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AMC MCQ - You Can Do It!!!!!❤️❤️ > Haematology > Flashcards

Haematology Flashcards

1
Q

Normal Hb levels

A

Male: 130 - 180 g/L|13.8 to 17.2
Female: 115 - 165 g/L | 12.1 to 15.1

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2
Q

Normal serum ferritin level

A

men: 24 -336 mg/L
women: 1 - 307 mg/L

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3
Q

Mean corpuscular count

A

80 - 100 fL

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4
Q

Platelet count

A

150 - 400 x 10^9/L

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5
Q

Bleeding time

A

2 - 8.5 mins

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6
Q

Prothrombin time (pt)

A

10 - 13 secs

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7
Q

Partial thromboplastin time (aPTT)

A

25 - 35 secs

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8
Q

Autosomal dominant

A
  • spherocytosis
  • hemorrhagic telangiectasia
  • Von Willebrand disease
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9
Q

Autosomal recessive

A
  • Factor 5 diseases
  • Fanconi’s anaemia
  • haemochromatosis
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10
Q

X-linked recessive

A

Haemophilia A
Haemophilia B
- Glucose-6-phosphate dehydrogenase deficiency

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11
Q

rise in platelet count causes

A

– Polycythemia vera.
– Hyposplenism due to splenectomy.
– Iron deficiency anemia.
– Correction of vitamin B12 and folic acid deficiency

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12
Q

microcytic anemia + . Seizures
+ peripheral neuritis + dermatitis

A

Vitamin B6 (pyridoxine) deficiency

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13
Q

vegan vegetarian deficiency

A

B12 deficiency

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14
Q

Vitamin B12 bsorbed by binding to

A

intrinsic factor

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15
Q

B12 deficiency causes what type of anaemia

A

pernicious anaemia

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16
Q

B12 deficiency conditions

A
  • Autoimmune gastritis
  • Terminal ileum disease
  • Gastrectomy
  • Metformin therapy
  • Coeliac disease
  • H.pyelori infection
  • Crohn disease
  • Postgastrectomy
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17
Q

weakness + fatigue + dizziness + palpitations + exercise intolerance + craving of ice/clay

A

Iron deficiency

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18
Q

increased MCV + neutropenia + thrombocytopenia + history of alcohol abuse + hypersegmentation of
the neutrophils

A

Folate deficiency

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19
Q

cheilosis + glossitis+ a variety of ocular problems + hx of biliary atresia/hepatitis

A

Folate deficiency

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20
Q

px around 70 + fatigue + tiredness + macrocytic anaemia

A

myelodysplasia

Myelodysplasia (Myelodysplastic Syndromes - MDS)

Overview:
Myelodysplastic syndromes (MDS) are a group of disorders caused by poorly formed or dysfunctional blood cells. They occur when the blood-forming cells in the bone marrow are damaged. This leads to low levels of one or more types of blood cells.

Symptoms:
- Fatigue
- Shortness of breath
- Unusual paleness (pallor) due to anemia
- Easy or unusual bruising or bleeding
- Frequent infections

Causes:
The exact cause of MDS is often unknown, but it can be linked to:
- Exposure to certain chemicals (e.g., benzene)
- Radiation therapy or chemotherapy for cancer
- Genetic mutations

Diagnosis:
- Blood Tests: Show abnormalities in the number and appearance of blood cells.
- Bone Marrow Biopsy: Examines the bone marrow to identify abnormalities.

Types:
MDS is classified based on the type of blood cells affected and specific genetic abnormalities. Some of the classifications include:
- Refractory anemia
- Refractory cytopenia with multilineage dysplasia
- Refractory anemia with excess blasts

Treatment:
- Supportive Care: Includes blood transfusions, medications to boost blood cell production, and antibiotics for infections.
- Drug Therapy: Medications like azacitidine and decitabine can help control symptoms.
- Stem Cell Transplant: May offer a potential cure, especially for younger patients with severe MDS.
- Clinical Trials: Participation in clinical trials for new treatments.

Prognosis:
The prognosis for MDS varies widely depending on the specific type, patient age, overall health, and response to treatment. Some patients may live for many years with minimal symptoms, while others may progress to acute myeloid leukemia (AML).

Lifestyle and Home Remedies:
- Follow a balanced diet
- Regular moderate exercise
- Avoid exposure to infections

Regular Monitoring:
Patients with MDS need regular follow-up with their healthcare provider to monitor their blood counts and adjust treatments as necessary.

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21
Q

myelodysplasia investigation

A

Bone marrow biopsy

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22
Q

Causes of macrocytic anemia

A

High MCV

megaloblastic anemias
- Vitamin B12 (cobalamin )
- folate deficiency
- myelodysplasia
vigorous reticulocytosis,
hypothyroidism,
chronic liver disease,
myelodysplastic syndrome

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23
Q

Common causes of microcytic anemia

A

Low MCV

iron deficiency
thalassemia,
anemia of chronic disease
sideroblastic anemia

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24
Q

difference between hemolytic anemia vs anemia of chronic disease

A

Low hepatoglobin

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25
Q

congenital developmental anomalies + progressive pancytopenia

A

Fanconi’s anaemia

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26
Q

Fanconi anaemia investigation

A

Diagnostic: Chromosome fragility test

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27
Q

Fanconi anaemia congenital abnormalities

A
  1. Hand and arm anomalies (misshapen,missing or extra thumbs or abnormalities of
    the radius)
  2. Skeletal anomalies of the hips, spine or ribs
  3. Skin discolouration (café au lait spots, hyper-pigmentation,
  4. Small head or eyes
  5. Low birth weight and subsequent short stature
  6. Missing or horseshoe kidney
  7. Gastrointestinal abnormalities including abnormal development of the
    oesophagus
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28
Q

sudden onset of jaundice + pallor, +
dark urine + with or without abdominal and back pain + fall in the haemoglobin concentration + “bite” cells

A

Glucose-6-phosphate dehydrogenase deficiency

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29
Q

acute haemolysis following ingestion of cotrimoxazole/primaquine

A

Glucose-6-phosphate dehydrogenase deficiency

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30
Q

Glucose-6-phosphate dehydrogenase deficiency dx

A

Heinz Bodies

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31
Q

helmet cells + Artificial (mechanical) valves placemenent

A

schistocytes Hemolytic anemia

32
Q

schistocytes Hemolytic anemia lab findings

A

Decreased serum haptoglobin level

33
Q

spherocytosis clinical features

A

1-Anaemia and jaundice.
2-Splenomegaly.
3-Positive family history of anaemia, jaundice, or gallstones.
4-Spherocytosis with increased reticulocytes.
5-Increased osmotic fragility.
6-Negative direct antiglobulin test (DAT).

34
Q

The outcome of splenectomy in a patient with spherocytosis

A

1- Spherocytosis persists after splenectomy, the cells survive longer in the circulation.
2-Decrease in reticulocytosis.
3- RBC fragility remains high resulting short life span of red blood cells
4- Fall in elevated bilirubin
5- In severely affected patients, life-threatening anaemia

35
Q

Spherocytosis gene defect

A

spectrin
ancyrin
protein 4.1

36
Q

fever + thrombocytopenia + low haemoglobin + acute renal failure + hallucination + haemolytic anaemia

A

Thrombotic thrombocytopenic purpura (TTP)

37
Q

immediate hemolytic reaction
secondary to a blood transfusion invesitgation

A

Positive Coombs test

38
Q

Thrombotic thrombocytopenic purpura (TTP) treatment

A
  • replacement fluid
  • fresh frozen plasma
39
Q

pruritis on hot bath + vertigo + tinnitus + headache + visual disturbances + hypertension + transient ischemic
strokes

A

Polycythaemia vera

40
Q

fever + maculopapular rash+ serum AST, bilirubin and alkaline phosphatase elevation post transplant

A

Graft-versus-host disease

41
Q

decreased serum albumin + hypercalcaemia + anaemia + bony lytic lesions/osteoporosis

A

Multiple myeloma

42
Q

CRAB

A

C - hypercalcaemia 13%
R - renal impairment 20–40%
A - anaemia 70%
B - bony lesions

43
Q

Multiple myeloma investigation

A

Initial: & diagnostic: serum and urinary
electrophoresis

44
Q

poor prognosis of multiple myeloma

A
  1. higher levels of beta-2 microglobulin
  2. lower levels of albumin
45
Q

hepatomegaly + weakness+ hyperpigmentation + atypical
arthritis + diabetes + impotence + unexplained chronic abdominal pain +
cardiomyopathy + Decreased production of FSH and LH + gynaecomastia + 90% are C282Y homozygotes

A

haemochromatosis

46
Q

Most common manifestation of cardiac
involvement in hemochromatosis

A

Congestive cardiac failure

47
Q

most common cause of death in hemochromatosis

A
  1. Liver disease
  2. cardiomypathy
48
Q

haemochromatosis investigation

A

Serum transferrin saturation
- >60% men
- 50$ women

49
Q

haemophilia A in pregnancy

A
  • measure Factor 8 level at 1st antenatal
    visit and at 32 weeks
  • majority develop normal level of factor 8 and do not require replacement
50
Q

-Malaise and pallor + Recurrent infection + Gingival hypertrophy + Fever, night sweats + -Normocytic normochromic anaemia + Thrombocytopenia + myeloblasts more than 20%

A

acute myeloid leukaemia (AML)

51
Q

conditions which can lead to the development of AML

A

-Trisomy 21 noted in Down syndrome.
-Fanconi anaemia.
-Ataxia-telangiectasia.
-Myeloproliferative syndromes.

52
Q

pallor + sweats + weight loss + bilateral axillary lymphadenopathy + massive Spleen and liver megaly

A

Chronic lymphocytic leukaemia (CLL)

53
Q

CLL management

A

1st line: corticosteroids such as prednisolone
chemotherapy if needed

54
Q

urticaria + stridor + hypotension during blood transfusion+ hx of recurrent infections

A

Immunoglobulin A deficiency

Immunoglobulin A (IgA) deficiency is the most common primary immunodeficiency disorder. It is characterized by a significant reduction or complete absence of serum and secretory IgA, which is the main antibody found in mucous secretions of the respiratory and gastrointestinal tracts.

55
Q

fatigue and weakness, dyspnea, and pallor + dysplasia + Anaemia with/o f bi- or
pancytopenia+ Macrocytosis + absolute neutropenia

A

Myelodysplasia

56
Q

common feature of autoimmune thrombocytopenia in
childhood

A

Antecedent viral illness

57
Q

microcytic anemia + increased concentration of hemoglobin A2

A

β-Thalassemia

58
Q

β-Thalassemia investigation

A

diagnostic: hemoglobin electrophoresis

59
Q

most profound adverse effect of chronic
transfusional iron overload in children with thalassemia?

A

Progressive hepatic cirrhosis

60
Q

sickle cell anaemia reduce iron overload

A
  • Subcutaneous deferoxamine
  • Splenectomy
  • ## Erythrocytopheresis
61
Q

earliest complication of sickle cell disease

A

Bone infarction

62
Q

decreased red cell, white cell and platelets counts

A

pancytopenia/aplastic anemia

63
Q

aplastic anaemia causes

A

NSAIDs
- Sulfonamides.
– Gold.
– Anti-epileptic drugs (carbamazepine, valproic acid, phenytoin).
– Nifedipine.
– Chloramphenicol.

64
Q

generalised weakness, low-grade fever and sore throat + normal haemoglobin + low neutrophil + low platelets + thyroid medicatiob

A

agranulocytosis

65
Q

Long-standing history of prolonged bleeding after trauma and history of menorrhagia in an otherwise healthy woman

A

Von Willebrand disease

66
Q

fever, night sweats, weight loss + painless generalized lymphadenopathy which becomes painful after alcohol consumption

A

f Hodgkin lymphoma (HL)

67
Q

f Hodgkin lymphoma (HL) highest risk of malignanc

A

Supraclavicular lyphadenopathy

68
Q

Hodgkin lymphoma (HL) diagnostic investigation

A

Lymph node excision biopsy

69
Q

non-Hodgkin lymphoma features

A

GI tract most common site
- 3% of all malignant gastric tumors
- Surgery alone can be considered adequate treatment that does not infiltrate beyond the submucosa
-

70
Q

incidence of thrombosis and bleeding in patients with myeloproliferative neoplasms?

