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TO DO HAEMATOLOGY Flashcards

1
Q

ANAEMIA
what are the causes of normoblastic macrocytic anaemia?

A
  • alcohol
  • reticulocytosis (haemolytic anaemia or blood loss)
  • hypothyroidism
  • liver disease
  • drugs (e.g. azathioprine)
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2
Q

ANAEMIA
what are the generic clinical features?

A

SYMPTOMS
- tiredness
- SOB
- headaches
- dizziness
- palpitations
- worsening other conditions such as angina, HF or peripheral arterial disease

SIGNS
- pale skin
- conjunctival pallor
- tachycardia
- raised respiratory rate

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3
Q

IRON DEFICIENCY ANAEMIA
what would iron studies show?

A
  • low iron
  • low ferritin
  • high transferrin
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4
Q

B12 DEFICIENCY
what are the causes?

A
  • autoimmune = pernicious anaemia (anti-parietal cell antibodies damage parietal cells + stop intrinsic factor)
  • malabsorption = coeliac disease, crohns disease, terminal ileum resection
  • malnutrition = lack of meat, poultry, milk + eggs
  • medications = PPIs, colchicine, metformin
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5
Q

B12 DEFICIENCY
which medications can cause B12 deficiency anaemia?

A
  • PPIs
  • colchicine
  • metformin
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6
Q

B12 DEFICIENCY
what are the clinical features that are unique to B12 deficiency anaemia?

A

SUBACUTE COMBINED DEGENERATION OF THE SPINAL CORD
- dorsal columns = sensory, vibration + proprioception loss
- lateral corticospinal tracts = UMN signs e.g. spastic paraparesis, brisk knee jerk + upgoing plantar
- spinocerebellar tract = ataxia

PERIPHERAL NEUROPATHY
- absent ankle jerk reflex

OPTIC NEUROPATHY
COGNITIVE IMPAIRMENT

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7
Q

B12 DEFICIENCY
what is the management?

A
  • dietary advice (eggs, meat, dairy, salmon)
  • hydroxocobalamin IM

if not dietary related (e.g. pernicious anaemia) = IM hydroxocobalamin given every 2-3 months

if dietary related = cyanocobalamin 50-150 micrograms daily or twice-yearly hydroxocobalamin injection

following treatment initiation, do FBC 7-10 days after to see Hb rise

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8
Q

FOLATE DEFICIENCY
what food is folate (folic acid) found in?

A

leafy green vegetables
legumes
fruits

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9
Q

FOLATE DEFICIENCY
where is folic acid absorbed?

A

in the jejunem

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10
Q

FOLATE DEFICIENCY
what are the causes?

A

MALNUTRITION (most common)
- lack of leafy green veg, legumes + fruits

ALCOHOL (most common)

MEDICATION
- methotrexate
- trimethoprim
- 5-fluorouracil
- anticonvulsants e.g. phenytoin

MALABSORPTION
- coeliac disease
- crohn’s disease
- small bowel resection (particularly jejunem)

PREGNANCY
- increased demand for folate
- can lead to neural tube defects

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11
Q

FOLATE DEFICIENCY
which medications can cause folate deficiency?

A
  • alcohol
  • methotrexate
  • trimethoprim
  • 5-fluorouracil
  • anticonvulsants e.g. phenytoin
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12
Q

FOLATE DEFICIENCY
what are the clinical features?

A

generic anaemia features
- lethargy
- pallor
- glossitis
- angular stomatitis

no neurological symptoms with folate deficiency alone

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13
Q

HYPOSPLENISM
what are the functions of the spleen?

A
  • activation of lymphocytes
  • removal of damaged/effete RBCs from circulation
  • sequestration of platelets for release during times of stress
  • site of haematopoiesis in utero
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14
Q

HYPOSPLENISM
what are the causes of functional hyposplenism?

A
  • coeliac disease
  • IBD
  • haematological malignancies (leukaemias, lymphomas, myeloproliferative disorders)
  • alcoholic liver disease (due to portal hypertension)
  • chronic graft-vs-host disease (secondary to bone marrow transplant)
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15
Q

HYPOSPLENISM
what are the investigations?

A

BLOODS
- FBC = thrombocytosis
- peripheral blood smear = Howell-Jolly bodies
- CT/MRI abdomen = atrophic/absent spleen

To consider
- pitted red cell count (PRC)

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16
Q

HYPOSPLENISM
what is the management?

A

IMMUNISATION
- vaccination to n.meningitidis, h.influenzae + s.pneumoniae
- annual flu vaccine

PROPHYLACTIC ANTIBIOTICS
- oral penicillins/macrolides if at high risk of pneumococcal infections

PATIENT EDUCATION
- comply with prophylactic measures
- wear medical bracelet
- avoid travel to malaria-endemic regions
- seek prompt medical attention if they develop signs/symptoms of infection

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17
Q

ALL
what are the risk factors?

A
  • previous chemotherapy
  • radiation exposure
  • down syndrome (20 x increased risk)
  • benzene exposure (painters, petroleum, rubber manufacturers)
  • family history
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18
Q

ALL
what are the clinical features?

A

SYMPTOMS
- fatigue
- loss of appetite
- easy bruising, prolonged bleeding + mucosal bleeding (due to thrombocytopaenia)
- bone pain (due to bone marrow infiltration)
- weight loss
- recurrent infections (due to neutropaenia)
- fever

SIGNS
- lymphadenopathy
- hepatosplenomegaly
- pallor
- flow murmur (due to anaemia)
- parotid infiltration
- testicular swelling
- CNS involvement (meningism + CN palsies)

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19
Q

ALL
what are the investigations?

A

BLOODS
- FBC = lymphocytosis, thrombocytopaenia + normocytic anaemia with low reticulocyte count
- blood film = lymphoblasts
- bone marrow aspiration + trephine biopsy = >20% lymphoblasts (is diagnostic)
- immunophenotype = CD10 indicates B-cell ALL
- cytogenic + molecular studies

To consider
- lumbar puncture
- CXR (to identify mediastinal mass

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20
Q

ALL
what is the management?

A
  • corticosteroids + chemotherapy
  • intrathecal therapy for CNS infiltration
  • often have maintenance therapy for 2 years

2nd line
- bone marrow transplant

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21
Q

AML
what are the risk factors?

A
  • increasing age
  • myelodysplastic syndromes
  • myeloproliferative neoplasms
  • previous chemotherapy or radiation exposure
  • benzene (painters, petroleum + rubber manufacturers)
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22
Q

AML
what are the clinical features?

A

SYMPTOMS
- fatigue
- loss of appetite (anorexia)
- bruising + mucosal bleeding
- weight loss
- fever
- recurrent infections

SIGNS
- pallor
- lymphadenopathy
- hepatosplenomegaly

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23
Q

AML
what are the investigations?

