HAEMATOLOGY Flashcards
ANAEMIA
what are the causes of normoblastic macrocytic anaemia?
- alcohol
- reticulocytosis (haemolytic anaemia or blood loss)
- hypothyroidism
- liver disease
- drugs (e.g. azathioprine)
B12 DEFICIENCY
what are the causes?
- 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
B12 DEFICIENCY
which medications can cause B12 deficiency anaemia?
- PPIs
- colchicine
- metformin
B12 DEFICIENCY
what are the clinical features that are unique to B12 deficiency anaemia?
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
HYPOSPLENISM
what are the functions of the spleen?
- activation of lymphocytes
- removal of damaged/effete RBCs from circulation
- sequestration of platelets for release during times of stress
- site of haematopoiesis in utero
HYPOSPLENISM
what are the causes of functional hyposplenism?
- 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)
HYPOSPLENISM
what is the management?
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
AML
what are the risk factors?
- increasing age
- myelodysplastic syndromes
- myeloproliferative neoplasms
- previous chemotherapy or radiation exposure
- benzene (painters, petroleum + rubber manufacturers)
CLL
what are the complications?
- hypogammaglobinaemia
- warm autoimmune haemolytic anaemia
- Richter transformation (into non-hodgkins lymphoma)
CML
which chromosome is present in 95% of patients with CML?
Philadelphia chromosome
forms a fusion gene BCR/ABL on chromosome 22 – has tyrosine kinase activity – simulate cell division
CML
what are the investigations?
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
CML
what is the management?
- tyrosine kinase inhibitor (imatinib)
- chemotherapy
- stem cell transplant if above fails
CML
why does the philadelphia chromosome cause CML?
Froms fusion gene BCR/ABL on chromosome 22 –> tyrosine kinase activity –> stimulates cell division
HODGKINS LYMPHOMA
what are the risk factors?
- EBV infection
- HIV
- autoimmune conditions (rheumatoid arthritis + sarcoidosis)
- family history
HODGKINS LYMPHOMA
how is it staged?
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
HODGKINS LYMPHOMA
what is the management?
- chemotherapy (ABVD)
- radiotherapy
- rituximab
NON-HODGKINS LYMPHOMA
what are the risk factors?
- HIV
- EBV
- h-pylori infection (associated with MALT lymphoma)
- Hep B + hep C infection
- exposure to pesticides
- exposure to trichloroethylene
- family history
NON-HODGKINS LYMPHOMA
what is the management?
depends on type + stage
may involve:
- watchful waiting
- chemotherapy (R-CHOP)
- monoclonal antibodies (rituximab)
- radiotherapy
- stem cell transplant
NON-HODGKINS LYMPHOMA
how is it staged?
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
DIC
what are the investigations?
FBC - thrombocytopaenia, anaemia + leukocytosis
Clotting studies - prolonged PT + APTT
Fibrinogen levels - decreased
D-dimer - raised
Blood cultures - identify cause
Blood film - schistocytes
HAEMOPHILIA
how is it inherited?
X-linked recessive - therefore primarily affects males
Haemophilia A = factor VIII deficiency
Haemophilia B = factor IX deficiency
HAEMOPHILIA
what are the investigations?
- 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
MULTIPLE MYELOMA
what are the investigations?
- 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
MULTIPLE MYELOMA
what are the main clinical signs?
old CRAB
- old = >75
- hypercalcaemia
- renal failure
- anaemia
- bone lesions
MULTIPLE MYELOMA
what is the diagnostic criteria?
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
PANCYTOPENIA
what are the causes?
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)
PANCYTOPENIA
what are the risk factors?
- co-morbid autoimmune diseases
- recent viral infections (HIV, EBV, CMV)
- malabsorption syndromes
- history of cancer
- family history of aplastic anaemia
PANCYTOPENIA
what are the clinical features?
