Final- new stuff Flashcards
Dexlansoprazole
PPI
MOA- irrevirsibly inactiavtes the hydrogen potassium adenosine triphosphate (H+/ K+/ ATPase) resulting in imparied acid secretion
Pro drug is protected by enertic coating ( dissoves in intestinal lumen abd is absorbed, carried to the parietal cells of the stomach for activation)
Can be taken with food
Onset of action2-3 hours, 3-4 days for maximal effect, duration of action 24 hours
Good for renal insufficiency patients
ADR- diarrhea, headache, abdominal pain, vitamin B12 deficiency, reduced absorption of iron, calcium, magnesium osteroperosis, fractures, C, diff, community aquired pneumonia
TAPER OFF- rebound hypersecretion
DDI- ketoconazole, intraconazole, atazanavir, rilpiverine, calicum caronate, iron salts
Pathophysiology of acne
Increased sebum production (caused by increased androgen levels)
Hyperkerinization (causes clogging of the follicle)
Colonization of P. Acnes (gram posititive anaerboe colonizes ans proliferates)
Release of inflmmatory mediators (papules, pustules)
Clobetasol propionate
Topical steroid-Ultra high potency
MOA- drecrease inflammation, modulate immune response and vasocontrict blood vessels to minimize redness, warmth and swelling
Potency determined by vasocontrictor assay (higher poteny more vasocotriction)
ADR- Skin atrophy, straie, rosacea, superfical infections, hypopigmentation, contact dermatitis, tolerance, tachyphylaxsis, systemic side effects (adrenalsupression, HTN, hyperglycemia)
Considerations high potency (groups 1-3)- not to be used in the face, groin, axilla, or under occlusions, better for thichker areas (palms and bottms of feet), use for the shortest duration possible, use for psoriasis, severe poison ivy, severe atopic detmatitis
Avobenzone
UVA
Polycarbophil
Bulk forming laxative
MOA- dissolves or swells in the intestional fluid, forming wmollient gels that facilitate the passage of intestional contents and stimulate peristalsis
DOC for constipation, goos for patients on low fiber diets
1-3 days onset to soften stool
Tretinoin
Topical Retinoid
MOA- stimuate epidermal cell trunover and decrease cell cohesiveness (unplug follicles , reduces inflammtion)
ADR- skin irritation, peeling, dryness, erythema, hyperpigmentation (more tretinoin> adapalene), acne may worsen with initial use (make take 3 months for full effect),
Consideratons- wear sunscreen, avoid UV light, apply at bedtime due to photosensitivity
Available in cream or gel
Azathioprines
Thiopurines
MOA- Purine antagonist→ inhibition of DNA/ RNA synthesis→ decreased T cell function→ immunosupression
Prodrug
ADR- N/V, bone marrow supression (leukopenia), hepatoxicity
DDI- allopurinal, feboxostate
Magnesium Citrate
Saline laxative- works in small and large intestine
MOA- draws water into the intestine, increasing intraluminal pressure, whihc acts as a stimulus to increase intestinal motility
Water evacuation within 1-6 hours
Do not use in patients with electrolyte disturbances, elders, patients with renal or cardiac issues ( uncontrolled hypertensionand CHF- salt content)
Salicylic acid
MOA- Keratolytic agent
Less effective vs. retinoids and BPO
ADR- peeling, dryness, burning
Methylnaltrexone
For opioid induced constipation
MOA- peripheral acting mu opioid receptor anatagonist, DOES NOT cross BBB (does not interfer with opiod use)
ADR- abdominal pain and/ or distension, diarrhea, headache, chills
DO NOT use with patients who have history of GI obstruction
Azelaic acid
MOA- normalizes keratinization and anti- inflammatory via reduction of p. acne
Use if you cannot tolerate other therapies
Dimenhydrinate
Anti-emetic- antihistamine and antimuscarinic bloackade (vestibular system) beneficial for nausea/ vomitting, motion sickness
Blocks more H1 then M1
ADR- first gen histamien ADR (constipation, dry mouth memory impairment)
Cyclosporine
MOA- calcineurin inhibitor→ drecreases transcription of IL-2, TNF- aplha, IL-4, etc
ADR- nephrotoxicity, HTN
Salfasazine
MOA- interferes with production of inflammatory cytokines. Modulates inflammation mediators derived from COX and lipoxygenase
Topical formuation- minimal systemic effect
CONTRAINDICCATED in those with salcylate allergy
SIte of action- large intestine
ADR- rash/ hypersensitivity, photosensitivity, hemolytic anemia, folate deficicency, pancreatitis, hepatitis
Monitor- CBC, LFT
Supplement with 1 mg dailty of folic acid
Finger tip method
1 FTU- 0.5g (500 mg)
Crisaborole
MOA- not fully elucidated; non steroidal inhibitor of PDE-4
Ointment
Mild to moderate atopic dermatitis
ADR- application related pain (burning, stinging)
Hitting which receptors causes stimulation of vomiting center?
- CNS (cortex, thalamus, hypothalamus, meninges)→ fear, anxiety, exciting causes stimuation of the vomitting center
- vestibukar center (balance, spacial awareness)→ Motion sickness caused by hitting H1 and M1 receptors causes nausea and vomitting
- Chemotigger zone- drugs hitting C2, NK and 5-HT3 receptors causes nausea and vomitting
- GI tract/ Heart- direct GI irrtants causes seratonin to be released (5-HT3 receptors) which stimulates the vomitting center
Oxybenzone
UVA+ UVB
Bismuth Subsalicylate
MOA- reacts with HCl to form bismuth oxychloride and salicylic acid
- Bismuth→ direct antimicrobial effect (H. pylori) used for travelers diarrhea
- Salicylic acid→ inhibits chloride secretion in intestine to reduce lipid content of stool (AVOID in aspirin allergy)
DO not use in children under 12 years old→ Reyes syndrome
ADR- blackening of tongue and stool (black tarry stool), tinnitus, dry stool, confusion
CHILDRENS PETO- NOT used for diarrhea its used for upset stomach
Fosaprepitant
NK recpotor antagonist (IV Only)
MOA- central blockade of NK receptors in the chemotrigger zone, blocks bnding of substance P
Coverted to aprepotant 30 min after infusion
ONLY used for prevention of chemotherapy induced nausea/ vomitting along with 5-HT3 antagonist and corticosteriods
ARR- Fatigue/ dizziness
CYP 3A4 substrate- combination with with CYP 3A4 inhibitor (Clarithromycin, Ketoconazole, Itraconazole, HIV protase inhibitors, Grapefruit Juice, diltizem, verapamil) can cause toxicity
Magnesium hydroxide
Saline laxative- works in small and large intestine
MOA- draws water into the intestine, increasing intraluminal pressure, whihc acts as a stimulus to increase intestinal motility
Water evacuation within 1-6 hours
Do not use in patients with electrolyte disturbances, elders, patients with renal or cardiac issues ( uncontrolled hypertensionand CHF- salt content)
Hydrocortisone
Topical steroid- low potency
MOA- drecrease inflammation, modulate immune response and vasocontrict blood vessels to minimize redness, warmth and swelling
Potency determined by vasocontrictor assay (higher poteny more vasocotriction)
ADR- Skin atrophy, straie, rosacea, superfical infections, hypopigmentation, contact dermatitis, tolerance, tachyphylaxsis, systemic side effects (adrenalsupression, HTN, hyperglycemia)
Considerations high potency (groups 6-7)- safest for prolonged use, large surface areas, face or other areas with thin skin, children, think dermatitis, diaper rash, rash on face/ eyelids, perianal inflammation
Octocrylene
UVB
Triamcinolone acetonide
Topical steroid- medium to high potency
MOA- drecrease inflammation, modulate immune response and vasocontrict blood vessels to minimize redness, warmth and swelling
Potency determined by vasocontrictor assay (higher poteny more vasocotriction)
ADR- Skin atrophy, straie, rosacea, superfical infections, hypopigmentation, contact dermatitis, tolerance, tachyphylaxsis, systemic side effects (adrenalsupression, HTN, hyperglycemia)
Considerations high potency (groups 1-3)- not to be used in the face, groin, axilla, or under occlusions, better for thichker areas (palms and bottms of feet), use for the shortest duration possible, use for psoriasis, severe poison ivy, severe atopic detmatitis
Zinc Oxide
UVA+ UVB
Mineral Oil
Lubricant
MOA- Soften fecal contents by coating them, therby preventing colonic reabsorption of fecal water
Safety concern of lipid pnuemonia (risk of aspiration, SOB)
1-3 days onset to soften stool
Olanzapine
D2 receptor antagonist
Hits D2, 5-HT1c, 5-HT3 (second line chemotherapy induced nausea/ vomitting)
ADR-Dystonia, akathesia, parkinsonian, sedation, hyperprolactinemia, hypotension, dry mouth
Octisalate
UVB
Sucralfate
Sucrose+ complexed aluminum hydroxide
MOA- mixes with HCl (DO NOT perscribe with PPIs) to form viscous paste that binds directly to ulcers and erosions- “physical barrier to protect stomach”, stimulates mucosal prostoglandin and bicarbonate secretion
Constipation (aluminum), aluminum toxicity in renal disease
Titanium dioxide
UVA+ UVB
Palonsetron
5-HT3 recepotr antagonist (IV ONLY)
Used for chemotherapy induced nausea/ vomitting
MOA- central bloakade of the chemotrigger zone and vomittng center. Peripheral blockage (Seratonin receptors in GI tract) of intestinal vagal and spinal afferent nerves→ drives antiemetic benefit (80% of seratonin is found in the GI tract)
Does not hit H1, M1 or D2 receptors not suitable for the treatment of motion sickness
Long half life (40 hours)- good for delayed nausea/ vomitting
Metabolism- CYP 2D6
ADR- Headache, dizziness, constipation,least likely to casue QTc prolongation (K+ channel blockade), Seratonin syndrome (Increase levels of seratonin)
Netupitant
NK recpotor antagonist
MOA- central blockade of NK receptors in the chemotrigger zone, blocks bnding of substance P
ONLY used for prevention of chemotherapy induced nausea/ vomitting along with 5-HT3 antagonist and corticosteriods
ARR- Fatigue/ dizziness
CYP 3A4 substrate- combination with with CYP 3A4 inhibitor (Clarithromycin, Ketoconazole, Itraconazole, HIV protase inhibitors, Grapefruit Juice, diltizem, verapamil) can cause toxicity
Rolapitant
NK recpotor antagonist
MOA- central blockade of NK receptors in the chemotrigger zone, blocks bnding of substance P
ONLY used for prevention of chemotherapy induced nausea/ vomitting along with 5-HT3 antagonist and corticosteriods
ARR- Fatigue/ dizziness
CYP 3A4 substrate- combination with with CYP 3A4 inhibitor (Clarithromycin, Ketoconazole, Itraconazole, HIV protase inhibitors, Grapefruit Juice, diltizem, verapamil) can cause toxicity
Fluticasone propionate
Topical steroid- medium to high potency
MOA- drecrease inflammation, modulate immune response and vasocontrict blood vessels to minimize redness, warmth and swelling
Potency determined by vasocontrictor assay (higher poteny more vasocotriction)
ADR- Skin atrophy, straie, rosacea, superfical infections, hypopigmentation, contact dermatitis, tolerance, tachyphylaxsis, systemic side effects (adrenalsupression, HTN, hyperglycemia)
Considerations high potency (groups 1-3)- not to be used in the face, groin, axilla, or under occlusions, better for thichker areas (palms and bottms of feet), use for the shortest duration possible, use for psoriasis, severe poison ivy, severe atopic detmatitis
Misoprostol
MOA- PGE1 anaglog- increases mucosal and bicarbionate secretion, enhances mucosal blood flow
Used for NSAID- related ulcers or labar induction (OB/ GYN)
Comes in combinaion product with diclofenac sodium
ADR- Diarrhea, enhanced uterine contractine, dont take if pregnant
Benzoyl Peroxide
MOA- antimicrobial (against P. acnes), anti-inflammatory, keratolytic effects
May inactivate some formularions of tretinoin, so avoid use or sperate times of administration
Efficacy is not concentration dependent
ADR- contact dermatitis, erythema, skin, dryness, peeling, bleaching
Mirtazapine
Anti-emetic- 5HT-3 antagonism and H1 antagonism
Used for cancer (nausea and vomitting), depressed and underweight people
Cinoxtane
UVB
lansoprazole
PPI
MOA- irrevirsibly inactiavtes the hydrogen potassium adenosine triphosphate (H+/ K+/ ATPase) resulting in imparied acid secretion
Pro drug is protected by enertic coating ( dissoves in intestinal lumen abd is absorbed, carried to the parietal cells of the stomach for activation)
Bioavailibity decreases with food (take on empty stomach 30-60 min beofre first meal)
Onset of action2-3 hours, 3-4 days for maximal effect, duration of action 24 hours
Good for renal insufficiency patients
ADR- diarrhea, headache, abdominal pain, vitamin B12 deficiency, reduced absorption of iron, calcium, magnesium osteroperosis, fractures, C, diff, community aquired pneumonia
TAPER OFF- rebound hypersecretion
DDI- ketoconazole, intraconazole, atazanavir, rilpiverine, calicum caronate, iron salts
Budesonide
Coricosteriods
pH controlled- entocort (pH5.5 more in the small intestine), uceris (pH> 7 more in large colon)
CYP 3A4 metabolite- watch for CYP 3A4
Opioid induced constipation
Opioids delys gastric emptying, interrupt bowel peristalsis, reduce intestinal secretion of fluid
Traditonal laxitives still first line