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Pharm 3 Flashcards

1
Q

MIC

A

The lowest concentration of an antimicrobial that will inhibit the visible growth of an organism

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2
Q

Post-antibiotic effect

A

Period of time after complete removal of an antibiotic during which there is no growth of the target organism

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3
Q

Patient specific antibiotic factors

A

Renal, hepatic function
Age
Size

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4
Q

Drug specific Abx factors

A

IV vs. PO
Bacteriostatic vs -cidal
Cost
Distribution

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5
Q

Bacterial resistance mechanisms

A

Inactivation by beta lactamases (+new/other -ases, ex carbapenemase)

New binding proteins w/ decreased affinity for Abx

Decreased permeability of bacterial cell wall

Modification of cell membrane constituents that prevent penetration

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6
Q

G+ aerobes

A

Staph, Strep, Enterococcus, Listeria

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7
Q

G- aerobes

A

E. coli, Klebsiella, Proteus, Pseudomonas, Moraxella

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8
Q

G+ anaerobes

A

Peptococcus, peptostreptococcus, Clostridium

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9
Q

G- anaerobes

A

Bacteroides, Fusobacterium, Prevotella

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10
Q

PCNs

A

Cell wall active-disrupt bacterial cell wall formation by inhibiting certain enzymes that create cross-linking –> activation of endogenous autolytic systems causes cell lysis and death (bacteriostatic)

Coverage: mostly G+, some G-

ADEs: hypersensitivity rxn, neutropenia, interstitial nephritis, CNS toxicity (seizures)

Peak concentration in 1-2 hr, most have wide distribution, minimal liver metabolism

Excretion by kidneys

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11
Q

Natural penicillins
Penicillin G, Penicillin V

A

Active against Strep, Enterococcus, some G+ anaerobes (peptococcus, peptostreptococcus)

Distribute to most tissues: lung, ascites, synovium, pericardium, soft tissues

Dose reduction for GFR <50
Most associated w/ ADEs

Drug of choice for syphilis, strep

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12
Q

Aminopenicillins

Ampicillin
Amoxicillin

A

Retain activity of naturals (More active against Enterococcus than other PCNs)
+
Extended G- coverage (H. flu, E. coli, K. pneumo)

Distributes to renal tissue, septic joints, ascitic fluid, CSF

Not very beta-lactamase stable

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13
Q

Penicillinase resistant PCNs

Oxacillin
Nafcillin
Dicloxacillin

A

Activity against: Strep good), Staph (excellent), Peptostrep
Very narrow, mostly just used for staph

No G- activity

Distributes to bone, septic joint effusions, cardiac tissue (endocarditis, septic joints)

Drug of choice for MSSA

Dose adjustment for severe HEPATIC impairment

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14
Q

Nafcillin

A

Penicillinase resistant PCN

Big sodium load when prepared IV. Caution in ascites/HF

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15
Q

Ureidopenicillins (Anti-pseudomonal penicillins)

Piperacillin

A

Always given w/ a beta lactamase inhibitor

Significantly improved activity against G- (Psuedomonas, Bacterioides) , some enterococcal activity, good anaerobe activity

No staph activity

Not very beta-lactamase stable

Distribution: pleural fluid, ascitic fluid, wound fluids

Dose adjustment for CrCl <50

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16
Q

Beta-lactam/Beta-lactamase inhibitors

Ampicillin/Sulbactam (Unasyn)
Amoxicillin/Clavulanic acid (Augmentin)
Piperacillin/Tazobactam (Zosyn)

A

Adds H. flu, M. cat, N. gonorrhea, B. fragilis coverage

Extends G+ and G- activity

Useful in mixed infections or for broad empiric coverage as a single agent

No antibiotic activity of its own

Good concentration throughout the body

Dose adjustment for CrCl < 50

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17
Q

Cephalosporins

A

Cell wall active: Disrupt bacterial cell wall formation by inhibiting certain enzymes that create cross-linking –> activation of endogenous autolytic systems to cause cell lysis and death

Activity variable across classes. None cover enterococcus

Some have MTT side chain which prolong PT/INR and may cause disulfram rxn w/ alcohol

1-3% cross reactivity w/ PCN allergy (maybe even less)

Rapidly absorbed, short T1/2, most excreted renally (ceftriaxone = liver metabolism)

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18
Q

1st Gen Cephalosporins

Cefazolin (IV)
Cephalexin, Cephadroxil (PO)

A

Good G+ coverage, limited G-, no anaerobes

Very active against strep and MSSA

Wide distribution throughout body (bone, skin, soft tissue) poor CSF penetration

Dose adjustment for CrCl < 50

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19
Q

Second Gen Cephalosporins: Group 1

Cefuroxime, Cefaclor

A

Very active against Strep, MSSA
Improved activity against G- (aerobes) BUT no G- anaerobes

variable CSF penetration (Cefuroxime penetrates well into CSF)

Dose adjustment in kidney disease

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20
Q

Second Gen Cephalosporins: Group 2 (Cephamycins)

Cefoxitin, cefotetan

A

Inferior activity against strep and MSSA BUT enhanced activity against G–

Preferred for “dirty” surgery (GI, GU,)

Dose adjustment in kidney disease

MTT side chain

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21
Q

Third Gen Cephalosporins

Anti-pseudomonal: Ceftazidime

Other: Cefotaxime, Ceftriaxone, Cefiximine, Cefpodixime

A

Anti-pseudomonals (Ceftazidime): excellent coverage G- aerobes (including pseudomonas), adequate Strep coverage (less than other cephalosporins)

Weak MSSA coverage (all 3rd gen)

Extensive distribution including good CSF penetration

Dose adjustment for decreased renal and hepatic function

Very broad coverage. Great for meningitis.

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22
Q

4th Gen Cephalosporins (Cefepime)

A

Staph/strep coverage comparable to earlier generation cephalosporins
Superior G- activity (including very good pseudomas aeruginosa coverage)

No MRSA

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23
Q

5th Gen Cephalosporins (Ceftaroline)

A

Widest spectrum: coverage of G-, G+, aerobic/anaerobic
MRSA coverage
Strep pneumo coverage

NO PSEUDOMONAL coverage

Restricted access because very broad and concerns for resistance if overused. Only for definitive therapy. Must consult ID

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24
Q

Thienamycins (-penems)

Imipenem
Ertapenem
Meropenem

A

Broadest coverage: G+ an G- aerobe coverage (except MRSA and E. faecium), most G- anaerobes

Meropenem has best pseudomonal coverage
Ertapenem: no pseudomonal but great against ESBLs

MOA: cell wall active, similar MOAs to PCN/Cephs
Pro: Post-Abx effect
ADE: N/V/D (IV)

Imipenem lowers seizure threshold, toxic metabolites. Always given w/ cilastatin to inhibit