SYMPTOMS
- fatigue
- recurrent infections
- epistaxis
- B symptoms (weight loss, fever, night sweats if malignancy)
SIGNS
- pallor
- petechiae
- splenomegaly
APLASTIC ANAEMIA
what is it?
bone marrow hypocellularity secondary to primary haematopoietic failure
type of pancytopaenia
APLASTIC ANAEMIA
what are the different causes?
- fanconi anaemia
- radiation
- carbimazole
- carbamazepine
- chloramphenicol
- chemotherapy
- benzene
FANCONI ANAEMIA
what is the inheritance pattern?
can be autosomal dominant or recessive
FANCONI ANAEMIA
what are the features?
- pancytopaenia in first decade of life
- organ hypoplasia
- bone defects (e.g. absent thumbs)
POLYCYTHAEMIA
what gene mutation is seen?
JAK2 gene
POLYCYTHAEMIA
what are the risk factors?
- age >40
- family history
- budd-chiari syndrome
POLYCYTHAEMIA
what are the clinical features?
SYMPTOMS
- headache
- pruritus
- erythromelalgia
- facial flushing
SIGNS
- splenomegaly
- palmar erythema
- plethoric complexion
- HTN
POLYCYTHAEMIA
what are the investigations?
- FBC = raised Hb + haematocrit
- U&Es + LFTs
- ABG (pO2 normal in primary but low in secondary)
- ferritin
- erythropoietin = (primary = low, secondary = raised)
- JAK2 mutation
POLYCYTHAEMIA
what is the management?
1st line = venesection (maintain haematocrit below 0.45)
hydroxyurea (in high risk patients)
aspirin 75mg
manage modifable CVD risk factors (diabetes, HTN, smoking, hyperlipidaemia)
ITP
what are the investigations?
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)
ITP
what is the management?
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
TTP
what is the pathophysiology?
- lack of ADAMTS13 protease causes platelet aggregation + activation of clotting
- leads to microthrombi in small vessels, platelet consumption + haemolytic anaemia
TTP
what are the risk factors?
- female
- obesity
- ethnicity (afro-caribbean)
- autoimmune diseases
- pregnancy
- HIV
- pancreatitis
- medications (quinine, clopidogrel)
TTP
what is the classic pentad of features?
- thrombocytopaenic purpura
- microangiopathic haemolytic anaemia
- neurological dysfunction (headache, confusion, seizures)
- renal dysfunction (AKI)
- fever
TTP
what are the clinical features?
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
TTP
what are the investigations?
- FBC - thrombocytopenia + normocytic anaemia
- U&Es - raised creatinine + urea
- blood film - schistocytes (fragmented red blood cells)
- ADAMTS13 activity
TTP
what is the management?
1st line = FFP
2nd line = plasma exchange
can also give high dose steroids, low dose aspirin and rituximab
HIT
what is the scoring system for working out the likelihood of having HIT?
4Ts test
- Thrombocytopenia (how low is platelet count?)
- Timing of reaction to heparin
- Thrombosis (signs of clot?)
- other causes of thrombocytopenia
THALASSAEMIA
what is the inheritance pattern?
autosomal recessive
THALASSAEMIA
what is the cause of beta thalassaemia?
gene mutation on chromosome 11
THALASSAEMIA
what are the different types of beta thalassaemia?
- 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
THALASSAEMIA
what are the clinical features of beta-thalassaemia major?
- 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
THALASSAEMIA
what are the investigations?
- 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
THALASSAEMIA
what is the management?
- 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)
THALASSAEMIA
what are the complications?
- heart failure
- hypersplenism
- aplastic crisis
- iron overload
- gallstones
SICKLE CELL DISEASE
what are the clinical features of a vaso-occlusive crisis?
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)
SICKLE CELL DISEASE
what is the presentation of a splenic sequestration crisis?
- abdominal pain (caused by splenomegaly)
- hypovolaemic shock
SICKLE CELL DISEASE
what is an aplastic crisis?
it is the temporary absence of the creation of new red blood cells
usually triggered by parvovirus B19
leads to significant anaemia (aplastic anaemia)
SICKLE CELL DISEASE
what are the clinical features of acute chest syndrome?
fever
SOB
chest pain
cough
hypoxia
CXR shows pulmonary infiltrates
SICKLE CELL DISEASE
what is the general long term management?
