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haem onc Flashcards

1
Q

Describe the PD and PK of Heparin

A

Binds and activates ATIII, causing inactivation of thrombin and factor Xa<div>Vd 5L</div><div>Protein binding complex and variable</div><div>Elimination is dose independent renal clearance and dose dependent depolymerisation</div><div>t1/2 1 - 2 hours</div><div>Reversible, give protamine 1mg for every 100units heparin given in past 4hrs</div>

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2
Q

Describe the PD and PK of Dabigatran

A

Direct thrombin inhibitor<div>Active metabolite accounts for 20% activity</div><div>Peak effect 2hrs</div><div>t1/2 12 - 14hrs</div><div>Vd 60L</div><div>35% protein bound</div><div>Not reversible, takes >12hrs to wear off</div><div>Consider RRT</div>

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3
Q

The major biochemical abnormalities associated with tumour lysis syndrome include

A

Hyperphosphatemia<div>Hyperkalemia</div><div>Hypocalcemia</div><div>Hyperuricemia</div><div>Metabolic acidosis</div>

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4
Q

Hemostatic resuscitation involves

A

Correcting hypothermia<div>Correcting acidosis</div><div>Treating coagulopathy early and aggressively</div><div>The use of blood products instead of isotonic crystalloid fluid aiming for limited volume replacement</div>

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5
Q

Methylprednislone is a …….

A

Glucocorticoid

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6
Q

Prednisolone dose equivelent vs methylprednisone, hyrdocortisone and dexamethasone

A

Pred: 1<div>Methylpred: 0.8</div><div>Hyrdrocortisone: 4</div><div>Dexamethasone: 0.2</div>

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7
Q

Parotiditis is cause by what? And via what mechanism?

A

ETOH liver disease<div>Due to fatty infiltration</div><div>In 70% of patients</div>

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8
Q

Sarcoidosis is syndrome causing what disease process?

A

Deposition of chronic inflammatory cells (granulomas) that form nodules in multiple organs.

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9
Q

Are sarcoid nodules caseating or not?

A

“No they aren’t”

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10
Q

What organs are effected by sarcoidosis?

A

Lung<div>Liver</div><div>Skin</div><div>Heart</div><div>Eyes</div><div>Blood</div><div>Lymph nodes</div><div>CNS</div><div>Exocrine glands</div>

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11
Q

What is the common treatment for sarcoid?

A

Prednisolone

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12
Q

MAG3 Scan: is also called?

A

Radioisotope renography

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13
Q

How does MAG3 work?

A

Tc99m-MAG3 are radiolabelled isotopes that are injected.

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14
Q

What is a MAG3 scan?

A

MAG3 clearance is well correlated to renal plasma flow.

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15
Q

How much of MAG3 injected is excreted into the tubules?

A

30-40%

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16
Q

What does PET stand for?

A

Positron emission topography

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17
Q

How does PET work?

A

It produces a 3D image by detecting pairs of gamma rays that are emitted by a tracer. This tracer is administered into the body and is attracted to highly metobolically active tissues.

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18
Q

Why is PET tracer attracted to biologically active tissues?

A

The tracer is called FDG, which is an analogue of glucose, and is this taken up by active cells

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19
Q

Suggested criteria for activation of Massive Transfusion Protocol

A

<p>Actual or anticipated 4 units RBC in <4hrs, +haemodynamics unstable, +/-anticipated ongoing bleeding</p>

<p>Severe thoracic, abdominal, pelvic, multiple long bone trauma</p>

<p>Major obstetric, gastrointestinal or surgical bleeding</p>

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20
Q

Blood product dosage in trauma

A

<p>Plt < 50 = 1 therapeutic dose</p>

<p>INR > 1.5 = FFP 15mL/kg</p>

<p>Fibrinogen < 1g/L = Cryoprecipitate 3 - 4g</p>

<p>Tranexamic acid = loading dose 1g over 10m then 1g over 8hrs</p>

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21
Q

Ticagrelor

A

<p>180mg load then 90mg BD</p>

<p>Reversible and non-competitive binding of ADP P2Y12 receptor</p>

<p>Prevents ADP-mediated GP IIb/IIIa activation therefore inhibiting aggregation</p>

<p>Absorption rapid, 36% bioavailability</p>

<p>Vd 88L, protein binding 99%</p>

<p>T1/2 parent drug ~ 7hrs, active metabolite 9hrs</p>

<p>Hepatic metabolism, excreted 58% faeces and urine 26%</p>

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22
Q

Prasugrel

A

<p>60mg load, 10mg OD</p>

<p>Prodrug converted to active metabolite</p>

<p>Irreversibly blocks the ADP P2Y12 receptor</p>

<p>Absorption rapid, 80% bioavailabilty</p>

<p>Vd 60L, protein binding 98%</p>

<p>Metabolism to active metabolite by serum esterases and CYP450</p>

<p>T1/2 7hrs</p>

<p>Excreted 68% urine and 27% faeces</p>

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23
Q

What blood products have high plasma volume components?

A

FFP<div>Plasma frozen within 24 hours (FP-24)</div><div>plasma</div><div>Cryo-reduced plasma</div><div>Apharesis platelets</div><div>Whole blood</div><div><br></br></div>

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24
Q

Definition of Cachexia is

A

Weight loss and skeletal muscle wasting due to illness where the body does not reduce catabolism (unlike starvation)

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25
List lab Ix to diagnose lymphoma?
Biopsy
Raised ALP, Ca and ACE levels.

26
Where does primary B cell lymphoma arise from?
Thymus.
27
When thoracic lymphoma is being considered what other imaging is required?
1. PET scan
2. CT Chest/Abdo/Pelvis
28
When considering a patient for chemotherapy what needs to be assessed?
Cardiac function (Echo) pre chemo.
29
What is Dabigatran?
It is a direct thrombin inhibitor.
30
What is the trade name for Dabigatran?
Pradaxa
31
Pharmacokinetics of Dabigatran?
Absorption - 3 -7% bioavailability
Distribtion - Pb 30%
Metabolism - Cleared unchanged
Excretion - Renally excreted (CI in those with CKI/AKI)
t1/2 12 hours
32
Describe the clinical use of Dabigatran? Advantages and disadvantages?
It is an oral anticoagulant (direct thrombin inhibitor) which has been studied for use in chronic intermittent AF.
Advantages: no INR requirment. 
Disadvantages: 
GI bleeds and extra-cranial bleeds in those . 75yo
inc risk of MI
inc risk of bleeding when transitioning from warfarin.
33
RELY/RECOVER
Comparing Dabigatran with Warfarin in chronic AF.
18000 patients and 2500 patients respectively
RELY - AF.
RECOVER - Recurrence of venous thromboembolism.
34
HITTS - Pretest probability

Thrombocytopaenia
PLT fall 50% and nadir >20 = 2 pts
PLT fall 30-50% and nadir 10 - 19,000micrmol/L = 1 pt
PLT fall <30% or nadir <10 = 0 pt

Timing of PLT count fall
Onset b/w d5 - 10, or <=d1 if prior heparin in last 30d = 2 pts
Onset prob bw d5-10, after d10 or fall <=d1 with prev heparin in last 30-100d = 1 pts
Onset at <4d without recent exposure = 0 pts

Thrombosis
New thrombosis / skin necrosis / acute systemic reaction after IV heparin bolus = 2 pts
Recurrent / progressvie / suspected thrombosis, non-necrskin lesion = 1pt
None = 0 pts

Other causes for thrombocytopaenia
None apparent = 2 pts
Possible = 1 pt
Definite = 0

Test interpretation
0 - 3: Low
4 - 5: Intermediate
6 - 8: Likely

35
What is is Vincristine? What class of drug is it?
It is a chemotherapeutic agent. It is an alkaloid.
36
What is vincristine commonly used to treat?
Non hodgkins lymphoma as part of CHOP
Hodkins are part of MOPP/COPP
ALL with dexemathosone
Rarely as an immunosuppressant in TTP
37
"What is vincristine's main SE?"
Peripheral neuropathy and hyponatremia
38
At what level platelets is TTP thought to be in remission?
150
39
What is found in TTP urinalysis?
Blood +
Protein +
40
What is deficient in TTP?
Deficiency of ADAMTS13
This is a protease
Which prevents aggregation
41
Risk factors for lumour lysis?
Large tumour burden
LDH > 1500
Extensive marrow involvement
ALL
Burkitt lymphoma
Chemo.
42
"
The following data refer to a 67-year-old male 8 days following initiation of treatment for acute leukaemia: 
a)  Give the underlying cause of the above abnormalities and give your reasoning to explain these findings. (20% marks)

b)  List the treatment options for this condition. (30% marks) 


"
a) Tumour lysis syndrome - Renal impairment with hyperkalaemia, hyperphosphataemia, hyperuraecamia and increased LDH

b) Resuscitation – Adequate IV hydration
Treatment of hyperkalaemia – Calcium chloride, bicarbonate if ECG changes, dextrose- insulin, dialysis, resonium??Renal replacement therapy – metabolic acidosis, hyperkalaemia and hyperphosphataemia Allopurinol??Rasburicase
43
Risks of 0 negative uncrossmatched blood administration.
Risks associated with 0-ve uncrossmatched:
Non ABO, Non Rh antigen/antibodies leading to allo-immunisation and delayed heamolytic reactions


44
List blood products and wether they require cross matching.
""
45
How to predict likelihood of HITTS?
"
4 T's is a scoring system for HITTS.

