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B & L > Patho > Flashcards

Patho Flashcards

1
Q

Excessive bleeding can result from:

A
  • Vessel abnormalities
  • Platelet abnormalities (deficiency or dysfunction)
  • Coagulation derangements
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2
Q

Primary Hemostasis

A
  • Platelet/ vascular problem
  • Onset: spontaneous, immediate after trauma
  • Sites: skin, mucous membranes
  • Form: petechiae, ecchymosis
  • Mucous membrane: common (nasal, oral, GI, GU)
  • Other sites: rare
  • Clinical examples: Thrombocytopenia, platelet defects, vWD, scurvy
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3
Q

Secondary Hemostasis

A
  • Coagulation factor problem
  • Onset: delayed after trauma
  • Sites: Deep tissues
  • Form: hematomas
  • Mucous membrane: less common
  • Other sites: joint, muscle, CNS, retroperitoneum
  • Clinical examples: Factor deficiency, liver disease, acquired inhibitors
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4
Q

Vascular abnormalities

A
  • Infections
  • Drug reactions (often related to hypersensitivity vasculitis due to immune complex deposition)
  • Scurvy, Ehler-Danlos (collagen defects in vessel walls)
  • Henoch-Schonlein purpura (immune complex deposition)
  • Hereditary hemorrhagic telangiectasia (Weber-Osler-Rendu Syndrome - dilated tortuous vessels that bleed easily
  • Amyloidosis (weakens vessel walls)
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5
Q

Causes of thrombocytopenia

A

Decreased production
Decreased survival
Sequestration
Dilution

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6
Q

Immune thrombocytopenia

A

> Destruction caused by deposition of antibodies or immune complexes on platelets
>Can be autoantibodies (recognize self antigens)
>Can be alloantibodies

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7
Q

Where do alloantibodies for thrombocytopenia come from?

A

> Can arise when platelets are transfused
Can arise when platelets cross placenta
>IgG from mother can cause fetal thrombocytopenia

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8
Q

Non-immune causes of decreased platelet survival in thrombocytopenia

A

> Mechanical injury- heart valves
Disseminated intravascular coagulation (DIC)
Thrombotic microangiopathies

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9
Q

Chronic Immune Thrombocytopenic Purpura (ITP)

A

> Caused by autoantibody mediated platelet destruction

|&raquo_space;Primary or idiopathic (diagnosis of exclusion)

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10
Q

Secondaries for Chronic ITP

A

> Systemic lupus erythematosis
HIV
B-cell neoplasms such as chronic lymphocytic leukemia
Many others

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11
Q

Pathogenesis of chronic ITP

A

> Autoantibodies most often directed against platelet surface glycoproteins IIb/IIIa or Ib-IX (typically IgG)
Anti-platelet Ab act as opsonins
>IgG Fc receptor recognition by macrophages in the reticuloendothelial system (spleen)
>Megakaryocytes may also be affected → further thrombocytopenia
>Splenectomy seems to help many patients (no more phagocytosis or autoantibody)

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12
Q

Clinical aspect of chronic ITP

A
  • Females <40
  • Insidious onset
  • Cutaneous bleeding (petechiae, ecchymoses, melena, hematuria, menorrhagia)
  • History of…easy bruising, nosebleeds, gum bleeding, soft tissue hemorrhages (with minor trauma)
  • Complications: subarachnoid or intracerebral hemorrhage
  • Uncommon: splenomegaly, lymphadenopathy
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13
Q

Labs of chronic ITP (diagnosis of exclusion)

A
  • low platelet count
  • large platelets on peripheral blood smear
  • normal or increased megakaryocytes in bone marrow
  • normal PT and PTT
  • platelet autoantibody tests
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14
Q

Treatment/prognosis of chronic ITP

A

> glucocorticoids (inhibit phagocyte function) (may respond, many relapse)
spontaneous remission within one or more years possible
splenectomy for severe thrombocytopenia (increased risk of infections)
immunomodulation (if splenectomy fails or is contraindicated)
>IVIG
>rituximab (anti-CD20 antibody)
peptides mimicking thrombopoietin (TPO-mimetics)

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15
Q

Acute ITP

A
  • mainly in children
  • likely triggered by viral illness (1-2 weeks post-illness)
  • self-limited mostly
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16
Q

Mechanisms of drug-induced thrombocytopenia

A

Direct destruction
Immune-mediated destruction
Drug instigates autoantibody (rarer)

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17
Q

Most common drugs causing drug-induced thrombocytopenia

A

> Bind platelet glycoproteins (IIb/IIIa)→ antibody recognition of antigenic determinants
>Quinine
>Quinidine
>Vancomycin

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18
Q

Heparin-induced thrombocytopenia (HIT)

A

Potentially deadly, arterial and venous thrombosis, limb loss or threatened loss, and/or pulmonary thromboembolism

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19
Q

Two types of HIT

A

> Type I: not usually clinically significant
>Rapid onset after therapy, likely secondary to platelet aggregating effect
Type II: (clinically significant - less common)
>Occurs 5-14 days after therapy initiation, sooner if pre-sensitized

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20
Q

Type II HIT

A

> Causes (paradoxical) thrombosis, not bleeding
(unfractionated heparin, but may still occur with LMWH -
almost never occurs with fondaparinux)
Mechanism
>Antibodies to heparin-platelet factor 4 (PF4) complex
»>PF4 is produced by activated platelets
>Antibody binding causes further platelet activation, even if thrombocytopenia
>Get aggregation and consumption, leads to prothrombotic state

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21
Q

HIV-Associated thrombocytopenia pathophysiology

A

> CD4 and CXCR4 on megakaryocytes
(can become HIV-infected >
leads to apoptosis and impaired platelet production)
B-cell hyperplasia/dysregulation leading to autoantibody formation against platelet GPIIb-IIIa (destruction in spleen)

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22
Q

Thrombotic Microangiopathies

A

> Caused by insults that lead to excessive platelet activation
>Deposit as thrombi in small blood vessels
>Cause microangiopathic hemolytic anemia
>Leads to widespread organ dysfunction
>Results in thrombocytopenia secondary to consumption
PT, PTT usually normal

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23
Q

Thrombotic Thrombocytopenic purpura (TTP) pentad

A 
Fever
microangiopathic hemolytic Anemia
Thrombocytopenia
Renal insufficiency
Neurologic symptoms (FATRN)
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24
Q

Hemolytic-uremic syndrome (HUS)

A
  • Children

- Lacks fever and neurologic symptoms

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25
Q

TTP pathophysiology

A

> ADAMTS13 (vWF metalloprotease) deficiency
>ADAMTS13 is normally responsible for degrading very high-molecular-weight multimers of von Willebrand factor (vWF)
>Without degradation, persistent multimers promote platelet activation and aggregation

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26
Q

Acquired form of TTP

A
  • More frequent

- Typically due to autoantibody that inhibits ADAMTS13

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27
Q

Hereditary form of TTP

A
  • Onset typically in adolescence, episodic symptoms

- Endothelial cell injury caused by other conditions may instigate or aggravate TTP

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28
Q

HUS pathophysiology

A

-Normal levels of ADAMTS13
-Typical: gastroenteritis with E. Coli
»produces Shiga-like toxin>
absorbed into circulation from damaged/inflamed GI mucosa >alters endothelial cell function >leads to platelet activation and aggregation
-Atypical: associated with defects, inherited or acquired, in:
»complement factor H (CFH)
»membrane cofactor protein (MCP or CD46)
»complement factor I (CFI)
»basis of platelet activation is unclear

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29
Q

HUS clinical/symptoms/treatment/pronosis

A

-Typical
»Mostly children and older adults
»Present with bloody diarrhea, followed by HUS a few days later
»Complete recovery with supportive care, but some may have irreversible renal damage or death
-Atypical
»Often remitting, relapsing course
»Treatment:
-Antibodies that inhibit activation of complement factor 5 for some inherited forms
-Immunosuppression for those with inhibitory autoantibodies

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30
Q

Bernard-Soulier Syndrome

A
  • Inherited adhesion defect
  • Autosomal recessive
  • deficiency in GPIb
  • clinically significant bleeding
  • Labs: markedly increased platelet size, moderate decrease in numbers
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31
Q

Glanzmann thromboasthenia

A
  • Inherited aggregation defect
  • Autosomal recessive
  • Deficiency or dysfunction in GPIIb/IIIa
  • bleeding tendency can be severe
  • Labs: platelets normal in number and size, solo w/o clumping
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32
Q

Secretion defects of storage pool disorders

A

Hermanski-Pudlak syndrome

Chediak-Higashi syndrome

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33
Q

Acquired platelet function disorders

A

Aspirin or nonsteroidal anti-inflammatory drugs
-Inhibits COX&raquo_space; required for TXA2
-Aspirin = irreversible inhibitor
Uremia
-impairs adhesion, aggregation, and granule secretion

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34
Q

Thrombin activates factors…

A

XI, V, and VIII

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35
Q

Factor VIII made in….

A

Liver sinusoidal and Kupffer cells and other areas

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36
Q

vWF made by…and is circulated and secreted into…

A

endothelial cells and megakaryocytes; subendothelial matrix

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37
Q

vWF plays a role in primary and secondary hemostasis, which involve ________ and ___________, respectively

A

platelet adhesion; stablizing fVIII

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38
Q

Von Willebrand Disease (VWD)

A
  • Most common inherited bleeding disorder
  • Generally associated with mild bleeding tendency
  • Clinically and molecularly heterogeneous
  • Mostly autosomal dominant, but rare autosomal recessive forms
  • VWF gene on chromosome 12p
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39
Q

Type 1 VWD

A
  • quantitative defects
  • Most common
  • Autosomal dominant (spectrum of mutations, including point substitutions that interfere with maturation or result in rapid clearance)
  • Mild to moderate vWF deficiency, generally mild disease
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40
Q

Type 3 VWD

A
  • quantitative defects
  • Autosomal recessive (usually deletions or frameshift mutations involving both alleles)
  • Very low levels of vWF, correspondingly severe clinical disease (some bleeding characteristics of hemophilia due to decreased stability of factor VIII)
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41
Q

Type 2 VWD

A
  • Qualitative defects

- 2A (most common, autosomal dominant, normal quantities of vWF > missense mutations lead to defective multimers)

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42
Q

VWD Labs

A

-Patients with vWD have platelet function defects despite normal platelet numbers (prolonged bleeding time)
-Plasma levels of active vWF are reduced
»Secondary decrease in factor VIII
»Prolonged PTT
-Wide variability in clinical expression, even within families

43
Q

VWD Treatment

A

-typically prophylactic
»Desmopressin (DDAVP) – stimulates vWF release
»Plasma concentrates with factor VIII and vWF

44
Q

Hereditary derangements typically involve….

A

A single factor

45
Q

Hemophilia A is a deficiency in…

A

Factor VIII

46
Q

Hemophilia B is a deficiency in…

A

Factor IX

47
Q

Acquired coagulation derangements involve….

A

Multiple coagulation factors

48
Q

Vitamin K deficiency infleunces coagulation factors…

A

Factors II, VII, IX, and X

Proteins S and C

49
Q

Disseminated intravascular coagulation involves…

A

Consumption of multiple factors

50
Q

Hemophilia A

A

-Most common hereditary disorder associated with life-threatening bleeding
-Factor VIII mutation(s) on chromosome X
»X-linked recessive inheritance
»Mostly affects males, with rare bleeding in heterozygous females
-30% without a family history (de novo mutation)

51
Q

Severity of Hemophilia A

A

<1% VIII activity: severe
2-5%: moderate
6-50%: mild

52
Q

Most severe mutation of Hemophilia A

A

Inversion involving X chromosome that abolishes synthesis of factor VIII

53
Q

Clinical signs of Hemophilia A

A
  • Easy bruising
  • Massive hemorrhage after trauma or procedures
  • Spontaneous hemorrhage (includes into joints - recurrent can cause joint deformities)
  • Petechiae absent
54
Q

Labs of Hemophilia A

A
  • Normal PT
  • Abnormal PTT
  • Factor VIII-specific assays required for diagnosis
55
Q

Hemophilia A treatment

A
  • Recombinant factor VIII (some develop antibodies»therapeutic challenge)
  • Previously, transfused with plasma-derived factor VIII»HIV
56
Q

Hemophilia B Characteristics

A
  • Not as common
  • Wide spectrum of mutations (X-linked recessive), variable severity
  • Prolonged PTT, normal PT (need factor IX testing)
  • Treat with RF IX
  • Christmas Disease
57
Q

Liver disease may be associated with…

A

-Reduced synthesis of factors and prolonged TT
-Decreased production of anticoagulant proteins
»can be associated with thrombotic or bleeding complications
-Severe = prolonged PT and PTT
-vitamin K-dependent proteins decreased
-can get inhibitor-like activity from abnormal fibrinogens

58
Q

Factors that limit coagulation

A
  • Dilution –blood flow washes out factors
  • Need for negatively charged phospholipid (provided by activated platelets)
  • Factors expressed by intact endothelium adjacent to injury
  • Fibrinolytic cascade
59
Q

Fibrinolytic cascade

A
  • Limits size of the clot, contributes to later dissolution
  • Plasmin – breaks down fibrin, interferes with its polymerization
  • Fibrinogen breakdown products (fibrin degradation/split products, fibrin-derived D-dimers) can be measured in thrombotic states
60
Q

Plasmin

A

-Generated from plasminogen by intrinsic pathway or plasminogen activators (t-PA)

61
Q

t-PA

A
  • Synthesized by endothelium
  • Active when bound to fibrin
  • Useful therapeutic agent – activity confined to sites of recent thrombosis
62
Q

Plasmin controlled by counter-regulatory factors once activated, like….

A

Alpha2-plasmin

63
Q

Three major anticoagulant systems that regulate enzymes of the coag protein system

A

Protein C/S system
-When activated, reduces thrombin formation, stimulates fibrinolysis, initiates inflammation to reduce thrombosis risk

Plasma serine protease inhibitor system – mainly antithrombin (AT III)

  • Inhibits factors IIa (thrombin) and Xa
  • Heparin interaction

TFPI- Tissue factor pathway inhibitor

64
Q

How does the endothelium limit coagulation?

A
  • Balance between anti- and pro-coagulant activities
  • Determines whether clot formation, propagation, or dissolution occur
  • Normal endothelium – antithrombotic effects via platelet inhibitory, anticoagulant, and fibrinolytic effects
  • Injured endothelium - loses many antithrombotic properties
65
Q

Platelet inhibitory effects of normal endothelium

A
  • Shields platelets from subendothelial collagen and vWF
  • Releases inhibitory substances – prostacyclin, NO, adenosine diphosphatase
  • Bind and alter activity of thrombin
66
Q

Anticoagulant effects of normal endothelium

A

> Shields from tissue factor in vessel wall

> Expresses factors that actively oppose coagulation

> > Thrombomodulin and endothelial protein C receptor
>Bind thrombin and protein C in a complex (causes thrombin to lose ability to activate factors and platelets, cleaves and activates protein C (with protein S, potent inhibitor of FVa and FVIIIa)

> > Heparin-like molecules
>Bind and activate antithrombin III, which inhibits thrombin and FIXa, Fxa, FXIa, FXIIa
>Heparin works by stimulating antithrombin III activity

> > Tissue factor pathway inhibitor (with protein S, binds and inhibits tissue factor /factor VIIa complexes)

67
Q

Fibrinolytic effects of normal endothelium

A

Synthesize t-PA

68
Q

Primary abnormalities involved in abnormal clotting (Virchow’s triad)

A

Endothelial injury
Stasis or turbulent blood flow
Hypercoagulability

69
Q

Prothrombotic changes in endothelial injury

A
  • Downregulate expression of thrombomodulin – modulator of thrombin activation
  • Downregulates other anticoagulants, such as protein C and tissue factor protein inhibitor
70
Q

Antifibrinolytic effects of endothelial injury

A
  • Activated endothelial cells secrete plasminogen activator inhibitors – limit fibrinolysis
  • Downregulate expression of tissue plasminogen activator
71
Q

Turbulence

A

causes endothelial injury and dysfunction

72
Q

Stasis

A

venous thrombi

73
Q

Both turbulence and stasis

A
  • Promote endothelial activation, enhance procoagulant activity
  • Disrupt laminar flow, platelets contact endothelium
  • Prevent washout and dilution of clotting inhibitors
74
Q

Examples of alterations to normal blood flow

A
  • Ulcerated atherosclerotic plaques
  • Aneurysms
  • Atrial dilation
  • Hyperviscosity
75
Q

Hypercoagulability/Thrombophilia

A
  • Any disorder that predisposes to thrombosis

- Primary (genetic) or secondary (acquired)

76
Q

Primary thrombophilias

A
  • Most common involve factor V Leiden and prothrombin
  • Also includes disorders with increased levels of factors VIII, IX, XI or fibrinogen
  • Less common include antithrombin III, protein C and protein S deficiencies
77
Q

Secondary thrombophilias

A
  • Frequently multifactorial

- Risks include stasis, vascular injury, hyperestrogenic state, malignancy, others

78
Q

Factor V Leiden

A
  • single nucleotide mutation in factor V
  • Not a factor deficiency, but an abnormal (mutated) form
  • Among those with recurrent DVTs, up to 60% have it
  • Mutation renders factor V resistant to cleavage by protein C, lose antithrombotic regulatory pathway
  • Heterozygotes – 5x increase of venous thrombosis
  • Homozygotes – 50x increase
79
Q

Prothrombin gene mutation

A
  • Single nucleotide change in prothrombin gene

- Leads to elevated PT levels, 3-fold increase of venous thrombosis

80
Q

Antithrombin deficiency

A
  • Hereditary – can present with DVT, PE

- Acquired – in DIC, liver disease, nephrotic syndrome, heparin therapy

81
Q

Protein C or S deficiencies

A
  • Both with genetic and acquired deficiencies

- Increased risk of thrombosis

82
Q

Antiphospholipid syndrome

A

-binding of antibodies to epitopes on proteins that are induced or “unveiled” by phospholipids
»Possibly associated with β2-glycoprotein I – associates with surfaces of endothelial cells and trophoblasts, and thrombin
»Induces a hypercoagulable state through uncertain mechanisms

83
Q

Clinical manifestations of antiphospholipid syndrome

A
  • recurrent thromboses
  • repeated miscarriages
  • cardiac valve vegetations
  • thrombocytopenia
  • Presentation can include pulmonary embolism, pulmonary hypertension, stroke, bowel infarction, renovascular hypertension, renal microangiopathy
84
Q

Primary Antiphopholipid syndrome

A
  • Hypercoagulable state, but no evidence of autoimmune disorder
  • Can follow exposure to certain drugs or infections
85
Q

Secondary antiphospholipid syndrome

A

-autoimmune diseases (SLE)

86
Q

Labs and Treatment for antiphospholipid syndrome

A
  • Prolonged PTT
  • Clotting, not bleeding
  • Treatment: anticoagulation and immunosuppression
87
Q

Arterial thrombosis

A
  • Usually begin at sites of turbulence or endothelial injury

- Frequently occlusive

88
Q

Venous thrombosis

A
  • Typically in areas of stasis
  • Almost invariably occlusive
  • Typically have more red cells than arterial – red or stasis thrombi
89
Q

Lines of Zahn

A

Laminations of a thrombosis that are pale platelet and fibrin deposits alternating with darker red cell-rich layers

90
Q

Postmortem lines of Zahn look like..

