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Haematology Flashcards

1
Q

Define ANAEMIA.

A

Anaemia is defined as haemoglobin less than what is considered “normal” for age and gender.

In males, normal Hb is between 135 to 180
In females, normal Hb is between 115 to 160

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2
Q

Describe CLINICAL SYMPTOMS of anaemia.

A 
✔️ fatigue
✔️ breathlessness (particularly on exertion)
✔️ palpitations
✔️ chest pain (particularly on exertion)
✔️ dizziness and lightheadedness
✔️ syncope
✔️ picca

Symptoms of underlying pathology
✔️ peripheral neuropathy –> B12 and / or folate deficiency
✔️ jaundice –> haemolytic anaemia
✔️ easy bruising –> aplastic anaemia
✔️ recurrent infections –> aplastic anaemia

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3
Q

Describe CLINICAL SIGNS of anaemia.

A 
CARDIOVASCULAR 
o tachycardia
o orthostatic hypotension
o systolic flow murmur
o wide pulse pressure
o signs of CHF

HEENT (head, ear, eyes, nose and throat)
o pallor of mucus membranes and conjunctiva
o ocular bruits
o spooning of the nails (onycholysis)
o angular stomatitis
o jaundice
o generalised pallor

DERMATOLOGY
o ecchymosis 
o petechiae 
o pallor of the creases 
o jaundice (if due to haemolysis) 
o nail changes
o glossitis

OTHER
o splenomegaly, hepatomegaly

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4
Q

Outline appropriate investigations for ANAEMIA.

A

Bedside Ix
✔️ ECG

Laboratory Ix
✔️ FBC + WCC
✔️ Inflammatory markers
✔️ Iron studies
✔️ B12 + folate levels
✔️ UECs
✔️ eLFTs (particularly unconjungated bilirubin)
✔️ coags
✔️ peripheral blood smear
✔️ haemolytic screen (LDH, haptoglobin, reticulocyte count)
✔️ Coombes Test (IgG and C3/C4)
✔️ electrophoresis (in the case of suspected thalassemia)

Imaging Ix
✔️ CXR (to look for CHF in severe anaemia)

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5
Q

What are the types of MICROCYTIC ANEAMIA?

A

✔️ iron deficiency anaemia
✔️ thalassemia
✔️ sideroblastic / lead poisoning
✔️ anaemia of chronic disease (~25% of cases)

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6
Q

Identify risk factors for IRON DEFICIENCY ANAEMIA.

A

REDUCED INTAKE / IMPAIRED ABSORPTION
✔️ dietary (i.e. vegan, vegetarian)
✔️ coeliac disease
✔️ gastric bypass surgery

INCREASED LOSS
✔️ acute haemorrhage
✔️ heavy periods (females)
✔️ malignancy

INCREASED USAGE
✔️ pregnancy
✔️ infancy
✔️ adolescents

NB. Any patient > 50 years of age with IDA and an unknown cause is presumed to have GI malignancy until proven otherwise; IDA in this age group ALWAYS warrants a gastrointestinal referral / follow up.

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7
Q

Outline the appropriate MANAGEMENT of IDA.

A
  1. identify and treat underlying cause
  2. iron replacement / supplementation
  3. prevention of recurrence
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8
Q

Explain ORAL IRON SUPPLEMENTATION to a patient.

A

The most common and practical way to supplement iron is via the oral route.

Iron tablets can be take once daily. Absorption is increased with Vitamin C and impaired with caffeine (e.g. coffee, tea). It is best to take oral supplements ~60 mins prior to eating.

It can take up to 3 months to replenish iron stores.

Gastrointestinal side effects are common in this medication, and include: 
✔️ constipation
✔️ black, tar-like stools
✔️ diarrhea
✔️ bloating
✔️ nausea and vomiting
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9
Q

Explain PARENTERAL IRON SUPPLEMENTATION to a patient.

A

Parental iron supplementation is appropriate for:
✔️ patients with symptomatic anaemia
✔️ patients with resistance to oral therapy
✔️ patients with malabsorption issues (e.g. Coeliac Disease)

There are two ways to delivery this medication:

  1. IM –> now rarely used
  2. IV –> well tolerated; requires supplementation every 3 to 6 months

All parental delivery options have a small risk of anaphylaxis and staining of the skin.

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10
Q

Explain BLOOD TRANSFUSION to a patient with IDA.