A

BLOODS
- FBC = leukocytosis, thrombocytopaenia + anaemia
- blood film = myeloblasts with AUER RODS
- clotting screen = DIC
- bone marrow aspirate + biopsy = >20% myeloblasts (diagnostic)
- cytogenic + molecular studies

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24
Q

AML
what is the management?

A
  • chemotherapy
  • corticosteroids

2nd line = stem cell transplant

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25
Q

CLL
what are the clinical features?

A

often asymptomatic

SYMPTOMS
- fatigue
- easy bruising + prolonged bleeding
- loss of appetite
- weight loss
- fever
- recurrent infection

SIGNS
- lymphadenopathy
- hepatosplenomegaly
- signs of anaemia

It can cause warm autoimmune haemolytic anaemia

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26
Q

CLL
what are the investigations?

A

BLOODS
- FBC = lymphocytosis (thrombocytopaenia + anaemia may be present)
- blood film = increased number of mature lymphocytes + SMUDGE CELLS
- immunoglobulins = hypogammaglobinaemia

To consider
- bone marrow biopsy
- lymph node biopsy
- Coombs test

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27
Q

CLL
what is the management?

A

EARLY DISEASE
- monitoring via blood every 3-12 months

ACTIVE +/- ADVANCED DISEASE
- chemotherapy
- allogenic stem cell transplant

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28
Q

CLL
what are the complications?

A
  • hypogammaglobinaemia
  • warm autoimmune haemolytic anaemia
  • Richter transformation (into non-hodgkins lymphoma)
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29
Q

CML
which chromosome is present in 95% of patients with CML?

A

Philadelphia chromosome

forms a fusion gene BCR/ABL on chromosome 22 – has tyrosine kinase activity – simulate cell division

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30
Q

CML
what are the clinical features?

A

SYMPTOMS
- fatigue
- weight loss, fever + night sweats
- SOB
- easy bruising + bleeding
- bone pain
- recurrent infections

SIGNS
- splenomegaly
- abdominal tenderness
- signs of anaemia
- pyrexia

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31
Q

CML
what are the investigations?

A

BLOODS
- FBC = leukocytosis, granulocytosis + anaemia (thrombocytosis seen in 30% of patients)
- blood film = increase is all stages of maturing granulocytes
- bone marrow biopsy = myeloblast infiltration
- cytogenic + molecular studies = PHILADELPHIA CHROMOSOME

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32
Q

CML
what is the management?

A
  • tyrosine kinase inhibitor (imatinib)
  • chemotherapy
  • stem cell transplant if above fails
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33
Q

CML
why does the philadelphia chromosome cause CML?

A

Froms fusion gene BCR/ABL on chromosome 22 –> tyrosine kinase activity –> stimulates cell division

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34
Q

HODGKINS LYMPHOMA
what are the risk factors?

A
  • EBV infection
  • HIV
  • autoimmune conditions (rheumatoid arthritis + sarcoidosis)
  • family history
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35
Q

HODGKINS LYMPHOMA
what are the clinical features?

A

often presents with painless lymphadenopathy

SYMPTOMS
- B symptoms (fever, weight loss + night sweats)
- Pel-Ebstein fever (intermittent fever every few weeks)
- pruritus
- dyspnoea

SIGNS
- lymphadenopathy (painless, hard, rubbery, fixed, contiguous spread)
- splenomegaly (rare)

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36
Q

HODGKINS LYMPHOMA
what are the investigations?

A

FBC - leukocytosis
LDH - often elevated
lymph node USS
lymph node biopsy - REED-STERNBERG CELLS (Owl’s eye nuclei)
staging imaging - CXR, CT neck, chest + abdomen + PET
immunophenotyping - reed-sternberg is CD15+CD30 positive

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37
Q

HODGKINS LYMPHOMA
how is it staged?

A

ANN ARBOR STAGING

1 = single lymph node region
2 = 2 or more lymph node regions on same side of diaphragm
3 = lymph node involvement on both sides of diaphragm
4 = involvement of one or more extralymphatic organs

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38
Q

HODGKINS LYMPHOMA
what is the management?

A
  • chemotherapy (ABVD)
  • radiotherapy
  • rituximab
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39
Q

TUMOUR LYSIS SYNDROME
what is it?

A

results from chemicals released when cells are destroyed by chemotherapy.
Results in:
- high uric acid
- high K+
- high phosphate
- low calcium

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40
Q

TUMOUR LYSIS SYNDROME
how can it be prevented?

A
  • good hydration + urine output
  • allopurinol to suppress uric acid levels
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41
Q

NON-HODGKINS LYMPHOMA
what are the risk factors?

A
  • HIV
  • EBV
  • h-pylori infection (associated with MALT lymphoma)
  • Hep B + hep C infection
  • exposure to pesticides
  • exposure to trichloroethylene
  • family history
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42
Q

NON-HODGKINS LYMPHOMA
what are the clinical features?

A

SYMPTOMS
- B symptoms (fever, weight loss + night sweats)

SIGNS
- lymphadenopathy (painless, hard, rubbery, fixed, non-contiguous spread)
- splenomegaly
- extranodal disease (bone marrow, thyroid, salivary gland, GI tract + CNS)

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43
Q

NON-HODGKINS LYMPHOMA
what are the investigations?

A

FBC - leukocytosis
LDH + uric acid - often raised
lymph node USS
lymph node biopsy
bone marrow biopsy

to consider
- staging imaging
- genetic testing
- immunophenotype

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44
Q

NON-HODGKINS LYMPHOMA
what is the management?

A

depends on type + stage
may involve:
- watchful waiting
- chemotherapy (R-CHOP)
- monoclonal antibodies (rituximab)
- radiotherapy
- stem cell transplant

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45
Q

NON-HODGKINS LYMPHOMA
how is it staged?

A

Lugano classification

1 = confined to 1 node or group of nodes
2 = in more than one group of nodes on same side of diaphragm
3 = affects lymph nodes on both sides of diaphragm
4 = widespread involvement, including non-lymphatic organs such as the liver or lungs

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46
Q

DIC
which organs are typically affected?

A

kidneys
liver
lungs
brain

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47
Q

DIC
what are the clinical features?

A

SYMPTOMS
- bleeding from wounds
- haematuria or haematochezia
- epistaxis or gingival bleeding
- dyspnoea
- chest pain

SIGNS
- petechiae or ecchymoses
- prolonged bleeding
- altered mental state
- focal neurological deficits (if cerebral involvement)

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48
Q

DIC
what are the investigations?

A

FBC - thrombocytopaenia, anaemia + leukocytosis
Clotting studies - prolonged PT + APTT
Fibrinogen levels - decreased
D-dimer - raised
Blood cultures - identify cause
Blood film - schistocytes

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49
Q

DIC
what is the management?

A

1st line
- treat underlying cause
- blood product transfusion (packed RBCs, FFP or platelets depending on blood results)
- anticoagulants = low dose heparin in severe disease

2nd line
- recombinant activated protein C (rhAPC)

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50
Q

DIC
what are the complications?

A
  • intracranial bleeding
  • life-threatening haemorrhage
  • multi-organ failure (renal failure, hepatic failure, ARDS)
  • gangrene or digital loss
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51
Q

HAEMOPHILIA
how is it inherited?

A

X-linked recessive - therefore primarily affects males

Haemophilia A = factor VIII deficiency
Haemophilia B = factor IX deficiency

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52
Q

HAEMOPHILIA
what are the investigations?

A
  • aPTT - prolonged
  • plasma factor VIII and IX levels - decreased or absent
  • mixing study
  • FBC - to rule out thrombocytopaenia
  • plasma von willebrand factor
    LFTs - to exclude liver disease
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53
Q

HAEMOPHILIA
what is the management?

A

MILD-MODERATE
- education
- avoidance of high risk activity
- joint strengthening exercises

SEVERE
- as above
- prophylactic clotting factors (IV replacement)

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54
Q

HAEMOPHILIA
what is the management of an acute haemorrhage?

A
  • ABCDE assessment
  • urgent haematology input
  • urgent clotting factor administration
  • antifibrinolytic agents (tranexamic acid)
  • desmopressin (in haemophilia A)
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55
Q

MULTIPLE MYELOMA
why does it cause hypercalcaemia?

A
  • caused by neoplastic cells releaseing cytokines
  • this causes activation of osteoclasts via RANK receptor
  • this leads to bone resorption, resulting in bone pain + lytic lesions on x-ray
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56
Q

MULTIPLE MYELOMA
how does it cause renal insufficiency?

A
  • deposition of light chains (Bence Jones proteins) in the kidney tubules
  • this disrupts kidney function
  • calcium deposition in the kidney also causes renal failure
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57
Q

MULTIPLE MYELOMA
how does it cause anaemia?

A
  • bone marrow infiltration by plasma cells results in reduced haematopoiesis
  • this leads to anaemia, thrombocytopaenia + leukopaenia
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58
Q

MULTIPLE MYELOMA
what are the clinical features?

A

CRAB
- hypercalcaemia
- renal failure
- anaemia
- bone lesions

SYMPTOMS
- hypercalcaemia (bones, stones, abdo groans, psychiatric moans)
- fatigue
- bleeding + bruising
- recurrent infections

SIGNS (due to amyloidosis)
- macroglossia
- carpal tunnel syndrome (Tinel’s + Phalens test positive)
- peripheral neuropathy

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59
Q

MULTIPLE MYELOMA
what are the investigations?

A
  • urine electrophoresis = BENCE-JONES PROTEIN
  • serum electrophoresis = monoclonal paraprotein band
  • bone marrow aspirate + biopsy (required for diagnosis)
  • FBC + blood film = anaemia, Rouleux formation (aggregation of RBCs)
  • U&Es (renal failure)
  • bone profile = hypercalcaemia + raised ALP
  • imaging = MRI (1st line) or CT (2nd line)
  • x-ray
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60
Q

MULTIPLE MYELOMA
what are the main clinical signs?

A

old CRAB

  • old = >75
  • hypercalcaemia
  • renal failure
  • anaemia
  • bone lesions
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61
Q

MULTIPLE MYELOMA
what would you expect to see on the x-ray?

A
  • lytic ‘punched-out’ lesions (pepper pot (raindrop) skull + vertebral collapse)
  • abnormal fractures
  • osteoporosis
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62
Q

MULTIPLE MYELOMA
what is the diagnostic criteria?

A

One or more biomarkers:
- bone marrow plasma cells >60%
- >1 focal lesion on MRI
- involved : uninvolved serum free light chain ratio >100

or evidence of end-organ damage (CRAB)
- hypercalcaemia
- renal insufficiency
- anaemia
- bone lesions

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63
Q

MULTIPLE MYELOMA
what is the management?

A

disease is incurable + has relapsing and remitting course

  • chemotherapy
  • stem cell transplant
  • bisphosphonates
  • radiotherapy
  • orthopaedic surgery to stabilise bones
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64
Q

PANCYTOPENIA
what are the causes?

A

REDUCED PRODUCTION IN BONE MARROW
- vitamin B12, folate or iron deficiencies
- aplastic anaemia
- myelodysplastic syndromes
- haematological malignancies
- bone marrow infiltration by metastatic cancer
- viral infections (HIV, parvovirus B19, CMV + EBV)

INCREASED DESTRUCTION
- splenic sequestration (TB, cirrhosis + malaria)
- autoimmune conditions (SLE, rheumatoid arthritis)

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65
Q

PANCYTOPENIA
what are the risk factors?

A
  • co-morbid autoimmune diseases
  • recent viral infections (HIV, EBV, CMV)
  • malabsorption syndromes
  • history of cancer
  • family history of aplastic anaemia
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66
Q

PANCYTOPENIA
what are the clinical features?

A

SYMPTOMS
- fatigue
- recurrent infections
- epistaxis
- B symptoms (weight loss, fever, night sweats if malignancy)

SIGNS
- pallor
- petechiae
- splenomegaly

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67
Q

APLASTIC ANAEMIA
what is it?

A

bone marrow hypocellularity secondary to primary haematopoietic failure
type of pancytopaenia

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68
Q

APLASTIC ANAEMIA
what are the different causes?

A
  • fanconi anaemia
  • radiation
  • carbimazole
  • carbamazepine
  • chloramphenicol
  • chemotherapy
  • benzene
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69
Q

FANCONI ANAEMIA
what is the inheritance pattern?

A

can be autosomal dominant or recessive

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70
Q

FANCONI ANAEMIA
what are the features?

A
  • pancytopaenia in first decade of life
  • organ hypoplasia
  • bone defects (e.g. absent thumbs)
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71
Q

POLYCYTHAEMIA
what gene mutation is seen?

A

JAK2 gene

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72
Q

POLYCYTHAEMIA
what are the risk factors?

A
  • age >40
  • family history
  • budd-chiari syndrome
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73
Q

POLYCYTHAEMIA
what are the clinical features?

A

SYMPTOMS
- headache
- pruritus
- erythromelalgia
- facial flushing

SIGNS
- splenomegaly
- palmar erythema
- plethoric complexion
- HTN

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74
Q

POLYCYTHAEMIA
what are the investigations?

