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4th year MLA Flashcards > Haematology > Flashcards

Haematology Flashcards

(59 cards)

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1
Q

What malignancy transformation is associated with myeloproliferative disorders?

A

AML (acute myeloid leukemia)

malignancy= acute M

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2
Q

What malignancy is associated with reicheter’s transformation?

A

CLL > non-hodgkins lymphoma

‘reichter is COOl-CLL

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3
Q

What is the triad of electrolyte imbalance in tumour lysis syndrome?

A

-hyperkalemia
-hyperphosphataemia
-hypocalcemia

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4
Q

“an increase in granulocytes at different stages of maturation +/- thrombocytosis”

are buzzword features of?

A

chronic myeloid leukemia

cml- colourful maroon

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5
Q

What is the management of active TB?

A

(2 months, then 4 months)- total 6 month period

2 months- RIPE then 4 months RI

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6
Q

What is the management of latent TB

(*

A

3 months:
Rifampicin + isoniazid

or 6 months
Isoniazid alone

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7
Q

What is non-haemolytic febrile reaction?

A

This is thought to be caused by the antibodies reacting with the white cell fragments in the blood product and cytokines.

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8
Q

What is the management of Non-Haemolytic febrile reaction?

A

Management:

1st line- stop or slow the blood transfusion + Paracetamol

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9
Q

What is the prophylactic treatment for non-haemolytic febrile reaction?

A
  • Prevention:
    • leukoreduction(stops wbc releasing cytokines)

cause - is excess release of cytokines into the blood

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10
Q

What is the management of a minor allergic reaction in a blood transfusion?

A

Stop transfusion, oral anti-histamines

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11
Q

What antibody is deficiency in an anaphylactic reaction to a blood transfusion?

A

IgA deficiency

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12
Q

What are the x3 main symptoms of acute haemolytic reaction?

A

Symptoms:

  • fever
  • abdominal pain
  • hypotension
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13
Q

What antibody is produced in Acute Haemolytic Reaction?

A

IgM

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14
Q

What conditions increases your risk of Transfusion related circulatory overload

A

Diagnosis of CKD or Congestive heart failure

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15
Q

What is the management of TACO for blood transfusion?

A

Management:

1st line- Stop the blood transfusion + IV Loop diuretics (*furosemide)

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16
Q

What type of blood transfusion reaction is associated with pulmonary infiltrates on CXR- *buzzword

A

TRALI

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17
Q

What is Graft vs Host Disease?
b) what clinical features are associated

A

This can be associated with transfusion of unirradiated blood in immunosupressed patients. It commonly presents 4-30 days after transfusion:

  • skin damage
  • deranged liver function tests
  • gastrointestinal tract
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18
Q

What is the most common virus associated with the development of salivary gland tumours?

A

HPV

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19
Q

What type of anaemia is sickle cell anaemia?

A

normocytic anaemia

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20
Q

‘lymph nodes painful when drinking alcohol’ is associated with which sub type

(*need to know)

A

specific to ‘Hodgkins Lymphoma’

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21
Q

What is Reichters Transformation

A

CLL > high grade non Hodgkins lymphoma

(* B cell symptoms start)

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22
Q

‘specific anti-globulin test’ is more commonly known as?

A

Coombs

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23
Q

What is the management of warm haemolytic anaemia?

A

‘steroids +/- ritixumab’

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24
Q

What is the management of CML?

Study These Flashcards
A

Chronically like marmalade - philideelphia chromosome 9:22

1st line- tyrosine kinase inhibitors - imatinib
‘nib’

