Biochemistry Mnemonics for USMLE Step 1: Amino Acids, Metabolism, Vitamins, and More
A ValueMD community study resource, originally shared on our forums and preserved here for students working through biochemistry for Step 1 and pre-clinical coursework.
Biochemistry is one of the most mnemonic-friendly subjects in the pre-clinical curriculum, largely because so much of it comes down to memorizing ordered sequences: cycles, pathways, classifications, and multi-letter acronyms. The collection below, built by the ValueMD student community, covers the highest-yield biochemistry mnemonics for amino acids, core metabolic pathways, vitamins, enzymes, and metabolic disease.
Educational note: these are student-built memory aids for exam review, not a substitute for a biochemistry textbook, First Aid, or your course material. A few entries below have been corrected or reordered for accuracy from the original forum thread; use them to reinforce concepts you’ve already studied.
Amino Acids
Essential Amino Acids
PVT. TIM HALL: Phenylalanine, Valine, Threonine, Tryptophan, Isoleucine, Methionine, Histidine, Arginine, Leucine, Lysine.
(“Pvt.” is short for Private, as in a military rank. Arginine and Histidine are considered semi-essential, since the body can synthesize small amounts but not enough during growth or illness.)
A related mnemonic used specifically for children, who need a slightly broader list: These Ten Valuable Amino Acids Have Long Preserved Life In Man: Threonine, Tryptophan, Valine, Arginine, Histidine, Lysine, Phenylalanine, Leucine, Isoleucine, Methionine.
Amino Acids That Form Acetyl-CoA or Acetoacetyl-CoA
A Lighter Lease (A-Ly-Tr-Le-Is): Acetyl-CoA/Acetoacetyl-CoA is fed by Lysine, Tryptophan, Leucine, and Isoleucine. Of these, Leucine and Lysine are the two amino acids that are purely ketogenic; tryptophan and isoleucine are both glucogenic and ketogenic.
Branched-Chain Amino Acids Used by Skeletal Muscle During Fasting
Muscles LIVe fast: Leucine, Isoleucine, Valine.
Creatine Phosphate Precursor Amino Acids
Nice GAMs: Glycine, Arginine, Methionine. (Creatine phosphate is a muscle energy store that spontaneously converts to creatinine, excreted in urine roughly in proportion to muscle mass, useful clinically for estimating muscle mass or kidney function.)
The Urea Cycle
Ordinarily, Careless Crappers Are Also Frivolous About Urination: the cycle proceeds Ornithine, Carbamoyl phosphate, Citrulline, (+ Aspartate joins), Argininosuccinate, (Fumarate leaves), Arginine, Urea.
Core Carbohydrate Metabolism
Glycolysis, Step by Step
Goodness Gracious, Father Franklin Did Go By Picking Pumpkins to Prepare Pies: Glucose, Glucose-6-phosphate, Fructose-6-phosphate, Fructose-1,6-bisphosphate, Dihydroxyacetone phosphate, Glyceraldehyde-3-phosphate, 1,3-Bisphosphoglycerate, 3-Phosphoglycerate, 2-Phosphoglycerate, Phosphoenolpyruvate (PEP), Pyruvate.
(“Did,” “By,” and “Pies” cue the “di-,” “bi-,” and “py-” prefixes of those three intermediates.)
The Citric Acid (Krebs) Cycle
Our City Is Kept Safe And Sound From Malice: Oxaloacetate, Citrate, Isocitrate, alpha-Ketoglutarate, Succinyl-CoA, Succinate, Fumarate, Malate.
A more detailed version that also captures citrate’s isomerization step: Oh! Citric Acid Is Of Course A Silly Stupid Funny Molecule: Oxaloacetate, Citrate, Aconitate, Isocitrate, Oxalosuccinate, alpha-Ketoglutarate, Succinyl-CoA, Succinate, Fumarate, Malate (“Silly” and “Stupid” distinguish succinyl-CoA from succinate).
Products of Complete Pyruvate Oxidation
4 Naked Fun 3 Coeds + 1 Guy: complete oxidation of pyruvate (through pyruvate dehydrogenase and the citric acid cycle) yields 4 NADH, 1 FADH2, 3 CO2, and 1 GTP.
Carbon Monoxide and the Electron Transport Chain
CO blocks CO: carbon monoxide inhibits cytochrome c oxidase (Complex IV).
Rotenone’s Site of Action
Rotenone is a site-specific inhibitor of Complex I.
Nucleic Acids and Gene Expression
DNA Bond Strength
Strong like crazy glue: cytosine and guanine pair with 3 hydrogen bonds (stronger), while adenine and thymine pair with only 2 (weaker). This matters in DNA replication, since the weaker A-T bonds are typically where the replication origin or primer sites form.
Purines vs. Pyrimidines
Pyrimidines are single-ring structures: Cytosine, Uracil, and Thymine. Purines are double-ring structures: Adenine and Guanine. A helpful shorthand: pyrimidines are “cut” from purines structurally, since they’re the smaller ring.
mRNA Splicing
Exons are expressed (they stay in the mature mRNA); introns are excised and degraded.
tRNA Shape
Transfer RNA (tRNA) is shaped like a capital letter “T.”
Mitochondrial DNA
Mitochondrial DNA is inherited maternally and has a notably high mutation rate: “mt DNA” as “Maternal Transfer, Mutates Tremendously.”
Enzymes
The Six Enzyme Classes
Over The HILL: Oxidoreductases, Transferases, Hydrolases, Isomerases, Ligases, Lyases.
Competitive vs. Non-Competitive Inhibition
With competitive inhibition, Km increases while Vmax stays the same (the reaction can still reach full speed at high enough substrate concentration). With non-competitive inhibition, Km stays the same while Vmax decreases (no amount of substrate can overcome the inhibitor).
The Golgi Complex
A SPAM: Adds mannose-6-phosphate to lysosomal proteins, Sulfates sugars and select tyrosines, assembles Proteoglycans, Adds O-oligosaccharides to serine/threonine, Modifies N-oligosaccharides on asparagine. (The Golgi also distributes proteins and lipids arriving from the ER.)
Signaling and Hormones
G Proteins and Their Receptors
QISS & QIQ: in order, alpha-1 (Gq), alpha-2 (Gi), beta-1 (Gs), beta-2 (Gs), and M1 (Gq), M2 (Gi), M3 (Gq).
Adrenaline’s Mechanism (Simplified)
A-B-C: Adrenaline activates Beta receptors, which increases Cyclic AMP.
Glucagon’s Function
Glucagon raises blood glucose through a cAMP-mediated signaling mechanism.
Insulin’s Function
Insulin drives both potassium and glucose into cells, which is why insulin (with glucose) is used clinically to temporarily lower dangerous serum potassium levels.
GnRH-LH-FSH Axis
The hypothalamus releases GnRH, which stimulates the pituitary to release LH and FSH; this axis is regulated by feedback from estrogen and testosterone.
Vitamins
Fat-Soluble Vitamins
KADE: Vitamin K, Vitamin A, Vitamin D, Vitamin E.
B Vitamins in Order
The Rhythm Nearly Proved Contagious: Thiamine (B1), Riboflavin (B2), Niacin (B3), Pyridoxine (B6), Cobalamin (B12). (This shorter list skips B5, B7, and B9, which are also essential B vitamins.)
Niacin (B3) Deficiency: Pellagra
The classic 4 D’s: Dermatitis, Diarrhea, Dementia, and Death if untreated.
Hypervitaminosis A
Increased Vitamin A makes you HARD: Headache, Hepatomegaly, Anorexia, Alopecia, Really painful bones, Dry skin/Drowsiness.
Folate Deficiency Causes
A FOLIC DROP: Alcoholism, Folate antagonists (e.g., methotrexate), Oral contraceptives, Low dietary intake, Infection (e.g., malabsorption from Giardia), Celiac sprue, Dilantin (phenytoin), Relative deficiency (increased demand, as in pregnancy or hemolysis), Old age, Pregnancy.
Metabolic and Genetic Disease
Acute Intermittent Porphyria: The 5 P’s
Pain in the abdomen, Polyneuropathy, Psychological/psychiatric abnormalities, Port-wine (dark/pink) urine, Precipitated by drugs such as barbiturates, oral contraceptives, and sulfa drugs.
Elevated BUN:Creatinine Ratio
ABCD: Azotemia (pre-renal), Bleeding (GI), Catabolic state, Diet (high-protein parenteral nutrition).
G6PD Deficiency: Oxidant Drugs That Trigger Hemolysis
AAA: Antibiotics (e.g., sulfamethoxazole), Antimalarials (e.g., primaquine), Antipyretics such as acetanilid (notably not aspirin or acetaminophen at normal doses).
Tangier Disease
Hallmark finding: large, orange tonsils, from HDL deficiency causing cholesteryl ester accumulation in tissue.
Glycogen Storage Diseases
The enzyme defects in Andersen disease (Type IV) and Cori disease (Type III) are easy to mix up: Andersen’s = Branching enzyme deficiency; Cori’s = Debranching enzyme deficiency.
