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PRESENTATION
NAME: AWAIS AHMED
SUBJECT :INTERNAL DISEASES
TOPIC : VITAMIN B 12 DEFICIENCY
GROUP: 6TH
SEMESTER : 8TH
ROYAL METROPOLITAN MEDICAL UNIVERSITY

introduction
Definition
physiology
pathology
causes
clinical menifestations

Diagnosis (lab test)
Treatment

summary

INTRODUCTION

​VITAMIN B12

its known as cobalamin it is a compound name
it is a water soluble vitamin
its essential vitamin required from food that we have to get it from animal products
such as (1 meat 2 fish 3 eggs 4 dairy products)
it can not be manufactured by humans
synthesis by bacteria not from vegetables

physiology

​vitamin B12 mechanism of absorption

actually gastric acid liberates vit B12 from animal products after it combines with intrinsic factor that produced by gastric parietal cells and it absorbed in the in the terminal ilium
(TERMINAL ILIUM)
it is a part of small intestine connect to the large intestine that help to absorb vit 11 12 and bile salts

storage and function Vit B 12

​storage

Liver is principal organ for storage of vit B 12 and also other organs such as btrain heart

​function

vitamin B 12 important for some enzyme for the conversion into its final products such as
(1) methylation of homocystein
(2) methyl malonyl coA mutase to succinyl co A
(3) Diuridine monophosphate to thymine monophasphate

Role of Vitamin B12

​(1) formation of RBC's
(2) synthesis of DNA
(3) neurological functions

vitamin B 12 deficiency

caused by

actually its kind of megaloblastic anemia in which deficiency of these 3 important subs:
(1) vitamin B 12
(2) folic acid
(3) perniciuos anemia
caused by
(1) poor diet
(2) compromised absorption
(3) most common is pernicious anemia
i

continue

pregnancy
gastric causes
(1) intrinsic factor
(2) gastrictomy
intestinal causes
(1) crohan's disease

​role of Vitamin B 12 in pregnancy

before 1 month of pregnancy we have to prescribe folic acid tablets to mother for prevention of ( neural tube defects in utero)
also it will contineu after birth
due to in after pregnancy increase demand of lactose that is important for health of baby

​Nieweg's hypothesis

deficiency of folic acid is not related with neurological disorders but B12 deficiency is associated with neurological lesions
example ;( sub acute degeneration of the spinal cord
And both related with megaloblastic anemia
actually folic acid concerd with DNA metabolism
The B 12 concerd with RNA as a deficiency of B!2 result will neurological lesions
Thymine(DNA)
uracil (RNA)

​epidiomology

cobalamin deficiency arises n vegans who do not eat meat fish eggs cheese and other animal products from diet
The largest group in the world consists of hindus
subnormal serum cobalamin levels are found in 50% of randomly selected young adults indian vegans.....

​according to Harrison's internal medicine 20th edition

clinical features

​phycological effects

methylmalonyl coA mutase requires vit B 12 as a co factor and if there's not enough vitamin B12 for this enzyme to function we get build up intermediatery ( methyl malonic acid) it will increases and damage the neurons that lead (axonal neuropathy)
affect (dorsal column medial leminniscus system)
Depression
Decrease cognition ( impaired memory dementia in older person

neurological effects

​if vit B12 deficiency more chronic lead

• symmetrical paraesthesia ( tingling and burning sensation both lower limbs

• shuffling gait ( parkinsonian like symptoms dragging feet)

• Dec two point discrimination

• dec proprioception ( dec ability to balance)

other symptoms

1. ​Anaemia ( macrocytic megaloblastic)

2. pallor ,fatigue

3. jaundice

4. melanin pigmentation

5. splenomegaly ( not in aplastic anaemia)
   

• yes

• decrease

• macrocytic

• increase

• yes

• increase

• increase

​vitamin B12

​Anemia?
Hb
which type?
MCV
Neurologial
Homocysteine
methylmalonic acid

Diffrencies between folate & B12

​Folate def

• yes

• decrease

• macrocytic

• increase

• No

• increase

• No

DIAGNOSIS

​SCHILLING TEST two ways

To find out cause and vitamin B 12 deficiency
(1)use radiolablled vit B 12
if excretion greater than 8 % i 24 hours patient have vit B 12 deficiency
if excre; less than 8 % it is normal patient

(2) use radiolabelled vit B12 + intrinsic factor
(a) excretion improve if deficiency
(b) excretion same this mean malabsorption

​continue

1. decrease Hb

2. RBC ( see macrocytosis) large in size

3. Anisocytosis (change in size )

4. poikilocytosis ( change in RBC shape )

5. see howel jowel bodies

6. MCV increase

7. leucocytes decrease

8. platelets decrease

9. serum B12 decrease

10. macro ovalocytes

​Blood test

​treatment

short course of vitamin B 12 course ( about 4 weeks )
it usually treated with injection of vitamin B 12 (hydroxocobalamin)
every day for 2 weeks unttil symptoms have improving
available in form
injection (hydroxocobalamin)
tablet ( cyanocobalamin) orally for 4 weeks

THANK YOU