A

Blood transfusion is indicated in the following patient groups:
✔️ acute blood loss due to haemorrhage
✔️ haemodynamically unstable
✔️ Hb < 70

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11
Q

Define ANAEMIA OF CHRONIC DISEASE.

A

Anaemia of chronic disease is an anaemia that arises due to impaired uptake and utilisation of iron as a result of increased inflammatory markers.

ACD is a diagnosis of exclusion, and should only be made when all other causes of anaemia have been appropriately investigated and ruled out.

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12
Q

Identify risk factors for ACD.

A

✔️ chronic kidney disease
✔️ chronic liver disease
✔️ malignancy
✔️ any inflammatory or rheumatological disease
✔️ endocrine disorders (e.g. T2DM, hypothyroidism, hypopituitarism, hypogonadism)

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13
Q

Briefly outline the pathophysiology of ACD.

A

Hepcidin is a key regulator of iron absorption. It is increased by:

  1. high levels of serum iron
  2. inflammatory cytokines (e.g. TNF-alpha, IL-1 and IL-6)

Chronic disease is associated with chronically elevated levels of inflammatory cytokines. These cytokines stimulate hepcidin production from the liver.

Hepcidin works to reduce iron absorption by inhibiting the transferrin iron transporter. Consequently, iron remains trapped as FERRITIN in the liver and macrophages. This means that whilst iron and ferritin levels in the body are HIGH, the iron cannot be utilised to synthesise haemoglobin.

ACD is characterised by: 
↑ ferritin
↑ serum iron
↓ TIBC 
↓ %age saturation

ACD is characterised as being a normocytic, normochromic anaemia.

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14
Q

Outline treatment options for ANAEMIA OF CHRONIC DISEASE.

A

Treatment of the underlying cause is paramount; inflammation is driving iron under-utilisation; must treat inflammatory component before any other treatment will be effective.

Treat anaemia in patients who would benefit from a higher haemoglobin –> oral iron supplementation first followed by parenteral iron.

EPO may be indicated in chronic renal failure.

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15
Q

Define MEGALOBLASTIC ANAEMIA.

A

Megaloblastic anaemia is a subset of macrocytic anaemia characterised by low circulating levels of B12 and folate. Both of these compounds MUST be obtained from the diet and are essential for both erythrocyte and neuronal cell production.

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16
Q

Describe some risk factors for B12 DEFICIENCY.

A

REDUCED INTAKE
✔️ dietary (e.g. vegan, vegetarian)
✔️ malnutrition

REDUCED GASTRIC ABSORPTION
✔️ pernicious anaemia
✔️ gastric by-pass surgery

REDUCED INTESTINAL ABSORPTION
✔️ Coeliac disease
✔️ Crohn’s disease
✔️ pancreatic insufficiency

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17
Q

Briefly describe the pathophysiology of PERNICIOUS ANAEMIA.

A

Pernicious anaemia is a sub-type of megaloblastic anaemia. This is an auto-immune condition in which auto-antibodies are produced against gastric parietal cells leading to lack of intrinsic factor secretion.

Intrinsic factor is required to stabilised Vitamin B12 as it passes through the bowel.

Reduced IF means that there is decreased ileal absorption of Vitamin B12. This condition may also be associated with other auto-immune pathologies.

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18
Q

Describe some risk factors for FOLATE DEFICIENCY.

A

REDUCED INTAKE
✔️ vegan diet
✔️ malnutrition
✔️ chronic / severe alcoholism

IMPAIRED ABSORPTION
✔️ IBD
✔️ Coeliac disease
✔️ short bowel syndrome

DRUGS
✔️ methotrexate
✔️ anti-convulsants (e.g. phenytoin)
✔️ oral contraceptive pill

INCREASED DEMAND
✔️ pregnancy
✔️ haemolysis
✔️ premature babies
✔️ haemodialysis
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19
Q

Outline the appropriate management of MEGALOBLASTIC ANAEMIA.

A

B12 SUPPLEMENTATION
✔️Vitamin B12 1,000 ug IM every two weeks for three courses and then every three months OR
✔️Vitamin B12 1,000 to 1,2000 ug PO –> watch for hypokalaemia and rebound thrombocytosis when treating severe megaloblastic anaemia

FOLATE SUPPLEMENTATION
✔️ folic acid 1 to 5 mg PO, once daily for 1 to 4 months (N.B. ALWAYS give Vitamin B12 supplementation FIRST)

20
Q

What is one complication of megaloblastic anaemia?

