Brainscape's Knowledge GenomeTM

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


See full index

Year 3 > Haematology > Flashcards

Haematology Flashcards

1
Q

def erythema

A

redness of the skin or mucous membrane due to capillary congestion (inflammation, injury or infection)

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

General signs of anaemia

A

Fatigue, weakenessm pale/yellowish skin, irregular heartbeats, SoB, dizziness/light-headedness, chest pain, cold hands and feet, headache

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

How is vit B12 absorbed (journey from mouth to blood)

A

Binds to transcobalamin I/haptocorrin/R protein/R factor produced by salivary glands
Haptocorrin-vitamin B12 complex is protected from acid degradation in stomach
In duodenum: pancreatic proteases degrade haptocorrin: free vit B12 binds to intrinsic factor (IF): B12-IF complex
In terminal ileum: cubilin receptors take up B12-IF complex by endocarditis-mediated absorption

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

If patient has iron, folate or vit B12 deficiency anaemia, what Qs should you ask to get to the bottom of it?

A
  • are they deficient in the diet
  • are they malabsorbed
  • are they producing it (renal failure, chronic diseases, bone cancers etc)
  • are they losing it (nose bleeds, cutting yourself)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do you give vit B12

A 
Orally
Injections (if issue with the stomach: intrinsic factor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do you do if a patient is in shock and is not anaemic

A

GIVE BLOOD
(May take a while for the blood to expand and dilate)

Assess clinically: pale and clammy, pulse, BP, level of consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Def haematocrit

A

Percentage of RBC i total blood (should be approx 40%)

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

How is Hb concertation measured and what are normal values

A

Lyse of RBC and measure of Hb concentration
Men: 130-180 g/L
Women: 115-165 g/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the reticulocyte count show

A

Amount of reticulocytes (RBC with RNA) in blood
If low: problem in production
If high: production is fine but RBC are being destroyed prematurely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Causes of hypochromic microcytic anaemia

A

Iron deficiency
Chronic disease (IL6 and hepcidin)
Sideroblastic anaemia
Thalassaemia

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

What are the haematinic deficiencies?

A

Iron
Folate
Vit B12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Haematinics and milk

A

Cows milk: contains folate but contains no iron and hinders its absorption
Goats milk: no folate but contains iron

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

Causes of iron deficiency anaemia

A

Diet
Malabsorption (coeliac disease, milk, tea)
Blood loss (menarche, GI bleeding, cancer, bleeding disorder)
(Pregnancy, rapid grow, premature birth, low birth weight)

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

Types of thalassaemia

A

Beta thalassaemia minor: one abnormal gene
Beta thalassaemia major: two abnormal genes
Alpha thalassaemia: 4 types (4 genes)
-1 gene delete:clinically silent
-2 genes deleted: alpha thalassaemia trait (mild hypochromic microcytic anaemia)
-3 gene deleted: Hb H disease (haemolytic disease)
-4 gene deleted: Bart’s Hydrops Fetalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does ferritin measure

A

Iron stores

But goes up in chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Signs and symptoms of iron deficiency

A

General symptoms of anaemiaa

Headaches (esp with activity)
Pica
Sore or smooth tongue
Brittle nails or hair loss
Koilonychia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

B12 deficiency anaemia causes

A
  • nutritional
  • malabsorption
    • gastric: surgery, pernicious anaemia
    • intestine: iléal résections fish tapeworm
  • alcohol excess

(Would get malabsorption in Crons, coeliac, CF but not bough to cause deficiency)

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

Folate deficiency anaemia causes

A 
Nutritional
Intestinal (coeliac, resection)
Excessive requirement (pregnancy)
Increase turnover (chronic haemolysis, severe skin disease)
Drugs (methotrexate, anticonvulsants )
Excess loss (dyalisis)
(Alcohol BUT beer good source of folate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Specific symptoms and signs seen in B12 and folate deficiency

A
  • insidious onset
  • mild jaundice and anaemia
  • Glossitis
  • angular Cheilitis (inflam of corners of mouth
  • neuropathy
    • peripheral (folate + B12)
    • sub-acute degeneration of the cord (B12)
    • optic (B12)
    • dementia (B12)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Iron tablet prescriptions caution and info for patient

A
  • be careful in diverticulosis and IBD because can exacerbate diarrhoea
  • can interact with antibiotics, levadopa, zinc, tetracyclins, calcium products, levothyroxins so don’t give them together (2 hour difference)
  • better absorbed on empty stomach, astobic acid helps with absorption + dpn’t take it with tea, eggs and milk products
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Def haemolytic anemia

A

Destruction of. RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Investigatons in haemolytic anaemia

