BL Practice Flashcards

1
Q

Is the first MTP involved in gout or CPDD?

A

Gout

remember gout is cool extremities and 1st MTP

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2
Q

Hemophilia A

  • what is it?
  • PT vs PTT?
  • Genetic disorder?
A

(VIII Deficiency)

most common

PT is normal, but PTT is prolonged.

X linked

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3
Q

Hemophilia B

  • what is it?
  • PT vs PTT?
  • Genetic disorder?
A

(Christmas/IX def)

PT is normal, but PTT is prolonged. (just like hem A)

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4
Q

Hemophilia C

  • what is it?
  • PT vs PTT?
  • Genetic disorder?
A

Factor XI Deficiency

AR

PT is prolonged, but PTT is normal.
(Opp of Hem A and B)

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5
Q

The most commonly used treatment options in ITP include:

A
Corticosteroids
Intravenous immunoglobulin (IVIG)
Splenectomy
Rituximab 
TPO (=thrombopoetin):
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6
Q

Desmopressin (DDAVP)

A

DDAVP stimulates release of von Willebrand factor and factor VIII from endothelial stores.It will temporarily increase levels of those factors 3 to 5 times.

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7
Q

Argatroban

A

direct thrombin inhibitor
- used to treat Heparin-induced thrombocytopenia syndrome (HIT) (platelets <50%)

can also use Lepirudin

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8
Q

anti jo Ab are associated with?

A

DM/PM

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9
Q

causes of a prolonged PT and PTT

A

Liver disease
Vit K def
Warfarin

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10
Q

Causes of a prolonged PTT more than protime

A

DIC

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11
Q

Serine Proteases

A
  1. Protein C
    1. Plasminogen
    2. t-PA (tissue plasminogen activator)
    3. u-PA (urokinase)

Plasmin

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12
Q

Inhibitors of fibrinolysis

A

PAI-1
alpha 2- antiplasmin
TAFI (an exopeptidase)

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13
Q

things factor XIII can do

A

aid TAFI and alpha 2- antiplasmin in fibrinolysis

  • link D-D in DEDs together
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14
Q

TFBI

A

plays a role in anticoagulation and in protection from atherosclerosis.

(part of the quaternary complex with Xa, VIIa, TF)

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15
Q

What to avoid if you have VWD?

A

aspirin, NSAID’s, other platelet inhibiting drugs

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16
Q

Platelet type excessive bleeding

A

nosebleed,
GI bleeding,
menorraghia

*top down

17
Q

Clotting factor

A

hemophilia,
joint bleed,
bleed into muscle or retroperitoneum

18
Q

lupus anticoagulant

A
  • Common acquired abnormality → Results in hypercoaguable state.
    • Causes Antiphospholipid Antibody Syndrome (APS) → in vivo thrombotic disorders)

*remember: This is due to lupus anticoagulant: an IgG antibody that reacts against the phospholipid in the platelet membrane and endothelial cells.
○ PTT will NOT correct when mixed with normal plasma.

19
Q

Arterial thrombi:

A

○ Occur in high shear stress
○ Primarily platelets, few RBCs (white thrombi)
○ If large enough, cause downstream ischemia
○ Thick, high pressure, muscular
○ High oxygen

20
Q

Venous thrombi

A
○ Slow blood flow
		○ Large amounts of fibrin with lots of RBCs (red thrombi)
		○ More common with increased age
		○ Thin, low muscle
		○ Oxygen poor
21
Q

Antithrombin deficiency:

A
  • Regulatory protein

* 60% of people w/ deficiency have recurrent venous thrombosis

22
Q

acquired disorders that are associated with recurrent venous or arterial thromboembolism.

A
  1. Antiphospholipid Antibody Syndrome (One of the more severe)
    1. Malignancy (Myeloproliferative disorders)
    2. Trauma
    3. Oral contraceptives
    4. Pregnancy
23
Q

antiphospholipid antibody syndrome

A

○ Can see both venous and arterial thrombosis

Clinical Criteria:
• Vascular thrombosis:
○ 1+ clinical episodes of thrombosis
• Complications of pregnancy:
○ 1+ unexplained death of fetus > 0 wks
○ 1+ premature births of neonates <10 wks

24
Q

LMWH

A

Subcutaneous, longer half life, better bioavailability