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Phase 2a > Haematology > Flashcards

Haematology Flashcards

1
Q

Two positions of a DVT?
Which is more dangerous?
Which is more common?

A

Proximal or distal
Proximal = dangerous
Distal = common

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2
Q

Two ways a DVT can happen?

Why is this important?

A

Provoked - by injury

Spontaneous - will need further management to prevent recoccurrence

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3
Q

Symptoms of a DVT? (5) Why?

Added symptoms if a PE has occurred? (5)

A

Inflammation, pain, swelling, redness, warmth around the area:
BECAUSE superficial veins being used

PE: dyspnoea, pleuritic chest pain, cough, cyanosis, shock

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4
Q

Risk factors for a DVT? (5)

A 
Elderly
Lack of movement
Hormones
Pregnancy
Cancer
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5
Q

How to diagnose a DVT?
Diagnostic
Test used to rule out?
Differentials for DVT? (2)

A

Usually: Ultrasound compression test
Sometimes: Venography
D-dimer
Cellulitis, CHF

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6
Q

How is a DVT treated:
Small clots?
Large clots?
Future management? (3)

A

Small clots may resolve on their own

Large clots: acute = LMW heparin or fondaparinux

Future: education, IVC filter, anticoagulant therapy (DOACs, heparins, warfarin)

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7
Q

What is the definition of anaemia?
How is it measured in practice?
Normal ranges for male and female?
Example of why this may not always represent a true anaemia

A

Reduced red cell mass

Male (131-166 g/L of Hb)
Female (110-147g/L of Hb)

Via haemoglobin concentration

Pregnancy: has a reduced Hb (due to increased plasma volume), but actually an increased RCM (red cell mass)

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8
Q

CAUSES classification of anaemia

4 types and examples of each

A
  • Haemorrhagic (blood loss): trauma, operation, ulcers, haemorrhoids
  • Haemolytic (increased destruction): sickle cell, malaria, autoimmune, PNH, enzymes, DIC
  • Hypoplastic (production failure): renal failure, PRCA, anaplastic
  • Dyshaemopoietic (production failure): chronic disease, thalassaemia, iron deficiency, folate and B12
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9
Q

RED BLOOD CELL SIZE classification of anaemia

3 types and big examples of each

A
  • Microcytic (<80) - Iron deficiency, Chronic disease, Thalassaemia, Sideroblastic anaemia (TICS)
  • Normocytic (80-100) - Chronic disease, Acute blood loss, combined haematinic

• Macrocytic (>100) - foetus, alcohol, hypothyroid, reticulocytosis, B12/folate, cirrhosis
FAT RBC

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10
Q

Name 4 causes of an iron deficiency anaemia
What would you see on a blood film?
Signs of iron deficiency? (4)

A

Dietary, parasites, menorrhagia, CANCER

Blood film: PENCIL SHAPE CELLS, HYPOCHROMIC

Brittle hair & nails, atrophic glossitis, kolionychia (spoon nails), angular stomatitis (inflammation at corners of mouth)

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11
Q

How does a sideoblastic anaemia work?

What does it look like on a blood film?

A 
Iron is available but unable to enter the RBC
Ringed sideroblasts (iron deposits with Prussian stain)
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12
Q

How does anaemia of chronic disease work?

Common in…?

A

Chronic disease uses up iron, stopping haemoglobin being formed
Common in hospitalised patients

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13
Q

Basic pathophysiology of a B12 or folate deficiency?

Key finding on blood film?

A

Problems with DNA synthesis in erythroblasts
Blood film:
Macrocytic cells w/ hypersegmented neutrophils

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14
Q

Name the two key enzymopathies?

A

G6PD deficiency & pyruvate kinase deficiency

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15
Q

G6PD:
Signs + symptoms (3)
What can cause a crisis?
Mainly affects…., why?

A

Often asymptomatic
Crisis: haemolysis, jaundice & anaemia
Crisis is precipitated by fava beans, infections or drugs

Mainly affects men, X-linked

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16
Q

Two membranopathies?
Symptoms?
Treatment?

A

Spherocytosis & elliptocytosis

Jaundice, gallstones, normally seen in childhood

Folic acid

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17
Q

What does PRV stand for?
What is it?
Association with what mutation?
Become more common with….

A

Polycythaemia rubra vera

Too many RBCs produced by bone marrow

Associated with JAK2 mutation (90% of cases)

More common with increasing age

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18
Q

Side effects of iron tablets?

