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Pathology Block 1 > Block 1 Coagulation > Flashcards

Block 1 Coagulation Flashcards

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1
Q

Anti-thrombotic factors produced by endothelial cells

A

PGI2, NO, heparin-like molecule, tPA, thrombomodulin

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2
Q

von Willebrand factor

A

Co-factor for platelet adhesion; produced by platelet a-granules, subendothelial CT, Weibel-Palade bodies of endothelium

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3
Q

Main factors secreted by platelets

A

Serotonin
TXA2
ADP

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4
Q

Fibrinogen

A

Cross-links platelets in primary hemostasis, co-factor for platelet aggregation

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5
Q

How are platelets activated?

A

Exposure to sub-endothelial BM thrombin (factor 2a)

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6
Q

Tissue factor/ extrinsic pathway of clotting cascade

A

Damaged endo = FVII leaves, contact TF, TF-FVIIa -> FXa + FVa -> IIa/ thombin -> fibrin

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7
Q

Contact/ intrinsic pathway of clotting cascade

A

Endothelial damage -> formation of kallikrein-FXII complex my HMWK -> FXIIa -> FXIa -> FIXa + FVIIIa -> FXa + FVa -> IIa/ thrombin -> fibrin

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8
Q

Bleeding time

A

Assesses platelets; 2-9 min nrl, prolonged = defect in platelet # or fxn

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9
Q

Normal platelet count

A

150k-300k/ul

*May appear low d/t post-draw clumping

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10
Q

PT (prothrombin time)

A

Add TF and Ca2+

Measures extrinsic/ TF pathway: FVII, FX, FV, FII, fibrinogen

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11
Q

Normal PT and APTT time

A

PT: 11-14 s
PTT: 25-35 s

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12
Q

APTT (activated partial thromboplastin time)

A

Add surface area and Ca2+

Measures intrinsic/ contact pathway: FXII, HMWK, PK, XI, IX, VIII, X, V, II, fibrinogen

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13
Q

Three main categories of bleeding disorders

A

Increase vessel fragility
Platelets (deficiency or dysfunction)
Coagulation factors

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14
Q

Symptoms of vessel wall abnormalities

A

Non-thrombocytopenic purpura/ petechiae in skin, mucous membranes
Occasionally joint, mm bleeds, menorrhagia, epistaxis, GI bleed, hematuria

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15
Q

Lab values for vessel wall abnormalities

A

Bleeding time, platelet count, PT, APTT all normal

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16
Q

Causes of vessel wall abnormalities

A

Infections -> vasculitis or DIC (meningococcemia, infective endocarditis, Rickettsioses)
Drug rxns -> Ab-Ag complex deposition
Impaired collagen formation (elderly, Cushing syndrome, scurvy, ED syndrome)

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17
Q

Henoch-Schonlein purpura

A

Vessel wall abnormality d/t systemic hypersensitivity of unknown cause
Deposition of Ag-Ab complexes in vessels -> purpuric rash, abdominal pain, polyarthralgia, acute glomerulonephritis

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18
Q

Hereditary hemorrhagic telangiectasia

A

Vessel wall abnormality of AD inheritance; dilated, thin-walled vessels bleed easily, commonly in nose, mouth, tongue, eyes, GI tract

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19
Q

Amyloid

A

Causes vessel wall abnormalities d/t perivascular deposition seen in plasma cell dycrasias -> mucocutaneous petechiae

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20
Q

Thrombocytopenia

A

Platelets

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21
Q

Causes of thrombocytopenia d/t decreased platelet production

A

Generalized BM disease, selective impairment of production, ineffective megakaryopoiesis

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22
Q

Specific causes of BM disease, impaired platelet production, ineffective megakaryopoiesis

A

BM: aplastic anemia, marrow infiltration (leukemia)
Imp: drugs (thiazides, alcohol), infections (HIV, measles)
Mega: megaloblastic anemia, myelodysplastic syndromes

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23
Q

Causes of thrombocytopenia d/t decreased platelet survival

A

Immunologic (auto-Abs and allo-Abs) and non-immunologic (mechanical)

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24
Q

Immunologic causes of thrombocytopenia

A

Ab against platelet membrane GPIIb-IIIa and Ib-IX
Auto-Abs: ITP, SLE, HIT, HIV/mono
Allo-Abs: blood transfusion, pregnancy

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25
Non-immunologic mechanical causes of thrombocytopenia
Artificial heart valves, malignant HTN with diffuse narrowing of vessels
26
Thrombocytopenia d/t sequestration and dilution
Seq: hypersplenism (normally stores 30-40%) Dil: blood stored >24 h has no platelets -> relative dilution w/ transfusion
27
ITP general characteristics
Immune thrombocytopenic purpura Primary acute or chronic, and secondary Auto-Abs against GP2a-3b or 1b-9 Long BT, nrl PT/APTT
28
Mechanism of ITP & histo findings
Plasma or bound auto-IgG against GP 2b-3a, Ib-9 -> spleen phago of opsonized platelets Prominent spleen germ center, increased BM megakaryos (immature, non-lobated nuc), megathrombocytes on PBS
29
Chronic ITP
Women
30
Acute ITP
Children, F=M Follow viral illness, self-limited to 6 mos Steroid therapy in severe cases 20% may -> chronic ITP, usually w/o viral prodrome
31
Secondary ITP
Due to a variety of conditions and exposures (e.g. HIT, HIV)
32
Drug-induced thrombocytopenia
Quinine, quinidine, sulfonamide ABs | Heparin: 5% pts (HIT)
33
Type 1 HIT
Occurs rapidly after therapy onset, mild and may resolve spont, d/t direct platelet-aggregating effect of heparin
34
Type 2 HIT
5-14 d post therapy onset, severe, Abs against heparin-platelet factor 4 complex; activated platelets -> thrombus
35
HIV-induced thrombocytopenia
Megakaryos have CD4 receptor, can be infected -> apoptosis = impaired platelet production Abs cross-rx with HIV-assc GP120 & direct against GP2b-3a complex, acting as opsonins
36
TTP symptoms
Thrombotic thrombocytopenic purpura Pentad: fever, thrombocytopenia, microangiopathic hemolytic anemia, transient neuro def, renal failure *Can result in consumption, hemolytic anemia
37
HUS symptoms
``` Hemolytic uremic syndrome No neuro symptoms Prominent acute renal failure Seen in children *Can result in consumption, hemolytic anemia ```
38
Cause, dx, and tx of TTP
ADAMTS-13 enzyme def, a vWF metalloprotease -> chains of vWF = microaggregates PT, APTT normal Tx: plasma exchange
39
Acquired vs. inherited TTP
Ac: have inhibiting antibody In: have inactivating mutation
40
Cause, dx of HUS
Kids: E. coli O157:H7 -> Shiga-like toxin damages endo -> aggregation *Bloody diarrhea precedes by 2-3 days Good prognosis with supportive care Adult: endo damage d/t drugs or radiation; poor prognosis PT/APTT normal
41
Bernard-Soulier syndrome
AR defect in platelet adhesion d/t deficiency of GP1b-9 (vWF receptor)
42
Glanzmann's thrombasthenia
AR defect in platelet aggregation d/t dysfunction GP2b-3a (bridges platelets by binding fibrinogen and vWF)
43
Impaired platelet secretion of TXA and ADP
Storage pool disorder/ disorder of secretion = no platelet activation
44
Aspirin & uremia -> thrombocytopenia
ASA: irreversible COX inh = no TXA2/PG for platelet aggregation and release rxns Uremia: not fully understood, several platelet fxn abnormalities
45
Symptoms of clotting factor deficiencies
Large post-traumatic ecchymoses, hematomas, or prolonged bleeding GI, GU, joint bleeding
46
Acquired clotting factor deficiencies
``` Vit K def (F2, 7, 9, 10) Liver disease (dec synth factors) DIC ```
47
Factor VIII
Produced by sinusoidal endothelial cells, Kupffer cells, glomerular and tubular renal epithelium Circulates with vWF
48
vWF
Multimers produced by endothelial cells and megakaryos In platelet alpha granules Dep in subendo matrix, promotes platelet adh via GP1b-9 Circulating: promotes platelet agg by binding activated GP2b-3a
49
Von Willebrand disease
1% frequency Mostly AD inheritance Quant (type 1, 3) and qual deficiencies (type 2)
50
Type 1, 2, 3 vWF disease
1: Quant, 70% cases, mild 2: Qual, 25% cases, mild-mod 3: Quant, AR, severe
51
Testing for vWF disease
Ristocetin agglutination test: AB promotes intxn vWF and GP1b-9 Types 1, 3 may have 2' FVIII def = prolonged PTT
52
Hemophilia A
``` Most common hereditary disorder a/w serious bleeding X-linked Reduction amt/act FVIII PTT prolonged, all else nrl Deep bleeding: jj, mm, intracranial ```
53
Hemophilia B/ Christmas disease
Factor IX def, X-linked Clinically indistinguishable from Hemophilia A PTT prolonged, all else nrl Tx: recombinant FIX
54
Hemophilia treatment
Lyophylized powder reconstituted at home or in hospital for IV admin Dosed to correct def to specific levels Prophylaxis to prevent bleeds Issues: venous access, cost, inhibitors
55
Protective mechanisms against thrombosis
Intact endothelium, neutralization of activated factors by circulating anti-coags Dilution of activated factors by blood flow Clearance of activated factors by liver Fibrinolysis
56
Natural circulating anti-coags
AT-3, protein C, protein S, TFP-I (tissue factor pathway [extrinsic] inhibitor)
57
Antithrombin 3
Interacts with HLM on endo to inactivate thrombin (2), 9, 10, 11, 12
58
Protein C
Main circulating anti-coag, complexed to protein S Affects Vit-K dep factors Activated by ™ on endo surface, inactivates 5a, 8a
59
TFPI
Secreted by endo and other cells, inactivates 10a, 7a
60
Fibrinolysis & testing for it
Dissolution of formed thrombi performed by plasmin | Tests: plasminogen level, fibrin degradation products (D-dimer)
61
tPA
Tissue-type plasminogen activator Urokinase-type plasminogen activator Inhibited by PAIs
62
Causes of thrombosis
Damaged endo cells, exposure of blood to subendo, act platelets or coagulation, inhibition of fibrinolysis, stasis
63
Predisposing factors of thrombus
Trauma, central catheters, deficiencies circulating anti-coags, endo damage, surgery
64
Acquired defects of endo surface function
Vascular injury, atherosclerosis, drug/ foreign substance
65
Thrombophilia
Predisposition to thrombus Features: thrombosis at young age, multiple family members with thrombosis, repeated episodes of thrombosis (esp in odd places)
66
Factor V Leiden mutation
2-15% Caucasians | Sub Q for R at position 506 = resistant to cleavage by protein C -> unchecked coagulation
67
Prothrombin mutation
1-2% population | G to A in 3' untranslated region of prothrombin gene -> elevated prothrombin levels
68
Hyperhomocytsteinemia
A/w premature atherosclerosis, mild elevations a/w arterial and venous thrombosis ? Due to inh AT3 and endo TM Gene polymorphisms identified
69
Congenital defects of circulating anti-coags
``` Plasminogen deficiency AT3 def (heterozygotes prone, venous thromb is adol/early adult) Protein C or S def ```
70
Homozygous protein C/S def symptoms & tx
Purpura fulminans (skin necrosis, DIC), immediate recognition and FFP transfusions
71
Heterozygous protein C/S def symptoms & risk factors
Venous thrombosis in adol/early adulthood | Compounded by pregnancy or birth control pills
72
Anti-phospholipid syndrome (Lupus anti-coag)
Ab against cardiolipin = prolonged PT, APTT No clinical bleeding, may cause recurrent venous or arterial thrombi, miscarriage, cardiac veg, thrombocytopenia *False + syphilis test
73
Causes of anti-phospholipid syndrome/ Lupus anti-coag
Idiopathic SLE and other collagen vascular diseases Post-viral Medication-induced
74
Features, location, complications of DVT
Pain, swelling, discoloration Extremities, pulmonary vessels, pelvic veins, other PE, post-phlebitic syndrome, bleeding from anti-coag
75
Managing thrombosis patients
Thrombolytic therapy, anti-coag, surgical clot removal, angioplasty, anti-platelet therapy, search for causative factors
76
Thrombolytic therapy
Activate fibrinolysis pathway to rapidly resolve thrombi, esp in arterial disease Risk: hemorrhage Requires plasminogen
77
Streptokinase/ urokinase
Activate plasminogen, like tPA
78
Heparin
``` Rapid reversible anti-coag b/c IV with short T1/2 Therapy before Coumadin Works via AT3 to inh 10a, 2a Target PTT = 1.5 upper normal limit *Measure hep levels directly ```
79
Safe heparin use includes:
Standard infusion rates Check AT3 levels Dedicated IV line Avoid: ASA, IM injections, trauma
80
LMWH (low mol weight heparin)
More specifically inh Xa, may be safer than standard hep | Outpatient therapy admin 1-2/day
81
Warfarin/Coumadin
Most common anti-coag Inhibits gamma carboxylation of 2, 7, 9, 10 (vit K antagonist) Oral, long T1/2 Metabolism affected by diet, meds
82
INR (international normalized ratio)
INR = (patient PT/ avg PT)^ISI ISI = international sensitivity index assigned to each TF batch *Corrects for variability in instrumentation and reagents
83
Safe use of Coumadin
Monitor INR, adjust every 4-5 days, discontinue heparin when therapeutic levels achieved
84
What drugs modify extrinsic/ TF pathway & intrinsic/ contact pathway?
TF: Warfarin (PET is WET), measured by PT CA: Heparin (PITT is a HIT), measured by PTT
85
Prophylactic ASA
Aspiring irreversibly acetylates COX, inhibits primary hemostasis; role in preventing arterial thrombosis
86
DIC
Acute, subacute, or chronic thrombohemorrhagic disorder | Activation coag pathway -> microthrombi; consumes platelets, fibrin, coag factors; secondary activation fibrinolysis
87
Mechanisms of DIC: release of tissue factor or thromboplastic substances
From placenta, mucus from adenocarcinoma (act FX, chronic), granules from acute promyelo leuk, G- sepsis (endotoxins -> monocytes IL-1, TNF = inc exp TF and dec TM)
88
Mechanisms of DIC: widespread endothelial injury
Meningococci, ricketssiae, trauma, burns
89
Symptoms of DIC and tx
Fibrin dep -> ischemia; microangiopathic hemolytic anemia; dyspnea, cyanosis, resp failure; convulsions, coma; oliguria, acute renal failure; circulatory failure; shock, death Tx: treat underlying cause

Pathology Block 1 (12 decks)

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