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Haematology Flashcards

1
Q

MCV?

A

Average cell size

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2
Q

RDW?

A

Red cell distribution width - measure of the range of variation of red blood cell volume

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3
Q

Reticulocytes?

A

Immature red cells

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4
Q

TIBC?

A

Total iron binding capacity - blood’s capacity to bind iron with transferrin

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5
Q

Haematocrit?

A

How many red cells in blood volume (% red cells) - if it decreases with Hb then it suggests decrease is dilutional

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6
Q

Mnemonic for remembering absorption?

A

DUDE IS JUST FEELING ILL BRO

Duodenum = iron
Jejunum = folate
Ileum = B12
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7
Q

Causes of micro, normo and macro-cytic anaemias

A 
Micro = iron, thalassaemia
Normo = chronic disease, sickle cell
Macro = B12/folate, ETOH, pregnancy
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8
Q

Signs of IDA?

A

Pallor
Severe –> hyperdynamic circulation (tachy, flow murmurs, cardiac enlargement, rectal bleeding)
Chronic –> koilonychia, atrophic glossitis, angular stomatitis, post-cricoid webs

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9
Q

Investigations in IDA?

A 
High = TIBC (clinging on to iron)
Low = Hb, MCV, ferritin, serum iron, transferrin saturation

Ferritin = acute phase reactant

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10
Q

Management of IDA?

A

Ferrous sulphate/ferrous fumerate TDS

3 wks to 1 month - should increase Hb by 20 - continue for 3 months

SEs = constipation, black stools, abdo pain, nausea

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11
Q

Causes of macrocytic anaemia?

A

DIETARY
Lack of intake, alcohol

MALABSORPTION
Stomach - pernicious anaemia –> no intrinsic factor. Also post gastrectomy.
Terminal ileum - Crohn’s disease

PREGNANCY

ANYTHING THAT KNACKS UP BONE MARROW

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12
Q

Signs in macrocytic anaemia?

A

Lemon tinge to skin (pallor + haemolysis)

Glossitis, angular stomatitis

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13
Q

Complications of macrocytic anaemia?

A

Neuropsychiatric - irritability, depression, psychosis, dementia
Neurological - paresthesia, peripheral neuropathy, subacute combined generation of spinal cord

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14
Q

Investigations in macro anaemia?

A 
High = MCV
Low = Hb, WCC, platelets, serum B12, reticulocytes (because production is impaired)
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15
Q

Intrinsic causes of haemolytic anaemias?

A

RBC membrane - hereditary spherocytosis/elliptocytosis

Hb synthesis - sickle cell disease, thalassaemia

RBC enzymes - G6PD deficiency, pyruvate kinase deficiency

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16
Q

Extrinsic causes of haemolytic anaemia?

A

Immune - incompatibility (newborn, transfusion), AI haemolytic anaemia

Non-immune - infections (malaria, black water fever, Clostridium welchii), chemicals (lead, drugs, toxins)

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17
Q

Investigations in haemolytic anaemia?

A

High = reticulocytes, bilirubin, LDH

Low = Hb, haptoglobin (what Hb binds to)

Others = Coomb’s test (AI causes)

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18
Q

Management of haemolytic anaemia

A

HAEMATOLOGY

Folic acid, steroids, rituximab, IVIG (IV immunoglobulins)
Transfusion therapy
EPO

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19
Q

Pathophysiology of sickle cell disease?

A

Normal Hb = 2 alpha 2 beta –> 1 deficient beta chain

Autosomal recessive - heterozygotes = sickle cell trait
homozygotes = SC disease

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20
Q

Investigations in sickle cell?

A

Hb = 60-90
MCV normal
RBC breakdown –> high reticulocytes and bilirubin

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21
Q

Presentation of SC disease?

A

Anaemia + vaso-occlusive crisis (precipitated by hypoxia, infection, dehydration, cold)

Pain crisis, splenic infarct, stroke, priapism

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22
Q

Management of sickle cell crisis?

A

O2, morphine, treat cause (fluid/abx)

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23
Q

Pathophysiology of thalassaemia?

