S18C228 - Acquired bleeding d/o Flashcards

1
Q

Platelet defects

A
  • quantitative (production, consumption, destruction)
  • qualitative
  • manifestations: nonpalpable petechiae, purpura, mucosal bleeding, menorrhagia, hemoptysis, hematuria, hematochezia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Platelet defects

A
  • quantitative (production, consumption, destruction)
  • qualitative
  • manifestations: nonpalpable petechiae, purpura, mucosal bleeding, menorrhagia, hemoptysis, hematuria, hematochezia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Transfusion threshold for platelets:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ITP

A

-ITP bleeds less at a lower platelet count than other causes of thrombocytopenia
-autoimmune dz causing rapid destruction of platelets
-Sx: purpura, petechiae
-normal bone marrow
-more common in younger children
-usually resolves in 1-2mo, chronic ITP lasts >3mo
-assoc with other autoimmune dz
-mild anemia may also be present
-smear shows large scant platelets
-tx: avoid ASA/NSAIDs, control BP, avoid procedures, prevent falls
>50 no tx
children >30 do not need hospitalization or tx usually
children 50 no tx
20-30 consider steroids
20 can be managed as out-pt if no bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Acquired thrombocytopenia: decreased production

A
  • marrow infiltration (tumor/infxn)
  • viral infx -rubella, HIV
  • drugs
  • radiation
  • vit B12/folate deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Acquired thrombocytopenia: increased destruction

A
  • ITP
  • TTP
  • HUS
  • DIC
  • viral infxn: HIV, mumps, varicella, EBV
  • drugs (heparin, protamine)
  • HELLP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acquired thrombocytopenia: sequestration

A
  • SCD

- cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Drugs that cause thrombocytopenia

A
  • heparin
  • sulfa
  • quinine
  • EtOH
  • ASA
  • indomethacin
  • acyclovir
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Drugs that impair platelet function

A
  • ASA
  • NSAIDs
  • glyocprotein IIb-IIIa agents (plavix)
  • PCN, cephalosporins
  • CCB
  • TCA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Platelet clumping

A
  • can occur in younger pts
  • results in a false thrombocytopenia count
  • is seen on a peripheral smear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ITP tx

A

-prednisone 60-100mg OD PO with taper
IVIG 1g/kg/d for 2d or anti-D for very low platelet counts and bleeding
-tranfuse platelets only if needed
-life-threatening bleed: methylpred 30mg/kg/d IV x3d, IVIG and platelet TFN after 1st dose of methylpred given
-RBC PRN
-conjugated estrogen can be considered for uterine bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Drug-induced thrombocytopenia

A
  • presents very similar to ITP

- HIT causes a drop in platelets but pts are paradoxically hypercoagulable due to platelet activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Things that cause qualitative platelet abnormalities

A
  • uremia
  • liver dz
  • DIC
  • antiplatelet Abs (ITP, SLE)
  • cardiopulmonary bypass
  • myeloproliferative d/o (CML, polycythemia vera)
  • dysproteinemia (MM, waldenstrom macroglobulinemia)
  • vW dz
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Transfusion threshold for platelets:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Acquired coag d/o: DIC pathophys

A
  • innappropriate and widespread activation of coagulation system
  • results in intravascular fibrin formation and activation of fibrinolytic system, clots breakdown, coag factors are consumed, bleeding ensues
  • pathophys: increased cytokines and activation of tissue factor (part of extrinsic pathway), leads to thrombin generation, small fibrin clots in microcirculation, leading to occlusion of small vessels and end organ dysfxn, consumption of platelets and coag factors
  • as well, tPA is activated and this leads to excessive activation of fibrinolytic activation and pathologic bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acquired thrombocytopenia: decreased production

A
  • marrow infiltration (tumor/infxn)
  • viral infx -rubella, HIV
  • drugs
  • radiation
  • vit B12/folate deficiency
17
Q

DIC - labs

A
  • prolonged PT
  • low platelets** quite sensitive
  • low fibrinogen (may remain normal however b/c it is an acute phase reactant)
  • elevated d-dimer (this helps differentiate DIC from other similar presentations)
  • increased LDH, decreased haptoglobin and smear with schistocytes (from hemolysis)
18
Q

