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Kirsty 3.1 > CPT2: Anaemia 2 > Flashcards

CPT2: Anaemia 2 Flashcards

1
Q

What is the most common type of anaemia?

A

Iron deficient Anaemia

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2
Q

What is iron deficient anaemia classed as based on morphology?

A

Microcytic anaemia

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3
Q

What is iron defiency anaemia?

What limits defines anaemia in men and women?

A

Iron defiency anaemia occurs in the more severe stages of iron defiency when the body is iron defient to the point RBC prodution is reduced.

According to NICE:

  • Men: Hb below 130g/L
  • Women: Hb below 120g/L (Non pregn)
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4
Q
  1. What is the pathologoly of IDA?
  2. Where does our source or iron come from and why?
  3. Where does iron absorption occur?
A
  1. Essentially it is a mismatch between the body’s iron requirements and iron absorption
  2. The body cannot “make” iron therefore dietary uptake essential
  3. Iron is mainly absorbed from duodenum and jejunum but absorption is very inefficient ~10% of total ingested
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5
Q

How would bowl cancer or an opperation in the bowl effect absorption of iron?

A

Would reduce iron up take and potentially lead to IDA

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6
Q

What food is iron more readily absorbed from and why?

What can be used to improve absorption

A
  • Iron bound to haem proteins found in meats is much better absorbed than iron from green vegetables.
  • Ascorbic acid (VitC) increases absorption from green vegetables
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7
Q

What causes IDA?

A
  1. Blood loss
  2. Diet
  3. Pregnacy
  4. Malabsorption
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8
Q

Causes of blood loss

A

Possible causes:

  • Surgery
  • Accident
  • Gynaecological causes–child birth/multiple pregnancies, menorrhagia. (Mensturation)
  • GI causes– Gastric erosion,IBD,GI cancer, Aspirin, NSAID’s
  • Parasitic infection (Hook worm)
  • Blood donation
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9
Q

What are the causes of IDA from diet?

A
  • Poor nutrition – 10-30% of pre-school aged children in UK living in inner cities affected. Milk fortified with iron given to inner city infants for first 18months.
  • Special diets – vegans
  • Inadequate dietary intake – Elderly, neonates
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10
Q

What forms can dietry iron be in? where are these found?

A

Dietary iron is found in two basic forms either as haem or non-haem iron.

  • Haem iron found: meat and meat products that are rich in two major haem-containing proteins, haemoglobin and myoglobin.
  • Non-haem: Vegetables etc
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11
Q

What is absorption and what is BA?

A
  • Absorption – uptake of a nutrient into the intestinal mucosa and its transfer into the body.
  • Bioavailability – proportion of a nutrient that is taken up and transferred by the intestinal mucosa.
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12
Q

What is haem absorption regulated by?

What is the most BA form of haem iron and where is this sourced from?

How much iron is absorbed each day?

A
  1. Uptake is mainly regulated by the NEED for iron.
  2. Haem iron is the most bioavailable form:
    1. 20-30% absorption from haem containing foods
    2. 1-10% absorption from non-haem sources
  3. Approx 1 mg/day absorbed from diet to replace lost iron.
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13
Q

When can iron absorption be increased and reduced?

A

Iron absorption may be :

  • Increased - if a person has a high intake of fish, or meat (red or white).
  • Reduced - if a person has a high intake of phytate (e.g. from wholegrain cereals), polyphenols (for e.g. from tea and coffee), calcium (dairy products)
  • Reduced - if the person is taking anything that raises the gastric pH (e.g. antacids/PPI’s).
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14
Q

What are inhibitors and promoters of non-haem iron absorption?

What can prevent the effect of inhibitors?

How do promoters work?

A

Inhibitors:

  • Phytates (wholegrain cereals, seeds, nuts)
  • Polyphenols, e.g. tannins (tea, coffee, cocoa, red wine)
  • Oxalate
  • Phosphorus
  • Calcium
  • Soy protein

Inhibitors of iron uptake can be degraded by milling, soaking, cooking, germination, fermentation and heat, thus increasing the amount of iron available for absorption.

​Promoters:

  • Ascorbic and citric acids (ferric => ferrous)
  • Cysteine peptides in meat

Ascorbic and citrus acids reduce ferric to ferrous iron (the form in which iron is taken up into the mucosal cells) and by forming a more soluble complex than iron alone.

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15
Q

Iron Rich food examples

A
  • Liver
  • Lean red meats, including beef, pork, lamb
  • Seafood: oysters, clams, tuna, salmon, and shrimp
  • Beans, including kidney, lima, navy, black, pinto,soy beans, and lentils
  • Iron fortified whole grains, including cereals, breads, rice, and pasta
  • Greens, including collard greens, kale, mustard greens, spinach, and turnip greens
  • Vegetables including broccoli, Swiss chard, asparagus, parsley, watercress, brussel sprouts
  • Chicken and turkey
  • Nuts
  • Egg yolks
  • Dried fruits, such as raisins, prunes, dates and apricots
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16
Q

Who is at risk of IDA?

A
  • Infants over 6 months, toddlers and adolescents. (Rapids growth/ development so high nutrient demand)
  • Menstruating women. (Due to blood loss)
  • Pregnant women.
  • Older people. (Insufficent intake)
  • People consuming diets low in iron and high in iron absorption inhibitors like phytate.
  • Individuals with high blood losses.
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17
Q

What can the effect of IDA in childhood be?

What can be done to help manage this?

A
  • Even mild IDA can have a long term detrimental influence on mental & psychomotor development
  • confounders - poverty, maternal education, prematurity.
  • The management of IDA through iron fortified foods or supplementation results in improved growth.
  • improvements in cognitive outcomes have been harder to define
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18
Q

Read

A
19
Q

What dietary advice should be given to patients?

A

Remind patients that;

  • Vitamin C – Increases absorption of iron from plant sources
  • Tannins (e.g. in tea) – Reduce iron absorption
  • Vegetarians
    • Advise to consume a source of vit C with meals
    • Drink tea between meals (doesnt act as inhibitor then)

VIT C IS ASCORBIC ACID

20
Q

What is malabsorption?

What are some potential causes?

A

Malabsorption is a disorder that occurs when people are unable to absorb nutrients from their diets

  • Coeliac disease
  • Gastrectomy
  • Helicobacter pylori infection
  • Gut resection (surgery)
  • Bacterial overgrowth
21
Q

How does Helicobater Pylore effect iron absoprtoin?

A

It can damage the tissue in your stomach and the first part of your small intestine (the duodenum). This can cause redness and soreness (inflammation).

Impares B12 absoption - B12 is required for RBC production.

As conditins advances blood loss occurs leading to IDA

22
Q

How doesCoeliac disease cause IDA

A

People with celiac disease get iron-deficiency anemia because they’re not absorbing enough iron from the food they eat. That’s because in celiac disease, eating gluten-containing foods causes your body to attack the lining of your small intestine, impairing your ability to absorb nutrients (including iron).

Automimmune disease

23
Q

How does pregnancy cause IDA?

What does the body do to try overcome this?

A
  • Physiological iron requirements - 3x higher
  • As pregnancy progressesàIncreasing demand
  • Gut increases absorption capacity to overcome increased demand
24
Q

What can be complications of IDA in pregn women?

A
  • Increased morbidity for (mother&infant)
  • Possibility of lower birthweight
  • Increased risk of preterm delivery
  • Maternal postpartum/postnatal depression
  • Infant iron deficiency (in 1st 3mo)
25
Q

What happens in IDA at molecular level?

A

Less iron in the circulation means than Iron does not bind to Hb. The formation of defective Hb then leads to microlytic, hypochromic RBC in the circulation

Microlytic - RBC smaller than normal

Hypochromic - Less Hb than normal and apear paler

26
Q

What do symptoms depend on?

What are examples of symptoms of IDA and iron defenciy?

A
27
Q

Clinical signs of IDA

A
  • No signs?
  • Pallor? - pale
  • Koionychis (brittle spoon shaped nails)
  • Cheiolsis (ulceration at the side of the mouth)
  • Cardiac signs
    • Tachycardia
    • Murmurs
    • Cardiac enlargement
28
Q

What are the steps in IDA management?

A
  • Confirm diagnosis
    • HCT, MCV, Hb
  • Assess (Investigation)
    • Clinical signs
  • Refer
    • E.g. to tropical medicine physician if hook worm (stool sample)
  • Treat
  • Advise
    • Pharmacological and non-pharmacological advice
  • Monitor
29
Q

What information is asked in a patient history?

A

weight loss - could indicate cancer

30
Q

What are examples of investigations you would carry out?

A
  • Visual signs- breathlessness, nails, skin colour
  • FBC
    • MCV
    • HCT
    • Hb
    • TIBC (total iron binding capacity)
    • Plasma Ferritan (iron store measuement)

Checking for causes:

  • GI –> endoscopy
  • Bleeding or parasitic infection –> urine and stool samples
31
Q

What are the steps of treatment?

A
  1. Ascertiain - type of anaemia
  2. Exclude any underlying causes
  3. Address any underlying causes - e.g. stop NSAIDs
  4. Iron supplementatoin
  5. Dierary advice
32
Q

What are the goals of treatment?

A
  • Correct underlying cause
  • Replenish iron store
  • Restore Hb to normal levels
33
Q

Why must care be taken with iron supplements?

A
  • There is no defined excretory pathways for excess iron from the body. Iron losses are therefore restricted to that stored in cells shed from the lining of the gastrointestinal and urinary tracts, skin and hair and losses through bleeding. This means it can easily build up.
  • Iron can become toxic to cells and tissues if in excess due to its ability to rapidly alter its oxidation state and generate oxygen radicals.
  • Body iron levels must be tightly regulated to avoid pathologies associated with both iron deficiency and overload.
34
Q

What types of toxicities is there and who do these tend to occur in?

A

Acute & sub-chronic toxicity

  • Tends to occur in children – accidental ingestion of supps.
  • High doses of 50-220mg/d can cause GI effects: constipation, nausea, diarrhoea and vomiting.

Chronic toxicity – chronic iron overload

  • Parenteral administration (therapeutic Fe or repeated blood transfusions).
  • Haemochromatosis – unregulated dietary absorption with gradual accumulation of iron in tissues. Leads to irreversible tissue damage.
35
Q

Prophylaxis

A
  • Used in the past in pregnancy together with folic acid
  • Now only if other risk factors present e.g. poor diet
  • Also appropriate in patients with: malabsorption, menorrhagia, partial or total gastrectomy, haemodialysis, low birth weight infants.
36
Q
  1. What route of iron supplements should be used?
  2. What preperations are available
  3. What does choice depend on?
  4. What is an important point to consider when switiching preperations
  5. What is reccomended dose of elemental iron?
A
  • Route of administration:
    • Oral preferred
    • IV - MHRA warning: Can have severe anaphylatic reaction and fatal reaction. Only used in specific circumstances by specific staff where resucitation equip available
  • Preparations:
    • m/r (not really any therapuetic benefit)
    • compound prep - folic acid and iron
      • Only recommended when need for folic acid
    • Iron salts

​

  • All iron salts have similar absorptance efficency and Hb regeneration rates effects there depends on costs and side effects
  • Beware different iron salts contain different doses of iron. Dose conversions will be needed when switching preperation!!!
  • 3-6mg/kg daily in 2-3 divided doses (up to 200mg)
37
Q
  1. What is an example of an iron salt preperation used?
  2. What is the reccomended dose?
  3. What are potential side effects?
  4. What is an alternative if they are intolerant?
A
  1. Ferrous sulphate (65mg elemental iron)
  2. Dose: 200mg 2-3 times daily for 3-6months
  3. ADR: nausea, abdominal cramps, diarrhoea, discoloured faeces
  4. If a patient is intolerant to ferrous sulphate change to ferrous gluconate (35mg elemental iron)
38
Q
  1. What is important to think about when deciding treatment?
  2. Why might ferrous gluconate be better?
  3. What is another alternative? Why might this not be any use?
A

Remember when making a drug selection:

it’s a balance between achieving patient concordance through minimising s/e’s AND ensuring adequate replenishing of iron stores

  • Ferrous gluconate 300 mg tablets – may be better tolerated than ferrous sulphate as there is less elemental iron content per tablet.
    • But remember then the patient is receiving less iron!
  • Ferrous fumarate tabs contain more elemental iron per tab than ferrous sulphate, therefore unlikely to be better tolerated.
39
Q

What counseling points should be given to patients newly started on Iron tablets?

A
  • Reassurance (black stools)
    • Reassure discolouration of stool (black) is normal
    • Explain bloody stool needs to be reported and investigated as is not due to iron tablets
  • Examples of common S/E’s
  • Compliance
    • Explain duration and encourage them to stick to treatment
  • •Diet
  • •Safe storage of tablets – toxic to children!
40
Q
A
41
Q

What to do if poor compliance?

A
  • If constipation present —> laxative use
  • If GI S/E’s —-> Recommend taking iron with or after meals.
  • Reduce dosage frequency (e.g. 1 or 2 tabs daily).
  • Try a different iron formulation or salt with a lower elemental iron content.
42
Q

Mointoring

A

Recheck haemoglobin levels (full blood count) after 2–4 weeks of iron supplement treatment to assess the person’s response. The haemoglobin concentration should rise by about 2 g/100 mL over 3–4 weeks.

If there is a lack of response, see the section on Inadequate benefit from initial iron treatment.

If there is a response, check the full blood count at 2–4 months to ensure that the haemoglobin level has returned to normal.

Once haemoglobin concentration and red cell indices are normal:

Continue iron treatment for 3 months to aid replenishment of iron stores, and then stop.

Then monitor the person’s full blood count every 3 months for 1 year.

Recheck after a further year, and again if symptoms of anaemia develop subsequently.

If haemoglobin or red cell indices drop below normal, prescribe iron supplements.

Further investigation is only necessary if haemoglobin or red cell indices cannot be maintained this way.

Consider an ongoing prophylactic dose in people who are at particular risk of iron deficiency anaemia.

43
Q
A

Kirsty 3.1 (47 decks)

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