Uiuc- Wallig, Exam 2- Veterinary Pathology-

Front 1

Define: Hyperemia

Back 1

Increased flow of blood in a tissue

Front 2

Causes of pathologic hyperemia

Back 2

1. accute inflammation
2. neovascularization

Front 3

Causes of physiologic hyperemia

Back 3

1. active muscles
2. GI tract after a meal
3. repro tract during estrus
4. blushing

Front 4

cardinal signs of inflammation

Back 4

1. rubor (redness)
2. calor (heat)
3. tumor (welling)
4. dolor (pain)

Front 5

Define Passive Congestion.

Back 5

distension of veins & venules with blood (also called passive hyperemia)

Front 6

local or regional congestion is caused by:

Back 6

impediment of venous flow (ex: thrombosis, external compression of a vein)

Front 7

systemic congestion is caused by

Back 7

heart failure

Front 8

appearance of congested tissue:

Back 8

dark red, purple, or blue

Front 9

Define: Cyanosis

Back 9

tissue is blue from congestion and deoxyhemoglobin (BEFORE death)

Front 10

Define: Hypostatic Congestion

Back 10

pooling of blood in dependent regions BEFORE death

Front 11

Define: Livor mortis

Back 11

postmortem lividity: dependent pooling of blood AFTER death

also called postmortem lividity

Front 12

appearance of liver in acute passive congestion:

Back 12

mildly swollen, dark red, oozes blood from cut surfaces

color contrast between congested centrilobular zones & less congested periportal zones gives a reticula rpattern, or 'nutmeg liver'

Front 13

appearance of liver with chronic passive congestion

Back 13

nutmeg pattern, reduced size, firm

Front 14

Define: Nutmeg liver

Back 14

a reticular pattern observed in the liver. often resulting from passive congestion

Front 15

Define: Jugular pulse

Back 15

distension & pulsation of jugular veins as a result of Right-Heart Failure

Front 16

T/F: Left heart failure, if prolonged, predisposes to right heart failure

Back 16

TRUE. increased pulmonary venous BP causes increased pulmonary arterial BP, which increases workload on the right heart, causing RHF.

Front 17

in LHR, increased pulmonary arterial BP directly causes:

Back 17

increased resistance to right cardiac output.

Front 18

T/F: Severe pulmonary effusion can be drained by the lymphatic vessels:

Back 18

False, it cannot be drained by lymphatics, which results in pulmonary edema. However, mild pulmonary effusion can be drained by the lymphatic tissues.

get effusion of fluid from blood vessels into alveolar spaces, which causes interference with gas exchange (get hypoxia & hypercapnia.... leading to acidosis)

Front 19

effusion of fluid from blood vessels into alveolar spaces during severe pulmonary effusion causes:

Back 19

hypoxia & hypecapnia... leading to acidosis

Front 20

appearance of chronic passive congestion in the lung:

Back 20

heavy, wet (oozes fluid & blood from cut surface), brown-tinged( because of hemosiderin within alveolar macrophages)

Front 21

Define: Hemorrhage by diapedesis

Back 21

leakage of erythrocytes across capillary walls

Front 22

Define: Heart failure cells

Back 22

Hemosiderin-laden macrophages within pulmonary alveoli secondary to CHRONIC passive congestion.

Note if severe enough, can impart a brown color to lung

Front 23

Define: Cor pulmonale

Back 23

RHF caused by pulmonary arterial hypertension.

Front 24

Causes of cor pulmonale:

Back 24

- emphysema
- pneumonia with vascular changes
- high altitude disease in cattle
- heartworm infestation in dogs

Front 25

Define: Dilation

Back 25

lumenal expansion within normal physiological limits

Front 26

Define dilation

Back 26

expansion of a lumen within normal physiological limits

Front 27

T/F Internal hemorrhage is outside of the body?

Back 27

False! it's inside the body

(always nice to have a confidence-booster)

Front 28

Define: melena

Back 28

when blood lost in the upper GIT turns dark black (tarry) as it is digested.

