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Pharmacology > Summer Exam 2 > Flashcards

Summer Exam 2 Flashcards

1
Q

What is the only depolarizing neuromuscular blocking drug?

A

Succinylcholine

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2
Q

What are the 2 major families of non-depolarizing neuromuscular blocking drugs?

A

Isoquinoline (tubocurarine) and steroid derivatives (pancuronium)

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3
Q

Half life and duration of action with drugs excreted by liver vs kidney (neuromuscular blockers)

A

Liver have shorter half lives and duration

Kidney have longer half-lives and durations (>35 minutes)

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4
Q

Succinylcholine MOA

A

2 molecules bind at nAChR opening ion channels causing depolarization, generating action potential in muscle resulting in brief contractions (agonist)
Keeps Na channel inactive for prolonged period resulting in flaccid paralysis

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5
Q

Uses of Succinylcholine

A

Placement of endotracheal tube at start of anesthetic procedure
Can control muscle contractions in status epileptics

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6
Q

Pharmacokinetics and AEs of Succinylcholine

A

Rapid metabolism by plasma cholinesterase, lasts ~5 minutes

AEs: hyperkalemia, arrhythmias, increased IOP and abdominal pressure

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7
Q

Uses of non depolarizing neuromuscular blockers (tubocurarine and pancuronium)

A

facilitate intubation and maintain skeletal muscle relaxation during surgery

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8
Q

MOA of non depolarizing neuromuscular blockers

A

One molecule binds to nAChR, inhibits channel activation preventing muscle cell depolarization causing flaccid paralysis (antagonist)

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9
Q

Order of paralysis

A

Small rapid muscles of face and eyes> fingers> toes>extremities> trunk> intercostals> diaphragm
Reversed as paralysis resolves

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10
Q

How do we reverse effect of Tubocurarine/pancuronuium

A

Administer cholinesterase inhibitors neostigmine or pyridostigmine; these are usually given with atropine or glycopyrrolate to void bradydysrhythmias
This increases amount of Each in synaptic cleft

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11
Q

What classes of drugs enhance effect of non depolarizing neuromuscular blocking drugs?

A

Aminoglycosides (gentamycin/tobramycin) and CCB (verapamil/ dihydropyrodinesal)

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12
Q

Which Non depolarizing neuromuscular blocker is the best?

A

Cisatracurium, does same thing as tubocurarine without histamine release or antimuscarinic effects, or hypotension

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13
Q

Pharmacokinetics of non depolarizing neuromuscular blockers

A

tubocurarine excreted by kidneys, rocuronium metabolized by liver, cisatracurium isn’t dependent on either

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14
Q

AEs of Tubocurarine

A

Histamine release, hypotension, prolonged apnea

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15
Q

General Anesthesia administration

A

given by inhalation or intravenously

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16
Q

What are the four stages of anesthesia and which do we want to avoid?

A

1-analgesia (decreased awareness of pain, consciousness impaired)
2- disinhibition (delirious, excited, amnesia, enhanced reflexes, may have retching and incontinence)
3- surgical anesthesia (unconscious with no pain reflexes, regular respiration and BP)
4- medullary depression (severe respiratory and cardiovascular depression requiring mechanical support-WANT TO AVOID!)

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17
Q

5 primary effects of general anesthetics

A

unconsciousness, amnesia, analgesia, inhibition of autonomic reflexes, skeletal muscle relaxation

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18
Q

Inhaled Anesthetics Names/MOA

A

*Fluranes!
Facilitate GABA mediated inhibition-blocks brain NMDA and ACh-N receptors
All decrease respiratory function, some vasodilate, some decrease cardiac output, some increase cerebral blood flow

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19
Q

Interactions and toxicities of inhaled anesthetics

A

Additive CNS depression with opioids and sedative hypnotics

Toxicity: extended effect on brain, heart/vasculature and lungs

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20
Q

Rapid acting Intravenous anesthetics

A

Amobarbital, thiamylal, etomidate, propfol, methohexital, thiopental (no longer available, execution drug)

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21
Q

Slow acting IV anesthetics

A

diazepam, ketamine, lorazepam, midazolam

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22
Q

Use of IV anesthetics

A

Facilitate rapid induction of anesthesia (helps avoid stage 2), preferred method of anesthesia induction in adults
BUT not ideal drugs o produce all and only the 5 anesthesia effects

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23
Q

MOA of IV anesthetics

A

GABA mediated inhibition at GABA receptors (enhances GABA activity) causing circulatory and respiratory depression and decreased ICP

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24
Q

Which IV anesthetic has less depressant action?

A

Medazolam

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25
Q

Pharmacokinetics of Barbiturates and Benzos as anesthetics

A

Benzos have slow onset but longer duration

Barbiturates have high lipid solubility so rapid onset and short duration

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26
Q

Toxicities of Medazolam

A

Post respiratory depression (reversed by flumazenil)

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27
Q

Which anesthetics have no analgesia and how do we make them work for general anesthesia?

