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RACP 2023 > HAEM > Flashcards

HAEM Flashcards

1
Q

DVT treatment duration?
- Proximal provoked
- Distal provoked
- Distal unprovoked

A
  • Superficial: LMWH, 4-6 weeks
  • Distal provoked: 6 weeks
  • Proximal provoked: 3 months
  • Distal unprovoked: 3 months

The common thrombophilias, factor V Leiden and prothrombin gene mutation don’t change timing

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2
Q

PE treatment duration?

A

Provoked:
- distal: 6 weeks
- proximal: 3 months
Unprovoked: 3-6 months
Submassive: 6-12 months
Massive: Indefinite
Permanent risk factor: Indefinite

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3
Q

Difference between anticoagulants?

A
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4
Q

What is assessed in renal transplant recipient?

A

CV
Resp
Substances
Infection
Malignancy
Psychosocial
PCKD

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5
Q

Risk of ESKD in renal transplant donor?

A

< 1% in white, young female

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6
Q

Where do immunosuppressants work
- Signal 1,2,3

A

Signal 1: Calcineurin inhibitors, ATG
Signal 2: CTLA4
Signal 3: Basiliximab

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7
Q

What diagnosis most likely to recur in renal transplant?

A

FSGS

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8
Q

Causes for delayed graft function in renal transplant?

A

ATN/AIN
Thrombosis
Drugs
Early disease recurrence
Obstruction
Rejection

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9
Q

Causes for worsening renal function < 12 months in renal transplant?

A

AKI
Thrombosis
rejection
BK polyoma nephropathy
RAS
Immunosuppressants

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10
Q

Causes for rejection in renal transplant + tx?
- Hyperacute (hours)
- Acute (days)
- Chronic

A

Hyperacute - preformed antibodies - removal
Acute - T cells - ATG/steroids
Chronic - antibody/cell OR disease recurrence OR drugs - Plasma exchange, IVIG, Ritux.Bortex

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11
Q

Causes for infection in renal transplant?

A

< 1 month: nosocomial; donor/recipient derived infections
1-6 months: opportunistic/ latent infection/ residual
> 6 months: community acquired

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12
Q

Causes for ESKD in renal transplant?

A

HTN
DM

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13
Q

Causes for cancer in renal transplant?

A

SCC
B lymphoproliferative disorders (EBV)

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14
Q

Causes for death with graft loss in renal transplant?

A

Early: CV
Late: cancer

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15
Q

Causes graft loss in renal transplant?

A

Early: thrombosis/rejection
Late: Chronic rejection/ allograft nephropathy from CNI

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16
Q

How does G6PD deficiency cause hemolysis?

A

G6PD enzyme involved in cell membrane
G6PD –> NADPH –> glutathione

Reduced glutathione –> can’t resistant oxidants

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17
Q

Drug causes of G6PD hemolysis?

A

Antimalarials
Rasburicase
Sulfur drugs
Aspirin
Vit K analogues

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18
Q

How does PNH cause hemolysis?

A

Lacks PIGA gene –> normally synthesis GPI –> protects from complement killing

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19
Q

How to differentiate extracorpscular and intracorpuscular hemolysis?

A

Intracorpuscular causes hemoglobinuria

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20
Q

Treatment for HUS?

A

Supportive
Eculizumab: C5

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21
Q

Which diseases do you usually use plasma exchange?

A

TTP
Cryoglobulinemia
AntiGBM

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22
Q

Sickle cell carriers manifestations?

A

Thromboses under extreme circumstances: heat, exercise –> rhabdo
2x risk VTE

23
Q

Treatment for Sickle Cell Disease + MoA?

A

Hydroxyurea: incr HbF –> antisickling effect

Transfusions +/- exchange

Keep warm

24
Q

Alpha/Beta thalassemia gene abnormalities + clinical result

A

Check notes

25
Q

PV treatment?

A

Aspirin OD: all
Aspirin BD: thrombosis, CV risk factors

LOW RISK: age < 60, no history thrombosis
- Aspirin

HIGH RISK: age > 60, history of thrombosis, PLTS > 1500 WCC > 15, uncontrolled symptoms
- Ruxolitinib
- Hydroxyrea
- Interferon

26
Q

ET treatment?