The full set of Types I through VI, in order: Von Gierke’s (I), Pompe’s (II), Cori’s (III), Andersen’s (IV), McArdle’s (V), Hers’s (VI).
Pompe Disease
A lysosomal storage disease caused by alpha-1,4-glucosidase (acid maltase) deficiency, classified as Type II glycogen storage disease.
Fabry Disease
Alpha-galactosidase A deficiency, X-linked recessive (affects males). Key features: angiokeratomas, burning pain in the extremities, elevated BUN from progressive renal failure, and foam cells in the glomeruli and tubules.
Phenylketonuria (PKU)
Caused by a deficiency of phenylalanine hydroxylase.
Galactosemia
Caused by a deficiency of galactose-1-phosphate uridyltransferase (GALT), tested clinically via the GALT enzyme assay.
Sickle Cell Disease
A single amino acid substitution: at the sixth position of the hemoglobin beta chain, valine replaces glutamic acid.
Acid-Base and Electrolytes
Nitric Oxide Synthesis
Arginine is the amino acid precursor to nitric oxide (NO); synthesis also requires NO synthase, calcium, and NADPH.
The Na+/K+ Pump
The pump moves 2 potassium ions into the cell and 3 sodium ions out, maintaining a high intracellular potassium concentration relative to sodium.
Normal Anion-Gap Metabolic Acidosis, by Potassium Level
With hyperkalemia (RAISE K+): RTA type 4, Aldosterone or mineralocorticoid deficiency, Iatrogenic causes (NH4Cl, HCl administration), obstructive uropathy, and early uremia.
With hypokalemia (ReDUCE K+): Renal tubular acidosis types 1 and 2, Diarrhea, Ureteral diversion into bowel, Carbonic anhydrase inhibitors, and post-hyperventilation.
Hemoglobin-Oxygen Dissociation Curve: Shift to the Right
CADET, face right: increased CO2, increased Acid (decreased pH), increased 2,3-DPG, increased Exercise, and increased Temperature all shift the curve right, favoring oxygen release to tissues.
The Malate-Aspartate Shuttle
Malate moves into the mitochondrion; alpha-ketoglutarate and aspartate move back out.
Metabolic Pathways That Span Both Cytoplasm and Mitochondria
HUG: Heme synthesis, the Urea cycle, and Gluconeogenesis all have steps occurring in both the cytoplasm and the mitochondria.
Structural Biochemistry
Collagen Synthesis, Concisely
COLLAGEN: Covalent cross-links, Vitamin C-dependent hydroxylation, Connective tissue and Cartilage, Chondroblast/osteoblast production, Copper as a cofactor for cross-linking, functions Outside the cell, Osteogenesis imperfecta as a disease of collagen defects, Lysyl hydroxylase and Lysyl oxidase in cross-link formation, Long triple-helical fibers found in Ligaments, Alpha chains held by hydrogen bonds, Ascorbate needed for hydroxylation of lysyl/prolyl residues, Glycine in every third position with Glycosylation via the Golgi, functions in the Extracellular matrix including the Eye, and defects causing Ehlers-Danlos syndrome, with an N-terminal propeptide in procollagen.
Dicarboxylic Acids (C2 through C10)
Oh My, Such Good Apple Pie, Sweet As Sugar: Oxalic, Malonic, Succinic, Glutaric, Adipic, Pimelic, Suberic, Azelaic, Sebacic.
Frequently Asked Questions
What’s the easiest way to remember the essential amino acids? “PVT. TIM HALL” covers all ten: Phenylalanine, Valine, Threonine, Tryptophan, Isoleucine, Methionine, Histidine, Arginine, Leucine, Lysine. Arginine and Histidine are considered semi-essential in adults.
What is the correct order of the urea cycle? Ornithine, Carbamoyl phosphate, Citrulline, then aspartate joins to form Argininosuccinate, fumarate leaves to form Arginine, and Arginine is finally cleaved to produce Urea (regenerating ornithine).
How do competitive and non-competitive enzyme inhibitors differ? Competitive inhibitors increase Km but leave Vmax unchanged, since enough substrate can outcompete the inhibitor. Non-competitive inhibitors leave Km unchanged but decrease Vmax, since the inhibitor’s effect can’t be overcome by adding more substrate.
What causes the hemoglobin-oxygen dissociation curve to shift right? Increased CO2, acid (lower pH), 2,3-DPG, exercise, and temperature all shift the curve right, meaning hemoglobin releases oxygen more readily to tissues, remembered as “CADET, face right.”
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