2. Anaemia Flashcards
(95 cards)
1
Q
What are the components of haemoglobin?
A
Haem and globin. They are both haemoproteins.
2
Q
Describe the structure of haemoglobin
A
Tetramer with 4 polypeptide pairs. There are two pairs of unlike polypeptide chains : 2 alpha pairs and 2 beta pairs.
3
Q
Where is the haems contained?
A
In a hydropbic compartments of the globins
4
Q
How many irons can fit on each haemoglobin?
A
4 Fe 2+
5
Q
What is the redox reaction?
A
Fe 2+ to Fe3+ (ferrous state to ferrate)
6
Q
In what oxidation state is iron when in circulation?
A
Fe2+
7
Q
Why is iron Fe2+ when in circulation?
A
in order to maintain osmotic equilibrium
8
Q
How to blood cells generate ATP?
A
Through the embden-meyerhof pathway
9
Q
How do red cells generate power?
A
Through NADPH though hexose-monophosphate pathway
10
Q
How is iron transferred around the body?
A
1) Iron binds to transferrin to form an iron-transferrin complex
2) Iron-transferrin complex transported to cells with transferrin receptors
11
Q
What is ferritin?
A
Stored iron
12
Q
Besides ferritin, what else can iron be stored as?
A
Haemosiderin
13
Q
Where is ferritin stored?
A
Spleen, liver, pancreas and bone marrow
14
Q
How many Fe mg does the western diet have?
A
10-15 mg-
15
Q
Where is the iron absorbed?
A
5 - 10% through small intestine
16
Q
Humans lose 1mg of iron a day. How?
A
through faeces, hair, skin, menstruation
17
Q
Where can iron be found in the diet?
A
Red meat - liver in particular (animal iron is more readily absorbed than plant-based iron)
Egg yolk
Fish - sardines, tuna, salmon
Cereals, Wholemeal bread
pluses, legumes, veg, nuts, prunes and fortified foods
18
Q
What is the meaning of anaemia?
A
To have below normal levels of haemoglobin
19
Q
What are the normal ranges of haemoglobin for males and females?
A
male 130-170g/L. Female 120-155g/L
20
Q
How is anaemia classified?
A
By the size of the red blood cells
21
Q
What is microcytic anaemia? Mean cell volume?
A
Small red cells. MCV= <78fl/L
22
Q
What is macrocytic anaemia? Mean cell volume?
A
Large red cells. MCV= >100fl/L
23
Q
What is normocytic anaemia? Mean cell volume?
A
Normal red cell. MCV = 77-100fl/L
24
Q
What kind of anaemia do microcytic cells cause?
A
Iron deficiency anaemia, thalassaemia, anaemia of chronic disease (and other haemoglobin disorders)
25
What are the two subcategories of macrocytic anaemia?
Megaloblastic anaemias and non-megaloblastic anaemias
26
What disorders/deficiencies may cause macrocytic megaloblastic anaemia?
B12 deficiency, Folic acid deficiency, and auto-immune disease (pernicious anaemia)
27
What is pernicious anaemia
anaemia caused by the auto-immune system
28
What disorders may cause macrocytic non-megaloblastic anaemia?
Liver disease, myeloidysplastic syndrome (MDS)
29
What kind of anaemias are caused by normoblastic cells?
Haemolytic, anaemia of chronic disease
30
If a patient suffers with acute blood loss, which kind of anaemia are they likely to have?
normocytic anaemia
31
What is the most common type of anaemia?
Iron deficiency anaemia
32
What are the two main causes of iron deficient anaemia?
Iron supply does not meet demand due to: Mean cell volume reduced, mean cell haemoglobin reduced.
33
What do microcytic anaemia red cells look like?
Central area of pallor is pale and empty. Small red cells.
34
What are the three main stages of iron deficient anaemia?
Iron repletes, iron depletes, iron deficient
35
What are the physical causes of iron deficient anaemia?
chronic blood loss due to menstrual cycles, gastrointestinal issues.