Front 29

What is the color of blood lost in the lower GIT?

Back 29

red

Front 30

When the rate of hemorrhage is slow, the body can survive more...
(a) internal hemorrhage than external
(b)external hemorrhage than internal

Back 30

A.... when the rate of hemorrhage is slow, the body is better at surviving when the hemorrhage is internal.

This is because blood constituents (fluid, protein, iron) can be recycled

Note: an exception to this is internal hemorrhage in critical locations (lungs, pericardial sac, and intracranially)

Front 31

When hemorrhage in the pericardial sac causes a build-up of external pressure, thus preventing cardiac filling, this is called_____.

Back 31

cardiac tamponade

Front 32

coughing caused by blood in airways _____ the hemorrhage:

(a) diminishes
(b) exacerbates

Back 32

B, coughing up blood exacerbates the hemorrhage.

Front 33

Why is intracranial hemorrhaging such a critical issue?

Back 33

the brain is in the rigid cranium, which cannot expand.

Front 34

How will intracranial hemorrhaging look grossly?

Back 34

- edematous brain & meninges
- cerebral gyri may be pressed flat
- cerebellum may herniate caudally out of the foramen magnum

Front 35

blue hemorrhage is caused by what?

Back 35

oxyhemoglobin & deoxyhemoglobin

Front 36

what is the cause of green hemorrhage?

Back 36

yellow + blue = green

yellow- from macrophages engulfing RBCs and forming bilirubin & biliverdin

dark red/blue- from oxyhemoglobin/deoxyhemoglobin

Front 37

what is the size of each of the following?
1- petechiae
2- ecchymoses
3- hematoma

Back 37

1- petechiae= pinpoint to few mm, multifocal

2- ecchymoses= several mm, multifocal

3= hematoma= large hemorrhage, usually 3-D.

Front 38

another word for contusion:

Back 38

bruise

Front 39

another word for petechiae or ecchymoses:

Back 39

purpura

Front 40

Define: Thrombocytopenia/thrombocytopathy

Back 40

reduced # or function of platelets

Front 41

T/F vasculitis is immune-mediated

Back 41

TRUE. precipitation of Ag-Ab complexes, which are chemotactic for neutrophils, result in vascular damage.

Front 42

T/F: Diffusely red tissue is indicative of hemorrhage

Back 42

FALSE!

It's indicative of: hyperemia, hypostatic congestion, Hb imbibition, and post-mortem lividity

Front 43

_____ is the disruption of RBCs and staining of tissues with free Hb

Back 43

Hemoglobin Imbibition

Front 44

what is the term used to describe hemorrhage into joints?

Back 44

hemoarthrosis

Front 45

Define: hyphema

Back 45

hemorrhage into anterior compartment of the eye.

Front 46

Define: Exsanguination

Back 46

severe acute hemorrhage, usually sufficient to cause death.

Front 47

What is the term used to describe systemic bleeding caused by deficiency of clotting factors?

Back 47

hemorrhagic or bleeding diathesis

Front 48

This term refers to EITHER hemorrhagic diathesis OR uncontrolled coagulation:

Back 48

coagulopathy

Front 49

during acute hemorrhage, the rapid compensation by the baroreceptor response leads to:

Back 49

peripheral vasoconstriction

Front 50

during cute hemorhage, a response from the renin-angiotension-aldosterone system causes:

Back 50

- vasoconstriction
- retention of Na & H2O

Front 51

the body's response to systemic hypotension (such as in acute hemorrhage) includes:

Back 51

1- compensation by baroreceptor response --> peripheral vasoconstriction

2-renin-angiotensin- aldosterone system --> vasoconstriction and retention of Na & H2O

3-release of ADH --> acts on nephron to promote water resorption

Front 52

Consequences of shock include:

Back 52

- decreased blood perfusion of tissues
- cellular hypoxia
- anaerobic metabolism
- acidosis
- cell death

Front 53

shock means:

Back 53

circulatory failure

Front 54

hypovolemic shock is caused by:

Back 54

-hemorrhage

-dehydration (diarrhea, vomiting, sweating, water deprivation)

Front 55

cardiogenic shock is caused by:

Back 55

heart failure

Front 56

septic shock can be caused by:

Back 56

- endotoxins
- Gram-positive bacteria
- fungal infections

Front 57

Neurogenic shock can be caused by:

Back 57

-anesthetic accidents
-CNS trauma

Front 58

anaphylactic shock is caused by:

Back 58

IgE binding of basophils & mast cells and the release of histamine & other vasoactive substances (arteriolar dilation results)

Front 59

non-progressive shock is also called:

Back 59

compensated shock

Front 60

during compensated shock, the decreased systemic BP initiates many compensatory measures. These include:

Back 60

Rapid Compensatory Measures=
- baroreceptor reflex (peripheral vasoconstriction)
-medullary reflexes
-catecholamine release from adrenals

Slower Compensatory Measures=
-renin-angiotensin cascade
-secretion of ADH from neurohypophysis

Front 61

Of the following, which is the least sensitive to hypoxia:

a. neurons
b. hepatocytes
c. renal epithelium
d. skeletal muscle
e.myocardiocytes

Back 61

D, skeletal muscle

Front 62

During uncompensated shock, the hypoperfusion of tissues causes hypoxia, which on the cellular level, causes:

Back 62

anaerobic cellular metabolism (less efficient production of ATP, adn causes systemic acidosis)

Front 63

Endothelial cells damaged from hypoxia release ___, which causes _____.

Back 63

Nitric oxide (NO)

systemic dilation of capillary beds

Front 64

hypoxic & acidotic damage to endothelium, combined with sludging of blood results in _______

Back 64

Disseminated Intravascular Coagulation (DIC)

Front 65

T/F: septic shock can be induced by injection of LPS alone.

Back 65

TRUE

Front 66

acute phase proteins are produced where?

Back 66

liver

Front 67

Clinical signs of shock include:

Back 67

-cold skin & etremities
-tachycardia (weak, rapid pulse)
-cyanotic mucous membranes
-slow capillary refill time
-weakness, disorientation

Front 68

What is Friedrickson-Waterhouse syndrome?

Back 68

adrenocortical hemorrhage & necrosis associated with septic shock.

occurs in people too.

Front 69

What is hemostasis?

Back 69

The arrest of bleeding.

Front 70

Hemostasis results in the formation of what?

Back 70

A hemostatic plug.

Front 71

What is a clotted mass of blood formed from the inappropriate activation of hemostatic mechanism?

Back 71

Thrombus

Front 72

What is a mass traveling in the blood stream?

Back 72

Embolism

Front 73

What are the great majority of emboli?

Back 73

Bits broken off of thrombi

Front 74

What is syneresis?

Back 74

Process of clot retraction that expels serum.

Front 75

What is the first step in hemostasis?

Back 75

Reflex vasoconstriction

Front 76

What is the second step in hemostasis?

Back 76

Activatin of platelets and formation of primary platelet plug

Front 77

What is the third step in hemostasis?

Back 77

Activation of coagulation cascases to form a terminal plug

Front 78

What is the fourth step in hemostasis?

Back 78

Confinement of platelet activity and coagulation to the site of injury

Front 79

What is the fifth step in hemostasis?

Back 79

Resolution of the hemostatic plug by fibrinolysis or fibrosis

Front 80

What do the multiple initiators in hemostasis do?

Back 80

activate platelets and coagulation factors, amplify cascades by feedback loops, inhibit platelets and coagulation factors, and dissolve fibrin

Front 81

How is hemostasis initiated?

Back 81

by alteration of the endothelium

Front 82

What are the two coagulation cascades?

Back 82

Intrinsic and extrinsic

Front 83

How do the coagulation cascades terminated?

Back 83

In a common pathway

Front 84

The terminal path of the coagulation cascades produces what?

Back 84

Thrombin and ultimately fibrin

Front 85

Most coagulation factors are _________ that are synthesized in the liver.

Back 85

proteins

Front 86

Coagulation profactors must be post-translationally modified in what way in order to be processed?

Back 86

In a vitamin K dependent process

Front 87

Each step in coagulation cascades consist of ____________________

Back 87

A complex of an activated coagulation factor and an inactivated coagulation factor

Front 88

Thrombosis is predisposed by?

Back 88

Virchow's Triad

Front 89

Define: Virchow's Triad

Back 89

1. Injury to vascular wall
2. Altered blood flow as a result of stasis or turbulence
3. Hypercoagulability

Front 90

Examples of Vascular Injury

Back 90

1. trauma
2. infection
3. Immune-mediated disease
4. degenerative/metabolic

Front 91

Mechanism of Vascular Injury

Back 91

exposes underlying collage or causes release of tissue factor from endothelium

Front 92

Mechanism of Stasis

Back 92

1. allows platelets to settle and contact endothelium.
2. prevents clotting factors from being swept away

Front 93

Causes of stasis:

Back 93

1. shock,
2. cardiac arrhythmias
3. prolonged immobility
4. focal myocardial fibrosis (area of non-contraction and focal stasis)
5. abnormally shaped RBC's which lodge in capillaries

Front 94

mechanism of turbulence

Back 94

disrupts laminar flow which allows platelets to contact endothelium

Front 95

causes of turbulence:

Back 95

1. cardiomyopathy
2. arterial aneurysms
3. stenotic or insufficient cardiac valves
4. erythrocyte abnormalities

Front 96

acquired hypercoagulable conditions: (4)

Back 96

1. nephrotic syndrome:
a. glomerular damage=
b. loss of small proteins in urine=
c. hypoalbuminemia, edema, and hypercoagulability from deficient AT-III
2. increasing age (decreased prostacyclin production)
a. dec PGI2=
b. incr tendency of platlet agregation
c. thats why older ppl take aspirin
3. vasculidites (arteritis or phlebitis)
a. from endothelial infection or immune-med damage
4. certain cancers may produce tissue factor

Front 97

inherited hypercoagulable conditions: (1)

Back 97

inherited deficiencies of anticoagulant proteins: AT-III, Protein C, Protein S

Front 98

Characteristics of Arterial Thrombosis

Back 98

1. often occlusive (infarction in endarterial supply, ex:renal cortex)
2. grow retrograde
3. "lines of Zahn" are seen histologically. Alternating laminae of pale fibrin and platelets, and darker erythrocytes

Front 99

Characteristics of venous thrombosis (phlebothrombosis)

Back 99

1. at autopsy, hard to distiguish from post-mortem clots
2. adhered to vascular wall, while post mortem not
3. postmortem clots usually have a dark red dependent portion, and a clear or tan, gelatinous superficial portion

Front 100

Fates of thrombi

Back 100

1. propagation (enlargement)
2. embolization (fragment into blood)
3. dissolution (by plasmin)
4. organization and recanalization
a. incorporation into wall and blood flow reestablished around it
b. occlusive, but undergoes fibrosis and vascular channels form through it
5. infection (fertile soil for bacteria)
a. septic vs bland

Front 101

Fates of emboli

Back 101

1. lodge (hard to distinguish from primary thrombus)
a. mult infarc or thrombi in kidney suggest emboli from left cardiac valves
2. 99% of emboli from thrombi but could also be foreign mat, gases, cartilage, lipid
3. Feline dilitative cardiomyopathy: form mural thrombi in left heart which may break and lodge in distal aorta

Front 102

define; saddle thrombis

Back 102

embolus lodged in vascular birfurcation

Front 103

define: infarct

Back 103

area of necrosis caused by occlusion of blood flow.

