

95
Q

stage 2 of shock

A

Decompensation
• Progressivedecreaseintissueperfusion
• Potentiallyreversibletissueinjuryoccurs
• Developmentofametabolic(lactic) acidosis, electrolyte imbalances, and renal insufficiency

96
Q

stage 3 of shock

A

Irreversible
• Irreversibletissueinjuryandorganfailure
• Ultimately resulting in death

97
Q

kidney shock pahtology

A
  • Acute tubular necrosis (acute renal failure)

* Oliguria and electrolyte imbalances occur

98
Q

lung shock pathology

A

Undergo diffuse alveolar damage (“shock lung”)

99
Q

intestines shock pathology

A
  • Superficial mucosal ischemic necrosis and hemorrhages

* Prolonged injury may lead to sepsis with bowel flora

100
Q

liver shock pathology

A

Undergoes centrilobular necrosis (“shock liver ”)

101
Q

adrenal shock

A
  • Undergo the Waterhouse-Friderichsen syndrome
  • Commonly associated with meningococcal septic shock
  • Bilateral hemorrhagic infarction
  • Acute adrenal insufficiency
102
Q

NON-Specific Vascular Wall

Response to Injury

A
  • Endothelial “activation”
  • Smooth Muscle cell roles

Development, growth, Remodeling

• Intimal “thickening”

103
Q

arteriosclerosis

A

thickening and loss of elasticity in arterial walls (general)

104
Q

monckeberg medial calcific sclerosis

A

calcific deposits in muscular arteries in persons over 50

105
Q

function of endothelial cells (9)

A

Maintenance of Permeability Barrier
• ElaborationofAnticoagulant,Antithrombotic, Fibrinolytic Regulators: Prostacyclin, Thrombomodulin, Heparin, Plasminogen •ElaborationofProthromboticMolecules: vWF, TF, Plasminogen activator inhibitor
• Extracellular Matrix Production (collagen,
proteoglycans)
• Modulation of Blood Flow and Vascular Reactivity
• Vasoconstrictors: endothelin, ACE
• Vasodilators: NO, Prostacyclin
• Regulation of Inflammation and Immunity
• Regulation of Cell Growth
• OxidationofLDL

106
Q

Prostacyclin … platelet activation

A

INHIBITS

107
Q

Thrombomodulin … thrombin

A

inhibits

108
Q

body’s main anticoagulant

A

heparin

109
Q

plasminogen is a precursor of what and what is its function?

A

precursor of plasmin dissolves fibrin!

110
Q

vessel growth and remodeling (5 aspects)

A

The sum total of all the factors and processes involved in tissue injury and the body’s ability to grow vessels, develop new pathways, and re- perfuse areas in response to tissue and/or blood vessel injury.

111
Q

intimal thickening

A

Intimal thickening is a NON-specific response to vascular (chiefly arterial) injury, and is they KEY feature in atherosclerosis as well.

112
Q

ArterioVenous Malformation (AVM)

A

= Arteriovenous fistulas (can be surgically produced for dialysis)
• Also called ArterioVenous Malformation (AVM)
• Common factor is abnormal communication between high pressure arteries and low pressure veins
• Usually congenital (malformation), but can be acquired by trauma or inflammation
• Most often described in the brain as an AVM
• Often asymptomatic or with hemorrhage or pressure effects

113
Q

Arteriolosclerosis

A

involving small arteries and arterioles, generally regarded as NOT strictly being part of atherosclerosis, but more related to hypertension and/or diabetes

114
Q

3 stages of Atherosclerosis

A

1) FATTY STREAK non-palpable, but a visible YELLOW streak)
2) ATHEROMA (plaque) (palpable)
3) THROMBUS (non-functional, symptomatic)

115
Q

morphologic progression of artheriosclerosis

A

• Macrophages (really monocytes) infiltrate
• Intimal “Thickening”
• Lipid Accumulation
• Streak
• Atheroma
• Smooth Muscle Hyperplasia and
Migration
• Fibrosis
• Calcification
• Aneurysm*
• Thrombosis

116
Q

Cholesterol (really cholesterol esters) makes macrophages

A

“foamy” and cause “clefts” extracellularly.

117
Q

pathogenesis of arterioschlerosis

A

Chronic endothelial injury
• LDL, Cholesterol in arterial WALL
• OXIDATION of lipoproteins
• Monocytes migrateendothelium*
• Platelet adhesion and activation
• Migration of SMOOTH MUSCLE from media to intima to activate macrophages (foam cells)
• Proliferation of SMOOTH MUSCLE and ECM
• Accumulation of lipids in cells and ECM

118
Q

major risk factors for arterioschlerosis

A

NON-modifiable
Increasing age
Male gender
Family history Genetic abnormalities

Modifiable
Hyperlipidemia Hypertension Cigarette smoking Diabetes

119
Q

minor factors for artheriosclerosis

A

Modifiable
Obesity
Physical inactivity
Stress (“type A” personality)
Postmenopausal estrogen deficiency
High carbohydrate intake
Alcohol
Lipoprotein Lp(a)
Hardened (trans)unsaturated fat intake Chlamydia pneumoniae

120
Q

Hyperlipidemia – Foamy Macrophage

A

Chiefly CHOLESTEROL, LDL»»HDL
• HDL mobilizes cholesterol FROM atheromas to liver
• Low Cholesterol Diet Is Good
• Unsaturated Fatty Acids Good
• Omega-3 Fatty Acids Good
• Exercise Good

121
Q

cholesterol clefts/esters

A

• Needle shaped washed out spaces in arteries, are cholesterol clefts, and can be nothing else, and like all other fat, yellow grossly, white microscopically.

