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Phase 2 > HAEMATOLOGY > Flashcards

HAEMATOLOGY Flashcards

1
Q

Neoplasm of plasma cells - associated conditions

A

Multiple myeloma (most common); Localised Plasmacytoma (when a more discrete plasma cell tumor develops in or out of bone, eg in airways); Waldenstroms Macroglobulinaemia (monocolonal proliferation of IgM plus lymphocytes)

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2
Q

Pathology of myeloma

A

Malignant proliferation of plasma cells that leads to the production of one Ig or free light chains.
=immune paresis - infection risk
=hyper viscosity in blood - eye problems
=bone lesions - fractures, pain, neuro involvement if spine
=bone resorption - hypercalcemia
=Increased Ig’s and free light chains in blood - can be deposited in tissues = amyloidosis, renal failure.

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3
Q

Presentation of myeloma

A

Bone pain - back pain, neuro involvement
Tiredness/ fatigue - anaemia
Confused/ thirsty - older pt, hypercalcaemia

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4
Q

Investigations for myeloma

A

Bloods:
FBC - anemia, neutropenia, thrombocytopenia
Blood film - stacked RBCs
U&Es - elevated urea and creatinine in renal damage
Serology - raised Ig’s - probably IgG’s

Urine:
Ig’s and free light chains

X-ray:
Bone lesions - lytic
Skull - pepper pot

MRI:
If needed for spine

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5
Q

Signs of myeloma

A

Anaemia - pale mucus membrane of eyes

Amyloidosis - red/ purple patches around eyes; tongue

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6
Q

Treatment of myeloma

A

Analgesia
Bisphosphonates for bones & fracture prevention
Anaemia - transfusion, EPO
Renal - rehydrate
Infections - anti-viral prophylaxis, may need IgG transfusion

Chemo/ steroids/ radiotherapy

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7
Q

Causes of microcytic anaemia

A
  1. Iron deficiency
  2. Chronic conditions (through changes in hepcidin?)
  3. Thalassemia
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8
Q

Causes of normocytic anaemia

A
  1. Acute blood loss (GI, or menses)
  2. Chronic conditions (through changes in marrow/ production)
  3. Combined haemantic deficiency
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9
Q

Causes if macrocytic anaemia

A
  1. B12/ folate deficiency
  2. Liver disease/ alcohol excess
  3. Hypothyroid (rarer)
  4. Other haematological:
    - Chemo
    - Haemolysis
    - Marrow failure - underlying blood disease/ aplastic cause
    - Marrow infiltration - myeloma, leukemia etc
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10
Q

Anaemia investigations

A

FBC, Film, MCV
Reticulcyte count (tell you about marrow activity & haematopoiesis), LFT, U&E’s. B12, folate, Iron.
Serology - Intrinsic factor antibodies - pernicious anaemia; Coeliac disease

If can’t get diagnosis from this, may need marrow biopsy.

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11
Q

Anaemia symptoms

A 
Tiredness/ fatigue
SOB
Faintness 
Palpitations 
Headache
Tinnitus
Anorexia
Angina  (if pre-existing coronary disease)
If severe - tachy, flow murmurs (systolic), cardiac enlargement
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12
Q

Anaemia signs

A 
Pallor - pale skin 
Pale mucous membrane - check eyes
Brittle nails - may have spoon shape 
Brittle hair
Ulcers at side of mouth
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13
Q

Anaemia managment

A

Treat the underlying cause, can use oral iron, b12, folate etc.
Some may need blood transfusion.

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14
Q

Examples of chronic diseases that cause anaemia

A

Chronic infection, vasculitis, rheumatoid, cancer, renal failure (EPO).
Inflammation causes hepcidin release, hepcidin inhibits ferroportin, t/f stored iron cant be used. Any chronic inflammatory disease may cause microcytic anaemia through this mechanism.

