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Internal Medicine pt. 2 > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

What are the functions of platelets?

A 
1- adhesion to damaged sub endothelium 
2- primary aggregation -> PG E2, F2, TXA2 
3- secretion of: 
- serotonin -> vasoconstriction 
- ADP -> secondary aggregation 
- PF3 -> coagulation 
- Retactozyme 
4- secondary aggregation by ADP 
- maintained by GpIIb/IIIa that binds fibrinogen
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2
Q

When is the decrease of platelets noticed clinically?

A
  • clinical petichae < 50 000

- serious bleeding < 20 000

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3
Q

What is the body’s natural coagulation system?

A

Extrinsic pathway
- factor 7 ——–> 10

Intrinsic pathway
- factor 12 -> 11 -> 9 -> 8 ——-> 10

Common pathway
- 10 -> 5 -> prothrombin to thrombin -> fibrinogen to fibrin

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4
Q

what is the body’s natural anticoagulation system?

A

1- intact endothelium -> prostacyclin & plasminogen activator
2- protein C & S -> C inhibits factor 5 & 8
3- Heparin cofactor II
4- tissue factor inhibitor -> extrinsic pathway
5- fibrinolytic system -> tPA
6- anti thrombin III
7- clearance of clotting factors by liver

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5
Q

What are the manifestations of defect in blood vessels or platelets?

A
  • skin -> petichea <3mm -> flat in platelet defect & raised edges in BV defect
  • mucous membranes -> epistaxis, bleeding gums, hematuria, hemoptysis
  • internal organs -> cerebral hemorrhage
  • spontaneous bleeding if platelets < 20 000
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6
Q

What is the clinical picture in case of coagulation system defect?

A
  • skin -> ecchymosis, hematoma
  • deep bleeding -> muscles & joints
  • external bleeding -> hematemesis, hematuria, hemoptysis
  • prolonged bleeding after cutting umbilical cord & circumcision
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7
Q

What are the investigations performed to differentiate between causes of bleeding?

A 
1- BV & platelet defect 
2- platelet defect 
3- coagulation defect 
4- anemia 
5- investigations foe the cause
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8
Q

What are the investigations that reveal BV/platelet defects?

A

BV & platelets

  • Bleeding time -> 2 - 4 min normally
  • Hess capillary fragility test -> inflate sphygnomanonmeter 80mmHg every 5 minus -> < 5 petichae may be seen normally

Platelets

  • spontaneous bleeding < 20 000
  • platelet function -> aggregation & adhesion by aggregometer & ADP content/PF3 activity
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9
Q

What are the investigations that reveal a coagulation defect?

A
  • clotting time: 5 - 10 mins normally
  • PTT -> 30 - 40s normally (common & intrinsic pathways)
  • PT -> 14s normally (common & extrinsic pathways)
  • INR -> patient PT/control PT
  • assay of serum level of clotting factors
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10
Q

What are the causes of vascular purpura?

A

Hereditary
1- hereditary hemorrhagic telangiectasia
-> autosomal dominant with impaired vasoconstriction
- treatment: Epsilon amino caproic acid

2- connective tissue disorder

  • Ehler Danlos -> hyperlaxity
  • Marfan syndrome -> aortic regurgitation & tall stature

Acquired
1- traumatic -> convulsions, malignant hypertension, cough
2- inflammatory -> Purpura fulminants, rickets, SLE, PAN
3- immunological -> anaphylactoid purpura
4- idiopathic -> Devil’s punch
5- mesynchymal weakness
- scurvy -> defective collagen synthesis due to vit C deficiency
- steroid & Cushing’s -> diminished collagen synthesis
- senile purpura

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11
Q

What is the etiology of anaphylactoid purpura?

A

allergic reaction to strep throat -> formation of immune complex (IgA + And + complement) -> capillaritis & arteriolitis

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12
Q

What is the clinical picture pf anaphylactoid purpura?

A
  • petichae on buttocks
  • arthralgia -> tender swollen joints
  • nephritic syndrome
  • GI bleeding
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13
Q

How is anaphylactoid purpura diagnosed & treated?

A
  • increased bleeding time
    • Hess capillary fragility test
  • anemia from bleeding
  • renal function impairment & RBC casts
    • autoantibodies

treatment

  • corticosteroids
  • symptomatic treatment
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14
Q

What are the causes of platelet defect purpura?

A

1- increased destruction -> hypersplenism, immunological
2- decreased production -> aplastic anemia, megaloblastic anemia, thiazides & imipenam
3- pooling -> splenomegaly & hypothermia
4- dilutional -> massive blood transfusions
5- increased consumption -> DIC

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15
Q

What is the etiology of ITP?

A

autoimmune disease characterized by IgG (ITP factor) -> antibodies that

  • increase removal of platelet by RES
  • decrease budding of megakaryocytes

could be associated with SLE, CLL, autoimmune hemolytic anemia

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16
Q

What is the presentation of ITP?

A

ACUTE

  • in children 2-9 years
  • spontaneous remission

CHRONIC

  • 20 - 40 years
  • females
  • remission & exacerbation

Clinical picture of purpura due to platelet defect

  • skin & mucous membranes -> epistaxis, gum bleeding, petichae
  • organs -> hematuria, hemoptysis, cerebral hemorrhage
  • spontaneous bleeding < 20 000
17
Q

What will be found on investigation of ITP?

A
  • increased bleeding time & + capillary Hess test
  • decreased platelet count
  • anemia
  • auto antibodies +ive
18
Q

How is ITP managed?

A

1- general measures -> avoid injury, trauma, surgery, & aspirin
2- steroids -> prednisone
3- immunosuppressive -> cyclophosphamide or azathiopnire
4- splenectomy -> in case of
- failed steroid therapy
- relapse after stopping steroids
- fulminant cases
5- IV IgG to block receptors of macrophages -> in emergencies only
6- plasmapheresis

19
Q

What is thrombocytosis & what are its causes?

A

platelets > 400 000

Primary

  • essential thrombocytosis
  • polycythemia vera
  • CML
  • myelofibrosis

Secondary
- post splenectomy

20
Q

What is the clinical picture & treatment of thrombocytosis?

A

CP
- thrombosis (increased platelets) + bleeding (defective platelet function)

Treatment

  • hydroxyurea
  • busulphan
  • alpha-interferon
  • treat the cause
21
Q

What are the causes of coagulation defects?

A

HEREDITARY

  • Hemophilia A -> factor 8
  • Hemophilia B -> factor 9
  • Parahemophilia -> factor 5
  • Afibrinnogenemia -> factor 1

ACQUIRED

  • Liver failure -> decrease in coagulation factors
  • Renal failure -> accumulation of toxins affects protein synthesis
  • Vitamin K deficiency -> defect in factors 1972
  • DIC -> consumption of coagulation factors & platelets
  • Drugs -> heparin
  • SLE
  • Hypothermia
22
Q

What is the etiology & clinical picture of hemophilia A?

A
  • X-linked recessive disease -> mostly affects men
  • deficiency in factor VIII (8)
  • always positive family history
  • females are carrier
  • most common CP -> hematoma & hemoarthrosis
23
Q

What are the investigations done for hemophilia A?

A
  • bleeding time, capillary fragility test & platelet count are normal
  • prolonged PTT -> because intrinsic pathway is affected (factor 8)
  • PT & TT are normal
  • decreased factor VIII level
  • microcytic hypochromic anemia
24
Q

How is hemophilia A treated?

A

1- replace factor VIII -> cryoprecipitate (factor VIII & fibrinogen II)

  • FFP or blood
  • AHF concentrates

2- Desmopressin -> increases release of factor VIII from endothelium

3- in case of Hemoarthrosis -> physical therapy, analgesia, & aspiration after givinng factor VIII

4- prophylaxis

  • genetic counseling
  • avoid trauma, unnecessary operations, anticoagulants, & aspirin
  • immunization against hepatitis & tetanus
  • AHG prophylaxis before surgery
25
Q

What is the difference between hemophilia A & B?

A

Hemophilia B

  • deficiency in factor 9
  • treated with plasma & factor IX concentrate

all the rest is the same

26
Q

What is the etiology for vitamin K deficiency?

A 
1- Decreased intake 
2- decreased flora synthesis 
- premature infants 
- prolonged intake of oral antibiotics 
3- decreased absorption
- obstructive jaundice 
- malabsorption syndrome 
4- decreased activation 
- liver cell failure 
- oral anticoagulants
27
Q

What is the clinical picture of vitamin K deficiency?

A

like hemophilia but without hemoarthrosis

  • skin -> ecchymosis & hematoma
  • internally -> bleeding in muscles & brain
  • externally -> hematemesis, hemoptysis, hematuria
  • anemia
  • CP of the cause
28
Q

How is vitamin K deficiency diagnosed with investigations?

A
  • normal bleeding time, Hess capillary fragility test, & platelet count
  • Clotting time, PTT, & PT are PROLONGED
  • assay of coagulation will show decreased factors 10, 9, 7, 2
29
Q

How is vitamin nK deficiency managed?

A
  • IV vitamin K
  • or plasma transfusion
  • treat the cause -> stop anticoagulants
30
Q

What is the presentation of DIC?

A

Thrombosis

  • thrombosis -> ischemia & organ failure
  • formation of fibrin network is circulation -> intravascular hemolysis

Bleeding

  • platelet consumption
  • coagulation factor consumption
  • FDP increase -> more bleeding
31
Q

What are the causes of DIC?

A
  • obstetric cause
  • cancer prostate
  • major surgery
  • incompatible blood transfusion
  • sepsis or other types of shock
  • fat embolism
  • burns
  • liver cell failure
32
Q

What is the clinical picture of DIC?

A 
1- Tissue ischemia 
- ARDS
- Respiratory failure 
- liver failure 
- peripheral ischemia 
2- Bleeding 
3- C/P of cause
33
Q

What will be found on investigation of DIC?

A

everything is increased except fibrinogen & platelet count

  • bleeding time, + Hess capillary fragility test
  • prolonged clotting time, PT, & PTT
  • decreased fibrinogen but increased FDPs
  • thrombocytopenia (decreased platelets)
  • intravascular hemolysis -> decreased heptaglobin & hemipixin
  • organ failure
  • all coagulation factors decreased
34
Q

What is the treatment of DIC?

A

depending on the dominant symptom if its bleeding or thrombosis

if BLEEDING -> replace coagulation factors only
1- plasma only
2- platelets if count is < 20 000
3- cryoprecipitate
4- epsilon aminocaproic acid & tranexamic acid in case of profuse bleeding

if THROMBOSIS
- give heparin ONLY if bleeding is NOT from major vessels

Internal Medicine pt. 2 (19 decks)

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