A

Lack organization, not attached to underlying wall, “chicken fat” upper portion

91
Q

Mural thrombi

A

Those occuring in hear chambers or aorta

92
Q

Heart valve thrombi

A

Vegetations

93
Q

Fate of the thrombus

A

> Propagation – accumulate additional platelets and fibrin, grow
Embolization – dislodge and travel to other sites
Dissolution
–Fibrinolysis, can lead to rapid shrinkage
–More resistant once cross-linking occurs (explains why t-PA works only early on)
Organization and recanalization - ingrowth of endothelial cells, can eventually re-establish continuity of a vessel

94
Q

Venous thrombosis (phlebothrombosis)

A
  • Most common in superficial or deep leg veins
  • Can cause congestion, swelling, pain, tenderness, lead to overlying ulceration
  • Deep veins thromboses can embolize – pulmonary embolism
  • Can be associated with hypercoagulable states, bed rest/immobilization, congestive heart failure, trauma, surgery, pregnancy, malignancy
95
Q

Arterial thrombosis

A

Atherosclerosis most common etiology – endothelial injury and abnormal blood flow

96
Q

Disseminated Intravascualr Coagulation (DIC)

A

-An acute, subacute or chronic thrombohemorrhagic disorder
-Characterized by excessive activation of coagulation and formation of thrombi in microvasculature
-Occurs as a secondary complication of many disorders
-Results in consumption of platelets, fibrin, and coagulation factors
»Secondary activation of fibrinolysis

97
Q

DIC Etiology and Pathogenesis

A
  1. exposure of tissue factor
  2. Combines with factor VII to activate Factors X and IX
  3. Activation of X leads to generation of thrombin
  4. Thrombin converts fibrinogen to fibrin
  5. Feeds back to activate factors IX, VII, and V
  6. Stimulates fibrin crosslinking
  7. Inhibits fibrinolysis
  8. Activates platelets
  9. Leads to stable clot
    -Thrombin is also bound to thrombomodulin, anticoagulant
    »Activates protein C, which inhibits factors V and VIII
98
Q

Widespread injury to endothelial cells can happen through…

A
  • Necrosis
  • Sepsis - mediated by TNF, induces tissue factor expression, decreases thrombomodulin, upregulates expression of adhesion molecules (attracts leukocytes)
  • Deposition of antigen-antibody complexes
99
Q

DIC most frequently associated with…

A

obstetric complications, malignancy, sepsis, major trauma

100
Q

Consequences of DIC

A

-Widespread deposition of fibrin in microvasculature (can lead to ischemia, microangiopathic hemolytic anemia)
-Consumption of platelets and clotting factors, activation of plasminogen (leads to hemorrhagic diathesis)
»Plasmin cleaves fibrin, digests factors V and VIII
»Fibrin degradation products inhibit platelet aggregation, fibrin polymerization, and thrombin

101
Q

Lab findings of DIC

A

-Prolonged PT, PTT
-Thrombocytopenia (generally mild)
-Presence of both thrombin and plasmin formation
»D-dimer test - measures plasmin-cleaved, insoluble, cross-linked fibrin that originally arose from thrombin cleavage
»Previously measured fibrin degradation (split) products – not as specific

102
Q

DIC Morphology

A
  • Thrombi (Brain, heart, lungs, kidneys, adrenals, spleen, liver, (decreasing order) but may be anywhere
  • Can cause infarcts, hemorrhage
103
Q

Clinical features of DIC

A

-Can be sudden
»50% associated with pregnancy, can be reversible with delivery
»33% with carcinomatosis
-Can get:
>Microangiopathic hemolytic anemia
>Dyspnea, cyanosis, respiratory failure
>Acute renal failure and oliguria
>Circulatory failure and shock
-Waterhouse-Friderichsen syndrome in meningococcemia (massive adrenal hemorrhages)
-Kasabach-Merritt syndrome (unusual DIC associated with giant hemangiomas)
-Best treated by managing the underlying disorder
-Variable prognosis

B & L (4 decks)

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