heme 3 Flashcards Preview

Hematology, oncology > heme 3 > Flashcards

Flashcards in heme 3 Deck (62)
Loading flashcards...
1
Q

Vitamin K deficiency labs

A

PT + INR prolonged + PTT normal or mildly prolonged (prolonged with severe vitamin k deficiency) + inciting factor

2
Q

what is d-dimer?

A

fibrin degradation product (or FDP), a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis

3
Q

Other reasons for elevated d-dimer

A

any acute or inflammatory process (eg, age >50 years, recent surgery or trauma, acute illness, pregnancy or postpartum state, rheumatologic disease, renal dysfunction [estimated glomerular filtration rate <60 mL/min/1.73 m2]), sickle cell disease, pulmonary disease

4
Q

life span of one red blood cell

A

120 days

5
Q

effect of prophylactic heparin on PTT

A

small, but significant, increase in aPTT (mean 38.6)

6
Q

lab profile of factor VIII deficiency

A

Prolonged PTT

7
Q

Effect of warfarin on PT and PTT

A

Typically prolongs the PT alone, but at high levels can prolong both tests.

8
Q

Effect of heparin on PT and PTT

A

Heparin typically prolongs the aPTT alone (because PT reagents contain heparin-binding agents that block heparin effect), but at high levels heparin can prolong both tests.

9
Q

Effect of direct thrombin inhibitors on PT and PTT

A

typically prolong both tests

10
Q

Effect of Xa inhibitors on PT and PTT

A

prolong the PT and aPTT, although these effects are variable

11
Q

Effect of liver disease on PT and PTT

A

Typically prolongs just PT, but also prolong PTTs in severe liver disease

12
Q

Describe the clotting cascade

A

https://upload.wikimedia.org/wikipedia/commons/thumb/b/b6/Coagulation_full.svg/400px-Coagulation_full.svg.png

13
Q

what is a lupus anticoagulant (pathophys)

A
  • Acquired autoantibody to phospholipids. Interacts with platelet membrane phospholipids, increasing adhesion and aggregation of platelets, which accounts for in vivo prothrombotic characteristics.
  • misnomer, as it is actually a prothrombotic antibody.
14
Q

Initial workup of prolonged PTT

A

Step 1 = Mixing study →
IF corrects = deficient clotting factor
IF remains abnormal = inhibitor present (ie lupus anticoagulant)
confirm presence with prolonged phospholipid-sensitive functional clotting testing (dilute Russell’s viper venom time, or the Kaolin clotting time)

15
Q

Concept of a mixing study

A

You’re looking for an inhibitor in plasma or a deficient clotting factor. Patient’s plasma is mixed with normal pooled plasma and the clotting is reassessed. If a clotting inhibitor such as a lupus anticoagulant is present, the inhibitor will interact with the normal pooled plasma and the clotting time will remain abnormal. However, if the clotting time of the mixed plasma corrects towards normal, the presence of an inhibitor such as the lupus anticoagulant is excluded, and instead a deficient quantity of clotting factor (that is replenished by the normal plasma) is likely.

16
Q

treatment of lupus anticoagulant

A

IF history of thrombosis + documented history of lupus anticoagulant twice → consider indefinite AC
IF no history of thrombosis → observation

17
Q

Prevalence of lupus anticoagulant

A

Relatively common (believed to be approximately 5% in adults, with a predominance among females of reproductive age).

18
Q

Why does renal disease cause coagulopathy

A

uremic platelet dysfunction

19
Q

Reversal agent for Xa inhibitors

A

Andexxa

20
Q

Problem with Xa inhibitor reversal agent

A

Not available on most pharmacy formularies

21
Q

Thrombotic risk of liver disease

A

Cirrhotics are coagulopathic but also hypercoagulable (protein c and s deficiency). This is why they still need heparin dvt ppx (from studies).

22
Q

Only case in which hypercoagulability workup would change management

A

High risk anti phospholipid syndrome, which requires coumadin

23
Q

Where are platelets produced?

A

Bone marrow, just like red and white cells.

24
Q

What is “treatment failure” from NOACs typically due to?

A

Nonadherence – patients missing doses. Due to short half life, you are at increased thrombotic risk by just missing a dose or two.

25
Q

Why you always need to calculate reticulocyte index

A

The problem arises because the reticulocyte count is not really a count but rather a percentage: it reports the number of reticulocytes as a percentage of the number of red blood cells. In anemia, the patient’s red blood cells are depleted, creating an erroneously elevated reticulocyte count.

