washed nation

Acidosis is

blood pH < 7.35 from excess H+ ions

alkalosis is

pH > 7.45 from an H+ deficit

Vmax

The maximum reaction velocity when all enzyme active sites are saturated with substrate

Pathway Inhibitors

Inhibitors slow enzymatic reactions, causing upstream intermediates to build up and downstream products to drop

Aerobic respiration

uses oxygen in the TCA cycle for high ATP

anaerobic respiration

reduces pyruvate to lactate to regenerate NAD+

Glycolysis

breaks down glucose in fed states via PFK-1

gluconeogenesis

builds glucose in fasting states using liver bypass enzymes

Cholesterol Excretion

Cholesterol cannot be broken down for energy and is eliminated by the liver into bile or converted to bile acids for fecal excretion

Sources of Ammonia

Ammonia comes from amino acid catabolism via glutamate deamination and intestinal bacterial protein breakdown

Fatty Acids and Mitochondrial Transport

Hydrocarbon chains ending in a carboxylic acid group that cross the inner mitochondrial membrane via the carnitine shuttle (CPT-I and CPT-II)

Fate of Acetyl-CoA

Enters the TCA cycle for ATP production, or forms ketone bodies in the liver when oxaloacetate is depleted

Vitamin Important to the PAP

Pantothenic acid (Vitamin B5) is required to synthesize Coenzyme A and the phosphopantetheine group

Ketone Body Production

Produced in the liver during prolonged fasting or uncontrolled diabetes when oxaloacetate is depleted for gluconeogenesis

Enzyme Regulated in Fatty Acid Synthesis

Acetyl-CoA Carboxylase (ACC) is the rate-limiting enzyme converting acetyl-CoA to malonyl-CoA.

Rate-Limiting Enzyme in Cholesterol Synthesis

HMG-CoA Reductase is the rate-limiting enzyme converting HMG-CoA to mevalonate.

Statins

block HMG-CoA reductase

Bile Acid Sequestrants

block bile reabsorption, forcing the liver to upregulate LDL receptors to lower plasma cholesterol.

Urea Cycle Purpose, Location, and TCA Connection

Converts toxic ammonia into urea across the mitochondria and cytosol, linking to the TCA cycle via fumarate

Importance of Aminotransferases

Transfer amino groups to alpha-ketoglutarate to form glutamate, acting as clinical biomarkers for tissue damage

Glutamate

collects amino groups

glutamine synthetase

binds free ammonia to glutamine for safe blood transport

PKU

is caused by phenylalanine hydroxylase deficiency causing cognitive deficits

high ammonia

causes cerebral edema and encephalopathy

Glucogenic amino acids

form pyruvate or TCA intermediates for gluconeogenesis

ketogenic amino acids

form acetyl-CoA or acetoacetyl-CoA

Makeup of the Cell Membrane

A phospholipid bilayer with hydrophilic heads and hydrophobic tails, interspersed with cholesterol, proteins, and carbohydrates

Simple Diffusion

Passive movement of small nonpolar molecules down a concentration gradient without transport proteins

Facilitated Diffusion

Passive transport of polar/charged molecules down a gradient via specific carrier or channel proteins

Clinical Correlation of Liposomes

Artificial phospholipid vesicles used for targeted drug delivery to increase tumor accumulation and reduce systemic toxicity

Symporters

move two molecules in the same direction across a membrane

antiporters

move them in opposite directions

Sodium-Potassium Pump

Uses ATP hydrolysis to pump 3 Na+ ions out and 2 K+ ions into the cell against their concentration gradients.

Clinical Correlation of the Na-Glucose Symporter:

SGLT reabsorbs glucose in the kidneys and gut, and SGLT2 inhibitors block it to treat Type 2 diabetes via glucosuria

Clinical Mechanism of Cystic Fibrosis

Mutations in the CFTR chloride channel impair Cl- and water transport, causing thick mucus in the lungs and pancreas

Ionotropic Receptors

Ligand-gated ion channels that alter membrane ion flux within milliseconds of ligand binding

G Protein-Coupled Receptors (GPCRs)

Seven-transmembrane receptors coupled to G proteins that trigger secondary messenger cascades in seconds to minutes

Enzyme-Linked Receptors

Receptors like tyrosine kinases that dimerize and autophosphorylate to trigger effects over minutes to hours.

Nuclear Receptors

Intracellular receptors that bind lipophilic ligands and alter gene transcription over hours to days

Clinical Correlations of Signaling Pathway Dysfunction

Mutations or dysregulation in cellular signaling pathways drive endocrine diseases, metabolic disorders, and cancer

Clinical Effects of Medications Having Different Signaling Pathways

Receptor kinetics dictate drug onset timing, ranging from milliseconds for ionotropic drugs to days for nuclear-acting steroids

Zymogens

Inactive enzyme precursors synthesized to prevent autodigestion of secretory organs until cleaved into active forms

Enzymes that Aid in Digestion

Digestive enzymes like pepsin, trypsin, amylase, and lipase break down dietary macronutrients for absorption

Vitamins

Essential organic nutrients classified as water-soluble coenzymes or fat-soluble compounds required from the diet

Digestive Enzymes in Stomach

Pepsin.

Digestive Enzymes in Pancreas/Intestine

Trypsin, chymotrypsin, elastase, carboxypeptidases (proteins); pancreatic amylase (carbohydrates); pancreatic lipase, colipase, bile salts (lipids); brush-border disaccharidases (lactase, sucrase, maltase).

Water-Soluble Vitamins (B-complex, C)

Function primarily as coenzymes; excess excreted in urine.

Thiamine (B1)

Beriberi, Wernicke-Korsakoff syndrome.

Vitamin C:

Scurvy (defective collagen hydroxylation)

Niacin (B3)

Pellagra (diarrhea, dermatitis, dementia)

Fat-Soluble Vitamins (A, D, E, K)

Require dietary fat and bile salts for efficient intestinal absorption; stored in liver/adipose tissue.

Vitamin A

Night blindness, epithelial keratinization.

Vitamin D

Rickets (children), osteomalacia (adults).

Vitamin K

Coagulation factor carboxylation defects leading to bleeding tendencies.

Chylomicrons

Transport dietary triglycerides and cholesterol from gut to peripheral tissues.

VLDL

Transport endogenous triglycerides from liver to peripheral tissues.

IDL

VLDL remnant; precursor to LDL.

LDL

Delivers cholesterol to peripheral tissues ("bad cholesterol"); high levels drive atherosclerotic plaque formation.

HDL

Performs reverse cholesterol transport, clearing excess peripheral cholesterol back to the liver ("good cholesterol").

Saturated fatty acids

contain single bonds only

unsaturated fatty acids

contain one or more double bonds (introducing kinks that increase membrane fluidity).