Front 104

Causes of Infarcts

Back 104

arterial or venous thrombosis

Front 105

describe infarcted tissue grossly

Back 105

necrotic tissue appears pale and edges reddened. A rim forms around the infarct as a result of vasodilation and neovascularization. Many infarcts are wedge-shaped or symmetrical, reflecting anatomy of vascular supply.

Front 106

describe infarcted tissue histologically

Back 106

necrotic

Front 107

define: white, pale, or anemic infarcts

Back 107

1. affected tissue is pale due to occlusion of arterial supply
2. occur most often in solid organs with end arterial supply (kidney, spleen, heart)

Front 108

define: red infarcts

Back 108

1. affected tissue is red or purple from hemorrhage or engorgement of veins
2. hemorrhage occurs in loose tissue (lung, liver) with dual blood supply (lung, intestine), or as a result of venous infarct (ovary, testis, spleen)
3. infarcts can also hemorrhage after lysis of the occluding thromboembolus

Front 109

define: septic and bland infarcts

Back 109

1. infarction may result from occlusion by septic embolus, thrombosis may be predisposed by septicemia or bacteria may invade thrombi and necrotic tissue
2. septic infarcts usually become abscesses

Front 110

What is von Willebrand's disease?

Back 110

an inherited deficiency of vWF which impedes formation of the primary platelet plug and associated coagulation. In such animals, prolonged bleeding but normal platelet count is seen.

note: highest prevalence is in Doberman pinscher

Front 111

a deficiency of factor VIII causes:

Back 111

Hemophilia A. it's a sex-linked trait

Front 112

a deficiency of factor IX causes:

Back 112

Hemophilia B, can be sex-linked

Front 113

Anticoagulant rodenticides inhibit ____, which is produced in the ____.

Back 113

Vitamin K, Liver

its production in the liver is inhibited, causing Vit. K-dependent coagulation factors in the blood to become depleted.

Front 114

These animals see sweet clover poisoning:

Back 114

livestock.

Front 115

Sweet clover poisoning contains onnocuous ______ chemicals

Back 115

coumarin

Front 116

Most coagulation enzymes are synthesized by the ______, and this organ's fialure can cause a terminal coagulopathy

Back 116

LIVER

Loss of 80% of liver can result in inadequate production of coagulation factors and terminal hemorrhagic diathesis

Front 117

The most common bleeding disorder in dogs and cats is______.

Back 117

Thrombocytopenia

Front 118

Define Thrombocytopenia:

Back 118

decreased numbers of platelets.

It can be due to increased destruction or decreased production of platelets.

Front 119

Increased destruction of platelets is one cause of Thrombocytopenia. What are some causes of the increased destruction?

Back 119

- immune mediated thrombocytopenia (IMTP)
-drug-induced thrombocytopenia
-administration of modified-live virus vaccines
-rickettsial infections
-viral infections

Front 120

Decreased production of platelets is one of two causes of Thrombocytopenia. What can cause this decreased production?

Back 120

- neoplasia effacing bone marrow
-aplastic anemia (chloremphenicol toxicosis)
-radiation

Front 121

Disseminated Intravascular Coagulation (DIC) is also called;

Back 121

consumption coagulopathy

Front 122

What are the two general mechanisms that can trigger DIC?

Back 122

1- excessive release of coagulation activating substances into circulation

2-widespread injury to endothelial cells

Front 123

Conditions that can result in DIC:

Back 123

-extensive necrosis
-shock
-vasculitis
-sepsis
-various cancers
-burns
-systemic viral diseases
-heat stroke
-snake bite
-acute pancreatitis
-polycythemia (incr. concentration in RBCs)
-the nephrotic syndroms (renal loss of AT-III)

Front 124

DIC can be clinically confirmed by:

Back 124

-elevated FDP's
-thrombocytopenia
-hypofibrinogemia
-presence of acanthocytes & schistocytes

Front 125

Hemostatic reaction usually takes place on ____________

Back 125

a phospholipid membrane usually provided by platelets in the presence of Ca++

Front 126

What must happen to coagulation profactors in order to be functional?