1. Thrombocytopenia - severity
2. Timing of platelet fall
3. Thrombosis or other sequalea
4. Other causes of thrombocytopenia

If there is a high degree of suspicion then don't wait for labratory confirmation.


"
46
4T scoring system?
Thrombocytopenia:
2 points > 50% fall OR
Lowest is 20 -100.
1 point 30 - 50% fall
0 points < 30% fall

Timing:
2 points if 5 - 10 days post
OR within 2 days of reexposured within 30 days initial exposure
1 point > 10 days

Thrombosis:
2 points new proven thrombosis
1 point progressive/recurrent thrombosis

Alternative cause:
2 points no other cause
1 point if there is a possible
0 points if definite other cause

0-3 unlikely
4-5 intermediate probability
6-8 highly likely

47
List DDx for pancytopaenia.
Decreased marrow function:
Aplasia
Acute leukemia
Myelodysplasia
Myeloma
Infiltration:
 - lymphoma
 - solid tumours
 - TB
Megaloblastic anaemia
Myelofibrosis
Haemophagocytic syndrome
(AAMI HMMM)

Destruction:
Trauma
Sepsis
Massive Haemolysis
Spenomegally
48
Compare and contrast:
Enoxaparin, Abciximab, Danaparoid, Aspirin.
""
49
ABC score in trauma.
Predicts need for massive transfusion.
No = 0
Yes = 1

ED SBP < 90 
ED HR > 120 bpm
Penetrating mechanism
Positive fluid on FAST scan

Score of 3 predicts 45% need for massive transfusion.

Score of 4 predicts 100% need for massive transfusion.
50
How to subclassify MACROCYTIC anaemia?
Megaloblastic - B12/Folate def.
Non megaloblastic - ETOH, low thyroid, drugs.

51
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54
Anaemic of chronic disease:
Describe findings.
Microcytosis (mild)
Normochromia
No reticulocytes.

55
How can anaeamia of chronic disease be distinguished from Fe def anaemia?
1. By a lack of increase in Hb when administered IV or PO iron.

2. Lack of increase in Serum Transferrin Receptor Concentration with IV or PO iron.
56
When is a bone marrow biopsy required in Fe def anaemia?
Occasionally required to assess total body iron stores
57
Micro/normo/macrocytic classification of anaemia.
""
58
What is the mechanism by which chronic inflammation causes iron deficiency anaemia?
Release of cytokines (specifically IL) causes:
1. Reduced release of iron from marrow and macrophages
2. Reduced absorption of iron from gut
3. Supressed erythropoeisis
59
Define Leukoerythroblastosis:
1. A leukoerythroblastic (or leucoerythroblastic) anemia is any anemic condition resulting from space-occupying lesions in the bone marrow; 

2. the circulating blood contains immature cells of the granulocytic series and nucleated red blood cells, frequently in numbers that are disproportionately large in relation to the degree of anemia. 

3. picture on blood film can be the bone marrow response to any irritation including marrow infiltration [causing immature red cells]. 

4. Marrow infiltrative disorders include myelomas, malignancy, myelofibrosis, 

5. It can also occur as a response to severe critical illness, such as trauma, septicemia, massive hemolysis, or severe megaloblastic anemia. 

7. Leukoerthyroblastic change refers to the presence of nucleated red blood cells and primitive white blood cells.

8. Seen in bone marrow failure, myelofibrosis and extramedullary hematopoiesis.
60
Howell-Jolly Bodies.
""
61
Classify anaemia.
""
62
Management of sickle cell crisis:
ABC
Keep sats > 96%
IVH
Adequate analgesia
Seek and treat precipitants
63
List diseases associated with target cells.
Hb-opathies
Fe deficiency
Spleen removal
Thalassaemia
Enzyme def - lecithin cholesterol acyl transferase
64
What is the standard therapy for venous sinus thrombosis?
Warfarin
65
When is endovascular thrombectomy used?
"Large vessel thrombus in ischaemic stroke.
Especially if recanalisation hasn't occured with thrombolysis, or if the patient is outside time window.
Can cause direct vascular damage or dissection.

CI:
Tortuous vessels
Coagulopathy
Established infarct
Contrast allergy
"
66
What causes raised APTT and normal PT/INR in the setting of DVT in a young male?
Heparin
Artefactual
Haemophilia A and B
Factor VII and XI deficiency
vWD
Lupus inhibitor
67
"
What?
When?
"
Target cells.
Found in defective Hb chain synthesis.

Haemotology (2 decks)

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