2,4 DNP
MOA: Uncouples OXPHOS, causing release of calcium from mitochondrial stores and preventing calcium re-uptake. Leads to free intracellular calcium and causes muscle contraction and hyperthermia
Lipid soluble. Dissociable proton with pKa near 7.2, so DNP picks up fromton in intermembrane space where H+ conc is high and carries it across the membrane, to dissociate in lower proton conc of the matrix. Makes it so cells cannot mainatin electrochemical gradient or synthesize ATP, which decreased ATP conc and increases electron transport and fuel oxidation.
Toxicity: Hyperthermia, muscle contraction, ect
Met: rapid, except in possible cases of liver disfunction

MOA: Acts directly on skeletal muscles by interfering with release of calcium ion from the sarcoplasmic reticulum (by antagonizing ryanodine receptors), prevents or reduces the increase in myoplastic calcium ion conc that activates the acute catabolic processes associated with malignant hypothermia. The muscle relaxation (bc less intracellular calcium) allows heat dissapation.
Use: Treat/prevent malignant hyperthermia, manage neuroleptic malignant syndrome, muscle spasticity, 2,4 dinitrophenol poisoning
BBW: Hepatotoxicity
Side Effects: Flushing, drowsiness, dysphagia, anemia
Met: Hepatic

NSAID. Decrease inflammation and pain by inhibiting prostoglandin formation by reversibly inhibiting COX-2 (and COX-1) enzymes via non-covalent binding to active site, which results in less PGE2 (decreased vasodilatino and vascular permeability).
Use: Acute Gout, osteoarthritis, ect
Can cause GI bleeding/peptic ulcers
Do not give if renal issue (causes lithium retention bc reducing its excretion from kidneys)
Can cause increased plasma renin and aldosterone, increase Na and K retentino (edema, HTN, hyperkalemia, hypernatremia)
FDA warning that can cause heart attacks or strokes

Depolymerization of microtubules (Prevents microtubule formation) decreases polymorphonuclear leukocytes (neutrophils) from migrating in response to leukotriene B4 (prevents chemotaxis)
Use: Acute and prophylactic treatment for gout inflammation
Don’t give with renal issues, bc is renally excreted
Characteristic side effect is diarrhea

MOA: Corticosteroid. Has some immunosupressive effects, which can decrease migration of leukocytes and reverse the increased capillary permeability. Mostly acts by targeting acute inflam by increasing the transcription of lipocortins (such as annexin 1) which bind and inhibit phospholipase A2, preventing the cleavage of arachidonic acid from membrane phospholipids. Inhibits expression of COX2.
Use: Used as immunosuppressant for autoimmune diseases and for acute Gout. Most commonly used glucocorticoid in cancer chemo. Also used in CLI, non-Hodgekin hymphoma. Treats symptoms of inflammation from pneumonia.
Toxicity: Peptic Ulcers and Cushings like symptoms: weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis, HTN, hyperglycemia, psychosis

Hyperurecemia treatment (aka prevent gout). Inhibits xanthine oxidase, interfering w/ conversion of hypoxanthine and xanthine to uric acid. Use: chronic gout prevention. Side Effects: Rashes, Hypersensitivity, ect

MOA: Inhibits renal tubular urate resorption; inhibits renal tubular penicillin secretion. Use: Chronic gout treatment and as penecillin adjunct. Do NOT use if in acute gout attack.

Long acting Insulin
Should never make you hypoglycemic when you are not eating, so do NOT use to cover the food someone is eating
Highest efficacy, variable cost
High hypoglycemic risk, weight gain
Caution for hypoglycemia if renal disease (kidneys and liver)
Side Effects: hypoglycemia

Intermediate Acting Insulin

Short acting Insulin
Regular body insulin. Give for DKA. Can give in IV.

Rapid acting Insulin (Lispro)
With a meal, and usually in the pumps (continuous SubQ devices)

Sensitizer used for DM2. MOA: Decreases hepatic glucose production (gluconeogenesis) and intestinal glucose absorption, increases insulin sensitivity and uptake in the periphery. Possible action by activating AMPK, inhibiting cAMP, and activating PKA to inhibit glycerophosphate dehydrogenase.
Use: first line diabetes drug. Long time safety, high efficacy, inexpensive, neutral/low of weight.
BBW: Lactic Acidosis.
Side Effects: diarrhea (improves over time), nausea, abdominal pain, low risk of hypoglycemia. Excreted unchanged from kidneys so if have kidney disease then are drug stacking, caution for lactic acidosis if renal or hepatic disease

SGLT2 inhibitor used for DM2.
MOA: Inhibits sodium-glucose cotransporter 2 (SGLT2), reducing glucose reabsorption and increasing urinary glucose excretion. SGLT2 is responsible for at least 90% of renal glucose reabsorption- blocking causes blood glucose to be eliminated thru the urine. Side Effects: low BP (bc additional water is eliminated by osmotic diuresis) , hypoglycaemia. Don’t use if renal failure.

MOA: Chemical salt of an alkaline ion (usually bicarbonate, hydroxide) and a counterion (aluminum,magnesium, calcium). Side Effects: All can cause hypokalemia, can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH

Proton Pump Inhibitor
MOA: Irreversibly inhibits the H+/K+ ATPase pumop in stomach parietal cells. Covaltently binds the cysteins on the extra-cytoplasmic surface of the H-K pump
Use: peptic ulcer, gastritis, GERD, zollinger-ellison syndrome
Metabolized by P450
Toxicity: inc risk of C difficile infectiona nd pneumonia. Dec serum MG+ with long-term use.

Histamine-2 receptor (H2) antagonist,
MOA: Reversible block of histamine H2 receptors, which causes dec H+ secretion from parietal cells. Take before eating.
Use: peptic ulcer, gastritis, mild esophageal reflux (GERD)
Toxicity: Decreases renal excretion of creatinine.

MOA: Binds penicillin-binding proteins (transpeptidases) and blocks transpeptidase cross-linking of peptidoglycan in cell wall. Activates autolytic enzymes. Wider spectrum of action than penicillin, penicillinase sensitive.
Use against the H pylori-> extended spectrum penicillin
Toxicity: Hypersensitivity, rash, pseudomembranous colitis
Mech of resistance: oenicillinase in bacteria cleaves beta-lactam ring

Antibiotic, protein synthesis inhibitor
MOA: Inhibits protein synthesis by blocking translocation; binds to 23S rRNA of the 50S ribosomal subunit. Bacteriostatic.
Use: atypical pneumonia, STIs, gram positive cocci, and B pertussis
Toxicity: Gastrointestinal motility issues, Arrhythmias caused by prolonged QT interval, acute cholestatic hepatitis, rash, eosinophilia. Increases serum conc of theophyllines, oral anticoagulants. Inhibit cytochrome P-450. Embryotoxic
Mech of resistance: methylation of 23 S rRNA biding site prevents binding of drug

NSAID, Generic Aleve.
Decreases inflammation and pain by reversibly inhibits COX enzymes (via non-covalent binding of active site) which results in decreased prostoglandin (PGE2) synthesis (dec vasodilation and vascular permeability)
Use: antipyretic, analgesic, anti-inflammatory.
Side Effects: Gastric ulcer(less mucous, more acid). Renal ischemia and interstitial nephritis (do not give if renal issue, prostaglandins vasodilate afferent arteriole). FDA warning of heart attacks/stroke.

Decreased inflammation and pain by inhibiting prostoglandin formation by reversibly inhibiting COX enzymes (1,2,3) via non-covalent binding to active site, which results in less PGE2 (dec vasodilatino and vascular permeability).
Use: antipyretic, analgesic, anti-inflammatory.
Toxicity: Gastric ulcer (less mucous, more acid)interstitial nephritis, renal ischemia (prostoglandins vasodilate afferent arteriole) so do not give with renal issues. FDA warning for strokes and heart attack.

Blood thinner, metabolized from prodrug to active drug by P450

Opioid Analgesic. MOA:act as angonist at opiod receptors to modulate synaptic transmission- open K+ channels, close Ca2+ channels-> dec synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P Use: pain, cough suppression, diarrhea, acute pulmonary edema, maintenance for heroin addicts. Adverse Effects: Addiction. Respiratory depression, constipation, miosis. NOTE: may increase the tone of sphincter of Oddi (not proven)

MOA: Corticosteroid.
Has some immunosuppressive effects
Mostly act by targeting acute inflammation by inhibiting phospholipase A2 via increased transcription of lipocortins (such as annexin 1), which binds/inhibits phospholipase (note phospholipase cleaves arachidonic acid from membrane phospholipids). Therefore decreases epithelial leaky-ness and causes less migration of leukocytes
Inhibits the expression of inducible COX-2
Use: Most commonly used glucocorticoids in cancer chemotherapy, used in CL, non-hodgekins lymphoma. Also used as immunosuppresants (eg autoimmune diseases, alcoholic hepatitis)
Toxicity: Peptic ulcers and Cushing-like symptoms: weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis, hypertension, hyperglycemia, psychosis

MOA: Competative nonselective phosphodiesterase inhibitor (raises intracellular cAMP, activates PKA, inhibits TNF and leukotrine synthesis, which reduces inflammation and innate immunity). Also improves RBC deformability, reduces blood viscosity. Also an antagonist at adenosine 2 receptors
Use: treat muscle pain in peripheral artery disease, alcoholic hepatitis
Side Effects: Dizziness, nausea, angina, aseptic meningitis. Contraindicated if have recent or risk factors for hemorrhage. Co-administerd with sodium thiopental can cause death by acute pulmonary edema

MOA: Long-acting opioid antagonist used for relapse prevention once detoxified.
Use: Heroin dependence, also alcohol dependence (Alcohol upregulates opioid receptors)

MOA: Inhibits acetaldehyde dehydrogenase (ALDH) which converts acetaldehyde to acetate, causing acetaldehyde to accumulate and contribute to hangover symptoms)
Use: to condition the patient to abstain from alcohol use

Oral Lactulose
MOA: Increases stool water content, increases stool acidity, trapping NH4 ions. Bacterial degradatino of lactulose results in an acidic pH, which inhibits the diffusinoof NH3 into the blood by causing the conversion of NH3 to NH4+. This also enhances the diffucsion of NH3 from the blood into the gut where conversino to NH4+ occurs, by producing an osmotic effect in colon w resulting distention promoting peristalsis. Reduces blood ammonia conc to reduce degree of portal systemic encephalopathy
Use: Constipation, portal systemic encephalopathy
Contraindications: galactosemia, caution if DM or colorectal electrocautery procedures
Side effects: Dehydration, abdominal discomfort

MOA: Exerts local anti-inflammatory effects, possibly by blocking cyclooxygenase and inhibiting prostoglandin production in the colon. Maybe also TNF.
Use: Ulcerative colitis maintenance
Side Effects: nephropathy, hepatotoxicity, headache, diarrhea

MOA: Antimetabolite. Purine analogue. An inosine analog that inhibts the enzymatic synthesis of purines (GMP and AMP) by preventing interconversion of IMP (inosine monophosphate) to A or G. A sulfer
Use: Immunosuppressive, used for acute lymphocytic leukemia, Crohn Disease, Ulcerative colitis.
Toxicity: myelosuppression. Also GI and liver effects.

MOA: Monoclonal antibody which binds and inhibits TNF (Tumor Necrosis Factor), reducing inflammation and altering immune response
a. Binds to soluble and transmembrane forms of TNF-alpha, inhibits/prevents effective binding of TNF with it’s receptors
b. Note: TNF -alpha induces proinflamm cytokines (IL-1 and 6), enhances leukocyte movement/migration by increasing the permeability fo the endothelial layer of blood vessels, and increases the release of adhesion molecules
Use: Autoimmune diseases such as: ankylosing spondylitis, Crohn, psoriasis, psoriatic arthritis, rheumatoid arthritis, Ulcerative colitis
BBW: Serious infection risk, lymphoma and other malignancies
Other side effects: sepsis, pneumonia, TB, hepatotoxicity, fever, myalgia, headache, fatigue, ect

Acetylated NSAID. Salicylate. Decrease inflammation and pain by inhibiting prostoglandin formation by irreversibly inhibiting COX enzymes via covalent acetylation of the active site, which results in less PGE2 (decreased vasodilatino and vascular permeability).
When act on inducible COX2 for is antinflammatory
When act on COX2 and CoX3 is analgesic
When act on COX-1 has side effects (GI bleeding bc less mucous and more acid)
Aspirin exacerbated respiratory disease, possible Reye’s Syndrome in children. Do not give if renal issue. Possible risk of hemorrhagic stroke.
In gout, aspirin interacts with the uric acid excretion/re-uptake (URAT1) and so is NOT used for ppl with gout

Generic Tylenol
Possible CNS specific action by inhibiting COX3 (splice variant of COX1)
Works on CNS, no anti-inflammatory properties, no effects on platelets, no GI toxicity, No Reye syndrome
Overdose can cause live damage

NSAID. Decrease inflammation and pain by inhibiting prostoglandin formation by reversibly inhibiting COX-2 enzymes via non-covalent binding to active site, which results in less PGE2 (decreased vasodilatino and vascular permeability). Note that this is relatively inducible COX-2 specific.
Do not give if renal issue
FDA warning that can cause heart attacks or strokes

Glucocorticosteroid. Has some immunosuppressive effects
Mostly act by targeting acute inflammation by inhibiting phospholipase A2 via increased transcription of lipocortins (such as annexin 1), which binds/inhibits phospholipase (note phospholipase cleaves arachidonic acid from membrane phospholipids)
Inhibits the expression of inducible COX-2
Can cause some stomach bleeding, Cushing-like symptoms

Glucocorticosteroid. Has some immunosuppressive effects
Mostly act by targeting acute inflammation by inhibiting phospholipase A2 via increased transcription of lipocortins (such as annexin 1), which binds/inhibits phospholipase (note phospholipase cleaves arachidonic acid from membrane phospholipids)
Inhibits the expression of inducible COX-2
Can cause some stomach bleeding

Competitive inhibition of HMG CoA reductase, which causes dec cholesterol synthesis. Decreased cholesterol levels cause an increase in LDL receptor synthesis (via SREBP activity) and overall causing a dec of LDL up to 60%, also inc HDL and dec TG
Use: drug of choice for LDL lowering, can consider co-administrations with other agents but increased side effects
Side effects: myopathy, hepatotoxicity

Cholesterol Absorption Inhibitor, blocking the transporter NPC1L1 in enterocytes. This decrased the absorptino of cholesterol, and causes dec LDL up to 20%, inc HDL, dec TGs.
Use: role in dual therapy when co-admin with statin
Side Effects: myopathy, elevated LFTs

PSK-9 inhibitors
Inhibit PSK-9, which targets LDL receptors for degradation. This means have more LDL receptors available and less cholesterol in the blood.

anti-TB medication that induces CYP and P-glycoprotein induction

Cimetidine, Grapefruit Juice
Inhibit CYP and P-glycoprotein induction (aka pts w statins should not have much grapefruit juice)

Second-generation sulfonylureas
Oral Antidiabetic Agent, Secretagogues
MOA: Bind to sulfonylurea receptor, which is part of ATP sensitive channel and block the K efflux, which causes membrane depolarization and Ca2+ influx, which causes insulin release
High efficacy, low cost
Moderate hypoglycemic risk, weight gain
Caution of hyperglycemia if in renal disease (kidney and liver)
Side Effects: Hypoglycemia

Thiazolidinediones (TZDs)
Oral Antidiabetic Agent Sensitizer, increase the glucose disposal by activating PPARgamma which increases the signal from insulin receptors in the peripheral tissue (combats insulin resistance)
High efficacy, low hypoglycemic risk, low cost
Side Effects: Edema, CHF, Fractures. Do not use of ALT is over 2,5 (3x normal)
Weight gain due to retention of fluids, so use caution for fluid overload if hepatic or renal disease or CHF

alpha-glucosidase inhibitors
Oral Antidiabetic Agent MOA: Saccharides that act as competitive inhibitors of enzymes (alpha-glucosidases of the brush border) needed to digest carbohydrates, which causes reduction of rate of digestion of carbohydrates
Side Effects: flatulence, diarrhea. Pneumatosis cystoides interstinalis. Possible hypoglycemia

GLP-1 (glucagon-like polypeptide-1) receptor agonists
Oral Antidiabetic Agent Potentiates incretin action
High efficacy, low hypoglycemic risk, loss of weight bc of delayed gastric emptying, high cost
Do not use if renal disease
Side Effects: Delayed gastric emptying, nausea improves w time, pancreatitis, SQ injection

DPP-4 (dipeptidyl peptidase-4) inhibitors
Oral Antidiabetic Agent MOA: Inhibit DPP-4 which degrades incretins, thereby increasing incretin action which causes increased secretion of insulin only when there is food present (aka glucose present) bc incretins are secreted when food is present.
Intermediate efficacy, low hypoglycemic risk, high cost
Neutral to weight
Excreted unchanged from kidneys, dose adjusted
Side effects rare: hypersensitivity, pancreatitis, Upper Respiratory Infection

SGLT2 (sodium glucose cotransporter 2) inhibitors
Oral Antidiabetic Agent MOA: Blocks the re-absorption for Glucose from the descending kidney tubule by inhibiting SGLT2
Intermediate efficacy, low hypoglycemic risk, loss of weight (and water), high cost
Decrease in BP (think about MOA)
Side Effects: Genical mycotic infections, UTIs, dehydration. Kidneys (lowest dose if renal disease)

Bile Acid Sequestrants
Ex: cholestyramine. Bile acid resin that removes bile acids from enterohepatic circulation.
Dec LEL upt o 28%, inc HDL, +/- TGs.
Use: second line agent for LDL lowering, used in young persons or co admin with statin. Also to decrease bile-acid caused secretory diarrhea
SE: can inc TG levels, GI distress, dec absorption of fat soluble vitamin

Gemfibrozol, fenofibrate
MOA: inc synthesis of LPL (by binding to nuclear receptor PPARalpha and increasing protein expression) which increases clearance of VLDL and CM from the blood and TGs to adipose. Also inc apo A1, dec apo CII in hepatocytes. Causes a Dec TG by 50%, Dec LDL, inc HDL
Use: drug of choise for hypertriglyceridemia, can be co-administerd w stating but inc myopathy
SE: dyspepsia, gallstones, myopathy

Binds to niacin receptor in adipose and decreased the HSL activity, which decreases FFAs, deceasing VLDL synthesis and therefore LDLs. Also causes a decreased ApoA1 clearance, which increases the HDL levels (which remove cholesterol from periphery and deliver to liver to be excreted as bile) Overall causes an Inc HDL, Dec TGs, dec LDL
Use: when interested in raising HDL, also lower LDLa dn TG.
SE: Flushing, hyperglycemia, hyperuricemia, GI distress, hepatotoxicity

Bactericidal, antiprotozoal.
MOA: Forms toxic free radical metabolites in the bacterial cell that damage DNA.
Use: First line for mild C Diff associated diarrhea, H pylori (wht PPI and clarithromycin)acute dysentery, Giardia, ect. Treats anaerobic infection below the diaphragm.
BBW: Carcinogenic. Severe flushing, tachycardia, hypotension with alcohol; headache, metallic taste

MOA: Antidiarrheal. Agonist at u-opioid receptors, slows gut motility by acting on circular and longitudinal intestinal muscles to inhibit peristalsis and prolong transit time. (Reduces fecal volume, increases viscosity, and diminishes fluid and electrolyte loss. Demonstrates antisecretory activity. Increases tone of anal sphincter. )
Poor CNS penetration (low addictive potential)
Met by cytochrome P450
Contraindications: possible C diff (recent antibiotic use, fever). Also alcohol within last 12 hrs.
Use: Diarrhea
Side Effects: nausea, constipation (associated w toxic megacolon)

MOA: Glycopeptide. Inhibits bacterial cell wall synthesis by blocking glycopeptide polymerization through binding tightly to D-alanyl-D-alanine portino of cell wall precursor
Use: First line for severe C Diff infection, give in a pulse tapered fashion (to allow time for the spore to be converted to fully functional toxin producing forma in which they can be killed). Also endocarditis, sepsis, ect. Not absorbed by GI, so for C diff do not give in IV.
Side Effects: Hypotension and flushing, erythmatous rash on face and upper body, nephrotoxicity

MOA: Antidiarrhea, Fiber Supplement, Laxative, Bulk-Producing. Psyllium is a soluble fiber, and absorbs water in the intestine to form a viscous liquid which promotes peristalsis and reduces transit time
Side Effects: Abdom cramps, ect

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