Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2A revision > haematology to work on COPY > Flashcards

haematology to work on COPY Flashcards

1
Q

Give 3 signs of anaemia

A
  1. Conjunctival pallor
  2. Hyper-dynamic circulation
  3. Tachycardia
  4. Systolic flow murmur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the specific signs of B12 deficiency/pernicious anaemia?

A

Inflamed tongue (glossitis), angular stomatitis, mild jaundice
Neurological - paraesthesia, psychological problems, ataxia
- dementia and visual disturbances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give 3 acquired causes of haemolytic anaemia

A
  1. Autoimmune
  2. Drug induced
  3. Secondary to systemic disease
  4. Malaria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Give 3 chronic complications of sickle cell disease

A
  1. Renal impairment
  2. Pulmonary hypertension
  3. Joint damage
  4. growth and development problems
  5. cardiomegaly, MI
  6. hepatomegaly
  7. retinopathy
  8. impaired placental blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the treatment for sickle cell disease

A
  • Precipitating factors should be avoided - e.g. infection, dehydration, cold
  • Folic acid
  • Acute attacks:
    - IV fluids
    - Analgesia
    - Oxygen
  • Possible blood transfusions
  • Oral hydroxycarbamide to reduce frequency of crises
  • Stem cell transplant

long term management

  • hydroxyurea - increases HbF levels so is used as prophylaxis
  • pneumococcal vaccine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the clinical features of G6PD deficiency?

A 
Most are asymptomatic 
Pallor
Fatigue
Palpitations
Shortness of breath
Jaundice 
Exacerbated by ingesting fava beans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name 3 things that can precipitate G6PD deficiency

A
  1. Broad beans / fava beans
  2. Infection
  3. Drugs - Primaquine, sulphonamide, quinolones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the secondary causes of absolute polycythaemia?

A

hypoxia

 - Smoking
  - Lung disease
 - Cyanotic heart disease
  - High altitude 
  - obstructive sleep apnoea

Excess EPO - renal disease

alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the clinical features of polycythaemia?

A 
Headaches and dizziness 
Itching
Fatigue
Tinnitus
Erythromelalgia – burning sensation in fingers and toes 
Hypertension 
Angina 
Hepatosplenomegaly (distinguishes 1o from 2o)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the treatment for polycythaemia?

A 
No cure
Treatment aim is to maintain normal blood count 
Venesection - relieves symptoms 
Low does aspirin 
Radioactive phosphorus in those over 70
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can cause decreased platelet production?

A
  1. Congenital causes (e.g. malfunctioning megakaryocytes)
  2. Infiltration of bone marrow (e.g. leukaemia)
  3. Alcohol
  4. Infection (e.g. HIV/TB)
  5. Reduced TPO
  6. Aplastic anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can cause increased platelet destruction?

A
  1. Autoimmune (e.g. ITP)
  2. Hypersplenism
  3. Drug related (e.g. heparin induced)
  4. DIC and TTP –> increased consumption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What can cause reduced platelet function?

A
  1. Congenital abnormality
  2. Medications - aspirin
  3. VWF disease
  4. Uraemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give 3 things that can cause coagulation disorders

A
  1. Vitamin K deficiency
  2. Liver disease
  3. Congenital - haemophilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is thrombotic thrombocytopenia (TTP)?

A
  • Widespread adhesion and aggregation of platelets leads to microvascular thrombosis and consumption of platelets
  • Occurs due to a reduction in ADAMTS-13 – a protease that is normally responsible for the degradation of vWF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the treatment for thrombotic thrombocytopenia (TTP)?

A
  • Plasma exchange (removed ADAMTS13 autoantibodies)
  • Splenectomy
  • IV steroids
  • IV methylprednisolone
  • IV rituximab
  • folic acid
  • platelet transfusion = contraindicated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give 3 causes of immune thrombocytopenia (ITP)

A 
Primary = viral infection (children)
Secondary (chronic, adults)  
  - Autoimmune conditions
  - Malignancies - CLL
  - Infections - HIV/Hep C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the management for immune thrombocytopenia (ITP)?

