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76 Cards in this Set

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LFTs - ALP
Indicates biliary obstruction and hepatic metastasis
LFTs - AST
Liver and skeletal muscle pathologies
LFTs - Albumin
If low, capillary leak
LFTs - ALT
If high, hepatitis
V. high ALP, high ALT
Problem in bile duct
Very high ALT, high ALP
problem in liver
Very very high ALT, high AST
Severe necrosis of liver
Very high ASP, high ALT
Alcoholic cirrhosis
Neutrophilia
Acute infection, inflammation, acute necrosis
Neutropenia
Viral infection, drug reactions
Causes of microcytic anaemia
Iron deficiency, thalassaemia (low MCV, raised RBC)
Causes of normocytic anaemia
Blood loss, chronic disease, bone marrow failure, renal failure, hypothyroidism, haemolysis, pregnancy
Causes of macrocytic anaemia
B12/folate deficiency, alcohol excess, reticulocytosis, myelodysplastic syndrome, marrow infiltration, hypothyroidism
Cause of anaemia in renal failure
Erythropoietin deficiency
What are Howell-Jolly bodies?
DNA nuclear remnants in RBCs. They are normally removed by the spleen and seen in post splenectomy and hyposplenism (sickle cell, coeliac, UC, Crohn's)
What are reticulocytes?
Young (therefore large) RBCs signifying active erythropoiesis. Increased in haemolysis and haemorrhage.
Lymphocytes are increased in
Acute viral infections, chronic infections, leukaemias and lymphomas
Atypical lymphocytes seen in...
Epstein-Barr virus infection
Lymphocytes are decreased in...
Steroid therapy, SLE, Legionnaire's, HIV, post chemo
Eosinophils are increased in...
Drug reactions (erythema multiform), allergies, parasitic infection, skin disease (pemphigus, eczema, psoriasis)
Most common cause of macrocytic anaemia
Pernicious anaemia, NOT B12 deficiency
Causes of megaloblastic anaemia
B12 and folate deficiency
Cause of sickle cell anaemia
Autoimmune substitution of Glu for Val at position 6 of the beta chain
Homo/heterozygote in SCA
Heterozygote = HbAS = sickle cell trait. Homozygote = HbSS = SCA
Expected blood results in SCA
Haemolysis, Hb ~ 6-9, Reticulocytes raised by 10-20%, raised bilirubin
Triggers of SC crises
Cold, dehydration, infection, hypoxia
Complication of SCA
Splenic infection therefore susceptibility to infection, poor growth, chronic renal failure, gallstones, retinal disease, iron overload, lung damage.
Management of chronic SCA
Hydroxycarbimide if crises are frequent, prophylactic antibiotics, bone marrow transplant
Management of SCA crisis
Prompt IV opiates, crossmatch, rehydrate, broad spectrum antibiotics, blood transfusion
Causes of hypocoagulability
Acquired - Anticoagulation with warfarin, liver failure, vitamin K deficiency, dengue fever, leukaemia.

Autoimmune - antiphospholipid syndrome

Genetic - Haemophilia, Von Willebrand's, Bernard-Soulier syndrome
Causes of hypercoagulability
Congenital - Factor V leiden

Acquired - antiphopholipid syndrome, heparin induced thrombocytopenia, paroxysmal nocturnal haemoglobinuria, cancers, nephrotic syndrome, pregnancy, oral contraceptive
Symptoms of hypercoagulability
DVT, PE, SOB, palpitations, collapse, shock, cardiac arrest, miscarriage (multiple = antiphospholipid syndrome), pre-eclampsia
Symptoms of hypocoagulability
Petechiae, purpura, melena, haematochezia, bleeding gums
How does heparin work?
Inactivates thrombin (IIa) and factor Xa at a slow rate. Heparin AT-III can also inactivate factors IX, XI, XII and plasmin
How does warfarin work?
Vitamin K antagonist therefore inactivates Vit K dependent clotting factors (II, VII, IX, X, protein C, protein S)
Describe the intrinsic pathway
Caused by damaged surface.

XII -> XIIa
XI -> XIa
IX -> IXa
X -> Xa

Prothrombin (II) -> Thrombin (IIa)

V -> Va

Fibrinogen -> Fibrin

Hence factor V leiden causes hypercoagulability
Describe the extrinsic pathway
Trauma

Tissue factor
X -> Xa

Prothrombin (II) -> Thrombin (IIa)

V -> Va

Fibrinogen -> Fibrin

Hence factor V leiden causes hypercoagulability
How and why do we test prothrombin time?
Addition of thromboplastin to the plasma to test the extrinsic system. It tests for abnormalities in factors I, II, V, VIII, IX, X, XI, XII
How and why do we test thrombin time?
Thrombin added to plasma to convert fibrinogen to fibrin. Prolonged by heparin treatment.
Normal time to haemostasis in bleeding time test?
10 mins
To correct anaemia or blood loss...
Use packed RBCs
To correct clotting defects/warfarin overdose...
Use FFP
Early transfusion complications
TRALI, bacterial infection, anaphylaxis, fluid overload, acute haemolytic reactions
Late transfusion complications
Viral infection, graft vs host disease, iron overload, post transfusion pupura
Tumour lysis syndrome
Caused by a massive destruction of cells leading to increased potassium, urate and renal impairment.
Signs and symptoms of ALL
Marrow failure: Anaemia, susceptibility to infection, bleeding.

Infiltration: Hepato and splenomegaly, lymphadenopathy, orchidomegaly, cranial nerve palsy
Investigations of ALL
Blast cells on blood film, mediastinal lymphadenopathy on CXR
Basic support in ALL
IV fluids, prophylactic antibiotics, allopurinol (prevent tumour lysis syndrome)
Chemotherapy in ALL
Remission induction via vincristine, prednisolone, L-asparaginase + daunorubicin

CNS prophylaxis - intrathecal methotrexate

Maintenance - mercaptopurine (daily), methotrexate (weekly), vincristine and prednisolone (monthly)
Differentiating symptoms in AML
Gum hypertrophy, CNS involvement is rare
Differentiation in CML is via...
Presence of the Philadelphia chromosome. Features of gout due to purine breakdown. WCC raised across the spectrum.
The commonest form of leukaemia is...
CLL
Rai stages of CLL
0 = Lymphocytosis alone = 13 yr

1= LCT + lymphadenopathy = 8yr

2- LCT + splen/hepat meg = 5yr

3= LCT + anaemia = 2yr

4 = LCT + platelets < 100 = 1yr
Signs of CLL
Enlarged, rubbery, tender nodes. Hepatosplenomegaly
Tests for CLL
High lymphocytes. Low Hb, neutrophils and platelets
Treatment of CLL
Fludarabine + cyclophosphamide
Treatment of CML
Imatinib
Characteristic cells of Hodgkin's lymphoma
Reed-Sternberg cells
Presentation in Hodgkin's lymphoma
Enlarged, rubbery PAINLESS cervical nodes (painful in CLL), alcohol induced lymph node pain,
Staging of Hodgkin's lymphoma
Is via the Ann Arbor system

1. Confined to single lymph node region

2. Two or more nodal areas on same side of diaphragm

3. Nodes on both sides of diaphragm

4. Spread beyond lymph nodes (liver or bone)
Treatment of Hodgkin's lymphoma
ABVD - Adriamycin, bleomycin, vinblastine, dacarbazine
Differentiating pathogenesis of non-Hodgkin's lymphoma
No Reed-Sternberg cells featured
Clinical features of Non-Hodgkin's lymphoma
Disease of the oropharyngeal lymphoid tissue (Waldeyer's ring) = difficulty breathing + sore throat.
Treatment of Non-Hodgkin's lymphoma
R-CHOP regimen: Rituximab, Cyclophosphamide, Hydroxydaunorubicin, Oncovin (trade name of vincristine) and Prednisolone
Classification of the myeloproliferative disorders.
RBCs = polycythaemia rubra vera

WBCs = chronic myeloid leukaemia

Platelets = Essential thrombocytopenia

Fibroblasts = Myelofibrosis
Signs and symptoms of polycythaemia rubra vera
headaches, dizziness, tinnitus, itchy after hot bath, burning sensation in peripheries, visual disturbances, gout due to raised urate from RBC turnover
Characteristic investigative result of myeloma is...
Monoclonal band (2/3 IgG, 1/3 IgA). Urine often contains Bence-Jones protein. Increased blast cells on bone marrow biopsy.
Symptoms of myeloma
Osteolytic pain, pathological fractures and hypercalcaemia (increased osteoclasts), anaemia, neutropenia, thrombocytopenia, recurrent bacterial infections, renal failure
Compatible blood for A+ patient
A+, A-, O+, O-
Compatible blood for A- patient
A-, O-
Compatible blood for B+ patient
B+, B-, O+, O-
Compatible blood for B- patient
B-, O-
Compatible blood for AB+ patient
Anything
Compatible blood for AB- patient
Anything negative
Compatible blood for O+ patient
O-, O+
Compatible blood for O- patient
O-