A

Black stools, constipation, diarrhoea, nausea, GI upset, abdominal pain

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19
Q

PRV:
Symptoms: (7)
Diagnosis: (2)
Treatment:

A

Symptoms: may be asymptomatic, itching after hot bath, erthromelagia (burning sensation in fingers and toes), facial plethora, splenomegaly, gout, headaches, dizziness

Diagnosis: Raised red cell mass on chromium studies & splenomegaly

Treatment: Keep haematocrit below 0.45, venesection, hydroxycarbamide (make HbF), aspirin

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20
Q

Why is sickle cell disease & thalassaemia more common in African populations?
Both what type of inheritance?

A

Aetiology note: Carrier is protected against malaria, hence Sub-Saharan Africa prevalence

Recessive inheritance

21
Q

SICKLE CELL ANAEMIA:
What is Haemoglobin S made of?
What is the problem with HbS

A

2 alpha, 2 beta-S (mutated)

HbS: deoxygenated area leads to polymerisation and deformation - intravascular haemolysis

22
Q

Investgiations of sickle cell anaemia?
3 main complications?
Basic management - acute and chronic?

A

Blood smear
Protein electrophoresis (shows HbS)
Sickle solubility chest (new-born screen)

Complications: Splenic infarction, poor growth, renal failure

Management:
ACUTE: analgesia, rehydration, possible blood transfusion (bronchodilators: salbutamol)
CHRONIC: hydroxycarbamide, prophylaxis for infections, bone marrow transplant

23
Q

3 categories in signs and symptoms of sickle cell anaemia, examples in each

A

Anaemia - enlarged cheeks, hair on end apperance on skull
Hepatomegaly (RBC production in liver)
Vaso-occlusion - dactylitis, pain crises, auto-splenectomy, strokes

24
Q

What can cause an aplastic crisis?

A

Parvovirus B19

25
Q

Basic principles of thalassaemia
Twp types of thalassaemia?
Main treatment:
General presents when?

A

Diminished synthesis of one or more globin chains - resulting in reduction

BETA: (reduced/absence beta chain production)
ALPHA: (reduced/absence alpha chain production)

Regular transfusions

Presents in childhood - pale, crying, failure to feed

26
Q

Three coagulation tests?

What does each measure? (intrinsic or extrinisic)

A
  • aPTT (activated partial thromboplastin time) - intrinsic
  • PTT (prothrombin time) - extrinsic
  • INR (international normalized ratio) formed from PTT
27
Q

Name 3 main DOACs/NOACs

A

apixiban
rivaroxaban
dabigatran

28
Q

What are the characteristic symptoms of a platelet disorder (4) vs a coagulation disorder (1)

A

PLATELET
Mucosal bleeding (epistaxis - nosebleed, gum bleeding, menorrhagia)
Easy bruising (ecchymosis)
Petechiae (small) and purpura (large)

COAGULATION
Deep tissue and joint bleeding

29
Q

What does VWF stand for?

What are it’s 3 main roles?

A

Von Willebrand Factor
• Bring platelets in contact with sub-endothelium
• Make platelets bind to each other
• Bind to factor 8 (protecting it from destruction)

30
Q

Two types of Haemophilia?
What factor is deficient in each?
Which is more common?
Genetic note?

A

Two types
• Haemophilia A - factor 8 deficiency (treated with IV factor 8)
• Haemophilia B - factor 9 deficiency

Haemophilia A is more common

X-linked recessive: mainly male

31
Q

Name 4 aetiologies of microangiopathic haemolytic anaemias?

A

TTP - thrombotic thrombocytopenic purpura

DIC - disseminated
intravascular coagulation

HUS - Haemolytic uremic syndrome

Valvular disease (stenosis or prosthetic)

32
Q

What is anaplastic anaemia?

3 key points of symptoms?

A

A rare stem cell disorder leading to pancytopenia and hypoplastic bone marrow

Anaemia (low Hb), Infection (low WBC), Bleeding (low platelets)

33
Q

Which is more common ITP or TTP?

What does each stand for?

A

ITP

Immune thrombocytopenic purpura (also idiopathic thrombocytopenic purpura)

Thrombotic thrombocytopenic purpura

34
Q 
Basic physiology of ITP?
Presentation in chronic?
Presentation in acute?
Normal symptoms?
Is there splenomegaly?
3 treatment points
"diagnosis of ..."
A

Autoimmune destruction of platelets by the spleen

Acute: children 2 weeks after infection
Chronic: females of reproductive age

Features: easy bruising, purpura, epistaxis
May be asymptomatic

No splenomegaly

Corticosteroids (prednisolone)
IV IG
Splenectomy

Diagnosis of exclusion

35
Q

What does DIC stand for?
Basic physiology?
Causes? (5)
Management principle?

A

Disseminated Intravascular Coagulation

Widespread clotting which consumes platelets and then causes bleeding

Causes: Malignancy, septicaemia, trauma, infections, haemolytic transfusion reactions

Treat underlying cause

36
Q

What gene/protein is TTP associated with?
Basic pathophysiology?
“The terrible pentad”?

A

Thrombotic thromobcytopenis purpura (TTP)

ADAMTS13 - normally inhibits vWF, loss of it causes platelets binding to vWF

Fever, Neurologic, Renal, Anaemia, Platelets

37
Q

What is multiple myeloma a cancer of?
Percentage in bone marrow?
3 types of multiple myeloma?
What is the name of the protein formed? What does it do?

A

Plasma cells

> 10%

Symptomatic
Asymptomatic (smouldering)
Monoclonal gammopathy of undertermined significance (MGUS) (not technically multple myeloma)

Paraprotein (light chain) - damages the kidney

38
Q 
What are the key symptoms of multiple myeloma?
Bloods would show:
FBC = ?
Normal antibodies = ?
Hyper or hypocalc = ?
Creatinine = ?
Bence Jones = ?
X-ray = ?
A

CRAB: hyperCalcaemia, Renal failure, Anaemia, Bone lesions (also infections, fatigue, back pain (spinal cord fracture), dehydration)
FBC = Anaemia, thrombocytopenia, low WBC?
Normal antibodies = decreased
Hyper or hypocalc = hypercalcaemia
Creatinine = Increased
Bence Jones = Increased (paraprotein in urine)
X-ray = Lytic bone lesions

39
Q

Staging of Hodgkin’s lymphoma?

A

Ann Arbor system
1: involvement of single lymph node region
2: two ore more lympho node regions on same side as diaphragm
3: involvement of lymph node regions on both sides of diaphragm
4: diffuse extralymphatic disease
A = absence of symptoms
B = symptoms present

40
Q

What is the common presentaiton of lymphoma?

A

Painless lymphadenopathy
Fever, weight loss, night sweats
Possible bowel obstruction and pancytopenia

41
Q

Two types of lymphoma - how do you distinguish between these two?

A

Hodgkin’s & Non-hodgkin’s

Hodgkin’s shows Reed-Sternberg cells under the microscope

42
Q

Note on incidence of Hodgkin’s lymphoma?

Key antibody treatment in lymphoma? CD__?

Association with what two viruses?

A

Bimodal - young adults and elderley

RITUXIMAB (CD20)

EBV & HIV

43
Q

Two categories in Non-Hodgkin’s lymphoma?
2 examples from each category?
Note on prognosis of each?

A

Low grade: follicular, MALT
Better treatment, slightly better prognosis

High grade: diffuse large B cell, Burkitt’s lymphoma
Slightly worse prognosis, more aggressive

44
Q

General symptoms of acute leukaemia? Pathophysiology behind 3 categories of these symptoms?

What percentage is needed for a leukaemia diagnosis?

A

Anaemia: tiredness, fatigue, pallor
Thrombocytopenia: bruising or bleeding
Leukopenia: infections

Increased in blast cells in bone marrow leads to crowding out:

Greater than 20% in bone marrow

45
Q

Two chromosomal associations with ALL?
ALL is normally found in…
Also an association with what syndrome?

A

9:22 Philadelphia
12:21
Normally found in childhood
Down’s syndrome

46
Q

What does ALL stand for?
Two major types of ALL?
What is ALL positively stained with to differentiate it from AML?

A

Acute lymphoblastic leukaemia

B-cell and T-cell

Nuclear staining for TdT

47
Q

Who is normally seen with AML?
What is the key finding on blood film?
Some examples of the subtypes?

A

Elderly

Auer rods (myeloperoxidase staining)

Varying maturation subtypes, promyelocytic, monocytic, etc…

48
Q

Chronic leukaemia symptoms?

A

Same as acute
Anaemia, thrombocytopenia & leukocytopenia
Not always symptomatic though

49
Q

CML is common in what age group?
What chromosomal abnormality? Explain this mechanism
What is it called when CML becomes AML? Common mechanism behind this?

A

Middle age

Philadelphia t(9;22)

Forms BCR-ABL gene which turns on Tyrosine Kinase, causing build-up (on-switch)

Called a BLAST CRISIS - often due to double of Philadelphia chromosome

Phase 2a (9 decks)

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