- Pain management - regularly prescribe medication for chronic pain
- hydroxycarbamide
- lifelong phenoxymethylpenicillin (if hyposplenic)
- regular vaccinations
- blood transfusion
- folic acid supplementation
MYELOPROLIFERATIVE DISORDERS
what are the different types?
- primary myelofibrosis
- polycythaemia vera
- essential thrombocythaemia
MYELOPROLIFERATIVE DISORDERS
what can they result in?
transformation into ALL
MYELOFIBROSIS
what is it?
a type of myeloproliferative disorder
a clonal haematopoietic stem cell disorder
is characterised by:
- bone marrow fibrosis
- extramedullary haematopoiesis
- splenomegaly (often)
MYELOFIBROSIS
what are the characteristics?
- bone marrow fibrosis
- extramedullary haematopoiesis
- splenomegaly (often
MYELOFIBROSIS
what are the risk factors?
- age >60
- JAK2 mutation
- polycythaemia vera
- essential thrombocythaemia
MYELOFIBROSIS
what are the clinical features?
SYMPTOMS
- fatigue
- weight loss
- night sweats
SIGNS
- anaemia
- massive splenomegaly
- hepatomegaly
MYELOFIBROSIS
what are the investigations?
- 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)
MYELOFIBROSIS
what is the management?
supportive care
- blood transfusions (for anaemia)
- erythropoiesis stimulating agents
Ruxolitinib (JAK2 inhibitor)
Chemotherapy (hydroxycarbamide)
allogenic stem cell transplant
ESSENTIAL THROMBOCYTHAEMIA
which cell line is affected?
megakaryocyte - high platelet count
ESSENTIAL THROMBOCYTHAEMIA
what is the management?
- aspirin
- chemotherapy (hydroxycarbamide)
- anagrelide
HAEMOLYTIC ANAEMIA
what are the inherited causes of haemolytic anaemia?
- hereditary spherocytosis
- hereditary elliptocytosis
- thalassaemia
- sickle cell anaemia
- G6PD deficiency
HAEMOLYTIC ANAEMIA
what are the acquired causes of haemolytic anaemia
autoimmune haemolytic anaemia
alloimmune haemolytic anaemia (transfusion reactions + haemolytic disease of the newborn)
paroxysmal nocturnal haemoglobinuria
microangiopathic haemolytic anaemia
prosthetic valve related haemolysis
HAEMOCHROMATOSIS
what is the inheritance pattern?
autosomal recessive
gene located on chromosome 6 - C282Y mutations
HAEMOCHROMATOSIS
what are the clinical features?
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)
HAEMOCHROMATOSIS
what are the investigations?
PRIMARY CARE
- serum ferritin
- fasting serum transferrin saturation (TS)
SECONDARY CARE
1st line
- serum transferrin saturation = elevated
- serum ferritin = elevated
- TIBC = low
- 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
HAEMOCHROMATOSIS
what is the management?
LIFESTYLE
- avoid alcohol
- low iron diet
PHLEBOTOMY/VENESECTION
- remove small amount of blood, initially weekly
IRON CHELATION
- desferrioxamine
FAMILY SCREENING
HAEMOCHROMATOSIS
what are the complications?
LIVER
- cirrhosis
- HCC
ENDOCRINE
- T2DM
- hypogonadism
CARDIAC
- dilated cardiomyopathy
- congestive heart failure
MSK
- pseudogout
- osteoporosis
DERMATOLOGICAL
- skin hyperpigmentation
BLOOD TRANSFUSION REACTIONS
what is the mechanism of action for acute haemolytic transfusion reactions?
ABO incompatibility
RBC destruction by IgM antibodies
BLOOD TRANSFUSION REACTIONS
what is the management for acute haemolytic transfusion reaction?
