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BDS2 - diseases of the blood > anaemia > Flashcards

anaemia Flashcards

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

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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
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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

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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)
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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)
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6
Q

what are haematinics

A

what makes haem

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7
Q

what are examples of haematinics

A
  • iron
  • vitamin b12
  • folic acid (folate)
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8
Q

what are some iron sources

A
  • meat
  • green leafy vegetables
  • iron tablets
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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
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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

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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
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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
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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

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14
Q

can vitamin b12 be made ourselves in our body

A

No. need bacteria to do it

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15
Q

how can someone be deficient in vitamin b12

A
  • can’t absorb it

- they’re diet is not including it

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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
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17
Q

what haematinics allow dna synthesis

A

folic acid and vitamin b12

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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

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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
Q

what happens with haematinics deficiencies

A
  • 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
Q

what is thalassaemia

A

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
Q

what causes thalassaemia

A
  • genetic mutation of globin chains
  • alpha chains = alpha thalasaemia (more common in Asians)
  • beta chains = beta thalasaemia (more common in Mediterranean’s
28
Q

what are the clinical effects of thalassaemia

A
  • 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
Q

how to manage thalassaemia

A
  • 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
Q

what is sickle cell anaemia

A

abnormal globin chains

31
Q

what happens in sickle cell anaemia

A

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
Q

is sickle cell anaemia a dominant trait

A

no

  • if heterozygous then the patient will have the trait but not the disease
  • if homozygous then the patient will have the disease
33
Q

in who is sickle cell anaemia most common

A

in African people

- those who have it in the UK will have African heritage

34
Q

what cause losses that cause anaemia

A
  • 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
Q

what causes increased demands that causes anaemia

A
  • 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
Q

how can the size of a RBC give a clue of the problem

A
  • microcytic = small RBC (iron deficient, thalassaemia)
  • macrocytic = large RBC (B12/folate deficient, cretics)
  • normocytic = normal RBC (bleed, renal, chronic disease)
37
Q

what are macrocytic RBC’s

A
  • 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
Q

what are microcytic RBC’s

A
  • smaller than they should be

- paler in colour due to lack of Hb pigment (hyochromic)§

39
Q

what are reticulocytes

A
  • 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
Q

what must you look at to diagnose anaemia

A
  • 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
Q

what are some clinical signs of anaemia

A
  • pale mucosa
  • smooth tongue (iron deficient)
  • beefy tongue (vit b12 deficient)
  • but often patients don’t have these signs
42
Q

anaemia signs

A
  • pale

- tacchycardia as RBC’s pushed faster round body

43
Q

anaemia symptoms

A
  • tired and weak
  • dizzy
  • shortness of breath
  • palpitations
  • sometimes get enlarged liver - rare
44
Q

what investigations are taken

A
  • 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
Q

what age group is git bleeding more common

A
  • in older patients
  • can start with a polyp then becomes malignant (carcinoma)
  • different ages have different reasons for bleeding
46
Q

treatment for anaemia

A
  • 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
Q

what are dental aspects to think about due to anaemia

A
  • 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

BDS2 - diseases of the blood (5 decks)

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