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15
Q

Causes of iron deficiency anaemia

A

Blood loss (GI bleed, menses)
Poor diet
Malabsoprtion
Hookworm (worldwide)

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16
Q

Causes of B12 deficient anaemia

A

Dietary - vegan
Malabsorption - think pernicious anaemia & problem with parietal cells (IF antibodies, autoimmune disease)
Congenital metabolic errors

17
Q

Blood results for microcytic anaemia

A

Low Hb (<115 f; <130 m) + MCV <76

18
Q

Blood results for normocytic anaemia

A

Low Hb (<115 f; <130 m) + MCV 76-96

19
Q

Blood results macrocytic anaemia

A

Low Hb (<115 f; <130 m) + MCV >96

20
Q

Physiological cause of macrocytic anaemia

A

Pregnancy

21
Q

Groups of anaemias based on pathology

A

Hypoplastic anaemias (problem with marrow function - cancers etc)
Dyshaematopoietic (problem with how RBCs are made; low iron, B12, folate, chronic disease etc)
Haemolytic (RBCs killed - infection/ malaria, blood disease)
Post hemorrhage (GI - IBD, menses etc)

22
Q

Pathological consequences of anaemia

A 
Myocardial fatty change
Fatty change in liver
Aggravate angina/claudication
Skin and nail atrophic changes
CNS cell death (Cortex and basal ganglia)
23
Q

What does TTP stand for, what is a distinguishing clinical feature of this disease that would differentiate it from HUS

A

Thrombotic thrombocytopenia purpura
Neurological involvement distinguishes this from HUS.
HUS - renal picture
TTP pathology - widespread microvascular thrombosis results in consumption of platelets leading to thrombocytopenia and secondary microvascular haemorrhage.

24
Q

How would you identify HUS on a blood film

A

Schistocytes - fragmented RBCs. Fragments occur from RBCs passing through damaged microvasculature

25
Q

What is a common autoimmune cause of TTP

A

Antibodies against ADAMTS13 protease.
It is a protease that breaks down von willebrand factor. Antibodies against it deplete it = deficiency = promote platelet rich thrombi.
Can also inherit as genetic mutation but rare.

26
Q

What is the action of warfarin

A

It is a vitamin K inhibitor.
Vitamin K is required for synthesis of clotting factors X, IX, VII, II
Factor VII is specific to the extrinsic coagulation pathway
Warfarin tf prevents clotting by inhibiting the extrinsic coagulation pathway

27
Q

What is the action of heparin

A

Heparin is an indirect inhibitor of Xa and IIa (thrombin)
Heparin binds to antithrombin - an enzyme that inhibits Xa and IIa
Bc heparin mainly acts on thrombin, it prevents clotting by inhibiting the indirect pathway

28
Q

Why is low molecular weight heparin used over unfractioned heparin

A

Better (longer) plasma half life, so can give less doses per day - 1-2 injections

29
Q

What is a DOAC and how does it work

A

Direct oral anticoagulant

Directly inhibits Xa and IIa

30
Q

What is factor II and factor I

A 
II = prothrombin
I = fibrinogen
31
Q

What is the function of the extrinsic and intrinsic coagulation pathways

A

Extrinsic gives a rapid burst of thrombin = useful for vessel rupture
Intrinsic gives a slow but longer lasting thrombin release = useful for inflammatory processes

32
Q

What are platelet rich thombus formed in arteries and fibrin rich thrombi formed in veins

A

Think of Virkows tria - flow, coagulation, endothelium
In arteries, damage to the endothelium is the main cause for thombi to form - in this case platelet plugging is the immediate response and predominates
In veins, there is no vessel damage, the problem is with blood flow (i.e. stasis bc of valves and low pressure) - this means that platelets arent activates but clotting factors bump into each other more, so you get fibrin formation without platelets - fibrin rich

33
Q

What is the fibrinolytic system

A

System that degrades firbin
Tissue plasminogen activation (from endothelium) - released on break to endothelium
Activates plasminogen -> plasmin
Plasmin degrades fibrin

34
Q

What drug would you give to a patient that was heamodynamically unstable because of a PE

A

Thrombolytic drug

Alteplase

Phase 2 (12 decks)

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