- immediate transfusion termination
- send blood for direct Coombs test, repeat typing + cross match
- fluid resuscitation with IV saline
BLOOD TRANSFUSION REACTIONS
what is the mechanism of action for non-haemolytic febrile reactions?
due to white blood cell HLA antibodies
BLOOD TRANSFUSION REACTIONS
what is the management for non-haemolytic febrile reactions?
- slow or stop transfusion
- paracetamol
- monitor
BLOOD TRANSFUSION REACTIONS
what is the mechanism of action for mild allergic reaction?
thought to be caused by foreign plasma proteins
BLOOD TRANSFUSION REACTIONS
what is the management for a minor allergic reaction?
- temporarily stop transfusion
- antihistamine (cetirizine)
- once symptoms resolve, transfusion may be continued with no need for further work up
BLOOD TRANSFUSION REACTIONS
what can cause anaphylaxis?
patients with IgA deficiency who have anti-IgA antibodies
BLOOD TRANSFUSION REACTIONS
what are the clinical features for transfusion-related acute lung injury (TRALI)?
- hypoxia
- fever
- HYPOTENSION
- pulmonary infiltrates on CXR
BLOOD TRANSFUSION REACTIONS
what is the mechanism of action for transfusion-related acute lung injury (TRALI)?
non-cardiogenic pulmonary oedema
thought to be secondary to increased vascular permeability caused by host neutrophils that become activated by substances in donated blood
BLOOD TRANSFUSION REACTIONS
what is the management for transfusion-related acute lung injury (TRALI)?
- stop transfusion
- supportive care
- oxygen
BLOOD TRANSFUSION REACTIONS
what are the clinical features of transfusion-associated circulatory overload (TACO)?
- pulmonary oedema
- HYPERTENSION
BLOOD TRANSFUSION REACTIONS
what is the management for transfusion associated circulatory overload (TACO)?
- slow or stop transfusion
- consider loop diuretic (furosemide)
- consider oxygen
SPHEROCYTOSIS
what is the inheritance pattern?
autosomal dominant
can be autosomal recessive (rarer)
SPHEROCYTOSIS
what are the clinical features?
SYMPTOMS
- fatigue
- dizziness
- palpitations
- RUQ pain (gallstones)
- neonatal jaundice
- failure to thrive
SIGNS
- splenomegaly
- signs of anaemia (conjunctival pallor)
- jaundice
- tachycardia
- flow murmur
SPHEROCYTOSIS
what is the management?
- phototherapy or exchange transfusion
- blood transfusion
- folic acid
- splenectomy (must be >6yrs old)
FEBRILE NEUTRPENIA
Give 4 risk factors for febrile neutropenia
- If the patient had chemotherapy <6 weeks ago
- Any patient who has had a stem cell transplant <1 year ago
- Any haematological condition causing neutropenia
- Bone marrow infiltration
- those on methotrexate, carbimazole and clozapine
FEBRILE NEUTROPENIA
what are the most common causes?
- staph. epidermidis
most commonly occurs 7-14 days after chemotherapy
FEBRILE NEUTRPENIA
what is given as prophylaxis?
fluoroquinolone - if they are suspected to be likely to have neutrophil count <0.5 x 109
FEBRILE NEUTRPENIA
what is the management?
- 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
DOACs
what is the mechanism of action?
Rivaroxaban, apixaban and edoxaban= direct factor Xa inhibitor
Dabigatran = direct thrombin inhibitor
DOACs
how are they excreted?
Rivaroxaban = majority liver
Apixaban = majority faecal
Edoxaban = majority faecal
Dabigatran = majority renal
DOACs
how can they be reversed?
Rivaroxaban + apixaban = andexanet alpha
Dabigatran = idarucizumab
Edoxaban = no reversal agent
LMWH
what is the mechanism of action?
activates antithrombin III
forms a complex that inhibits factor Xa
LMWH
how can it be reversed?
- protamine sulfate
UNFRACTIONATED HEPARIN
what is the mechanism of action?
- activates antithrombin III
- forms a complex that inhibits thrombin, factors Xa, IXa, Xia and XIIa
WARFARIN
what are the side effects?
