anaemia Flashcards
(47 cards)
1
Q
what is anaemia
A
reduction in haemoglobin in the blood- but not necessarily decrease in red blood cells
- the Hb concentration of the patient is below normal for the population
2
Q
what can cause anaemia
A
- reduced production of RBC’s (RBC’s should last 120 days and Hb be recycled in that time but if reduced RBC then less HB in the body)
- increased losses
- increased demand
3
Q
what are the 2 situations that produces anaemia
A
1 - reduced normal red cells production
2 - normal amount of RBC’s but not enough HB to go inside
4
Q
what happens in the 1st situation that produces anaemia
A
- reduced normal red cells production
- bone marrow failure
- making rbc’s but not enough
- aplastic anaemia (acellular as not making cells)
5
Q
what happens in the 2nd situation that produces anaemia
A
- normal amount of RBC’s but not enough Hb to go inside
- could be problem with harm production or globin chain production
- deficiency in Fe, folate and vitamin B12
- abnormal globin chains (thalassemia, sickle cell anaemia)
- chronic inflammatory disease (rheumatoid arthritis)
6
Q
what are haematinics
A
what makes haem
7
Q
what are examples of haematinics
A
- iron
- vitamin b12
- folic acid (folate)
8
Q
what are some iron sources
A
- meat
- green leafy vegetables
- iron tablets
9
Q
how is iron absorbed
A
- complex process
- change iron type to another to be absorbed
- type of iron in meat is good as it is easier to enter the cell as it is in the blood containing haem form
- once in the cell, it is stored as ferritin then transferred to the blood to be made into haem again
10
Q
why do you measure ferritin in the blood instead of iron
A
it is more stable and so gives a better prediction of how much iron is in the blood
11
Q
what are some disease that can affect iron absorption
A
- small intestine diseases = make it difficult to absorb
- achlorhydia = lack of stomach acid so no conversion of non-haem iron to haem iron, can be drug induced by proton pump inhibitors as these get rid of all acid in stomach
- coeliac disease = lose the small villi on the surface of endothelial wall of cell so lose surface area so less ability to absorb
12
Q
how can iron be lost
A
- from anything that makes you bleed
- gastric ulcers and erosions = bleed into the gut is not obvious as it is chemically changed to black in the GIT so not noticeable in stool
- inflammatory bowel disease = Crohn’s disease, ulcerative colitis (expose surface of connective tissue causing bleeding)
- bowel cancer = colonic cancer, rectal cancer
- haemorrhoids = can be noticed as blood doesn’t pass through GIT so still seen as red in stool
13
Q
how can vitamin b12 be taken
A
- difficult to get outside of animal products
- milk, eggs, cheese, chicken, fish, meat and yoghurt etc
14
Q
can vitamin b12 be made ourselves in our body
A
No. need bacteria to do it
15
Q
how can someone be deficient in vitamin b12
A
- can’t absorb it
- they’re diet is not including it
16
Q
how is vit b12 used in the body
A
- intrinsic factor combines with vitamin b12 in the stomach
- receptors at the end of the ileum are designed to pick up the intrinsic factor and vit b12
- vitamin b12 can be stored in the liver for 3 years
17
Q
what haematinics allow dna synthesis
A
folic acid and vitamin b12
18
Q
when would you think that there is an absorption problem
A
if both the folic acid and intrinsic factor are down in concentration - then not diet problem of lack of vitamin b12
19
Q
how is vitamin b12 usually replaced
A
with an injection
20
Q
how can you get vitamin b12 deficiency
A
- lack of intake
- lack of intrinsic factor = autoimmune stomach disease, pernicious anaemia (don’t make intrinsic factor), gastric disease
- disease of the terminal ileum = Crohn’s disease, receptors don’t work
21
Q
what are the sources of folic acid
A
- 12 foods rich in folate
- leafy greens, asparagus, brocoli, papaya and oranges, avocado, seeds and nuts, Brussel sprouts, beans pease and lentils, okra, cauliflower, beets and bell peppers
22
Q
how can you be folic acid deficient
A
- lack of intake = peculiar diet habits
- absorption failure = jejunal disease (coelia disease), usually seen co-deficient with iron
- can lead to neural tube defects in foetus
23
Q
how is the neural tube defected
A
- folic acid deficiency
- folic acid is needed for nerve maturation = children with spina bifida usually due to lack of folic acid during pregnancy
- spina bifida = neural tube not closed properly so spinal cord open to world through a hole
- defects can’t be fixed
24
Q
how to you determine which haematinic a patient is deficient in
A
take blood tests
25
what happens with haematinics deficiencies
- can be deficient in these without any effect on the Hb yet