A 
FBC with reticulocytes (high)
Blood film (macrocytic)
Bilirubin/lactic dehydrogenase (goes up)
Coomb’s test (DAT) (for immune haemolytic anaemia)
EMA binding
Glucose-6-phosphate dehydrogenase levels
Haemoglobin identification
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name some Haemolytic anaemia and the defects

A

Congenital

  • RBC membrane: hereditary elliptocytosis and sperocytosis
  • RBC enzyme deficiency: G^PD, pyruvate kinase
  • RBC Hb disorders: thalassaemia, sickle cell disease

Acquired:

  • auto-immune haemolysis (AIHA)
  • Wilson’s disease (copper deficiency)
  • others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hereditary spherocytosis:

  • aetiology
  • clinical presentation
  • Diagnosis
  • treatment
  • what it looks like on blood film
A

Aetiology:

  • autosomal dominant
  • abnormalities of RBC membrane proteins Spectrin and Actin

Clinical presentation:
-neonatal jaundice
-complicated by gallstones
(Blood film: micro-spherocytes (small, round dense RBC) and polychromatic macrocytes)

Diagnosis:

  • family history, FBC, reticulocyte count, blood film
  • if family history but FBC and blood film are normal: EMA-binding (fluorescence would be weaker)

Treatment:

  • regular folate
  • possible splenctomy and cholecystectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Glucose-6-phosphate dehydrogenase deficiency

  • aetiology
  • presentation
  • treatment
A

Aetiology:
-often family history OR history of neonatal jaundice (X linked)

Presentation

  • normally well between attacks
  • sudden onset of
    • feeling unwell + lack of energy
    • pale and jaundice + backache
    • passing dark urine

Treatment

  • avoid triggers :
    • fava and broad beans
    • anti-malarial drugs, aspirin, many other drugs
    • moth balls
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Sickle cell disease

  • aetiology
  • clinical presentation/complications
  • management/prevention
A

Aetiology
-beta globin variant (HbSS(/HbAS)): co -dominant autosomal recessive

Clinical presentation

  • Vaso-occlusive crisis (artérioles in bone)
  • stroke/death
  • sickle cell chest (fat emboli in lungs)
  • sequestration crisis
    • pulmonary hypertension
    • multi organ failure
  • Anaemia

Management:
Long term: keep warm, hydrated, eat well, hydroxyurea (switch to HbF)
take penicillin and folic acid, Pneumovax, Primary and secondary stroke prevention (use transcranial Doppler for detection, regular transfusions, stem cell transplant
-during crisis: analgesia, IV fluids, transfusion (severe cases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Management of Beta thalassaemia major

A

Long term blood transfusion and Iron chelation (Desferrioxamine or desferasirox)
or stem cell transplantation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Autoimmune Haemolytic anaemia

  • types
  • causes
  • diagnosis
  • treatment
A

Types: warm and cold

Causes:

  • warm: idiopathic, secondary to rheumatoid disease, lymphoma, chronic lymphatic leukaemia, drugs, ovarian teratoma
  • cold: idiopathic, secondary to EBV virus, mycoplasma pneumonia, ulcerative colitis

Diagnosis: confirming haemolysis, blood film, positive Coomb’s test (IgG in warm and complement in cold)

Treatment:
-warm: steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Affect of hepcidin on iron

A

Hepcidin degrades ferroportin

Ferroportin stimulates:

  • enterocyte Fe release
  • marrow macrophage Fe release

High transferrin saturation, IL6 increases Hepcidin
Low TFR saturation, TMPRSS6 (liver protein), GDF15 (RBC haemolysis, hypoxia decreases Hepcidin

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

Why can you get iron overload in chronic haemolysis

A

In haemolytic anaemia, increase in levels of growth differentiation Factor 15 (GDF15): which promotes iron absorption by inhibiting hepcidin

31
Q

Early sign of microcytic anaemia (esp caused by vit B12 and folic acid deficiency)

A

Hyper segmentation of neutrophils

32
Q

Coomb’s tests:
What it is
When do you use it

A

Antiglobulin test: look for antibodies to RBC

  1. Indirect antiglobulin test: ab to parties serum (used in cross matching blood)
  2. Direct antiglobulin test (DAT): detects ab to own serum (used in autoimmune haemolytic anaemia)
33
Q

What do you order for coagulation tests

A 
Prothrombin time (PT)
Activated partial thromboplastin time (APTT)
APTT 50:50
Fibrinogen levels
(Thrombin time)
34
Q

Which tests measures extrinsic pathway of clotting cascade

A 
Prothrombin Time:
II
V
VII
X
TF
Warfarin
35
Q

Which tests measures the intrinsic pathway of clotting cascade

A 
APTT
VIII
IX
X
XI
XII
VWD

More?

36
Q

Factor VIII deficiency disorder

A

Haemophilia A

37
Q

Factor IX deficiency disorder

A

Haemophilia B

38
Q

Which factor are vit K dependent

A

II, VII, IX, X

Protein C and S

39
Q

Diagnostic triad of bleeding disorders

A
  1. Personal history of bleeding
    - bruising, epistaxis, GIT, menses, urine
    - surgical and dental history, cuts and injuries
  2. Family history of bleeding
    - Known bleeding disorders
    - bleeding in family members
  3. Supportive lab tests
    - platelets
    - coagulation
    - clot stability
40
Q

What do you do for platelet tests

A

FBC
Microscopy
PFA (platelet function assay)

41
Q

What can the APTT 50:50 test show

A

If prolonged PT or APTT

And with 50:50 mixture:
If correct: factor deficiency
If fails to correct: factor inhibitor

42
Q

Haemophilia A

  • aetiology
  • clinical features
  • investigations
  • management
A

Aetiology
-Factor VIII deficiency, X linked

Clinical features (same as haemophilia B)

  • severe (levels of <1 IU/dL): frequent spontaneous bleeding (into joints and muscles). Can dad to crippling joint deformity
  • moderate (levels 1-5 IU/dL): sever bleeding post surgery + occasional spontaneous bleeds
  • mild (>5 IU/dL): bleeding post surgery + injury

Investigations:

  • personal and family history
  • prolonged APTT and reduced FVIII

Management:

  • RICE (rest, immobilise, cool, elevate)
  • factor VIII (3 times a week)
  • for mild Haemophilia: desmopressin (DDAVP): releases stores of FVIII
  • tranexamix acid (anti-fibrinolytic): oral
43
Q

Haemophilia B

  • aetiology
  • clinical features
  • investigations
  • management
A

Aetiology:
-factor IX deficiency, X linked

Clinical features (same as haemophilia A)

  • severe (levels of <1 IU/dL): frequent spontaneous bleeding (into joints and muscles). Can dad to crippling joint deformity
  • moderate (levels 1-5 IU/dL): sever bleeding post surgery + occasional spontaneous bleeds
  • mild (>5 IU/dL): bleeding post surgery + injury

Investigations:

  • personal and family history
  • prolonged APTT and reduced FIX

Management:

  • RICE
  • FIX (twice a week)
  • tranexamix acid (anti-fibrinolytic): oral
44
Q

Von Willebrand’s disease

  • aetiology
  • types
  • clinical presentation
  • diagnosis
  • management
A

Aetiology
-defective platelet function and FVIII deficiency

Types:

  • 1: partial quantitative deficiency of vWF (inherited autosomal dominant)
  • 2: qualitative abnormality of vWF (inherited autosomal dominant)
  • 3: complete deficiency of vWF (inherited recessive)

Clinical features:

  • type 1 and 2: mild features (bleeding post trauma +surgery, epistaxis and ménorragie, mucocutaneous)
  • type 3: severe bleeding, rarely joint and muscle bleeds of Haemophilia (mucocutaneous)

Diagnosis:

  • test FVIII, vW ag, vW activity
  • VW activity:vW protein ratio
    • type 1 >0.6
    • type 2 <0.6
Treatment:
-type 1: DDVAP + tranexamic factor
-type 2: vWFactor/?DDVAP (but NOT for Type 2b)
-type 3: VWFactor
\+iron
45
Q

Virchow’s triad what is it?

A

Factors that contribute to thrombosis:

Stasis of blood flow, endothelial injury and hypercoagulability

46
Q

VTE prevention in hospitals

A 
(Risk assessment tool)
Early annulation 
1. Mechanical 
-anti-embolism stockings OR
-intermittent pneumatic compression sleeves (for surgery)
2. Pharmacological 
-LMWH (SC)
-UFH (low dose unfractionated heparin) (IV)
-DOACs (oral)
NOT warfarin
47
Q

VTE risk factors

A

Age, BMI, varicose veins, air travel, immobility, pregnancy, precious VTE, thrombophilia, oestrogen therapy, plasminogen deficiency

Trauma/surgery, cardiac/resp failure, malignancy, recent MI/stroke, acute illness/infection, IBD, sickle cell

48
Q

DVT

  • symptoms/signs
  • investigations
  • differential diagnosis
A

Symptom/signs
-unilateral painful, red/hot, swollen calf (>3cm compared to unaffected leg), engorged superficial veins, ankle oedema, present Homan’s sign, cyanotic discoloration

Investigations:

  • DVT Wells score
  • proximal leg vein ultrasound, if low risk or can’t be done w/in 4h do
  • D-dimer, if pos: anticoagulants