A

Subacute degeneration of the spinal cord (SDSC).

21
Q

Define APLASTIC ANAEMIA.

A

Aplastic anaemia is characterised by hypocellularity of bone marrow, resulting in pancytopenia (normocytic anaemia + thrombocytopenia + leukopenia).

Diagnosis is via BONE MARROW BIOPSY which confirms < 25% cellularity.

22
Q

Identify risk factors for APLASTIC ANAEMIA.

A

✔️ idiopathic
✔️ drug-induced
✔️ toxin-induced
✔️ ionising radiation
✔️ post-viral infection (e.g. CMV, EBV, HBV, HIV)
✔️ auto-immune (e.g. SLE, GVHD)
✔️ other (e.g. pregnancy, anorexia nervosa)

23
Q

Describe clinical features of APLASTIC ANAEMIA.

A 
ANAEMIA
✔️ fatigue, lethargy, malaise
✔️ dyspnoea on exertion
✔️ palpitations
✔️ angina

THROMBOCYTOPENIA
✔️ easy bruising
✔️ purpura or petechiae

LEUKOPENIA
✔️ opportunistic infections
✔️ recurrent infections

OTHER
✔️ hepatosplenomegaly

24
Q

Outline the management of APLASTIC ANAEMIA.

A
  1. Remove the offending agent
  2. Supportive care
    a. red blood cell transfusions, platelet transfusions, antibiotics
  3. Immunosuppression (for idiopathic aplastic anaemia)
    a. cyclosporine
  4. Allogenic bone marrow transplant
  5. Growth factors (e.g. TPO receptor agonist)
25
What are FOUR features that are universal to all types of haemolytic anaemia?
1. ↑ reticulocyte count 2. ↑ LDH 3. ↑ unconjugated bilirubin 4. ↓ haptoglobin
26
Identify key features of INTRAVASCULAR HAEMOLYISIS.
✔️ schistocytes on blood film ✔️ increased free serum haemoglobin ✔️ reduced haptoglobin ✔️ hemoglobinuria (Hb in urine) ✔️ hemosiderinuria (hemosiderin in urine) ✔️ methemalbuminemia (heme + albumin in serum)
27
Describe key features of WARM AUTOIMMUNE HAEMOLYTIC ANAEMIA.
``` Antibody: IgG Temperature: 37°C Causes: idiopathic DAT / Coombe's Test: positive for IgG Blood Film: spherocytes Management: corticosteroids, immunosuppression ```
28
Describe key features of COLD AUTOIMMUNE HAEMOLYIC ANAEMIA.
Antibody: IgM Temperature: 4°C Causes: post-viral infection DAT / Coombe's Test: negative for IgG; positive for complement Blood Film: agglutination Management: stay in warm climates; rituximab agents; plasma exchange
29
Describe clinical signs relevant to HAEMOLYTIC ANAEMIA.
✔️ jaundice ✔️ dark urine ✔️ cholelithiasis (pigmented stones) ✔️ iron overload in significant / extreme extravascular haemolyisis ✔️ iron deficiency in significant / extreme intravascular haemolysis
30
Describe key features of ACUTE LYMPHOCYTIC LEUKEMIA (ALL).
Age Group: children < 6 years of age; second peak ~40 years of age Cell Lineage: B cells and / or T cells Key Symptoms: anaemic (fatigue, weakness, lethargy, dyspnea, dizziness), leukopenia (opportunistic infections, recurrent infections), thrombocytopenia (easy bruising, easy bleeding), bone pain, splenomegaly Histology: large lymphocytes with oval nucleus, coarse and clumped chromatin, scanty cytoplasm, thrombocytopenia Management and Prognosis: management involves four stages of chemotherapy (1) . introduction phase (2) . eradication phase (3) . maintenance phase (4) . prophylaxis
31
Describe key features of ACUTE MYELOID LEUKAEMIA (AML).
Age Group: adults > 60 years of age Cell Lineage: myeloid cells Key Symptoms: anaemic (fatigue, weakness, lethargy, dyspnea, dizziness), leukopenia (opportunistic infections, recurrent infections), thrombocytopenia (easy bruising, easy bleeding), bone pain, splenomegaly, gum hypertrophy and bleeding Histology: Aur Rods; myeloblasts on blood film Management and Prognosis: average life expectancy following diagnosis is between 12 to 24 months
32
Describe key features of CHRONIC LYMPHOCYTIC ANAEMIA (CLL).