A
  • FBC = raised Hb + haematocrit
  • U&Es + LFTs
  • ABG (pO2 normal in primary but low in secondary)
  • ferritin
  • erythropoietin = (primary = low, secondary = raised)
  • JAK2 mutation
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75
Q

POLYCYTHAEMIA
what is the management?

A

1st line = venesection (maintain haematocrit below 0.45)
hydroxyurea (in high risk patients)
aspirin 75mg
manage modifable CVD risk factors (diabetes, HTN, smoking, hyperlipidaemia)

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76
Q

ITP
what is immune thrombocytopenic purpura (ITP)?

A

autoimmune disorder where platelets are destroyed by antibodies, leading to low platelet counts and increased risk of bleeding.

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77
Q

ITP
what is the difference in disease course for children and adults?

A

CHILDREN
- triggered by recent viral infection
- follows an acute course
- typically resolves within 6 months

ADULTS
- chronic

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78
Q

ITP
what are the causes?

A

PRIMARY ITP - no underlying clear cause

SECONDARY ITP
- SLE
- CLL
- drugs (penicillin, heparin, quinine)
- viruses (HIV, hep C, varicella zoster, CMV)
- pregnancy

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79
Q

ITP
what are the risk factors?

A
  • female
  • increasing age
  • co-morbid autoimmune diseases
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80
Q

ITP
what are the clinical features?

A

SYMPTOMS
- bruising
- epistaxis
- menorrhagia

SIGNS
- petechiae (<4mm bleed into skin)
- purpura (4-10mm bleed into skin)
- ecchymosis (>10mm bleed into skin)
- mucosal bleeding

cutaneous bleeding is more common on lower limbs

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81
Q

ITP
what are the investigations?

A

considered a diagnosis of exclusion

  • FBC = isolated thrombocytopaenia
  • peripheral blood smear = assess platelet size

to consider
- bone marrow aspiration
- blood-borne virus serology (hep C + HIV)

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82
Q

ITP
what is the management?

A

CHILDREN
- 1st line = conservative management
- 2nd line = corticosteroids if platelets <10

ADULTS
- 1st line = oral corticosteroids
- 2nd line = IVIg

platelet transfusions are not commonly used as the transfused platelets will be destroyed by antibodies

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83
Q

TTP
what is thrombotic thrombocytopaenic purpura (TTP)?

A

thrombi form in small vessels which uses up platelets

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84
Q

TTP
what are the causes?

A

Hereditary
autoimmune (post-infection, drug induced, SLE, HIV)

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85
Q

TTP
what is the pathophysiology?

A
  • lack of ADAMTS13 protease causes platelet aggregation + activation of clotting
  • leads to microthrombi in small vessels, platelet consumption + haemolytic anaemia
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86
Q

TTP
what are the risk factors?

A
  • female
  • obesity
  • ethnicity (afro-caribbean)
  • autoimmune diseases
  • pregnancy
  • HIV
  • pancreatitis
  • medications (quinine, clopidogrel)
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87
Q

TTP
what is the classic pentad of features?

A
  • thrombocytopaenic purpura
  • microangiopathic haemolytic anaemia
  • neurological dysfunction (headache, confusion, seizures)
  • renal dysfunction (AKI)
  • fever
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88
Q

TTP
what are the clinical features?

A

SYMPTOMS
- confusion
- seizures
- headache
- bleeding (menorrhagia, epistaxis, prolonged bleeding, severe internal bleeding)
- chest pain (myocardial ischaemia)
- abdominal pain (mesenteric ischaemia)

SIGNS
- coma
- fever
- jaundice
- puerperal rash

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89
Q

TTP
what are the investigations?

A
  • FBC - thrombocytopenia + normocytic anaemia
  • U&Es - raised creatinine + urea
  • blood film - schistocytes (fragmented red blood cells)
  • ADAMTS13 activity
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90
Q

TTP
what is the management?

A

1st line = FFP
2nd line = plasma exchange

can also give high dose steroids, low dose aspirin and rituximab

91
Q

TTP
what are the complications?

A
  • renal failure
  • neurological damage
  • death (if untreated)
92
Q

HIT
what is the scoring system for working out the likelihood of having HIT?

A

4Ts test
- Thrombocytopenia (how low is platelet count?)
- Timing of reaction to heparin
- Thrombosis (signs of clot?)
- other causes of thrombocytopenia

93
Q

THALASSAEMIA
what is it?

A

condition caused by a genetic defect in protein chains that make up haemoglobin

defects in alpha-globin chains = alpha thalassaemia
defects in beta-globin chains = beta-thalassaemia

94
Q

THALASSAEMIA
what is the inheritance pattern?

A

autosomal recessive

95
Q

THALASSAEMIA
what is the cause of alpha-thalassaemia?

A

gene mutation on chromosome 16

96
Q

THALASSAEMIA
what is the cause of beta thalassaemia?

A

gene mutation on chromosome 11

97
Q

THALASSAEMIA
what are the different types of beta thalassaemia?

A
  • beta thalassaemia trait (thalassaemia minor) = 1 normal + 1 abnormal gene, mild microcytic anaemia
  • beta thalassaemia intermedia = 2 defective genes OR 1 defective + 1 deletion gene, microcytic anaemia
  • beta thalassaemia major = homozygous for deletion, no functioning beta-globin, severe anaemia, failure to thrive
98
Q

THALASSAEMIA
what are the clinical features of beta-thalassaemia major?

A
  • anaemic symptoms (fatigue, weakness, SOB, palpitations)
  • failure to thrive
  • hepatosplenomegaly
  • neonatal jaundice

BONE FEATURES
- frontal bossing (prominent forehead)
- enlarged maxilla (prominent cheekbones)
- depressed nasal ridge (flat nose)
- protruding upper teeth

99
Q

THALASSAEMIA
what are the investigations?

A
  • Hb electrophoresis (diagnostic)
  • FBC = microcytic anaemia with reticulocytosis
  • blood film = microcytic, hypochromic erythrocytes, target cells + Howell-Jolly bodies

to consider
- skull x-ray = hair-on-end appearance in beta thalassaemia intermedia + major

100
Q

THALASSAEMIA
what is the management?

A
  • regular blood transfusions (when Hb <70 or symptomatic)
  • iron chelation (DESFERRIOXAMINE)
  • hydroxycarbamide (increase HbF)
  • folate supplementation
  • splenectomy
  • stem cell transplantation (only curative option, recommended in severe disease)
101
Q

THALASSAEMIA
what are the complications?

A
  • heart failure
  • hypersplenism
  • aplastic crisis
  • iron overload
  • gallstones
102
Q

SICKLE CELL DISEASE
what are the clinical features of a vaso-occlusive crisis?

A

Presents with pain + swelling in hands or feet but can affect chest, back or other areas.
It can be associated with fever.
BONE
- dactylitis
- avascular necrosis
- osteomyelitis

LUNGS
- acute chest syndrome (dyspnoea, chest pain, hypoxia, pulmonary infiltrates on CXR)

SPLEEN
- along with sequestration, can cause autosplenectomy

CNS
- stroke

GENITALIA
- priapism (very common)

103
Q

SICKLE CELL DISEASE
what is a splenic sequestration crisis?

A

RBCs block blood flow within the spleen
It causes an acutely enlarged + painful spleen
It can lead to severe anaemia + hypovolaemic shock

104
Q

SICKLE CELL DISEASE
what is the presentation of a splenic sequestration crisis?

A
  • abdominal pain (caused by splenomegaly)
  • hypovolaemic shock
105
Q

SICKLE CELL DISEASE
what is an aplastic crisis?

A

it is the temporary absence of the creation of new red blood cells
usually triggered by parvovirus B19
leads to significant anaemia (aplastic anaemia)

106
Q

SICKLE CELL DISEASE
what usually triggers an aplastic crisis?

A

infection with parvovirus B19

107
Q

SICKLE CELL DISEASE
what is the management of an aplastic crisis?

A

supportive
blood transfusions if necessary
usually resolves spontaneously within a week

108
Q

SICKLE CELL DISEASE
what is the management of a splenic sequestration crisis?

A

SUPPORTIVE
- blood transfusions
- fluid resuscitation

  • splenectomy in recurrent cases
109
Q

SICKLE CELL DISEASE
what is acute chest syndrome?

A

occurs when vessels supplying the lungs become blocked
it is a medical emergency with high mortality

110
Q

SICKLE CELL DISEASE
what are the clinical features of acute chest syndrome?

A

fever
SOB
chest pain
cough
hypoxia

CXR shows pulmonary infiltrates

111
Q

SICKLE CELL DISEASE
what is the management of acute chest syndrome?

A
  • analgesia
  • good hydration (IV fluids may be required)
  • antibiotics/antivirals
  • blood transfusions for anaemia
  • incentive spirometry
  • respiratory support
112
Q

SICKLE CELL DISEASE
what is the general long term management?

A
  • Pain management - regularly prescribe medication for chronic pain
  • hydroxycarbamide
  • lifelong phenoxymethylpenicillin (if hyposplenic)
  • regular vaccinations
  • blood transfusion
  • folic acid supplementation
113
Q

MYELOPROLIFERATIVE DISORDERS
what are the different types?

A
  • primary myelofibrosis
  • polycythaemia vera
  • essential thrombocythaemia
114
Q

MYELOPROLIFERATIVE DISORDERS
what can they result in?

A

transformation into ALL

115
Q

MYELOFIBROSIS
what is it?

A

a type of myeloproliferative disorder
a clonal haematopoietic stem cell disorder

is characterised by:
- bone marrow fibrosis
- extramedullary haematopoiesis
- splenomegaly (often)

116
Q

MYELOFIBROSIS
what are the characteristics?

A
  • bone marrow fibrosis
  • extramedullary haematopoiesis
  • splenomegaly (often
117
Q

MYELOFIBROSIS
what are the risk factors?

A
  • age >60
  • JAK2 mutation
  • polycythaemia vera
  • essential thrombocythaemia
118
Q

MYELOFIBROSIS
what are the clinical features?

A

SYMPTOMS
- fatigue
- weight loss
- night sweats

SIGNS
- anaemia
- massive splenomegaly
- hepatomegaly

119
Q

MYELOFIBROSIS
what are the investigations?

A
  • FBC = low Hb, low WCC
  • peripheral blood smear = teardrop poikilocytes + aniosocytosis (differing cell sizes)
  • bone marrow biopsy = increased fibrosis (collagen deposition) + abnormal cell lines, dry tap

To consider
- urate + LDH
- molecular testing (JAK2)

120
Q

MYELOFIBROSIS
what is the management?

A

supportive care
- blood transfusions (for anaemia)
- erythropoiesis stimulating agents

Ruxolitinib (JAK2 inhibitor)

Chemotherapy (hydroxycarbamide)

allogenic stem cell transplant

121
Q

MYELOFIBROSIS
what are the complications?

A

progressive bone marrow failure
thrombosis + DIC
haemorrhage
transformation to leukaemia

122
Q

ESSENTIAL THROMBOCYTHAEMIA
which cell line is affected?

A

megakaryocyte - high platelet count

123
Q

ESSENTIAL THROMBOCYTHAEMIA
what is the management?

A
  • aspirin
  • chemotherapy (hydroxycarbamide)
  • anagrelide
124
Q

ESSENTIAL THROMBOCYTHAEMIA
what is the difference between essential thrombocythaemia + thrombocytosis?

A

thrombocythaemia - high platelet count that isn’t related to another condition

thrombocytosis = high platelet count because of another condition

125
Q

ESSENTIAL THROMBOCYTHAEMIA
what are the clinical features?

A
  • signs + symptoms of blood clots
126
Q

HAEMOLYTIC ANAEMIA
what are the inherited causes of haemolytic anaemia?

A
  • hereditary spherocytosis
  • hereditary elliptocytosis
  • thalassaemia
  • sickle cell anaemia
  • G6PD deficiency
127
Q

HAEMOLYTIC ANAEMIA
what are the acquired causes of haemolytic anaemia

A

autoimmune haemolytic anaemia
alloimmune haemolytic anaemia (transfusion reactions + haemolytic disease of the newborn)
paroxysmal nocturnal haemoglobinuria
microangiopathic haemolytic anaemia
prosthetic valve related haemolysis

128
Q

HAEMOLYTIC ANAEMIA
What is the management for haemolytic anaemia

A

Treat according to the cause

Dietary = folate and iron supplementation
AI cause = immunosuppression
Surgical = splenectomy

129
Q

HAEMOCHROMATOSIS
what is the inheritance pattern?

A

autosomal recessive

gene located on chromosome 6 - C282Y mutations

130
Q

HAEMOCHROMATOSIS
which organs does it most commonly affect?

A
  • liver
  • pancreas
  • heart
131
Q

HAEMOCHROMATOSIS
what are the risk factors?

A

middle age (40-50yrs)
male gender
family history
history of chronic transfusion (only relevant in acquired haemochromatosis)

132
Q

HAEMOCHROMATOSIS
what are the clinical features?

A

SYMPTOMS
- early symptoms = lethargy, arthralgia (hands) + erectile dysfunction
- loss of libido (hypogonadism due to cirrhosis + pituitary dysfunction)
- polyuria + dysuria (T2DM)

SIGNS
- skin hyperpigmentation (bronze skin)
- arthritic joints
- testicular atrophy
- features of chronic liver disease (hepatomegaly)
- features of heart failure (peripheral oedema)

133
Q

HAEMOCHROMATOSIS
what are the investigations?