Back 126

Must be post-translationally modified in a Vitamin K dependent process in order to be functional

Front 127

What are the Vitamin K dependent clotting factors?

Back 127

Prothrombin (II), VII, IX, X

Front 128

Vitamin K deficiency is rare or common?

Back 128

Rare

Front 129

What inhibits the action of Vitamin K in the production of coagulation factors?

Back 129

Coumarin (Warfarin)

Front 130

Hemostatic events initiate_______

Back 130

Inflammation, specifically secretion of vasoactive amines and chemotatic factors and increased expression of leukocyte adhesion molecules

Front 131

What is the anticoagulant state?

Back 131

Normal resting state of blood and endothelium

Front 132

What forms a barrier to prevent platelets and clotting factors from exposure to underlying procoagulant factors?

Back 132

Endothelium

Front 133

Resting endothelium expresses ______________

Back 133

An antiplatelet, anticoagulant, and fibronolytic phenotype

Front 134

In the procaogulant state of hemostasis, what is secreted and what is it?

Back 134

Endothelin (vasoconstrictor)

Front 135

What happens to endothelial cells in the procoagulant state?

Back 135

Endothelial cells are retracted to expose underlying collagen, tissue factor, and vWF

Front 136

The endothelium in the procoagulant state secretes ____________

Back 136

Plasminogen activator inhibitor (PAI)

Front 137

What is a neuorgenic reflex that occurs in response to endothelial injury and also causes secretion of endothelin?

Back 137

Transient vasoconstriction

Front 138

What happens when platelets are exposed to collagen and other subendothelial factors?

Back 138

They become activated and adhere to collagen via vWF

Front 139

What do platelet secretory granules secrete?

Back 139

ADP, thromboxane (TXA)2, Ca++, vasoactive amines, coagulation factors, and growth factors (PDGF, TGF-beta)

Front 140

T/F Early platelet adhesion during stasis is reversible?

Back 140

T

Front 141

Aggregation of platelets that are activated in hemostasis form what?

Back 141

The primary platelet plug

Front 142

What causes the primary platelet plug to grow?

Back 142

ADP, TXA2

Front 143

Where is tissue factor located?

Back 143

Endothelial membranes

Front 144

What happens when endothelium is damaged, as far as tissue factor is concerned?

Back 144

Tissue factor is exposed to plasma

Front 145

What happens when plasma is exposed to tissue factor?

Back 145

Extrinsic coagulation cascade is initiated

Front 146

What activates the intrinsic coagulation cascade?

Back 146

Exposre of sunendothelial collagen and High Molecular Weight Kininogen

Front 147

What happens when fibrinogen is converted to fibrin?

Back 147

Fibrin polymerization

Front 148

Thrombin is absorbed to _____

Back 148

Fibrin

Front 149

Fibrin is inactivated in the blood by ___________

Back 149

AT-III

Front 150

What increases the activity of AT-III?

Back 150

Heparin

Front 151

Heparin is secreted by _________ and __________

Back 151

basophils and mast cells

Front 152

How are platelet aggregation and and coagulation confined to the region of endothelial damage?

Back 152

Endothelial secretion of inhibiting and fibrinolytic factors adjacent to the injury and by blood flow

Front 153

What happens to plasminogen trapped within clots?

Back 153

It is slowly converted to plasmin by the action of tissue plasminogen activator (t-PA)

Front 154

Breakdown of fibrin forms __________

Back 154

Fibrin degradation products

Front 155

Fluid accumulation in the peritoneal cavity

Back 155

hyroperitoneum or acites

Front 156

Fluid accumulation in the thorax

Back 156

hydrothorax

Front 157

Fluid accumulation within the pericaridal sac

Back 157

hydropericardium

Front 158

Generalized edema, usually in the fetus

Back 158

anasarca

Front 159

Some things that lead to edema (there are 9 in the notes!)

