Haematology Prep Flashcards

1
Q

What investigations should be done on patients over 50 presenting with back pain?

A

Serum protein electrophoresis and CRP to check for multiple myeloma

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2
Q

What are the common symptoms of multiple myeloma?

A
  1. Osteolytic bone lesions causing backache, pathological fractures, and vertebral collapse (hypercalcaemia may cause symptoms)
  2. Anaemia, neutropenia, thrombocytopenia may result from marrow infiltration by plasma cells - causing ANAEMIA, INFECTION and BLEEDING
  3. Recurrent bacterial infections
  4. Renal impairment
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3
Q

What investigations are performed in a patient with suspected myeloma?

A

FBC = normocytic normochromic anaemia, raised calcium, raised creatinine, raised urea and raised albumin
Serum/urine electrophoresis
X-ray = punched out lesions, vertebral collapse, features of osteoporosis
Bone marrow aspirate and biopsy (diagnostic)

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4
Q

What is the treatment for multiple myeloma?

A

Supportive = analgesia and biphophonates (zoledronic acid) for bone pain. EPO for anaemia. IV immunoglobulin injections for infection
Chemotherapy

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5
Q

What do the presence of bence jones protein in the urine suggest?

A

Myeloma

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6
Q

What are presence of reed sterberg cells on blood film indicative of?

A

Hodgkins lymphoma

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7
Q

What investigations are performed in suspected hodgkins lymphoma? What is the treatment?

A
Excisional lymph node biopsy
FBC = low Hb, low platelets. WBC high or low
U+E usually normal
ESR raised 
CXR = mediastinal mass
Reed sternberg cells on blood film

Chemoradiotherapy

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8
Q

Describe the ann arbor staging system for lymphoma.

A
1 = confined to single lymph node region
2 = 2 or more nodal areas on same side of diaphragm
3 = involvement of nodes on both sides of diaphragm
4 = spread beyond lymph nodes
A = no systemic spread
B = systemic symptoms within last 6 months
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9
Q

What investigations are performed in suspected PVD?

A

Need to exclude - DM, anaemia, arteritis, renal disease etc.
Measure ABPI (PVD = 0.5-0.9, critical limb ischaemia = less than 0.5)
Colour duplex USS
MR/CT angiogram

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10
Q

What are the 4 parts of the Fontaine criteria?

A
  1. Asymptomatic
  2. Intermittent claudication
  3. Rest pain
  4. Ulceration/gangrene/tissue loss
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11
Q

How is PVD managed?

A

STOP SMOKING

  • treat HTN and high cholesterol
  • prescribe clopidogrel/aspirin to slow disease progression and reduce CV risk
  • manage claudication = exercise programme and cilostazol
  • PTA (percutaneous transluminal balloon angioplasty) or bypass graft
  • amputation (gabapentin given for phantom limb pain)
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12
Q

What are causes of a (i) prolonged PT (ii) prolonged APTT?

A

(i) warfarin, liver disease, factor 7 deficiency

(ii) vW disease, heparin, deficiency of factors 8, 9, 11

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13
Q

What are causes of a prolonged PT and APTT?

A
  1. severe Vit K deficiency e.g. liver disease, malnutrition, low fibrinogen
  2. Deficiency of prothrombin, fibrinogen or factors 5 or 10
  3. Direct factor Xa inhibition e.g. rivaroxaban
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14
Q

If a patient has a prolonged PT or APTT, the test is redone with a 50:50 mix of normal plasma. What does it mean if it (i) corrects (ii) fails to correct?

A

(i) factors deficiency

(ii) factor inhibitor

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15
Q

What is haemophilia A a deficiency of? How is it diagnosed? What is the management?

A

Factor 8 deficiency causing prolonged APTT and low factor 8 assay
Treatment = recombinant factor 8, desmopressin

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16
Q

What is haemophilia B a deficiency of? How is it managed?

A

Factor 9 deficiency

Manage with recombinant factor 9

17
Q

What investigations are performed in suspected vW disease?

A

Prolonged APTT, low factor 8 and low vW antigen

18
Q

What are the 3 types of vW disease? How are each of these treated?

A

TYPE 1 = reduced amount of normal vW protein. Treatment = desmopressin (DDAVP) and tranexamic acid
TYPE 2a = abnormal underactive vW protein. Treat with vWF and maybe desmopressin (DDAVP)
TYPE 2b = abnormal overactive vW protein. treat with vWF (NOT DDAVP)
TYPE 3 = little or no vW protein. treat with vW factor

19
Q

What is the (i) 1st line investigation and (ii) management of a suspected ruptured AAA?

A

(i) abdominal USS
(ii) 1. Summon vascular surgeon + anaesthetist
2. ECG, bloods = amylase, Hb, crossmatch, catheterise
3. IV access 2 large bore cannulas = treat shock with O- blood. Keep SBP under 100mmHg to prevent further rupture
4. Take straight to theatre
5. Prophylactic Abx = cefuroxime + metronidazole
6. Surgery = EVAR (endovascular aneurysm repair)

20
Q

When is elective surgery used for an unruptured AAA?

A

If aneursym is 5.5cm or more OR if it is symptomatic

- EVAR

21
Q

If patients have an unruptured AAA under 5.5cm, what is done?

A

Monitor under surveillance

  • 3 month intervals if 4.5 to 5.4cm
  • annually if 3 to 4.4cm
22
Q

What is the difference between Type A and B aortic dissections? Remember to include treatment.

A
A = involving the ascending aorta, irrespective of site of tear. All with type A should be considered for surgery = get URGENT cardiothoracic advice
B = not involving ascending aorta. Can be managed medically, with surgery being reserved for distal dissections that are leaking, ruptured, or compromosing other organs. 
Management = crossmatch 10 units blood. ECG + CXR. CT/MRI or TOE. Take to ITU keep SBP at about 100-110 mmHg. Give labetolol plus morphine IV
23
Q

When should you suspect a haemolytic anaemia?

A

If there’s reticulocytosis, mild macrocytosis, increased bilirubin and urobilinogen.
Often mild jaundice

24
Q

What do investigations show in a patient with sickle cell anaemia?

A

Hb 60-90 g/L
Raised bilirubin, reticulocytes
sickle solubility test +ve
Hb electrophoresis

25
How do you manage chronic sickle cell disease?
Get help from a haemotologist Hydroxycarbamide if frequent crises Splenic infarction leads to hyposplenism. Prophylaxis, in terms of ABx + immunosuppression should be given Febrile children risk sepsis. Avoid admission with ABx Bone marrow transplant can be curative but remains controversial
26
How do you treat beta thalassaemia?
Promote fitness, healthy diet. Folate supplements Regular lifelong transfusions Iron chelators (deferiprone + desferrioxamine) to prevent raised iron. Large does of asorbic acid - increasing urinary excretion of iron Splenectomy if hypersplenism persists Hormonal replacement for endocrine complications Histocompatible transplant can offer the chance of a cure.