Increased demands due to growth or pregnancy
Malabsoption form stomach (due to gastrectomy)
Poor diet
36
How quickly do the clinical features of iron-deficient anaemia arise?
slowly
37
What are the clinical features of iron-deficient anaemia
pallor, fatigue, brittle hair and nails, dysphagia (issues swallowing) glossitis (tounge swelling), abnormal appetite, lassitude (lethargy) and trachychardia
38
What are the laboratory findings when studying a blood sample of an iron-deficient anaemia patient
hyperchromic (pale red cells)
microcytic cells
raised platelet count
Bone marrow will show absence of ferritin
Erythroblasts will be ragged/have an irregular cytoplasm
There is a reduced serum ferritin level and low serum iron levels
Raised serum transferrin receptors present (due to no transferrin binding to it)
39
What is the treatment for iron deficient anaemia?
Oral iron tablet taken 3x a day for 4-6 months.
| IV iron for patients with malabsorption (which is the true cause of the illness)
40
What response would you expect to see after treating iron-deficient anaemia?
You would expect a an increase in reticuloctye formation and circulation after 7 days of treatment
41
What is the function of B12?
Coenzyme for 2 biochemical reactions:
1) methylation from homocystein to methionine
2) converts methylmalomyl coA to succinyl co A
42
What would happen is the coenzyme reactions of B12 could not occur?
Less precursors for DNA synthesis and myelin production (for myelin sheath)
43
What is the effect of abnormal DNA synthesis on RBC production?
Erythroblasts in bone marrow show abnormal maturation (maturation arrest - they are premature)
The maturation of the nucleus of the cell is delayed in relation to the cytoplasm
No reticuloctye production
44
How many mg of B12 do adults require per day?
1ug
45
How many mg of B12 would you expect in the normal, balanced diet?
10-15ug
46
How long is B12 stored for?
2-4 years
47
Where is B12 stored in the body?
In the liver
48
Describe the process of absorption of B12 by the body
B12 absorbed in the illium of the small intestine by binding to intrinsic factors that have been secreted by the stomach. (ileum has receptors for these intrinsic factors so B12 absorbed when attatched)
49
How is B12 transported through the body?
Travels through blood plasma when bound to transcobalamin
50
How is B12 lost from the body?
Faeces and bile excretions
51
What are the dietry sources of B12?
```
Animal based produce:
liver, kidney, heart, red meat
clams, oysters, seafood,
Egg, cheese, milk, yoghurt,
fortified foods
```
52
What are the main causes of B12 deficiency? (6)
Inadequate diet: vegans
Malabsoption: 1) due to gastrectomy (removal of stomach). 2) intrinsic factor deficiency so no absorption in ileum
Intestinal issues: Crohn's, tape worm, ileal resection (due to crohns)
Excess utilisation of B12: 1)pregnancy 2)haematological disorder
Liver disease
Drug treatment
53
What type of anaemia are you likely to experience with a B12 deficiency?
Megaloblastic anaemia
54
What is megaloblastic anaemia
Type of macrocytic anaemia where DNA does not pass the G2 phase so continuously divides (leading to macrocytosis)
55
What are the clinical features of megaloblastic anaemia (B12 deficiency)
```
Slow onset
Mild jaundice
Glossitis
Tingling of hands and feet
Reduced platelet count
Raised biliruben levels
Low serum B12
Hypercellular bone marrow (maturation arrest)
Raised serum methiomalonic acid and homocytein levels
```
56
Treatments of B12 deficiency?
1mg of hydroxycobalamin injected intramuscularly everyday 3 days until 6 injections have been given in total. Thereon after its just 1 every 3 months unless cause of B12 deficiency is resolved.
57
What can be given alongside B12 treatment? Why?
K+ given at same time as B12 in severe cases as some people will die suddenly due to sudden drop in K+
58
What is B12 neuropathy?
subacute degernation of the cord: progressive damage to peripheral sensory nerves (spinal cord, brain, peripheral nerves)
59
Describe what the clinical features of B12 neuropathy would be
Clinical features mainly affect lower limbs. Tingling feet, difficulty walking (abnormal gait), falling often, optic atrophy, psychiatric conditions
60
What is the cause of B12 neuropathy
Accumulation of homocystein and reduction in methionine in nervous tissues
This causes defective myelination of myelin
Abnormal fatty acids form around cell and nerves
61
What is pernicious anaemia?
It is an autoimmune disease where auto antibodies attack gastric parietal cells. Parietal cells secrete intrinsic factors that bind to B12 and are later absorbed by the ileum. If parietal cells are attacked there will be no resorption of B12.