- haemorrhage
- teratogenic (can be used in breastfeeding)
- skin necrosis
- purple toes
WARFARIN
how would you manage INR > 8?
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
WARFARIN
how would you manage INR 5-8?
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
ADP RECEPTOR INHIBITORS
give some examples?
- clopidogrel
- prasugrel
- ticagrelor
- ticlopidine
ADP RECEPTOR INHIBITORS
what is the mechanism of action?
- inhibit binding of ADP to P2Y12 receptor (antagonist)
- this blocks platelet activation and aggregation
ASPIRIN
what is the mechanism of action?
- blocks cyclo-oxygenase 1 and 2
- this prevents thromboxane A2 formation
- this reduces the platelets ability to aggregate
ASPIRIN
what does it interact with?
- warfarin
- steroids
- oral hypoglycaemics
ANTIPLATELETS
what is the 1st and 2nd line antiplatelet for peripheral arterial disease?
1st line
- clopidogrel (lifelong)
2nd line
- aspirin (lifelong)
MALARIA
what are the clinical features?
SYMPTOMS
- cyclical fever
- headache
- weakness
- myalgia
- arthralgia
- anorexia
- diarrhoea
- abdominal pain
- nausea and vomiting
SIGNS
- hepatosplenomegaly
- jaundice
- pallor
MALARIA
what are the clinical features of severe disease?
- GCS<11
- oliguria
- acidosis
- hypoglycaemia
- respiratory distress
- hypotension
- seizures
- spontaneous bleeding (DIC)
- parasitaemia >10%
MALARIA
what are the investigations?
- 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
MALARIA
what is the management?
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
MALARIA
what are the complications?
- AKI
- hypoglycaemia
- metabolic acidosis
- severe anaemia
- DIC
- sepsis
- blackwater fever
- ARDS
- cerebral malaria
TYPHOID
what are the risk factors?
- poor sanitation
- poor hygiene
- travelling to developing regions
TYPHOID
what are the clinical features?
SYMPTOMS
- high fever
- weakness and myalgia
- bradycardia
- abdominal pain
- constipation
- headaches
- vomiting
- skin rash with rose-coloured spots (common in exams)
- confusion
TYPHOID
what are the investigations?
- 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
TYPHOID
what is the management?
- antibiotics (azithromycin or ceftriaxone)
- infection control measures
TYPHOID
what are the complications?
- osteomyelitis (esp in sickle cell anaemia)
- GI bleeding/perforation
- rarely, meningitis
DENGUE
what are the clinical features?
- 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)
AUTOIMMUNE HAEMOLYTIC ANAEMIA
what are the differences between warm and cold autoimmune haemolytic anaemia?
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
AUTOIMMUNE HAEMOLYTIC ANAEMIA
what is the presentation?
- fatigue
- pallor
- jaundice
- SOB
- Raynaud (cold AIHA)
AUTOIMMUNE HAEMOLYTIC ANAEMIA
what are the investigations?
- FBC (anaemia, elevated reticulocytes)
- raised LDH
- LFTs (raised bilirubin)
- direct Coombs (presence of antibodies on RBCs)
AUTOIMMUNE HAEMOLYTIC ANAEMIA
what is the management?
1st line = prednisolone
2nd line = rituximab
treat underlying conditions
blood transfusions in severe anaemia
G6PD
what is the pattern of inheritance?
x-linked recessive
G6PD
what are the clinical features?
- anaemia
- intermittent jaundice
- gallstones
- splenomegaly
only get symptoms when they have been in contact with a trigger
G6PD
what are the triggers?
- fava beans
- antimalarials (primaquine, chloroquine)
- antibiotics (NITROFURANTOIN, sulfonamides, chloramphenicol, ciprofloxacin)
- NSAIDs
- infection
G6PD
what are the investigations?
- G6PD enzyme assay (diagnostic)
- blood film (HEINZ BODIES)
- FBC = anaemia, reticulocytosis, raised bilirubin)
G6PD
what is the management?
- avoid triggers
- supportive care during haemolytic episodes (hydration, pain relief, blood transfusions)