A

PRIMARY CARE
- serum ferritin
- fasting serum transferrin saturation (TS)

SECONDARY CARE
1st line
- serum transferrin saturation = elevated
- serum ferritin = elevated
- LFTs = deranged due to liver deposition
- HbA1c = elevated due to damage to pancreatic beta cells
- initial screening (requires FBC, transferrin, serum ferritin + serum iron)

genetic testing
- C282Y + H63D mutations

liver biopsy
- show iron accumulation using Prussian blue (Perls) staining

ECG

Joint x-rays = show chondrocalcinosis

134
Q

HAEMOCHROMATOSIS
what is the management?

A

LIFESTYLE
- avoid alcohol
- low iron diet

PHLEBOTOMY/VENESECTION
- remove small amount of blood, initially weekly

IRON CHELATION
- desferrioxamine

FAMILY SCREENING

135
Q

HAEMOCHROMATOSIS
what are the complications?

A

LIVER
- cirrhosis
- HCC

ENDOCRINE
- T2DM
- hypogonadism

CARDIAC
- dilated cardiomyopathy
- congestive heart failure

MSK
- pseudogout
- osteoporosis

DERMATOLOGICAL
- skin hyperpigmentation

136
Q

BLOOD TRANSFUSION REACTIONS
what is the mechanism of action for acute haemolytic transfusion reactions?

A

ABO incompatibility
RBC destruction by IgM antibodies

137
Q

BLOOD TRANSFUSION REACTIONS
when do symptoms appear for acute haemolytic transfusion reaction?

A

within minutes

138
Q

BLOOD TRANSFUSION REACTIONS
what are the clinical features for acute haemolytic transfusion reaction?

A

symptoms appear within minutes of transfusion starting

  • fever
  • abdominal pain
  • chest pain
  • agitation
  • hypotension
139
Q

BLOOD TRANSFUSION REACTIONS
what is the management for acute haemolytic transfusion reaction?

A
  • immediate transfusion termination
  • send blood for direct Coombs test, repeat typing + cross match
  • fluid resuscitation with IV saline
140
Q

BLOOD TRANSFUSION REACTIONS
what are the complications for acute haemolytic transfusion reaction?

A
  • DIC
  • renal failure
141
Q

BLOOD TRANSFUSION REACTIONS
what is the mechanism of action for non-haemolytic febrile reactions?

A

due to white blood cell HLA antibodies

142
Q

BLOOD TRANSFUSION REACTIONS
how does non-haemolytic febrile reaction present?

A

fever
chills

143
Q

BLOOD TRANSFUSION REACTIONS
what is the management for non-haemolytic febrile reactions?

A
  • slow or stop transfusion
  • paracetamol
  • monitor
144
Q

BLOOD TRANSFUSION REACTIONS
what is the mechanism of action for mild allergic reaction?

A

thought to be caused by foreign plasma proteins

145
Q

BLOOD TRANSFUSION REACTIONS
what is the management for a minor allergic reaction?

A
  • temporarily stop transfusion
  • antihistamine (cetirizine)
  • once symptoms resolve, transfusion may be continued with no need for further work up
146
Q

BLOOD TRANSFUSION REACTIONS
what can cause anaphylaxis?

A

patients with IgA deficiency who have anti-IgA antibodies

147
Q

BLOOD TRANSFUSION REACTIONS
what is the management for anaphylaxis?

A
  • stop transfusion
  • IM adrenaline
  • antihistamine
  • corticosteroids
  • bronchodilators
148
Q

BLOOD TRANSFUSION REACTIONS
what is transfusion-related acute lung injury (TRALI)?

A

characterised by development of hypoxaemia/ acute respiratory distress syndrome (ARDS) within 6 hours of transfusion

149
Q

BLOOD TRANSFUSION REACTIONS
what are the clinical features for transfusion-related acute lung injury (TRALI)?

A
  • hypoxia
  • fever
  • HYPOTENSION
  • pulmonary infiltrates on CXR
150
Q

BLOOD TRANSFUSION REACTIONS
what is the mechanism of action for transfusion-related acute lung injury (TRALI)?

A

non-cardiogenic pulmonary oedema
thought to be secondary to increased vascular permeability caused by host neutrophils that become activated by substances in donated blood

151
Q

BLOOD TRANSFUSION REACTIONS
what is the management for transfusion-related acute lung injury (TRALI)?

A
  • stop transfusion
  • supportive care
  • oxygen
152
Q

BLOOD TRANSFUSION REACTIONS
what is transfusion-associated circulatory overload (TACO)?

A

fluid overload resulting in pulmonary oedema

153
Q

BLOOD TRANSFUSION REACTIONS
what is the mechanism of action for transfusion associated circulatory overload (TACO)?

A
  • excessive rate of transfusion
  • pre-existing HF
154
Q

BLOOD TRANSFUSION REACTIONS
what are the clinical features of transfusion-associated circulatory overload (TACO)?

A
  • pulmonary oedema
  • HYPERTENSION
155
Q

BLOOD TRANSFUSION REACTIONS
what is the management for transfusion associated circulatory overload (TACO)?

A
  • slow or stop transfusion
  • consider loop diuretic (furosemide)
  • consider oxygen
156
Q

BLOOD TRANSFUSION REACTIONS
which pathogens are at risk of being transmitted in platelets?

A

staph epidermidis
b.cereus

this is because platelets are stored at room temperature, which increases the risk of bacterial proliferation

157
Q

BLOOD TRANSFUSION REACTIONS
which prions are at risk of being transmitted in blood transfusions?

158
Q

SPHEROCYTOSIS
what is it?

A

inherited haemolytic anaemia
autosomal dominant

159
Q

SPHEROCYTOSIS
what is the inheritance pattern?

A

autosomal dominant

can be autosomal recessive (rarer)

160
Q

SPHEROCYTOSIS
what is the pathophysiology?

A
  • defect in RBC membrane proteins
  • RBCs appear spherical
  • there is accelerated degradation of RBCs in spleen, resulting in normocytic anaemia
  • splenomegaly occurs as spleen has to work harder
  • haemolysis increases bilirubin, which increases risk for gallstones + cholecystitis
161
Q

SPHEROCYTOSIS
what are the clinical features?

A

SYMPTOMS
- fatigue
- dizziness
- palpitations
- RUQ pain (gallstones)
- neonatal jaundice
- failure to thrive

SIGNS
- splenomegaly
- signs of anaemia (conjunctival pallor)
- jaundice
- tachycardia
- flow murmur

162
Q

SPHEROCYTOSIS
what are the investigations?