62
What is the prevalence of pernicious anaemia?
Affects more women than men (1.6:1). Patients tend to be over the age of 60 and although common to all races, most common to northen europeans
63
What secondary disease can result from pernicious anaemia?
Carcinoma of the stomach
64
What is folic acid the parent group of?
the folates
65
What does pteroglutamic acid refer to?
Folic acid
66
What vitamin is folic acid?
B9
67
How long is folic acid stored for?
3 months
68
Can humans synthesise folic acid?
No
69
When preparing food that is rich in folic acid, what must you not do to it?
Cook it: folic acid is heat sensitive and is destroyed by cooking
70
Where is folic acid absorbed?
Jejunum
71
What causes folic acid deficiency
malfunction of the small intestine: coeliacs disease, crohns disorder, tropical sprue
72
What is the role of folic acid?
Required for metabolic reactions: homocystein to methionene, serine to glycine, DNA precursor synthesis
Necessary for the production of new cells
Substrates are important for reactions that involve B12 (homocystine to methionene and methylolmalomyl coA to Succinyl Co A)
73
What does folic acid deficiency hinder?
Cell division and DNA synthesis
74
What are the sources of folic acid?
Leafy veg (spinach), turnip, lettuce, liver, beans, peas, breakfast cereals, bananas, melon, lemons
75
What are the cinical features of folic acid deficiency?
Same as B12 but less severe but does not cause neuropathy
76
How quickly do symptoms appear?
Quickly as there arent as many reserves
77
What causes folic acid deficiency?
Usually dietry - alcoholism or intestinal disorders
78
When can demand for folic acid increase?
Pregnancy and during rapid cell division (cancer)
79
What kind of disorder is spina bifada?
neural tube defect
80
What cuases spinal bifada?
B12 or folic acid deficiency in early pregnancy. The lower the serum B12 or folate, the greater the incidence.
Homocystein builds up in the featus and impairs myelination of protiens and lipids
81
What is the treatment for spina bifada?
No treatment just dietry supplements in early pregnancy
82
What other abnormalities can arise from B12/folic acid deficiency?
- sterility of either sex
- abnormal morphology of cervix, bladder and other epithelia
- cleft lip/pallate in feotus/newborn (folic acid supplements at conception/early pregnancy)
- melanine pigmentation problems
- CV and malignent disease
83
What is normocytic anaemia?
Normal sized red cells but just not enough of them
84
What causes normocytic anaemia?
Acute blood loss and premature destruction of red cells
85
What would cause the premature distruction of red cells?
Haemolytic anaemia or chronic disease
86
What are 3 diseases associated with haemolytic anaemia?
sickle cell, autoimmune disorders and hereditary spherocytosis
87
What 4 kinds of heritary disease can cause haemolytic anaemia?
rheumatoid athritis, cancer, kindey disease or drug treatment
88
What is haemolytic anaemia?
increased rate of RBC breakdown
89
What are the two subcatercategories of haemolytic anaemia?
Hereditary or aquired
90
What causes hereditary haemolytic anaemia? (3)
1) Red cell membrane defects: sperocytosis which causes RBC to be shperical as opposed to biconcave. Ellipotosis where RBC are elliptical shape.
2) Defective red cell metabolism: G6PD deficiency. Pyruvate kinase deficiency.
3) Disorders of haemoglobin synthesis: sickle cell, thallasaemia
91
What are the two subcategories of acquired haemolytic anaemia?
Extra corpuscular and environmental
92
What causes extracorpuscular haemolytic anaemia?
haemolytic disease of a newborn, autoimmune haemoltic anaemia, DIC and heart valve replacement
93
What casues environental haemolytic anaemia?
Drug induced, march haemoglocinuria and infetion of malaria, ecoli
94
What are the clinical effects of haemolyic anaemia?
Pallor, mild fluctating jaundice
95
What would lab findings show if looking at haemolytic anaemia blood?
increased RBC breakdown: biliruben will be raised, hepatoglobin reduced. (hepatoglobin is binded to released haem and taken to spleen)
increased RBC production: increased reticulocytosis, bone marrow erthythrocyte hyperplasia (bone marrow enlarged due to extra production of RBC produced in its marrow)
Damaged red cells: morphology shows fragments, microspocytes and elliptocytes.
