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MANCHESTER YEAR 3 > Haematology Prep > Flashcards

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
Q

How do you manage chronic sickle cell disease?

A

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
Q

How do you treat beta thalassaemia?

A

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.

MANCHESTER YEAR 3 (11 decks)

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