Back 159

inflammation, heart failure, pulmonary disease, renal disease, hepatic disease, gastrointestinal disease and pancreatic disease, neoplasia, malnutrition, certain types of parasitism

Front 160

Edema can the be the result of?
(4 different situations)

Back 160

blood pressure, osmotic pressure, endothelial integrity, lymphatic drainage

Front 161

Consequences of edema vary according to severity and location. What are three locations in the body that edema can form in and what happens if edema is there?

Back 161

1. skin=room to swell
2. brain=no room
3. lung=intereferes with gas exchange

Front 162

Edema in the lungs can lead to...

Back 162

hypoxia, hypercapnia, acidosis

Front 163

What is the gross appearance of tissues with edema?

Back 163

swollen
heavy
wet
widening of fascial planes
gelatinous (pitting edema)

Front 164

Appearance of inflammatory edema vs. noninflammatory edema

Back 164

inflammatory: dark, gelatinous
noninflam: pale yellow and watery

Front 165

Histological appearance of edema?

Back 165

thickening, widening of tissue
clear, empty spaces bt collagen fibers and cells
lymphatic vessels are dilated
alveolar spaces are bigger than they should be

Front 166

Unclassified fluid?

Back 166

effusion

Front 167

effusion with low protein and low cellularity

Back 167

transudate

Front 168

effusion with high protein and high cellularity

Back 168

exudate

Front 169

an effusion with high protein and low cellularity or low protein and high cellularity

Back 169

modified transudate (has properties between exudate and transudate)

Front 170

Dissolved particles?

Back 170

solute

Front 171

liquid that particles are in?

Back 171

solvent

Front 172

where does exchange of water always occur?

Back 172

in beds of capillaries or small venules

Front 173

osmotic pressure due to proteins is called?

Back 173

colloid osmotic pressure or oncotic pressure

Front 174

the majority of colloidal osmotic pressure is due to what protein? synthesized where?

Back 174

albumin, synthesized in liver

Front 175

What grows aroud the clot in hemostasis?

Back 175

Endothelium

Front 176

Which pathway is more rapid and more easily activated in hemostasis?

Back 176

Extrinsic pathway

Front 177

Which pathway in hemostasis is more important in extensive injuries?

Back 177

Intrinsic pathway

Front 178

T/F Vitamin K is a coagulation factor

Back 178

F

Front 179

Where is vWF located?

Back 179

Circulation and subendothelial matrix

Front 180

where are hydrostatic pressures greatest?

Back 180

arteriolar side of capillary

Front 181

where are hydrostatic forces lowest?

Back 181

in the interstitium

Front 182

things that tend to pull water out of vessels?

Back 182

blood pressure and osmotic pressure

Front 183

things that tend to pull water into blood?

Back 183

hydrostatic pressure

Front 184

Is there a difference bt the composition of normal lymph fluid and normal interstitial fluid?

Back 184

not much difference in the composition

Front 185

Does dehydration cause net flow of water into or out of the interstitium?

Back 185

out of interstitium into capillaries

Front 186

Does accute hemorrhage cause net flow of water into or out of the capillaries?

Back 186

into the capillaries out of the interstitium

Front 187

what causes edema by increasing blood pressure?

Back 187

1. hyperemia
2. local passive congestion

Front 188

Is hyperemia a local or systemic process?

Back 188

local

Front 189

when edema results from increased venous blood pressure instead of increased arterial blood pressure, this is called?

Back 189

local passive congestion

Front 190

Heart failure has the same effects as local passive congestion, except?

Back 190

it is regional or systemic, not local

Front 191

How can RHF lead to ascites?

Back 191

RHF-->passive congestion of liver-->increase portal venous bp-->increased mesenteric and intestinal venous bp-->ascites

Front 192

How can decompensated left heart failure lead to death?

Back 192

LHF-->pulmonary edema-->interference with gas exchange--> hypoxemia-->further depression of cardiac function-->death

Front 193

hypoproteinemia is generally synonymous with?

Back 193

hypoalbuminemia

Front 194

Things that cause hypoproteinemia by decreasing protein synthesis?

Back 194

1. protein malnutrition
2. end stage liver disease

Front 195

Things that cause hypoproteinemia by increasing protein loss?

Back 195

1. parasitism
2. renal disease (a. glomerular amyloidosis, b. glomerulonephritis)
3. gastrointestinal disease
4. extensive cutaneous burns

Front 196

Things that cause edema by impairing lymph drainage?

Back 196

1. lymphangitis or lymphadenitis
2. blockage of lymph vessels by invasive or metastatic cancer

Front 197

what is the sequence of events of inflammatory edema?

Back 197

1. damage to endothelium
2. leakage of protein across capillary walls
3. increased interstitial colloid osmotic pressure
4. fibrin strands form on serosal surfaces

Front 198

Presence of fibrin is proof of?

Back 198

damaged leaky endothelium

Front 199

high protein in edema stains what color?

Back 199

pale pink

Front 200

What does vWF do?

Back 200

Anchors platelets to subendothelial collagen

Front 201

If vWF levels are insufficient, what happens to factor VIII levels?

Back 201

Factor VIII levels may also be suboptimal

Front 202

In hemostasis, fibrinogen is also known as ______

Back 202

I

Front 203

In hemostasis, Ia is also known as __________

Back 203

Fibrin

Front 204

In hemostasis, II is also known as ___________

Back 204

Prothrombin

Front 205

In hemostasis, Thrombin is also known as _________

Back 205

IIa

Front 206

In hemostasis, tissue factor is also known as ___________

Back 206

Thromboplastin, Factor III

Front 207

In hemostasis, Xa is also known as ____________

Back 207

Prothrombin activator

Front 208

In hemostasis, Hageman factor is also known as __________

Back 208

XII

Front 209

In hemostasis, V is also known as ___________

Back 209

Proaccelerin

Front 210

In hemostasis, fibrin stabilizing factor is also known as ______________

Back 210

XIII

Front 211

What is the order of the intrinsic coagulation cascade in hemostasis?

Back 211

1. Contact activation with collagen 2. Factor VII is turned in Factor VIIa in presence of HMWK 3. XIIa converts XI to XIa 4. XIa converts IX (K dependent) to IXa 5. IXa converts X to Xa 6. Xa is part of the common pathway

Front 212

What is the order of the extrinsic coagulation cascade in hemostasis?

Back 212

1. Release of a tissue factor complex from damaged cells 2. Factor VII converted to Factor VIIa 3. Factor VIIa converts X to Xa 4. Xa is part of common pathway

Front 213

What is the order of the common coagulation cascade in hemostasis?

Back 213

1. Factor Xa from either intrinsic or extrinsic cascade 2. Factor Xa converts prothrombin (K dependent) to thrombin 3. Thrombin converts fibrinogen to fibrin 4. Fibrin monomers spontaneously form linear fibrin polymers 5. Fibrin polymers are strengthened and form numerous covalent cross-links by the action of fibrin stabilizing factor.

Front 214

GUARANTEED EXAM QUESTION:
what starts coagulation in vivo?

Back 214

tissue factor

Front 215

GUARANTEED EXAM QUESTION:
what is the most critical step in coagulation?

Back 215

thrombin formation

Front 216

GUARANTEED EXAM QUESTION: why can't factor 10 leak out of tissue?

Back 216

because it is immediately destroyed

Front 217

GUARANTEED EXAM QUESTION:
The major antithrombotic effect is against which factors?

Back 217

10a and 2a

Front 218

GUARANTEED EXAM QUESTION:
______ can be measured in circulation, and are indicative of fibrin degradation (that an active clot was formed)

Back 218

D-Dimers

Front 219

GUARANTEED EXAM QUESTION:
Measuring D-dimers in the circulation is a measure of _____ degradation.

Back 219

Fibrin (NOT fibrinogen)

Front 220

What are the Vitamin K-dependent coagulation factors?

Back 220

2, 7, 9, 10, PC, PS