A

Normal globin chains, but not enough - autosomal recessive
Alpha/Beta, Trait/Major

Homozygous = major (disorder) - 2 chains deleted
Heterozygous = trait (healthy carrier) - 1 chain deleted

Alpha major = death in utero (b/c only have fHb)
Beta major = severe anaemia

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24
Q

Presentation of thalassaemia?

A

Trait = often asymptomatic

B major = severe anaemia at 4-6 months (babies have HbF)
Characteristic facial features, splenomegaly, pallor, failure to thrive, stunted growth, HF

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25
Presentation and treatment of haemochromatosis?
Iron overload (symptoms develop in middle age, later in females because of periods) Bronze diabetes --> bronze deposits in skin, hepatic dysfunction, diabetes, gonadal dysfunction, cardiac problems Treatment = venesection (once a week --> every few months)
26
Too little and too many white cells?
Too little = leucopenia (99% neutropenia) | Too many = leucocytosis
27
Definitions of neutropenia?
``` <1.5 = neutropenia <1 = infection <0.5 = immediate review ```
28
Causes of neutropenia?
REDUCED PRODUCTION Marrow aplasia/infiltration, viral infections, TB, drugs (antimetabolites, sulphonamides, carbimazole, sulfasalazine) INCREASED CONSUMPTION Septicaemia (neutrophils used up), hypersplenism (neutrophils destroyed), autoimmune destruction of neutrophils (SLE, Felty's syndrome)
29
Presentation of neutropenic sepsis?
7-10 days post-chemo | Fevers, rigors, malaise, hypothermia, hypotension, tachycardia, dizziness, reduced urine output
30
What is the MASCC risk score?
Assesses risk of complications during febrile neutropenic episode
31
What is involved in a neutropenic sepsis screen?
``` Bloods - FBC, LFT, U+E, CRP, lactate Cultures - line and peripheral cultures Swabs, viral swabs Sputum culture Urine analysis and culture Stool analysis and culture CXR ```
32
Management of neutropenic sepsis?
Empirical antibiotic therapy - TAZOCIN or VANC/AZTREONAM ?G-CSF
33
Differentials for leucocytosis?
Primary haem problem (cancer) or a secondary response (infection) NEUTROPHILIA Infection (rarely >30), CML (>200, really high), others (steroid use, post-op, MI, DKA) LYMPHOCYTOSIS Viral (infectious mono), CLL/ALL/NHL LEUCOSTASIS Emergency --> ischaemia
34
Too little and too many platelets?
Too little = thrombocytopenia | Too many = thrombocytosis
35
Definition of thrombocytopenia?
<100 in reality... For surgery - should be over 100 >30 asymptomatic <10 worrying
36
Causes of thrombocytopenia?
IMMUNE - ITP, drug induced (HEPARIN - 5-10 days after), SLE, post-transfusion ``` Dilutional Haemolytic uraemic syndrome Cancer DIC Decreased production (low numbers megakaryocytes - radiation) ```
37
Presentation of thrombocytopenia?
Bleeding tendency - spontaneous purpura/ecchymoses, mucous membrane bleeding, nose bleeds, menorrhagia, PPH Rare (< 30) - retinal/subconjunctival haemorrhage, GI bleeding, intracranial bleeding
38
Thrombocytosis?
Differentiate between primary cause or secondary reactive cause ``` Primary = myeloproliferative neoplasm Secondary = acute phase reactant (rarely >1000) ```
39
Rough definition of leukaemias, lymphomas, myeloma?
Leukaemia = malignant cells in marrow Lymphoma = malignant cells in LNs Myeloma = plasma cell malignancy Myelodysplasias = not enough cells, Myeloproliferative = too many cells
40
Acute myeloid leukaemia?
Older adults (65-70) - 80% under 50 get complete remission, 30% cure with chemo post-remission Symptoms of anaemia, thrombocytopenia, neutropenia Infections (bacterial/fungal) Fever DIC Infiltration of extramedullary sites (lymphadenopathy, hepatosplenomegaly, CNS involvement, gingival infiltration)
41
Acute lymphoblastic leukaemia?
