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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
PV treatment?
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
ET treatment?
Old = hydroxyurea + aspirin CVS/ mutation= aspirin Thrombosis = BD aspirin CHECK NOTES
27
Rate of transformation MGUS --> MM
1%
28
Definition MGUS
Clonal plasma cells < 10% NO CRAB M protein < 3
29
Definition MM
CRAB/ lesion/ high FLC Clonal plasma cells > 20%
30
Marker that is strongest predictor of survival in MM?
Beta-2 microglobulin
31
Which diseases are associated with lymphoma development? How
Burgdella Burgdorfi HIV EBV HCV H pylori HTLV Usually inhibit tumour suppressor genes/ inhibit apoptosis/ cause unregulated growth
32
Risk factors for lymphoma development?
Immunosupression Transplant Medications: azathioprine/ MTX Chemo
33
Explain Ann Arbor staging?
I: localised II: spread on one side of diaphragm III: spread to other side of diaphragm IV: extranodal
34
Key features of HL?
Bimodal distribution Curable
35
CD markers of Reed Sternberg cells?
CD 15 and 30
36
Non-chemo treatment options for HL?
CD 30 target: Brentuximab vedotin PD-1
37
Follicular lymphoma translocation?
t(14:18) --> BDL2 association
38
Non chemo agent used for indolent lymphomas?
CD-20
39
Hepcidin MoA?
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
Fe absorption and transferring?
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
B12 metabolism:
Check notes
42
Folate metabolism:
Check notes
43
Thrombocytosis causes?
44
Thrombocytopenia causes?
45
Leukocytosis causes?
46
Neutropenia causes?
47
Aplastic anaemia treatment?
○ Antithymocyte globulin: § SE's: serum sickness, infusion reaction ○ Cyclosporine ○ Eltrombopag TPO agonist
48
Diagnosis Fe deficiency
Serum ferritin <30 ng/mL ● Transferrin saturation ≤19 percent,
49
MGUS to MM development rate?
~1% of patients per year with MGUS go on to develop myeloma
50
Difference between MGUS, smouldering myeloma and MM?
Check notes
51
What is Caplacizumab?
Antibody against vWF
52
What is · Romiplastim/ Eltrombopag + what is it used in?
Refractory TPO
53
Auer rods significance?
Not always present but if they are, virtually certain (APML) § Myeloperoxidase reaction + : indicates that the blasts are myeloid
54
What is differentiation syndrome?
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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