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Summer 3 > Bleeding GK > Flashcards

Bleeding GK Flashcards

1
Q

What are the 2 clotting D/O we need to know?

A

Hemophilia A (Factor 8 Def)

Hemophilian B (Factor 9 Def)

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2
Q

Hemophilia A is what factor deficiency?

A

8

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3
Q

Hemophilia B is what deficiency?

A

Factor B

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4
Q

What are the 4 types of platelet disorders?

A
  1. dysfunction (acquired or congenital)
  2. splenic sequestration
  3. increased destruction
  4. impaired production
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5
Q

What are the 3 signs of bleeding disorders on physical exam?

A
  1. Petechiae <2mm
  2. Purpura 2-10 mm
  3. Ecchymosis >1cm
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6
Q

What is petechiae?

A

focal areas of subcutaneous bleeding

DO NOT BLANCHE with pressure

may occur in periorbital areas after vomiting/coughing

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7
Q

What is purpura?

A

palpable or nonpalpable

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8
Q

What 5 lab studies should you order for a pt with suspected bleeding disorder?

A

CBC (platelet count)

Peripheral smear

PT/INR, aPTT

bleeding time

fibrinogen

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9
Q

What does the platelet count look at?

A

# of platelets (thrombocytes) per cubic ml of blood

looks at quantity, not quality.

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10
Q

What is the normal platelet count?

A

150,000-400,000

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11
Q

What lab value is considered thrombocytopenia?

A

<100,000

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12
Q

What can happen if the platelet count is <40,000?

A

prolonged bleeding from vascular injury can occur

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13
Q

What can happen if platelet count is <20,000?

A

spontaneous bleeding

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14
Q

What does bleeding time measure?

A

measures time for hemostasis (stopping of blood flow)

screens for microvasculature and platelet function

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15
Q

Prolonged bleeding time occurs in what 2 disorders?

A

platelet disorders (von wildebrand’s disease)

severe thrombocytopenia

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16
Q

What is the 1st hemostatis response when vessel injury occurs?

A

spastic contraction of the damaged microvessels (vasoconstriction)

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17
Q

What is the 2nd hemostatic response when vessel injury occurs?

A

platelets adhere to the affected area (platelet plug formation)

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18
Q

What is the 3rd hemostatic response when vessel injury occurs?

A

initiation of coagulation cascade

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19
Q

Vasoconstriction is also known as what

A

vascular spasm

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20
Q

Vasoconstriction

A

happens immediately

smooth muscle on damaged vessels will constrict which reduced blood flow to the area (limits blood loss)

Collagen is exposed which promotes platelets to adhere to the injury site.

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21
Q

Primary hemostasis in platelet plug formation

A

platelets clump together through platelet adhesion: adhere to damaged endothelium, form platelet plug & degranulate (thromboregulation)

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22
Q

what is platelet plug formation activated by?

A

glycoprotein: vWF

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23
Q

What do platelets release once they adhere to exposed collagen?

A

ADP & TAz (thromboxane) to activate more platelets and increase the effect of vasoconstrictionq

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24
Q

Seconday Hemostasis

A

once platelet plug has been formed, clotting factors are activated = “coagulation cascade”

Leads to formation of fibrin (from inative fibrinogen) = fibrin mesh produced all around platelet plug to hold it in place.

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25
Q

Secondary Hemostasis is comprised of what 3 pathways?

A

intrinsic pathway

extrinsic pathway

common pathway

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26
Q

PT (prothrombin time) is prolonged with abnormalities in which pathway?

A

prolonged with abnormalities in extrinsic pathway (or common)

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27
Q

PT is used to monitor what?

A

warfarin (coumadin) therapy

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28
Q

What does PT assess?

A

liver function/damage

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29
Q

PTT or aPTT is prolonged in what abnormality?

A

intrinsic pathway abnormalities

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30
Q

PTT is used to monitor what?

A

unfractionated hepatin therapy

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31
Q

What conditions will you see an abnormal PTT with?

A

hemophilia

vW disease

liver damage

Vit K deficiency

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32
Q

T/F: INR is a more accurate reflection of PT

A

True

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33
Q

What is INR?

A

standardized ratio of prothrombin time compared to a control

results are independent of reagents or methods used

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34
Q

What is the Goal INR level dependent on?

A

underlying need for anticoagulation

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35
Q

What is INR used to monitor?

A

warfarin anticoag therapy

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36
Q

Characteristics of clotting disorders?

A

associated with excessive or repetitive bleeding at unusual sites (joints, muscles, GI, GU tract) with normal activity.

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37
Q

clotting disorders are classified as either ________ or _________.

A

clotting disorders are classified as either congenital or acquired.

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38
Q

What are the 2 congenital clotting disorders?

A

Hemophllia A & B

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39
Q

What is christmas disease?

A

Hemophilia B (Factor 9)

40
Q

Which hemophilia is most common?

A

Hemophilia A (Factor 8 deficiency)

41
Q

Both are X-linked recessive

predominately affects males

can affect females born to affected father and carrier mother

What dz?

A

Hemophilia A & B

42
Q

Dz severity correlates with factor levels

Which dz?

A

Hemophilias

43
Q

Clinical Px of Hemophilia A & B

A

most = asx for first few months of life

1st episode of sx bleeding: occurs after newborn period but within 1st 2 years of life (spontaneous or with minimal injury)

severe pain in weight-bearing joints (hemophilic arthropathy)

Repeated episodes of bleeding

44
Q

MC sites of bleeding in Hemophilia

A

Joints

muscles

skin

GI, GU

spontaneous hemarthrosis = sign of severe dz

45
Q

Lab studies for Hem A

A

platelet count: nml

PT: nml

aPTT: prolonged (can be normal in prolonged disease)

Factor 8 assay

46
Q

Hem A mgmt

A

Factor 8 concentrate administration/infusions

Desmopressin (DDAVP)

47
Q

Pt education for Hem A

A

avoid trauma, high risk activity

avoid certain meds (ASA)

genetic counseling

48
Q

Potential causes of low platelets

A

recent infection

platelet consumption syndrome

immune d/o

chronic liver dz

bleeding

49
Q

potential causes of high platelets

A

cause of significant inflammation

significant infection

abnormal peripheral smear

essential thrombocytosis sx

iron deficiency anemia

inappropriate clotting or bleeding

metastatic malignancy

50
Q

is acquired or congenital a more common cause of platelet dysfunction?

A

acquired: drugs, uremia, alcoholism, myeloproliferative disease

51
Q

What will lab studies show for dysfunctional platelets?

A

normal count and morphology

prolonged bleeding time

52
Q

mgmt for dysfunctional platelet disorders

A

discontinue offending agent

hemodialysis in uremic cases

platelet TF if serious bleeding

53
Q

What causes sequestering platelet disorders?

A

splenomegaly/hypersplenism = thrombocytopenia

post-splenectomy = ractive (thrombocytosis)

54
Q

Increased platelet destruction disorder (autoimmune)

A

ITP (idiopathic thrombocytopenic purpura)

55
Q

increased platelet consumption disorders

A

TTP (thrombotic thrombocytopenic purpura)

HUS (hemolytic-uremic syndrome)

DIC (disseminated intravascular coagulation)

56
Q

Pathophys of ITP

A

reduced platelet llifespan due to antibody mediated destruction of platelets

57
Q

What are the 2 types of ITP?

A

Primary: due to autoimmune mechanisms leading to platelet destruction and platelet underproduction that is not triggered by an associated condition.

Secondary: associated with another condition: HIV, Hep C, SLE, CLL

58
Q

What type of ITP?

self limited

common in children (2-4 yrs old)

IgG associated

prior viral URI

A

Acute ITP

59
Q

What type of ITP?

females > males

peak incidence 20-50 y/old

insidious onset

associated with other autoimmune dz, HIV

A

Chronic ITP

60
Q

CPx of ITP

A

can be asx

peteichiae

pupura

hemorragic bullae on skin & mucus membranes

SAH, ICH

splenomegaly should NOT be present

61
Q

Lab studies for ITP

A

thombocytopenia: Plt <20

Coag studies = nml

BM: increased megakaryocytes

Dx of exclusion

62
Q

ITP Mgmt

A

avoid platelet antagonists (NSAIDs, ASA)

Acute ITP: resolves spontaneously, may require steroids/splenectomy

Chronic ITP: high-dose prednisone or dexamethasone, IVIG, If refractory: splenectomy, danazol

63
Q

Emergency ITP tx

A

stop bleeding

platelet TF

64
Q

Life-threatening complication of exposure to heparin

results from an autoantibody directed against endogenous platelet factor 4 (PF4) in complex with heparin.

What dz?

A

Heparin-induced thrombocytopenia (HIT)

65
Q

Removal of IgG-coated platelets by macrophages of the reticuloendothelial system (eg, spleen, liver, bone marrow)

What dz?

A

HIT

66
Q

what is HIT associated with?

A

arterial and venous thrombosis (hypercoagulable)

67
Q

tx for HIT

A

STOP HEPARIN

68
Q

etiology of TTP

A

Idiopathic

Infection/autoimmune/malignancy: Includes HIV

Drugs

Pregnancy/post-partum

Stem-cell transplant

Shigatoxin producing E. Coli – follows bloody diarrhea prodrome

69
Q

TTP CPx

A

abrupt onset: can be acute, chronic, relapsing

fever, toxic-appearing

fatigue

abdominal patin (pancreatitis common)

HA, AMS, focal neuro deficits (waxes and wanes)

Skin pallor, petechiae, purpura, jaundice

20-50 year olds

70
Q

Endothelial layer of small vessels is damaged and results in fibrin deposition and platelet aggregation (platelet consumption)

As RBCs travel through damaged vessels, they are fragmented which results in intravascular hemolysis.

Pathophys of what dz?

A

Microangiopathic hemolytic anemia + thrombocytopenia

71
Q

Children with atecedent E Coli infection

MHA(microangiopathic hemolytic anemia + thrombocytopenia)

Mainly seen in infants and chlidren (MC follows E coli infection)

W/o neurologic findings

Which dz?

