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Haemotology > haem onc > Flashcards

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
Q

List lab Ix to diagnose lymphoma?

A

Biopsy<div>Raised ALP, Ca and ACE levels.</div><div><br></br></div>

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26
Q

Where does primary B cell lymphoma arise from?

A

Thymus.

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27
Q

When thoracic lymphoma is being considered what other imaging is required?

A
  1. PET scan<div>2. CT Chest/Abdo/Pelvis</div>
28
Q

When considering a patient for chemotherapy what needs to be assessed?

A

Cardiac function (Echo) pre chemo.

29
Q

What is Dabigatran?

A

It is a direct thrombin inhibitor.

30
Q

What is the trade name for Dabigatran?

A

Pradaxa

31
Q

Pharmacokinetics of Dabigatran?

A

Absorption - 3 -7% bioavailability<div>Distribtion - Pb 30%</div><div>Metabolism - Cleared unchanged</div><div>Excretion - Renally excreted (CI in those with CKI/AKI)</div><div>t1/2 12 hours</div>

32
Q

Describe the clinical use of Dabigatran? Advantages and disadvantages?

A

It is an oral anticoagulant (direct thrombin inhibitor) which has been studied for use in chronic intermittent AF.<div>Advantages: no INR requirment.</div><div>Disadvantages:</div><div>GI bleeds and extra-cranial bleeds in those . 75yo</div><div>inc risk of MI</div><div>inc risk of bleeding when transitioning from warfarin.</div>

33
Q

RELY/RECOVER

A

<div>Comparing Dabigatran with Warfarin in chronic AF.</div>

<div>18000 patients and 2500 patients respectively</div>

<div>RELY - AF.</div>

<div>RECOVER - Recurrence of venous thromboembolism.</div>

34
Q

HITTS - Pretest probability

A

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

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

<p><strong>Thrombosis<br></br></strong>New thrombosis / skin necrosis / acute systemic reaction after IV heparin bolus = 2 pts<br></br>Recurrent / progressvie / suspectedthrombosis, non-necrskin lesion = 1pt<br></br>None = 0 pts</p>

<p><strong>Other causes for thrombocytopaenia<br></br></strong>None apparent = 2 pts<br></br>Possible = 1 pt<br></br>Definite = 0</p>

<p><u>Test interpretation<br></br></u>0 - 3: Low<br></br>4 - 5: Intermediate<br></br>6 - 8: Likely</p>

35
Q

What is is Vincristine? What class of drug is it?

A

It is a chemotherapeutic agent. It is an alkaloid.

36
Q

What is vincristine commonly used to treat?

A

Non hodgkins lymphoma as part of CHOP<div>Hodkins are part of MOPP/COPP</div><div>ALL with dexemathosone</div><div>Rarely as an immunosuppressant in TTP</div>

37
Q

“What is vincristine’s main SE?”

A

Peripheral neuropathy and hyponatremia

38
Q

At what level platelets is TTP thought to be in remission?

A

150

39
Q

What is found in TTP urinalysis?

A

Blood +<div>Protein +</div>

40
Q

What is deficient in TTP?

A

Deficiency of ADAMTS13<div>This is a protease</div><div>Which prevents aggregation</div>

41
Q

Risk factors for lumour lysis?

A

Large tumour burden<div>LDH > 1500</div><div>Extensive marrow involvement</div><div>ALL</div><div>Burkitt lymphoma</div><div>Chemo.</div>

42
Q

“<img></img><div>The following data refer to a 67-year-old male 8 days following initiation of treatment for acute leukaemia:</div><div><div>a) Give the underlying cause of the above abnormalities and give your reasoning to explain these findings. (20% marks)</div><div><br></br></div><div>b) List the treatment options for this condition. (30% marks)</div><div><br></br></div></div><div><br></br></div>”

A

<div>a)Tumour lysis syndrome - Renal impairment with hyperkalaemia, hyperphosphataemia, hyperuraecamia and increased LDH</div>

<div><br></br></div>

<div>b)Resuscitation – Adequate IV hydration</div>

<div>Treatment of hyperkalaemia – Calcium chloride, bicarbonate if ECG changes, dextrose- insulin, dialysis, resonium??Renal replacement therapy – metabolic acidosis, hyperkalaemia and hyperphosphataemia Allopurinol??Rasburicase</div>

43
Q

Risks of 0 negative uncrossmatched blood administration.

A

<div>Risks associated with 0-ve uncrossmatched:</div>

<div>Non ABO, Non Rh antigen/antibodies leading to allo-immunisation and delayed heamolytic reactions</div>

<div><br></br></div>

<div><br></br></div>

44
Q

List blood products and wether they require cross matching.

A

“<img></img>”

45
Q

How to predict likelihood of HITTS?

A

“<div>4 T’s is a scoring system for HITTS.</div><div><br></br></div><div>1. Thrombocytopenia - severity</div><div>2. Timing of platelet fall</div><div>3. Thrombosis or other sequalea</div><div>4. Other causes of thrombocytopenia</div><div><br></br></div><div>If there is a high degree of suspicion then don’t wait for labratory confirmation.</div><div><br></br></div><br></br>”

46
Q

4T scoring system?

A

Thrombocytopenia:<div>2 points > 50% fall OR</div><div>Lowest is 20 -100.</div><div>1 point 30 - 50% fall</div><div>0 points < 30% fall</div><div><br></br></div><div>Timing:</div><div>2 points if 5 - 10 days post</div><div>OR within 2 days of reexposured within 30 days initial exposure</div><div>1 point > 10 days</div><div><br></br></div><div>Thrombosis:</div><div>2 points new proven thrombosis</div><div>1 point progressive/recurrent thrombosis</div><div><br></br></div><div>Alternative cause:</div><div>2 points no other cause</div><div>1 point if there is a possible</div><div>0 points if definite other cause</div><div><br></br></div><div>0-3 unlikely</div><div>4-5 intermediate probability</div><div>6-8 highly likely</div><div><br></br></div>

47
Q

List DDx for pancytopaenia.

A

<b>Decreased marrow function:</b><div>Aplasia</div><div>Acute leukemia</div><div>Myelodysplasia</div><div>Myeloma</div><div>Infiltration:</div><div>- lymphoma</div><div>- solid tumours</div><div>- TB</div><div>Megaloblastic anaemia</div><div>Myelofibrosis</div><div>Haemophagocytic syndrome</div><div>(AAMI HMMM)</div><div><br></br></div><div><b>Destruction:</b></div><div>Trauma</div><div>Sepsis</div><div>Massive Haemolysis</div><div>Spenomegally</div>

48
Q

Compare and contrast:<div>Enoxaparin, Abciximab, Danaparoid, Aspirin.</div>

A

“<img></img>”

49
Q

ABC score in trauma.

A

Predicts need for massive transfusion.<div>No = 0</div><div>Yes = 1</div><div><br></br></div><div>ED SBP < 90</div><div>ED HR > 120 bpm</div><div>Penetrating mechanism</div><div>Positive fluid on FAST scan</div><div><br></br></div><div>Score of 3 predicts 45% need for massive transfusion.</div><div><br></br></div><div>Score of 4 predicts 100% need for massive transfusion.</div>

50
Q

How to subclassify MACROCYTIC anaemia?

A

Megaloblastic - B12/Folate def.<div>Non megaloblastic - ETOH, low thyroid, drugs.</div><div><br></br></div>

51
Q

“<img></img>”

A

“<img></img>”

52
Q

“<img></img>”

A

“<img></img>”

53
Q

“<img></img>”

A

“<img></img>”

54
Q

Anaemic of chronic disease:<div>Describe findings.</div>

A

Microcytosis (mild)<div>Normochromia</div><div>No reticulocytes.</div><div><br></br></div>

55
Q

How can anaeamia of chronic disease be distinguished from Fe def anaemia?

A
  1. By a lack of increase in Hb when administered IV or PO iron.<div><br></br></div><div>2. Lack of increase in Serum Transferrin Receptor Concentration with IV or PO iron.</div>
56
Q

When is a bone marrow biopsy required in Fe def anaemia?

A

Occasionally required to assess total body iron stores

57
Q

Micro/normo/macrocytic classification of anaemia.

A

“<img></img>”

58
Q

What is the mechanism by which chronic inflammation causes iron deficiency anaemia?

A

Release of cytokines (specifically IL) causes:<div>1. Reduced release of iron from marrow and macrophages</div><div>2. Reduced absorption of iron from gut</div><div>3. Supressed erythropoeisis</div>

59
Q

Define Leukoerythroblastosis:

A

<div>1. A leukoerythroblastic (or leucoerythroblastic) anemia is any anemic condition resulting from space-occupying lesions in the bone marrow;</div>

<div><br></br></div>

<div>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.</div>

<div><br></br></div>

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

<div><br></br></div>

<div>4. Marrow infiltrative disorders include myelomas, malignancy, myelofibrosis,</div>

<div><br></br></div>

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

<div><br></br></div>

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

<div><br></br></div>

<div>8. Seen in bone marrow failure, myelofibrosis and extramedullary hematopoiesis.</div>

60
Q

Howell-Jolly Bodies.

A

“<img></img>”

61
Q

Classify anaemia.

A

“<img></img>”

62
Q

Management of sickle cell crisis:

A

ABC<div>Keep sats > 96%</div><div>IVH</div><div>Adequate analgesia</div><div>Seek and treat precipitants</div>

63
Q

List diseases associated with target cells.

A

Hb-opathies<div>Fe deficiency</div><div>Spleen removal</div><div>Thalassaemia</div><div>Enzyme def - lecithin cholesterol acyl transferase</div>

64
Q

What is the standard therapy for venous sinus thrombosis?

A

Warfarin

65
Q

When is endovascular thrombectomy used?

A

“Large vessel thrombus in ischaemic stroke.<div>Especially if recanalisation hasn’t occured with thrombolysis, or if the patient is outside time window.</div><div>Can cause direct vascular damage or dissection.</div><div><br></br></div><div>CI:</div><div>Tortuous vessels</div><div>Coagulopathy</div><div>Established infarct</div><div>Contrast allergy</div>”

66
Q

What causes raised APTT and normal PT/INR in the setting of DVT in a young male?

A

Heparin<div>Artefactual</div><div>Haemophilia A and B</div><div>Factor VII and XI deficiency</div><div>vWD</div><div>Lupus inhibitor</div>

67
Q

“<img></img><div>What?</div><div>When?</div>”

A

Target cells.<div>Found in defective Hb chain synthesis.</div><div><br></br></div>

Haemotology (2 decks)

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