Freeman Flashcards

1
Q

What is the incidence of Factor 5 Leiden? HOw does this affect your risk if you are heterozygous or homozygous for it?

A

hyper coagulability risk
Incidence: 3-8%
Hetero: 8X risk
Homo: 20X risk

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

What are some of the things that affect your mechanical flow dynamics?

A
prior sites of thrombus
compression due to obesity
chemical
*nicotine
*vasoconstricting agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some modifiable risk factors for coagulation?

A
Obesity
Sedentary life-style
Travel
OCP
Pregnancy
Surgery
        *elective, particularly
	ortho
Smoking
Prior DVT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are som unmodifiable risk factors for coagulation?

A
Factor V Leiden
Prothrombin Gene Mutation
Malignancy
Surgery
        *emergent
Chronic Illness
Lupus Anticoagulant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the treatment for acute thrombogenesis?

A

Warfarin + Heparin

Heparin for 7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which factors are Vit K dependent?

A

2, 7, 9, 10
Proteins C& S
**Vit K carboxylates the N terminus of these factors to activate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the half life of Factor X?

A

48 H

Note: this is a coagulant.

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

What is the half life of Protein C?

A

6 hours

Note: this is an anticoagulant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why is it that you have to treat patients struggling with coagulation with heparin for a full 7-10 days?

A

b/c the factors that are alive & active take some time to die.
4-5 half lives.
This equals out to 7-10 days. Otherwise: just get a blood clot a few days later.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What affects the course of Warfarin?

A

based on the etiology of the thrombogenic event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When do you sometimes see lupus anticoagulants?

A

may be seen at the time of acute thrombotic events (acute phase reactants)

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

How is a lupus anticoagulant identified in lab? In vitro & in vivo?

A

In vitro: prolongs PTT

in vivo: procoagulant.

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

When a patient is taking both heparin & warfarin…when should the warfarin be instituted?

A

it can be initiated at the same time as heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

66yo male admitted to Med Center w/hypotension, tachycardia, & fever.
W/U reveals gram(+) septicemia 2/2 staph aureus. Echocardiogram reveals mass in ‘upper’ R-ventricle. Nurses report patient ‘oozing’ from all iv sites.
EXAM: b/L foot amputations
No obvious source of skin
breakdown/infections
LABS: PT 13.3 secs (nl: 11-12.2 secs)
1:1 mixing study: PT normalizes

PMHx: DMII; no h/o cardiac dz.

D/C’ed 3 weeks earlier for gram(+) sepsis @ that time.
What’s going on?

A

the normalizing with the mixing study shows that this person probably has a factor deficiency
seems to be suffering from heparin inducted thrombocytopenia
**seems to have endocarditis after a staph aureus septicemia that induced DIC

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

Same pt
On admit, platelet count 175K (Nl: 150-400K)
Started on LMWH (Lovenox) prophylactically on admit; next day, platelets are 45K.

The ICU team requests Heme consult regarding recommendations for anticoagulant agent of choice; they suspect HIT. Cardiology suggests treatment of thrombus.

Your recommendations?
What should be done for this patient?

A

stop the heparin!

treat the endocarditis
DIC will go away…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain what happens in type I HIT.

A
  • *Modest, transient decrease in platelets 2/2 heparin-induced platelet agglutination.
  • *Self-limited; plt counts can return to normal while heparin is continued.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Explain what happens in Type II HIT.

A

A drug-induced, immune-mediated response 2/2 abs directed against heparin-plt factor 4 complete that results in a 50% or greater drop in platelet counts
**Severe thrombocytopenia w/bleeding is rare!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

HIT is less likely with which type of heparin? When is HIT usu seen?

A

usu seen after major surgery where large volumes of heparin are required
less likely with low molecular weight heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What Should be considered in all recently hospitalized patients returning w/acute thrombosis w/in 1-2 weeks of their hospital stay?

A

HIT

shows thrombocytopenia & thrombosis!

20
Q

What is the testing done for HIT? What is the treatment?

A

Testing: radiolabeled platelet-serotonin release assay
Rx: direct thrombin inhibitors

21
Q

Why is there both thrombosis & thrombocytopenia in HIT?

A

blood clots being made
consumption of platelets
also autoimmune destruction of heparin-platelet 4 complex

22
Q

How do you measure the effectiveness of 10a inhibitors?

A

measure 10a

measure D-dimer

23
Q

What is the pathophysiology of DIC?

A

Widespread activation of the clotting cascade causing a consumption of clotting factors and platelets w/resultant bleeding.

Microvascular compromise 2/2 to thrombin formation results in tissue ischemia w/resultant end-organ damage, particularly of liver & kidneys.

24
Q

DIC is triggered by diseases that promote the expression of tissue factor (transmembrane glycoprotein). Give some examples.

A
  • Gram(-) septicemia
  • damaged cerebral tissue
  • APL (promyelocytic leukemia) awa other liquid/solid malignancies.
  • Placental tissue from obstetric catastrophes
  • Snake venoms
  • Acute hemolytic transfusion rxns
  • Hypotension from any cause can result in endothelial cell damage(CABG, etc.
  • Massive Tissue Injury: trauma;burns; hypothermia
25
Q

What is the cause of activation of the coagulation cascade in DIC?

