# pixorize.com

> AI-optimized mirror of pixorize.com containing 50 pages totalling 14,404 words of clean markdown content, structured data, and semantic HTML. Original source: https://pixorize.com/. Last updated: 2026-06-10T00:49:55.432Z.

Each page is available as HTML (with JSON-LD structured data) and Markdown (text-only, ideal for LLMs and RAG).

## Homepage

- [Memorize Anything](/content/site-root.html): We turn complex facts into easy-to-remember, visual stories. Use mnemonics to gain an edge on high-stakes exams. (135 words)

## Articles & Blog Posts

- [Electron Transport Chain (ETC)](/content/view/7183/index.html): The electron transport chain, or the ETC for short, is a series of proteins found along the inner membrane of the mitochondria. The ETC plays a major role in aerobic respiration in the cell. 

There are 5 main protein complexes of the ETC to know. The first is complex I, also known as NADH dehydrogenase. Complex I receives two electrons from the high energy NADH, oxidizing the molecule to form NAD. Complex I then transfers both electrons to Ubiquinone, forming its high energy form, UQH2. The energy created through this transfer is harnessed to simultaneously pump four protons from the mitochondrial matrix into the intermembrane space. Complex I can be blocked by the actions of rotenone.

On the other hand, Complex II, also known as Succinate dehydrogenase, receives two electrons from FADH2, oxidizing the molecule to its low energy form, FAD. Like complex I, complex II transfers both of these electrons to ubiquinone, turning it into the high energy UQH2. However, unlike Complex I, Complex II does not pump any protons across the inner membrane.

Next, Complex III, also known as cytochrome reductase, transfers electrons from ubiquinone to cytochrome C. Because cytochrome C can only accept one electron at a time, two molecules of cytochrome C are actually needed to unload each ubiquinone molecule from Complex I and II. Using the energy of this reaction, Complex III also pumps four protons from the mitochondrial matrix into the intermembrane space. Complex III is blocked by the actions of antimycin A.

Afterwards, Complex IV, also known as cytochrome oxidase, then transfers electrons from Cytochrome C to oxygen, producing water as a byproduct. Through this transfer, complex IV can pump an additional two protons across the inner membrane into the intermembrane space. Complex IV can be blocked by cyanide, carbon monoxide, or by azide.

Complexes I through IV help create a proton gradient with a high concentration of protons in the intermembrane space. These protons flow down their concentration gradient to return to the mitochondrial matrix via Complex V, formally known as ATP synthase. In other words, Complex V uses the energy generated from the release of this proton gradient to create ATP! ATP is a high energy molecule used as a generic power source in the cell. This process of phosphorylating ADP to form ATP is known as oxidative phosphorylation.  Complex V can be directly blocked by the actions of oligomycin.

In addition, a few uncoupling agents work to cause leakage of protons from the intermembrane space, destroying the proton gradient and blocking the production of ATP. A few uncoupling agents to know include aspirin, thermogenin from brown fat, as well as 2,4-DNP. (925 words)
- [Citric Acid Cycle (TCA Cycle)](/content/view/7189/index.html): The Citric Acid cycle, also known as the Krebs cycle or tricarboxylic acid (TCA) cycle, is a biochemical pathway that plays a central role in cellular respiration.

Although many biomolecules like fats, proteins, and others can be broken down to enter this cycle, the classic metabolite is pyruvate derived from glycolysis.  Pyruvate must first be converted into acetyl-CoA, by the pyruvate dehydrogenase complex, in a reaction that requires 5 cofactors, including Vitamin B1 AKA thiamine, Vitamin B2 AKA riboflavin, Vitamin B3 AKA niacin, Vitamin B5 AKA pantothenic acid, as well as lipoic acid. This pyruvate dehydrogenase complex also produces 1 molecule of NADH and carbon dioxide. This step is irreversible and is a site of regulation.

Acetyl-CoA is the actual starter molecule that enters the citric acid cycle. Acetyl-CoA combines with oxaloacetate to form citrate, in a reaction that is catalyzed by citrate synthase. This step is irreversible and is hence a site of regulation.

Next, aconitase catalyzes the conversion of Citrate to cis-aconitate, and then quickly to Isocitrate.

Isocitrate dehydrogenase then catalyzes the formation of alpha-ketoglutarate from isocitrate, producing 1 molecule of NADH and carbon dioxide in the process. This step is also irreversible and is therefore a regulatory step. Notably, isocitrate dehydrogenase is inhibited by high levels of ammonia.

Afterwards, the alpha-ketoglutarate is converted into succinyl-CoA in a reaction catalyzed by  alpha-ketoglutarate dehydrogenase. Alpha-ketoglutarate dehydrogenase is a complex that requires the same 5 factors as pyruvate dehydrogenase complex: namely, vitamin B1, B2, B3, B5, and lipoic acid. This reaction also produces 1 molecule of NADH and carbon dioxide. This step is also irreversible and is regulated.

Next, Succinyl-CoA is converted into Succinate, forming 1 molecule of GTP and releasing CoA in the process.

In the next step, Succinate dehydrogenase converts succinate to fumarate, generating 1 molecule of FADH2 in the process.

Next, fumarase converts fumarate to malate.

Finally, Malate dehydrogenase reforms oxaloacetate from malate, generating 1 molecule of NADH in the process. Oxaloacetate can then be reused in the cycle by combining with another molecule of acetyl-CoA.

In total, the citric acid cycle produces 3 molecules of NADH, 1 molecule of FADH2, and 1 molecule of GTP per unit of acetyl-CoA that enters. If we account for pyruvate as the starting point before acetyl-CoA, this adds 1 more molecule of NADH produced. These electron carriers then feed their electrons into the electron transport chain, which ultimately generates ATP via oxidative phosphorylation. Since the citric acid cycle is coupled to oxidative phosphorylation -- and hence oxygen -- the pathway is inhibited in anaerobic environments. This makes this cycle an important part of aerobic metabolism. (721 words)
- [Glycolysis](/content/view/7174/index.html): Glycolysis is a metabolic pathway that breaks down sugar to produce high energy molecules, like ATP and NADH. All of the reactions in glycolysis occur in the cytoplasm of cells.

The pathway begins with glucose, which is converted by either hexokinase or glucokinase to produce glucose-6-phosphate. This step consumes 1 molecule of ATP, and is an important irreversible and regulatory step that functions to trap glucose inside the cell. Notably, hexokinase is inhibited by its direct product, glucose-6-phosphate, while glucokinase is inhibited by an intermediate further downstream, fructose-6-phosphate.

In the next step, glucose-6-phosphate is converted to form fructose-6-phosphate.

Afterwards, PFK1 catalyzes the conversion of fructose-6-phosphate into fructose-1,6-bisphosphate.  This irreversible reaction consumes another molecule of ATP, and serves as the rate-limiting step of glycolysis. This reaction is therefore highly regulated: it is stimulated by AMP and fructose-2,6-bisphosphate, but is inhibited by ATP and citrate.

Next, aldolase acts on fructose-1,6-bisphosphate, creating one molecule of G3P and one DHAP intermediate. The DHAP is quickly converted into another molecule of G3P. This generates a total of 2 molecules of G3P.

Each molecule of G3P is then converted into 1,3-BPG, forming 1 molecule of NADH in the process. 

This 1,3-BPG is then converted by PG kinase to form 3-PG. This reaction produces 1 molecule of ATP.

The 3-PG is then converted into 2-PG.

Afterwards, enolase converts 2-PG to form PEP, which is an unstable, high-energy intermediate.

Finally, pyruvate kinase irreversibly converts PEP to pyruvate, forming another molecule of ATP in the process. This reaction is stimulated by Fructose-1,6-bisphosphate, and is inhibited by alanine, ATP, and glucagon.

At a higher level, all of the steps can be organized into two distinct phases: an initial investment phase and a later payoff phase. In the investment phase, 2 molecules of ATP are invested to break down each molecule of glucose into 2 molecules of G3P. In the later payoff phase, the 2 molecules of G3P are both turned into pyruvate, producing 4 molecules of ATP and 2 molecules of NADH. This means that glycolysis produces a net yield of two ATP, two NADH, and two pyruvate molecules. (654 words)
- [De Novo Purine Synthesis](/content/view/4386/index.html): De novo purine synthesis is a biochemical pathway that creates purine nucleotides from simple molecules. This can be contrasted against purine salvage, which recycles purines nucleotides after partial degradation.

De novo purine synthesis begins with the precursor molecule Ribose-5-phosphate (R5P) . R5P is then converted to its high energy, "activated" form, PRPP . This form enables the transfer of phosphoribosyl groups (such as R5P). This R5P transferred from PRPP forms the pentose sugar of the eventual purine nucleotide.

Next, PRPP undergoes a series of reactions that require aspartate, glycine, THF, and glutamine. Through these steps, PRPP is converted into IMP (inosine monophosphate), the purine precursor molecule. The conversion of PRPP to IMP can be inhibited by the drug 6-MP (6-mercaptopurine) as well as by its prodrug azathioprine.

Finally, IMP can be converted to either AMP (adenosine monophosphate) or GMP (guanine monophosphate). The latter reaction is especially important, as the drugs mycophenolate and ribavirin inhibit the enzyme IMP dehydrogenase, which converts IMP to GMP. (281 words)
- [Vitamin B7 (Biotin)](/content/view/3765/index.html): Vitamin B7 (Biotin) is a water-soluble vitamin, important in metabolism as a cofactor for several important carboxylase enzymes. Enzymes dependent on biotin include pyruvate carboxylase, acetyl-CoA carboxylase, and propionyl-CoA carboxylase.

Biotin deficiency is rare, but it can be induced by antibiotic usage or excessive consumption of raw egg whites. In particular, the avidin in egg whites binds and sequesters biotin. Patients with a biotin deficiency typically present with dermatitis, diarrhea, and alopecia. (239 words)
- [Vitamin B6 (Pyridoxine)](/content/view/3763/index.html): Vitamin B6 (Pyridoxine) refers to a group of water-soluble vitamins important in metabolic reactions via its active form, PLP (pyridoxal 5′-phosphate). PLP is involved in a number of enzymatic reactions, including transamination, decarboxylation, that of glycogen phosphorylase. PLP is also involved in neurotransmitter synthesis, cystathionine synthesis, histamine synthesis, heme synthesis, and gene expression.

Given its important physiologic roles, Vitamin B6 deficiency can present with many signs and symptoms. Examples include neuropathy (paresthesias), convulsions and a sideroblastic anemia secondary to ALA synthase dysfunction. Vitamin B6 deficiency can be caused by a variety of reasons, but classically is seen in the setting of oral contraceptive or isoniazid use. (299 words)
- [Vitamins B9 and B12 Deficiencies](/content/view/3950/index.html): Megaloblastic anemia is a macrocytic anemia caused by deficiencies of either Folate (Vitamin B9) or Cobalamin (Vitamin B12). Megaloblastic anemia is characterized by the presence of hypersegmented neutrophils (>5 lobes) in peripheral blood smears, and labs reveal elevated homocysteine levels. Despite these similarities, there are distinguishing characteristics between folate and cobalamin deficiency.

Cobalamin (B12) deficiency is characterized by neurologic symptoms, as myelin synthesis is impaired in a syndrome known as subacute combined degeneration. Specifically, the lateral corticospinal tract, spinocerebellar tract, and dorsal columns are affected. Labs show elevated methylmalonic acid (MMA) levels, a finding not observed in folate deficiency.

Contrastingly, Folate (B9) deficiency is more common and occurs faster than B12 deficiency, as the liver has a smaller reserve pool of folate. Folate deficiency is common in alcoholics, and is often seen in conjunction with Vitamin B1 (Thiamine) Deficiency. (352 words)
- [Vitamin K Biochemistry](/content/view/4014/index.html): Vitamin K is a fat-soluble vitamin synthesized by intestinal bacteria. Vitamin K is activated by the enzyme epoxide reductase to its reduced form, which acts as a cofactor for gamma-carboxylation of glutamic acid residues on blood clotting proteins. Therefore, Vitamin K plays an important role in coagulation (formation of blood clots), as there are a number of such vitamin K-dependent coagulation factors: including factors II, VII, IX, X, as well as protein C and S. (223 words)
- [Vitamin D Deficiency and Excess](/content/view/4062/index.html): Vitamin D imbalances can occur as deficiency or excess. Vitamin D deficiency is usually caused by low sun exposure. Importantly, infants are at risk due to low sun exposure and low levels of Vitamin D in breast milk. The clinical effects of Vitamin D deficiency mainly stem from decreased calcium and phosphate levels, leading to poor mineralization of bone, which presents as rickets in children and osteomalacia in adults. Other lab findings include increased alkaline phosphatase (ALP), a marker for compensatory bone resorption to restore calcium levels. Likewise, increased PTH levels are also observed, thought to be a compensatory response to hypocalcemia.

Vitamin D excess is rare, and mainly results from overconsumption. However, one rare but commonly tested cause is granulomatous disease, since epithelioid macrophages may express α-1 hydroxylase (usually only found in the kidney), which converts vitamin D to its active form, calcitriol. Symptoms of Vitamin D excess include hypercalcemia, GI symptoms, and altered mentation. (399 words)
- [Vitamin B3 (Niacin) Biochemistry](/content/view/3716/index.html): Vitamin B3 (Niacin) is a water-soluble vitamin which serves a key role as a precursor of the coenzymes NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate). Found in foods, niacin is also used pharmacologically as a treatment for lipid disorders, specifically for its ability to raise HDL ("good" cholesterol) and lower VLDL and LDL ("bad" cholesterols). The synthesis of niacin requires a number of factors, including tryptophan, Vitamin B2 (Riboflavin), and Vitamin B6 (Pyridoxine). (222 words)
- [Medicine & USMLE Subscriptions](/content/subscribe/index.html): Purchase a Pixorize subscription for the USMLE Step 1. (132 words)
- [Zinc](/content/view/3963/index.html): Zinc is an essential trace element that is required for the function of a wide variety of enzymes and transcription factors. One such enzyme requiring zinc is collagenase III, an enzyme involved in wound healing. Notably, a coordinated zinc icon is also required for zinc fingers, which are important DNA-binding structural motifs.

Since zinc plays such an important biological role, zinc deficiency leads to a number of characteristic signs and symptoms. Related to its role in collagenase III, zinc deficiency classically presents with delayed wound healing. Furthermore, zinc deficiency is characterized by decreased adult hair, notably in the axillary, facial, and pubic regions. It also leads to a number of sensory problems, such as anosmia (loss of smell) and dysgeusia (loss of taste). Zinc deficiency can also lead to liver problems, as it predisposes patients to alcoholic cirrhosis. Another notable characteristic is hypogonadism.

An important disease to note is acrodermatitis enteropathica, a metabolic disorder that affects zinc uptake through the bowel mucous membrane. It is characterized by a perioral, perianal, and perianal rash. (335 words)
- [De Novo Pyrimidine Synthesis](/content/view/4541/index.html): De Novo Pyrimidine Synthesis describes the biochemical pathway used to make pyrimidine nucleotides from building blocks in the cell.

Pyrimidine Synthesis begins with glutamine and carbon dioxide, which combine to form carbamoyl phosphate, in a reaction catalyzed by CPS2. Carbamoyl phosphate then combines with aspartate to form orotic acid, through steps that can be inhibited by leflunomide. Afterwards, orotic acid reacts with PRPP to form UMP, in a reaction that is impaired in orotic aciduria.

UMP is then phosphorylated to UDP, which has two possible fates: it can be converted into the pyrimidine nucleotide, CTP, or undergo reduction by ribonucleotide reductase (RNR) to dUDP. Notably, RNR can be inhibited by the drug, hydroxyurea. dUDP is then dephosphorylated to dUMP, which in turn undergoes methylation by thymidylate synthetase to form dTMP.

Thymidylate synthetase can be blocked by the drug, 5-fluorouracil (5-FU), or by its prodrug, capecitabine. Thymidylate synthetase also requires the cofactor N5,N10-methylene-THF, whose regeneration can be blocked by DHFR antagonists such as pyrimethamine, methotrexate, and trimethoprim. The reduction in THF by methotrexate can be reversed by leukovorin (folinic acid), which serves as an alternative source for N5,N10-methylene-THF (leukovorin rescue).

Find De Novo Pyrimidine Synthesis and more Biochemical Pathways among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (258 words)
- [Purine Salvage](/content/view/4414/index.html): Purine Salvage is a biochemical pathway that recycles partially degraded purine bases to reform purine nucleotides.

Purine salvage begins with the free nitrogenous bases, hypoxanthine and guanine. Guanine combines with PRPP to form GMP, whereas Hypoxanthine combines with PRPP to form IMP. IMP can then be interconverted with AMP. Therefore, salvage of AMP occurs through hypoxanthine. 

Both salvage reactions with PRPP are catalyzed by HGPRT  (hypoxanthine guanine phosphoribosyltransferase). Notably, Lesch-Nyhan Syndrome is caused by a defect of HGPRT and impairs purine salvage.

A less common purine salvage pathway begins with adenine, since adenine is not usually produced by purine degradation. Adenine combines with PRPP to form AMP, in a reaction catalyzed by APRT (adenine phosphoribosyltransferase).

Find Purine Salvage and more Biochemical Pathways among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (181 words)
- [Vitamin B1 (Thiamine) Biochemistry](/content/view/3680/index.html): Thiamine (Vitamin B1) is a water-soluble vitamin and an important constituent of TPP (thiamine pyrophosphate), a cofactor found in several important dehydrogenase reactions. Specifically, TPP is an important cofactor for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, and branched-chain ketoacid dehydrogenase. Besides dehydrogenase reactions, TPP also serves an important role as a cofactor for transketolase. (220 words)
- [Vitamin A (Retinol) Biochemistry](/content/view/3794/index.html): Vitamin A is a group of fat-soluble compounds that includes retinol, retinal, retinoic acid, and several provitamin A carotenoids (notably beta-carotene) found in leafy greens. Vitamin A is an antioxidant, and it has a number of functions.  These functions include growth and development, cell differentiation and immune maintenance, the formation of visual pigments, and the treatment of acne (isotretinoin) and measles. ATRA (all-trans retinoic acid), a form of vitamin A, is used to treat the APL, also known as acute promyelocytic leukemia (subtype of AML). (247 words)
- [Vitamin B12 (Cobalamin) Biochemistry](/content/view/3764/index.html): Vitamin B12 (Cobalamin) is a water-soluble vitamin important in many metabolic reactions. Cobalamin plays roles as a cofactor for the enzymes methionine synthase and methylmalonyl-CoA mutase. It is important in the nervous system for its role in myelin synthesis, as well as in the bone marrow for the maturation of red blood cells. Vitamin B12 is primarily obtained from the diet in meat products, as it is synthesized by the gut bacteria in animals. Before cobalamin can be absorbed, however, parietal cells in the stomach must first secrete intrinsic factor. Intrinsic factor then binds to cobalamin, after which it can be absorbed in the terminal ileum. (259 words)
- [Cori Cycle](/content/view/4270/index.html): The Cori Cycle, also known as the Lactic Acid Cycle, is a biochemical pathway that is used to manage lactate, which is produced by anaerobic metabolism during muscular activity or in the absence of oxygen (e.g. hypoxemia).

In muscle, glucose is converted into pyruvate through glycolysis, producing ATP in the process. Pyruvate is then converted into lactate by the enzyme lactate dehydrogenase (LDH). Most tissues including muscle have no mechanism to metabolize excess lactate, so they export the lactate to the bloodstream. If left unmanaged, the resulting accumulation can lead to lactic acidosis.

The organ responsible for metabolizing lactate is the liver. The liver contains enzymes necessary for gluconeogenesis, providing a method to convert accumulated lactate and pyruvate into glucose. This glucose can then be exported back out to tissues, which can then use it for additional energy. This full circle of glucose and lactate forms the cycle.

However, the Cori Cycle requires a net loss of 4 ATP to function, so it is not an infinite energy machine. Specifically, 6 ATP are used for gluconeogenesis in the liver, and 2 ATP are yielded by glycolysis in muscle. In other words, the Cori Cycle moves energy from the liver to the muscle, and lactate vice versa, at the expense of 4 ATP. (333 words)
- [Vitamin B3 (Niacin) Deficiency and Excess](/content/view/3816/index.html): Niacin (Vitamin B3) imbalances in the body may present as deficiency or excess. Mild niacin deficiency presents with glossitis, and severe deficiency is characterized by the clinical syndrome of pellagra, which includes the constellation of dermatitis, dementia, diarrhea, and potentially death. Niacin excess is rare, and is typically observed after administering niacin to treat lipid disorders. Symptoms of excess notably include facial flushing responsive to aspirin, flares of gout (hyperuricemia), and occasionally, hyperglycemia (high blood sugar). (234 words)
- [Vitamin A (Retinol) Deficiency and Excess](/content/view/4026/index.html): Vitamin A (Retinol) imbalances include syndromes of deficiency and excess.

Vitamin A deficiency has a number of characteristic clinical findings, including night blindness (nyctalopia), bitot spots, dry scaly skin (xerosis cutis), and keratomalacia (corneal liquefaction).

Vitamin A excess is more common than deficiency, and chronic hypervitaminosis A is characterized by dry skin, joint pain, pseudotumor cerebri, and hepatomegaly. Acute vitamin A toxicity presents with nausea/vomiting and vertigo. Crucially, vitamin A is teratogenogenic, and prescription of retinol-containing drugs should be carefully considered in sexually-active and pregnant women. (308 words)
- [Vitamin K Deficiency](/content/view/4025/index.html): Vitamin K deficiency typically presents with bleeding or hemorrhage. Causes include insufficient intake (malnourishment) or insufficient production by gut flora. Specifically, Crohn's disease, cystic fibrosis, and other causes of pancreatic insufficiency can lead to poor absorption of this fat-soluble vitamin. Insufficient production by gut flora is of particular concern in newborns, as their sterile intestines are unable to synthesize vitamin K. This leads to a condition known as hemorrhagic disease of the newborn, which is characterized by increased PT (and PTT) but normal bleeding time. Likewise, prolonged antibiotic use (broad-spectrum) may disturb gut flora, which again may lead to impaired synthesis of vitamin K and subsequent deficiency. (283 words)
- [Alanine (Cahill) Cycle](/content/view/4613/index.html): The Alanine or Cahill Cycle is the biochemical pathway for shuttling amino groups from the muscle to the liver.

In the muscle, amino groups are produced from the breakdown of amino acids. α-ketoglutarate accepts these amino groups, and is converted into glutamate after accepting an amino group. Glutamate then transfers the amino group to pyruvate, producing alanine in a reaction catalyzed by the enzyme, alanine transaminase, better known as ALT (see Pyruvate Metabolism). Alanine can then exit to the bloodstream to reach the liver.

At the liver, alanine is taken up and converted into pyruvate. This involves the removal of an amino group, catalyzed by alanine transaminase (ALT) working in reverse. The amino groups are transferred to α-ketoglutarate, producing glutamate. Glutamate then contributes the amino groups in ammonia for the Urea Cycle, where they are packaged for elimination. The pyruvate produced in the liver is then used for gluconeogenesis, making glucose. This glucose is exported to the bloodstream, and some of it ends up back in the muscle, finishing the cycle.

Find Alanine (Cahill) Cycle and more Biochemical Pathways among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (239 words)
- [Homocysteine Metabolism](/content/view/4806/index.html): Homocysteine can be metabolized down two different pathways: (1) methylation to methionine, (2) or transsulfuration to cystathionine with the eventual formation of cysteine.

Production of methionine from homocysteine is catalyzed by methionine synthase, which requires the Vitamin B9 (Folate)-derived 5-MTHF and Vitamin B12 (Cobalamin). Therefore, decreases in either folate or cobalamin can lead to increases in homocysteine (see Vitamins B9 and B12 Deficiencies). Notably, 5-MTHF is regenerated by MTHFR, and defects in MTHFR can lead to excess homocysteine and homocystinuria (see Homocystinuria - coming soon).


Production of cystathionine and eventually cysteine occurs through a different set of reactions. Namely, cystathionine synthase combines homocysteine and serine to produce cystathionine, using Vitamin B6 (Pyridoxine) as a cofactor. The cystathionine is then cleaved to produce cysteine. 

Find this Homocysteine Metabolism mnemonic and more Biochemical Pathways mnemonics among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (193 words)
- [Catecholamine Synthesis & Breakdown](/content/view/4681/index.html): Catecholamine Synthesis is a biochemical pathway used to produce dopamine, norepinephrine, and epinephrine. This process takes place in the adrenal medulla as well as the post-ganglionic fibers of the sympathetic nervous system.

The pathway begins with phenylalanine, which is converted into tyrosine. This reaction is catalyzed by the enzyme phenylalanine hydroxylase, and requires the cofactor, BH4 (tetrahydrobiopterin) . Notably, this reaction is impaired in patients with Phenylketonuria.

Next, tyrosine is converted into DOPA, by the enzyme tyrosine hydroxylase. Tyrosine hydroxylase also requires a BH4 cofactor. Afterwards, DOPA is converted into dopamine, by the enzyme DOPA decarboxylase. This reaction requires Vitamin B6 (Pyridoxine) as a cofactor, and can be blocked by the drug, carbidopa.

Subsequently, dopamine is converted into norepinephrine. This reaction is catalyzed by dopamine beta-hydroxylase, and requires Vitamin C (Ascorbic Acid) as a cofactor. Finally, norepinephrine is methylated by PNMT, producing epinephrine. This reaction requires SAM  as a cofactor, and can be stimulated by cortisol.

Catecholamine Breakdown is a separate biochemical pathway used to metabolize and eliminate catecholamines. Dopamine is degraded into homovanillic acid, while norepinephrine and epinephrine are first converted into metanephrines by the enzyme COMT. These metanephrines are then further degraded into vanillylmandelic acid, a reaction catalyzed by the MAO enzymes.

Find this Catecholamine Synthesis Mnemonic and more Biochemical Pathways Mnemonics among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (273 words)
- [Vitamin C (Ascorbic Acid) Deficiency and Excess](/content/view/3745/index.html): Vitamin C (Ascorbic Acid) imbalances can occur as either deficiency or excess. Deficiency of Vitamin C results in the clinical syndrome of scurvy. Symptoms include easy bleeding, swollen gums, weakened immune response, anemia, and coiled or “corkscrew” hairs. The bleeding abnormalities can manifest as bruising, petechiae, hemarthrosis, subperiosteal and perifollicular hemorrhages. Vitamin C excess is rare and presents clinically with fatigue, nausea/vomiting, calcium oxalate kidney stones, and increased risk for iron toxicity (hemochromatosis). (235 words)
- [Vitamin D Biochemistry](/content/view/4063/index.html): Vitamin D (calciferol) is a fat-soluble vitamin that exists in a number of different forms. Ergocalciferol (D2) is a less potent form of vitamin D found in plants, whereas cholecalciferol (D3) is a more potent form synthesized in the skin upon exposure to sunlight. In addition, dairy products may be fortified with vitamin D3.

After ingestion or synthesis, vitamin D (calciferol) undergoes hydroxylation in the liver to form 25-hydroxy Vitamin D (calcidiol), the inactive storage form of vitamin D. Later, calcidiol undergoes further hydroxylation in the kidney, forming the biologically-active form: 1,25-dihydroxy vitamin D (calcitriol). **Errata: video mentions "peritubular capillaries" in the kidney. 1,25 alpha-hydroxylase acts in the proximal tubules of the kidney. For examination purposes, knowing the kidney as the site of activation is sufficient.

Active vitamin D (calcitriol) operates at the kidneys, GI tract, and bone to control calcium and phosphate levels. At low levels, it leads to increased bone mineralization. At high levels, it leads to increased bone resorption, thereby increasing calcium and phosphate levels. (310 words)
- [Fatty Acid Breakdown (Carnitine Shuttle)](/content/view/4263/index.html): Fatty Acid Breakdown is a biochemical pathway involving the Carnitine Shuttle, used to metabolize fatty acids into molecules that can be harnessed for energy. This process usually occurs in the liver.

The pathway begins with fatty acids and coenzyme A (CoA), which are combined to form acyl-CoA. This Acyl-CoA is then shuttled via carnitine into the mitochondrial matrix, a process that can be inhibited by high levels of malonyl-CoA.

Inside the mitochondrial matrix, acyl-CoA dehydrogenase performs beta-oxidation, converting acyl-CoA into acetyl-CoA. Acetyl-CoA is a versatile molecule used to produce ketone bodies for export, or ATP via the Kreb’s Cycle for intracellular use.

Find Fatty Acid Breakdown and more Biochemical Pathways among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (172 words)
- [Pyruvate Metabolism](/content/view/4329/index.html): Pyruvate can be metabolized in many different reactions by the body. The four most important reactions include its conversion into (1) oxaloacetate, (2) alanine, (3) lactate, and (4) acetyl-CoA.

The first is the conversion of pyruvate into oxaloacetate, a reaction catalyzed by pyruvate carboxylase with the co-factor, Biotin (Vitamin B7).

Second, pyruvate can undergo transamination via ALT (alanine transaminase) into alanine, using Vitamin B6 (pyroxidine) as a cofactor.

Third, pyruvate is turned into lactate by lactate dehydrogenase (LDH), which uses the Vitamin B3 (Niacin)-derived NADH, generating NAD+ in the process.

Finally, pyruvate gets converted into acetyl-CoA by pyruvate dehydrogenase. This reaction is catalyzed by the pyruvate dehydrogenase complex, which requires 5 cofactors: Vitamins B1, B2, B3, B5, and lipoic acid. It also converts NAD+ to NADH in the process.

Find Pyruvate Metabolism and more Biochemical Pathways among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (193 words)
- [HMP Shunt (Pentose Phosphate Pathway)](/content/view/4957/index.html): The HMP Shunt, also known as the Pentose Phosphate Pathway or the Phosphogluconate Pathway, is a biochemical pathway that serves as an alternative metabolic pathway for glucose. 

The first phase is oxidative and irreversible. Glucose-6-phosphate (G6P) is converted via series of steps into Ribulose-5-phosphate. The most important catalytic enzyme is Glucose-6-phosphate Dehydrogenase (G6PD), which produces NADPH in the process. This is the major source of NADPH in the cell, and decreased NADPH can be seen in G6PD Deficiency.

The second phase is non-oxidative and reversible, and involves transketolase as a major enzyme. Ribulose-5-phosphate is converted into Ribose-5-phosphate, which can undergo further reactions to produce Fructose-6-phosphate and Glyceraldehyde-3-phosphate. Ribose-5-phosphate is an important precursor to PRPP in the Purine and Pyrimidine Synthesis pathways. Of note, the action of transketolase requires Vitamin B1/Thiamine as a cofactor.

Find this HMP Shunt mnemonic and more mnemonics for Biochemical Pathways among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (207 words)
- [Vitamin B1 (Thiamine) Deficiency](/content/view/3653/index.html): Thiamine (Vitamin B1) Deficiency is common in alcoholics and malnourished patients. The clinical picture of Vitamin B1 deficiency is known as beriberi, of which there are two main types: dry beriberi and wet beriberi. Dry beriberi describes neurological symptoms, and includes Wernicke encephalopathy and Korsakoff syndrome. Classically, Wernicke encephalopathy is characterized by confusion (encephalopathy), ataxia, and nystagmus. Korsakoff syndrome is a more severe finding that includes confabulations. Radiographic imaging of these patients typically reveals lesions at the mamillary bodies and thalamus. Wet beriberi describes cardiovascular effects of thiamine deficiency, and can include high output heart failure and dilated cardiomyopathy. (280 words)
- [Vitamin B9 (Folate)](/content/view/3695/index.html): Vitamin B9 (Folate) is a water-soluble vitamin that plays a key role as a component of THF (tetrahydrofolate). THF serves a key role in methylation reactions, such as those required for DNA and RNA synthesis. Folate is present in leafy green vegetables, and it is absorbed in the jejunum of the small intestine. (174 words)
- [Vitamin B2 (Riboflavin)](/content/view/3681/index.html): Vitamin B2 (Riboflavin) is a water-soluble vitamin which serves an important role as a precursor for the flavin coenzymes, including flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD). These flavins serve as cofactors in a number of redox reactions. One of the major enzymes requiring flavins (FAD+) as a cofactor is succinate dehydrogenase, which plays major roles in the Citric Acid Cycle and electron transport chain. In patients with riboflavin deficiency, cheilosis and corneal vascularization are characteristic findings. (202 words)
- [Kwashiorkor and Marasmus](/content/view/4594/index.html): Kwashiorkor and Marasmus are diseases of severe malnutrition, which are rare in developed countries but sometimes observed in developing countries. Kwashiorkor is a disease caused by protein deficiency, presenting with swelling of the belly (secondary to edema), skin lesions, fatty change of the liver, and anemia. Marasmus describes generalized muscle wasting caused by a deficiency of all nutrients, or a total caloric deficiency. It can be seen in people with poor intake, although cancer-related muscle wasting may also be described as marasmus. (221 words)
- [Vitamin B5 (Pantothenic Acid)](/content/view/3682/index.html): Vitamin B5 (Pantothenic Acid) is a water-soluble vitamin which serves a key role in the synthesis of CoA (coenzyme A), a cofactor in many metabolic reactions. It is also plays a role in fatty acid synthesis, as it is a cofactor for the enzyme fatty acid synthase (FAS). Vitamin B5 Deficiency is rare, and primarily presents with symptoms of gastroenteritis (diarrhea), with possible adrenal insufficiency, dermatitis, or alopecia. (192 words)
- [Vitamin E (Tocopherol/Tocotrienol)](/content/view/3779/index.html): Vitamin E refers to a group of fat-soluble vitamins including tocopherol and tocotrienol, for which the exact biological function is poorly understood. An excess of Vitamin E has been found to alter the function of vitamin K, enhancing warfarin's anticoagulant effects. Vitamin E deficiency can cause neurological problems, specifically affecting the spinocerebellar tract and dorsal columns. Deficiency can also lead to the finding of acanthocytosis (red blood cells with spiked cell membranes). As an antioxidant, deficiency of Vitamin E can lead to oxidative damage to red blood cells, resulting in hemolytic anemia. (240 words)
- [Visual MCAT Review](/content/mcat/index.html): We turn complex MCAT topics into easy-to-remember visual stories. Use mnemonics to gain an edge and get into medical school. (761 words)
- [Vitamin C (Ascorbic Acid) Biochemistry](/content/view/3717/index.html): Vitamin C (Ascorbic Acid) is a water-soluble vitamin important as a cofactor for hydroxylase enzymes. It is a cofactor for dopamine beta-hydroxylase, facilitating the conversion of dopamine to norepinephrine. Vitamin C is also involved in collagen synthesis, as a cofactor for hydroxylation of proline and lysine residues. As an antioxidant, Vitamin C also plays an important role in the reduction of iron (III) to iron (II), which is required for enteric absorption of iron. This property also makes vitamin C useful as an ancillary treatment for methemoglobinemia. (222 words)
- [Ethanol Metabolism](/content/view/4298/index.html): Alcohol  or Ethanol Metabolism occurs in the liver through several steps, beginning with ethanol (alcohol), proceeding through acetaldehyde, and ending with acetate (acetic acid), which is excreted in the urine.

First, ethanol can be metabolized into acetaldehyde in 3 ways. The most important way is through alcohol dehydrogenase in the cytoplasm, which is blocked by the drug, fomepizole. Alcohol dehydrogenase operates via zero-order kinetics, which means that it operates at a constant rate regardless of how much alcohol is present (amount ingested). Less important enzymes include CYP2E1 in the microsome, or catalase in the peroxisome.

The acetaldehyde is then metabolized into acetate through the actions of aldehyde dehydrogenase. The drug disulfiram is given to discourage drinking, as it blocks aldehdye dehydrogenase and leads to the build-up of the toxic intermediate: acetaldehyde.

The metabolism of alcohol usually generates 2 molecules of NADH from NAD+, which increases the NADH to NAD+ ratio. The increase in this ratio leads to a number clinical findings, such as lactic acidosis, fasting hypoglycemia, hepatosteatosis, and ketogenesis.

Find Ethanol Metabolism and more Biochemical Pathways among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (235 words)
- [Sorbitol (Polyol) Pathway](/content/view/4871/index.html): The Sorbitol Pathway, also called the Polyol Pathway, is a two-step process that converts glucose to fructose. The pathway contributes to diabetic complications affecting the eyes, kidneys, and nerves.

First, glucose is converted into sorbitol, in a reaction catalyzed by aldose reductase. This reaction also uses NADPH, producing NADP+ in the process.

Second, sorbitol is converted into fructose by sorbitol dehydrogenase. This reaction produces NADH from NAD+ in the process.

Deficiencies in sorbitol dehydrogenase activity cause sorbitol accumulation in high glucose states, such as in diabetes mellitus. The major tissues with poor sorbitol dehydrogenase activity are the lens, retina, kidney, and schwann cells of the peripheral nervous system. Sorbitol accumulation contributes to cataracts, retinopathy, renal failure, and peripheral neuropathy, respectively.

Find this Sorbitol (Polyol) Pathway mnemonic and more Biochemical Pathways mnemonics among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (190 words)
- [Purine Excretion](/content/view/4408/index.html): Purine Excretion describes the series of reactions used to excrete the free purine bases, hypoxanthine and guanine, in the event that they are not salvaged (see Purine Salvage).

The pathway begins with the purine bases, hypoxanthine and guanine, which are then converted into xanthine. Xanthine is then converted to uric acid, in a reaction catalyzed by xanthine oxidase. The xanthine oxidase enzyme can be inhibited by the drugs allopurinol and febuxostat. These drugs prevent the formation of uric acid and are commonly used to treat gout.

Uric acid clearance by the kidney plays a major role in purine excretion, and clearance is enhanced by the drugs probenecid and rasburicase. In contrast, aspirin has been shown to reduce clearance of uric acid.

Find Purine Excretion and more Biochemical Pathways among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (187 words)
- [Hartnup Disease](/content/view/3903/index.html): Hartnup Disease is an autosomal recessive metabolic disorder characterized by a dysfunction in the neutral amino acid transporter. This defect causes decreased absorption of nonpolar amino acids, specifically tryptophan. Since tryptophan is important for the synthesis of Vitamin B3 (Niacin), patients with Hartnup disease will also present with signs and symptoms consistent with Niacin Deficiency), with pellagra-like symptoms. Since clinical findings are primarily due to niacin/tryptophan deficiency, niacin supplementation and/or a high-protein diet can be used to treat the disease. (214 words)
- [Fatty Acid Synthesis (Citrate Shuttle)](/content/view/4245/index.html): Fatty Acid Synthesis is a biochemical pathway which uses the Citrate Shuttle to produce palmitate, a fatty acid, from other molecules.

First, citrate from the mitochondrial matrix is shuttled to the cytosol via the citrate shuttle. This citrate is then converted by ATP citrate lyase into Acetyl CoA.

Afterwards, Acetyl-CoA is turned into Malonyl-CoA via the Vitamin B7 (Biotin)-dependent Acetyl-CoA carboxylase enzyme.

Finally, this Malonyl-CoA is converted into Palmitate, a 16-C fatty acid at the end of this pathway. 

Find Fatty Acid Synthesis and more Biochemical Pathways among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (149 words)
- [404](/content/browse/index.html): Score higher on exam day with Pixorize's visual mnemonics. (6 words)
- [Thionamides (PTU vs Methimazole)](/content/view/6040/index.html): Propylthiouracil, shortened as PTU, and Methimazole are thionamide drugs that are used in the treatment of hyperthyroidism. They work by inhibiting the enzyme thyroid peroxidase, which prevents the organification or coupling of oxidized iodide to thyroglobulin in order to form thyroid hormones. PTU specifically also has a second mechanism of blocking the peripheral conversion of T4 to T3. All of these mechanisms are useful in the treatment of hyperthyroidism. An adverse effect of both drugs is bone marrow suppression, which presents in a variety of ways, including agranulocytosis and anemia. PTU specifically may cause life-threatening hepatotoxicity, while methimazole specifically acts as a teratogen during pregnancy. Due to these side effects, methimazole is preferred over PTU for the treatment of hyperthyroidism, except during pregnancy. (315 words)
- [Galactose Metabolism](/content/view/5170/index.html): Galactose metabolism is a series of reactions used by the body to process galactose. There are two major pathways which you should remember for test day.

In the first pathway, galactose is converted to galactitol, in a reaction catalyzed by aldose reductase.

In the second pathway, galactose is first converted into galactose-1-phosphate by the enzyme, galactokinase. Next, Galactose-1-phosphate is converted to glucose-1-phosphate, in a reaction catalyzed by a UDP transferase enzyme. In order to keep this reaction running, 4-epimerase is needed to regenerate certain intermediates. Finally, glucose-1-phosphate can enter into the normal glucose metabolism pathways, such as glycolysis and glycogenesis.

Deficiencies in galactokinase can cause Galactokinase Deficiency. Deficiencies in UDP transferase or epimerase can cause Galactosemia. (162 words)
- [Purchase Subscription](/content/purchase/10/index.html): Score higher on exam day with Pixorize's visual mnemonics. (80 words)
- [Urea Cycle](/content/view/4325/index.html): The Urea Cycle is a biochemical pathway that occurs in the liver to eliminate excess nitrogen as urea. Nitrogen is delivered in high amounts to the liver (refer to Cahill Cycle), and begins in this pathway as ammonia.

Ammonia combines with carbon dioxide to form carbamoyl phosphate, in a reaction catalyzed by the mitochondrial enzyme, CPS1.

Carbamoyl phosphate is then combined with ornithine to produce citrulline, in a reaction catalyzed by another mitochondrial enzyme, ornithine transcarbamylase. Notably, Ornithine Transcarbamylase Deficiency can block the urea cycle, leading to hyperammonemia.

Citrulline and aspartate are converted into argininosuccinate, and this reaction occurs via the argininosuccinate synthetase enzyme. Argininosuccinate is then broken down by argininosuccinase, to form arginine and fumarate.

Arginase splits arginine into urea and ornithine. The urea is excreted in the urine, thereby eliminating nitrogen, whereas the ornithine is regenerated, completing the urea cycle.

Find Urea Cycle and more Biochemical Pathways among Pixorize's visual mnemonics for the USMLE Step 1 and NBME Shelf Exams. (206 words)
- [Account Recovery](/content/recover-account/index.html): Score higher on exam day with Pixorize's visual mnemonics. (14 words)
- [sitemap-xml.html](/content/sitemap-xml.html) (1,292 words)

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