A

Imidazoles (etomidate) and phenols (propofol)

Combine with opioids like fentanyl

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28
Q

Ketamine MOA

A

Blocks excitation by glutamate at NMDA receptors

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29
Q

Goals of OA Treatment

A

Pain relief, can’t reverse damage

improve joint mobility, limit impairment, improve quality of life

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30
Q

First line in OA

A

Acetaminophen, exercise, weight loss, can do nonselective NSAIDs if low GI bleed risk

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31
Q

What is the max dose/monitoring for acetaminophen?

A

4g/day

monitor liver function

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32
Q

What to do in OA if acetaminophen fails?

A

topical (capsaicin) or oral NSAIDs, topical have less GI effects
Ketoprofen if over 75

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33
Q

Third line agents in OA

A 
Tramadol
Injected steroids (alternate first line in knee and hip)
Duloxetine
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34
Q

NSAIDs compared to acetaminophen in OA

A

Better pain relief but higher risk of GI, renal and cardiovascular issues

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35
Q

What drug classes reduce the risk of GI events compared to acetaminophen?

A 
Cox2 inhibitors (except diclofenac)-celecoxib
PPIs and misoprostol (causes miscarriages) significantly reduce risk in those taking NSAIDs
Nonacetylated salicylates (choline salicylate and trisalicylate)
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36
Q

Which drug is NSAID of choice in high CV risk?

A

Naproxen>ibuprofen, but these have high GI risks

Cox 2 inhibitors have the most risk

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37
Q

MOA of Prostacyclin

A

inhibits platelet aggregation and causes vasodilation

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38
Q

AEs of NSAIDs

A

GI Bleed, abnormal liver function, renal insufficiency/failure, asthma
Monitor CBC, serum creatinine and LFTs

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39
Q

In knee OA what do we give if acetaminophen is contraindicated?

A 
Topical NSAIDs (voltaren or diclofenac), steroid injection or tramadol
Can give duloxetine if those don't work
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40
Q

Hand OA treatment guidelines

A

If over 75, topical NSAIDs/capsaicin are first line, second line you combine with tramadol
If under 75, ORAL NSAIDs are first line but can do topical also, combine with tramadol for second line

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41
Q

Common joints in OA

A

Neck, back, hips and knees

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42
Q

Common joints in RA

A

Feet and hands, symmetrical and bilateral, can be anything in extremities

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43
Q

Physical exam signs of RA

A

ulnar deviation of fingers, swan neck deformity, synovitis, nodules

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44
Q

Goal of RA treatment

A

Early treatment to avoid irreversible damage (DMARDS for disease modification)

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45
Q

First line RA treatment

A

Methotrexate (DMARD) within 3 months

Can give NSAIDs/steroids as adjunctive therapy, esp in established disease

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46
Q

What to monitor with methotrexate?

A

Folic acid levels (prescribe together), mouth sores/stomatitis

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47
Q

When do we use anti-TNF biologics?

A

Early disease with high activity and poor prognosis factors

Usually combine with methotrexate

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48
Q

Common INITIAL combo treatments for RA

A

MTX with etanercept or infliximab (#1) or sulfasalazine with pred

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49
Q

Combo treatments for mod-high RA disease activity

A

MTX plus hydroxychloroquine
MTX plus leflunomide
MTX plus sulfasalazine

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50
Q

Triple combination RA therapy meds

A

MTX + sulfasalazine + hydroxychloroquine (all nonbiologics)

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51
Q

Methotrexate MOA

A

Inhibits cytokine production and purine biosynthesis, stimulates release of adenosine (anti-inflammatory) Also a folic acid antagonist
Dosed once weekly

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52
Q

Contraindications of Methotrexate

A

PREGNANCY/NURSING

Liver disease, immunodeficient, leukopenia, thrombocytopenia, CrCl <40, effusions

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53
Q

Toxicities of Methotrexate

A

Stomatitis (mouth/gum sores) first, high LFTs, thrombocytopenia, pulm fibrosis and pneumonitis

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54
Q

Leflunomide MOA

A

Inhibits pyramiding synthesis leading to decreased lymphocyte proliferation inflammation
Comparable to MTX but worse side effects

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55
Q

Contraindications of Leflunomide

A

Liver disease, pregnancy

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56
Q

Toxicities of Leflunomide

A

Hair loss, bone marrow toxicity, hepatotoxicity, GI

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57
Q

Hydroxychloroquine MOA/Use

A

Dampens antigen-antibody relational inflammation sites

Used in MILD RA r in combo treatment for more severe

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58
Q

Toxicities of Hydroxychloroquine

A

Ocular (decreased night/peripheral vision), N/V/D (take with food), rash, HA, vertigo, insomnia
NOT myelosuppresive or toxic to liver/kidneys

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59
Q

Sulfasalazine MOA

A

Cleaved into sulfapyridine and 5-aminosalicylic acid in the colon, absorbed rapidly in GI tract but 2 month onset

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60
Q

Sulfasalazine AEs

A

NVD, anorexia, rash, serum-sickness, leukopenia, hair loss, stomatitis, high LFTs, SKIN yellow-orange color

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61
Q

Sulfasalazine Interactions

A

Binds iron decreasing its absorption, stops warfarin effects (contraindicated w/ warfarin)

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62
Q

Tofacitinib/Baricitinib Uses/MOA

A

Mod-severe RA that are intolerant to MTX

JAK (tyrosine kinase) inhibition reducing cytokine signals suppressing immune system

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63
Q

JAK inhibitors AEs

A

serious infections, malignancies, elevated LFTs and lipids

Check for latent TB, no live vaccines with treatment

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64
Q

Which RA drugs are not commonly used anymore due to AEs and lack of benefit?

A

Azathioprine, cyclosporine, cyclophosphamide

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65
Q

What are biologic DMARD drug names?

A

TNFs: Adalimumabm certolizumab, golimumab, infliximab, etanercept
IL6: tocilizumab, sarilumab
B cells: Ritixumab
T cells: Abatacept

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66
Q

TNF-a MOA

A

Block pro inflammatory cytokines TNF-a

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67
Q

TNF-a AEs and Contraindications

A

MS like illness/exacerbation of MS, increased risk of lymphoproliferative cancer (high lymphocytes)
Contraindicated in CHF

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68
Q

Why do we give methotrexate with inflixumab?

A

To prevent formation of antibody response to the drug

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69
Q

IL-6 DMARD MOA

A

Attaches to IL-6 receptors preventing cytokine from interacting with them
Always used in combo treatments

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70
Q

IL-6 DMARD AEs

A

Increased risk of infection, ^ plasma lipids, ^LFTs, risk of perforation
Check for TB and no live vaccines

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71
Q

Ritixumab MOA and Use

A

Binds to and depletes peripheral B cells

Added to MTX when patient fails MTX or TNF treatment

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72
Q

Ritixumab AEs

A

Histamine reaction- give methylprednisolone, acetaminophen or antihistamines prior to avoid
No live vaccines

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73
Q

Abatacept MOA

A

Binds to CD80/86 on T cells to prevent costimulation needed for them to work

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74
Q

Abatacept AEs

A

Nasopharyngitis, cough, back pain, HTN, dyspepsia, UTI, extremity pain
No live vaccines

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75
Q

What vaccine do patients starting biologic DMARDS get early?

A

Herpes zoster-given at age 50 instead of 60

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76
Q

What drugs can cause hyperuricemia?

A

Diuretics, nicotinic acid, salicylates, alcohol, ethambutol, cyclosporine, levodopa, pyrazinamide

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77
Q

What are first line treatments for gout?

A

NSAIDs (indomethacin, naproxen or sulindac), steroids, colchicine (within 24-36 hours of onset)

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78
Q

Colchicine MOA

A

Inhibits microtubule assembly decreasing macrophage migration and phagocytosis
Inhibits leukotriene B4 decreasing inflammation

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79
Q

Colchicine AEs

A

Dose dependent diarrhea, N/V, myelosuppression, reversible neuromyopathy
Can cause hypersensitivity reactions and gout exacerbation

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80
Q

Colchicine Interactions

A

Adjust dose when used with CYP3A4 and P-glycoprotein inhibitors
Inhibits secretion of methotrexate

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81
Q

Steroid Use in Gout

A

Can do medal dose pack, IM triamcinolone with oral pred, intraarticular kenalog if 1-2 joints involved and combined with NSAID/colchicine/pred

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82
Q

Steroid AEs in Gout

A

Adrenal suppression, growth inhibition, muscle wasting, osteoporosis, salt retention, glucose intolerance, behavioral changes

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83
Q

Chronic Gout Treatment

A

Colchicine, Probenicid (uricosuric) or allopurinol/feboxustat
Last resort: pegloticase or rasburicase

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84
Q

Medication used for gout associated with malignancy?

A

Rasburicase

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85
Q

What meds do we use while starting gout prophylaxis?

A

Colchicine 1-2x/day
Low dose NSAIDs + PPI
<10mg pred/day
One of these for 3-6 months after target uric acid levels reached

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86
Q

Allopurinol MOA

A

Irreversibly inhibits xanthine oxidase and lowers uric acid production
1st line gout prophylaxis, but starts low and increase!