A
  • FBC = normocytic anaemia + raised MCHC
  • blood film = spherocytosis
  • Coomb’s test = negative

to consider
- EMA binding test
- cryohaemolysis
- gel electrophoresis
- osmotic fragility test

163
Q

SPHEROCYTOSIS
what is the management?

A
  • phototherapy or exchange transfusion
  • blood transfusion
  • folic acid
  • splenectomy (must be >6yrs old)
164
Q

SPHEROCYTOSIS
what are the complications?

A
  • gallstones
  • aplastic crisis
  • bone marrow expansion
  • post-splenectomy sepsis
165
Q

FEBRILE NEUTROPENIA
What is the definition of febrile neutropenia?

A

neutrophil count <0.5 x109 with either temp >38.0 or other signs + symptoms of sepsis

166
Q

FEBRILE NEUTRPENIA
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
167
Q

FEBRILE NEUTROPENIA
what are the most common causes?

A
  • staph. epidermidis

most commonly occurs 7-14 days after chemotherapy

168
Q

FEBRILE NEUTRPENIA
what is given as prophylaxis?

A

fluoroquinolone - if they are suspected to be likely to have neutrophil count <0.5 x 109

169
Q

FEBRILE NEUTRPENIA
what is the management?

A
  • do not wait for WBC
  • empirical antibiotics (piperacillin with tazobactam (tazocin))
  • if central line access, add vancomycin
  • if still febrile after 48hrs change antibiotic to menopenem +/- vancomycin
  • if not responding after 4-6 days investigate for fungal infection
170
Q

DOACs
what are the indications?

A
  • prevention of stroke in non-valvular AF (with other risk factors e.g. prior stroke, HTN, DM, HF, >75)
  • prevention of VTE following hip/knee surgery
  • treatment of DVT and PE
171
Q

DOACs
what is the mechanism of action?

A

Rivaroxaban, apixaban and edoxaban= direct factor Xa inhibitor
Dabigatran = direct thrombin inhibitor

172
Q

DOACs
how are they excreted?

A

Rivaroxaban = majority liver
Apixaban = majority faecal
Edoxaban = majority faecal
Dabigatran = majority renal

173
Q

DOACs
how can they be reversed?

A

Rivaroxaban + apixaban = andexanet alpha
Dabigatran = idarucizumab
Edoxaban = no reversal agent

174
Q

LMWH
what is the mechanism of action?

A

activates antithrombin III
forms a complex that inhibits factor Xa

175
Q

LMWH
how can it be reversed?

A
  • protamine sulfate
176
Q

UNFRACTIONATED HEPARIN
what is the mechanism of action?

A
  • activates antithrombin III
  • forms a complex that inhibits thrombin, factors Xa, IXa, Xia and XIIa
177
Q

UNFRACTIONATED HEPARIN
what are the side effects?

A
  • bleeding
  • heparin induced thrombocytopenia
  • osteoporosis
178
Q

UNFRACTIONATED HEPARIN
how is it monitored?

A

APTT (activated partial thromboplastin time)

179
Q

UNFRACTIONATED HEPARIN
how is it reversed?

A

protamine sulfate

180
Q

WARFARIN
what general things can interact with warfarin?

A
  • liver disease
  • antiepileptics (phenytoin, carbamazepine)
  • rifampicin
  • st Johns wort
  • chronic alcohol intake
  • smoking
  • cranberry juice
  • NSAIDs
  • antibiotics (ciprofloxacin, clarithromycin, erythromycin)
  • isoniazid
  • amiodarone
  • allopurinol
  • SSRIs (fluoxetine, sertraline)
  • sodium valproate
181
Q

WARFARIN
what are the side effects?

A
  • haemorrhage
  • teratogenic (can be used in breastfeeding)
  • skin necrosis
  • purple toes
182
Q

WARFARIN
how would you manage INR > 8?

A

MAJOR BLEED OR REQUIRE SURGERY
- stop warfarin
- give IV vitamin K
- give dried prothrombin complex concentrate (PCC) or Fresh frozen plasma (FFP) if PCC is unavailable

MINOR BLEED
- stop warfarin
- IV vitamin K
- repeat vitamin K dose after 24hrs if INR still too high
- restart warfarin when INR<5

NO BLEED
- stop warfarin
- oral vitamin K
- repeat vitamin K dose after 24hrs if INR still too high
- restart warfarin when INR <5

183
Q

WARFARIN
how would you manage INR 5-8?

A

MINOR BLEED
- stop warfarin
- give IV vitamin K
- restart warfarin when INR<5

NO BLEED
- withhold 1-2 doses of warfarin
- reduce subsequent maintenance dose

184
Q

ANTIPLATELETS
what are the different types?

A

aspirin
adenosine diphosphate (ADP) receptor inhibitors = clopidogrel

185
Q

ADP RECEPTOR INHIBITORS
give some examples?

A
  • clopidogrel
  • prasugrel
  • ticagrelor
  • ticlopidine
186
Q

ADP RECEPTOR INHIBITORS
what is the mechanism of action?

A
  • inhibit binding of ADP to P2Y12 receptor (antagonist)
  • this blocks platelet activation and aggregation
187
Q

ADP RECEPTOR INHIBITORS
what are the interactions?

A

clopidogrel interacts with PPIs

188
Q

ASPIRIN
what is the mechanism of action?

A
  • blocks cyclo-oxygenase 1 and 2
  • this prevents thromboxane A2 formation
  • this reduces the platelets ability to aggregate
189
Q

ASPIRIN
what does it interact with?

A
  • warfarin
  • steroids
  • oral hypoglycaemics
190
Q

ANTIPLATELETS
what is the 1st and 2nd line antiplatelet for ACS?

A

1st line
- aspirin (lifelong) + ticagrelor (12 months)

2nd line
- clopidogrel (lifelong)

191
Q

ANTIPLATELETS
what is the 1st and 2nd line antiplatelet for PCI?

A

1st line
- aspirin (lifelong) + prasugrel /ticagrelor (12 months)

2nd line
- clopidogrel (lifelong)

192
Q

ANTIPLATELETS
what is the 1st and 2nd line antiplatelet for TIA?

A

1st line
- clopidogrel (lifelong)

2nd line
- Aspirin (lifelong) + dipyridamole (lifelong)

193
Q

ANTIPLATELETS
what is the 1st and 2nd line antiplatelet for ischaemic stroke?

A

1st line
- clopidogrel

2nd line
- aspirin (lifelong) + dipyridamole (lifelong)

194
Q

ANTIPLATELETS
what is the 1st and 2nd line antiplatelet for peripheral arterial disease?

A

1st line
- clopidogrel (lifelong)

2nd line
- aspirin (lifelong)

195
Q

MALARIA
what are the risk factors?