A
  • first line = Corticosteroid (prednisolone) or IV immunoglobulin - IV IgG
  • second line = Splenectomy or immunosuppression (rituximab)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Give 3 signs of haemolytic anaemia

A
  1. Pallor
  2. Jaundice
  3. Splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give 2 specific symptoms of iron deficiency anaemia

A
  1. Koilonychia - spoon nails
  2. Brittle hair and nails
  3. Atrophic glossitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give 3 causes of neutrophilia

A
  1. Infection
  2. Inflammation
  3. Cancer
  4. CML = primary cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give 3 causes of lymphocytosis

A
  1. Viral infection
  2. Inflammation
  3. Cancer
  4. CLL = primary cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give 3 causes of thrombocytosis

A
  1. Infection
  2. Inflammation
  3. Cancer
  4. Essential thrombocythaemia = primary cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Give 3 causes of neutropenia

A
  1. Underproduction = marrow failure, marrow infiltration, marrow toxicity (e.g. drugs)
  2. Increased removal = autoimmune, Felty’s syndrome, cyclical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Give 2 causes of thrombocytopenia

A
  1. Production failure - marrow suppression, marrow failure

2. Increased removal - immune response (ITP), consumption (DIC), splenomegaly

26
Q

Give 4 risk factors for febrile neutropenia

A
  1. If the patient had chemotherapy <6 weeks ago
  2. Any patient who has had a stem cell transplant <1 year ago
  3. Any haematological condition causing neutropenia
  4. Bone marrow infiltration
  5. those on methotrexate, carbimazole and clozapine
27
Q

What is hyper viscosity syndrome?

A

Increase in blood viscosity usually due to high levels of immunoglobulins

28
Q

What 3 blood test values would be increased in someone with polycythaemia?

A
  1. Hb
  2. RCC
  3. PCV
29
Q

what are the clinical features of chronic lymphoblastic leukaemia (CLL)?

A
  • often no symptoms
  • may be anaemic
  • weight loss, sweats, anorexia
  • hepatosplenomegaly
  • enlarged, rubbery, non-tender nodes
30
Q

what are the risk factors for folate deficiency?

A
  • elderly
  • poverty
  • alcoholic
  • pregnant
  • crohn’s/coeliac
31
Q

what are the risk factors for pernicious anaemia?

A
  • female
  • elderly
  • fair hair and blue eyes
  • blood group A
  • thyroid and addison’s disease
32
Q

what is the clinical presentation of folate deficiency?

A
  • may be asymptomatic
  • may present with anaemia symptoms
  • glossitis
  • no neuropathy
33
Q

what investigations should be undertaken in folate deficiency?

A
  • blood count and film = megaloblastic, RBCs macrocytic
  • low serum and red cell folate low
  • serum bilirubin may be raised
34
Q

what is the management for acute attacks in sickle cell anaemia?

A

IV fluids
analgesia
oxygen
antibiotics

35
Q

what is the treatment for G6PD?

A
  • blood transfusion

- stop exacerbating drugs

36
Q

what investigations should be undertaken for polycythaemia?

A
  • blood count = raised WBC and platelets
  • raised Hb
  • JAK2 mutation on genetic screen
  • bone marrow biopsy - proliferation of granulocytes and megakaryocytes
  • low serum EPO
37
Q

which investigations should be undertaken for immune thrombocytopenia purpura (ITP)?

A
  • bone marrow examination = thrombocytopenia with normal/increased megakaryocytes
  • platelet autoantibodies
38
Q

what are the causes of thrombotic thrombocytopenic purpura (TTP)?

A 
idiopathic
autoimmune e.g. SLE
cancer
pregnancy
drug related
39
Q

what is the management for von Willebrand’s disease?

A
  • Education on bleeding risks
  • Stop any antiplatelet drugs and NSAIDs
  • Tranexamic acid - used for minor bleeds
  • Combined oral contraceptive to control menorrhagia in women
  • Desmopressin -> increases vWF levels
  • Platelet transfusions can be helpful in some
  • Family screening should be offered
40
Q

what are the causes of aplastic anaemia?

A
  • inherited
  • idiopathic
  • benzene
  • chemotherapeutic drugs
  • antibiotics
  • infections - EBV, HIV and TB
41
Q

what investigations are undertaken for aplastic anaemia?

A
  • blood cell count
    • pancytopenia and low reticulocyte count
      bone marrow examination
    • hypocellular with increased fat spaces
42
Q

what is the treatment for aplastic anaemia?

A
  • treat cause
  • antibiotics for neutropenia
  • RBC transfusion and platelets
  • bone marrow transplant
  • immunosuppressive therapy
    - ATG and ciclosporin if under 40
43
Q

what are the investigations for von Willebrand’s disease?