A

Endotoxin
IL-1
TNF alpha
**tissue factor is released in response to the presence of these cytokines

26
Q

What are the characteristic lab findings in patients with DIC?

A

Prolonged PT/PTT or both.
Thrombocytopenia
Decreased fibrinogen levels
Increased D-dimer

27
Q

What are some disorders of coagulation that can lead to bleeding?

A

platelet disorders

factor disorders

28
Q

What are some disorders of organ systems that can lead to bleeding?

A

renal failure
liver failure
hematopoietic
coronary artery issues

29
Q

What are some drugs that could cause bleeding?

A
GP IIb/IIIa inhibitors(Plavix)
COX I inhibitors(ASA)
Heparin
Coumarins
OTC
*Ginko
*Ginseng
30
Q

What is the appropriate drug to treat bleeding due to renal failure? What does it do?

A

DDAVP

releases factor 8 from weibel palace bodies in endothelial cells of blood vessels

31
Q

What are the possible causes of a prolonged PT?

A

malnutrition
liver disease (due to decreased synthesis of Vit K factors)
coumadin

32
Q

What are the possible causes of a prolonged PTT?

A

lupus anticoagulant/acquired factor inhibitors
vWD
Factor 8/9 deficiency or inhibitor
heparin

33
Q

If a mixing study is not corrective…what are you thinking?

A

there is an inhibitor present

**next step: check specific factor assays

34
Q

If a mixing study is corrective…what are you thinking?

A

deficiency of a factor

perform a factor assay

35
Q

DDAVP is contraindicated in which condition ?

A

type II von wilebrand’s disease

36
Q

What’s the deal with factor 8?

A

there are 2 different molecules
one is for vwd & binds to endothelial cells
another is used for hemophilia treatment & has a different mechanism & is a procoagulant

37
Q

Can a baby with possible vwd have a circumcision?

A

yes
b/c some of the good factor 8 from the mom will have crossed the placenta
the babies shouldn’t bleed for a few months

38
Q

What are the different ways that you can get vwd?

A
Inherited;  autosomal dominant
Type 1:  Quantitative deficiency
Type 2:  Qualitative deficiency
Type 3:  Total deficiency Acquired
 *lymphoproliferativd disorders: can create antibodies to factor 8
*Monoclonal gammopathies
 *MPS, particularly ET: ET—essential thrombocytosis
*Mechanical (Heidi’s Syndrome)
39
Q

How is vwd inherited? WHat does it look like clinically?

A

aut dom

mucosal oozing after surgery or trauma

40
Q

How is hemophilia inherited? What does it look like clinically?

A

x-linked

clinically spontaneous hemarthroses

41
Q

Hemophilia B is also known as what?

A

Factor 9 problem

Christmas!

42
Q

Patient presents w/symptomatic AS. During w/u, he is found to have microcytic anemia. FOBT is (+). PTT is prolonged @ 12.9(nl 11.7); 1:1 mixing study corrects PTT to 10.8. EGD (-) but colonoscopy reveals (3) polyps in R-colon. Capsule endoscopy reveals scattered, slightly bleeding av-malformations in ileum. To Rx the condition, you order…..

  1. DDAVP intranasal spray during acute bleeding episodes.
  2. Factor VIII replacement during acute bleeding episodes.
  3. R-hemicolectomy
  4. Aortic Valve Replacement
  5. Partial small bowel resection.
  6. Amicar 1 gm q6HRs to seal clots @ site of small vessel bleeds (anti-fibrinolytic).
A

Aortic Valve Replacement

43
Q

What is Heyde’s Syndrome?

A

A syndrome caused by aortic valve stenosis resulting in GI bleeding @ sites of colonic angiodysplasia w/exaggeration of bleeding 2/2 mechanical destruction of ultra-large von Willebrand factor molecules(acquired vWD).

44
Q

A 36 year old male presents not the emergency department with a 36 hour history of headache and intermittent episodes of aphasia. He has no significant past medical history and takes no medications. Other symptoms include intermittent low-grade fevers with temperatures to 38.5°C. On examination, he has mild left sided weakness without other abnormalities. Initial laboratory examination reveal moderate renal insufficiency, a hemoglobin of 9.2 g/dl, and a platelet count of 42 x 109/L. Coagulation tests are normal. Examination of the peripheral blood smear reveal frequent red cell fragments. The lactate dehydrogenase level is approximately 4 times the upper limit of normal.
Which of the following is the most likely cause of this patient’s disorder?
Disseminated intravascular coagulation
Drug-associated toxic reaction
A hereditary form of thrombotic thrombocytopenic purpura
An acquired antibody-mediated microangiopathic disorder

A

C. TTP
disorder can be due to autoantibody against ADAMTS13, involved in vwfactor processing.
microvascular fibrin deposition & thrombocytopenia associated with hemolysis

treat with plasmapheresis

45
Q

What is quintad in TTP?

A
Fever
MSΔ’s
Renal insufficiency
Microangiopathic HA
Thrombocytopenia
46
Q

What are the lab abnormalities seen in TTP?

A

Anemia/thrombocytopenia
Very Raised LDH
Raised serum creatinine
Peripheral Smear: schistocytes

47
Q

What are some possible causes of acquired ADAMTS-13 antibodies?

A
E coli
idiopathic
autoimmune disease
drug associated
bloody diarrhea prodrome
pregancy, postpartum
hematopoietic cell transplantation