Age Group: adults > 70 years; males > females Cell Lineage: B cells Key Symptoms: asymptomatic (25% of patients), lymphadenopathy, splenomegaly, hepatomegaly, B symptoms, immune dysregulation, bone marrow failure Histology: Smudge Cells Management and Prognosis: median survival is > 9 years; 5% of CLL undergo malignant transformation into aggressive Large B Cell Lymphoma
33
Describe key features of HODGKIN'S LYMPHOMA.
Age Group: young adults (males ~ 35 years of age) Cell Lineage: B Cell Lymphocytes Classification: nodular lymphocytic predominant; classical (nodular sclerosing, mixed cellularity, lymphocyte predominant, lymphocyte deplete) Pathophysiology: EBV infection is associated with ~50% of cases --> causes a chromosomal translocation between Chromosome 8 and 14; MYC protein Histology: Reid Steinberg Cells (RS) cells Clinical Presentation: pruritis, alcohol induced pain, painless lymphadenopathy, splenomegaly (50%) +/- hepatomegaly, mediastinal mass, systemic B symptoms (e.g. fever, nightsweats, weight loss) ``` Management: ABVD chemotherapy regime ✔️A - adriamycin ✔️ B - bleomycin ✔️ V - vinblastine ✔️ D - decarbazine ``` ``` Complications: the complications of HL are mainly associated with chemotherapy side effects and include ✔️ infertility ✔️ cardiotoxicity ✔️ pulmonary toxicity ✔️ secondary malignancy ✔️ thyroid disorder ```
34
Define NON-HODGKIN'S LYMPHOMA and outline how it is classified.
Non-hodgkin's Lymphoa pertains to any lymphoma that does NOT show RS cells on histology. Classification: ✔️ indolent - follicular lymphoma, small cell lymphocytic lymphoma, mantle cell lymphoma ✔️ aggressive - diffuse large B cell lymphoma ✔️ highly aggressive - Burkitt's lymphoma
35
Outline the complications of treatment for NHL.
``` ✔️ neutropenia --> opportunistic infection ✔️ thrombocytopenia --> bleeding risk ✔️ nausea + vomiting ✔️ mouth ulcers ✔️ hair loss ✔️ fatigue ```
36
Define MYELOPROLIFERATIVE DISORDER.
Myeloproliferative disorders include four conditions characterised by excessive production / uncontrolled proliferation of various cells as a result of genetic mutations to selective genes. There are four conditions that fit into the MPD umbrella: 1. polycythemia rubra vera 2. essential thrombocytosis 3. chronic myeloid leukemia 4. idiopathic myelofibrosis All of these conditions have the potential to develop into ACUTE MYELOID LEUKAEMIA.
37
``` ESSENTIAL POLYCYTHEMIA RUBRA VERA ✔️ definition ✔️ mutation ✔️ clinical presentation ✔️ appropriate investigations and findings ✔️ management ```
DEFINITION: essential PRV is a condition characterised by excessive proliferation of erythrocytes, resulting in both elevated haemoglobin +/- thrombocytosis. MUTATION: JAK2 CLINICAL PRESENTATION: ✔️ facial plethora ✔️ erythema and oedema of the hands and feet ✔️ pruritis ✔️ hepatomegaly ✔️ splenomegaly ✔️ thrombotic complications (e.g. stroke, VTE, MI) INVESTIGATIONS: must exclude secondary causes of polycythemia (e.g. dehydration, renal failure, EPO use) MANAGEMENT: phlebotomy until Hct <45% ✔️ aspirin ✔️ allopurinol (as required, for gout) ✔️ anti-histamines (as required, for pruritis)
38
``` CHRONIC MYELOID LEUKEMIA ✔️ definition ✔️ mutation ✔️ clinical presentation ✔️ appropriate investigations and findings ✔️ management ```
DEFINITION: CML is a type of myeloproliferative condition characterised by uncontrolled proliferation of immature myeloid cells. This results in increased immature within the bone marrow and decreased capacity of the bone marrow for other cell lineages, resulting in anaemia, leukopenia and thrombocytopenia. MUTATION: Philadelphia Chromosome (translocation between Chromosome 9 and 12, resulting in the BCR-ABL gene) ``` CLINICAL PRESENTATION: ✔️ asymptomatic ✔️ fatigue, lethargy ✔️ lymphadenopathy ✔️ splenomegaly (LUQ pain) ✔️ B symptoms (fever, weight loss, night sweats) ``` APPROPRAITE INVESTIGATIONS: ✔️ peripheral blood smear ✔️ bone marrow biopsy ✔️ cytology
