Download MBBS Important Topics Biochemistery Cases

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Important Topics Biochemistery Cases for MBBS 1st Year Important Topics, MBBS 2nd Year Important Topics, MBBS 3rd Year Important Topics & MBBS Final Year Important Topics.

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MBBS 2021 Important Topics and Materials for 1st Year, 2nd Year, 3rd Year and Final Year

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Biochemistry Case

Kwashiorkor
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Condition: 2-3 year child
Low Serum Albumin (N.R= 3.4-5.0 gm%)
Low Serum total Protein (N.R = 6-8 gm%)
Hypoalbuminemia, edema, diarrhoea
Treatment:
1. Balanced diet with good quality of protein
2. Vitamin & Iron supplement to correct Anaemia
3. Frequent oral Feeding & Mineral Supplement
Marasmus
Conditions: Children 1 yr. or Less than 1 yr.
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deficiency of Calories
Manifestation: (प्रकटीकरण)
Serum albumin is Normal
Hb is Less than Normal.
Muscle Wasting, Weight loss, Weakness
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Wrinkled skin
No edema,
No Fatty liver
Treatment:
Nutrition rich in calories, Protein, vitamin,

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Gout - (Nucleic Acid Metabolism.)
Condition: Pain & swelling In joints
↑ blood uric acid - (N.R- 3.0-7.0mg%)
disorder of Purine catabolism.
Hyperurecemia
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Reasons:
1. Hyperactivity of PRPP Synthase & PRPP Amido transferase
2. Deficiency of HGPRTase
Treatment:
1. Allopurinol competitively Inhibit Xanthine oxidase, thus reduce uric acid formation
2. Colchicine & NSAIDS like Indomethacin.
3. Reduce Intake of dietary Protein like meat, Liver, tea, coffe, Sea Foods
4. Avoid Alcohol & High Protein diet
5. Consume Plenty of H₂O.
Lesh Nyhan syndrome
Condition: Bitting fingers, lip,
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Joint Pain
Neurological symptoms
Increased serum uric acid level.
Reason: deficiency of Hypoxanthine Guanine Phosphoribosyl Transferase (HGPRT)
X-linked recessive disorder (Only Male affected)
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concerned (संबधित) Pathway:
Guanine HGPRTase GMP
PRPP ppi
Hypoxanthine HGPRTase IMP.
PRPP PPI

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Sickle cell Anaemia
Condition: Crescent Shaped RBCs
Electrophoresis - Hbs Band.
Slightly Anemic (Low Haemoglobin).
Reasons:
1. Glutamic acid replaced by valine at 6th Position of B-Chain Of HbA
Lab. Test:
1. Sickle Test.
2. Demonstration of sickled RBC in smear
3. Haemoglobin, electrophoresis
Factors: ↓O₂ Tension, ↑ CO₂ concentration.
↓PH (Acidosis), ↑2,3-BPG Concentration

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Manifestation:
1. Hemolytic anaemia
2. Tissue damage & Pain in bone (chest, Abd).
3. ↑ed susceptibility to Infection i.e. Malaria
4. Premature death.

