One-page cheat sheet: Fat-soluble vitamins (A, D, E, K)

Fat-soluble vitamins are classic USMLE bait because they travel together (with fat), fail together (in malabsorption), and show up together in “weird bruising + night blindness” style stems. Here’s a one-page, shareable cheat sheet for A, D, E, K with mnemonics, one-liners, and the highest-yield associations.

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The Big Picture (What makes ADEK “fat-soluble”?)

Key rule: A, D, E, K are absorbed with dietary fat and require bile salts → problems when fat absorption is impaired.

High-yield causes of deficiency (think: “can’t absorb fat”):

• Pancreatic insufficiency (e.g., cystic fibrosis, chronic pancreatitis) → low lipase
• Cholestasis / biliary obstruction (e.g., gallstones, PBC/PSC) → low bile salts
• Celiac disease or other small bowel malabsorption
• Orlistat (blocks pancreatic lipases) → ADEK deficiency risk
• Bariatric surgery (malabsorptive procedures)

Storage: Fat-soluble vitamins are stored in the liver and adipose → deficiencies develop more slowly than water-soluble ones (but toxicity risk is higher, especially A and D).

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Visual / Mnemonic Device (fast recall)

“A DEK” = A is DEKing out your body

• A = A vision/epithelium (“Aye!”)
• D = D bones (calcium/phosphate)
• E = Erythrocytes & neurons (oxidative protection)
• K = Klotting (coagulation)

One-liner anchor:
“ADEK need fat to get in; if fat can’t get absorbed, neither can ADEK.”

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One-Page Table: What each vitamin does, deficiency, and classic USMLE clues

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Vitamin A (Retinoids): “Vision + epithelium”

The one-liner

Vitamin A keeps you seeing at night and keeps epithelium from turning into dry, keratinized pavement.

Highest-yield facts

• 11-cis-retinal is part of rhodopsin in rods → low A = night blindness (often the earliest clue).
• Deficiency causes:
  • Xerophthalmia (dry eyes)
  • Bitot spots (foamy, keratinized conjunctival plaques)
  • Hyperkeratosis
  • ↑ susceptibility to infections (impaired mucosal barriers, immune function)
• Toxicity (classic Step association):
  • Teratogenic (important: pregnancy counseling)
  • Hepatotoxicity
  • Pseudotumor cerebri (increased intracranial pressure symptoms)

Stem triggers

• “Child with poor diet + trouble seeing in dim light”
• “Dry eyes + foamy conjunctival patches”

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Vitamin D: “Build bone; regulate calcium/phosphate”

The one-liner

Vitamin D raises calcium and phosphate absorption to mineralize bone—too little bends bones; too much calcifies everything.

Pathway (USMLE-level)

• Skin: UV converts precursor → cholecalciferol (D3)
• Liver: 25-hydroxylation → 25-OH D
• Kidney: 1α-hydroxylation → 1,25-(OH)$_2$ D (calcitriol)
  Stimulated by PTH and low phosphate (classically tested)

Deficiency findings

• Rickets (kids): bone deformities, bowed legs, rachitic rosary
• Osteomalacia (adults): bone pain, fractures, low mineralization

Toxicity

• Hypercalcemia symptoms: kidney stones, abdominal pain/constipation, neuropsychiatric changes
• Can cause soft tissue calcifications

Stem triggers

• “Dark-skinned person, little sun exposure, bone pain”
• “Chronic kidney disease + bone issues” (impaired activation)

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Vitamin E: “Antioxidant for RBCs and neurons”

The one-liner

Vitamin E protects membranes from oxidative damage—without it, RBCs pop and long tracts malfunction.

Deficiency = 2 buckets

• Hematologic: hemolytic anemia, fragile RBCs (oxidative damage)
• Neurologic: posterior column/spinocerebellar signs
  • Ataxia
  • Loss of vibration/proprioception
  • Peripheral neuropathy

Stem triggers

• “Premature infant” (limited stores) or “fat malabsorption + neuro symptoms”
• “Hemolysis with acanthocytes” (membrane abnormalities)

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Vitamin K: “Clotting factor activation”

The one-liner

Vitamin K activates clotting factors via γ-carboxylation—low K means you can’t clot, so PT/INR rises.

Must-know list

Vitamin K–dependent factors: II, VII, IX, X, protein C, protein S
Mnemonic: “1972 + C&S” (as in years, not labs)

Mechanism tested on Step

• Vitamin K is a cofactor for γ-glutamyl carboxylase → adds carboxyl groups so factors can bind Ca$^{2+}$ and attach to phospholipid surfaces.

Deficiency scenarios

• Newborns: sterile gut (no bacterial synthesis) + low vitamin K in breast milk → hemorrhagic disease of newborn
  → prevent with vitamin K injection
• Broad-spectrum antibiotics: wipe out gut flora (less menaquinone)
• Fat malabsorption: obstructive jaundice, pancreatic insufficiency

Drug tie-ins (very testable)

• Warfarin inhibits vitamin K epoxide reductase → ↓ active vitamin K → ↑ PT/INR
• Warfarin effect is first seen with protein C decline (short half-life) → transient hypercoagulability early.

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Rapid-Fire USMLE Associations (quick review bullets)

• Fat malabsorption → deficiency of ADEK (think biliary obstruction, CF, celiac, orlistat).
• Night blindness + Bitot spots → Vitamin A deficiency
• Bone pain + fractures + low sunlight/CKD → Vitamin D deficiency
• Hemolytic anemia + neuro signs in malabsorption → Vitamin E deficiency
• Bleeding + ↑ PT/INR (especially newborn/antibiotics/cholestasis) → Vitamin K deficiency
• Toxicity risks: mainly A and D (stored, accumulate)

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Mini Self-Check (30 seconds)

1. Patient with CF develops neuropathy and hemolysis → which vitamin? E
2. Newborn bleeding without prophylaxis → which vitamin? K
3. Night blindness and xerophthalmia → which vitamin? A
4. Osteomalacia in CKD → which vitamin pathway impaired? D activation in kidney