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87
Q

Allopurinol AEs

A

Pruritus, rash, ^LFTs, acute hypersensitivity syndrome in first few months (esp in asians)

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88
Q

Febuxostat MOA/Uses

A

Reversibly inhibits xanthine oxidase

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89
Q

Feboxustat AEs/Contraindications

A

Contraindicated with azathioprine
LFT increase, nausea, arthralgia, rash
Monitor LFTs, renal function and rate levels

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90
Q

Medication used for refractory/tophaceous gout

A

Pegloticase- recombinant porcine (pig) like uricase that metabolizes uric acid to allantoin

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91
Q

First Line drugs for generalized anxiety disorder

A

Duloxetine, escitalopram, paroxetine, sertraline (SSRIs), venlafaxine (SNRI)

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92
Q

First line drugs for panic disorder

A

SSRIs and venlafaxine

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93
Q

First line drugs for social anxiety disorder

A

Escitalopram, fluvoxamine, paroxetine, sertraline, venlafaxine

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94
Q

Buspirone MOA

A

Selective anxiolytic- partial agonist at 5HT receptors, minimal CNS depressant effects

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95
Q

Pharmacokinetics of Buspirone

A

Slow onset (1 week), forms active metabolite, interacts with CYP3A4 inducers and inhibitors

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96
Q

Buspirone Indications

A

Generalized anxiety disorders (2nd line but better than benzos), safe in pregnancy

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97
Q

Buspirone AEs

A

GI distress, tachycardia, paresthesia

minimal tolerance development

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98
Q

Which anxiolytic causes QT prolongation?

A

Citalopram (used in panic disorder and social anxiety disorder)

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99
Q

Which drug is the best for rapid treatment of suicidal ideation?

A

Ketamine (used to be midazolam)

100
Q

What is the best treatment course when a depression med doesn’t work?

A

Add a second drug to augment the original, could be better than changing drugs or increasing doses

101
Q

First line in major depression disorder

A

SSRIs

102
Q

MAOI Mech of Action

A

Inhibit monoamine oxidases that metabolize norepinephrine and serotonin MAO type A and dopamine MAO type B

103
Q

Tricyclic MOA

A

block reuptake transporters of norepinephrine and serotonin

104
Q

SSRI MOA

A

Selectively inhibit serotonin (5HT) transporters with only modest effects on other neurotransmitters

105
Q

SNRI MOA

A

block norepinephrine and 5HT transporters, but lack alpha blocking, anticholinergic and antihistamine actions of tricyclics

106
Q

5HT2 Receptor antagonist MOA

A

Structurally related drugs that block subgroup of serotonin receptors with only minor effects on amine transporters

107
Q

Pharmacokinetics/monitoring of antidepressants

A

Rapid oral absorption, metabolized in liver and cleared in kidney, tightly bound to plasma proteins
Monitor CrCl, GFR, LFTs

108
Q

Tricyclic Indications

A

MDD, chronic pain, insomnia, enuresis, OCD

Triptylines or ipramines

109
Q

Tricyclic AEs

A

alpha block (hypotension, anticholinergic), sedation, weight gain (muscarinic black), seizures and arrhythmias

110
Q

Tricyclic with least AEs

A

Nortiptyline, but LOTS of norepinephrine

111
Q

Monoamine Oxidase Inhibitors Indications

A

unresponsive MDD, anxiety, panic disorder

Segiline used for parkinsons

112
Q

MAOI Interactions/AEs

A

Causes hypertension with tyramine (cheese, soy, beer, dry sausage)-try not to prescribe!
Serotonin syndrome
Can cause hypotension and insomnia

113
Q

SSRI Indications

A

all depression/anxiety type things and bulimia

114
Q

SSRI Interactions

A

Long half life

Lithium, TCAs, warfarin, alprazolam, theophylline have increased blood levels

115
Q

What are the top SSRI picks?

A

Escitalopram- NONE OF THE AES!

Fluoxetine, has norepinephrine but can cause seizures

116
Q

Black box warning of antidepressants

A

Increased suicidality- monitor behavioral changes and mental status

117
Q

AEs of SSRIs

A

Fluoxetine-anorexia and nausea
Fluvoxamine- somnolence/sleepy
Paroxetine- anticholinergic effects
ALL- Insomnia, anxiety, serotonin syndrome, sexual dysfunction

118
Q

SNRI Indications/drug names

A

MDD, GAD, pain disorders (duloxetine), stress incontinence, menopause
Venlafaxine, desvenlafaxine, levomilnacipran, duloxetine

119
Q

AEs of SNRIs

A

Desvenlafaxine- hyperlipidemia
Duloxetine and levomilnacipran- orthostatic hypotension
Venlafaxine- hypertension
all: CV changes (^BP, pulse), insomnia, sexual dysfunction, serotonin syndrome

120
Q

5HT Antagonist Indications

A

MDD and hypnosis (trazodone)

ALL are -azodones

121
Q

5HT Antagonist AEs

A

Nefazodone- clitoral priapism, liver toxicity
Trazodone- bad in depression good for sleep
Vilazodone- decreased libido, serotonin syndrome
Mirtazapine- weight gain
Bupropion- seizure

122
Q

Supplements used in depression

A

Omega 3 fatty acids (EPA>DHA)
St Johns Wort
SAMe
Folate

123
Q

Pharmacokinetics of Antipsychotics

A

Lipid soluble so they can enter CNS
metabolized by liver enzymes to active metabolite, renal eliminated
Long plasma half life

124
Q

AEs for Antipsychotics (first gen vs second)

A

Both have tremors, stiffness, cogwheeling, muscle dystonia, tar dive dyskinesia, but second gen isn’t as bad
first gen ineffective for negative symptoms, but second gen is

125
Q

Which 3 antipsychotics are most chosen/first line in schizo and what are their main AEs?

A

Aripiprazole-no big AEs
Haloperidol- Parkinson like syndrome (extrapyramidal)
Risperidone- hyperprolactinemia
Ziprasidone

126
Q

What AEs do we monitor for in all antipsychotics?

A

Akathisia (anxiety), hyperprolactinemia at every visit
tardive dyskinesia Q3M for 1st gen and 6M for 2nd
Weight gain

127
Q

AEs in Clozapine

A

agranulocytosis- monitor weekly for 6 months

sialorrhea (drooling)

128
Q

AEs in Loxapine

A

bronchospasm, lots of other respiratory issues-its inhales!

129
Q

AEs in Olanzapine Pamoate monohydrate

A

post injection sedation/delirium syndrome

130
Q

Agents used to treat extrapyramidal side effects (Parkinson like syndrome)

A

Antimuscarinics, antihistamines, dopamine agonist, benzos, B blockers

131
Q

When is clozapine recommended in schizos?

A

if patient is suicidal

132
Q

How long do you treat schizo patients?

A

at least 12 months after remission of first episode, many recommend at least 5 years, many require lifetime of small dose

133
Q

How do we switch antipsychotic drugs?

A

Taper one down over 1-2 weeks while we taper the other up

134
Q

Acute Mania Bipolar Treatment

A

Lithium and valproate are first line

carbamazepine, lots of prines and idones

135
Q

Bipolar maintenance treatment

A

Lithium, aripiprazole, olanzepine, lamotrigine

136
Q

Meds for bipolar depression

A

Quetapine, lurasidone

137
Q

Lithium MOA

A

reduces excitatory (dopamine and glutamate) but increases inhibitory (GABA) neurotransmission

138
Q

Pharmacokinetics of Lithium

A

distributed in total body water, excreted in urine

Monitor sodium, it can substitute it!

139
Q

Interactions with Lithium

A

Clearance decreased by thiazides and NSAIDs

140
Q

Lithium AEs

A

Tremor (one of the first signs of toxicity), edema, hypothyroidism, renal dysfunction
Pregnancy cat D

141
Q

What happens if lithium replaces sodium in the body?

A

Increased urination/loss of water
Inhibits GSK3 increasing COX2 expression and PGE synthesis>diminished vasopressin activity and decreased AQP2 levels on apical membrane

142
Q

Treatment of hypomania

A

Lithium, valproate or carbamazepine first, can add bento for short term adjust therapy

143
Q

Mania Treatment

A

2-3 drug combos! lithium, valproate or SGA plus benzo +/- antipsychotic
don’t combine antipsychotics

144
Q

Depressive episode treatment in bipolar

A

lithiumm, quetiapine, lurasidone

in severe can add carbamazepine or antidepressant if needed, then try 3 drug combos

145
Q

What is the main receptor responsible for vomitting?

A

Mu

146
Q

What are the 4 important sources of afferent input to vomiting center and their receptors?

A

1- chemoreceptor trigger zone (Dopamine D2, opioids and serotonin 5HT and NK receptors)
2- vestibular system (muscarinic M1 and histamine H1 receptors)
3- vagal and spinal afferent nerves (5HT receptor, effeced by chemo and radiation)
4- CNS (psychiatric disorders, stress and anticipatory vomitting)

147
Q

Antacid Use and products

A

simple nausea/vomitting

Sodium bicarb, calcium carbonate, magnesium hydroxide, aluminum hydroxide

148
Q

Serotonin Antagonists as antiemetics Drugs and uses

A

Drugs end in -setron

Used for vagal stimulation (post sx), chemo

149
Q

Which serotonin 5 HT drugs have long half life and whats the benefit?

A

Palonosetron, better for chemo and delayed nausea, but only when given ahead of time, better when combined with steroid

150
Q

Pharmacokinetics of 5HTs

A

Extensive hepatic metabolism, eliminated by renal/hepatic, dose reduction NOT required for old/renal insufficient, but in liver insufficient ondansetron needs to be changed

151
Q

What is the most common use of 5HT antiemetics?

A

Post op and post-radiation N/V, good for whole body/abdominal radiation

152
Q

AEs of Serotonin antagonists

A

Headache, constipation, dizziness

Small risk of QT prolongation esp with dolasetron

153
Q

Serotonin Antagonist Antiemetic Interactions

A

Other drugs may reduce hepatic clearance, increasing half life

154
Q

Substance P/Neurokinin 1 Receptor antagonist Uses/ AEs

A

Helps with delayed emesis

Causes diarrhea, hiccups, headache, constipation

155
Q

Which drug is good for motion sickness (vestibular)?

A

Antihistaminic-anticholinergics (dimenhydrinate and diphenhydramine)

156
Q

Dimenhydrinate AEs

A

Drowsiness, confusion, blurred vision, dry mouth, urinary retention
Don’t use in elderly!

157
Q

Prochlorperazine vs promethazine

A

Promethazine is better bc no hard shell, you can adjust size of pill, also no prolonged QT interval/sedation or tar dive dyskinesia, only drowsiness

158
Q

Antiemetic use/AEs of Benzos

A

Mostlyfor anticipatory N/V like anxiety, chemo
Causes dizziness, sedation, appetite change, memory impairment
They are controlled substances! Level 4

159
Q

Antiemetics in Pregnancy

A

1st line: pyridoxine +/- doxylamine

Persistent vomitting should get fluids with B6/thiamine (B6 is good antiemetic also)

160
Q

Drug for refractory N/V or hyperemesis in pregnancy

A

Corticosteroids (methylpred)

161
Q

What do the 2 classes of acid disorder meds do?

A

1-reduce intragastric acidity

2-promote mucosal defense

162
Q

What are antacids/what do they do?

A

Weak bases that react with gastric HCl to form salt and water
Sodium bicarb, calcium carbonate, magnesium or aluminum hydroxide

163
Q

Sodium bicarb MOA and AEs

A

Reacts rapidly with HCl to produce CO2 and NaCl

Causes belching, metabolic alkalosis, fluid retention

164
Q

Calcium Carbonate MOA and AEs

A

Reacts slowly w/ HCl forming CO2 and CaCl2

Causes belching, metabolic alkalosis, hypercalcemia, renal insufficiency

165
Q

Magnesium/Aluminum Hydroxide MOA and AEs

A

Reacts slowly with HCl to form magnesium or aluminum chloride and water
Does not cause gas
Can cause osmotic diarrhea, constipation, renal insufficiency

166
Q

Antacid interactions

A

Reduces absorption of many other drugs

Should not be given within 2 hours of TCAs, fluoroquinolone, Itraconazole, iron

167
Q

H2 Receptor Antagonist/H2 Blockers Names and Pharmacokinetics

A

all end in -tidine
first pass hepatic metabolism (except nizatidine), renal secretion, dose reduction in severe real insufficiency and elderly

168
Q

H2 Blocker MOA

A

Competitive, selective inhibition of H2 receptors in parietal cell to suppress acid secretion stimulated by histamine, gastrin and cholinomimetic agents
Diminished effect of acid secretion by gastrin or acetylcholine in parietal cell

169
Q

What is the most effective H2 blocker?

A

Famotidine (Pepcid)

170
Q

Which H2 blocker works for allergies?

A

Cimetidine

171
Q

H2 Blocker prescription vs OTC doses

A

Prescription doses are higher and given BID, maintain acid inhibition for 10 hours
OTC inhibit acid for less than 6 hours (more is better!)

172
Q

H2 Blocker Uses

A

GERD, PUD, NID, Prevention of stress-related gastritis bleeding

173
Q

H2 Blocker AEs

A

Diarrhea, headache, fatigue, myalgia, constipation (all are rare)-NO GAS!
Mental status changes
Cimetidine causes gynecomastia/galactorrhea
Avoid in pregnancy!

174
Q

H2 Blocker Interactions

A

Cimetidine interacts with a LOT

Nizantidine and Famotidine have almost no interactions-choose these!

175
Q

Which PPI is the best choice?

A

Pantoprazole

176
Q

PPI Administration

A

give 30-60 minutes before a meal, preferably breakfast bc food decreases bioavailability, and they inactivate ACTIVE pumps

177
Q

PPI pharmacokinetics

A

Rapid first pass systemic hepatic

irreversible inactivation causes 18 hours for synthesis of new pumps

178
Q

What is the best drug class for acid suppression?

A

PPIs

179
Q

PPI AEs

A

Diarrhea, headache, abdominal pain
vitamin/mineral deficiencies (B12, iron, calcium, magnesium>osteoporosis)
Resp infections, pneumonia, C dif
Rebound dyspepsia/heartburn

180
Q

PPI Interactions

A

Pantoprazole has no interactions!

Others alter drug absorption, omeprazole inhibit metabolism of warfarin

181
Q

Mucosal Protective Agent Examples

A

Sucralfate, prostaglandin analogs, bismuth

182
Q

Sucralfate

A

Neg charged, binds to pos charged proteins in base of ulcers forming barrier, stimulates mucosal prostaglandin and bicarb secretion
Mixed in water and drank, creates viscous paste

183
Q

Sucralfate Uses and AEs

A

Prevention of stress related bleeding

Causes constipation, some aluminum absorption, impairs other med absorption (take 2-4 hours apart from other meds)

184
Q

Prostaglandin Analog-Misoprostol Pharmacokinetics

A

Rapidly absorbed, metabolized to active free acid, half life <30 mins, excreted in urine
Must dose 3-4 times/day

185
Q

Misoprostol MOA

A

Acid inhibitory and mucosal protective

Stimulates mucus and bicarb secretion, enhances mucosal blood flow, reduces histamine stimulated cAMP production

186
Q

Misoprostol Uses

A

Helps in child birth (causes uterine contractions)

NSAID ulcer reduction

187
Q

Misoprostol AEs

A

Diarrhea and cramping, uterine contractions (don’t use in pregnancy)

188
Q

Bismuth Compounds (2)

A

Bismuth subsalicylate- nonprescription

Bismuth substrate potassium- prescription that has metronidazole and tetracycline to treat H pylori

189
Q

Bismuth Pharmacokinetics

A

Bismuth subsalicylate undergoes rapid dissociation in stomach allowing salicylate absorption, excreted in urine
<1% bismuth absorbed-excreted in stool

190
Q

Bismuth MOA

A

Coats and protects ulcers
Bismuth subsalicylate reduces frequency and liquidity in diarrhea
Direct antimicrobial activity against H pylori

191
Q

Bismuth Uses

A

Dyspepsia, diarrhea, H pylori infection

192
Q

Bismuth AEs

A

Black stool, dark tongue, renal insufficiency, encephalopathy, tinitis

193
Q

H pylori treatment options

A

Bismuth quadruple therapy (PPI +bismuth subsalicylate +metronidazole +tetracycline)- cheapest, but bismuth and tetracycline interact
PPI based triple therapy (PPI +claritho/azithromycin + bismuth)

194
Q

What kind of medications can selectively stimulate gut motor function?

A

Prokinetic agents (erythromycin, metoclopramide/raglan)

195
Q

Gastrointestinal Motility Drug Classes

A

Cholinomimetic Agents, metoclopramide, macrolides

196
Q

Cholinomimetic Agent Examples

A

Bethanecol (Stimulates muscarinic M3 receptors)

Neostigmine (acetylcholnesterase inhibitor)

197
Q

Cholinomimetic AEs

A

Excessive salivation, nausea, vomiting, diarrhea, bradycardia

198
Q

Cholinomimetic Agent Uses

A

Symptomatic GERD, delayed gastric emptying from post-surgery disorders, diabetic gastroparesis, non-ulcer dyspepsia, prevention of vomitting

199
Q

Metoclopramide MOA

A

Dopamine D2 receptor antagonist, inhibits smooth muscle stimulation resulting in anti-nausea and antiemetic action (increases LES pressure, esophageal peristalsis, gastric emptying)

200
Q

Metoclopramide AEs

A

SLUDGE, tardive dyskinesia, extrapyramidal effects, elevated prolactin

201
Q

Macrolide Cholinomimetic MOA

A

Erythromycin: Directly stimulates motion receptors on GI smooth muscle and promotes onset of migrating motor complex
Tolerance builds rapidly

202
Q

Erythromycin Uses (motility)

A

Beneficial in gastroparesis, helps with upper GI hemorrhage to promote gastric emptying of blood before endoscopy

203
Q

What can help prevent constipation?

A

High fiber diet, adequate fluid intake, regular exercise

204
Q

Constipation Treatment

A

Symptomatic-treat underlying cause (osmotic laxative, stimulant laxative, dietary fiber, etc)

205
Q

Bulk forming Laxatives

A

Meta-mucil: Hydrophilic colloids that absorb water forming bulky, emollient gel that promotes peristalsis
Made with psyllium and methylcellulose>lots of gas

206
Q

Stool Surfactant Agents (softeners)

A

Docusate- Mix aqueous and fatty materials in intestines
Mineral Oil-dangerous when taken orally, stops water absorption from stool, can be mixed with juices, aspirin can cause pneumonia

207
Q

Osmotic Laxatives

A 
Soluble but non-absorbable compounds that result in stool liquidity due to increase in fecal fluid
Magnesium hydroxide (milk of magnesia)
208
Q

Sorbitol and Lactulose

A

Non-absorbable sugars used to prevent or treat chronic constipation, good with liver failure
Cause farts and cramps

209
Q

Sodium Phosphate Issues

A

Causes severe electrolyte disorder (hyper phosphatemia/natremia, hypocalcemia/kalemia)>cardiac arrhythmias or renal failure

210
Q

Polyetheylene Glycol

A

Nonabsorbable osmotically active sugar w/ sodium sulfate, sodium chloride, sodium bicarb and potassium chloride-no electrolyte or fluid shifts, no gas or cramps-SAFE! but takes 1-3 days
Chronic constipation

211
Q

Cathartic Laxatives

A

Direct stimulation of enteric nervous system and colonic electrolyte and fluid secretion
Usually used long term for bed-bound long term care facilities

212
Q

Anthraquinone Derivatives

A

Aloe, Senna, cascara- occur naturally in plants, given orally or rectally
Causes brown pigmentation of colon (melanosis coli) and may be carcinogenic

213
Q

Diphenylmethane Derivative

A

Bisacodyl/ducolax
Minimal systemic absorption so safe for short or long term use
Given orally or rectally

214
Q

Opioid Induced Constipation Treatment

A

Methylnaltraxone (palliative care), alvimopan (in hospital), naloxegol

215
Q

Food with acute diarrhea

A

If no signs of severe dehydration don’t withhold food, it may control problem in osmotic diarrhea but not secretory
If uncontrollable vomiting is present then withhold food

216
Q

Oral rehydration solutions

A

DONT USE GATORADE! unless mix with water to lower osmolality

lower osmolality improves dehydration faster

217
Q

When should we not use antidiarrheals?

A

Bloody diarrhea, high fever or systemic toxicity

218
Q

Types of opioid antidiarrheals

A 
Opioid agonists (constipating effects)
Loperamide (no addiction potential, doesn't cross BBB)
Diphenoxylate (CNS effects, dependence potential)
219
Q

Adsorbent antidiarrheals

A

Kaolin-pectin, polycarbophil, attapulgite

Remove toxins, nutrients, drugs and digestive juices from bowel

220
Q

Bile salt binding resins

A

Cholestyramine ,colestipol, colesevelam (doesnt effect absorption of other drugs)

221
Q

Antisecretory antidiarrheals

A

Somatostatin, octreotide

222
Q

Somatostatin MOA

A

14amino acids released in GI tract from paracrine and D cells, enteric nerves and hypothalamus
Inhibits secretion of hormones, reduces fluid secretion, slows GI motility and inhibits gallbladder contraction

223
Q

Octreotide- AEs and what it does

A

Effects motility

AEs: steatorrhea, nausea, abdominal pain, flatulence, diarrhea, bradycardia

224
Q

Treatment of IBS-C

A

soluble fiber (psyllium/ispaghula) or polyethylene glycol (PEG) are first line
2nd: lubiprostone, guanylate cyclase-C agonist (linaclotide, plecanatide)
last resort: tegaserod

225
Q

PEG Benefits and AEs

A

Improves constipation but not abdominal pain

Causes bloating and abdominal discomfort

226
Q

Lubiprostone MOA/Uses

A

Stimulates chloride channel increasing chloride-rise fluid secretion and stimulating intestinal motility
Used in women >18 with contraception (not okay in pregnancy)

227
Q

Linaclotide MOA/Uses

A

Stimulates intestinal fluid secretion and transit time

Used for persistent constipation, relives abdominal pain

228
Q

Plecanatide MOA

A

Increase cGMP resulting in chloride and bicarb secretions into intestine increasing fluid and GI transit time

229
Q

Plecanatide Box warning

A

Risk of serious dehydration in peds patients

230
Q

Plecanatide AEs

A

Diarrhea, dizziness, UTI, increased AST/ALT, sinusitis

Not recommended in pregnancy

231
Q

Tegaserod

A

Increased number of CV deaths, only used emergency IBS-C treatment in women <55

232
Q

IBS-D Treatment

A

Loperamide first line
Bile acid sequestrants 2nd line
5HT receptor antagonists (ondansetron/alosetron), Eluxadoline

233
Q

Loperamide MOA

A

Inhibits peristalsis, decreasing still frequency and consistency
Doesn’t help bloating or abdominal discomfort

234
Q

Eluxadoline MOA

A

Mixed mu and kappa opioids receptor agonist and delta-opioids receptor antagonist, acts locally to reduce abdominal pain and diarrhea

235
Q

Eluxadine AEs

A

Constipation, nausea, abdominal pain, CNS depression

lots of risk, try to avoid!

236
Q

Bile acid sequestrants

A

Cholestyrmine, colestipol, colesevelam

Causes bloating, flatulence, abdominal discomfort and constipation

237
Q

Alosetron Uses

A

Last resort in women with severe IBS-D

Reduces abdominal pain, cramps, urgency and diarrhea, reduces number of bowel movements/day

238
Q

Alosetron AEs

A

Constipation, ischemic colitis,

239
Q

Chronic abdominal pain in IBS

A

tricyclics

240
Q

Antispasmodics in IBS

A

Diclomine and hyoscyamine-anticholinergic effects

241
Q

Key to Acute Pancreatitis Treatment

A

Early and aggressive fluid resuscitation, symptomatic treatment

242
Q

Medications that cause pancreatitis

A 
Aces, arbs, thiazides, furosemide
steroids
bactrim
valproic acid
statins
243
Q

Medication to avoid in pancreatitis treatment

A

Demerol

244
Q

Malabsorption treatment in Chronic pancreatitis

A

Pancreatic enzyme supplementation

Reduce intake of fates

245
Q

Chronic Pancreatitis Treatment

A

Enzymes (lipase!) for malabsorption and pain; plus either H2 blocker or PPI

246
Q

Celiac Disease Treatments

A 
Avoid gluten (wheat, barley, rye), can eat rice, corn, soy, amaranth, potato, oats
Supplement deficiencies

Pharmacology (7 decks)

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