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Flashcards in Heme Emergencies Deck (18)
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1
Q

WHat are the 3 phases of hemostasis?

A
  • primary: vasoconstriction and platelet plug
  • secondary: coagulation (factors)
  • tertiary: fibrinolysis
2
Q

Kids who get their wisdome teeth pulled and get dry sockets, what type of disorder is most likely?

A

-vonWillebrands

they are oozers, usually vWF deficient.

3
Q

When would we check the D-dimer levels? What is D-dimer?

A

-when we think we are clotting, D-dimer is the measure of fibrinolysis

4
Q

Where are all pro-coagulants synthesized?

A

all pro-coagulants are synthesized in the liver, EXCEPT for vWF this is synthesized in the endothelium)

5
Q

What is the only thing to break down clots?

A

tPA

6
Q

What does protein C do? S?

A
  • acts as an anticoagulant by inactivating factors V and VIII
  • S breaks down fibrin into fibrin degredation products(D-dimer) that act as anticoagulants
7
Q

Physiology of Fibrinolysis

A
  • plasminogen binds firbin and tissue plasminogen activator (tPA)»> leading to conversion of plasminogen to active plasmin.
  • plasmin cleaves fibrin strand at multiple sites and releases fibrin degradation products (D-dimer)
8
Q

Hemophilia
Signs
What pathway is impaired?
what test will be prolongated? normal?

A
  • *Swollen, painful joints
  • local bleeding out of proportion with injury
  • any other bleeding

Impaired synthesis of functioning of the intrinsic pathway (VIII, IX, XI, and XII)

Prolongation of the aPTT and the Pt will remain normal

-Patients with hemophilia do not bleed more profusely or more quickly but bleed for a longer time.

Hemophilia A=VIII
Hemophilia B=IX
(x-linked recessive)

9
Q

Lab findings of Hemophilia A

hemophilia b?

A

A:
PTT prolonged
reduced factor VIII
Normal vWF

B:
PTT prolonged
reduced factor IX

10
Q

Physical Exam findings in -Platelet Defects/Deficiences

  • Coagulataion Factor Defects
  • Any bleeding disorder
A

Platelet:
-prolonged superficial bleeding, epistaxis, gingival and mucosal bleeding, purpura, petechiae

Coagulation:
-cannot effectively reinforce platelet-initiated hemostasis, recurrent bleeding into deep structures, muscles, joints, and retroperitoneum.

Any:
-ecchymosis, GI bleeding, Menorrhagia

11
Q

Physical exam findings of anemic pt

A
  • pallor, skin and conjunctiva
  • tachycardia
  • systolic murmurs (Cardiac output is higher b/c you are compensating for lack of O2)
  • tachypnea at rest
  • hypotension
12
Q
Vitamin K
Source
required for synthesis of?
Most commonly seen in? (who)
Antidote for what drug?
A

green veggies

required for synthesis of factors II, VII, IX, X, and Protein C and S
extrinsic

Alcoholics! and chronic kidney disease, poor diet, malabsorption

Warfarin! (managing high INR values)

13
Q

Von Willebrands Disease
signs and symptoms
Lab findings

A
excessive menstrual and postpartum bleeding
GI bleeding
epistaxis
gingival bleeding
easy bruising
UNCOMMON for joints to be involved
Lab-
prolonged bleeding time
PTT may be prolonged
PT and platelets normal
Factor VIII decreased
vWF levels low
  • ingestion of aspirin can precipitate bleeding that may not have occurred otherwise
  • some pts remain asymptomatic
14
Q
Vitamin K
Source
required for synthesis of?
Most commonly seen in? (who)
Antidote for what drug?
A

green veggies

required for synthesis of factors II, VII, IX, X, and Protein C and S
extrinsic

Alcoholics! and chronic kidney disease, poor diet, malabsorption

Warfarin! (managing high INR values)

15
Q

Aspirin
inhibits what?
effects last for how long

A

IRREVERSIBLY inhibits cyclooxygenase in platelets

Effects last for 7 days

16
Q

When distinguishing between HUS and TTP, what symptoms would help?

A

HUS has more renal manifestations because it has different vascular beds. (No neuro symptoms)

TTP will have neurologic Sx and not always renal failure.

17
Q

How to distinguish between HUS and DIC

A

Coags are normal in HUS and not in DIC

18
Q

Sx of DIC

A

-bleeding: petechia, ecchymosis, blood in urine, stool, vomitus, sputuem

  • renal dysfunction
  • hepatic dysfunction
  • shock
  • thromboembolism
  • cns involvement