A

HUS (Hemolytic Uremic syndrome)

72
Q

Cpx of HUS

A

Abdominal pain & bloody diarrhea 5-10 days prior to onset

Like TTP (anemia, thrombocytopenia, fatigue), but CNS involvement is less common

If neuro symptoms predominate: TTP

If renal failure predominates : HUS

73
Q

How do you differentiate between TTP and HUS?

A

TTP: neuro sx predominate

HUS: renal failure predominates

74
Q

Most commonly adults

Microangiopathic hemolytic anemia

Thrombocytopenia

Renal dysfunction

Severe CNS symptoms

Fever

TTP or HUS?

A

TTP

75
Q

Mostly children

Microangiopathic hemolytic anemia

Thrombocytopenia

Acute renal failure

No CNS symptoms

TTP or HUS?

A

HUS

76
Q

Lab studies for TTP-HUS

A

Microangiopathic hemolytic anemia:

Reticulocytosis

Increased LDH, indirect bilirubin

Negative coombs test

Thrombocytopenia

Schistocytes (helmet cells) on peripheral smear

Normal coagulation tests (separates TTP from DIC)

renal insufficiency

77
Q

TTP-HUS Management (adults)

A

Corticosteroids

Plasmapheresis

Rituximab for refractory cases

High-risk mortality

78
Q

TTP-HUS mgmt in children

A

IVF, electrolyte repletion

79
Q

Potentially life threatening condition in which proteins which control blood clotting become overactive.

Pathophys of what dz?

A

DIC

80
Q

First, you get extensive thrombosis.

Then as clotting factors and platelets are used up, bleeding/hemorrhage may occur.

Widespread platelet consumption.

Patho of which dz?

A

DIC

81
Q

What dz is typically associated with severe underlying systemic illness?

A

DIC

82
Q

Widespread activation of the coagulation cascade–>increased fibrin clots which entrap platelets–>microthrombi cause RBC destruction and small vessel occlusion –> massive consumption of platelets, fibrin, and coagulation factors –> results in uncontrolled bleeding.

Mechanism of what dz?

A

DIC

83
Q

Clinical conditions associated with which dz?

•Sepsis

  • Trauma
  • Cancer (myeloproliferative disorders, solid tumors)
  • Obstetrical complications (amniotic fluid embolus, abruption)
  • Vascular disorders (giant hemangioma, aortic aneurysm)
  • Reactions to toxins (snake venom, drugs, amphetamines)
  • Immunologic disorders
  • Severe allergic reactions
  • Hemolytic transfusion reactions
  • Transplant rejection
A

DIC

84
Q

DIC Clinical Px

A
  • Variable, onset may be acute or gradual
  • Patients VERY sick with bleeding/clotting: Bleeding>clotting
  • Multiple organ systems affected
  • Hemorrhage and/or thrombosis
85
Q

What is the origin of hemorrhage in DIC?

A

microvasculature:

  • petechiae
  • bleeding from venipuncture sites or surgical wounds
  • GI, lung, obstetrical bleeding
86
Q

DIC lab studies

A

•Decreased platelets

•Increased PT & PTT

•Decreased fibrinogen

•Increased fibrinolysis –> results in increased fibrin degradation products

•Increased D-dimer (very sensitive): Fibrin degradation product, Assesses fibrinolysis

•Microangiopathic hemolytic anemia present in 25% of cases

•Peripheral smear: schistocytes

87
Q

DIC Mgmt

A

quick recognition and aggressive tx of underlying cause

TF support:

  • Cryoprecipitate (fibrinogen replacement)
  • FFP (coagulation factors)

•Platelet transfusion

•RBC transfusion

88
Q

•Autosomal dominant (affects males & females)

•Most common congenital coagulopathy (1/100)

Reduced levels of factor VIII antigen or risocetin cofactor

What dz?

A

Von Willebrand’s Dz

89
Q

Causes of acquired vW dz

A

MC: bone marrow malignancies

valproic acid, SLE

90
Q

Von Willebrand factor serves what two main functions?

A

Facilitates platelet adhesion by linking platelet membrane to vascular subendothelium

Serves as a plasma carrier for Factor VIII

91
Q

what is the result of low level of vWF or defect?

A

bleeding

92
Q

Cpx of vW Dz

A
  • Bleeding (nasal, sinus, vaginal, GI)
  • Spontaneous hemarthrosis and soft-tissue bleed less common than in hemophilia A
  • Bleeding worse with ASA, decreases with estrogen/pregnancy
93
Q

vW Dz Labs

A

•Prolonged bleeding time: Helps differentiate vW disease from hemophilia: Bleeding time is normal in hemophilia

•Low vWF (fancy confirmatory test): must test at different times

•INR normal

94
Q

vW Dz mgmt

A

•Desmopressin acetate (DDAVP) for Type 1: Releases stored vWF from endothelial cells

•Factor VIII infusion

•Humate-P: Derived from human plasma & Contains both factor VIII and vWF

95
Q
A

Summer 3 (12 decks)

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