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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
Q

Monobactams (aztreonam)

A

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

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26
Q

Non Beta-Lactam, Cell Wall Active: Glycopeptides (Vancomycin)

A

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

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27
Q

Aminoglycosides

Gentamycin
Tobramycin
Amikacin
Streptomycin

A

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

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28
Q

Tetracyclines

Tetracylcine
Doxycycline
Minocycline

A

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

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29
Q

Macrolides

Erythromycin
Clarithromycin
Azithromycin

A

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

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30
Q

Erthromycin

A

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

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31
Q

Azithromycin/Clarithromycin

A

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

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32
Q

Lincosamides (Clindamycin)

A

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)

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33
Q

Fluoroquinolones

Ciprofloxacin (bone/UTI)
Levofloxacin (both)
Moxifloxacin (atypical resp)

A

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

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34
Q

Sulfas

Trimethoprim/sulfamethoxazole (Bactrim)

A

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

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35
Q

Nitroimidazoles (Metronidazole)

A

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

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36
Q

Oxalinediones (Linezolid)

A

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

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37
Q

Lipopeptides (Daptomycin)

A

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

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38
Q

CURB-65

A

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

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39
Q

Typical CAP pathogens

A

H flu
Chlamydia
Strep pneumo

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40
Q

Atypical PNA pathogens

A

CML:
Chlamydia
Mycoplasma
Legionella

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41
Q

Empiric CAP therapy: non-ICU

A

Macrolide (ex: azithromycin) + beta-lactam (cephalosporin, PCN, penem, etc)

Ex: Azithro + cephtriaxone
Azithro + ertapenem

OR

Fluoroquinolone alone (levo or moxifloxacin)

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42
Q

Empiric CAP therapy: ICU

A

Cephalosporin (Ceftriaxone) OR Ampicillin-Sulbactam + Fluoroquinolone

if PCN allergy: moxi or levo + aztreonam

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43
Q

CAP treatment modifying factors

A

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

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44
Q

HAP common pathogens

A

E coli, Klebsiella pneumo, Staph, Psueodomonas
Anaerobes (d/t aspiration)

Watch for multi drug resistant organisms

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45
Q

HAP tx (low risk mortality)

A

No MRSA risk factors
Pip/Tazo (Zosyn) OR
Cefipime OR
FQ (Levofloxacin) OR
Penem (Meropenem/imipenem)

MRSA risk factors
Add vanco or linezolid

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46
Q

VAP empiric tx

A

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
Q

Aspiration pneumonia

A

Primarily anaerobic in nature. Direct therapy towards mouth flora

Lincosamide (Clinadamycin) + FQ

48
Q

Primary, Type I Osteoporosis

A

loss of trabecular bone with estrogen loss

49
Q

Primary, Type II Osteoporosis

A

loss of trabecular and cortical bone w/ inefficient remodeling (d/t diet, age, physical activity)

50
Q

Secondary osteoporosis

A

D/t systemic illness or meds

51
Q

Calcium products

A

Dietary preferred
Take supplements <500 mg w/ meals
Eliminated unabsorbed via GI tract

ADE: N/C
Interactions: Binding w/ FQs/Tetracycline Abx

52
Q

Vitamin D

A

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
Q

Bisphosphonates

A

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
Q

PTH analog (Teriparatide)

A

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
Q

SERMS (Raloxifene)

A

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
Q

Calcitonin

A

3rd line tx for osteoporosis
inhibits osteoclast
Nasal or SQ
ADE: N/V, flushing, injection site rxns
Avoid in hypocalcemia

57
Q

Estrogen products

A

Short term symptom mgmnt of osteoporosis Inhibit osteoclast activity via estrogen receptor
ADE: HA, depression, N/V, cramps, hypertension, VTE, bleeding, breast CA

58
Q

CKD

A

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
Q

Anemia of CKD

A

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
Q

Secondary hyperparathyroidism of CKD

A

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
Q

Phosphate binders

A

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
Q

Vitamin D products

A

Inhibits PTH secretion & promotes GI Ca absorption
Calcitriol, Paricalcitol, Doxercalciferol
ADE: Hypercalcemia

63
Q

Calcimimetic agent

A

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
Q

Hyperkalemia in CKD

A

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
Q

Metabolic acidosis in CKD

A

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
Q

Bicarb replacement

A

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
Q

Hyperthyroid

A

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
Q

Thioureas (MMI, PTU)

A

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
Q

Nonselective beta blockers (propranolol)

A

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
Q

Iodines/iodides

A

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
Q

Thyroid storm

A

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
Q

Hypothyroid

A

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
Q

Levothyroxine

A

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
Q

Myxedema coma

A

Life threatening decompensated hypothyroidism
Causes: trauma, infection, HF, drug induced
Presentation: AMS, hypoventilation, hypothermia
Tx: IV thyroid hormone replacement, empiric Abx, corticosteroids

75
Q

Metformin

A

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
Q

Sulfonylureas (Gliperizide, glimepiride, glyburide)

A

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
Q

Meglitinide (Repaglinide)

A

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
Q

TZDs (pioglitazone, rosiglitazone)

A

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
Q

DPP4 inhibitors (Sitagliptin, Saxafliptin)

A

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
Q

SGLT2 inhibitors (Canagliflozin, empagliflozin)

A

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
Q

Acarbose

A

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
Q

Basal insulin dosing

A

10 units daily or 0.1-0.2 units/kg daily

Titrate by 2 units every day 3 days to target A1C

83
Q

Prandial insulin dosing

A

Start w/ 1 dose @ largest meal (if A1C above goal w/ appropriately titrate basal dosse)
increase by 1-2 units twice weekly

84
Q

Insulin dosing options

A

2/3 NPH + 1/3 regular
OR
50% basal, 50% prandial divided into 3 meals daily

85
Q

GLP 1 analogs (injectable) ( Liraglutide, Exanatide)

A

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
Q

Rapid acting insulin

A

Lispro
Aspart
Glulisine

15 min onset

87
Q

Short acting insulin

A

Regular (Humulin)

60 min onset

88
Q

Intermediate acting insulin

A

2-4 hr

89
Q

Long acting insulin

A

Glargine (Lantus)

4-5 hr onset, 24 hr duration
No pea

90
Q

GERD:

A

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
Q

PUD

A

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
Q

Antacids

A

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
Q

H2 antagonists

A

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
Q

PPI

A

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
Q

Reglan (Metoclopramide)

A

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
Q

Sucralfate

A

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
Q

Misoprostol

A

PGE1 analog, stimulates production of mucus and bicarb, Cryoprotection.
ADE: abd pain, diarrhea, spontaneous abortions, bleeding in postmenopause
Contraindications: women of childbearing age

98
Q

H. pylori therapy

A

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
Q

Phenothiazines (Prochlorperaine, promethazine)

A

MOA: DA antag @ CT
ADE: sedation, dry mouth, urinary retention, blurred vision, EPS

100
Q

Benzamides (Metoclopramide, trimethobenzamide)

A

MOA: inhibits DA in GI/CTZ, +reglan aids motility in gastric paresis
ADE: sedation/ EPS

101
Q

5HT3 antagonist (Ondansetron, granisetron)

A

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
Q

Benzos (Ativan)

A

prevent limbic input from reaching vomiting center
Anticipatory nausea, anxiety

ADE: sedation, amnesia, akithesia

103
Q

Corticosteroids (Dexamethasone)

A

MOA unknown, for chemo-induced vomiting
ADE: mood changes, increased appetite, weight gait

104
Q

Antihistamines, anticholinergics

A

Inhibit cholinergic receptors which decreases stimulation of vomiting center
ADE: sedation, dry mouth, blurred vision

105
Q

Aprepitant (Emend)

A

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
Q

Antiperistaltic agents (Loperamide, diphenoxylate)

A

Slow GI motility

Caution in infectious diarrhea, avoid in children
ADE: sedation, CNS effects

107
Q

Adsorbants (Polycarbophil, Bismuth)

A

Absorbs water, no systemic absorption
Less effective, but fewer ADEs than anti-motility agents
ADE: fullness, bloating gas

108
Q

Anti-secretory (Bismuth subsalicylate)

A

Antisecretory, antimicrbial, and absorbant properties
Toxicity-broken down to salicylate, watch if on ASA or other anticoags
ADE: black stool, tongue darkening, tinnitus

109
Q

Bulk forming laxatives (polycarbophil, methylcellulose)

A

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
Q

Surfactants -docusate sodium (Colace)

A

1-3 days to work

Preventative, esp to prevent straining
Facilitates mixture of fats, aqueous materials

Do not give w/ mineral oil–toxicity!

111
Q

Saline laxatives (Mag citrate, sodium phosphate, milk of magnesia)

A

1-6 hr onset

Mostly used for evacuation of bowels prior to diagnostic exams

Caution in hypertension, sodium restricted diets, renal dysfunction

112
Q

Osmotics (lactulose, sorbitol, glycerin)

A

Metabolized to solutes in GI tract, moves water osmotically and facilitates propulsion and evacuation

113
Q

Stimulants (Bisacodyl, Senna)

A

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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