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Metabolic Acidosis
Condition: Untreated diabetic mellitus lead to excessive production of keto acid.
- Low - serum Bicarbonate, PH, PCO₂
- Fall in cardiac output, so BP ↓
- deep sighing respiration - Kussmaul's breath
NaHCO₃ / H₂CO₃ = 20/1
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Treatment:
1. Insulin administration.
2. Na Bicarbonate to Neutralise acids
3. In Renal failure - dialysis
Metabolic Acidosis: ↓ Bicarbonate (HCO₃)
Respiratory Acidosis: ↑ Carbonic acid (H₂CO₃)
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Metabolic Alkalosis: ↑ Bicarbonate (HCO₃)
Respiratory Alkalosis: ↓ Carbonic acid (H₂CO₃)
Hyperthyroidism
Condition: Swelling in Neck
Elevated T3 & T4
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Low TSH
Sweating, Loss of wt., Palpitation
Lab:
↑ total and free T3 & T4
↓ TSH (Thyroid stimulating Hormone)
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↓ TBG (thyroxine Binding Globin)
↑ Radioactive Iodine uptake.
↑ BMR
Causes:
- Enlarged Thyroid Gland (exophthalmic Goiter)
- Weight Loss
- ↑BMR, Uncouples oxidative Phosphorylation, Block ATP Synthesis, High Consumption of O₂, Librates Heat
Manifestation: (प्रकटीकरण)
↑ HR, Tremors, Anxiety, Loss of Wt, ↑ Appetite, sweating
Nervousness, Irritability, ↑ BMR, ↑T3 & T4, ↓TSH.
Treatment:
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Surgical Removal
Radioactive Iodine Therapy
Drug like Carbimazole
Hypothyroidism
Condition: Enlarge thyroid Gland.
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decreased T3 & T4
Increased TSH.
Manifestation:
Cretinism (children) - Poor Physical, Mental, sex. Growth
Myxoedema (adult) - Bagginess under eye, Mental & Physical slowing, puffing face.
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Low pulse rate, Gain wt, sensitivity to cold, Dry skin, sluggish behaviour, ↓Appetite
Lab:
↓ total & Free T3 & T4
↑ TSH
↓ Radioactive Iodine Uptake
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Treatment:
Administration of Thyroxine.
Fatty liver
Condition: Serum cholesterol & Serum T.G level
Anorexia
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Causes:
1. Excessive mobilization of fat from Adipose tissue e.g. diabetic mellitus & Starvation
2. excessive Intake of calories
3. Impaired mobilisation of fat due to
  Deficiency of EFA
  Deficiency of Lipotropic factor
4. Alcoholism
5. Toxin like CCl₄, Chloroform, orotic acid, Puromycin, yellow Phosphorous, Aresenic.
6. Deficiency of essential Amino acid Antioxidant (Vit E, Se)
7. endocrine Factor e.g. Insulin, ACTH, Thyroid H.
Test:
1. liver function Test:
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  ↑ serum bilirubin
  ↑ SGPT
  ↑ SGOT
  ↑ LDH
  ↑ ALP
2. Lipid profile:
  ↑ S. cholesterol
  ↑ LDL Cholesterol
  ↑ T.G
  ↑ HAL Cholesterol.
Mechanism:
Ingestion of Alcohol.
Formation of (NADH+H⁺)
Oxaloacetate → Malate
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Acetyl-CoA
↓
Increased Pool used
Factor that prevent fatty Liver:
1. Choline
2. Methionine & betaine
3. Lecithin
4. casein.
5. Antioxidant like vit E & selenium
6. Vit. B12 & folic acid.
7. omega-3- fatty acid - (esterification of cholesterol)
Treatment:
Stoppage of Alcohol.
Weight Control
Control of diabetes
Hyperlipidemia
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Nutritional Support
Atherosclerosis
Condition:
characterized by thickening of Hardening of arteries due to Accumulation of cholesterol & Other lipid in Atrial wall resulting Narrowing of Lumen.
Biochemical changes:
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Hypercholesterolemia
↓ HDL.
Risk factor:
Hypercholesterolemia ↑200 mg%.
↑ LDL cholesterol ↑150 mg%.
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Obesity
Smoking
High consumption of Fat
Hypertension
Stress
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Lack & Physical exercise
Treatment:
Drug - Lovastatin, simvastatin. Inhibit Cholesterol Synthesis by Inhibiting HMG-CoA reductase
Diet
- PUFA (veg. oil & fish oil)
- Green leafy vegetable
- Avoid sucrose
- Garlic oil Contain Allyl thiosultinate which ↓ Cholesterol, LDL, ↑ HDL
- Antioxidant Like Vit. E, vit. C & β-Carotene.
ketoacidosis
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Ketone Bodies are:
Acetoacetate
β-OH butyrate
Acetone
Explantation:
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Acetoacetate & β-OH-Butyrate - Strong Acid
↓
depletes Alkali reserve
↓
Causes → Metabolic Acidosis
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In ketosis:
electrolyte (Imbalance) & (dehydration) because Ketone Body, Nation, Glucose, are Lost in Urine
Myocardial Infarction (MI)
Nicotine causes Transient constriction of coronary! Carotid artery. It also decrease HDL & causes Accumulation of CO that causes endothelial Cell Injury.
Risk Factor:
- Hypercholesterolemia ↑200mg%
- ↑ Serum T.G ↑100 mg%
- ↑LDL > 150 mg%.
- ↓ HDL < 35 mg%
- LDL: HDL ratio>3.5
- Hypertension
- smoking
- Diabetes mellitus
- sedentary life
- obesity
- Alcoholism
Prevention:
- Physical exercise
- consumption OF PUFA
- Fibre diet ↓ cholesterol absorption
- No Smoking
- Moderate Alcohol Consumption.
- Antioxidant. Vit E, Vit.c, β-Carotene.
- Garlic & Fenugreek seed - ↓ cholesterol.
Diabetic ketoacidosis (DM+ ketoacidosis)
Condition: deep breathing with Fruity odour
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Excessive thirst
Polyurea with ketone bodies
Biochemical Investigation:
1. Urine:
  Benedict Test - to detect sugar in Urine
  Rothera's Test - to detect K.B in urine
2. Blood:
  Blood sugar estimation- for degree of Hyperglycemia
  Blood Ketone Body - for severity of (ketoacidosis)
  Blood Urea- May be raised.
3. Plasma electrolyte:
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  K- Normal
  HCO₃-↓
  Na- Usually ↓
  H⁺-↑
  P - Usually ↑
Metabolic changes:
1. Hyperglycemia & Glycosuria
2. ketoacidosis
3. electrolyte Imbalance
4. Dehydration

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Diabetes Mellitus
Condition: Glycosuria, polyuria, loss of wt, Polydipsia, Polyphagia, Polyuria
Biochemical Test:
- Urine Benedict Test
- Blood Sugars - Fasting, PP, GTT
- Lipid profile- (serum cholesterol, T.G & HDL)
- HbA1C.
Glycosuria
Diabetic Glycosuria
Renal Glycosuria
Alimentary Glycosuria
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emotional Glycosuria
experimental Glycosuria
Pathologic Glycosuria
Glycosuria of pregnancy
Toxic Glycosuria

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Type-I/Insulin dependent diabetes Mellitus
- Lack of insulin due to obstruction of pancreatic beta cell due to:
  - Viral infection
  - Autoimmune disorder
Onset-(शुरुवात)
at about 14 yr of age (Juvenile)
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5-10% Symptoms- (Hyperglycemia with Glycosuria & ketoacidosis)
- Polyuria (Frequent Urination)
- polydyspia (excessive Thirst)
- Polyphagia (excessive Hunger)
- Loss of weight / weakness, Tiredness
- Not obese.
Treatment:
Administration of exogenous Insulin is required.
Type-II/Non-Insulin dependent diabetes Mellitus
- decreased sensitivity of target cell to insulin. (Inadequate insulin receptor)
90-95% Onset:
After age 40 year (Adult onset diabetes).
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Symptoms
Similar with Ketoacidosis is Absent
Treatment:
- diet control. exercise weight reduction
- drug that Increases insulin sensitivity- Thiazolidinediones & Metformin.
Blood Glucose estimation:
- GOD-POD
- Folin-Wu Method
diabetes insipidus
Condition:
urine Benedict - -ve
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Blood Glucose Level - Normal.
Specific Gravity- less than Normal.
Polyuria, Polydypsia.
Causes:
1. Lack of Antidiuretic H (ADH) / Vasopressin.
2. Deficient action of ADH on its Target cell
Lab:
1. Fluid & food are withheld for 24 Hours
2. Body wt, plasma, urine osmolarity measured
Galactosemia - प्रश्न मध्ये direct असेल.
Symptoms - Mental Retardation & cataract, liver & kid. damage, Hepatosplenomegaly & Jaundice
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Defective enzyme- Galactose-1-phosphate uridyl Transferase.
Galactose
ATP
Galactokinase
ADP
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Galactose-1-P
UDP Glu.
Gal-1-P uridyl Transferase
Glu-1-P + UDP Galactose
UDP-Galactose epimerase.
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UDP-Glucose
Biochemical Test:
1. estimation of Galactose-1-P-uridyl transferase in RBC (Normal -4-30 Units /gm of Hb)
2. Blood Galactose level ↑ed.
3. Blood sugar level ↓ed (Hypoglycemia)
4. Galactosuria
5. Albuminuria & Aminoaciduria.
Role:
Synthesis of Breast and glycoprotein mucopolysacchride & Proteoglycans
Lactose Intolerance / Milk Intolerance
Abdominal discomfort, feeling of diarrhoea after taking milk.
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Cause:
- deficiency of lactase enzyme
- Accumulate in Intestine
- Indigestion Abdominal Cramps
- flatulence & diarrhoea
Treatment: total Restriction of Milk