122
Q

NON ATHEROSCLEROSIS VASCULAR DISEASES (5)

A

•HYPERTENSION •ANEURYSMS
•VASCULITIDES • VEIN DISORDERS
• NEOPLASMS

123
Q

Causes of renal hypertension (7)

A

Renal
• Acute glomerulonephritis
• Chronic renal disease
• Polycystic disease
• Renal artery stenosis
• Renal artery fibromuscular dysplasia
• Renal vasculitis
• Renin-producing tumors

124
Q

causes of endocrine hypertension

A

Endocrine
• •
•
•
•
Adrenocortical hyperfunction
(Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, licorice ingestion)
Exogenous hormones (glucocorticoids, estrogen [including pregnancy- induced and oral contraceptives], sympathomimetics and tyramine- containing foods, monoamine oxidase inhibitors)
Pheochromocytoma, acromegaly, HYPO-thyroidism (myxedema), HYPER-thyroidism
pregnancy-induced

125
Q

causes of cardiovascular hypertension

A

• Coarctation of aorta, polyarteritis nodosa (or other vasculitis)
• Increased intravascular volume

126
Q

CO is influenced by (4)

A

BLOOD VOLUME
atriopeptin
Na
mineralocorticoids

CARDIAC FACTORS

127
Q

what constricts? (5)

A 
angiotensin II
catecholamines
thromboxane
endothelin
leukotrines
128
Q

dilators (3)

A

NO
kinins
prostoglandins

129
Q

local factors that affect peripheral resistance

A

pH, hypoxia

autoregulation

130
Q

local factors that affect peripheral resistance

A

pH, hypoxia

autoregulation

131
Q

neural factors that affect peripheral resistance

A

dilators-alpha adrenergic

constrictors-beta adrenergic

132
Q

the juxtaglomerular cells release the enzyme renin….

A

If the perfusion of the juxtaglomerular apparatus in the kidneys decreases

133
Q

renin cleaves

A

• Renin cleaves an inactive peptide called
angiotensinogen, converting it into angiotensin I.

134
Q

Angiotensin I is then converted to angiotensin II by

A

angiotensin-converting enzyme (ACE), which is found mainly in lung capillaries.

135
Q

Angiotensin II is the major bioactive product of the renin-angiotensin system. Angiotensin II acts as

A

an endocrine, autocrine/ paracrine, and intracrine hormone.

136
Q

Often, benign or “malignant” hypertension is described as two different types of changes in arterioles, usually renal. These are described as…

A

1)Benign: Hyalization of arteriole wall
2)Malignant: Fibrinoid necrosis and “onion skinning” of arteriole wal

137
Q

true v false aneurysm

A

difference between a TRUE (endothelial expansion) and FALSE (NO endothelial expansion) aneurysm

138
Q

Non-atherosclerotic causes of aneurysms (5)

A

Congenital
• Luetic(Syphilitic)
• Traumatic
• “Mycotic”(Mis-leadingTerm) • 2° To Vasculitis

139
Q

Non-atherosclerotic causes of aneurysms

A

Congenital
• Luetic(Syphilitic)
• Traumatic
• “Mycotic”(Mis-leadingTerm) • 2° To Vasculitis

140
Q

2 main causes of aneurysms

A

1) atherosclerosis
2) cystic medial degeneration (necrosis), can be familial

141
Q

Most abdominal aortic aneurysms (AAA) occur

A

between the renal arteries and the bifurcation of the aorta

142
Q

Dissection

A

i.e., blood or hemorrhage disrupting the wall of a large artery) can be both a cause or an effect of an aneurysm.

143
Q

Vasculitides

A

inflammation of the blood vessels that causes changes in the blood vessel walls.

144
Q

Why are arteritides highly linked to autoimmune diseases

A

Because there are rarely any known causative external (i.e., infectious) pathogens, and many are associated with known auto- antibodies.

145
Q

“Temporal” Arteritis aka, Giant Cell Arteritis, GCA

A

• Mainly Arteries Of The Head And Temporal Arteries Are The Most Visibly, Palpably, And Surgically Accessible
• Blindness Most Feared Sequelae
• Granulomatous Wall Inflammation Diagnostic
• Often Associated With Marked ESR Elevation To Be Then Known As Polymyalgia Rheumatica
• Anti-neutrophil Ab’s Often Positive

146
Q

Takayasu Arteritis

A

• Involves aortic arch and other heavily elastic arteries, i.e., chief thoracic aorta branches, most commonly young Asian women
• FEMALES

SF test 8 (1 decks)

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