Penetrate most tissues, including bone, meninges

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25
Monobactams (aztreonam)
Covers G- aerobes (including pseudomonas) No G+ No anaerobes Good substitute for aminoglycosides in pt at risk for toxicity Widely distributed, often used in combo w/ clindamycin, macrolides Dose reduce in renal insufficiency
26
Non Beta-Lactam, Cell Wall Active: Glycopeptides (Vancomycin)
Binds to D-alanyl-D-alanine terminal residue in growing peptidoglycan chain, inhibiting cell wall synth Bacteriocidal Activity against G+ aerobes: strep, staph (including MRSA, MRSE), enterococcal spp No G-, no anaerobes (except oral vanco for C. diff) ADE: red mans syndrome, neutropenia, nephrotoxicity, ototoxicity Distributes to CSF and widely to other tissues
27
Aminoglycosides Gentamycin Tobramycin Amikacin Streptomycin
Most toxic antibiotic class MOA: Binds to 30S ribosomal subunit which decreases protein synth. Increases misreading of mRNA Covers aerobic G- (including pseudomonas) No anaerobe, no G+ Synergistic w/ cell wall active beta lactams (Vanco) for MRSA, MSSA, Enterococcus, Pseudomonas Good penetration into urine, CSF, lungs BBW: nephro/ototoxic. Need drug level monitoring 100% excreted by kidneys
28
Tetracyclines Tetracylcine Doxycycline Minocycline
MOA: Reversibly binds to 30S subunit on ribosome, preventing protein synth Bacteriostatic @ therapeutic concentrations Good coverage of G+ and G- aerobes, except pseudomonas No G- anaerobes Doxy: good for MRSA cellulitis atypical pneumonia pathogens Penetrates brain/CSF in small amounts ADE: photosensitivity, decrease skeletal growth in children, GI, hepatotoxicity, vertigo, worsening of renal failure Separate from milk/antacids by 2-4 hr window Esophageal irritant: drink lots of water and take sitting upright
29
Macrolides Erythromycin Clarithromycin Azithromycin
Good coverage G+ aerobes (erythro best) Good coverage G- aerboes (azithro best) Good atypical PNA coverage (legionella, mycoplasma, chlamydia) and typical pna (H. flu, M. cat) H pylori Clarithro/azithro active agaisnt MAC No coverage G- anaerbobes
30
Erthromycin
Macrolide Best in its class for G+ aerobe coverage, worst for G- aerobes many drug interactions due to metabolism through the CYP450 enzyme system ADEs: abd cramps/N/V/D, thrombophlebitis, cholestatic hepatitis Poor penetration in body tissues Short T1/2. Dose adjustment in hepatic/renal failure
31
Azithromycin/Clarithromycin
Macrolides, best in class for G- aerobes, less coverage of G+ aerobes No G- anaerobes Both cover H pylori and MAC Azithro: long T1/2 (5 days), less QTc prolongation than other macrolides ADE: less GI side effects than erythro, tinnitus/dizziness Penetrate well into many tissues, including lungs/alveolar macrophages
32
Lincosamides (Clindamycin)
Binds to 50S ribosomal subunit, decreases protein synth Active against staph (MSSA and MRSA), strep, G- anaerobes (B fragilis group), G+ anaerobes, toxoplasmosis No activity against G- aerobes Penetrates bone, bile, most body tissues but NOT CSF ADE: GI intolerance, hepatotoxicity, neutropenia/thrombocytopenia, esophageal irritation (drink w/ lots of water and sitting uprignt)
33
Fluoroquinolones Ciprofloxacin (bone/UTI) Levofloxacin (both) Moxifloxacin (atypical resp)
Inhibits DNA gyrase (inhibit DNA synthesis and breakage of bacterial DNA) All active against G- aerobes Cipro and Levo active against pseudomonas ***only oral agents available to treat pseudomonas Variable against G+ aerobes: MSSA, Moxi/Levo better coverage of Strep No G- anaerobes Also: atypical PNA ADE: GI, HA/dizziness, phototoxicity, increased LFTs, tendon rupture, QTc prolongation Renal dose adjustments needed. Contraindicated in peds and pregnancy Avoid w/ dairy, antacids for 2-4 hr window
34
Sulfas Trimethoprim/sulfamethoxazole (Bactrim)
Inhibit bacterial folic acid synth, inhibiting cell growth *One of only oral drugs for MRSA cellulitis Good activity G- and G+ aerobes (Except pseudomonas, Group A strep, enterococcus) No G- anaerobes Penetrates well into most tissues, CSF levels 40% of serum levels ADE: crystalluria (hydrate well), increases INR in patients on warfarin, increases phenytoin levels, hyperkalemia, GI intolerance, SJS, anemia, neutropenia Avoid in HD patients. Dose adjust in renal failure
35
Nitroimidazoles (Metronidazole)
bacteriocidal: enters cell, reduced to free radicals which damage DNA covers all anaerobes (including C diff, H pylori) No aerobe coverage ADE: disulfram rxn w alcohol, increased INR w/ warfarin, metallic taste, GI disturbance, dark urine, reversible neutropenia
36
Oxalinediones (Linezolid)
Bacteriostatic: binds to 50S ribosomal subunit, inhibits early phase protein synth Broad coverage! G+pathogens (including VRE) Staph (including MRSA) Strep (including PCN resistant strains) ADE: diarrhea, nausea, taste perversion, increased LFTs, thrombocytopenia No hepatic/renal dose adjustment
37
Lipopeptides (Daptomycin)
Bacteriocidal: Binds to bacterial cell membranes, causing rapid depolarization of membrane potential --> leads to inhibition of protein, DNA and RNA synthesis G+ activity including VRE, MRSA 1st bacteriocidal drug against resistant bugs Widely distributed to tissues except lungs Dose reduce in renal insufficiency
38
CURB-65
Each 1 point for determining PNA site of treatment: Confusion Uremia/BUN > 20 Resp Rate > 30 BP < 90/60 65 years or older 0-1 = home >3 = possible ICU
39
Typical CAP pathogens
H flu Chlamydia Strep pneumo
40
Atypical PNA pathogens
CML: Chlamydia Mycoplasma Legionella
41
Empiric CAP therapy: non-ICU
Macrolide (ex: azithromycin) + beta-lactam (cephalosporin, PCN, penem, etc) Ex: Azithro + cephtriaxone Azithro + ertapenem OR Fluoroquinolone alone (levo or moxifloxacin)
42
Empiric CAP therapy: ICU
Cephalosporin (Ceftriaxone) OR Ampicillin-Sulbactam + Fluoroquinolone if PCN allergy: moxi or levo + aztreonam
43
CAP treatment modifying factors
IF structural lung disease: add antipseudomonal agent (Cefipime, pip/tazo, imipenem, meropenem) PLUS macrolide/ FQ(levo/cipro ) BL allergy: FQ +/- vanco CAP MRSA: Vanco or Linezolid + FQ
44
HAP common pathogens
E coli, Klebsiella pneumo, Staph, Psueodomonas Anaerobes (d/t aspiration) Watch for multi drug resistant organisms
45
HAP tx (low risk mortality)
No MRSA risk factors Pip/Tazo (Zosyn) OR Cefipime OR FQ (Levofloxacin) OR Penem (Meropenem/imipenem) MRSA risk factors Add vanco or linezolid
46
VAP empiric tx
Cover MRSA: linezolid, vanco Cover pseudomonas -Beta lactam: zosyn OR 3rd gen ceph OR penem OR aztreonam -Non-beta lactam: FQ(cipro/levo) OR aminoglycosides (amikacin, tobramycin, gentamycin)
47
Aspiration pneumonia
Primarily anaerobic in nature. Direct therapy towards mouth flora Lincosamide (Clinadamycin) + FQ
48
Primary, Type I Osteoporosis
loss of trabecular bone with estrogen loss
49
Primary, Type II Osteoporosis
loss of trabecular and cortical bone w/ inefficient remodeling (d/t diet, age, physical activity)
50
Secondary osteoporosis
D/t systemic illness or meds
51
Calcium products
Dietary preferred Take supplements <500 mg w/ meals Eliminated unabsorbed via GI tract ADE: N/C Interactions: Binding w/ FQs/Tetracycline Abx
52
Vitamin D
Dietary, UV exposure preferred Supplemented w/ cholecalciferol, calcitrol in susceptible pt ADE: Hypercalcemia: promotes absorption of Ca from SI Decreases PTH and bone resorption
53
Bisphosphonates
1st line osteoporosis therapy Binds to bone, inhibits osteoclast activity Renally excreted ADE: nausea, abd discomfort, rare jaw necrosis/femur fx Interactions: antacids Avoid in renal impairment, esophageal obstruction
54
PTH analog (Teriparatide)
Stimulates osteoblasts, increases renal tubular reabsorption of Ca, increasing bone mass/density SQ for 18-24 months ADE: HA/LH, hypotension, palpitations, transient hyperca Avoid in hx skeletal malignancy or bone mets
55
SERMS (Raloxifene)
Estrogen R agonist in bone and antagonist @ breast/uterus. Slow rate of bone loss Highly protein bound ADE: hot flash, flushing, leg cramps, VTE
56
Calcitonin
3rd line tx for osteoporosis inhibits osteoclast Nasal or SQ ADE: N/V, flushing, injection site rxns Avoid in hypocalcemia
57
Estrogen products
Short term symptom mgmnt of osteoporosis Inhibit osteoclast activity via estrogen receptor ADE: HA, depression, N/V, cramps, hypertension, VTE, bleeding, breast CA
58
CKD
Structural (blood/protein in urine) and/or functional (decreased GFR) damage to kidneys over at least 3 months Causes: hyperglycemia, uncontrolled HTN/HLD Loss of renal function is slow Microalbuminuria = high prognostic factor for progression of CKD GFR <120 = damage 60-90 = modeerate kidney function <30 = ESRD Things to watch: Anemia, secondary hyperparathyroidism, hyperkalemia, acidosis, nutrition
59
Anemia of CKD
Decreased EPO production Decreased RBC survival Iron deficiency Blood loss (via GI or dialyzer) Target goal Hgb 11-13/Hct 33-36% EPO products and iron *Always correct iron prior to or in conjunction w EPO therapy
60
Secondary hyperparathyroidism of CKD
Decreased renal elimination of phosphate, decreased production of active vitamin D Increased serum phos = decreased Ca --> increased PTH production in response to decreased Ca and active vitamin D --> PTH increases Ca mobilization from bone Goals of therapy: Serum phos 2.7-5.5 Serum Ca 8.4-9.5 (adjust for albumin) Serum PTH 35-300 (dependent on CKD stage) Serum vit D >30 ng/mL
61
Phosphate binders
Binds phosphorus in the gut, complex is subsequently eliminated in the feces Must be taken with meals to optimize binding effect Initiate when Phos >4.5 If serum Ca x PO product < 55 --> calcium containing product If serum Ca x PO product >55 --> nonabsorbable polymer (sevalamer)
62
Vitamin D products
Inhibits PTH secretion & promotes GI Ca absorption Calcitriol, Paricalcitol, Doxercalciferol ADE: Hypercalcemia
63
Calcimimetic agent
Designed to activate the Ca-SR on the PT glands Receptors become more sensitive to the binding of extracellular Ca, which then inhibits PTH Cinacalcet (Sensipar®) ADE: N/V, hypocalcemia Can be used in combination with Vit D analogs and phosphate binders
64
Hyperkalemia in CKD
Diminished renal potassium excretion + Redistribution of K+ into extracellular fluid due to metabolic acidosis Tx depends on serum K+ level as well as presence of ECG changes Therapy usually initiated when K+ > 6 mmol/L
65
Metabolic acidosis in CKD
In normally functioning kidneys H+ ion is generated to facilitate absorption of filtered bicarbonate. In the diseased kidney there is a decrease in H+ ion production and subsequently reduced bicarb absorption Reduced bicarb absorption is responsible for the development of metabolic acidosis Contributes to osteodystrophy and muscle loss Tx: dialysis, bicarb replacement
66
Bicarb replacement
Dose (mmol) = 0.5 L/kg x (22- pt serum bicarb) Initial replacement = 1/2 total dose daily to prevent excess Na intake Maintenance = 10-20 mmol daily
67
Hyperthyroid
Etiology: Graves, pituitary/toxic adenomas, drug induces (amiodarone) Presentation: weight loss, heat intolerance, tachycardia, warm/moist skin Dx: high T4, low TSH, radioactive iodine studies, thyroid related Antibodies (Grave's)
68
Thioureas (MMI, PTU)
MOA: inhibit iodination and synthesis of thyroid hormones, block T3/T4 conversion in periphery. MMI more potent than PTU Both have slow (4-6 week) onset ADE: hepatotoxicity, arthralgia, fever, rash, agranulocytosis Teratogenicity: PTU safe in 1st trimester, MMI in 2nd-3rd trimester
69
Nonselective beta blockers (propranolol)
For symptomatic control of hyperthyroidism. Blocks hyperthyroid manifestations mediated by beta-adrenergic receptors and can block T4/T3 conversion ADE: bradycardia, hypotension, cardiac ischemia
70
Iodines/iodides
MOA: inhibit release of stored TH, decreases vascularity of thyroid gland prior to surgery Indicated before surgery, after ablative therapy, in thyroid storm ADE: metallic taste, burning mouth
71
Thyroid storm
Life-threatening decompensated thyrotoxicosis Causes: Trauma, infections, noncompliance with pharmacotherapy, severe inflammation of thyroid Tx: thiourea, iodide therapy, beta blockers for tachycardia, tylenol for fever, IV corticosteroids
72
Hypothyroid
Causes: Hashimotos, iodine deficiency, secondary (pituitary insufficiency), iatrogenic Presentation: cold intolerance, weight gain, bradycardia, areflexia Dx: low T4, elevated TSH, thyroid antibodies present Screen all patients > 60 years
73
Levothyroxine
Start @ 1.6 mcg/kg/day ideal body weight Give in AM on empty stomach Highly protein bound (100%) 4-6 weeks to reach peak effect Hepatic metabolism to T3, eliminated in urine ADE: hyperthyroidism, tachyarhthymias, increased risk fx
74
Myxedema coma
Life threatening decompensated hypothyroidism Causes: trauma, infection, HF, drug induced Presentation: AMS, hypoventilation, hypothermia Tx: IV thyroid hormone replacement, empiric Abx, corticosteroids
75
Metformin
1-2% Reduction in A1C 1st line for T2DM MOA: decreases hepatic gluconeogenesis, increases insulin sensitivity and glucose uptake into tissues ADE: N/V/D, B12 deficiency, BBW for lactic acidosis Contraindications: renal impairment, metabolic acidosis Concentrates in liver, kidney, GI Category B in pregnancy No weight gain, low risk hypoglycemia as monotherapy, can use as adjunct w/ other agents
76
Sulfonylureas (Gliperizide, glimepiride, glyburide)
1-2% reduction in A1C MOA: binds to receptors on pancreatic beta cell, depolarizes membrane and stimulates insulin secretion ADE: hypoglycemia, weight gain, must take w/ food Contraindications: poor renal function, hepatic insufficiency
77
Meglitinide (Repaglinide)
0.5-1.5% reduction in A1C MOA: similar to sulfas w faster onset of action ADE: hypoglycemia, weight gain, URI Contraindications: concomitant use w/ gemfibrozil
78
TZDs (pioglitazone, rosiglitazone)
0.5-1.4% MOA: increases insulin sensitivity of adipose tossue Delayed (1-3 month) onset ADE: weight gain, edema, bone rx, worsening HF, myalgia, increased LFTs Contraindications: NYHA Class III/IV HF
79
DPP4 inhibitors (Sitagliptin, Saxafliptin)
0.5-0.8% reduction in A1C MOA: inhibits breakdown of GLP 1 secreted during meals which increases insulin secretion, decreases glucagon secretion, and promotes satiety Monitor s/sx pancreatitis
80
SGLT2 inhibitors (Canagliflozin, empagliflozin)
0.3-1% reduction A1C MOA: increases urinary glucose excretion by blocking normal reabsorption in proximal convoluted tubule ADE: increased urination, UTI hypotension, increased risk bone fx Contraindicated in renal impairment
81
Acarbose
MOA: decreases absorption of glucose from intestine to bloodstream by slowing breakdown of large CHO into smaller, easier to absorb sugars ADE: flatulence, diarrhea, abd pain, LFTs Contraindications: IBD, colonic ulcerations, intestinal obstructions
82
Basal insulin dosing
10 units daily or 0.1-0.2 units/kg daily Titrate by 2 units every day 3 days to target A1C
83
Prandial insulin dosing
Start w/ 1 dose @ largest meal (if A1C above goal w/ appropriately titrate basal dosse) increase by 1-2 units twice weekly
84
Insulin dosing options
2/3 NPH + 1/3 regular OR 50% basal, 50% prandial divided into 3 meals daily
85
GLP 1 analogs (injectable) ( Liraglutide, Exanatide)
MOA: analog of human GLP-1 that increases glucose dependent insulin secretion, decreases glucagon secretion, and decreases gastric emptying. ADE: N/V/D, hypoglycemia, acute renal impairment Monitor for pancreatitis
86
Rapid acting insulin
Lispro Aspart Glulisine 15 min onset
87
Short acting insulin
Regular (Humulin) 60 min onset
88
Intermediate acting insulin
2-4 hr
89
Long acting insulin
Glargine (Lantus) 4-5 hr onset, 24 hr duration No pea
90
GERD:
Decreased basal LES pressure --> LES relaxation Impaired esophageal clearance Decreased acid clearance, delayed gastric emptying Severity r/t amount of time esophagus exposed to acid and pepsin Tx: avoid aggravating factors: diet, exercise, pregnancy, tight clothing, smoking cessation OTC antacids, H2 blockers, PPIs Complications: esophagitis, strictures, Barrett's esophagus
91
PUD
Gastric, duodenal ulcers Common causes: H. pylori, NSAIDs, stress-related Tx: dietary/lifestyle changes, eradicate H pylori, relieve pain/heal ulcers and erosions OTC antacids, H2 blockers, PPIs Misoprostol for NSAID induced PPI Triple therapy (or alt) for H pylori induced
92
Antacids
Neutralize acid by increasing gastric pH. Inhibits conversion of pepsinogen to pepsin. May also stimulate production of mucosal prostaglandins Symptomatic relief only, does not provide healing Types: aluminum, magnesium, Ca, bismuth Suspensions superior to capsules/tablets. Thoroughly chew and take w full glass of water Decreases absorption of H2 antagonists, ampicillin, phenytoin, iron, FQs, tetracycline Soln: separate from other meds/food by at least 2 hr Quick onset, short duration. Can mask other issues Accumulation in renal disease
93
H2 antagonists
Inhibit histamine receptors on parietal cells, decreased secretion of hydrogen ions. Indication: DU (4-8 wks), GU/GERD (8 weeks) 1st line for tx of chronic mild-moderate GERD. Intended only for short term use BUT if long term therapy required, H2 antago preferred over PPI ADE: HA, diarrhea, Monitor renal function
94
PPI
Irreversible inhibition of H/K/ATPase pump on parietal cells (the final step of acid secretion) 1st line for moderate-severe GERD, preferred over H2 blockers for H pylori and erosive esophagitis Take 30-60 min before 1st meal of the day. Do not crush or chew ADE: risk of fracture, hypomag, C diff diarrhea, CAP, HA Pantoprazole has fewest drug interactions because not CYP mediated
95
Reglan (Metoclopramide)
Unclear MOA, stimulates motility in upper GI, prokinetic agent, increases LES tone and peristalsis. Only for use after confirmed diagnosis ADE: Galactorrhea, diarrhea, EPS, depression/drowsiness (DA driven ADEs) Contraindications: Parkinsons, obstruction Monitor renal function Interactions: anticholinergics, MAO-I, Levodopa
96
Sucralfate
Promote mucosal defense, react w/ hydrochloric acid in stomach to form a paste that binds to surface of ulcer. Barrier allows ulcer to heal No acid reducing capacity Useful as adjunct therapy, not alone
97
Misoprostol
PGE1 analog, stimulates production of mucus and bicarb, Cryoprotection. ADE: abd pain, diarrhea, spontaneous abortions, bleeding in postmenopause Contraindications: women of childbearing age
98
H. pylori therapy
Clarithro based triple therapy: PPI + clarithromycin + amoxicillin // PPI + clarithromycin + metronidazole OR In escalating resistance: Bismuth quadruple therapy: Bismuth + metro + tetra + PPI OR PPI/Levo/Amoxicillin --> best in terms of adherence/resistance
99
Phenothiazines (Prochlorperaine, promethazine)
MOA: DA antag @ CT ADE: sedation, dry mouth, urinary retention, blurred vision, EPS
100
Benzamides (Metoclopramide, trimethobenzamide)
MOA: inhibits DA in GI/CTZ, +reglan aids motility in gastric paresis ADE: sedation/ EPS
101
5HT3 antagonist (Ondansetron, granisetron)
MOA: inhibits 5-HT in vomiting center ADE: HA, malaise, constipation, hypotension, EPS (rare), anorexia Overall well tolerated but prolonged QTc w/ doses >16 mg, now contraindicated. Correct hypoMag and hyperK
102
Benzos (Ativan)
prevent limbic input from reaching vomiting center Anticipatory nausea, anxiety ADE: sedation, amnesia, akithesia
103
Corticosteroids (Dexamethasone)
MOA unknown, for chemo-induced vomiting ADE: mood changes, increased appetite, weight gait
104
Antihistamines, anticholinergics
Inhibit cholinergic receptors which decreases stimulation of vomiting center ADE: sedation, dry mouth, blurred vision
105
Aprepitant (Emend)
Substance P/Neurokinin 1 receptor antagonist in GI tract and CTZ Primarily for chemo induced N/V Effective as combo w/ steroid and 5HT3 antag
106
Antiperistaltic agents (Loperamide, diphenoxylate)
Slow GI motility Caution in infectious diarrhea, avoid in children ADE: sedation, CNS effects
107
Adsorbants (Polycarbophil, Bismuth)
Absorbs water, no systemic absorption Less effective, but fewer ADEs than anti-motility agents ADE: fullness, bloating gas
108
Anti-secretory (Bismuth subsalicylate)
Antisecretory, antimicrbial, and absorbant properties Toxicity-broken down to salicylate, watch if on ASA or other anticoags ADE: black stool, tongue darkening, tinnitus
109
Bulk forming laxatives (polycarbophil, methylcellulose)
1-3 days to onset Preferred med since not systemically absorbed. Holds water in stool, swells, increases stool bulk which then stimulates intestinal movement ADE: flatulence
110
Surfactants -docusate sodium (Colace)
1-3 days to work Preventative, esp to prevent straining Facilitates mixture of fats, aqueous materials Do not give w/ mineral oil--toxicity!
111
Saline laxatives (Mag citrate, sodium phosphate, milk of magnesia)
1-6 hr onset Mostly used for evacuation of bowels prior to diagnostic exams Caution in hypertension, sodium restricted diets, renal dysfunction
112
Osmotics (lactulose, sorbitol, glycerin)
Metabolized to solutes in GI tract, moves water osmotically and facilitates propulsion and evacuation
113
Stimulants (Bisacodyl, Senna)
stimulates colonic contractions --> evacuation Bisacodyl (Dulcolax): 6-12 hr onset Do not use every day!! risk paralytic ileus Senna (ExLax): 6-12 hr onset More gentle/preferable over bisacodyl

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