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G6PD deficiency → Hemolytic Anaemia
condition:
Hb-reduced
Unconjugated Bilirubin - ↑
Antimalarial drug- Primaquine
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Red Colour Urine
defect: G6PD- (Glucose-6-phosphate dehydrogenase)
First enzyme in HMP Shunt.
Test:
1. Intravascular Hemolysis
2. Estimation of G6PD level in RBC
Glutathione (GSSG)
NADPH
reduction
(GSH)
↓
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Protect RBC
Oxidative
Hepatic Jaundice (Hb Metabolism)
Normal serum Bilirubin- 0.2-1.0 mg%.
Urinary finding:
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Urinary Bilirubin - Present ↑(conj. & unconj.)
Urinary Bile salt- Absent
Urinary BPG- ↑ed (N=> 0.4-6mg/24h)
Cause:
Stool- clay coloured (Absence of SBG)
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Urine - dark coloured (Increased UBG)
Hemolytic Jaundices (Hb. Metabolism)
- unconjugated Bilirubin Increased.
- Total Bilirubin increased but less than 6 mg
- All enzymes are in Normal Range
- excessive Break down of RBC after treatment of malaria. The heme degraded to form excess of bilirubin which can't be effectively conjugated & Hence increase in Unconjugated billirubin
Feature
(↑SGPT) Normal ALP
Test: Vanden Bergh Test.
Causes - sickle cell Anemia
Incompatible blood Transfusion
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G6PD deficiency.
Thalassemia
Malaria
drug. eg - Sulphasalazine & dapsone
Neonatal Jaundice (Physiological Jaundice).
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Causes- (Hb Metabolism)
Increased Hemolysis & defective conjugation of bilirubin.
Complication-
↑ in unconjugated bilirubin.
when level exceed 20 mg %, it cross BBB & Cause brainage damage- Kernicterus
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Treatment-
Phototherapy.
Obstructive Jaundice (Hb Metabolism)
- Bilirubin Present
- UBG Absent
Manifestation - Pain in Abdomen, Jaundice, enlargement of Head of Pancreas, Itching & fever
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Cause:
- Gall Stone
- Carcinoma of Pancreas
- stricture of bile duct
- Hepatitis
- Alcohol
- Cirrhosis
- secondaries in liver
- Hodgkin disease
- Bacterial Infection
Enzyme for diagnosis:
- Increased level of serum Alkaline Phosphate
- SGPT Increased
Urinary finding:
Urinary bilirubin - Present (Fouchet's & Gmelins test +ve)
Urinary bile salt - present (Hay's Sulphur test +ve)
Urinary UBG - Absent (Ehrlich test Negative)
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Colour of urine- Dark (↑bilirubin)
Fecal SBG- Absent
Colour of Stool- Chalky white, Pale @ Clay coloured
Phenylketonuria (PKU)
Condition: (Autosomal Recessive Gene)
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Mousy odour to urine.
excreation of phenyl Pyruvate.
mental retardation, eczema, seizures
Why Mousy odour?
Phenylalanine X Tyrosine
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Transaminase
Phenyl Pyruvate
Redo
Decarboxylation
Phenyl Lactate
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Phenyl Acetate
conjugation
Phenyl Acetylglutamine
Acculumation & lead to Mousy odour
Test:
1. FeCl₃ Test
2. Guthrie's Test
Normal plasma level - 1-2 mg%
In PKU level of Phenylalanine - 20-65mg%
prenatal diagnosis with DNA Probe
effect:
1. Mental Retardation grow Properly
2. walk & Talk seizure
3. Psychosis & Tremors
Types:
PKU type I -deficiency of Phenylalanine Hydroxylase
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PKU type II -defect in H₂- biopterin reductase
PKU type III-defect in H₂- biopterin Synthesis
Management:
1. Low Phenylalanine diet. Milk & Milk Product are totally withdrawn.
2. Supplement of Tyrosine.
3. Give Serotonin & DOPA to restore their deficiency
Parkinson's disease
- Parkinson's disease (Shaking Palsy) because the treatment include carbidopa & γ- Methyl dopa.
Cause:
to decreased production of dopamine
Manifestation:
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Tremors, rigidity, expressionless face, lethargy, Involuntary movement.
Albinism - (Protein Metabolism)
Condition: Lack of Pigmentation (Hypo-Pigmentation)
Blue eye & White hair
Defective enzyme - Tyrosinase required for synthesis of Melanin.
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Derived Compound:
1. Melanin.
2. Catecholamine - dopamine, epinephrin & Norepi
3. Thyroid H- T3 & T4
4. Tyramine
Biochemical Reaction:
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Tyrosine
↓ Tyrosinase (Cu+2)
DOPA
↓ Tyrosinase (Cu+2)
Dopaquinone
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↓ Decarboxylation
Indole quinone
↓ Polymerisation
Melanin.
Manifestation:
1. Hypopigmentation of skin, Hair, eye
2. Photo Phobia ( Intolerance to Light)
↑ed sensitivity to Light
↑ed chances of skin cancer
Diminished Visual Acuity & Nystagmus
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Types:
1. Ocular Albinism - Affect only eye & Not Skin
2. Oculo-Cutaneous Albinism- ↓ Pigmentation.
Alkaptonuria (P.M)
Urine-coke like colour (Black)
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Arthritis
deficient enzyme- Homogentisate oxidase enzyme.
Biochemical Rxn-
Phenylalanine
↓ Phe-Hydroxylase deficiency causes pku
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Tyrosine
P-Hydroxy-Phenyl Pyruvic Acid
Accumulates Homogentiste
in Blood & tissue
Excreated in Urine
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4 Maleyl Acetoacetate
4-fumazyl acetoacetate
Fumarate Acetoacetate
Treatment- No specific treatment
Provide Low protein diet with low Phenylalanine & Tyrosine Content.

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Hartnup disease (P.M)
Symptoms: Pellagra, Mental Retardation & excessive Urinary excreation of Tryptophan.
Deficiency of Tryptophan & Lead to decreased synth. of serotonin & Niacin (NAD+ & NADP+)
Diagnosis- (Dbeemeyers Test)
1. ↑ed urinary excreation & Tryptophan
2. ↑ed excreation of Indole Acetic acid.
Treatment:
High protein diet with supplement of Niacin
Maple syrup Urine disease (MSUD) (p.m)
Urine smell like Burnt sugar
defective enzyme-α-keto acid dehydrogenase
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Urinary finding- ↑ excreation & branched chain A.A
Diagnosis - Urine +2,4-dinitro Phenyl Hydrazine in HCl.
Roth couple ring
Chromatography
Vit.A
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condition- diminished vision of light.
Low Plasma retinol level.
Finding:
1. Impaired vision.
2. Nightblindness (Nyctalopia)
3. xerophthalmia - dryness of conjunctiva & cornea
4. keratomalacia - Corneal Ulceration & degen
5. Bie fitot spot - White opaque spot on Conjunctiva
Cycle-
ROA-
Adult - 2500-3500 IU
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children- 1500-2000 IU.
Infant - 1000 IU
Pregnancy & Lactation - 3000-4000 IU.
Source-
Rich source- cod liver Oil, & Animal liver
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Good source- Milk & Milk Product, egg yolk, yellow-Green fruit vegetable,
Precursor of vit. A is Beta-Carotene It is yellow Pigment in fruit act as Antioxidant.
VIT-D
Condition: Bone deformities
(Low Ca+2, P, Calcitriol) (High ALP) (High PTH)
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Bone Fracture → Low bone density.
disease - Rickets
Type:
- Renal Rickets - seen in chronic Renal failure
- Resistant Rickets - resistant to vit.D
- Hypophosphatemic rickets - due to defective renal Ah,
- 2° Rickets -due to malabsorption state
- Drug Induced Rickets - Anticonvulsants
Investigation:
- low serum calcium (N.R- 9-10 mg%)
- Low Serum phosphate (N.R- 3-4 mg%)
- Low serum calcitriol (N.R- 25-60 pg%)
- High ALP (N.R- 3-13 KA Unit)
Treatment:
1. Food rich in vit.D like fish, liver oil, egg, yolk, liver & Mushroom
2. Vit.D Supplements
3. Food rich in calcium & phosphorus
  e.g - milk
Manifestation:
1. Bossing of forehead.
2. Bow leg
3. knocked leg/knee
4. Soft & pliable bone
5. Pigeon chest
6. Delay in Chest formation
7. Protruding Abdomen (pot belly)
8. Increased ALP
9. Low. Serum ca+2
10. Low- Serum phosphate
11. Thickening of Wrist & Ankle
Hormone:
7-dehydrocholesterol
UV light (skin)
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Cholecalciferol
25-Hydroxylase (liver)
25-OH-Cholecalciferol
1-α-Hydroxylase (Kidney)
1,25 DHCC
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Calcitriol.
Acts on Intestinal mucosa, bone to ↑ ca+2
Thiamine (B1) - Anorexia, Neuropathy, Muscular Weakness
↑ed Pyruvate level, Memory loss.
Diagnosis: Wernickes encephalopathy / Wernicke's Korsakoff syndrome / Beri-Beri.
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Active form- Thiamine Pyrophosphate (TPP)
Pyruvate PDH → Acetyl-CoA
TPP, FAD, COA, NAD
α-Ketoglutarate α-ketoglutarate dehydro. complex → Succinyl-CoA
TPP, FAD, COA, NAD, lipoate
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Source:
Germinated seed, Unrefined cereals, Nuts & Pulses, Beans, Lentils, Milk, liver, Egg, meat
ROA:
Adult - 1.2-1.5 mg
Children - 0.7-1.2 mg
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Infant - 0.3-0.5 mg
Pregnancy & Lactation - 1.5-1.6 mg
Diagnosis:
1. Measurement & Blood Thiamine, Pyruvate & lactate level

This post was last modified on 24 July 2021

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