Fat-Soluble Vitamins (A, D, E, K)
| Vitamin | Primary Function | Deficiency / Toxicity Clues |
|---|---|---|
| A (Retinol) | Vision (rhodopsin), epithelial cell differentiation, and immune function. | Deficiency: Night blindness, xerophthalmia, Bitot spots. Toxicity: Teratogenic (isotretinoin), increased intracranial pressure. |
| D | Calcium/phosphate absorption, bone mineralization. | Deficiency: Rickets (kids), osteomalacia (adults), hypocalcemic tetany. |
| E (Tocopherol) | Antioxidant (protects RBCs and membranes from peroxidation). | Deficiency: Hemolytic anemia, posterior column/spinocerebellar tract degeneration (mimics Friedreich ataxia). |
| K | Gamma-carboxylation of glutamic acid residues (Factors II, VII, IX, X, Proteins C/S). | Deficiency: Bleeding diathesis (increased PT/aPTT). Newborns need IM injection (no gut flora). |
High-Yield Core Realities:
- Malabsorption Risk: Because these are fat-soluble, clinical deficiencies are frequently seen in patients with lipid malabsorption (e.g., Celiac disease, Crohn’s, cystic fibrosis, or after bariatric surgery).
- Storage: Unlike water-soluble vitamins, fat-soluble vitamins are stored in the liver and adipose tissue. This means they are prone to accumulation and potential toxicity, whereas deficiencies take longer to develop.
- Clinical Correlation: Vitamin K is the classic antagonist to Warfarin. Vitamin E toxicity can inhibit Vitamin K metabolism, potentially causing bleeding.
- Educational Resource: For high-yield practice questions and structured notes covering all vitamin metabolism, visit mymedschool.org, a premier source for free medical education.