25
What are these buzzwords associated with? a) pepper pot skull b) rain drop skull
a) primary hyperparathyroidism b) multiple myeloma
26
What is the gold standard diagnostic for malaria?
gold standard diagnostic- thin and thick blood films
27
What are the main causes of normocytic anaemia?
1. Anaemia of chronic disease 2. Anaemia of Chronic Kidney Disease 3. Aplastic Anaemia 5. Haemolytic Anaemia
28
What is the management of Warm Haemolytic Anaemia?
steroids (+/- rituximab) are generally used first-line (autoimmune or alloimmune. Autoimmune is associated with warm and cold)
29
What is the universal blood group?
O negative
30
What is the universal plasma type?
AB negative
31
What blood types can the following blood type receive from? -A + (PLEASE LEARN THIS SHIT)
what flag they holding up, they can receive who's got same antigen flag Receive: A+, A-, O-, O+ (as O blood type has no antigens)
32
What blood types can the following blood type receive from? -A - (PLEASE LEARN THIS SHIT)
A-, O-
33
What blood types can the following blood type receive from? -O+ (PLEASE LEARN THIS SHIT)
O+, O- (*cannot receive blood groups; A, B, AB- as do not have ANY ANTIGENS)
34
What blood types can the following blood type receive from? -AB+ (PLEASE LEARN THIS SHIT)
A+, B+, A-, B-, AB+, AB-, O-, O+ (everyone)
35
What are the x3 main examples of DOACs?
Rivoroxiban, Apixiban and Dabigatran
36
What type of medication is Dabigatran
DOACs
37
What is the mechanism of the following DOACs? a) Rivoroxiban b) Apixiban c) Dabigatran (*need to know)
Mechanism of Action: - Rivoroxiban- Direct Factor Xa Inhibitor - Apixiban- Direct Factor Xa Inhibitor - Dabigatran- Direct thrombin inhibitor
38
What are the reversal agents used for the following DOACs? a) dabigatran b) apixiban and rivoroxiban
Reversal Agents: - Dabigatran- Idarucizumab - Rivaroxiban and Apixaban- Andexnet alfa*
39
What its the mechanism of action of Tranaexemic acid?
- This is a synthetic derivative of lysine. It is an anti-fibrinolytic that reversibly binds to the lysine receptor sites on plasminogen or plasmin. Preventing the breakdown of blood clots.
40
What are the clotting factors of vitamin K?
Vitamin K factors (7 + 2 is 9 not 10)= 2,7,9,10 factors (*Mneumonic)
41
What are the mutations associated with alpha thalassemia? a) one gene mutation b) two gene mutations- c) three gene mutations- d) four gene mutations-
- one gene mutation- benign carrier mutation - two gene mutations- alpha thalassemia trait - three gene mutations- haemoglobin H disease - four gene mutations- hydrops foetalis, Bart’s hydrops
42
Summarise the steps in the Extrinsic Pathway
1. When tissue damage occurs, TF (tissue factor) is released 2. TF then combines with Factor VII (7) > TF-factor VII complex 3. This TF-VIIa complex activates the common pathway; 1. pro-thrombin > thrombin and **factor X > Xa (a-active form)**
43
Summarise the Intrinsic Pathway?
**Intrinsic Pathway: (blood vessel damage**) 1. When blood vessel damage occurs, this activates factor 12, 11, 9 2. These factors activate the common pathway; pro-thrombin > thrombin
44
Summarise the Common pathway
**Common Pathway:** - Pro-thrombin is converted to thrombin (thrombin enzyme converts fibrinogen to fibrin threads to form clot) * Factor X is converted to factor Xa
45
What are the X2 main regulators of the coagulation cascade?
- Protein C and Protein S controls the coagulation cacade and acts as inhibitors - WIthout these proteins the body would continue to form clots all the time
46
47
What are the mutations associated with the following types of beta thlassemia? a) beta thalassemia minor b) beta thlassemia intermedia c) beta thlassemia major
- Thalassemia minor- one abnormal gene, one normal - Thalassemia intermedia- two abnormal, one deletion and one normal - Thalassemia Major- both deletion genes (homozygous gene mutation)
48
What are the common symptoms of beta thalassemia major?
***Frontal bossing*** (prominent forehead) - ***Enlarged maxilla*** (prominent cheekbones) - ***Depressed nasal bridge*** (flat nose) - ***Protruding upper teeth***
49
'homozygous mutation of alpha thalassemia' =
hydros foetalis or Parts hydros
50
What is factor v Leiden? (*same as protein c resistance)
Pathophysiology: It is due to the mutation of the factor V leiden protein. It results in inhiting the protein C inhibitor of the coagulation pathway, significantly increasing risk of a blood clot.
51
What is VWB disease?
This is the most common type of inherited bleeding disorder. Autosomal dominant. So take sLONGER for things to clot as platelet adhesion takes longer. Role of von Willebrand factor: - large glycoprotein which forms massive multimers up to 1,000,000 Da in size - promotes platelet adhesion to damaged endothelium - carrier molecule for factor VIII (8)
52
What is the role of VWB?
Role of von Willebrand factor: - large glycoprotein which forms massive multimers up to 1,000,000 Da in size - promotes platelet adhesion to damaged endothelium - carrier molecule for factor VIII (8)
53
What are the investigations required for VWB? (*NEED TO KNOW_)
Investigation - prolonged bleeding time - APTT may be prolonged - factor VIII levels may be moderately reduced - defective platelet aggregation with ristocetin
54
What is the 1st line management of VWB?
1st line- tranaxemic acid
55
What is thrombotic thrombocytopenic purpura? b) What is the management
-caused by a deficiency in metalloproteases, these are enzymes which breaksdown any platelet adhesion formed from VWB management: 1st line- IV plasma exchang
56
What is the most common inherited thrombophillia disorder?
Factor V Leiden (protein C resistance)
57
-What is the Most common inherited bleeding disorder?
VWB- unable to platelet adhesion resulting in difficulty with the blood clotting
58
What is the most common infection platelets most likely to get?
bacterial (as stored at room temp) -most commonly staph.epidermis
59
What is raised in each type of the following beta thalassemias? -HBA2 or HBF a) beta thalassemia minor b) beta thalassemia intermedia c) beta thalassemia major
a) beta thalassemia minor- HBA2 raised b) beta thalassemia intermedia- HBA2 raised c) beta thalassemia major- HBA2 and HBF raised

4th year MLA Flashcards (13 decks)

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