Anaemia I Flashcards

1
Q

What happens to Hb according to the following factors?

a) Increasing age
b) Men
c) Smokers
d) Altitude + what effect does altitude have on EPO?

A

a) Decreases
b) Increases (due to hormones)
c) Increases to account for CO
d) Increases + increases EPO due to hypoxia.

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2
Q

PREGNANCY + ANAEMIA

1A) What affect does pregnancy have on Hb?
1B)In which trimester(s) is it affected?

2A) What affect does pregnancy have on plasma volume?
2B) Why is this an advantage?

3) What risk does having a high Hb have in pregnancy?

A

Decreases
2nd/3rd trimester - baby taking up more O2

Dilutes (increases)
Blood loss from birth is diluted so you lose less RBC.

3) Pre-eclampsia

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3
Q

1) Where in the world is anaemia most prevalent?

2) What factors increase the prevalence here?

A

1) Sub saharan Africa (>40%)
2) Low dietary iron,
worse post-natal care,
have more children.

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4
Q

HAEMOGLOBIN

1) HbA consists of?
2) HbF consists of?
3) Which has a higher affinity for oxygen + why?
4) Does myoglobin have a higher affinity + why?

A

1) 2 alpha + 2 beta
2) 2 alpha + 2 gamma
3) HbF - to allow oxygen to cross the placenta
4) Yes - to offload oxygen to muscles.

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5
Q
Features of Anaemia: 
P?
P?
P ?
T?
S?
C?
A
Pallor 
Peripheral oedema 
Palpitations 
Tachycardia 
SOB (esp. on exertion)
Confusion (esp. in elderly)
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6
Q

IRON-DEFICIENCY ANAEMIA

1) What is the minimum amount of iron required to make RBC?
2) Features: K,A,V?
3) What histological findings would you find?
4) Affect on ferritin/serum iron?
5) What is ferritin?

A

1) 4g
2) Koilonychia (spoon nails)
angular stomatitis
pharyngeal/oesophageal varices (dysphagia)
3) microcytic hypochromic (pale) anaemia w/ small RBC that have large central pallor. pencil cells ( long, thin RBC)
4) low and low
5) intracellular protein that stores iron - acts as a buffer that stores + releases.

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7
Q

IRON-DEFICIENCY ANAEMIA Causes

Four main causes

1) If you only need 1mg of Fe per day, what physiological causes mean your susceptible to anaemia?
2) Who gets a dietary deficiency?
3) What diseases lead to malabsorption of iron?
4) What type of blood loss would lead to iron deficient microcytic anaemia?

A

1) periods where demand is higher:
- Infancy (growing)
- Menstruation (losing blood)
- Pregnancy (blood for foetus)
2) Vegetarians - most iron absorption from meat.
3) Coeliacs, crohn’s and malignancy
4) Chronic and slow - acute is normocytic anaemia.

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8
Q

IRON-DEFICIENCY ANAEMIA Tx

1) how do you treat physiological anaemia?
2) How do you treat males + post menopausal women?
3) What determines Tx for pre-menopausal women + what would the consequential Tx be?

A

1) Iron (oral)
2) Ix: colonoscopy or barium enema
3) GI Symptoms?
- If Y: colonoscopy or barium enema,
- if N: iron (oral)

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9
Q

What is MCV?
Unit?
How do you differ between micro-, normo- and macrocytic?

A
Mean Cell Volume 
Femtolitre (1fL ) 
Micro = <83 
Normo = 83-96 
Macro = >96
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10
Q

CLASSIFICATION OF ANAEMIA:
(following microcytic, normocytic or macrocytic?)

a) iron deficiency anaemia?
b) thalassaemia?
c) anaemia of chronic disease?
d) acute blood loss?
e) haemolysis?
f) liver disease/alcohol excess?
g) Vit B12/folate deficiency?
h) Hypothyroidism?

A

a) micro
b) micro
c) micro + normo
d) normo
e) normo + macro
f) macro
g) macro
h) macro

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11
Q

ANAEMIA OF CHRONIC DISEASE

1) what affect does macrophages have on iron?
2) By how long does it shorten RBC survival?
3) 4 main causes: M, E, C, K?
4) Tx?

A

1) destroys iron therefore failure of iron transport from reticuloendothelial system
2) 120 to 105 days
3)
- Malignancy (reduce RBC production)
- Endocrine disorders
- Chronic infection
- Kidney failure - less EPO - anaemia
4) Treat underlying cause + give EPO/iron supplements

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12
Q

VIT B12 DEFICIENCY

1) What is the role of Vit B12?
2) Where is it found + who is this a problem for?
3) What type of anaemia does this cause?
4) What is the role of IF in B12 absorption + where is IF made?
5) Causes of B12 deficiency - D, M, P?
6) Why is there a delay in signs of low B12?

A

1) DNA synthesis and maturation of developing RBC in marrow.
2) animal produce - vegans
3) MEGALOBLASTIC macrocytic anaemia
4) IF protects B12 in stomach + helps its absorption in terminal ileum, IF made in gastric parietal cells.
5) Dietary, Intestinal malabsorption (crohns), pernicious anaemia (low IF)
6) Liver has large stores.

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13
Q

FOLATE DEFICIENCY

1) where is folate absorbed?
2) From what foods can you source it from?
3) Low folic acid leads to what type of anaemia?
4) Causes of folate deficiency?

A

1) Jejunum
2) Nuts, cereals and veg.
3) MEGALOBLASTIC macrocytic
4) Dietary, malabsoprtion (crohns) and pregnancy (^utilisation)

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14
Q

What clinical features are specific to Vit B12 + folate deficiency?

A
Jaundice (^RBC breakdown) 
Glossitis 
Neuro deficits (parasthesia + cognitive deficit
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15
Q

What is the Tx for Vit B12 + folate?

Which do Tx do you administer first: folate or B12 + why?

A

1) Tx underlying cause
2) Vit b12 iM Injection
3) oral folic acid

B before F
As you can get severe neuro problems otherwise

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16
Q

What MEGAloblastic changes do you see in Vit B12 + folate deficiency?

A

RBC progenitor have REALLY BIG nuclei (low B12 means DNA replication is stopped so nuclei gets bigger and bigger) .

Neutrophils have 7-8 lobes instead of 2-3 for same reason.

17
Q

HAEMOLYTIC DISEASE OF NEWBORN

1) what type of sensitivity reaction is it?
2) WHat type of rhesus does ma + pa have to be?
3) WHat rhesus does first baby have to be?
4) In response what does mother do + leaving what type of antibodies in her blood after delivery?
5) What type of resus does second child have to be ?
6) What happens as a result?

A

1) Type II
2) if father is Rh+ and mother is Rh-
3) +ve
4) anti Rh antibodies production
5) +VE
6) anti-Rh antibodies will cross placenta and damage fetal RBC

18
Q

HAEMOLYSIS

1) Def? - Two types?
2) Normal to have low level of haemolysis - what compensates this?

A

1) ^ destruction of RBC - intravascular (RBC rupture in vessels - ^ free Hb). Extravascular (^clearance in reticuloendothelial system)
2) EPO

19
Q

HAEMOLYTIC ANAEMIA

What is a classic feature of:

1) extravascular haemolysis?
2) - for chronic haemolysis?
3) - for intravascular haemolysis?
4) In all types of haemolysis?

A

1) Splenomegaly
2) Gallstones
3) Haemaglobinuria
4) Anaemia + Jaundice

20
Q

Name four inherited causes of haemolytic anaemia?

A

Inherited:

1) Hereditary Spherocytosis (spherical RBC - autosomal dominant - on blood smear RBC have lost central pallor
2) Glucose - 6 - phosphate dehydrogenase deficiency: X-linked recessive, enzyme protects against oxidative stress.
3) Pyruvate Kinase deficiency - autosomal recessive - causes haemolysis
4) Hb problem - sickle cell or thalassaemia.

21
Q

What does MAHA stand for?

Why does it cause acquired haemolytic anaemia?

A

Microangiopathic haemolytic anaemia

RBC get sliced by passing through small vessels.

22
Q

DIAGNOSING HAEMOLYTIC ANAEMIA

How:

1) prove that RBC production is increased?
2) prove that ^^RBC destruction?

3) What do you see on blood film for
a) MAHA
b) HS + autoimmune haemolytic anaemia?
c) Tx for HELLP + what does HELLP stand for?
4) Coomb’s test show?

A
1) 
Reticulocytosis (^young RBC) 
Polychromasia (reticulocytes have blue tinge) 
Folate deficiency (due to ^^RBC turnover) 
2) 
^unconjugated bilirubin 
^LDH 
low haptoglobins (cells that mop up Hb) 
Haemoglobinuria 

3)
a) Red cell fragments = MAHA
b) Spherocytes/loss of central pallor = HS or autoimmune haemolytic anaemia
c) Tx: baby delivery, Haemolysis, Elevated Liver enzymes + low platelets

4) Look for immune cause, if +ve = autoimmune cause.

23
Q

HAEMOGLOBINOPATHY

1) What is haemoglobinopathy?
2) Alpha + beta subunit are on which chromosomes + how many of each?
3) How many alpha and beta do you get from parents?
4) alpha or beta problems more common?
5) What are the two most common haemoglobinopathies?
6) Alpha + beta affect whom?
7) Defects in beta occur when?

A

1) Inherited genetic defect of Hb
2) 2 alpha on 16 + 1 beta on 11
3) 4 alpha + 2 beta
4) beta - less of them
5) Sickling disorders + thalassaemia
6) Alpha = foetal + adult, beta = adult
7) 6 months (when switch from HbF to HbA occurs)