A
  • FBC
  • Fibrinogen level
  • Platelet count - normal
  • Clotting screen- Plasma vWF decreased
  • Factor VIII levels - can be decreased as vWF is not present to protect it
44
Q

what are the investigations for haemophilia B?

A
  • Normal prothrombin time
  • Prolonged activated partial thromboplastin time
  • Low factor IX levels
  • Endoscopy if GI bleed suspected
45
Q

what is the treatment for malaria?

A
  • Chloroquine for non-falciparum malaria
  • Oral quinine sulphate for falciparum
  • Add IV quinine dihydrochloride for severe disease
    Do not treat those with G6PD deficiency
    Need specialist help
46
Q

what is the pathophysiology of anaemia of chronic disease?

A

● Decreased release of iron from bone marrow to developing erythroblasts
● Inadequate erythropoietin response to anaemia – decreased RBC survival

47
Q

what are the side effects of erythropoietin treatment?

A

flu-like symptoms,
hypertension,
raised platelets,
thromboembolism

48
Q

what are the main causes of aplastic anaemia?

A
  • inherited - Fanconi’s anaemia
  • idiopathic- benzene, toulene, glue sniffing
  • chemotherapeutic drugs
  • antibiotics
  • infections - EBV, HIV, TB
49
Q

what is the long term management for sickle cell anaemia?

A
  • hydroxyurea - increases the HbF levels and is used in the prophylactic management of sickle cell anaemia to prevent painful episodes
  • pneumococcal vaccine
50
Q

how is heparin treatment reversed?

A
  • proteamine
51
Q

Describe the treatment for symptomatic myeloma

A 
Bone pain = analgesia 
Bisphosphonates (zolendronate)   
Blood transfusion - for anaemia
Fluids and dialysis - renal failure
Chemotherapy 
Stem cell transplant
52
Q

what are the clinical features of AML?

A
  • Anaemia -> breathlessness, fatigue, pallor
  • low WCC = Infection
  • low platelets = bleeding/bruising
  • Hepatosplenomegaly
  • Peripheral lymphadenopathy
  • Gum hypertrophy
  • Bone marrow failure and bone pain
53
Q

what are the clinical features of CML?

A
  1. Symptomatic anaemia
  2. Abdominal pain = splenomegaly
  3. Weight loss, tiredness, palor
  4. Gout - due to purine breakdown
  5. Bleeding - due to platelet dysfunction
  6. fever and sweats in absence of infection
54
Q

What is the treatment for CML?

A
  • Chemotherapy
  • Tyrosine kinase inhibitors, e.g. Imatinib - Given orally
  • Stem cell transplant
55
Q

what are the clinical features of ALL?

A
  • Anaemia = breathlessness, fatigue, pallor
  • Low WCC = Infection
  • low platelets = bleeding and bruising
  • Hepatosplenomegaly
  • Peripheral lymphadenopathy
  • CNS involvement - headache, cranial nerve palsies
  • SVC obstruction, dilated superficial chest veins
  • Bone marrow failure and bone pain
56
Q

What is the treatment for ALL?

A
  • Blood and platelet transfusion
  • Chemotherapy
  • Steroids
  • Allopurinol to prevent tumour lysis syndrome
  • Intrathecal drugs, e.g. methotrexate
  • Acute control of infections with IV antibiotics
  • Neutropenia makes this high risk
  • Stem cell transplant
57
Q

Describe the treatment for AML

A
  • Blood and platelet transfusions
  • IV fluids
  • Allopurinol to prevent tumour lysis
  • Infection control with IV antibiotics
  • Chemotherapy
  • Steroids
  • Sibling matched allogenic bone marrow transplant
58
Q

What is the diagnostic test for multiple myeloma

A

Serum/urine electrophoresis

59
Q

what is DIC?

A

pathological activation of coagulation cascade
fibrin in vessel walls
there is platelet and coagulation factor consumption

60
Q

give 3 causes of DIC?

A

sepsis
trauma
malignancy

61
Q

what is the affect of DIC on blood results

TT, PTT, APTT and fibrinogen

A

TT, PTT, APTT all increase

fibrinogen decreases

62
Q

what is the most common trigger of sickle cell crisis?

A

parvovirus B19

Phase 2A revision (38 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions