Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a diseases > Haematology > Flashcards

Haematology Flashcards

1
Q

What is the clinical presentation of iron deficiency anaemia?

A

Anaemia:

  • Fatigue
  • Low energy
  • Pallor
  • Dyspnoea on exertion.

Deficiency of iron:

  • Pica (appetite for non-food items).
  • Hair loss
  • Restless leg syndrome
  • Nail abnormality (spooning, flattening, thinning).
  • Angular stomatitis.
  • Glossitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the histological presentation of iron deficiency anaemia?

A
  • Microcytic, hypochromic.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the risk factors for iron deficiency anaemia?

A
  • Pregnant.
  • Vegan/vegetarian.
  • Menorrhagia.
  • Coeliac.
  • Excessive NSAID use (causes peptic ulcers).
  • CKD (low erythropoietin).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the diagnostic tests for iron deficiency anaemia?

A
  • FBC: Low RBCs, low MCV, low MCH (mean corpuscular haemoglobin).
  • Blood smear: Microcytic, hypochromic.
  • Low reticulocytes.
  • Low serum iron and low serum ferratin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the treatment for iron deficiency anaemia?

A
  • 1st line: Ferrous sulfate (orally).
  • 2nd line: IV iron (used if ferrous sulfate is intolerated or the individual has IBD.)
  • RBC transfusion. Used if the individual begins to present with symptoms of CV compromise (chest pain, dyspnoea on rest).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is pernicious anaemia?

A
  • Autoimmune disorder.
  • Destruction of the parietal cells of the stomach (that secrete IF) and production of intrinsic factor antibodies.
  • Causes malabsorption of B12, as If is required for the cotransportation process used for B12 absorption.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the symptoms of pernicious anaemia?

A

Anaemia:

  • Fatigue
  • Lack of energy
  • Pallor
  • Dyspnoea on exertion.

B12 deficiency:
- Neurological problems (peripheral neuropathy and dementia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the histological presentation of pernicious anaemia?

A
  • Macrocytic, megaloblastic (presence of large, immature RBCs).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the risk factors for pernicious anaemia?

A
  • Old age (reduced stomach acid secretion).
  • FH.
  • Autoimmune endocrine disorders (e.g. Hashimoto’s thyroiditis).
  • Coeliac disease.
  • IBD (crohns, UC).
  • Partial/complete stomach resection.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the investigations used to confirm diagnosis of pernicious anaemia?

A

FBC - MCV increased, MCHC normal.

Blood film - Shows macrocytic, megaloblastic RBCs.

Intrinsic factor antibody test - Presence of these antibodies proves pernicious anaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the treatment for pernicious anaemia?

A
  • Give hydroxocobalamin, a B12 analogue (1st line)
  • If there are neuro symptoms, refer to neurology/haematology.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the risk factors for folate-deficiency anaemia?

A
  • Pregnancy/lactation.
  • Old age.
  • Chronic alcohol abuse.
  • Low folate diet.
  • FH.
  • Coeliac disease.

Use of certain drugs:
- Trimethoprim.
- DMARDS (sulfasalazine, methotrexate).
- Anticonvulsants.
(therefore these drugs are contraindicated in pregnancy).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the histology of folate-deficiency anaemia?

A
  • Macrocytic, megaloblastic anaemia.
  • Hypersegmented neutrophils

NOTE: same as pernicious anaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the clinical presentation of haemolytic anaemia?

A

Anaemia:

  • Fatigue
  • Lack of energy
  • Pallor
  • Dyspnoea on exertion

Folate deficiency:

  • Angular stomatitis.
  • Glossitis
  • Painful swallowing.
  • NO NEURO SYMPTOMS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the investigations used to diagnose folate-deficiency anaemia?

A
  • FBC. Raised MCV and MCHC.
  • Blood film. Macrocytic, megaloblastic cells with hypersegmented neutrophils.
  • Serum folate: 1st line screening tool.
  • RBC folate: Gold standard. More sensitive than serum folate, but more expensive/complex.
  • Serum B12. Should be done to exclude pernicious anaemia, which can be masked by folate supplementation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the treatment for folate-deficiency anaemia?

A
  • Folic acid oral (1st line).
  • Consider RBC transfusion if severely anaemic.
  • Women planning/currently pregnant should be taking folic acid to reduce risk of neural tube defects.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is haemolytic anaemia?

A

A number of conditions that occur due to increased destruction of RBCs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the symptoms of haemolytic anaemia?

A

Anaemia:

  • Fatigue
  • Lack of energy
  • Pallor
  • Dyspnoea on exertion.

Haemolysis:
- Jaundice (due to bilirubin released from erythrocyte breakdown).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What type of anaemia is haemolytic anaemia?

A
  • Normocytic usually.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the differentials for haemolytic anaemia?

A
  • Blood loss.
  • Transfusion reaction.
  • Underproduction anaemia. Caused by reduced production of RBCs rather than increased breakdown. Will therefore have a low reticulocyte count (would be high in haemolytic anaemia).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the risk factors for haemolytic anaemia?

A
  • FH.
  • Autoimmune disorders (especially SLE).
  • CLL
  • Cephalosporins.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the investigations used to diagnose haemolytic anaemia?

A

FBC - Reduced Hb, increased MCH due to high amount of reticulocytes.

Blood film - High reticulocyte count, lots of abnormal RBC’s.

Coomb’s test - If positive indicates an autoimmune cause of haemolytic anaemia.

Consider ANA if SLE suspected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the treatment for haemolytic anaemia?

A
  • If symptomatic, use RBC transfusion.
  • Give folic acid, as increased rates of reticulocytosis will deplete folic acid stores more quickly.
  • If coomb’s test +ve, give prednisolone (reduces production of autoantibodies that drive RBC breakdown in autoimmune haemolytic anaemia).
  • If caused by a drug (commonly cephalosporins) give prednisolone and discontinue the drug.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is sickle cell anaemia?

A
  • Hereditary deformation of RBC’s as a result of faulty Hb molecule formation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the clinical presentation of sickle cell anaemia?

A
  • Vaso-occlusion. Early childhood acute pain in the hands and feet due to small vessel occlusion.
  • In adults, pain in the long bones, ribs, spine and pelvis too.
  • OFTEN SYMPTOMS OF ANAEMIA DO NOT APPEAR AS HbS HAS A LOW OXYGEN AFFINITY.
  • If they do appear, anaemic symptoms are:
  • Tiredness
  • Fatigue
  • Dyspnoea
  • Palpitations
  • Headache
  • Faintness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the pathophysiology of sickle-cell anaemia?

A
  • Changes in sequence of haemoglobin subunit causes faulty structure.
  • Distorts erythrocyte shape, making them sickle shaped.
  • Sickle cell RBC’s block vessels easily, and are easily destroyed.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the investigation used for sickle cell anaemia?

A
  • Usually identified in neonatal screening.
  • Otherwise, identified by presence of sickle cells on blood film.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the treatment for sickle cell anaemia?

A
  • Anaphylactic penicillin until 5 years old (children). Because they are at substantially increased risk of invasive pneumococcal infection.
  • Hydroxycarbamide. Manages the pain.
  • Potentially blood transfusion.
  • Bone marrow stem cell transfusion if disease severe - still a very new treatment.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the alternative name for folic acid?

A

B9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the clinical presentation of a DVT?

A
  • Often will have progressed to PE before clinical presentation.

Classical features include:

  • Limb pain and tenderness.
  • Calf swelling.
  • Raised skin temperature.
  • Pitting oedema.
  • May resemble cellulitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the pathophysiology of DVT?

A
  • Thrombus formation in the deep vein.
  • May then embolise and flow up into the pulmonary circulation, before becoming stuck and causing a PE.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the thrombotic risk factors?

A
  • Obesity
  • Family history
  • Male
  • Smoking
  • Age
  • Cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the investigations used in a suspected DVT?

A

If Well’s score <2:

  • D-dimer testing. If negative, DVT ruled out.
  • If positive, arrange a venous ultrasound.

If Well’s score ≥2:
- Venous ultrasound straight away, before D-dimer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the treatment for a DVT?

A

Until DVT confirmed/ruled out:

  • apixaban (1st line)
  • If not tolerated, offer LMWH (2nd line).

When confirmed:

  • Continue apixaban
  • Encourage mobilisation as soon as possible.
  • Compression stockings.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the 4 different types of leukaemia? And what are they?

A
  • Acute lymphoblastic leukaemia (ALL). ACUTE malignant transformation of a clone of LYMPHOID PROGENITOR CELLS.
  • Chronic lymphoblastic leukaemia (CLL). CHRONIC malignant transformation of a clone of MATURE LYMPHOID CELLS.
  • Acute myeloid leukaemia (AML). ACUTE malignant transformation of a clone of MYELOID PROGENITOR CELLS.
  • Chronic myeloid leukaemia (CML). CHRONIC malignant transformation of a clone of MYELOID CELLS.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the typical presentation of ALL?

A
  • Fatigue
  • Dizziness
  • Palpitations
  • Bone pain
  • Hepatosplenomegaly

Bone marrow failure causes:

  • Anaemia (due to overpopulation of bone marrow with lymphoblastic cells).
  • Bleeding
  • Infection
  • ALL also has a propensity to include the CNS.
37
Q

What is the pathophysiology of ALL?

A
  • Uncontrolled proliferation of precursor B and T cells.
  • Leukaemic cells accumulate in the bone marrow, peripheral blood and other tissues.
  • Overproduction of leukaemic cells leads to reduced RBCs, platelets and neutrophils.
38
Q

What are the risk factors for ALL?

A
  • Genetic (Down’s syndrome 20x risk).
  • Environmental. Benzene compounds, drugs (alkylating agents) and radiation exposure.
39
Q

What is the most common cancer in children?

A
  • Acute lymphoblastic leukaemia (ALL).
40
Q

What are the investigations used to assess ALL?

A
  • FBC. Anaemia, leukocytosis, thrombocytopenia may be found.
  • Peripheral blood smear. Presence of leukaemic lymphoblasts indicates ALL.
  • Bone marrow aspiration. Look for presence of leukaemic lymphoblasts.
41
Q

What is the treatment for ALL?

A

Chemotherapy:
- Prednisolone (corticosteroid) AND cyclophosphamide (immunosuppressant) AND vincristine (alkaloid chemo drug) AND doxorubicin (anthracycline antibiotic).

  • Potentially use methotrexate (antimetabolite immunosuppressant) depending on type of AML.
42
Q

What is the prognosis for children with ALL?

A
  • Only 1/5 die from it. Prognosis very good.
43
Q

What is the clinical presentation of chronic lymphoblastic leukaemia (CLL)?

A
  • Early on, it will often be asymptomatic with lymphocytosis (increased white cell count).

Later on, will become symptomatic:

  • Anaemia
  • Bleeding and infection due to bone marrow failure.
  • Rubbery lymph nodes.
44
Q

What is the histological presentation of CLL?

A

Smudge cells.

45
Q

What is the pathophysiology of CLL?

A
  • Uncontrolled proliferation of mature T/B cells.
  • Autoimmune haemolysis may occur, causing anaemia.
46
Q

What is the aetiology of CLL?

A
  • Mutation (11q or 17p deletion).
47
Q

What is the epidemiology of CLL?

A
  • Most common leukaemia in western world.
  • Usually affects older people.
48
Q

What are the diagnostic tests for CLL?

A

FBC: Anaemia, raised white cell count.

Blood film: smudge cells.

49
Q

What is the treatment for CLL?

A

If asymptomatic, watch and wait.

When symptomatic:
- Chemotherapy.

CLL is incurable.

50
Q

What are the symptoms of AML?

A
  • Fatigue
  • Dizziness
  • Palpitations
  • Hepatosplenomegaly

Bone marrow failure causes:

  • Anaemia
  • Bleeding
  • Infection
51
Q

What is the histological presentation of AML?

A
  • Auer rod cells.
52
Q

What is the pathophysiology of AML?

A
  • Accumulation of leukaemic myeloid blast cells in the bone marrow, peripheral blood and other tissues.
  • There is also a reduction in erythrocytes, platelets and neutrophils.
53
Q

What is the aetiology of AML?

A
  • Can transform from myelodysplasia.
  • Can be genetic.
54
Q

What is the epidemiology of AML?

A
  • Most common in older adults.
55
Q

What are the investigations used to diagnose AML?

A

Peripheral blood film:

  • Anaemia
  • Thrombocytopenia
  • Auer rods

Bone marrow aspirate:
- Leukaemic blast cells

56
Q

What is the treatment for AML?

A
  • Chemotherapy
  • For severe/relapsing AML, consider stem cell transplant.
57
Q

What is the clinical presentation of CML?

A
  • Insidious onset
  • Fever
  • Weight loss
  • Sweating
  • Anaemia
  • HUGE SPLENOMEGALY
  • Untreated, will last 3-4 years before disease progresses to AML.
58
Q

What is the pathophysiology of CML?

A
  • CML lasts around 3-4 years, before blast formation begins.
  • Blast formation causes AML, leading to rapid death if untreated.
59
Q

What is the aetiology of CML?

A
  • Genetic. Philadelphia chromosome translocation in 95% of cases.
60
Q

What is the epidemiology of CML?

A

Most common in the elderly.

61
Q

What are the investigations used to diagnose CML?

A

FBC: Anaemia, raised white cells.

Cytogenetics: Philadelphia chromosome.

62
Q

What is the treatment for CML?

A

If in chronic stage, 1st line is imatinib (tyrosine kinase inhibitor).

When blast phase/acute phase reached, chemotherapy is 1st line.

63
Q

What is lymphoma?

A

Malignant tumour of the lymphatic system.

64
Q

What are the two types of lymphoma? What differentiates the two?

A

Hodgkin’s lymphoma. Reed-Sternberg cells present.

Non-Hodgkins lymphoma. No Reed-Sternberg cells present.

65
Q

What are the symptoms of lymphoma?

A
  • Painless, rubbery lymph node enlargement.
  • Hepatosplenomegaly.
  • Puritus
  • Fatigue
  • Alcohol induced pain in the affected nodes.

Typical cancer symptoms:

  • Weight loss
  • Fever
  • Night sweats
66
Q

What is the aetiology of non-Hodgkin’s lymphoma?

A
  • Usually unknown.
  • Could be H. Pylori in mucous associated lymphoid tissue lymphoma.
  • Could be EBV in Burkitt’s lymphoma.
67
Q

What is the aetiology of Hodgkin’s lymphoma?

A
  • Often unknown.
  • Could be previous EBV infection.
68
Q

What is the epidemiology of both Hodgkin’s and non-Hodgkin’s lymphoma?

A
  • Hodgkin’s more common in young adults.
  • Non-Hodgkins is more common in older people (rare before 40).
69
Q

What are the diagnostic tests used for lymphoma?

A
  • Lymph node biopsy. Will show Reed-Sternberg cells (Hodgkin’s lymphoma) or not (non-Hodgkin’s lymphoma).
  • CT scan is used for staging the cancer.
  • FBC. Check for anaemia.
70
Q

What is the treatment for Hodgkin’s lymphoma?

A
  • Radio + chemo (often doxorubicin).

As disease progresses, treatment will be made more aggressive.

71
Q

What is the treatment for non-Hodgkins lymphoma?

A
  • Chemotherapy + radiotherapy.
72
Q

Which form of lymphoma has a worse prognosis?

A
  • Hodgkin’s lymphoma has a worse prognosis than non-Hodgkin’s lymphoma.
73
Q

How is myeloma different to leukaemia?

A
  • In myeloma, cancerous cells generally remain in the bone marrow.
  • In leukaemia, cancerous cells will circulate in the blood.
74
Q

What is malaria?

A
  • Infection by plasmodium transmitted by mosquitos.
75
Q

What is the clinical presentation of malaria?

A

If infected with plasmodium falciparum, presentation occurs usually in the first month.

Other types of malaria can incubate much longer than this.

No specific symptoms, but symptoms can include:

  • Fever
  • Chills
  • Rigors (shivering + rise in temperature).
  • Cough
  • Myalgia
  • Splenohepatomegaly

If severe:

  • Impaired consciousness
  • SOB
  • Bleeding
  • Fits
  • Hypovolaemia
76
Q

What is the pathophysiology of malaria?

A
  • Mosquito bite.
  • Sporozoites in the mosquito saliva travel to the liver, where they mature.
  • Eventually, the sporozoites rupture and are released back into the blood.
  • Invade RBC’s and undergo asexual reproduction to create more sporozoites, which more mosquitos can pick up…
  • And the cycle continues.
77
Q

What is the pathophysiology of malaria?

A
  • Infection by plasmodium (usually plasmodium falciparum).
78
Q

What is the epidemiology of malaria?

A
  • Poor, pregnant, old and young all at more risk.
  • Consider if recently travelled abroad.
79
Q

What is the investigation used to diagnose malaria?

A
  • Giemsa stained thick and thin blood smears.
  • Will detect the malaria parasites inside the RBCs.
80
Q

What is the treatment for malaria?

A

If infection is with plasmodium falciparum:

  • Quinine sulfate + doxycycline (as will usually be resistant to chloroquine).
  • Chloroquine phopshate if not resistant.

If malaria infection is caused by another pathogen:
- Chloroquine is first line.

81
Q

What is thalassaemia?

A
  • Anaemia due to defective subunit of the haemoglobin complex.
82
Q

What are the two types of thalassaemia?

A
  • Alpha and beta.
  • Determined by the subunit that has been affected.
83
Q

What is the clinical presentation of thalassaemia?

A

Variable.
- Alpha tends to present in utero, whereas beta in infancy.

  • Heterozygotes can be asymptomatic, whereas homozygotes may have severe symptoms such as failure to thrive and bone deformities.
84
Q

What type of anaemia is thalassaemia?

A

Microcytic.

85
Q

What is the pathophysiology of thalassaemia?

A
  • Defective versions of either alpha or beta subunits of haemoglobin.
  • The globin chains within the erythrocytes precipitate and cause cell damage/death.
86
Q

What is the aetiology of thalassaemia?

A
  • Genetic. Homozygotes have severe anaemia, heterozygotes can vary.
87
Q

What is the diagnostic testing used for thalassaemia?

A
  • Firstly identify microcytic anaemia (blood film).
  • Either genetic testing or haemoglobin electrophoresis.
88
Q

What is the treatment for thalassaemia?

A
  • If iron too high: desferrioxamine
  • Blood transfusions if required.

IF THALASSAEMIA SEVERE, USE BONE MARROW TRANSPLANT!

89
Q

What are the potential complications of thalassaemia?

A
  • Iron overload
  • Endocrine dysfunction.

Phase 2a diseases (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions