Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
199 Cards in this Set
- Front
- Back
Gram + cocci |
stains purple
thick peptidoglycan, cell wall + single phospholipid layer |
|
Gram - Bacilli
|
stains red
Think peptidoglycan sandwiched btw 2 phospholipid layers |
|
Clusters of Cocci (+)
|
staphylococchi
|
|
Pairs of Cocci (+)
|
Strep Pneumoniaie
|
|
Chains of Cocci (+)
|
Group A & B strep; viridans streptococci
|
|
Pairs and Chains of Cocci (+)
|
enterococcus species
|
|
Bacilli (+)
|
bacillus species, listeria
|
|
Cocci (Gram -)
|
Morzella, neisseria
|
|
Bacilli (Gram -)
|
e coli, enterobacter sp, citrobacter, serratia, salmonella, shigella, acinetobacter helicobacter, pseudomonas aeruginosa
|
|
SPACE bugs:
|
serratia, pseudomonas aeruginosa, acinetobacter helicobacter,
citrobacter, enterobacter sp. |
|
Above the diaphram anaerobes
|
Peptococcus sp., Peptostreptococcus sp., Prevotella, Veilonella, Actinomyces
|
|
Below the diaphram anaerobes
|
Clostridium perringes, tetani, and difficile
Bacteroides fragilis, disantonis, ovatus, thetaiotamicron Fusobacterium |
|
Atypical Bacteria
|
Legionella pneumophila, Mycoplasma pneumonia or hominus, Chlamydia
pneumoniae or trachomatis |
|
spirochetes
|
Treponema pallidum (syphilis), Borrelia burgdorferi (Lyme)
|
|
What are things to think about when picking an antibiotic?
|
1. antimicrobial spectrum of activity (common bacter based on site of infection.)
2. Cutlure!!! 3. Organism susceptibility 4. Site of infection (will the antibiotic get to the source of infection?) |
|
Narrow-spectrum
|
Act only on a single or limited group of microorganisms
|
|
Extended spectrum
|
effective against gram positive organisms and also a significant number of gram neg organisms
|
|
Broad spectrum
|
agents that effect a wide variety of microbial special. May precipitate superinfections
|
|
Important factors to consider
|
– Minimum inhibitory concentration (MIC)
– Minimum bactericidal concentrations (MBC) – Institution’s Antibiogram |
|
Minimum Inhibitory Concentration
|
Lowest concentration
of antibiotic that inhibits bacterial growth • Effective antimicrobial therapy should have an antibiotic concentration greater than the MIC |
|
Bacteriostatic (Static = STOP)
|
• Arrest the growth and replication of bacteria at
serum levels achievable in the patient • Limits the spread of infection while the immune system attacks the pathogen |
|
Bactericidal (Cidal = KILL)
|
• Kills the bacteria
• Total number of viable organisms decreases |
|
Factors that influence penetration to the CSF
|
1. Lipid solubility of drug (high lipophilicity=more)
2. Molecular weight of the drug (small = more) 3. Protein binding of the drug (less = more) 4. inflammation of the BBB (inflam = leaky) |
|
Agents that are LESS micro-organism specific
|
can be associated with a significant amount of toxicity (AMINOGLYCOSIDES)
|
|
Empiric (broad spectrum)
|
• Usage of antimicrobial agents before the pathogen
responsible for a particular illness is known • Agents selected based on clinical experience • Early intervention improves outcomes and mortality in certain infections |
|
Narrow spectrum - treatment of documented pathogen
|
Ideally using the least narrow‐spectrum agent
available |
|
pharmacodynamics
|
what the drug does to the body
|
|
Concentration-dependent killing
|
certain ATB show significant inc in bactericide as the concentration of the ATB inc (Cmax). achieve high peak levels resulting in rapid killing of the pathogen
(aminoglycosides, fluoroquinolones) |
|
Time dependent killing
|
clinical eff is best predicted by % of time the blood concentrations of the drug remains about MIC.
AUC: MIC ratio indicates efficacy....inc the concentration does not inc the rate of kill |
|
post antibiotic effect (PAE)
|
persistent suppression of microbial growth the occurs after levels of antibiotic have fallen below the MIC.
|
|
combination therapy advantages
|
synergism (2+2 = 5)
ensure appropriate empiric overage of resistant organisms |
|
combination therapy disadvantages
|
interfering mechanisms of action.
overuse of antibiotics resulting in resistance |
|
mechanisms of resistance
|
1. genetic alterations (spontaneous mutations of DNA), DNA transfer of drug resistance
2. Altered expression of proteins |
|
Altered expression of proteins
|
1. modification of target sites
2. decrease accumulation (dec uptake or inc efflux) 3. enzymatic inactivation |
|
Superinfections
|
1. broad spectrum agents and/or combinations of agents can lead to alterations of the normal microbial flora.
2. permits overgrowth of opportunistic organisms |
|
Inhibitors of bacterial cell wall synthesis
|
B-Lactams (PCN, cephalosporins, monobactams, carbapenems)
Vancomycin |
|
B-Lactams
|
Mechanism of action
-interfere with cell wall synthesis by binding to PCN binding proteins located in bacterial cell walls -bactericidal -cross allergenicity except aztreonam |
|
Aminopenicillins
|
developed to inc activity against gram negative aerobes
|
|
carboxypencillins (carbenicillin, ticarcillin)
|
developed to further inc activity against resistant gram neg aerobes
|
|
Ureidopenicillins (piperacillin, azlocillin)
|
develop to further inc activity against resistant gram neg aerobes
|
|
B-lactamase inhibitor combos (unasyn, augmentin, timentin, zosyn)
|
developed to gain or enhance activity against B-lactamase producing organisms (gram + = staph aureus) (gram - h. influ, ecoli, )
|
|
3rd gen cephalosporins
|
even less active against gram + but have greater activity against gram neg.
|
|
Carbapenems
|
Most broad spectrum of activity of all antimicrobials
|
|
B-Lactam Resistance
|
Production of beta-lactamase enzymes
-hydrolyzes beta lactam ring causing inactivation. -Alteration of outer cell membrane leading to decreased penetration |
|
B-Lactam Pharmacokinetics
|
-Widely distributed into tissues
-PCN only get into CSF in presence of inflamed meninges -Time about MIC correlates with efficacy |
|
B-Lactam elimination
|
-kidneys....
all B-lactams have short eliminations half-lives except for ceftriaxone |
|
B-Lactam adverse effects
|
inc LFT, n/v/d/cdiff.
Interstitial nephritis. ETOH intolerance, phlebitis, hypokalemia, Na+ overload |
|
Mechanism of Action of vanco
|
inhibits bacterial cell wall synthesis, inhibits synthesis and assembly of the second state of peptidoglycan polymers. Bactericidal.....except for enteroccoccus
|
|
What classification of bacteria is vancomycin good for
|
Gram +
|
|
Vancomycin pharmacokinetics
|
Time-dependent killing
-time about MIC correlates with efficicy |
|
Vancomycin absorption
|
absorption from GI tract is negligible after oral administration except in pt with intense colitis. IV Therapy!
|
|
Red-man syndrom
|
flushing, pruritis, rash, r/t rate of infusion. resolves spontaneously after discontinuation. premed with benadryl
|
|
inhibitors of protein syn
|
tetracycl. aminoglycosides. macrolides. clinda. streptogramm.
|
|
Tetracyclines mechanism of action
|
inhibit bacterial protein syn by binding to 30S ribosomal subunit.....bacteriostatic
|
|
Tetracycline pharmacok
|
Time dependent.
AVOID acid suppressants and dairy products |
|
Tetracycline Distribution
|
widely distributed with good tissue pene into synovial fluid,with minimal CSF peen
|
|
tetracycline elimination
|
excreted unchanged in urine....require dosage adjustment in renal insuff.
|
|
Tetracycline adverse effects
|
GI, hypersen., photosensitivity, hepatox. Effects on calcified tissue
|
|
What does tetracycline do to preg/kids
|
bone and teeth deposition in growing....dont use in preg or kids <8
|
|
Linezolid
|
time dependent
-absorption 100% bioav IV and PO 30% CSF penetration -no adjustment for renal insuffien |
|
Adverse effects of linezolid
|
GI, HA, Thromboctopenia, reversible optic and periph. neuropathy
|
|
Daptomycin
|
rapidly bactericidal against gram +
Ind. SSTI, bacteremia, endocarditis |
|
Adverse reactions for daptomycin
|
elevated CK
|
|
metabolism of daptomycin
|
inactivated by pulmonary surfactant
|
|
Mechanism of action of fluoroquinolones
|
inhibit bacterial topoisomerases which are req for DNA synthesis. Bactericidal
|
|
Adverse effects of Fluoroquinolones
|
GI, CNS, Hepatotoxicity, Cardiac (QT prolong), tendonitis may damange growing cartilage
|
|
Who do you not use fluoroquinolones
|
children <18 year old
|
|
Metronidazole mechanism of action
|
inhibit dna synthesis. bactericidal
|
|
Amphotericin B mechanism of action
|
target fungal cell membrane. concentration dependent
|
|
mechanism of action of flucytosine
|
enters fungal cells via cytosine-specific permease
fungistatic |
|
Adverse effects of flucytosine
|
neutropenia, thrombocytopenia, bone marrow depression, hepatic dysfunction, GI
|
|
Mechanism of action of azoles
|
targets fungal cell membrane. fungistatic. time dependent
|
|
valtrex
|
converted to acyclovir after oral administration and first pass
|
|
amantadine
|
dopamine agonist used to manage parkinsons disease
|
|
rimantidine
|
hydrophilic analog of amantidine with reduced CNS adverse effects
|
|
Mech of action of amantadine and rimantadine
|
inhibit viral M2 protein to block viral replication
|
|
Oseltamivir and zanamilvir
|
inhibits new viruses from infecting cells. Activity against both influenza a and b
|
|
geriatrics absorption
|
compounds requiring active transp may have delayed absorption d/t dec in blood flow
|
|
GI changes with age |
reduction in acid
reduction in blood flow enzyme activity reduction in gastric emptying and bowel motility |
|
d/t dec in lean body mass and inc in total body fat % can
|
inc volume of distribution of lipid sol drugs and thus drug accumulation, toxicity
|
|
D/t dec in total body water and dec in serum albumin
|
most common binding protein to acidic drugs, can result in inc of free drug concentration; thus dec dose in drugs that are highly protein bound
|
|
geriatric prob with elimination
|
Changes in renal function- single most important physiologic causative factor in ADRs
-dec nephrons -dec blood flow -dec GFR -inc in sclerosed glomeruli |
|
Creatinine cleawrance in older
|
dec by ab 10% per decade after age 40
|
|
Resting heart rate, stroke volume, and cardiac output decline
|
slows absorption, distribution, and excretion of drugs
|
|
Impaired response of baroreceptors (concentrated in the internal carotid arteries and
aortic arch) to pressure changes |
resulting in BP instability, esp. w/ position Δ
|
|
Effects of drugs on CNS more variable r/t
|
↓ blood supply, changes in the blood-brain
barrier (allowing fat-soluble drugs to permeate the brain), ↓ in acetylcholine, dopamine, and serotonin → potentiating ADRs. Number and sensitivity of receptor sites altered → resulting in declines in neurotransmitter function and increased sensitivity of older adults to ADRs |
|
resp capacity dec
|
dec elimination of volatile drugs....such as inhalation anesthetics
|
|
total body water dec
|
inc concentrations of watersol drugs
|
|
drugs affected or that exacerbate changes
|
TCA, phenothiazines, anticholinergics, ETOH, ASA, psychoactive, diuretics, anti HTN, insulin, corticosteroids
|
|
Rate of ADRs inc exponentially in patients taking
|
>4 drugs
|
|
Beers Criteria
|
Studies confirm that inappropriate medication use remains a serious problem for the
elderly. Criteria for Potentially Inappropriate Medication Use in Older Adults |
|
adult levels of acidity not reached until
|
3 to 7 years
|
|
pediatric tbw
|
neonate = 70%
|
|
storage of drugs where in children?
|
teeth and bones
|
|
BBB in children
|
inc permeability in premature infant
|
|
metabolism in peds
|
slower in infants than older children. Liver immaturity in neonates
|
|
CYP 450 in peds
|
function at 50-70% of adult function
|
|
liver metabolism in peds
|
surpasses adult function starting at 2 years up to 10-12 years. could need higher dose or more frequent dosing than adultu
|
|
At what weight switch to adult dose?
|
40-50 kg...note if dose is divided BID TID etc>!!!
|
|
tetracyclines and peds
|
teeth staining
|
|
Asa and peds
|
reyes syn
|
|
valproic acid and peds
|
liver toxicity <2 yrs
|
|
pregnancy contraindications for medds
|
lisinopril, acutane, warfarin
|
|
common hazards in preg
|
rubella vaccine, caffeine, nicotine
|
|
most important thing about teratogenicity is
|
timing of exposure; embryonic phase 3-8 weeks most critical
|
|
Hale's Lactiation risk categories
|
L1 is safest, L 4 is possibly hazardous
|
|
Drug dosage for chemo is
|
prescribed based on BSA
|
|
Leukemic or other tumor cells find sanctuary in t
|
tissues such as CNS. THEREFORE
pt may require irradiation of the craniospinal axis or intrathecal .....additionally drugs may be unable to penetrate certain areas of solid tumors |
|
Combination drug chemo is more successful than single drug
|
results in higher response rates....use non overlapping host toxicities...dont want to use 2 drugs that are liver toxic
|
|
tamoxifen
|
estrogen antagonist.
classified as a selective estrogen-receptor modulator. used prophylactically in high risk women. approved for 5 yrs of use. poss stimulation of premalignant lesions d/t estrogenic prop |
|
Dextromethorphan
|
inc abused in high doses as a hallucinogen by adolescent.
>5-10x the rec dose. Since many of these products contain tyl. antihistamines and other can OD |
|
rebound congestion from
|
decognestant nasal sprays >3 days
|
|
Improper, long term use of antacids can cause
|
constipation, impaction in elderly, hypophosphatemia
|
|
laxative abuse
|
fluid and electrolyte disturbances
|
|
Insomnia, nervousness and restlessness from
|
sympathomimetics or caffeine in OTC products
|
|
Echinacea
|
enhance immune function in colds. anti inflammatory effects. anti bac, anti fung, anti viral
|
|
garlic
|
effects choleterol biosynthesis, has antioxidant prop.
lipid-lowering potential |
|
prob with ginkgo
|
antiplatelet properties and should not be used in combination with antiplatelet or anticoagulants
|
|
Coenzyme Q10
|
Modest ischemic heart disease prevention
|
|
anterior pituitary gland
|
anterior pit hormones stimulate production of hormones by peripheral endocrine glands or liver....
|
|
Except of anterior pituitary prolactin
|
prolactin acts directly on target
|
|
posterior pit hormones
|
synthesized in hypothalamus. trans via neurosecretory fibers and released by post pit lob. Hormones act directly on target tissues once released into circulation
|
|
anterior pit
|
GH, FSH, LH, ACTH, TSH, prolactin
|
|
post pit
|
oxytocin, ADH
|
|
principal hormone responsible for lactation
|
req appropriate serum levels of estrogens, progestins, corticosteroids and insulin
|
|
What inhibits prolactin?
|
dopamine
|
|
hyperprolactinemia causes
|
-prolactin-secreting adenomas;
medications: SSRI, dopamine antagonists, haldol and metoclopramid.... because they are inhibiting dopamine receptors |
|
elevated prolactin inhibits secretion of GnRH
|
amenorrhea and galactorrhea....
|
|
vasopressin antagonists
|
treatment of euvolemic or hypervolemic hyponatremia
|
|
cholesterol is converted to what by steroids
|
prenenolene
|
|
Clucocorticoid mech of action
|
receptor is intercellular
|
|
metabolic effects of glucocorticoid physiologic effects
|
regulate carbohydrate, protein, fat metabolism,
|
|
in a fasting state with glucocorticoid
|
-stimulate gluconeogenesis and glycogen synthesis (body needs to feed brain)
-release of amino acids via muscle catabolism -inhibition of peripheral glucose uptake (insulin release) -Stimulation of hormone sensitive lipase and lipolysis |
|
Catabolic and antianabolic effects of glucocorticoids
|
lymphoid and connective tissue, skin, bone, muscle....
dec muscle mass weakness and thin skin osteoporosis |
|
Cortisol is bound?
|
90% to corticosteoid binding globulin...
inc in preg, hyperthyroidism dec in hypothyroid, protein deficiency |
|
what causes reduced clearance of cortisol
|
estrogens, liver disease, anorexia, protein-cal malnutrition, pregnancy, hypothyroidism
|
|
mineralocorticoids
|
have salt retaining properties
|
|
hydrocortisone
|
only glucocorticosteroid that has salt retaining properties
|
|
Addisons disease supplement
|
with hydrocortisone-equivalent must be given daily
|
|
Acute adrenal insufficiency
|
hydrocortisone IV 100 mg
fluid replacement taper hydrocortisone gradually to goal of 30 -50 daily |
|
Risk with >7.5 mg predisone equivalent daily for > 3 weeks
|
-intact HPD axis with <5mg/day prednisone equ
-intact HPA axis with duration < 5 day |
|
glucocorticoid synthesis inhibitors and antagonists primarily used for
|
cushings syndrome and adrenal carcinomas
|
|
Aminoglutethimide
|
blocks conversion of cholesterol to pregnenolone, reducing synthesis of all hormonally active steroids
|
|
Ketoconazole
|
inhibits several steps in glucocorticoid synthesis at high doses
|
|
Mifepristone
|
glucocorticoid receptor antagonist
|
|
Mifepristone
|
glucocorticoid receptor antagonist
|
|
Short cosyntropin stimulation test
|
-diagnosis of addisons disease
-250 mcg cosyntropin IV or IM -plasma cortisol measured at 0 , 30, 60 min |
|
dexamethasone suppression test
|
diagnosis of cushings syndrome.
-1 mg dexamethasone administered PO at 11pm. plasma cortisol measured at 8am >5 mcg/dl indicative of cushings syndrome |
|
what stimulates the RAAS?
|
hypotension
hyponatremia Badrenergic activity CNS excition |
|
inhibitors of RAAS
|
-hypertension
-hypernatremia -angiotension II -Vasopressin -potassium -Calcium -medications |
|
Aldosterone
|
*sodium retention and potassium excretion
-primary mineralcorticoid |
|
Fludrocortisone
|
-synthetic mineralcorticoid
|
|
Adverse effects of mineralocorticoid
|
hypernatremia, fluid retention, hypokalemia, alkalosis, hypertension, CHF exacerbation
|
|
Spironolactone
|
-aldosterone and adrogen antagonist
-competitively inhibits aldosterone biosynthesis in adrenal gland -primary aldosteronism 50-100mg/day |
|
Eplerenone
|
aldosterone antagonist
-primary aldersteronism 50 mg BID |
|
Drospirenone
|
aldosterone antagonist and progestin
-contraceptive |
|
Conversion of T4 to T3 is inhibited by
|
Radiocontrast media
Beta blockers corticosteroids amiodarone illness starvation |
|
recommended daily iodide
|
150 mcg
|
|
myxedema coma treatment
|
levothyroxine IV loading dose 300-400 mcg followed by IV daily dose 50-100 mcg
|
|
Treatment for hyperthyroidism
|
Pharm -
thioamides. methimazole.& propylthiouracil -iodides.. Symptom management Beta blockers |
|
Thioamides mechanism of action
|
inhibit thyoid peroxidase-catalyzed rxns
block iodine organification block coupling of iodotyrosines block peripheral conversion of T4 to T3 |
|
iodides mech of action
|
inhibit thyroid hormone release.
dec size and vascularity of hyperplastic gland |
|
what is the preferred treatment for pt >21 yo
|
radioactive iodine
|
|
Beta Blocker mechanism of action
|
symptomatic relief by offsetting sympathetic sx
propranolol inhibits peripheral conversion of T4 to T3 |
|
Treatment for thyroid storm
|
sx: propranolol 40-80 mg
inhibit thyroid hormone release inhibit thyroid hormone synthesis inhibit peripheral conversion of T4 to T3...hydrocortisone 50 mc IV |
|
Functions of insulin
|
inhibit hepatic gluconeogenesis
-facilitat glucose transport into cells inhibit glycogenolyssi -stimulate protein synthesis |
|
diagnosis of diabetes
|
C-peptide : measure of insulin secretion; type I DM (undetectable); type II DN (normal or elevated)
autoantibodies : islet cell, insulin, glutamic acid decarboxylate, tyrosine phosphatase |
|
goals of management with peak prandial glucose
|
<180 mg/dL ; 1-2 hrs after meals
|
|
MOA: Insulin secretagogue
|
Binds to receptors on the pancreatic β‐cells leading to
membrane depolarization with subsequent stimulation of insulin secretion |
|
Sulfonylureas
|
Highly protein bound
– NSAIDs, sulfonamides • Metabolism – Hepatic – Renal excretion • Allopurinol, probenecid, NSAIDs, sulfonamides • Glipizide – Shortest half‐life (2‐4 hours) |
|
Contraindications to sulfonylureas
|
Hypersensitivity to sulfonamides
– Patients with hypoglycemia unawareness – Poor renal function • Glipizide and its active metabolites are not renally eliminated |
|
Biguanides MOA
|
reduce hepatic gluconeogenesis
-inc insulin sensistivity of peripheral tissue |
|
Adverse effects of metformin
|
– Nausea, vomiting, diarrhea, epigastric pain
– Rarely • Decreased vitamin B12 • Lactic Acidosis – Black Box Warning – Acidosis, anion gap, nausea, vomiting, increased respiratory rate, abdominal pain, tachycardia, shock – Smallest risk of hypoglycemia • Metabolism – Renal excretion as active compound |
|
Meglitinides MOA
|
insulin secretagogue...dosed with meals
|
|
Thiazolidinediones (TZDs) MOA
|
Peroxisome proliferator‐activated
receptor γ agonist – Increases the expression of genes responsible for glucose metabolism – Results in improved insulin sensitivity |
|
black box warning for TZDs
|
Increased risk of heart failure
|
|
α‐Glucosidase Inhibitors MOA:
|
slows the absorption of glucose from the intestines into vasculature
|
|
contraindications with α‐Glucosidase Inhibitors
|
IBD, colonic ulcerations, intestinal obstruction
|
|
Dipeptidyl Peptidase‐4 Inhibitors MOA
|
inhibits the breakdown of glucagon like peptide secreted druing meals
– Increases pancreatic insulin secretion – Limits glucagon secretion – Slows gastric emptying – Promotes satiety |
|
Bile Acid Sequestrants MOA
|
– Unknown action on blood glucose
– Used in conjunction with other medications • Colesevelam – Only one with FDA indication |
|
contraindications with bile acid sequestrants
|
constipation, dypepsia, n/v
|
|
Amylin analog MOA
|
synthetic amylin
• Amylin is co‐secreted with insulin • Effects similar to GLP‐1 analog |
|
patients on beta blockers and hypoglycemia
|
may only have sweating
|
|
Neuropathic pain
|
Tricyclic antidepressant
• Amitriptyline, desipramine • Dosing lower than used for depression • Limitations – anticholinergic side effects – Anticonvulsant • Gabapentin, lamotrigine, pregabalin • Pregabalin has FDA indication for neuropathic pain – SSRI / SNRI • Paroxetine, citalopram, duloxetine • Duloxetine has FDA indication for neuropathic pain |
|
Concentration gradient:
|
Increasing the
concentration gradient increases the mass of drug transferred per unit time just as in diffusion across other barriers |
|
Dosing schedule
|
D/T physical properties,
skin can act as a reservoir for many drugs "local half-life" may be long enough to permit oncedaily application of drugs with short systemic half-lives (corticosteroids) |
|
occlusion
|
application of plastic wrap to hold the drug and its vehicle in close contact with skin
|
|
Considerations in vehicle selection
|
Solubility of active agent in the vehicle
Rate of release of the agent from the vehicle Ability of the vehicle to hydrate the stratum corneum (enhancing penetration) Stability of the therapeutic agent in the vehicle Interactions (chemical and physical) of the vehicle, the skin and the active agent. |
|
Ability of the vehicle to prevent evaporation
increases from the least |
in tinctures and wet dressings and greatest in ointments
|
|
Typically, acute inflammation with oozing,
vesiculation, and crusting is best treated with |
drying preparations such as tinctures, wet
dressings, and lotions |
|
Chronic inflammation with xerosis, scaling,
and lichenification is best treated w/ |
lubricating vehicles (creams / ointments)
|
|
Tinctures, lotions, gels, foams, and
aerosols are convenient for application to |
the scalp and hairy areas.
|
|
Antibiotic-corticosteroid combinations may be useful
|
in treating diaper dermatitis, otitis externa, and`
infected eczema |
|
First line
treatment in scabies |
permethrin 5% cream....prutitis may persist for weeks.
|
|
Podophyllin
|
Soluble in lipids - therefore distributed widely, including CNS
Major uses: Tx of condyloma acuminatum, penile and anogenital warts |
|
Minoxidil:
|
Topical minoxidil (Rogaine) - effective in
reversing hair loss associated w/ androgenic alopecia (Vertex balding more responsive than frontal balding) MOA on hair follicles unknown |
|
Eflornithine (Vaniqa)-
|
effects step in biosynthesis of
polyamines Polyamines required for cell division growth... Topical - effective in reducing facial hair growth in approx. 30% of women when applied twice daily for 6 months of therapy Hair growth returns to pretreatment levels 8 weeks after discontinuation. |
|
Tretinoin – (Retin-A) external use only
Retinoic acid- the acid form of vitamin A |
effective topical treatment for acne
Improves photodamageed skin, discolorations MOA: promotes cell turnover of normal follicle and comedones Skin more susceptible to irritation for sunburn, wind, cold or dryness Metabolized by the skin |
|
Sucralfate:
|
complex of aluminum hydroxide and sulfated sucrose
• binds to positively charged groups in proteins of both normal and necrotic mucosa • forms complex gels with epithelial cells • Creates a physical barrier that impairs diffusion of HCl and prevents degradation of mucus by pepsin and acid. • Stimulates prostaglandin release, mucus and bicarbonate output |