A
  • typically mucocutaneous
  • Bleeding is usually less severe and less frequent than thrombosis
  • Arterial
    thromboses are more common than venous thrombosis
  • Strokes are more frequent followed by myocardial infarction and peripheral arterialocclusion

Myeloproliferative neoplasms (MPNs) are a group of diseases characterized by the overproduction of blood cells. The main types are polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). Here’s a simplified explanation of their pathophysiology:

  • JAK2 Mutation: The JAK2 V617F mutation is found in about 95% of PV cases and 50-60% of ET and PMF cases. This mutation leads to the continuous activation of the JAK-STAT signaling pathway, which promotes excessive blood cell production.
  • CALR and MPL Mutations: CALR (calreticulin) mutations are present in 20-25% of ET and PMF cases, and MPL (myeloproliferative leukemia virus oncogene) mutations are found in 5-10% of these patients. These mutations also activate pathways that lead to increased blood cell production.
  • Excessive Red Blood Cells: In PV, the mutation leads to the overproduction of red blood cells, increasing blood viscosity (thickness), which can cause sluggish blood flow and a higher risk of clot formation.
  • Symptoms: Headaches, dizziness, visual disturbances, and a ruddy complexion are common. Aquagenic pruritus (itching after exposure to water) is also characteristic.
  • Excessive Platelets: ET is marked by the overproduction of platelets. While these platelets are numerous, they are often dysfunctional, leading to an increased risk of both clotting and bleeding.
  • Symptoms: Many patients are asymptomatic, but symptoms can include headaches, visual disturbances, and erythromelalgia (burning pain and redness in the hands and feet).
  • Bone Marrow Fibrosis: In PMF, abnormal blood cells stimulate fibroblasts in the bone marrow to produce excess fibrous tissue, leading to scarring (fibrosis) of the bone marrow.
  • Symptoms: This fibrosis impairs the bone marrow’s ability to produce blood cells, causing symptoms like anemia, fatigue, and splenomegaly (enlarged spleen) due to the body compensating by producing blood cells in the spleen and liver.
  • Thrombosis (Clot Formation): Due to increased blood viscosity in PV and dysfunctional platelets in ET, there is a high risk of thrombosis, which can lead to deep vein thrombosis, pulmonary embolism, strokes, and heart attacks.
  • Bleeding: Despite the increased number of platelets in ET, their dysfunction can lead to an increased risk of bleeding, particularly in extreme thrombocytosis (very high platelet counts).
  • Disease Transformation: MPNs can transform into more aggressive diseases, such as acute myeloid leukemia (AML) or secondary myelofibrosis, which have poorer prognoses.
  • Phlebotomy: For PV, to reduce red blood cell mass and lower blood viscosity.
  • Medications:
    • Hydroxyurea: Used in PV and ET to reduce blood cell production.
    • Low-Dose Aspirin: To reduce the risk of thrombosis in PV and ET.
    • JAK Inhibitors (e.g., Ruxolitinib): Particularly useful in PMF to reduce spleen size and alleviate symptoms.
  • Monitoring and Risk Management: Regular monitoring of blood counts and careful management of symptoms and complications.

Understanding these basic concepts can help demystify the pathophysiology of MPNs and the rationale behind their treatment. For more detailed information, refer to the RACGP guidelines on MPNs oai_citation:1,RACGP - Myeloproliferative neoplasms oai_citation:2,RACGP - Performing therapeutic venesection in a doctor’s surgery.

71
Q

best test to monitor heparin therapy

A

Activated partial thromboplastin time (aPTT)

72
Q

DVT in the presence of thrombocytopenia

A

heparin induced thrombocytopenia

73
Q

types of heparin induced thrombocytopenia

A

Type 1 : first 2 days after exposure, platelet count normalizes with continued heparin therapy. non-immune

Type 2: typically occurs 4-10 days after
exposure, immune-mediated disorder
- Venous limb gangrene
- Bilateral adrenal hemorrhagic infarction
- Skin lesions at injection sites
- Acute systemic reactions following an i- ntravenous heparin bolus

74
Q

heparin induced thrombocytopenia management

A

discontinue and avoid all heparin products immediately

75
Q

Renal failure reflected by oliguria and abdominal pain following invasive diarrhoea

A

hemolytic uremic syndrome (HUS).

AMC MCQ - You Can Do It!!!!!❤️❤️ (50 decks)

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