Kids (most commonly) - Philadelphia chromosome (Ph1) --> poor outcome. Good remission/cure rates. Acute illness over several days, tiredness or non-specific aches over several weeks/months. BONE MARROW FAILURE --> anaemia, thrombocytopenia (bleeding), bacterial infection ACCUMULATION OF LEUKAEMIC CELLS --> bone/joint pain, hyperleukocytosis --> CNS involvement; tissue deposits of leukaemic cells --> gum hypertrophy, stomatitis; hepatosplenomegaly, lymphadenopathy, bone tenderness
42
Chronic myeloid leukaemia?
Median age 65 yrs. 95% have philadelphia chromosome. Usually remains stable for years then transforms to more malignant fatal disease. Only bone marrow transplantation is curative. REALLLY high WCC; splenomegaly, weight loss, sweats, anaemia, bleeding.
43
Chronic lymphocytic leukaemia?
Median age 69 years Insidious onset - when symptoms present disease is advanced 'B' symptoms - lethargy, weight loss, fever, night sweats Infections, anaemia, thrombocytopenia Symmetrical, non-tender lymphadenopathy Hepatosplenomegaly Skin lesions (HZV, pruritis)
44
Histology and spread of Hodgkin's lymphoma?
Histology = polymorphic - Reed-Steenberg cells diagnostic Spread = predictable - step by step to contiguous LNs, starting in neck usually.
45
Histology and spread of Non-Hodgkin's lymphoma?
Histology = monomorphic - malignant cells most numerous. Spread = random
46
Aetiology and epidemiology of Hodgkin's/Non-Hodgkins?
Hodgkins = unknown aetiology; bimodal distribution (many are young) Non-Hodgkins = unknown aetiology (EBV, h.pylori, HIV, hep C); median age = 50, increasing with age.
47
What are B symptoms?
Indicate poor prognosis in lymphoma Fever, night sweats, weight loss
48
Lymphadenopathy in Hodgkin's?
Painless - single group of nodes (cervical/supraclavicular)
49
Lymphadenopathy in non-Hodgkin's?
Painless (generalised; visceral) - typically disseminated at presentation
50
Symptoms in Hodgkin's
``` B symptoms (25%) Pruritis Chest discomfort/cough/dyspnoea Anaemia Immune dysfunction ``` ETOH-induced LN pain
51
Symptoms in non-Hodgkin's
B symptoms Anaemia Infections Purpura
52
Staging system in Lymphoma?
Ann Arbor System
53
Investigations in lymphoma?
LN biospsy Blood - film, FBC/ESR, U+E, LFT, bone profile, LDH (worse prog in non-hodgkin's), HIV serology Chest radiography Staging with contrast (CT neck to pelvis or PET/CT) Bone marrow biopsy
54
Management of Hodgkin's?
Localised = RTx Disseminated = high-dose chemotherapy (+/- stem cell transplantation)
55
Management of Non-Hodgkin's?
INDOLENT Local RTx = first line; watchful waiting if asymptomatic, rituximab, chemo AGGRESSIVE Usually HIV +ve; R-CHOP regimen; chemo/radioT; bone marrow/stem cell transplantation
56
What is myeloma?
Malignant proliferation of plasma cells Presence of paraproteins in blood or urine Associated organ dysfunction
57
What are paraproteins?
Abnormal immunoglobulin light chains --> damage kidneys by forming protein casts in renal tubules
58
How does myeloma cause bone pain/hypercalcaemia?
Abnormal plasma cells screte factors which activate osteoclasts Lytic lesions, bone pain, hypercalcaemia
59
Risk factors for myeloma?
Age, male, afro-caribbean, +ve FH, obesity, diet
60
Mneominc for myeloma?
CRAB HyperCalcaemia Renal failure Anaemia Bone lesions
61
Presentation of myeloma?
Bone pain (spine, ribs, pepper pot skull) Anaemia/thrombocytopenia (normocytic normochromic) Renal failure (uraemic symptoms, itching/muscle cramps, SoB/oedema) Infection Neurological (hypercalcaemia, hyperviscosity, peripheral neuropathy)
62
Bloods in myeloma?
FBC - anaemia, neutropenia, thrombocytopenia U+E - creatinine, hypercalcaemia ESR - persistently raised Blood film - Rouleaux formation Protein electrophoresis --> bence jones protein (blood and urine)
63
Imaging in myeloma?
Skeletal survey --> x-rays of skull, axial skeleton and proximal long bones (lytic lesions)
64
What is the intrinsic pathway and what measures its time?
XII, XI, IX, VIII aPTT
65
What is the extrinsic pathway and what measures its time?
TF + VII PT
66
What is haemophilia A/B deficiency of?
``` A = FVIII B = FIX ```
67
What is prolonged in haemophilia?
aPTT
68
How is haemophilia inherited?
X-linked recessive (only affects males - can have female carriers)
69
How does haemophilia present?
Haemarthroses and soft tissue bleeds after trauma or spontaneously
70
What is vWD? How is it inherited?
Congenital deficiency of vWF Autosomal dominant
71
What does vWF do? How does vWD present?
Is a cofactor essential for platelet adhesion and transport of factor VIII Prolonged APTT, low levels of factor VIII and IX Asymptomatic usually, and diagnosed following perioperative bleeding. Haemarthroses, soft tissue haematomas, epistaxis and menorrhagia.
72
What can liver disease do to bleeding?
Increase INR, low platelets
73
What can renal disease do with bleeding?
Uraemic bleeding --> affects platelet function
74
Causes of DIC?
Malignancy, infection, obstetric complications
75
How does DIC happen?
Trigger --> release of THROMBIN --> activation of platelets and clotting factors --> these are used up and form microthrombi Fibrinolytic system activates in response to thrombi --> unregulated fibrinolysis THROMBOTIC AND HAEMORRHAGIC FEATURES
76
What is antithrombin III deficiency?
AT III inhibits thrombin, fXa, fXIIa, fXIIIa and fIXa Autosomal dominant deficiency of this --> recurrent thrombosis and thromboembolism
77
What is protein C deficnecy?
Protein C = vit K dependent protease which inactivates fVIII and fV and stimulates fibrinolysis deficiency ---> THROMBOPHILIA
78
What is protein S deficiency?
Protein S = regulates protein C on surface of endothelial cells (needs Ca2+ as cofactor) deficiency --> THROMBOPHILIA
79
Packed red cells - how much do they increase Hb and how long over?
1 unit lasts 4 hours 1 unit --> Hb increased by 10-15, given over 3 hours
80
Platelets - how much do they increase by and how long over?
1 unit --> plts increase by 20, given over 30 minutes. lasts 24-48 hours in body
81
What are the special requirements for blood?
Hep E negative - CMV negative - transplant patients Irradiated blood - chemo/prego/immunosuppressed ALWAYS ASK WHETHER PATIENT HAS ANY SPECIAL REQUIREMENTS
82
Additional treatments in transfusion?
Furosemide (if overloaded) | K+ treament --> can increase K+ because is intracellular and can damage cells
83
Name some acute transfusion reactions?
Febrile non-hemolytic transfusion reaction (FNHTRs) Bacterial contamination Transfusion related acute lung injury (TRALI) Transfusion-related circulatory overload (TACO) Allergic/anaphylactic reaction
84
Management of FNHTR?
Slow or temporarily stop transfusion PCM Monitor closely Can occur up to 2 hours after. Less common now due to leucodepleted blood.
85
Management of bacterial contamination?
Stop transfusion Urgent supportive care - IV abx Call haem - send unit back to lab
86
Presentation of TRALI?
Antibodies in donor blood react with patients neutrophils, monocytes or pulmonary endothelium Within 2 hours of transfusion Severe breathlessness, cough + frothy sputum Hypotension, fever, rigors
87
Management of TRALI?
Stop transfusion Supportive managment - O2, ICU if required Remove donor from panel
88
Presentation of TACO?
Acute pulmonary oedema Acute resp distress, tachycardia, hypertensive, positive fluid balance
89
Managment of TACO?
Stop/slow transfusion Oxygen/diuretic therapy Careful monitoring and critical care if required
90
Management of allergic reaction?
Slow transfusion Antihistamine (oral/IV) - chlorphenamine Monitor closely
91
Management of anaphylaxis transfusion reaction?
STOP TRANSFUSION | Anaphylaxis algorithm

- FINALS (24 decks)

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