Acquired thrombocytopenia: sequestration

A
  • SCD

- cirrhosis

19
Q

Drugs that cause thrombocytopenia

A
  • heparin
  • sulfa
  • quinine
  • EtOH
  • ASA
  • indomethacin
  • acyclovir
20
Q

Drugs that impair platelet function

A
  • ASA
  • NSAIDs
  • glyocprotein IIb-IIIa agents (plavix)
  • PCN, cephalosporins
  • CCB
  • TCA
21
Q

Platelet clumping

A
  • can occur in younger pts
  • results in a false thrombocytopenia count
  • is seen on a peripheral smear
22
Q

ITP tx

A

-prednisone 60-100mg OD PO with taper
IVIG 1g/kg/d for 2d or anti-D for very low platelet counts and bleeding
-tranfuse platelets only if needed
-life-threatening bleed: methylpred 30mg/kg/d IV x3d, IVIG and platelet TFN after 1st dose of methylpred given
-RBC PRN
-conjugated estrogen can be considered for uterine bleed

23
Q

Drug-induced thrombocytopenia

A
  • presents very similar to ITP

- HIT causes a drop in platelets but pts are paradoxically hypercoagulable due to platelet activation

24
Q

Things that cause qualitative platelet abnormalities

A
  • uremia
  • liver dz
  • DIC
  • antiplatelet Abs (ITP, SLE)
  • cardiopulmonary bypass
  • myeloproliferative d/o (CML, polycythemia vera)
  • dysproteinemia (MM, waldenstrom macroglobulinemia)
  • vW dz
25
Q

Acquired coag d/o: liver dz

A
  • liver produces many factors (except VIII) so get a deficiency in factors
  • will have a prolonged PT
  • also affects bile acid production which is needed for absorption of vit K
  • also get portal HTN and splenic sequestration
  • get increased fibrinolysis b/c of decr synthesis of alpha2-plasmin inhibitor
  • difficult to distinguish hepatic coagulopathy from DIC: both have decr platelets, decr coag factors, hypofinbrinogenemia however D-dimer only mildly elevated in liver dz

-if actively bleeding: PRBC, vit K, FFP (For factors), cryoprecipitate (for fibrinogen

26
Q

Acquired coagulation d/o: renal dz

A
  • uremic toxins
  • dialysis induced thrombocytopenia
  • abn clotting factors
  • quantitative and qualitative platelet dysfxn
  • preventative measures: B12, folate, iron, erythropoietin
27
Q

Acquired coag d/o: DIC

A

-

28
Q

Acquired coag d/o: DIC clinic features

A
  • bleeding, thrombosis, purpura fulminans, multi organ failure (aLOC, gangrene, oliguria, lung injury, ARDS)
  • both heomrrhage and thrombosis occur but usually one predominates depending on the individual, more commonly bleeding
  • purpura fulminans (arterial and venous thromboses), seen in bacteremia
29
Q

DIC - labs

A

-prolonged PT
-low platelets** quite sensitive
-low fibrinogen (may remain normal however b/c it is an acute phase reactant)
-elevated d-dimer
-

30
Q

DIC - tx

A
  • supportive
  • tx underlying illness
  • fluid, PRBC, inotropes, vit K, folate
  • plateltes, fibrinogen, coag factors if bleeding
  • goal to raise fibrinogen to 100-150mg/dl with cryoprecipitate
31
Q

DIC - causes

A
  • infxn
  • cancer
  • leukemia
  • trauma
  • pregnancy
  • vascular dz
  • envenomation
  • ARDS
  • transfusion rxns
32
Q

Factor VIII inhibitor

A
  • develop in pts with hemophilia A but can also be spontaneous
  • pts w/o previous bleeding hx who develop factor VIII inhibitors present with massive spontaneous bruises and hematomas
  • normal PT, normal thrombin clotting time and greatly prolonged aPTT that does not correct with mixing
  • tx: steroids, IVIG, rituximab, factor VIII, IX, pasmapheresis