1. Hypertension
1.1. Angiotensin Convertin Enzyme Inhibitors (ACE)
1.1.1. Captopril
1.1.2. Inhibit the angiotensin concerting enzyme which blocks the production of angiotensin II
1.2. Angiotensin II Receptor Blockers
1.2.1. Iosartan
1.2.2. prevents the action of angiotensin II by blcoking the receptors
1.3. Thiazide Diurectics
1.3.1. Thiazide-Type
1.3.1.1. Hydrocholothiazide
1.3.2. Thiazide-like
1.3.2.1. Chlorthialidone
1.3.3. prevent reabsorption of Na and Cl in the distal tubule by inhibiting sodim chloride cotransporter, reducing blood volume.
1.4. Calcium Channel Blockers
1.4.1. Dihydropyridines
1.4.1.1. amlodipine
1.4.2. non-dihydropyridines
1.4.2.1. phenylalkylamine
1.4.2.1.1. Verapamil
1.4.2.2. benzothiaxepine
1.4.2.2.1. ditiazem
1.4.3. Inhibit voltage gated calcium channels to reduce calcium influx into vascular smooth muscle cells to decrease cardiac contractiona and contriction of arteries
2. Diabetes
2.1. Sulfonylurea
2.1.1. Glyburide
2.1.2. Glimepiride
2.1.3. Blocks Potassium Channel, causing depolarization, leading to voltage sensitve calcium chanel. This action allows beta cells to fuse to membrane and release insulin.
2.1.4. side effects
2.1.4.1. hypoglycaemia
2.1.4.2. weight gain
2.2. Biguanide
2.2.1. Metformin
2.2.2. Inhibits hepatic gluconeogenesis, increasees insulin sensitivity, improve glucose uptake by skeletal cells
2.2.3. improve glucose uptake by skeletal cells
2.2.4. reduced net glucose uptake across the intestinal wall
2.2.5. Side effects
2.2.5.1. Gastrointestinal irration (diarrhea, cramps, vomiting, and nausea)
2.2.5.2. Lactic acidosis (rare)
2.3. Alpha-Glucosidase Inhibitors
2.3.1. Acarbose
2.3.2. inhibits alphaglucosidase which breaks down starch and disaccarides to glucose to facilitate absorption through intestinal wall
2.3.3. side effects:
2.3.3.1. GI, abdominal or stimach pain, diarrhea, farting
2.4. Incretin Mimetics
2.4.1. Exenatide
2.4.1.1. twice per day
2.4.1.2. peptide like
2.4.2. Drugs that look like Incretin, hormones released released into gut, modulates insulin response which acccounts for up to 60% of total insulin secreted.
2.4.2.1. Glucagon-like-peptide-1 (GLP-1)
2.4.3. side effects:
2.4.3.1. GI problems
2.4.3.2. Acute pancreatitis
2.4.3.3. risk of hypoglycemia
2.4.3.4. may increase risk of thyroid cancer
2.5. Thiazolidin Ediones (TZD)
2.5.1. Rosiglitazone
2.5.2. Pioglitazone
2.5.3. Highly selective agonsit for (activate them) PPARy receptors regulate transcription of insulin responsive genes involved in teh control of glucose production, trnasport and utilization
2.5.4. side effects:
2.5.4.1. fluid retention leading to congestive heart failure
2.5.4.2. increased risk of fractures
2.5.4.3. macular edema
3. Anticancer
3.1. Alkylating Agents
3.1.1. Cyclophosphamide
3.1.2. Bind DNA creating covalent bonds, crosslinks DNA, prevents unwinding of DNA molecules, decreasing protein synthesis
3.2. Epipodophyllotoxins
3.2.1. Etoposide
3.2.2. Inhibit topoisomerase II, enzyme responsible for DNA breaks, therby inhibiting DNA synthesis
3.3. Antimetabolites
3.3.1. 5-Fluorouracil (5FU)
3.3.2. structurally simular nucelotide bases, incorperated into DNA/RNA infereing with function and synthesis. May also inhibit syntheiss of protein or DNA
3.4. Antitumour Antibiotics
3.4.1. Doxorubicin
3.4.2. insert between DNA base pairs, uncoil DNA helix, inhibit DNA and RNA synthesis, may also inhibit polymerase
3.5. Alkylating Agent AND Antitumour Antibiotic
3.5.1. Streptozocin
3.5.2. Naturally occuring, undergoes spontaneous decomposition, reactive methylcarbonium ions which alkylate DNA, interstrand cross links and inhibits mitosis.
3.6. Camptothecins
3.6.1. Irinotecan
3.6.2. Bind toposiomerase I, enzyme responsible for reversible single strand breaks in DNA during DNA replication, prevent religation of DNA strand. CELL DEALTH results (S phase)
3.7. Vinca Alkaloids
3.7.1. Vincristine
3.7.2. Prevent polymerization of tubulin to form microtubules (prevents mitosis)
3.8. Endocrine therapy
3.8.1. aromatase inhibitors
3.8.2. Letrozole
3.9. Taxanes
3.9.1. promte assembly and stabilization of microtubules, thus inhibiting cell replication
3.9.2. Docetaxel
4. Gastrointestinal
4.1. Intestinal Diseases
4.1.1. Constipation
4.1.1.1. Bulk Laxatives
4.1.1.1.1. water absorpting fiber produces distention in the colon stimulating the GI tract to induce a movement
4.1.1.1.2. Metamucil, dietary fiber
4.1.1.2. Osmostic Laxatives
4.1.1.2.1. uses poorly absorbed salts or fatty acids to stimulate distention to induce bowel movement
4.1.1.2.2. Saline Purgatives like Magnesium sulfate or hydroxide
4.1.1.3. Contact/Stimulant Laxatives
4.1.1.3.1. Compounds that stimulate smooth muscle to defecate
4.1.1.3.2. Ex-lax (sennosides)
4.1.2. Diarrhea
4.1.2.1. Fluid and Electrolytes
4.1.2.2. Opiods
4.1.2.2.1. Loperamide
4.1.2.2.2. Diminish propulsive activity allowing more time for water absorption
4.2. Gastic Diseases
4.2.1. Antacids
4.2.1.1. ALOH3, CaCO3
4.2.1.2. Direct neutralizaiton of excess acid.
4.2.1.3. Side Effects:
4.2.1.3.1. carbonate based-beltching
4.2.1.3.2. aluminum consipation
4.2.1.3.3. magnesium diarrhea
4.2.2. H2 receptor antagonists
4.2.2.1. Cimetidine
4.2.2.2. competeive, slective block of histamine H2 receptors. Reduced acid secretion drom reduced ATPase producing H+
4.2.2.3. Side effects:
4.2.2.3.1. Diarrhea
4.2.2.3.2. Headache
4.2.2.3.3. Drowsiness
4.2.3. PPIs
4.2.3.1. Omeprazole
4.2.3.2. Irreversible inactivation of ATPase. Prodrug, activated in areas of concentrated acid.
4.2.3.3. side effects:
4.2.3.3.1. headache
4.2.3.3.2. abdominal pain
4.2.3.3.3. diarrhea
4.2.4. Misoprostol
4.2.4.1. effective in NSAID induced ULCERS, artifically restores PGE function in the body
4.2.4.2. Side effects
4.2.4.2.1. induction of labour
4.2.4.2.2. diarrhea or cramping
4.2.5. Sucralfate
4.2.5.1. aluminum hydroxide sulfated sucrose complex that releases acid sulfated sucrose molecules which bind to links and charged groups forming a viscous, sticky protective gel that prevents further damange
4.2.5.2. side effects
4.2.5.2.1. constipation due to aluminum cations
5. Autonomic
5.1. Ophthalmic
5.1.1. aqueus humour is the target which can fix glaucoma
5.2. Sympatholytics
5.2.1. block/reduce sympathetic activity. Through binding to adrenergic receptors or decreaseing teh amount of sympathetic neurotransmitter released into the synpase
5.2.1.1. propranolol
5.2.1.2. clonidine
5.3. Sympathomimetics
5.3.1. Stimulate sympathetic nervous system. Directly act on adrenergic receptors (adrenline) by increaseing the amount of sympathetic neurotransmitter in the synapse. It can occur through inhibiting reuptake and increaseing the NT release
5.3.1.1. adrenaline
5.3.1.2. noraephinephrine
6. Antimicrobial
6.1. B-Lactam Antibiotics
6.1.1. Penicillin
6.1.2. inhibit synthesis of bacterial peptidoglycan cell wall
6.2. Macrolides
6.2.1. Azithromycin
6.2.2. inhibit bacterial protein snthesis by binding *reversibly* to 50S subunit of bacterial ribosomes
6.3. Aminoglycosides
6.3.1. Gentamicin
6.3.2. inhibit bacterial protein synthesis by irrevesibly binding to 30S and 50S ribosomal subunits to stop RNA synthesis/
6.4. Tetracyclines
6.4.1. Doxycycline
6.4.2. Inhibit bacterial protein synthesis by binding *reversibly* to the 30S subunits of bacterial ribosome
6.5. Sulfonamides
6.5.1. Sulfamethoxazole
6.5.2. interfere with folic acid synthesis by inhibiting dihydropteroate synthetase and preventing addiiton of PABA into folic acdi
6.6. Quinolones
6.6.1. Ciprofloxacin
6.6.2. inhibits DNA Gyrase/topoisomerase to inhibit relazation of supercoiled DNA to inhibit bacterial DNA replication
6.7. Glycopeptides
6.7.1. Vancomycin
6.7.2. inhibit cell wall synthesis in GRAM POSITIVE BACTERIA by bindint to D-aanyl-D-alanine termunus of cell wall precursor untis
6.8. Oxazolidineones
6.8.1. Linezolid
6.8.2. inhibit protein synthesis by binding at the **P site** of the 50S ribosomal subinits