A

Old = hydroxyurea + aspirin
CVS/ mutation= aspirin
Thrombosis = BD aspirin

CHECK NOTES

27
Q

Rate of transformation MGUS –> MM

A

1%

28
Q

Definition MGUS

A

Clonal plasma cells < 10%
NO CRAB
M protein < 3

29
Q

Definition MM

A

CRAB/ lesion/ high FLC
Clonal plasma cells > 20%

30
Q

Marker that is strongest predictor of survival in MM?

A

Beta-2 microglobulin

31
Q

Which diseases are associated with lymphoma development? How

A

Burgdella Burgdorfi
HIV
EBV
HCV
H pylori
HTLV

Usually inhibit tumour suppressor genes/ inhibit apoptosis/ cause unregulated growth

32
Q

Risk factors for lymphoma development?

A

Immunosupression
Transplant
Medications: azathioprine/ MTX
Chemo

33
Q

Explain Ann Arbor staging?

A

I: localised
II: spread on one side of diaphragm
III: spread to other side of diaphragm
IV: extranodal

34
Q

Key features of HL?

A

Bimodal distribution
Curable

35
Q

CD markers of Reed Sternberg cells?

A

CD 15 and 30

36
Q

Non-chemo treatment options for HL?

A

CD 30 target: Brentuximab vedotin
PD-1

37
Q

Follicular lymphoma translocation?

A

t(14:18) –> BDL2 association

38
Q

Non chemo agent used for indolent lymphomas?

A

CD-20

39
Q

Hepcidin MoA?

A

Produced by liver
Regulates plasma iron, iron absorption, release of Fe from macrophages involved in iron recycling and storage
WORKS ON MACROPHAGES AND ENTEROCYTES
§ Binds to ferroportin
§ Impaired absorption and release from stores –> decreased plasma iron by forcing it to be sequestered in cells
□ Makes ferroportin become internalised preventing release from enterocytes
□ Traps iron
§ Reduces expression of ferroportin on basolateral surface of enterocytes
□ Can’t transfer Fe
Causes of increased hepcidin synthesis
§ Inflammation –> causes low transferrin
§ Infection
Causes of decreased hepcidin
§ Fe deficiency
HAEMACHROMOTASIS: IMPAIRMENT OF HEPCIDIN

40
Q

Fe absorption and transferring?

A

Absorption
- Absorbed from diet
○ Duodenum
○ Proximal small intestine
- Active erythropoiesis and/or iron deficiency increase absorption
- Iron overload and systemic inflammation decrease absorption.
- Brush border
○ Ferric Fe converted to ferrous form
○ DMT-1 transporter
- Or release from stores (bound to transferrin)

Transferrin-iron complex
- Free iron is toxic
- Circulates in plasma
- Comes into contact with transferrin receptor on marrow erythroid cells
- Complex absorbed
- Fe released and used for heme synthesis
- Transferrin complex recycled to surface of cell –> circulation
- Negatively controlled by hepcidin

41
Q

B12 metabolism:

A

Check notes

42
Q

Folate metabolism:

A

Check notes

43
Q

Thrombocytosis causes?

A
44
Q

Thrombocytopenia causes?

A
45
Q

Leukocytosis causes?

A
46
Q

Neutropenia causes?

A
47
Q

Aplastic anaemia treatment?

A

○ Antithymocyte globulin:
§ SE’s: serum sickness, infusion reaction
○ Cyclosporine
○ Eltrombopag
TPO agonist

48
Q

Diagnosis Fe deficiency

A

Serum ferritin <30 ng/mL
● Transferrin saturation ≤19 percent,

49
Q

MGUS to MM development rate?

A

~1% of patients per year with MGUS go on to develop myeloma

50
Q

Difference between MGUS, smouldering myeloma and MM?

A

Check notes

51
Q

What is Caplacizumab?

A

Antibody against vWF

52
Q

What is · Romiplastim/ Eltrombopag + what is it used in?

A

Refractory TPO

53
Q

Auer rods significance?

A

Not always present but if they are, virtually certain (APML)
§ Myeloperoxidase reaction + : indicates that the blasts are myeloid

54
Q

What is differentiation syndrome?

A

Happens often within 3 weeks APML treatment

□ Promyelocytes differentiate, attacks endothelium
□ Fever, edema, weight gain, hypoxia with lung infiltrates, pleurpericardial effusion, renal and hepatic dysfunction
□ Mx: dex 10mg BD, delay chemo; resstart when symptoms resolved

RACP 2023 (17 decks)

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