39
``` ESSENTIAL THROMBOCYTOSIS ✔️ definition ✔️ mutation ✔️ clinical presentation ✔️ appropriate investigations and findings ✔️ management ```
DEFINITION: essential thrombocytosis is a myeloproliferative disorder characterised by excessive production of platelets. MUTATION: JAK2 mutation ``` CLINICAL PRESENTATION: ✔️ asymptomatic ✔️ arterial and venous thrombus ✔️ pregnancy complications ✔️ vasomotor symptoms (e.g. headache, dizziness, syncope) ``` MANAGEMENT: low dose aspirin
40
``` IDIOPATHIC MYELOFIBROSIS ✔️ definition ✔️ mutation ✔️ clinical presentation ✔️ appropriate investigations and findings ✔️ management ```
DEFINITION: idiopathic myelofibrosis is a myelodysplastic condition characterised by proliferation of fibroblasts within the bone marrow. This leads to suppression of other cell line, giving rise to a pancytopenia and extra medullary haematopoiesis. MUTATION: JAK2 ``` CLINICAL PRESENTATION: ✔️ anaemia --> severe fatigue ✔️ splenomegaly ✔️ hepatomegaly ✔️ B symptoms (e.g. fever, night sweats, weight loss) ✔️ recurrent infection ✔️ opportunistic infection ✔️ bone and joint pain ``` MANAGEMENT: ✔️ JAK2 enzyme inhibitor ✔️ allogenic stem cell transplant (potentially curative)
41
Define MULTIPLE MYELOMA.
Multiple myeloma is a condition characterised by production of a monoclonal malignant immunoglobulin (usually M protein) from a malignant Plasma B Cell. Whilst monoclonal disease is the most common, biclonal disease can exist.
42
Describe the clinical presentation of MULTIPLE MYELOMA.
C = calcium (renal stones, abdominal pain and constipation, depression / mood changes, pathological fractures, increased urinary frequency) R = renal failure A = anaemia (fatigue, lethargy, pallor) B = bone pain (pathological fractures, bony tenderness over the spine)
43
Identify causes for THROMBOCYTOPENIA.
Thrombocytopenia is defined as platelet count < 150 x 10^9 / L. Thrombocytopenia can be thought of in terms of: 1. reduced platelet production 2. increased platelet consumption REDUCED PLATELET PRODUCTION: ✔️ aplastic anaemia ✔️ bone marrow failure (e.g. idiopathic myelofibrosis, radiation induced) ✔️ liver failure (due to reduced TPO) ✔️ chronic alcoholism (combination of impaired liver function and bone marrow suppression) ``` INCREASED PLATELET CONSUMPTION: ✔️ DIC ✔️ splenomegaly ✔️ idiopathic thrombocytopenia ✔️ autoimmune destruction ```
44
Identify causes for THROMBOCYTOSIS.
Thrombocytosis is defined as platelet count > 400 x 10^9 / L. ``` Thrombocytosis may be due to: ✔️ essential thrombocytosis ✔️ significant bleeding / haemorrhage ✔️ malignancy ✔️ acute sepsis / severe infection ```
45
Define VON WLLEBRAND DISEASE.
VWD is an autosomal recessive condition characterised by quantitative or qualitative deficiency of von Willebrand Factor (vWF). There are two functions of vWF in haemostasis: ✔️ facilitates platelet binding to sub endothelial collagen ✔️ stabilises Factor VIII in circulation Because vWF has roles in both primary and secondary haemostasis, a deficiency can manifest with symptoms of either. There are three types of VWD: 1. mild quantitative issue 2. mild qualitative issue 3. severe quantitative issue
46
Outline clinical features of VON WILLEBRAND DISEASE (VWD).
``` ✔️ menorrhagia (females) ✔️ epistaxis ✔️ genitourinary bleeding ✔️ easy bruising ✔️ post operative bleeding ✔️ post dental surgery bleeding ```
47
Describe appropriate management of VWD.
1. desmopressin --> stimulates production of vWF and Factor VIII from endothelial cells 2. TXA --> helps stop bleeding

Medicine (AH1) (7 decks)

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