26
Q

What type and screen generally screens for

A

ABO
Rh
some other atypical antibodies

27
Q

typical premedication before IVIG

A

acetaminophen and diphenhydramine

28
Q

IVIG side effect profile

A

can have severe adverse effects, both localized and systemic.

29
Q

What are hemagglutinins?

A

glycoproteins which cause red blood cells (RBCs) to agglutinate or clump together. (Note that agglutination is one of three steps in the more complex process of coagulation.)
- anti-A and anti-B antibodies are considered hemagluttinins

30
Q

May Thurner Syndrome

A

Iliac vein compression syndrome. compression of the common venous outflow tract of the left lower extremity may cause discomfort, swelling, pain or clotting in the iliofemoral veins. It is caused by left common iliac vein compression by the overlying right common iliac artery.

31
Q

Evans syndrome clinical features

A

AIHA + thrombocytopenia

32
Q

When do schistocytes occur in hemolytic syndromes

A

intravascular syndromes

33
Q

examples of intravascular hemolysis

A

1) prosthetic valves
2) MAHA — microangiopathic hemolytic anemia (TTP, HUS, DIC)

34
Q

First step on boards if stem sounds like TTP

A

peripheral smear (don’t send ADAMST13 level, takes too long)

35
Q

Risk for spontaneous brain bleed happens at what platelet level

A

10

36
Q

How to exclude pseudo thrombocytopenia

A

Draw blood into citrated tube rather than EDTA tube

37
Q

First step on boards if looks like ITP and platelets aren’t severely low

A

Repeat CBC outpatient

38
Q

Next step after SPEP shows polyclonal gammopathy

A

NO FURTHER TESTING

39
Q

Differential for polyclonal gammopathy

A

Inflammatory disorders
Infections
Liver disease (60%)
Reactive processes

40
Q

EPO should be avoided in…

A

patients with a curable malignancy

41
Q

Presentation of hemoglobin C trait

A
  • asymptomatic
42
Q

Presentation of hemoglobin C disease

A
  • mild hemolytic anemia, splenomegaly, borderline anemia
43
Q

how to differentiate Hgb C from hgb A2 disease

A
  • citric acid agar
44
Q

Second most common cause of enzyme-deficient hemolytic anemia after G6PD

A

Pyruvate kinase deficiency (PKD)

45
Q

Management of PKD

A

most affected individuals don’t need treatment

46
Q

PKD inheritance

A

Autosomal recessive

47
Q

Clinical features of Hbs-Beta thalassemia

A
  • typically clinically indistinguishable from SCD
48
Q

electrophoresis pattern of SCD

A
  • pretty much all HbS, no HbA
49
Q

RDW in thalassemia

A
  • typically low (red cells are homogeneous)
50
Q

Lab test to distinguish thalassemia from iron deficiency aside from electrophoresis

A

ZPP (zinc protoporphyrin)

51
Q

How to diagnosis alpha-thalassemia trait

A
  • NOT electrophoresis

- sequencing

52
Q

RBC count in mild thalassemia

A
  • commonly normal or elevated (unclear reason)
53
Q

Management of drug induced AIHA

A
  • stop drug and supportive care (not immunosuppression)
54
Q

Most common cause of drug-induced AIHA

A

cephalosporins

55
Q

hereditary elliptocytosis clinical features

A

hemolytic anemia (defect in RBC membrane protein and cytoskeleton that predisposes a pt to hemolytic anemia)

56
Q

sequela of copper deficiency

A

sideroblastic anemia

57
Q

clinical features of copper deficiency

A

sensory ataxia + neuropathy + muscle weakness

58
Q

C3 and IgG pattern most commonly seen with warm AIHA

A

IgG+, C3+

59
Q

antibody patter for cold agglutinin disease

A

IgG negative C3 positive

60
Q

Pyruvate kinase deficiency clinical presentations

A
  • neonatal janducie
  • chronic hemolytic anemia
  • iron overload
  • coombs negative hemolytic anemia
61
Q

what is transient erythroblastopenia of childhood? clinical features?

A
  • transient or temporary red cell aplasia (self limiting)

- otherwise healthy child abruptly develops severe anemia

62
Q

MCV in anemia from hypothyroidism

A

macrocytosis

Decks in Hematology, oncology Class (218):