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Medicine > Haematology > Flashcards

Haematology Flashcards

1
Q

Describe Amyloidosis

A

A group of disorders characterised by extracellular deposition of a protein in abnormal fibrillar form, which is resistant to degeneration.

Can be primary (AL amyloid) or Secondary (AA amyloid) or familial.

Diagnosis is made with biopsy and postive Congo Red staining with red-green birefringence under polarised light microscopy.

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2
Q

What are Bence Jones proteins

A

Ig light chains excreted by kidney in excess in some patients with myeloma.

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3
Q

What are the causes of macrocytic anaemias?

A

Megaloblastic causes: Folate deficiency, B12 deficiency, anti-folate drugs e.g (phenytoin)

Normoblastic causes: alcohol, liver disease, hypothyroidism, pregnancy, reticulocytosis, myelodysplasia, cytotoxic drugs,

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4
Q

What are the causes of microcytic anaemias?

A
  • iron deficiency anaemia (most common)
  • thalassaemia
  • sideroblastic anaemia (very rare)
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5
Q

What are some causes of a normocytic anaemia?

A
  • acute blood loss
  • anaemia of chronic disease
  • renal failure
  • bone marrow failure
  • hypothyroidism (may be macrocytic)
  • Haemolysis ( may be macrocytic)
  • pregnancy
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6
Q

Describe iron-deficiency anaemia, it’s causes, diagnostic tests and treatment

A

Commonest cause of anaemia with microcytic hypochromic RBC’s

Causes:
•blood loss e.g menorrhagia or GI bleeding
•poor diet
•malabsorption
• hookworm in tropics

Signs: conjunctival pallor, lethargy, koilonychia, atrophic glossitis, angular cheilosis

Tests: FBC shows decreased MCV, MCH and ferritin (confirms diagnosis)

Treatment: ferrous sulphate 200mg BD PO follow up FBC if no response consider sideroblastic anaemia if Hb improves but MCV still low consider thalassaemia

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7
Q

What are the Side effects of oral ferrous sulphate?

A
  • nausea
  • abdominal discomfort
  • diarrhoea or constipation
  • black stools
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8
Q

Describe anaemia of chronic disease (secondary anaemia)

A

2nd most common anaemia after IDA most common anaemia in inpatients Due to 3 problems:
•poor use of iron in erythropoiesis
•cytokine-induced shortening of RBC survival
•decreased production of and response to erythropoietin

tests: FBC shows normocytic anaemia with normal or raises ferritin.

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9
Q

Describe myeloproliferative disorders

A

Causes by proliferation of a clone of haemopoetic myeloid stem cells in the marrow.

Classified depending on the cell type which is proliferating:

RBC - polycythaemia rubra Vera
WBC - chronic myeloid leukaemia
PLT - essential thrombocythaemia
Fibroblasts - myelofibrosis

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10
Q

What are some causes of thrombocytopenia?

A

May be due to decreased marrow production:
•aplastic anaemia
•megaloblastic anaemia
•marrow infiltration (e.g. Myeloma, leukaemia)
•marrow suppression (cytotoxics, radiotherapy)

Or may be due to excess destruction of platelets:
-immune causes:
•ITP
•SLE
•CLL
-Non-immune causes:
•TTP or HUS
•DIC
•hypersplenism
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11
Q

Describe Immune/Idiopathic Thrombocytopenic Purpura (ITP), its symptoms, tests, and management.

A

Caused by anti-platelet antibodies, may be acute (commonly self-limiting disease in children ~2 weeks post infection) or chronic (seen mainly in young/middle-aged women).

Symptoms:

  • Acute ITP presents wth bruising, purpura, petechiae. Usually history of recent gastroenteritis or URTI.
  • Chronic ITP presents with varying history of bleeding, purpura, epistaxis, menhorragia.

Tests: bone marrow biopsy shows increased megakaryocytes and anti platelet antibodies

Treatment:

  • none if mild, gradual resolution over 3 months.
  • if symptomatic or platelets less than 20, immunosuppression to keep platelets above 30 e.g Prednisolone 1mg/kg/d
  • if no response or relapse splenectomy cures
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12
Q

Describe disseminated intravascular coagulation, it’s causes, and treatment

A

Widespread activation of coagulation leading to consumption of clotting factors and platelets with increased risk of bleeding. Fibrin strands fill small vessels Haemolysing RBCs.

Causes: malignancy, sepsis, trauma, obstetric events

Treatment:

  • replace platelets if less than 50, cryoprecipitate to replace fibrinogen, FFP to replace coagulation factors.
  • Activated protein C reduces mortality in DIC with severe sepsis or multi-organ failure.
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13
Q

Describe MyeloDysplastic Syndrome (MDS)

A

A heterogenous group of disorders that manifest as marrow failure with risk of life-threatening infection and bleeding.

May be primary or secondary due to chemotherapy or radiotherapy. 30% transform to acute leukaemia.

Ix: pancytopenia, increased marrow cellularity, ringed sideroblasts

Rx: multiple transfusions
Erythropoietin +/- G-CSF
Immunosuppressives (ciclosporin or antithymocyte globulins)
Allogenic SCT
Thalidomide analogues eg lenalidomide
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14
Q

What are the main types of Leukaemia?

A

Leukaemia divides into 4 main types depending on the cell line involved.

Lymphoid:

  • Acute Lymphoblastic Leukaemia (ALL)
  • Chronic Lymphocytic Leukaemia (CLL)

Myeloid:

  • Acute Myeloid Leukaemia (AML)
  • Chronic Myeloid Leukaemia (CML)
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15
Q

Describe tumour lysis syndrome, its risk factors and preventative measures.

A

Caused by a massive destruction of cells leading to release of K+, Urate, and then kidney injury.

Increased risk if levels of LDH are increased, Creatinine increased, urate increased or WCC >25

Prevention with high fluid intake and allopurinol pre-cytotoxics
Rasburicase - in high risk

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16
Q

Describe Acute Lymphoblastic Leukaemia and its tests

A

A malignancy of lymphoid cells, affecting B or T lymphocyte cell lines.
Uncontrolled proliferation of immature blast cells with BM failure and tissue infiltration

Commonest cancer of childhood.

Tests: Blasts cells

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17
Q

Describe Acute Myeloid Leukeamia and its tests

A

Neoplastic proliferation of blast cells derived from marrow myeloid elements. Associated with MDS. Symptoms are of Marrow failure and infiltration
DIC in APML t(15:17)

Tests: Auer rods, cytogenetic analysis

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18
Q

Describe Chronic Myeloid Leukaemia and its tests.

A

uncontrolled clonal proliferation of myeloid cells. It accounts for 15% of leukaemias. Occurs most often between 40-60yrs.

Philadelphia chromosome t(9:22) BCR/abl

Features: flaws, gout, bleeding, abdo discomfort

Tests: Increase WCC, low Hb
Increase urate, b12
BM hypercellular

Rx:imatinib/dasatanib/nilotinib. Hydroxycarbamide

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19
Q

Describe Chronic Lymphocytic Leukaemia and its tests.

A

Accumulation of mature B cells that have escaped programmed cell death
Rai staging
Can transform to Richter’s transformation

Tests: marked increased in lymphocytes, later autoimmune haemolysis, marrow infiltration
decreased Hb, Neutrophils and platelets.

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20
Q

Describe Sepsis (+/-Neutropenia), the sepsis six, and severe sepsis signs.

A

is a potentially fatal complication of anti-cancer treatment (particularly chemotherapy). Identify with Quick Sepsis Related Organ Failure Assessment (qSOFA) with 2 or more of the following.

  • SBP less than 100mmHg
  • RR >22
  • new altered mental state.

Do the sepsis six:

  • high-flow oxygen
  • IV antibiotics
  • IV Fluid challange (hartmann’s)
  • Catheter and UO monitoring
  • Serum lactate
  • Blood cultures

Regularly screen for signs of severe sepsis:

  • SBP less than 90mmHg
  • SpO2 less than 90% despite high flow oxygen
  • INR >1.5 or APTT >60s
  • Plt less than 100
  • UO less than 0.5ml/kg/hr
  • lactate >2.0mmol/L
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21
Q

What is GCSF?

A

Granulocyte-colony stimulating factor is a protein that stimulats the bone marrow to make WBCs

22
Q

Describe lymphoma

A

Disorders caused by malignant proliferation of lymphocytes , which accumulate in the lymph nodes causing lymphadenopathy, but may also be found in peripheral blood or infiltrate organs. They are histologically classified into Hodgkins and Non-hodgkins depending on the presence of characteristic cells with mirror-image nuclei called Reed-Sternberg cells.

23
Q

What is the management of a high INR, in the context of a patient on warfarin with major bleeding?

A
  • Stop Warfarin
  • IV Vitamin K 5mg
  • Prothrombin complex concentrate (FFP if unavailable)
24
Q

What is the management of a high INR, in the context of a patient on warfarin with minor bleeding and INR > 8.0?

A
  • Stop warfarin
  • Give intravenous vitamin K 1-3mg
  • Repeat dose of vitamin K if INR still too high after 24 hours
  • Restart warfarin when INR less than 5
25
Q

What is the management of a high INR, in the context of a patient on warfarin with no bleeding and INR > 8.0?

A
  • Stop warfarin
  • Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
  • Repeat dose of vitamin K if INR still too high after 24 hours
  • Restart when INR less than 5
26
Q

What is the management of a high INR, in the context of a patient on warfarin with minor bleeding and INR 5.0-8.0?

A
  • Stop warfarin
  • Give intravenous vitamin K 1-3mg
  • Restart when INR less than 5
27
Q

What is the management of a high INR, in the context of a patient on warfarin with no bleeding and INR 5.0-8.0?

A
  • Withhold 1 or 2 doses of warfarin

- Reduce subsequent maintenance dose

28
Q

Describe Haemophilia A its presentation and tests

A

Factor VIII defiency (x linked recessive) though high rate of new mutations so may be no family history.

Presentation depends on severity but is often early in life or after surgery/trauma with bleeds into joints leading arthropathy and bleeding into muscles causing haematomas (increased pressure can lead to nerve palsies and compartment syndrome)

Tests: increased APTT, decreased factor VII

29
Q

Describe Haemophilia B

A

Factor IX deficiency also know as Christmas disease, inherited x-linked recessive behaves clinically like haemophilia A

30
Q

Describe Von Willebrand disease and the role of Von Willebrand factor

A

It is a bleeding disorder There are over 20 types of disease the most common is type I which is an autosomal dominant deficiency of vWF.

Von Willebrand factor (vWF) has 3 roles in clotting:

  • To bring platelets into contact with exposed subendothelium
  • to make platelets bind to each other
  • to bind to factor VII, protecting it from destruction in the circulation
31
Q

What are the causes of thrombophilia?

A

Thrombophilia is an inherited or acquired coagulopathy predisposing to thrombosis usually venous: DVT, PE

Inherited causes:
•factor V Leiden increase 
•prothrombin increase
•protein C and S deficiency
•anti-thrombin deficiency

Acquired causes:
•Pill/HRT
•antiphospholipid syndrome

32
Q

What are the causes of haemolytic anaemia?

A

Acquired:
•immune - drug induced (penicillin, quinine), autoimmune haemolytic anaemia, paroxysmal cold haemoglobinuria
•microangiopathic haemolytic anaemia - HUS, TTP, DIC, pre-eclampsia
•infection - malaria
•paroxysmal nocturnal haemoglobinuria

Hereditary:
•enzyme defects- G6PD deficiency, pyruvate deficiency
•membrane defects - Hereditary spherocytosis
•haemoglobinopathy - sickle cell disease, thalassaemia

33
Q

Describe Glucose-6-phosphate dehydrogenase (G6PD) deficiency and it’s presentation.

A

X-linked RBC enzyme defect. Mostly affecting males in the Mediterranean, Africa and Middle/Far East. Mostly asymptomatic, but may get oxidative crises due to decreased glutathione production.

Presentation: Rapid anaemia and jaundice, precipitated by drugs (primaquine, aspirin, sulphonamides), broad beans, or illness.

34
Q

Describe B-Thalassemia and its treatment.

A

Usually caused by point mutations in the B-globin genes on chromosome 11 leading to decreased production or its absence. Can be split into Thalassemia minor/trait, intermedia and major.

Minor and intermedia do not require transfusions but may be anaemic. healthy diet fitness and folate supplements help.

Thalassemia Major require regular blood transfusions and usually presents in 1st year of life. with extramedullary haemopoiesis causing characteristic skull bossing. Also require iron-chelators to prevent iron overload.

35
Q

What are the available anti-coagulants and which are used therapeutically and prophylactically

A

Prophylactic: Most commonly used is LMWH e.g. dalteparin, enoxaparin, tinzaparin. It inactivates Factor Xa It has longer half-life than heparin and response is more predictable meaning it needs only be taken once or twice daily and no monitoring is usually required.

Therapeutic: First line is LMWH and depending on cause warfarin is given in combination. LMWH is continued until INR >2.2 and until day 5 as warfarin has an initial prothrombotic effect.

36
Q

Describe paraproteinaemia

A

Presence in the circulation of immunoglobulins produced by a single clone of plasma cells. There are six major categories:

  • Multiple myeloma
  • Waldenstroms macroglobulinaemia
  • Primary Amyloidosis
  • Monoclonal gammopathy of uncertain significance
  • paraproteinemia in lymphoma or leukaemia (seen in 5% CLL)
  • Heavy chain disease
37
Q

Describe Sickle-cell anaemia and its crises’

A

it is an autosomal recessive disorder causing production of abnormal beta-globin chains due to an amino acid substitution of glutamate to valine. Heterozygotes have sickle cell trait which is protective against malaria as cells sickle when deoxygenated.

signs and symptoms:

  • Haemolysis is usually well tolerated
  • Vaso-occluive ‘painful’ crises common due to microvascular occlusion. Often affects marrow causing sever pain but can happen in gut (mesenteric ischaemia) CNS (stroke, seizures) or limbs (ulcers, avascular necrosis, dactylitis)
  • aplastic crisis, this is due to parvovirus B19 with sudden reduction in marrow production, usually self-limiting.
  • sequestration crises, mainly affects chilren as the spleen has not yet undergone atrophy. There is pooling of blood in the spleen +/- liver with organomegaly severe anaemia and shock
38
Q

Describe myeloma, its symptoms, tests and diagnosis.

A

Myeloma is a type of plasma cell dyscrasia (PCD). Plasma cell dyscrasias are due to an abnormal proliferation foa signl clone of plasma or lymphoplasmacytic cells leading to secretion of immunglobulin ultimately leading to dysfunction of many organs. Bence-Jones proteins present in 2/3 of urine.

Symptoms + Signs:

  • Osteolytic bone lesions (backache)
  • Hypercalcaemia
  • Anaemia, Neutropenia or thrombocytopenia (marrow infiltration)
  • recurrent bacterial infections
  • renal impairment (due to light chain deposition)

Tests:
FBC, U+E, serum and urine electrophoresis. Xrays in case of bony pain shows punched out lesions, vertebral collapse. osteoporosis. Marrow biopsy.

Diagnosis depends on:

  • monoclononal protein band in serum or urine electrophoresis
  • increased plasma cells on marrow biopsy
  • evidence of end organ damage e.g. hypercalcaemia, renal insufficiency, anaemia.
  • bony lesions.
39
Q

What are the causes of pancytopenia?

A

Pancytopenia is a reduction in all the major cell lines: red cells, white cells and platelets. Causes are due to:

  • Decreased marrow production i.e aplastic anaemia, infiltration (e.g. acute leukaemia, myelodysplasia, myeloma, lymphoma, solid tumours, TB) megaloblastic anaemia, paroxysmal nocturnal haemoglobinuria, myelofibrosis, SLE
  • peripheral destruction: hypersplenisn.
40
Q

Describe Aplastic anaemia, its symptoms, causes and management.

A

it is a rare stem cell disorder leading to pancytopenia and hypoplastic marrow.

Symptoms:Presents with features of anaemia, infection or bleeding.

Causes:Most cases are due to autoimmune, triggered by drugs or radiotherapy.

Management:

  • Bone marrow biopsy needed for diagnosis,
  • treatment is supportive in milder cases otherwise bone marrow transplant may be needed.
41
Q

Describe heavy chain disease in the context of paraproteinaemia

A

This is where neoplastic cells produce free Ig heavy chains. alpha chain disease is the most important, causing malabsorption from infiltration of small bowel wall. It may progress to lymphoma.

42
Q

Describe Protein C+S deficiency

A

These vitamin K-dependent factors act together to cleave and so neutralise factors V & VIII. Heterozygotes deficient for either protein risk thrombosis. Skin necrosis also occurs. Homozygous deficiency for either protein causes neonatal purpura fulminans, fatal if untreated.

43
Q

Describe Antithrombin deficiency

A

Antithrombin is a co-factor of heparin, and inhibits thrombin. heterozygotes risk is greater than protein C or S deficiency by ~4-fold. Homozygosity is incompatible with life.

44
Q

What are some causes of polycythaemia

A

May be absolute (increased RBC mass) or Relative (Normal RBC mass and decreased plasma volume)

Relative may be acute and due to dehydation (e.g. alcohol or diuretics)

Absolute causes may be primary (polycythaemia Rubra vera) or secondary due to hypoxia (e.g. high altitudes, chronic lung disease, cyanotic congenital heart disease, heavy smoking) or inappropriate erythropoietin secretion (e.g. renal carcinoma, hepatocellular carcinoma. Testosterone replacement can cause polycythaemia

45
Q

Describe agranulocytosis and some common drug causes

A

Granulocytes (neutrophils, basophils, eosinophils) stop being made. It may present as a sore throat before a fatal infection so warn all patients to report any fever when starting a risk drug. If presents stop drug, and GCSF may have a role.

Important drugs to note are:

  • Clozapine
  • anti-thyroid e.g. Carbimazole
  • anti-epileptics
  • cytotoxics
46
Q

What are some causes of a lymphocytosis?

A
  • Acute viral infection
  • Chronic infection e.g. TB, Brucella, Hepatitis, Syphilis
  • Leukaemias and lymphomas, especially chronic lymphcytic leukaemia (often presents as incidental finding on FBC)
47
Q

Describe Hodgkin’s Lymphoma, its symptoms, tests, and management.

A

Malignant proliferation of lymphocyte with characteristic mirror-image nuclei called Reed-Sternberg Cells. Peak incidence in young adults and elderly. It is the leading cause of malignancy if aged 15-24yrs.

Symptoms: Often presents with enlarged, painless, non-tender, rubbery superficial lymph nodes, typically cervical (60-70%), also axillary or inguinal. Node size may increase and decrease spontaneously and nodes can become matted. 25% have constitutional upset e.g. Fever, weight loss, night sweats, pruritis, and lethargy. There may be alcohol induced lymph node pain.

Tests: Bloods, FBC (anaemia, lymphocytosis), film, ESR (raised), LFT, LDH (raised in increased cell turnover), Urate, Ca2+/Image guided needle biopsy + CT/MRI for staging

Treatment:
-Chemoradiotherapy, increases risk of secondary malignancy Common course is ABVD Adriamycin, Bleomycin, Vinblastine, Dacarbazine.

48
Q

What are some causes of neutropenia?

A
  • Viral infections
  • drugs (e.g. Post chemotherapy, cytotoxic agents, carbamazepine, Sulfonamides
  • Severe sepsis
  • neutrophil antibodies (SLE, Haemolytic anaemia)
  • hypersplenism e.g. Feltys
  • bone marrow failure
49
Q

Describe the basic interpretation of coagulation studies.

A

Two main coagulation pathways studied are the APPT and PT.

APPT = XII, XI, IX, VIII, X, V, II
PT = VII, X, V, II

Therefore if PT is increased and APPT is normal then the problem lies early in the cascade e.g. Factor VII, If APPT is raised and PT is normal then the factor lies early in the APPT cascade e.g. XII, XI, IX, VIII. If both are raised the problem lies with the late common part of the cascade e.g. X, V, II.

Mixing studies allows to further differentiation of the cause, normal plasma is added to the sample which should correct an abnormality if deficiency is an issue. If it does not correct the problem then an inhibitor is the cause of the prolonged bleeding time.

50
Q

Complications of blood transfusions

A

Immediate
- immune mediated: haemolytic (ABO mismatch), febrile reaction (HLA antibodies), Rhesus incompatibility
- non-immune mediated: Bacterial infections
Late
- Immune: Graft vs host disease, TRALI, TACO, thrombocytopaenia
- non-immune: Hypocalcaemia, hyperkalaemia, CCF, infections (Viral and prions)

Medicine (21 decks)

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