A
  • travel to endemic area
  • absent chemoprophylaxis
  • absent use of mosquito net
  • pregnancy
  • extremes of age
  • immunocompromise
196
Q

MALARIA
what are the clinical features?

A

SYMPTOMS
- cyclical fever
- headache
- weakness
- myalgia
- arthralgia
- anorexia
- diarrhoea
- abdominal pain
- nausea and vomiting

SIGNS
- hepatosplenomegaly
- jaundice
- pallor

197
Q

MALARIA
what are the clinical features of severe disease?

A
  • GCS<11
  • oliguria
  • acidosis
  • hypoglycaemia
  • respiratory distress
  • hypotension
  • seizures
  • spontaneous bleeding (DIC)
  • parasitaemia >10%
198
Q

MALARIA
what are the investigations?

A
  • thick and thin blood films
  • rapid diagnostic test (RDT)
  • FBC = anaemia
  • clotting screen = PT may be prolonged
  • U&Es = AKI from dehydration + hypotension
  • LFTs = unconjugated hyperbilirubinaemia + deranged ALT/AST
  • blood glucose = hypoglycaemia
  • urinalysis
  • ABG = metabolic acidosis (in severe disease)

to consider
- PCR for malaria
- CXR
- HIV test
- CT head

199
Q

MALARIA
what is the management?

A

UNCOMPLICATED FALCIPARUM
- oral chloroquine/hydroxychloroquine (if chloroquine sensitive)
- oral artemether/lumefantrine (if chloroquine resistant)

SEVERE FALCIPARUM
- 1st line = IV artesunate
- 2nd line = IV artemether
- supportive care (IV fluids, airway protection, control of seizures, blood products)

NON-FALCIPARUM
- 1st line = oral chloroquine or hydroxychloroquine
- oral primaquine if p.vivax or p.ovale

200
Q

MALARIA
what are the complications?

A
  • AKI
  • hypoglycaemia
  • metabolic acidosis
  • severe anaemia
  • DIC
  • sepsis
  • blackwater fever
  • ARDS
  • cerebral malaria
201
Q

ENTERIC FEVER
what is it?

A

refers to typhoid and paratyphoid infections

202
Q

TYPHOID
what causes typhoid?

A

salmonella typhi

203
Q

TYPHOID
how is it spread?

A

through faecal oral transmission

204
Q

TYPHOID
what are the risk factors?

A
  • poor sanitation
  • poor hygiene
  • travelling to developing regions
205
Q

TYPHOID
what are the clinical features?

A

SYMPTOMS
- high fever
- weakness and myalgia
- bradycardia
- abdominal pain
- constipation
- headaches
- vomiting
- skin rash with rose-coloured spots (common in exams)
- confusion

206
Q

TYPHOID
what is the onset of symptoms following exposure?

A

symptoms generally appear 6-30 days after exposure
it’s typically a gradual onset

207
Q

TYPHOID
what are the investigations?

A
  • blood culture
  • stool culutre
  • bone marrow aspirate culture (gold standard)
  • ECG (esp if bradycardic)
  • bloods (FBC, U&Es, CRP, ABG/VBG, LFTs, group and save, cross match, clotting)
  • imaging
208
Q

TYPHOID
what is the management?

A
  • antibiotics (azithromycin or ceftriaxone)
  • infection control measures
209
Q

TYPHOID
what are the complications?

A
  • osteomyelitis (esp in sickle cell anaemia)
  • GI bleeding/perforation
  • rarely, meningitis
210
Q

DENGUE
what is the cause of dengue fever?

A

dengue virus (RNA virus)
transmitted by Aedes aegypti mosquito

211
Q

DENGUE
what is the incubation period?

212
Q

DENGUE
what are the clinical features?

A
  • fever
  • headache (often retro-orbital)
  • myalgia, bone pain and arthralgia (break bone fever)
  • facial flushing
  • maculopapular rash

SIGNS
- haemorrhagic manifestations (positive tourniquet test, petechiae, purpura/ecchymosis, epistaxis)
- warning signs (abdominal pain, hepatomegaly, persistent vomiting, ascites, pleural effusion)

213
Q

DENGUE
what are the investigations?

A

FBC, U&Es, LFTs
- leukopaenia
- thrombocytopaenia
- raised aminotransferases

DIAGNOSTIC TESTS
- serology
- nucleic acid amplification tests for RNA
- NS1 antigen test

214
Q

AUTOIMMUNE HAEMOLYTIC ANAEMIA
what are the different types?

A
  • warm autoimmune haemolytic anaemia
  • cold autoimmune haemolytic anaemia
215
Q

AUTOIMMUNE HAEMOLYTIC ANAEMIA
what are the differences between warm and cold autoimmune haemolytic anaemia?

A

WARM
- most common
- IgG
- occurs at body temperature
- occurs at extravascular sites e.g. spleen
- triggered by autoimmune disease or malignancy

COLD
- IgM
- occurs at 4 degrees
- occurs at intravascular sites
- mostly triggered by infection

216
Q

AUTOIMMUNE HAEMOLYTIC ANAEMIA
what is the presentation?

A
  • fatigue
  • pallor
  • jaundice
  • SOB
  • Raynaud (cold AIHA)
217
Q

AUTOIMMUNE HAEMOLYTIC ANAEMIA
what are the investigations?

A
  • FBC (anaemia, elevated reticulocytes)
  • raised LDH
  • LFTs (raised bilirubin)
  • direct Coombs (presence of antibodies on RBCs)
218
Q

AUTOIMMUNE HAEMOLYTIC ANAEMIA
what is the management?

A

1st line = prednisolone
2nd line = rituximab

treat underlying conditions
blood transfusions in severe anaemia

219
Q

G6PD
what is it?

A

genetic disorder causing a defect in G6PD
makes cells more vulnerable to reactive oxygen species, leading to haemolysis

220
Q

G6PD
what is the pattern of inheritance?

A

x-linked recessive

221
Q

G6PD
what are the clinical features?

A
  • anaemia
  • intermittent jaundice
  • gallstones
  • splenomegaly

only get symptoms when they have been in contact with a trigger

222
Q

G6PD
what are the triggers?

A
  • fava beans
  • antimalarials (primaquine, chloroquine)
  • antibiotics (NITROFURANTOIN, sulfonamides, chloramphenicol, ciprofloxacin)
  • NSAIDs
  • infection
223
Q

G6PD
what are the investigations?

A
  • G6PD enzyme assay (diagnostic)
  • blood film (HEINZ BODIES)
  • FBC = anaemia, reticulocytosis, raised bilirubin)
224
Q

G6PD
what is the management?

A
  • avoid triggers
  • supportive care during haemolytic episodes (hydration, pain relief, blood transfusions)

MY REVISION - ALL TO DO (21 decks)

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