PHARMACOLOGY
· Anti-muscarinic
· Motion Sickness; preoperatively to reduce secretions
· Anti-muscarinic toxicities (mydriasis & cycloplegia; decreased secretions & sweating; flushing; bradycardia (low doses); tachycardia (high doses); urinary retention; drowsiness, hallucinations, coma)
Typical
Anti-psychotics (Chlorpromazine, Haloperidol, Thioridazine)
· Dopamine antagonists
· Schizophrenia; psychosis
· Lactation; Extrapyramidal effects (parkinsonism, akathisia (motor restlessness), tardive dyskinesia (lip smacking, jaw movements, etc.)); anti-cholinergic effects (antimuscarinic, alpha-antagonistic (orthostatic hypotension), and anti-histamine (sedation)). Toxicities are a tradeoff—higher extrapyramidal effects coincide with lower anticholinergic effects and vice-versa. The higher the extrapyramidal effects, the higher the potency (haloperidol > chlorpromazine > thioridazine)
Atypical
anti-psychotics (Clozapine)
·
Dopamine antagonist
·
Schizophrenia; psychosis
·
NO extrapyramidal effects or lactation;
agranulocytosis (fatal); Neuroleptic Malignant Syndrome (catatonia, autonomic
instability, stupor); anti-cholinergic effects as above
· Act at mu, kappa, delta receptors in CNS
· Analgesia; Antitussive (Codeine); opiate addiction (Methadone); antidiarrheal (loperamide)
· CNS depression; nausea; respiratory depression; constipation; urinary retention; dependence
Opiate Mixed
Agonists-Antagonists (Pentazocine)
·
Same as agonists but will cause withdrawal in
those dependent on agonists
Opiate Antagonists
(Naloxone, Naltrexone)
·
Block opiate receptors
·
Narcotic overdose (no effect if used alone)
Erythropoietin
·
Increases RBC production in marrow
·
Anemia associated with renal failure
RU486 (Mifepristone)
·
Progestin antagonist
·
Early-term abortion
·
Uterine bleeding, possible incomplete abortion
·
Alpha-glucosidase inhibitor—decreases absorption
of glucose
·
NIDDM; adjunct to insulin in IDDM
·
Flatulence; diarrhea; abdominal cramping
·
Angiotensin II antagonist
·
Hypertension
·
Similar to ACE inhibitors but no cough
(decreased bradykinin activation)
· Inhibit cholinesterase
· Diagnosis (edrophonium); long-term treatment (Neostigmine, Pyridostigmine); open-angle glaucoma; reversal of non-depolarizing nm blockade
· Fasciculations & weakness
·
GnRH analog à
desensitization of pituitary receptor à
decreased FSH, LH secretion
·
Prostate Cancer
·
Transient excess testosterone production
(prevent by combining with flutamide); impotence, hot flashes, tumor flare
· Blocks inhibitory effects of testosterone on GnRH release
· Combo with leuprolide
·
Inhibits Cholesterol à
pregnenelone conversion (like metyrapone)
·
Metastatic breast cancer (decreased estrogen)
·
Induces
P450; transient CNS depression; rash
·
Decreases gluconeogenesis; improves lipid
profile (HDL rises, LDL falls)
·
NIDDM – lower risk of hypoglycemia
·
GI side effects; lactic acidosis (rare);
long-term interference w B12 absorption
· Absorbs water and softens stool à bulk à peristalsis
· Constipation
Mechanism, clinical use, and toxicity of dermatologic agents:
CORTICOSTEROIDS: Synthesized in the zona fascilculata of the adrenal cortex. Cortisol and Cortisone produced.
1) Glucocorticoids are catabolic. They influence carbohydrate and fat metabolism to insure adequate delivery of glucose to brain and tissues.
2) Decrease intestinal uptake of calcium; increase renal excretion of calcium (contribute to osteoporosis).
3) Supress the inflammatory response –
Decrease edema, fibrin deposition, capillary dilatation, leukocyte migration
and phagocytic activity. Inhibit
prostaglandin and leukotriene production by inhibiting phospholipase A2.
4) Include:
Cortisone (short acting), Prednisone (intermediate acting), Prednisolone
(similar to prednisone but no hepatic metabolism for activity),
Methylprednisolone (similar to prednisolone but better anti-inflamatory and
less mineralocorticoid effects), Triamcinolone (5x more potent than cortisol),
Dexamethasone (long acting)
& Beclomethasone (long acting available as aerosol).