- if these deficiencies are left untreated, they will eventually lead to anaemia = low Hb
26
what is thalassaemia
normal haem production but change in globin production - genetic
- make normal amounts of haem but the globin chains that wrap up haem are deficient
27
what causes thalassaemia
- genetic mutation of globin chains
* alpha chains = alpha thalasaemia (more common in Asians)
* beta chains = beta thalasaemia (more common in Mediterranean's
28
what are the clinical effects of thalassaemia
- most people go through life not knowing
- chronic anaemia
- marrow hyperplasia = skeletal deformities, as bone having to make more RBC's it grows and changes shape
- spleenomegaly = if more RBC's wrong then spleen needs to remove these faster so increases in size
- cirrhosis
- gallstones = more recycling of haem in body than normal
29
how to manage thalassaemia
- blood transfusions = but need to ensure not to give an iron overload as that then causes more problems
- if patient is coping, then best not to treat it
30
what is sickle cell anaemia
abnormal globin chains
31
what happens in sickle cell anaemia
globin chains change shape in low O2 environment
- go from flat to bent, means rbc's can't get through capillaries and cause cause blockages leading to hypoxia or tissue ischaemia (pain and necrosis)
32
is sickle cell anaemia a dominant trait
no
- if heterozygous then the patient will have the trait but not the disease
- if homozygous then the patient will have the disease
33
in who is sickle cell anaemia most common
in African people
| - those who have it in the UK will have African heritage
34
what cause losses that cause anaemia
- normal red cells but fewer number due to bleeding =usually GI bleeding
- abnormal red cells = decrease in RBC life span so need to make RBC quicker, autoimmune, hereditary (unusual)
35
what causes increased demands that causes anaemia
- pregnancy = you expand blood volume from 5-6litres so need to make more RBC to cope with expanding volume, conc. will be diluted
- malignant disease = in tumours, patients tend to have more RBC's whereas in pregnancy they have fewer in proportion to blood volume but still more than before
36
how can the size of a RBC give a clue of the problem
- microcytic = small RBC (iron deficient, thalassaemia)
- macrocytic = large RBC (B12/folate deficient, cretics)
- normocytic = normal RBC (bleed, renal, chronic disease)
37
what are macrocytic RBC's
- bigger than meant to be
| - have a bigger spread of different sizes of RBC's = in a normal blood sample, distribution should be even
38
what are microcytic RBC's
- smaller than they should be
| - paler in colour due to lack of Hb pigment (hyochromic)§
39
what are reticulocytes
- almost mature RBC's
- still got some bit inside them
- released early into circulation to replace the losses (reticulocytosis)
- will raise mean cell volume (size)
- in a microscope you will see purple fragments in them which mature RBC's don't have
40
what must you look at to diagnose anaemia
- what is the Hb
- what are the RCC and HCT (HCT = cells to liquids)
- is it cell deficiency or Hb formation deficiency
- what is the MCV
41
what are some clinical signs of anaemia
- pale mucosa
- smooth tongue (iron deficient)
- beefy tongue (vit b12 deficient)
- but often patients don't have these signs
42
anaemia signs
- pale
| - tacchycardia as RBC's pushed faster round body
43
anaemia symptoms
- tired and weak
- dizzy
- shortness of breath
- palpitations
- sometimes get enlarged liver - rare
44
what investigations are taken
- history
- FBC - full blood count to get ferritin and folate and fit b12
- FOB (faecal ocult blood) = looks for changes Hb, able to identify blood that's been changed black in stool
- endoscopy/colonoscopy = go right through GIT to see bleeding
- renal function = if kidney not working then no RBC will be getting made as it makes erythropoietin
- bone marrow examination
45
what age group is git bleeding more common
- in older patients
- can start with a polyp then becomes malignant (carcinoma)
- different ages have different reasons for bleeding
46
treatment for anaemia
- need to treat cause before anything else
- replace haematinics
* iron sulphate 200mg tablets for 3 month
* 1mg IM vit b12 x6 then 1mg/2 months
* 5mg folic acid daily
- transfusions needed if production failure
- erythropoietin needed if production failure due to renal failure
47
what are dental aspects to think about due to anaemia
- GA = need to think about O2 capacity
- deficiency states = Fe usually, mucosal atrophy, candidiasis, ROU, dysaesthesia (abnormal sensation when touched)
- check haematinics in mucosal diseases
- sickle cell disease
* check all patients of negroid background before GA
* do sickle dex test even is no anaemia
