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Module 10 > Homeostasis > Flashcards

Homeostasis Flashcards

1
Q

what is the normal hemostatic process (3)

A

1. vasoconstriction: local neurohumoral factors induce a transient vasoconstriction

1. primary hemostasis: platelets adhere to exposed extracellular matrix (ECM) via von Willebrands factor and are activated undergoing shape change and granule release. released ADP and thromboxane A2 –> further platelet aggregation to form the primary hemostatic plug

3. secondary hemostasis: local activation of coagulation cascade results in fibrin polymerization, cementing platelets into definitive secondary hemostatic plug

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2
Q

how do platelets cause coagulation

A

cell membrane has phospholipids

enzymes in phospholipids is where coagulation will occur

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3
Q

what are the regulatory mechanisms in normal hemostatic process

A
  1. thrombus and antithrombotic events: release of tissue type plasminogen activator (t-pa) (fibrinolytic) and thrombomodulin (interfering with coagulation cascade), limit the hemostatic process to the site of injury

good control of clot formation

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4
Q

what are the activities of endothelial cells that favour thrombosis

A

damage –> allows platelet adhesion –> held together by fibrinogen

injury or activation of endothelial cells results in a procoagulant phenotype that augments local clot formation

membrane bound tissue factor: extrinsic coagulation sequence

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5
Q

what are endothelial cell activities that inhibit thrombosis

A

antithrombin III inactivates thrombin and factors Xa and IXa

tissue factor pathway inhibitor: inactivates tissue factors VIIa and Xa

intact endothelial cells serve primarily to inhibit platelet adherence and blood clotting

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6
Q

what are the 3 mechanisms that platelets undergo after injury and encounter of the ECM

A
  1. adhesion and shape change
  2. secretion
  3. aggregation
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7
Q

what stimulates the formation of a primary hemostatic plug

A

released ADP

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8
Q

what stabilizes and anchors the aggregated platelets

A

fibrin deposition

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9
Q

what do platelets expose

A

phospholipid complexes that are important in the intrinsic coagulation pathway

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10
Q

what do injured or activated endothelial cells expose

A

tissue factor which triggers extrinsic coagulation cascade

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11
Q

what is the process of coagulation

A

series of enzymatic conversions turning inactive proenzymes into activated enzymes

produces thrombin –> converts plasma fibrinogen into insoluble fibrin

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12
Q

how is the coagulation cascade divided

A
  1. instrinsic
  2. extrinsic
  3. common pathway
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13
Q

what does activation of the coagulation system also activate

A

the fibrinolytic system

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14
Q

what does the fibrinolytic system generate

A

plasmin

plasmin breakdown fibrin and interferes with its polymerization

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15
Q

what are the fibrin split products produced when plasmin breaks it down

A

D-dimers

fibrin degradation products

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16
Q

what is free plasmin converted to

A

rapidly complexes to alpha2-plasmin inhibitor and is inactivated

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17
Q

what is thrombocytopenia

A

decreased circulating platelets in the peripheral circulation

at risk for spontaneous hemorrhage

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18
Q

what are the clinical presentations of thrombocytopenia

A
  1. epitaxis
  2. ecchymoses: hemorrhagic bruises
  3. petechiae: pin point hemorrhages
  4. hematuria
  5. hematochezia: fresh blood in feces
  6. hyphema: bleeding in chamber of eye
  7. melena: partially digested blood in feces
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19
Q

when does hemorrhage soley due to thrombocytopenia occur

A

not usually until Plt = <50 x 10^9/L

pretty low before there is clinical signs

(reference is 200-500x 10^9/L)

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20
Q

how is thrombocytopenia diagnosed

A
  1. CBC
  2. smear examination: check for platelet aggregates, morphology and size
  3. manual platelet count: if numbers fall below the sensitivity of automated machine
21
Q

what are the causes of thrombocytopenia (4)

A
  1. increased destruction (primary (idiopathic) or secondary immune mediated destruction)
  2. decreased production: marrow disorders
  3. increased consumption: DIC, thrombosis
  4. increased sequestration: hypersplenism (rare)
22
Q

what are platelet disorders

A

have enough platelets but can’t do their job properly

23
Q

what are the clinical signs of platelet disorders

A

mucosal bleeding, hematuria, petechiae (not typical of vWD), ecchymoses

clinical signs may vary

but platelet numbers are normal

24
Q

how are platelet disorders diagnosed

A

platelet function test

buccal mucosal bleeding time (should stop in <4mins)

25
Q

what is factor VIII-von Willebrand factor (vWF) complex and how does it form and wherei is it present

A

factor VIII is synthesized in the liver and kidney and vWF is made in endothelial cells and megakaryocytes

the two associate to form a complex in the circulation

also present in the subendothelial matrix of normal blood vessels and the alpha granules of platelets

26
Q

what occurs to factor VIII-von Willebrand factor (vWF) complex when there is an endothelial injury (4)

A
  1. exposure of subendothelial vWF causes adhesion of platelets primarily via glycoprotein lb platelet receptor
  2. circulating vWF and VWF released from the alpha granules of activated platelets can bind exposed subendothelial matrix, further contributing to platelet adhesion and activation
  3. activated platelets form hemostatic aggregates; fibrinogen (and possibly vWF) participate in aggregation through bridging interactions with the platelet receptor gpIIb/III
  4. factor VIII takes part in the coagulation cascade as a cofactor in the activation of factor X on the surface of activated platelets
27
Q

what is a platelet function disorder

A

Von Willebrands disease

28
Q

what is von willebrands disease caused by

A

caused by quantitative and functional deficiencies in vWF

29
Q

what are the 3 types of von willebrands disease

A
  1. partial quantitative disorder
  2. loss of large molecular weight
  3. abscence
30
Q

what is the most common inherited disorder of hemostasis in dogs

A

von willebrands disease

31
Q

how is VWD disease evaluated

A
  1. BMBT (not specific for VWD)
  2. quantitative assay –> ELISA for vWF;Ag, reported as percentage of normal (<50% indicates vWF deficiency)
  3. functional assays: ristocetin cofactor assay, VWF collagen binding assay
32
Q

what is thrombocytosis

A

blood platelet concentration above reference interval

33
Q

what causes thrombocytosis (3)

A
  1. reactive thrombocytosis –> increased production (inflammation, iron deficiency, blood loss, nonhemic neoplasia)
  2. redistribution: physiologic (exercise, epinephrine)
  3. hemic neoplasia (involves platelet line): primary essential thrombocythemia, acute megakaryocytic leukemia
34
Q

what are the two types of clotting disorders

A
  1. acquired: vitamin K deficiency, severe hepatic disease, DIC
  2. hereditary: X-linked deficiency hemophilia A (FVIII) and B (FIX), FVII deficiency beagles
35
Q

how can bleeding manigest as in clotting disorders

A
  1. hematomas
  2. GI tract and urinary bleeding
  3. hemarthrosis
36
Q

what are examples of hereditary clotting disorders

A
  1. hemophilia A (FVIII) most common (dogs, cats, horses)
  2. hemophilia B (FIX): X-linked traits, males affected, hemarthrosis, hematomas
37
Q

how are clotting disorders diagnosed

A

both types cause prolongation of intrinsic/common pathway tests

specific diagnosis can be achieved testing with specific factor deficient plasma

38
Q

what are examples of acquired coagulopathies

A
  1. vitamin K deficiency: biliary obstruction, infiltrative bowel disease (inflammatory or cancer of bowel –> gut lining is thicker and makes it difficult for nutrients to be absorbed)
  2. vitamin K antagonism: coumadin (warfarin), 2nd generation anticoagulant rodenticides, affects FII, FVII, FIX, FX
39
Q

how are acquired coagulopathies diagnosed

A

in vitro tests

prolongation of PT (prothrombin time) and aPTT (activated partial thromboplastin time)

normal TCT (thrombin clotting time)

40
Q

what do in vitro clotting tests reqiure

A
  1. tissue factor for extrinsic pathway
  2. contact activator for intrinsic pathway
  3. exogenous source of phospholipids and calcium
41
Q

what parts of the pathway do the following tests analyze:

  1. activated partial thromboplastin time
  2. thrombin clotting time
  3. prothrombin time
A
  1. intrinsic/common pathway
  2. common pathway
  3. extrinsic/common pathway
42
Q

how is fibrinogen measured

A

modified claus method (thrombin initiated clotting rate)

rate of clot formation in diluted citrated plasma with addition of high concentration thrombin solution

43
Q

what does it mean that fibrinogen is a positive acute phase protein

A

sensitive indicator of inflammation

fibrinogen is

44
Q

whats virchow’s triad

A
45
Q

what is disseminated intravascular coagulation

A

an acquired syndrome characterized by the intravascular activation of coagulation with loss of localization resulting from different causes

it can originate from and cause damage to the microvasculature which if sufficiently severe can produce organ dysfunction

DIC is always a secondary phenomenon

46
Q

what are primary disease conditions that can lead to DIC

A
  1. neoplasia
  2. systemic inflammation
  3. endotoxemia
  4. sepsis
47
Q

how is DIC initiated

A

massive tissue trauma causes exposure of huge amounts of tissue factor

some conditions can induce TF expression

abberant expression of TF by intravascular cells (monocytes, tumour cells)

48
Q

what is the pathophysiology of disseminated intravascular coagulation

A
49
Q

how is DIC diagnosed

A

CBC: thrombocytopenia

  1. clotting times: aPTT and PT clotting times prolonged, hypofibrinogenemia
  2. elevated D-dimers (dogs)

Module 10 (27 decks)

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