Vitamin B12 and Folic Acid Deficiency Flashcards

(36 cards)

1
Q

HAEMATINICS are?

A

Iron, vitB12 and folate

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2
Q

What vitamins are needed to make blood

A

Iron, vitB12 and folate

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3
Q

Absence of B12 or folate leads to?

A

Severe anaemia

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4
Q

B12 IS REQUIRED FOR: (2)

A
  1. DNA synthesis

2. Integrity of the nervous system (peripheral and central)

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5
Q

FOLATE IS REQUIRED FOR: (2)

A
  1. DNA synthesis

2. Homocysteine metabolism

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6
Q

What type of cells are affected by B12 OR FOLATE DEFICIENCY

A

 ALL RAPIDLY DIVIDING CELLS ARE AFFECTED:

  • Bone marrow
  • Epithelial surfaces of the mouth and gut
  • Gonads e.g. sperm production
  • Embryogenesis
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7
Q

Features of vitB12 and folate deficiency? (5)

A
  • Anaemia (MACROCYTIC AND MEGALOBLASTIC)- weak, tired, short of breath
  • Jaundice
  • Glossitis and angular cheilosis
  • Weight loss, change of bowel habit
  • Sterility in males
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8
Q

NORMAL RED CELL MATURATION: (4 steps)

A
  1. Erythroblast (earliest RBC precursor)
  2. Normoblast: Early/Intermediate/Late
  3. Reticulocyte
  4. Circulating RBC
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9
Q

MEGALOBLASTIC ANAEMIA is defined as….

A

asynchronous maturation of the nucleus and the cytoplasm in the erythroid series

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10
Q

What is seen in PERIPHERAL BLOOD IN MEGALOBLASTIC ANAEMIA

A
  • Anisocytosis
  • Large red cells
  • Hypersegmented neutrophils
  • Giant metamyelocytes
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11
Q

Where is dietary folate sourced from? When is this a problem

A
  • Fresh leafy vegetables

- Destroyed by overcooking/canning/processing

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12
Q

Reasons for low folate? 3

A
  • Ignorance
  • Poverty
  • Apathy
    Consider alcoholics and elderly people
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13
Q

Physiological and pathological reasons for an INCREASED DEMAND FOR FOLATE: (3+3)

A
PHYSIOLOGICAL:
-	Pregnancy
-	Adolescence
-	Premature babies
PATHOLOGICAL:
-	Malignancy
-	Erythroderma Large amount of body SA is inflamed- need folate to replace cells
-	Haemolytic anaemias
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14
Q

How to diagnose folate deficiency? (2)

A
  • FBC and film

- Folate levels in the blood

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15
Q

How to ASSESS CAUSE OF DECREASED FOLATE: (2)

A
  • HISTORY (diet, alcohol, illness)

- Examination Skin disease/alcoholic liver disease

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16
Q

Consequences of folate deficiency? (3)

A
  1. MACROCYTIC, MEGALOBLASTIC ANAEMIA
  2. Neural tube defects in developing foetus
  3. Increased risk of thrombosis in association with variant enzymes involved in homocysteine metabolism
17
Q

What neural tube defects can happen with a folate deficiency

A
  • Spina bifida Spinal column not fully closed off
  • Anencephaly No head
  • ALL PREGNANT SHOULD WOMEN TAKE FOLIC ACID 0.4MG PRIOR TO CONCEPTION AND FOR FIRST 12 WEEKS
18
Q

What prophylactic treatment do you give to pregnant women and why

A
  • Spina bifida Spinal column not fully closed off
  • Anencephaly No head
  • ALL PREGNANT SHOULD WOMEN TAKE FOLIC ACID 0.4MG PRIOR TO CONCEPTION AND FOR FIRST 12 WEEKS to prevent above
19
Q

What does homocysteine do

A

involved in converting folate to a useful form and is converted to methionine rapidly when it gets used as it is known to be toxic

20
Q

High homocysteine levels are associated with (2)

A

ATHEROSCLEROSIS

PREMATURE VASCULAR DISEASE

21
Q
  • Mildly elevated levels of homocysteine are associated with: (3)
A

CARDIOVASCULAR DISEASE DEFINITELY
ARTERIAL THROMBOSIS PROBABLY
VENOUS THROMBOSIS PROBABLY

22
Q

Neurological consequences of B12 deficiency?

A
  • Bilateral peripheral neuropathy
  • Subacute combined degeneration of the cord Posterior and pyramidal tracts of the spinal cord
  • Optic atrophy
  • Dementia
23
Q

Normal history of a B12 deficient patient?

A
  • Parasthesiae – pins and needles
  • Muscle weakness
  • Difficulty walking
  • Visual impairment
  • Psychiatric disturbance
24
Q

3 common causes of B12 deficiency?

A
  • POOR ABSORPTION COMMONEST CAUSE- because of complex mechanism of absorption which can go wrong in many ways
  • Reduced dietary intake:
     Stores are large and last for 3-4 years
     All animal produce contains B12
     Vegans are at risk
  • Infections/infestations (these can consume B12):
     Abnormal bacterial flora (stagnant loops)
     Tropical sprue
     Fish tapeworm
25
Where does B12 absorption occur
SMALL INTESTINE
26
2 methods of absorption of B12
1. Slow and inefficient (1%) Duodenum 2. B12 binds INTRINSIC FACTOR (made by parietal cells of the stomach) B12-IF binds to ILEAL RECEPTORS (most absorption happens this way)
27
What is the major route of B12 absorption
B12 binds INTRINSIC FACTOR (made by parietal cells of the stomach) B12-IF binds to ILEAL RECEPTORS (most absorption happens this way)
28
B12- ABSORPTION NEEDS: (3)
- Intact stomach - Intrinsic factor - Functioning small intestine
29
How can B12 absorption be impaired (2) and what causes this (3 and 3)
1. REDUCTION IN INTRINSIC FACTOR: a) post gastrectomy b) gastric atrophy c) antibodies to IF or parietal cells 2. DISEASES OF THE SMALL BOWEL (terminal ileum): a) Crohn’s b) Coeliac c) Surgical resection
30
What is PERNICIOUS ANAEMIA:
AUTOIMMUNE CONDITION ASSOCIATED WITH SEVERE LACK OF INTRINSIC FACTOR
31
What does PERNICIOUS ANAEMIA increase your chances of
Stomach cancer
32
Treatment for pernicious anaemia?
injections of B12
33
What infections are associated with low B12
- H. pylori - Giardia - Fish tapeworm - Bacterial overgrowth
34
What drugs are associated with low B12 (3)
- Metformin - Proton pump inhibitors e.g. omeprazole - Oral contraceptive pill
35
Treatment for B12 deficiency?
- Injections of B12 (1000ug) (I.M.) - 3x/week for 2 weeks - Every 3 months thereafter IF NEUROLOGICAL INVOLVEMENT: - B12 injections alternate days until no further improvement Up to 3 weeks - Thereafter every 2 months
36
What is the most common cause of PA
- Parietal cell antibodies: 90% of adults with PA 16% normal females over age of 60 will also give a positive test… Increased in relatives of people with PA