5) Toxicity:
a) Skin:
hirsutism, skin thinning,
poor wound healing, striae, acne and purpura.
b) Other: hyperglycemia, hypertension,
cataracts, glaucoma, peptic ulcer
disease, osteoporosis, and increased susceptibility to infection.
RETINOIDS:
1) Used to treat the following dermatologic diseases: Acne, psoriasis, icthyosis and has a potential benefit in early skin cancers (actinic keratosis)
2) Toxicity: in skin it can cause desquamation, dry skin and pruritus, erythema.
ANTIFUNGALS:
1) Polyene antibiotics are fungicidal against both filamentous and yeastlike fungi including Histoplasma, Blastomyces, Coccidioides, Cryptococcus, Candida, Aspergillus and Sporothrix. Polyenes interact with sterols in the cytoplasmic membrane of fungi leading to rapid leakage of small molecules and death. Sensitive fungi have ergosterol in their membranes.
a) Amphotercin B: Broad spectrum to treat systemic fungal infections. Side effects: Fever, chills, impaired renal function, anemia, thrombocytopenia.
b) Nystatin (Mycostatin): Similar to A but used primarily in topical preparations. Use in Candida infections and prophylaxis.
2) Imidazoles: Block the synthesis of fungal cell membrane ergosterols.
a) Miconazole & Clomitrazole: Miconazole is the only imidazole that can be administered IV; clotrimazole is only used topically.
i) Intravenous miconazole is rarely used due to toxicity. Treats ringworm, vulvovaginal candidiasis
b) Ketoconazole: Oral administration only. Causes gynecomastia.
3) Miscellaneous:
a) Flucytosine: Administer with amphotercin B
in the treatment of cryptococcal meningitis and other systemic infections
(synergistic).
b) Griseofulvin: Binds to keratin, treat
Tineas (capitis, corporis etc),
Other new pharmacologic agents:
1) Erythopoietin (EPO): RBC growth factor. Produced in kindneys. Recombinant form available (epoietin alpha).
a) Use for tx of Anemia 2nd to renal failure or zidovudine (AZT) use HIV patients.
b) Use for tx of Anemia 2nd to chemo, or to stimulate rbc production prior to surgery or to facilitate autologous donation.
c) Side effects: Clotting of dialysis tubing and hypertension.
2) RU486 (Mifrepristone): Abortificen. Blocks progesterone receptors and thereby progesterone support of pregnancy. 80% effective, 95% if used with prostaglandins.
a) Complications include incomplete abortion (2%), ongoing pregnancy (1%), hemorrhage during D&C (<1%).
Know About......
1) Complications of empiric antibiotic use:
a) Resistance: Must take into account susceptibility patterns of local settings. Must distinguish between community vs. nosocomial infection, and must take into account the patient’s immune status.
b) Fungal Infections: Due to destruction of normal flora. (candidiasis).
c) Other complications: C. Diff è Pseudomembranous colitis. Gentamicinè ototoxicity (must monitor levels), Sulfonamides and Penicillinè allergic reactions.
2) Secondary effects of other drugs:
a)
Heparin è osteoporosis with chronic use. Thombocytopenia –
usually transient and mild.
b) Thiazides èHyperlipidemia, hypokalemia.
3) Drugs that block/increase
hepatic drug metabolism:
a)
Cimetidine: Histamine analog that cab reduce hepatic blood flow and slow clearance of other drugs
and also reduces activity of cytochrome p-450
b) Ethanol: Chronic use induces
hepatic microsomal enzymes and may enhance metabolism of other drugs.
c)
Phenobarbital: Increased phenobarbital levels in patients that have
ethanol, chloramphenicol or valproic acid on board, since it has microsomal
enzyme metabolism.
d) Phenytoin (Dilantin): same as
Phenobarb and ETOH èMetabolized by microsomal enzymes.
e)
Rifampin: Causes jaundice and hepatotoxicity,
also interacts with C p-450 system.
4) Fundamental Pharmacodinamics:
a)
Partial
agonists/agonist: Drugs that bind to receptors and stimulate them.
b) Antagonists: are drugs that bind to receptors and
decrease or block the effect of an agonist. They do not stimulate the
receptors.
i)
Competitive
antagonist: Reversibly binds to the receptor and prevents binding of the
agonist.
ii) Non competitive antagonist: Usually binds to the
receptor irreversibly and prevents any agonist action.
c)
Efficacy:
Maximal effect produced by a drug.
d) Potency: Activity of a drug compared to a
reference standard; depends on the drug’s ability to reach the receptors and
its affinity to the receptor.
5) Drug efficacy and potency as demonstrated on
dose-response curves:
a)
ED50
(effect dose)- Dose
which produces half-maximal response (ie., observed effect seen in 50% of
patients); used as a measure of potency (the lower the ED50, the more potent
the drug).
b) TD50 (toxic dose)-
Minimum dose which produces a specific toxic effect in 50% of individual (or
animals).
c)
LD50 (lethal dose)-
Minimum dose which kills 50% of animals.
d) Therapeutic
index- Ratio of dose required to produce a toxic effect to the dose needed for a therapeutic
effect. Used as an indication of drug safety. Expressed as :
TI= TD50 or TI= LD50 You want drugs with a high therapeutic index (low
ED 50 ED50 side effects at usual doses).
6) Pharmacogenetics: drugs whose metabolism is affected by inheritance:
a) Isoniazid: Most commonly used drug for the treatment of TB.
i) Inhibits biosynthesis of mycolic acids.
ii) Metabolized in the liver (acetylated); speed of acetylation and consequently isoniazid’s half life is genetically determined (fast vs. slow acetylators).
7. Treatment of Anemia
1. Iron – absorbed in the duodenum and proximal jejunum. Iron deficiency seen in premature infants, pregnant and lactating women. Ferrous oral salts can be given; give for 3-6 months to replenish iron stores. IV iron can also be given.
2. Iron toxicity
a. N/V, cramps, constipation, diarrhea – dose-related so decrease the dose
b. Acute toxicity – seen in kids, necrotizing gastroenteritis followed by shock, lethargy, dyspnea
c. Chronic iron toxicity - hemochromatosis
1. Vitamin B12 (normally obtained in meats), requires intrinsic factor for absorption (pernicious anemia decreases absorption), gastrectomy also decreases absorption. B12 is stored in the body (years supply)
a. B12 deficiency also shows nervous defects
b. B12 shots can be given if oral absorption is a problem
c. Folate will NOT correct neurological features, but WILL help with the anemia
2. Folic Acid – from green leafy veggies, body stores of folate are lower (1-6 months)
a. Deficiency doesn’t have neurological deficits
b. Folic acid is well absorbed orally
1. Erythropoietin – used for renal failure, bone diseases, chemotherapy
a. Toxicity – too rapid increase in hematocrit can lead to HTN, thrombotic complications
2. Colony stimulating factors (G-CSF, GM-CSF)
a. Increase recovery after myelosuppressive chemotherapy or BMT
8. Prevention/treatment of cerebrovascular disease
1. Irreversibly blocks cyclooxygenase, = inhibits thromboxane (TxA2) formation from platelets
2. Only requires a small daily dose
1. Inhibits platelet aggregation (inhibits ADP pathway)
2. Decreases TIAs, completed strokes, unstable angina pectoris
3. Diarrhea in 20%, leukopenia in 1% (must monitor white count)
1. Streptokinase – cheap, allergic reactions possible
2. Urokinase
3. Tissue plasminogen activators (t-PA) – expensive, from recombinant DNA
9. Treatment of rheumatoid arthritis
A. Drugs that alter Pain
1. Aspirin – 1st line drug, GI problems
2. NSAIDS -
3. COX-2 inhibitors – less GI problems
1. Methotrexate and immunosuppressives – more toxic side effects
2. Gold – dermatitis is common side effect
10. Vaccines: indications, potential side effects
1. Active immunization – antigen is given so host develops antibodies (long protection)
a. Give to children
2. Passive – immunoglobins are given (short term protection)
a. Give to those recently exposed (Tetanus, Botulinum, HBV, Rabies) or to travelers (Polio, tetanus, Measles, diphtheria)
1. Giving live attenuated vaccines may cause the disease (eg. Polio vaccine)
2. Killed vaccine will not cause the disease
3. Allergic reactions are possible
11. Chemotherapeutic agents: risk of possible secondary cancer