Differential diagnosis:
Cellulitis, ruptured bakers’s cyst, muscle haematoma

49
Q

PE

  • sign/symptom
  • investigations
  • ECG findings/ABG
A

Signs and symptoms:

  • asymptomatic, acute SoB, pleuritic chest pain, Haemoptysis,dizziness, syncope
  • Pyrex is, cyanosis, tac hypnoses, tachycardia, hypotension, raised JVP, pleural rub/effusion

Investigations::

  • two-level PE Wells score
  • CT pulmonary angiogram, if can’t be carried out straight away (w/in 1h)
  • anticoagulants followed by CTPA

ECG findings: sinus tachycardia, AF, right heart strai (RBBB, right axis deviation), S1Q3T3 pattern

ABG hypoxia/T1RF

50
Q

VTE treatment

A

LMWH or fondaparinux
(If patient high risk of bleeding: UFH)

Start warfarin and when INR>2, stop LMWH

51
Q

What are the different fates of thrombus

A

Dissolution (fibrinolysis)
Propagation
Recanaliation
Embolisation

52
Q

def embolus

A

Material which is transported in the blood and lodged at different site
Can be gaseous or solid

53
Q

Causes of normocytic anaemia

A 
Acute blood loss
Chronic disease (or decreased MCV)
Bone marrow failure
Renal failure
Hypothyroid (or increased MCV)
Haemolysis (or increased MCV)
Pregnancy
54
Q

Causes of macrocytic anaemia

A 
B12/ folate deficiency 
Alcohol excess
Reticulocytosis
Cytotoxics
Myelodyaplastic syndromes 
Marrow infiltration 
Hypothyroidism 
Anti folate drugs
55
Q

what is the cell based model of haemostasis

A

initiation
amplification
propagation

56
Q

what is disseminated intravascular coagulation

A

process of clotting and fibrinolysis dysregulated: widespread clotting and bleeding

57
Q

how does DIC occur (pathophysiology)

A

release of procoagulant materials (i.e. TF) or via cytokine pathways (inflame response):
widespread coagulation activation leads to platelet and coagulation depletion + dysregulated fibrinolytic activation

58
Q

causes of DIC

A
  • malignant disease
  • septicaemia
  • haemolytic transfusion reactions
  • obstretic causes
  • trauma, burns, surgery
  • liver disease
  • snake bite
59
Q

what is D dimer a breakdown product of?

A

fibrin

60
Q

treatment of DIC

A
  • keep warm
  • sort out causes
  • reverse drugs:
    • clotting factors
    • fresh frozen plasma
    • platelets
    • blood transfusion?
  • -> TRANSFUSION PROTOCOL
61
Q

what are the different levels of the neck

A
  1. submandibular triangle

sternomastoid muscle divided into 3 areas:

  1. skull base to hyoid bone
  2. hyoid bone to circa cartilage
  3. cricoid cartilage to clavicle
  4. posterior triangle
  5. around thyroid cartilage
62
Q

what is the normal shape of a lymph node, and what is abnormal

A

normal: oval shaped
abnormal: football shape

63
Q

when does lymphadenopathy become relevant clinically?

A
  • adult: >1cm or 1.5 at level 2
  • paediatrics: > 2cm
  • any node w/ associated head neck symptoms that are persistent
64
Q

what are causes of lymphadenopathy?

A
  • inflammation (infection TB, HIV, bacterial etc)

- malignant (metastatic, lymphoma)

65
Q

what imaging techniques are good for what cervival lymphadenopathy

A

US: thyroid and benign nodes

CT: primary disease below hyoid

MRI: primary disease above hyoid

66
Q

what investigations to do in cervical lympadenopathy?

A

-full herd and neck exam including endoscopy
-imaging: US, CT, MRI, PET
biopsy FNA core

67
Q

risk factors for tonsil and tongue cancer

A

smoking
drinking
HPV

68
Q

salivary gland lump differentials

A
  • stones (recurrent tender with meals
  • tumour (persistent slow grown)
  • malignant (rapid growth , pain)
69
Q

what primary sites metastasise to cervical nodes

A

breast, stomach, lung, pancreas and thyroid

70
Q

what diseases have bilateral hi mar lymphadenopathy

A
  • lymphoma
  • glandular fever
  • TB
  • disseminated malignancies
  • sarcoid
  • ?
71
Q

presentation of tuberculous lymphadenopathy

A

chronic, painless mass in the neck (cold abscess)

may rupture through the skin forming chronic discharging sinus

72
Q

Hodgkin’s disease: age affected

A

bimodal distribution
15-30
50+

73
Q

types of Hodgkin’s disease by histological classification

A
  • lymphocyte predominant
  • nodular sclerosis (bands of collagen)
  • mixed cellularity
  • lymphocyte depleted

Year 3 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions