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Pharm II: Block 1 Flashcards

1
Q

Which neuromuscular blocking agent is the DOC in renal/hepatic Dz?

What neuromuscular blocking agent is metabolized into Laudanosine?

A

Cisatracurium

Atracurium

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2
Q

Define Acute Pain

A

Self limiting/nociceptive result from injury

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3
Q

Define Non-Cancer Chronic Pain

A

Nociceptive, neuropathic or both that impacts daily living and persists greater than 3mon

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4
Q

Define Chronic/Malignant Cancer Pain

A

Life threatening condition pain w/ multi-modal cause

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5
Q

What are the 5 steps of the pain process?

A

Transduction- damage creates AP in peripheral nerve
Conduction- AP activates Na channels
Transmission- peripheral to CNS by primary afferent nociceptor
Modulation- reduces transmission via downward projection
Perception- awareness produced by sensory signals

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6
Q

What types of medications stop ascending pain pathways?

What types of medications stop descending inhibitory pathways?

A

Aspirin, Non-opioid analgesics

Opioid analgesics

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7
Q

Describe the Inflammatory pain process?

A

Protective and assists w/ healing by discouraging use
Activates immune system
Tenderness promotes repair
Stimulated by Macrophage, Mast, Neutrophil, Granulocytes

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8
Q

What classes of drugs are used to alter the perception of pain in the brain?

A

Opioids
A2 agonists
TCAs
SSRI/SNRI

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9
Q

What classes of drugs are used to alter the modulation of pain in the descending modulation?

A

TCAs

SSRI/SNRI

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10
Q

What classes of drugs are used to alter the transmission of pain in the dorsal root ganglion?

What classes of drugs are used to alter the transmission of pain in the peripheral nerve?

A

LAs, A2 agonists

LAs, Opioids

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11
Q

What classes of drugs are used to alter the transduction of pain in the peripheral nerve?

A 
LAs
Capsaicin
Anticonvulsant
NSAIDs
ASA
Acetaminophen
Nitrate
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12
Q

What 5 classes of drugs can be used as adjuvant agents to reduce opioid burden?

A 
TCAs- Amit, Nortri, Desipramine
SSRI/SNRI- Dulox, Venlafax, Milnaciparn
Anticonvulsant- Gaba, Pregaba
Local anesthetic- Lidocaine
Counter irritant- Capsaicin
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13
Q

Where are COX 1, 2 and 3 most commonly found?

A 
COX-1= platelets, stomach and endothelium
COX-2= inflammatory cells and kidneys
COX-3= CNS (thermoregulatory control)
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14
Q

What are the undesireable and desired effects of COX-1 and COX-2 inhibition?

A

COX 1= Undesired= gastrotoxicity, Desired= antithrombic

COX-2= Undesired= HTN, Na retention, prothrombotic, Desired= anti-inflammatory, analgesic

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15
Q

What is the primary route of Acetaminophen metabolism?

What is the secondary route and what is adversely formed?

A

Glucuronidation and Sulfation to renal

3A4, 2E1, N-hydroxylation
Produces NAPQI- normally combined w/ glutathione and excreted renally

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16
Q

What three types of PTs/scenarios are at an increased risk of forming NAPQI?

A

Supratherapeutic doses (+4gm/24hrs)
Heavy alcohol/liver Dz (>3 drinks/day)
Malnutrition/Fasting

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17
Q

What are the three phases of an acetaminophen OD?

A

First 24hrs- GI Sxs, N/V
24-72- abd pain, liver tenderness, inc transaminase, decreased urine, jaundice
4 - 14 days- resolution or liver failure to death

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18
Q

What is the antidote to an Acetaminophen OD?

A

Charcoal regardless of lab wait times
N-acetylcysteine- metabolizes acetaminophen to cysteine which is glutathione precursor
Acetadote- injectable
Mucomyst- inhalation

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19
Q

N-Acetylecysteine is used in PTs w/ probable hepatotoxicity in what scenarios?

A

Single ingestion 150mg/kg or 7.5g total regardless of weight

Unknown ingestion time and >10mcg/mL

Hx of APAP ingestion and any evidence of liver injury

PTs w/ delayed +24hrs presentation w/ lab evidence of liver injury

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20
Q

What’s the max dose of acetaminophen per day?

A 
Adults- max 3gm/day
Elderly- <2gm/day
Acetaminophen/opioid combo- 325mg/pill
Infants/Children- 160mg/5ml
Children Melt Away- 80mg
Children- 10-15mg/kg/dose Q4-6
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21
Q

What is Aspirin’s effect on platelets?

What are the external uses of aspirin?

A

Anti-platelet due to irreversible COX inhibition

Salicyclic acid- acne, corns, callus, warts
Methyl salicylate- arthritis, sports rubs

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22
Q

As selectivity for COX 1 increases ? changes?

As selectivity for COX 2 increases ? changes?

A

Platelet aggregation is more prominent

Beneficial effects of platelet aggregation decrease, more CV risk

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23
Q

What is the list/precedence of treatment for PTs w/ CV Dz needing pain control?

A 
Acetaminophen
Aspirin
Tramadol
Opioids- short term
Non-acetylated salicylates
NSAIDS w/ low COX 2 selectivity
NSAIDS w/ some COX 2 selectivity
COX 2 selective agents
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24
Q

What type of PTs are at high risk of developing ulcers from NSAIDS?

Which ones are at moderate risk?

A

High- Hx of complicated ulcer

Mod- +65y/o, high dose NSAID, uncomplicated ulcer Hx, concurrent use of aspirin, corticosteroids, or anticoagulatns

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25
Q

PTs w/ low, moderate or high CV and/or GI ulcer risks receive what treatment regiments?

A

High CV, High ulcer= only alternative therapy
High CV, mod/low ulcer= Naproxen and PPI/Misoprostol

Low CV, High ulcer= alternative therapy or COX-2 inhibitor and PPI/Misoprostol
Low CV, Moderate ulcer= NSAID and PPI/Misoprostol
Low CV risk, Low ulcer= NSAID only at lowest effective dose

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26
Q

What are the 3 phases of Salicylate Toxicity?

A

1- N/V, tachypnea, HA, tinnitus; <150mg/kg
2- metabolic acidosis, respiratory compensation; 150-300mg/kg
3- sever K and BiCarb depletion, dehydrated, metabolic acidosis/respiratory compensation; >300mg/kg

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27
Q

How is Salicylate Toxicity treated?

A 
No antidote
Primary treatment= replenish BiCarb
Activated charcoal and lavage
O2 and E+
Glucose if AMS despite glucose levels
Start dialysis
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28
Q

What are the pros and cons of using non-acetylated salicylates?

A 
Effective anti-inflammatory
Effective analgesics
Less effect on platelets
Lower GI bleeds
Less renal toxicity

Con- less analgesic effect than aspirin

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29
Q

When is the use of non-acetylated salicylates preferred?

A

COX-1 inhibition needs to be avoided
PTs w/ asthma
Thrombocytopenia
Renal dysfunction

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30
Q

What are the uses and contraindications of using Ketorolac?

A

Decreases opioid requirement by 25-50% when treating mild-mod pain for less than 5 days
Cataract extraction, refractive surgery, ocular itching from allergic conjunctivitis

Don’t use in peds PTs, bleeding risk, w/ NSAIDS, renal impairment, Delivery
PBNDR

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31
Q

What is the max amount of Ibuprofen for adults and kids per day?

A

3200mg

2400mg

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32
Q

What effects do prostaglandins have in the eyes?

A

Meiosis
Increased vascular permeability in blood-ocular barrier
Pressure changes

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33
Q

What are the three ocular NSAIDS and their uses?

A

Flurbiprofen- inhibits operative meiosis
Diclofenac- post-op inflammation and photophobia
Keterolac- ocular itching and post-op inflammation

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34
Q

What type of NSAID is best for PTs w/ renal insufficiency?
Which one has the least CV events?
Which one has the lowest GI bleeds?

A

Non-Acetylated salicylates
Naproxen
Celecoxib

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35
Q

What effect do endogenous opioid peptides have on opioid receptors?

A

Opioid receptors= GPCRs

Peptides bind and inhibit adenylyl cyclase by controlling ion gating

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36
Q

What does a decreased amount of Ca2 influx in the presynaptic cleft do to pain?

A

Inhibits nociceptive input from periphery to spine
Activates descending inhibitory paths
Alters limbic activation

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37
Q

What medications inhibit the ascending pain pathway from nociceptors?

What medications inhibits the descending pain pathway?

A

Aspirin and non-opioids

Opioid analgesics

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38
Q

What are Mu, K, D and K receptors and their location?

A

Mu- most analgesic properties; U1- analgesia, U2- respiratory depression, sedation, euphoria
K- contribute to analgesic properties
D- located peripherally and selective for enkephalins

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39
Q

Opioid receptors are located in what three areas of the body?

A

CNS
Peripheral nerves
GI tract

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40
Q

Functions of Mu receptors

A

Supra/spinal analgesia, sedation, inhibits respiration, slowed GI motility, modulates hormone/neurotransmitter release

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41
Q

Functions of D receptors

A

Supra/spinal analgesia

Modulates hormone/neurotransmitter release

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42
Q

Function of K receptors

A

Supra/spinal analgesia
Psychotomimetic effects
Slows GI transit

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43
Q

Define Physical Dependence

Define Addiction

A

PTs use of drug is required for well being

Loss of control over drug use

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44
Q

Define Pseudo-Addiction

A

Under treatment of chronic pain leading to addiction-like behavior

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45
Q

What are the S/Sxs of opioid withdrawal?

A 
CACAIN
Anxiety
Irritability
N/V/D
Chills, aches, cramps
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46
Q

CNS excitation from opioids is from the stimulation of ? receptor?

The use of ? drug can cause myoclonus/seizure like activity in renal failure PTs

A

Kappa- causes dysphoria

Meperidine- Demerol

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47
Q

What side effect to opioid use does not go away with tolerance/continued use?

What can be used for the adverse nausea effect of opioids?

A

Miosis, constipation

Corticosteroid
Antihistamine,
Metoclopramide
Serotonin antagonist

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48
Q

What three opioids are most likely to cause allergic reactions?

What two have fewer histamine related reactions?

A

Codeine, Morhpine, Meperidine

Oxy, Fentanyl

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49
Q

What are the Sxs of Opioid Allergy

What are the Sxs of Pseudoallergy and what drug is most likely to cause it

A

IgE/T-Cell induced hives, rash, erythema, HOTN, bronchospasm, angioedema

Flush, Itch, Sweats, Hives, HTON
Morphine

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50
Q

What are Sxs of opioid toxicity?

A

Confusion, Hallucinations, Agitation, Respiratory depression, Dreams

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51
Q

Caution is needed when using opioids for ?

A 
Pure with weak agonists
Head injuries
Pregnancy
Pulmonary, liver, renal impairments
Endocrine dz
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52
Q

What is the most common used opioid used as prescription to suppressive the cough center of the brain?

What is the OTC derivative of this drug?

A

Codeine

Dextromethorphan

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53
Q

What is the least lipophilic of the common opioids prescribed?

A

Morphine- small amount crosses BBB and will cross placenta

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54
Q

What two drugs can be given if PT has adverse reactions to morphine?

A

Diphenhydramine

Hydroxyzine

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55
Q

How are the pharmacokinetics of Hydromorphone better than morphine?

Can all providers prescribe hydromorphone?

A

Better PO absorption, more fat soluble

Extended release is REMS drug, requires training Q2yrs

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56
Q

What is the sequence of best to worse binding affinity of morphine and it’s derivatives?

A

Hydromorphone
Morphine
Hydrocodone

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57
Q

What is Oxycodone metabolized into?

What is so special about polyethylene oxide form of oxy?

A

Noroxycodone and oxymorphone

Turns gummy when contacts w/ water

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58
Q

What are the adverse effects of mixed opioid ant/agonists?

A

Psychomimetic response
Precipitates withdrawal
Ceiling effect on respiratory/analgesic
Lower abuse potential

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59
Q

When are Fentanyl patches indicated for use?

A 
Severe chronic pain
PTs w/ opioid tolerance of +1wk on:
>60mg Morphine/day
>30mg PO Oxycodone/day
>8mg PO Hydromorphone/day
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60
Q

Characteristics of the Fentanyl derivatives Alf/Suf/Remifentanil?

All three share what characteristics?

A

Alf- rapid onset/short duration
Suf- slower onset than Fentanyl but lasts same time
Remi- rapid onset but shortest duration, ONLY available by infusion

No infusion accumulation

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61
Q

What drug is classified as a Diphenylheptane?

What two drugs are classified as Benzomorphans?

A

Methadone

Pentazocine and Dipenoxylate

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62
Q

What types of PTs can not receive Tapentadol?

In order for Naloxone to have a systemic effect in can’t be taken through what route and but when it is, what for?

A

Renal dysfunction

Not systemic if PO- opioid induced constipation

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63
Q

Consider giving Naloxone to what PTs?

A 
Hx of Intox/OD
Suspected Hx of abuse/non-medical use
Methadone/Buprenorphine use d/o
>50mg of PO morphine or equivalent
Rotated from one opioid to another
Smoke, Respiratory, Hepatic, Renal, Heart, Alcohol, Benzo, Sedative, Anti-Depressants
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64
Q

When should Naloxone be given to a suspected OD PT?

A 
Respiratory/CNS depression
Pinpoint pupils in difficult to arouse PT
Cyanosis
Death rattle
Bradycardia/HOTN
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65
Q

What is the MOA of Naltexone

What is it used for?

A

Mu competitive antagonist that competes but doesn’t displace opioids

Longer duration for opioid/alcohol dependence

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66
Q

What is the sequence of most hydrophilic to most lipophilic opioids?

A 
Morphine
Oxycodone
Oxymorphone
Hydromorphone
Methadone
Fentanyl
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67
Q

What are the two combo forms of Naltrexone and their use?

What are the contraindications for using Naltrexone

A

Morphine- post-op pain w/out abuse potential
Buproprion- weight management

Opioid analgesic
PT w/ pos UA

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68
Q

Why are TCAs are used in pain management and which ones are used?

A

Block reuptake of 5HT and NE
Amitriptyline- off label
Nortriptyline
Desipramine

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69
Q

Why are SSRIs/SNRIs used in pain management and which ones are used?

A

Block reuptake of 5HT and NE
Duloxetine- DM neuropathy, Fibromyalgia
Milnacipran- Fibromyalgia
Vanlafaxine- Neuropathic pain

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70
Q

Why are anti-convulsants used in pain management and which ones are used?

A

Decreases neuron excitability
Gabapentin- Post-Herpetic neuralgia, Neuropathic pain
Pregabalin- Diabetic neuropathy, Fibromyalgia, Post-herpatic Neuralgia

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71
Q

Why are local anesthetics used in pain managements and which ones are used?

Why are counter irritants used?

A

Lidocaine 5%: post-herpetic neualgia, Allodynia

Deplete substance P

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72
Q

Non-addicted opioid PTs should be tapered off by how much/how quickly?

How long of a taper do PTs taking opioids PRN need?

A

20-50% of original dose

None

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73
Q

What are reasons to change opioids?

A

Lack of response
Adverse effects
Change in PT status- dysphagia
Cost/personal preference

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74
Q

What is the gold-standard opioid?

For PTs taking long acting opioids, short acting meds should be given for break through pain and at ? dosage?

A

Morphine

10-15% of TDD Q1-2hrs

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75
Q

Define Primary HAs

Define Secondary HAs

A

Migraine, Tension, Cluster, Other (cough, exertion)

Head/neck trauma, Cranial/cervical vascular d/o, Infection, Psych d/o

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76
Q

What are the unique characteristics of migraines?

A 
Usually unilateral
Pulsating and aggravated w/ activity 
Nausea
Photo/Phono phobia
4-72hrs
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77
Q

What are the unique characteristics of tension HAs?

A 
Bilateral
Pressing/Tightening that doesn't worsen w/ activity
No nausea
Rare photo/phonophobia
Minutes-days
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78
Q

What are the unique characteristics of cluster HAs?

A

Men
Boring/Piercing that causes PT to be restless/agitated during episode
Ipsilateral Sxs
Occur frequently and last 15m-3hrs

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79
Q

What does the “SNOOP” acronym for finding secondary HAs stand for?

What does “POUND” acronym stand for when searching for migraines?

A

Systemic Neurologic Onset (sudden) Onset (late)
Pattern

Pulsatile, One-day, Unilateral, N/V, Disabling

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80
Q

When/why does a provider go SNOOPing for HA causes?

A 
Acute onset of 1st/worst in life
HA w/ meningitis Sxs
Inc SBP +210 or DPB +120
Dec pulse/tender temporal artery
Pain worse w/ laying down
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81
Q

What are the Dx criteria for a migraine w/out an aura?

A

5 attacks
Last 4-72hrs
2 of: unilateral, pulsating, intensity, aggravated by activity causing avoidance
1 of: N/V/both, photo/phono phobia

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82
Q

What are the Dx criteria for a migraine w/ an aura?

A

2 attacks
One aura Sxs: visual, sensory, speech, motor, brain stem, retinal
Two of: one aura Sx spreads over 5min or two Sxs occur in succession; Aura Sxs last 5-60min; Each aura Sx lasts 5-60min; One Sx is unilateral, Aur followed by HA in 60min

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83
Q

More than 50% of migraines are genetically caused by ?

A

Familial hemiplegic migraines- mutations in CACNL1A4 genes on Chromosome 19

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84
Q

Why is 5HT an important mediator of migraines?

A

Stimulation- triptans
Antagonizers- methysergides
Prevent uptake/release- CCBs
Inhibit serotogenic raphae neurons- Valproate

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85
Q

Pain from migraines originates from ?

A

Trigeminovascular system- regulated by serotonin neurons; activation causes release of vasoactive neuropeptides CGRP, Substance P and Neurokinan A that cause vasodilation and dural plasma extravasation which leads to inflammation

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86
Q

What are the 4 Phases of Migraine HAs?

A

1 Premonitory Sxs- hrs to day before onset, most commonly neurologic Sxs, psychosocial, autonmic or constitutional Sxs
2 Aura- Pos or Neg (most common) sensory or motor Sxs that precede the HA by 60min
3 HA- usually early morning or upon waking, most w/ nausea
4 Resolution- fatigue, mood, tender scalp and impaired concentration

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87
Q

How are migraine HAs cared for across attacks?

A

HA 1-3: Tx w/ NSAID
Unresponsive Tx in 2 or more HAs= 4th HA Tx w/ triptan
Caution for Serotonin Syndrome

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88
Q

How are migraine HAs cared for during attacks?

How is migraine care stratified?

A

HA Tx w/ NSAID, no response in 2hrs= Tx w/ triptan

HA Dx MIDAS Grade 2= Tx w/ NSAID
HA Dx MIDAS Grade 3-4= Tx w/ triptan

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89
Q

When treating migraines across, within or stratified across attacks, how is “successful response” defined?

A

Pain reduced from 3-4 down to 0-1

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90
Q

What are the Non-Specific, Specific and Miscellaneous acute migraine agents?

A

Non-Specific: analgesics, NSAIDs
Specific: Ergotamines, Triptains
Misc.: Butorphanol nasal spray, Anti-emetic (metoclopramide)

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91
Q

What may be a useful FIRST choice drug for acute migraines in PTs w/ mild-mod attacks or can’t take NSAIDs or ASA?

A

Acetaminophen, consider w/ caffeine

Inferior pain free response to other NSAIDs and ASA

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92
Q

What is the MOA of Butalbital in Fioricet and Fiorinal

A

Short acting barbiturate
APAP/Butalbital/Caffeine- not scheduled
ASA/Butalbital/Caffeine- scheduled

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93
Q

What is the DOC for mild/mod migraine attacks?

How long should use of this drug be limited to?

A

NSAIDs- Ibuprofen, Naproxen, Excedrin
Contra to NSAID: Acetaminophen (not for gastritis, ulcer, renal dz, bleeding d/o)

Less than 15 days/mon

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94
Q

Ergotamine must be given with ?

What are the adverse effects?

A

Caffeine and rectally

Constriction leading to vascular ischemia, gangrene, tonic-clonic convulsion and mania/hallucinations

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95
Q

What are the administration considerations for Ergotamine?

A

Pre-treat w/ antiemetic and start at first sign of attack

Rectal better tolerated than PO but less effective than triptans

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96
Q

When is the use of Dihydroergotamine a reasonable choice for HA management?

A

Mod-severe HA and NSAID trial/non-opioid analgesic fails
IV w/ anti-emetic for PTs w/ severe migraines
Overall preferable over Ergotamine

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97
Q

What 3 Triptans have the highest likelihood of consitent success?
Which two are slower and have lower efficacy?
Major side effect?

A

Riza, Ele, Almo (Ele has best short term/sustained benefit)
Nara, Frova
Serotonin Synd.

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98
Q

What are the advantages of Sumatriptan and Zolmitriptan?

When is nasal spray form more useful?

A

Number of dosing formulas

Faster onset and more useful for PTs w/ vomiting

9 days or less/mon

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99
Q

What is unique about the first dose of a Triptan?

A

Done in clinic w/ EKG w/ VS on PTs that are suspected to have CAD (HTN, hypercholesterol, obese, diabetic, smoker)

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100
Q

What is the clinical triad of Serotonin Syndrome?

A

Cognitive, Neuromuscular/Autonomic dysfunction

D/c offender
Benzos- anxiety/seizure
Cooling blankets for hyperthermia
Cyproheptadine- 1st gen anti-histamine

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101
Q

Name the 7 applicable Triptans and related comments

A

Almo- Sulfa group, dec dose w/ 3A4 inhibs, desmethyl metabolite
Ele- not metabolized by MAO, don’t use w/in 72hrs 3A4 inhibitors
Frova- not metabolized by MAO
Nara- not metabolized by MAO
Riza- dec dose by 5mg if PT is taking Propanolol
Suma
Zolmi- desmethyl metabolite w 2/3 potency of parent form

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102
Q

What anti-emetics are used during migraines?

A

Metoclopramide- most efficacious for N/V from migraine; significant EPS s/e
Anti-Psychotics- dopamine/serotonin antagonists (Chlorpromazine, Prochlorperazine)
5HT3 Antagonists- not efficacious, high adverse HA (Ondansetron, Granisetron)

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103
Q

What are the most, intermediate and least efficacious meds for migraine treatment?

A

Most- Aspirin, Excedrin, Ibuprofen, Triptan
Intermediate- Acetaminophen, Naproxen, Midrin, Butorphanol, Ergotamine, DHE + anti-emetic
Least- Fioricet/Fiorinal

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104
Q

Medication Overuse HA are AKA ?

How are they best avoided?

A

Analgesic Rebound HA from daily analgesic/triptans that cause 5HT down regulation

Limit migraine therapies to 2 days/wk

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105
Q

What are the criteria for migraine prophylaxis?

How long does it take to assess efficacy?

A

+4 HA/mon or duration >12hrs

1-2mon

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106
Q

What are the first line migraine prophylactics for pattern, heart, depression/insomnia or seizure/MD PTs?

A

Predictable- NSAID at time of HA
HTN/Angina/Anxiety- BB (Verapamil if BB contraindicated)
Depressed/Insomnia- TCA
Seizure/Manic Depressive- anticonvulsant

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107
Q

Which anti-convulsants can be used for migraine prophylaxis?

A

Divalproex- N/V, Asthenia, Weight gain, Hair loss, Tremor, Liver Dz, Preg Cat D, less GI than Valproate

Valproate- kidney stones, N/V, Asthenia, Weight gain, Hair loss, Tremor, Liver Dz, Preg Cat D

Topiramate- Kidney stones, Parasthesia, Weight loss, Metabolic acidosis, Sedation, Altered taste, Cleft lip/palate

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108
Q

What Triptans are used for migraine prophylaxis?

A

Frova, Zolmi, Nara

Contraindicated in PTs w/ ischemic heart dz, uncontrolled HTN, CV dz

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109
Q

Naratriptan is best used for ? types of migraines?

A

Short term prevention from menstrual associated migraine

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110
Q

Which BBs are used for migraine prophylaxis?

A

Propan, Tim, Aten, Meto
Fatigue, Tired, Dizzy, Impotence, No for Asthma PTs, Raynauds, caution w/ diabetic, may worsen depression

T/A/M- not first line BBs but may be sued w/ other therapies for PTs w/ anxiety, HTN or angina.

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111
Q

What CCBs are used for migraine prophylaxis?

Which NSAID can be used?

A

Verapamil
S/e= constipation, HOTN, bradycardia, worsening CHF
may not be seen for 8wks

Naproxen- Prevent predictable HAs

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112
Q

When is Botox A considered for migraines?

Why is Mg considered for phrophylaxis?

A

PTs w/ +15 HA days/mon or lasting +4hrs

Pregnancy

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113
Q

What is the most common type of primary HA?

A

Tension- pain originates from myofascical factors and peripheral sensitization of nociceptors

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114
Q

What are the pharmaceuticals of choice for tension HAs?

A

DOC- Acetaminophen, NSAIDs
Limit use to 9 days or less/mon
Muscle relaxants

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115
Q

When is prophylaxis considered for tension HAs?

What med is used?

A

+2/wk, +3hrs, disabliing

DOC- Amitriptyline @ bedtime
Adverse- Anti-Ach, Weight gain, OHOTN, Arrhythmias

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116
Q

What is the suspected cause of cluster HAs?

A

Hypothalamic dysfunction- altered circadian rhythms

Lab reports of abnormal melatonin, GH, testosterone and prolactin

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117
Q

What type of HA is the most severe of the primary HAs?

How is their presentation different than migraine PTs?

A

Cluster- occur at night, spring/fall w/ ipsilateral Sxs

PTs sit and rock or pace holding head

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118
Q

What is the criteria for cluster HAs?

A

5 attacks lasting 15-180min

Attack occurs w/ ipsilateral Sx

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119
Q

How are cluster HAs treated?

A

First line- Oxygen 100% by re-breather
Sumatriptan- SubQ/intranasal- most effective
Zolmitriptan, less effective but better tolerated
Ergotamine derivatives- DHE has quickest result and repeated use can break cycles but risks make them rarely used

120
Q

What medication is used as prophylaxis for cluster HAs?

A

DOC- Verapamil
2nd Line- Lithium, can be used w/ Verapamil
(monitor trough, thyroid and renal)

121
Q

What meds are used as transitional prophylaxis between cluster HAs?

A

Prednisone

Dihydroergotamine

122
Q

What is the most common form of osteoporosis?

Where does it usually effect and what are the two types?

A

OA- leading cause of disability in older adults; Primary/Idiopathic is most common

Knee, Hip, Thumb
Localized- one or two sites
Generalized- three or more sites

123
Q

Most preventable risk factor for OA is ?

When shaking hands w/ PTs that have OA in their hand, what might be felt?

A

Obesity

Herberden nodes

124
Q

What topical NSAIDs can be used for OA?

A

Diclofenac Gel- only FDA approved for hand or knee
Diclofenac Na- knee OA
Topical Salicylates- modest short term Tx of OA
Capsaicin- muscle/joint pain, diabetic/post-herpatic neuralgia

125
Q

What is the MOA of Topical Salicylates?

What are they used for?

A

Local COX 2 inhibition

Short term Tx of OA

126
Q

What are the clinical uses of capsaicin topicals?

What are the adverse effects?

What are the precautions?

A

Muscle/joints pain or Diabetic/post-herpatic neuropathic pain but must be used 4x/day

Temporary burning

Eyes, mouth, groin

127
Q

What is the MOA of Corticosteroids?

What are the adverse effects?

A

Suppresses leukocytes and reverses capillary permeability

Hyperglycermia, Edema, HTN, Dyspepsia, Adrenal suppresion

128
Q

What is the use of Glucosamine?

A

Stimulates proteoglycan production which is in articular cartilage.
Hyaluronic acid is lube/shock absorber of synovial fluid

129
Q

What is the use of Chondroitin sulfate?

A

Glucosamine and Aminosugars that add tensile strength to cartilage
Increases hyaluronic concentration and viscosity

130
Q

What are the precautions of using Glucosamine and Chondroitin?

A

Safe/tolerated when used at dose x 2yrs
Interacts w/ warfarin
PO glucosamine causes kidney issues
Shellfish allergy

131
Q

What are the adverse reactions of Glucosamine/Chondroitin?

What is one underlying perk in its MOA?

A

GI Sxs, Not FDA approved

No blood sugar increases

132
Q

RA is primarily mediated activity by ? cell

How are the activated?

A

T-cells

Macrophages activated by cytotoxins (IL-1, TNF-a)
Increases inflammatory mediators (CRP, histamine, prostaglandins)
Increased chondrocytes/osteoclasts which increase cartilage/bone degredation

133
Q

What lab results will be see in PTs w/ RA

What are the extra-articular involvements of RA?

A

+ RF, Elevated CRP and ESR

Nodules, Vasculitis, Pulmonary, Ocular, Cardiac, Felty’s Syndrome- splenomegaly and neutropenia

134
Q

How is RA controlled and what is used for pain relief?

A

Dz control= DMARDS and Biologics

Pain- NSAIDs, analgesics, glucocorticoids

135
Q

What class meds are used for the treatment of RA?

A

NSAIDs
Steroids
DMARDs- Methotrexate, Ankylating agents, Anti-malrials, Biologics
Duloxetine- FDA approved to treat MSK pain

136
Q

What is the first med used for the immediate treatment of pain and inflammation of RA and can be used as adjunct while DMARDs accumulate?

A

NSAIDs- Ibuprofen, Meloxicam, Nabumetone, Naproxen

137
Q

What drugs are used as “bridge” therapy while waiting for DMARD therapeutic effect?

What are the mainstay of treatment?

A

Corticosteroids

DMARDs- started w/in first 3mon of Sxs and can reduce mortality

138
Q

What are the traditional DMARDs used?

What Biologics are used w/ DMARDs?

A

Methotrexate, Leflunomide, Hydroxychloroquine, Sulfasalazine

TNF-a Inhibitor
Non-TNF-a Co-Stimulation modulators
Biosimilar DMARDs

139
Q

When are DMARD combos used?

A

Sx early Dz of Mod-High activity that is non-responsive to traditional DMARD monotherapy

140
Q

What are the adverse effects of Methotrexate?

What is monitored for in both Methotrexate and Leflunomide?

A

GI- most common
W/ chronic use: Leukopenia, Cirrhosis, Pneumonia-Like Sxs

CBC w/ platelets, AST/ALT

141
Q

What is Methotrexates reversal agent?

What is Leflunomide’s reversal agent?

A

Leucovorin

Cholestyramine

142
Q

What are the adverse effects of Leflunomide?

What is the MOA of Hydroxychloroquine?

A

GI, Allopecia, Hepatic, Peripheral neuropathy

Inhibits movement of neutrophils and eosinophils

143
Q

What is Hydroxychloroquine used for?

What are the adverse effects of it?

A

Anti-malarial, RA, Lupus

Decreased vision, required eye exam Q6mon
GI
Derm

144
Q

What is the MOA of Sulfasalazine

What is it used for?

A

Prodrug cleaved in intestine to decrease IgA and IgM

Mild RA to decrease radiologic progression of Dz
UC

145
Q

What are the adverse effects of Sulfasalazine use?

What are the interactions it can have?

A

GI, Rash, Photosensitivity

Dec sulfasalazine absorption which binds to Fe in gut
Displaces warfarin

146
Q

What is the MOA of biologic DMARDs?

What are they used for?

A

Block cytokines or prevent stimulation needed to activate T-cells

PTs that don’t respond to first line agents (meth) or combo agents

147
Q

All biologic DMARDs increase risk of ?

What is their black box warning?

A

Infection

Anti-TNF-a can cause increased lympho-proliferative/CAs in kids and adults

148
Q

What are the predisposing factors of gout?

A

Loop/Thiazide diuretics
Salicylates- no ASA, use NSAIDs
Calcineurin Inhibitors- Cyclosporine/Tacrolimus- impairs renal excretion
Chemo Drugs- Hydroxyures- rapid cell lysis
Niacin
XOIs

149
Q

What meds are used for acute gout flared?

What meds are used for urate lowering therapy/chronic suppression

A

NSAIDS, Colchicine, Glucocorticoids

XOIs, Uricosuric Agents, Uricase

150
Q

When is Celecoxib an option for gout treatment?

What meds are used for PTs w/ severe pain, polyarticular attack, or gout in multiple large joints?

A

PTs w/ contraindications (GI) and/or intolerant to typical NSAIDs

Colchicine and NSAID
Colchicine and Oral Corticosteroid
Intra-articular steroids

151
Q

What is the first line meds for acute gouty attacks in the first 24hrs

What 3 meds have FDA approval for treating acute gout attacks?

A

NSAID and Colchicine (only used in first 36hrs of onset)

Naproxen, Indomethacin, Sulindac
Indo/Nap- DOC for flares

152
Q

What is the MOA of Colchicine?

What is it use for?

A

Binds to tubulin and inhibits neutrophils associated w/ gout Sxs

Treat flares
Prophylaxis for flares

153
Q

What are the adverse effects of Colchicine?

A

Renal/Hepatic failure
Drug interactions
N/V/D
Bone marrow suppression- suppresses fast growing cells in <1% of PTs

154
Q

What are the three classes of drugs used for chronic gout suppression?

A

XOIs- Allopurinol, Febuxostat
Uricosuric agents- Probenecid, Lesinurad
Uricase/Urate Oxidase- Pegloticase

155
Q

What are the indications for giving ULTs?

What is the first line used?

A

Tophi on exam/imaging
Two or more acute gouty attacks/year
CDK Stage 2 or worse
Hx of Urolithiasis

XOI- Allopurinol, Febuxostat
Alternaitves if at least one XOI is contraindicated, ineffective or intolerable: Probenacid, Pegloticase

156
Q

What is the MOA of Allopurinol/Febuxostat

Fout flares can occur after initiating meds, what meds are used upon initiation?

A

Inhibits uric acid synthesis by inhibiting xanthin oxidase which is converts xanthine into uric acid

NSAIDs or Colchicine

157
Q

What are common adverse effects of XOIs?

What are the pros/cons of Febuxostst?

A

Rash, Leukopenia, Thrombocytopenia, Diarrhea, CV event, Drug fever

40mg= 300mg of Allo
Higher dose had better tolerance and more success
More expensive/no generic
Higher risk of thrombo emoblic events

158
Q

What are the MOA of Probenecid/Lesinurad

A

Weak organic acids that inhibit tubule urate anion exchanger that control urate absorption
Reduced B-lactam Abs and reduces excretion of other meds

159
Q

What are the clinical uses of Uricosuric Agents?

What are the adverse effects?

A

Probenecid- taken BID as an alternative/additive to ULT Tx if XOIs aren’t enough, contrainidcated, intolerable
Lesinurad- must only be used daily in combo w/ XOIs

Acute gouty attack- prophylact w/ NSAIDs or Colchicine
GI intolerance
Uric acid stone formation

160
Q

What are the contraindications and interactions of Uricosuric Agents?

A

Don’t give to PTs w/ uric acid crystals in UA
PTs must hydrate

Interact w/ renally cleared meds
Reduced/rendered useless by Salicylates (no change in uric acid levels when used w/ Aspirin)

161
Q

What is the MOA of Pegloticase?

What is it used for?

A

Recombinant Urate Oxidase that catalyzes oxidation of uric acid into allantoin

Severe gout Dz refractory to traditional urate lowering therapies

162
Q

What are the adverse effects of Pegloticase?

What PTs are contraindicated from receiving it?

A

Flares for first 3mon
Infusion reactions
HF exacerbation

G6PD deficiency

163
Q

What are the first line options of pharmacologic prophylaxis for gout?

How long should prophylaxis last?

A

Cochicine, NSAIDs, PPI
Alternative: oral corticosteroids

6mon
3mon after target serum levels are reached and no tophi are present w/ serum monitoring Q2-5wks

164
Q

PTs return to medical and serum urate goals have not been met, what are the next steps?

A

Titrate single XOI to max dose
Add Uricosuric to XOI: Probenecid, Losartan, Fenofibrate (Losartan and Fenofibrate are off-label but recommended 2nd line)
If still not reached, add Pegliticase (only in severe Dz and PT is refractory/intolerant to other ULT)

165
Q

What is intrinsic factor’s use in the stomach?

What stimulates HCl production?

A

Located in parietal cells of gastric glands and aids in absorption of B12

PPump at parietal cell by Ach, Histamine or Gastrin

166
Q

What makes up the protective substances for the GI?

What is their role?

A

Prostaglandins E1, E2 and I2 (prostacyclin)

Inhibit basal/stimulated gastric acid secretion

167
Q

On the stomach picture, what meds are linked to H Pylori, M1, ATPase, H2 and PG?

A 
H Pylori- Bismuth, ABX
M1- M antagonist
ATPase- Omerprazole
H2- H2 antagonist
PG- misoprosotol
168
Q

All GERD PT treatment starts with what steps?

A

Diet, Lifestyle
Mild- 1 or less episode/wk= H2 inhibitor and antacid.
After 4wks, if Sxs aren’t controlled, switch to PPI

GERD that’s >1/wk- start w/ PPI
If Sxs return, restart therapy

169
Q

What are the non-invasive tests for H Pylori?

What are the invasive tests?

A

F Ag test
Urea breath test
Serologic

Endoscopy w/ biopsy

170
Q

How are H pylori ulcers treated?

A

PPI
Triple therapy- Clarithromycin Amoxicillin (alt- metronidazole if allergic to PCN)
Quad therapy- PTs that can’t take Clarithromycin; Tetracycline, Metronidazole, Bismuth Subsalicylate

171
Q

How long is H pylori ulcer treatment conducted for?

What follow on test must be done on all PTs?

A

14 days of ABX
If PUD remains, continue PPI x 4-8wks (duodenal) or 8-12wks (gastric)

Erradication testing- UBT or stool Ag
Must be off PPIx x 2wks prior

172
Q

What is in Sequential Therapy after H Pylori triple therapy?

A

Clarithromycin, PPI, Tinidazole/Metronidazole x 10 days

Effective erradication of H Pylori in treatment naive PTs

173
Q

What is the next step for PTs that are H Pylori treatment failures?

A

Culture

Rescue therapy- Levofloxacin, Amoxicillin, and PPI x 2wks

174
Q

How are NSAID induced ulcers treated?

A

D/c
If d/c isn’t an option- switch to APAP or non-acetylates salicylate
COX-2 inhibitor- Celecoxib (last line)
PPI or MIsoprostol

175
Q

How are stress ulcers managed prophylactically?

A

PPI, H2RA
IV PPI is equivalent to high dose IV H2RA
IV preferred in PTs w/ feeding tubes

176
Q

What is the MOA of antacids?

What are their use in clinic?

A

Weak bases that neutralize acids by forming Na/H2O

1st line therapy for intermittent Sxs (less than 2x/wk)
Break through therapy for PTs on PPI/H2RA therapy

177
Q

What are the adverse effects of antacids?

What drugs do they interact with?

A

Constipation due to Al/Ca, diarrhea from Mg, accumulation of metal elements in kidneys

Chelation- avoid Fluroquinolones and TCAs
Toxicity- HIV meds (Ralte/Saquinavir)

178
Q

What is the MOA of Sodium BiCarb?

When should caution be taken during use?

A

Reacts w/ HCl to form CO2 and NaCl
CO2 released by belching or causes bloating

Metabolic alkalosis
High Na content, caution w/ HTN/CFH

179
Q

What are the benefits of using Calcium Carbonate as an antacid?

What adverse effects can happen?

A

Less neutralization activity

Metabolic alkalosis
Hypercalcemia

180
Q

What is the MOA of Magnesium Hydroxide?
What is an adverse effect?
When is it not used?

A

Reacts w/ HCl to form MgCl and H2O as an antacid or laxative
Osmotic diarrhea
Renal insufficiency

181
Q

What is the MOA of Aluminum Hydroxide?

What are the adverse effects?

A

Reacts w/ HCl to form AlCL and H2O
Constipation
Renal insufficient shouldn’t take it

182
Q

What two forms of antacids are often used together to reduce the impact on bowel function?

How does Aluminum Hydroxide and Magnesium Trisilicate work?

A

Mg/Al Hydroxide and Simethicone
Simethicone relieves flatulence

Alfinic acid that forms foamy layer above stomach contents to reduce reflux

183
Q

What is the MOA of H2RAs?

What are the adverse effects?

A

Competitively block histamine from binding to H2 receptors on parietal cells to inhibit gastric acid and secretion

CNS and confusion- most common
Prolonged cimetidine use- rare gynecomastia

184
Q

What drugs interact with H2RAs?

A

Cimetidine- competes w/ meds and creatinine for tubular secretion in kidney

185
Q

What are the diasdvantages of Cimetidine?

A

First H2 blocker

Endocrine effects- anti-androgen
Competes w/ meds and creatinine for tubular secretion in kidney

186
Q

What are the characteristics of the H2RA Ranitidine

A

Few s/e w/ good efficacy
150mg BID
Preferred H2RA for IV use

187
Q

What med is an antacid and H2 antagonist combo?

Nizatidine has comparable efficacy as other H2RAs, what is it’s con?

A

Famotidine

Expensive

188
Q

What is the disadvantage of PPIs

What drugs fall into this class?

A

Most expensive agents for GERD management

-prazole
Panto, Ome, Esome, Rabe, Lanso, Dexlanso

189
Q

What is the MOA of PPIs?

What is the adverse risk of taking these?

A

Prodrug that irreversibly bind to H/K/ATPase pump to suppress H+

Fx risk, Hypomagnesiaemia, C Diff, Community acquired pneumonia

190
Q

What interactions do PPIs ahve?

A

FDA recommends avoiding Ome and using Pantoprazole as alternative
Drugs w/ pH dependent absorption: Ketoconazole, Itraconazole, Protease inhibitors

191
Q

What are the mucosal protective agents?

What are they used for?

A

Sucralfate- covers/protects ulcers and stimulates prostaglandin release but reqs acid for activation

Heals ulcers, not as effective as H2 blockers/PPIs
Mainly- preventing stress related bleeding

192
Q

Why is Sucralfate use limited?

What are the mucosal protective agents?

A

Multiple doses/day, Large tablets, needs for meal/drug seperation

Misoprostol
Bismuth Subsalicylate

193
Q

What is the MOA of Misoprostol?

What are they used for?

A

E1 prostaglandin analog w/ antisecretory and mucosal protective properties

Preventing NSAID induced ulcers, not used widely due to adverse profile and multiple daily doses

194
Q

What are the adverse effects of Misoprostol?

What are the contraindications of use?

A

Diarrhea, Abd pain

Pregnancy X

195
Q

What are the Prokinetic Agents?

A

Metoclopramide

Erythromycin

196
Q

What is the MOA and use of Metoclopramide

A

Dopamine antagonist that stimulated upper GI w/out effecting secretions while enhancing tissue effect to ACh to enhance motility and blocking 5HT receptors for anti-emetic effect

Reflux, N/V from chemo, Impaired GI emptying

197
Q

What are the adverse effects of Metoclopramide?

A

CNS- drowsy, restless

EPS- parkinsonian features

198
Q

What is the MOA and use of Erythromycin as a prokinetic

What are the adverse effects?

A

Stimulate GI smooth muscles and promotes onset of migrating motor complex
IV for PTs w/ gastroparesis
Cramping and bacterial resistance

199
Q

Where is the vomiting center located in the brain?

What 4 sources of afferent input can stimulate it?

A

Medulla

Solitary Tract Nucleus- dopamine/5HT3 receptors
Vestibular apparatus- H1 /muscarinic cholinergic receptors
Chemo Trigger Zone- 5HT3, D2 H1 and M1, Opioid receptors
Cerebral cortex- sight, smell, emotions

200
Q

What causes vomiting undigested food hours after eating?

What causes vomiting immediately after meals?

What causes vomiting in mornings after breakfast?

A

Gastroparesis, Gastric outlet obstruction

Bulimia, Psychogenic causes

Pregnancy, Uremia, Alcohol, Increased ICP

201
Q

What anti-emetics are used for general medical use?

Which ones are used for chemo induced vomiting?

A

Phenothiazines, Serotonin antagonists

Phenothiazines, Serotonin antagonists, NK1 antagonists, Dronabinol

202
Q

What anti-emetics are used for post-op vomiting?

Which ones are used for motion sickness?

A

Serotonin antagonists, Scopolamine

Antihistamines, Scopolamine

203
Q

Which anti-emetics are used for pregnancy induced vomiting?

Which one is used for gastroparesis?

A

Phosphorylated Carbohydrates, Pyridoxine, Antihistamines

Metocopramide

204
Q

What are the 5HT3 Antagonists?

What is given with them?

A

Ondansetron, Granisetron, Dolasetron,
Palonosetron

Corticosteroids- Dexamethasone, Methylprednisolone

205
Q

What is the MOA of 5HT3 antagonists?

What are they used for?

A

Block presynaptic serotonin receptors on vagal fibers and vomit center and CTZ

Post-op N/V (Ondansetron)
Chemo N/V w/ Corticosteroids
Radiation N/V

206
Q

What are the most common s/e from 5HT3 antagonist use?

A

HA, Dizzy, Constipation

Small QTc prolongation especially w/ Dolasetron use

207
Q

What is the MOA of anti-histamines?

What are the 1st Generation Antihistamine?

A

Block vestibular apparatus H1s preventing N/V from motion sickness, all have drowsiness and anti-Chl s/e
Pregnancy Cat-A

Meclizine, Diphenhydramine, Dimenhydrinate, Doxylamine/Pyridoxine (B6)

208
Q

What is the MOA of Phenothiazines?

What two drugs are included?

A

Block D/M/H receptors in CTZ for anti-emetic effect given PO, IV, IM, rectal (not SubQ)

Prochlorperazine- N/V
Promethazine-N/V/Motion Sick

209
Q

What are the adverse effects of Phenothiazines?

A

HOTN, Restlessness, EPS, Drowsy

210
Q

What is unique about Promethazine’s administration route?

What class of drug is it?

A

No Sub-Q, IV needs to be diluted to prevent tissue necrosis

1st generation Antihistamine

211
Q

What is the MOA and use for Scopolamine?

A

Cholinergic antagonist w/ more lipophilic/central effects

Motion sickness
Surgery adjunct- blocks short term memory formation
Blocks salivation

212
Q

What needs to be monitored in PTs taking Scopolamine?

What are the adverse effects?

A

HR, Temp, Urine output

Excessive Anti-Chl effects

213
Q

What is the MOA of Butyrophenones?

What are they used for?

A

Droperidol
Blocks dopamine receptors in CTZ of CNS

No longer used as antipsychotic
Post-Op N/V
Endoscopy/surgery sedation in combo w/ opiod/benzos

214
Q

What are Adverse Effects of using Butyrophenones?

A

EPS, Dystonia, Drowsy, Aggitation, Confusion

215
Q

What Benzamide is used and what is it’s MOA and use?

A

Metoclopramide
Trimethobenzamide

Blocks emetic impulse to CTZ w/out EPSx like Metoclopramide

Apomorphine pre-treatment of Parkinson’s
Post-op N/V
Gastroenteritis nausea

216
Q

When are cotricosteroids used for N/V?

What two are used?

A

Chemo induced N/V w/ 5HT3 antagonists

Dexamethasone
Methylprednisolone

217
Q

When are Benzos used for N/V?

What two are used?

A

Prior to chemo to reduce anticipatory N/V caused by anxiety

Lorazepam
Diazepam

218
Q

What two Cannabinoids are used for N/V and what are the info facts on them?

A 
Dronabinol- synthetic, 
Unresponsive Chemo nausea 
AIDS anorexia
Potentiates psychoactive agents
Store @ 46-59*F

Nabilone- C-2
Synthetic, nausea from chemo that’s refractory to other anti-emetics

219
Q

What are the NK1s used for N/V

A

Aprepitant
Fosaprepitant
Netupitant/Palonosetron

220
Q

Facts of Aprepitant

A

Blocks postrema in medulla
Modulates Sub. P
Augments 5HT3 receptor

Used w/ 5HT3 antagonists and steroids for acute/delayed Cisplatin-induced emesis

221
Q

Facts of Fosaprepitant

A

Prodrug, converted to Aprepitant 30m after infusion

Used for Mod-High emetogenic chemo

222
Q

Facts of Netupitant/Palonosetron

A

Netupitant- antagonist of Substance P and NK1 receptors

Palonsetron- 5HT3 antagonist

223
Q

All NK1s used for N/V have what similar adverse characteristic?

A

Multiple CYP3A4 interactions

224
Q

What are the 4 types of diarrhea?

A

Secretory- large volume w/ E+
Altered motility- ANS s/o (DM, Post-Vagotomy, Hyperthyroid, IBS, Addisons)
Osmotic- hyperosmolar gradient in intestine from carb malabsorption, lactase deficiency, fat malabsorption, short bowel syndrome
Inflammatory- IBD, C Diff, E Coli, Shigella, Neoplasm

225
Q

Criteria for mild, moderate and severe diarrhea

How are mild and moderate treated?

A

3 or less, 4 or more, 6 or more

Mild- hydrate, lactose free diet, avoid caffeine
Mod- anti-motility, rehydrate

226
Q

What ABX are used for Traveler’s diarrhea?

A

Fluoroquinolones
Azithromycin
Rifaximin- only owrks in colon

227
Q

What ABX treats IBS diarrhea dominant disease?

A

Rifaximin

228
Q

What drugs are used for treating ABX associated diarrhea (C Diff)?

A

Metronidazole, PO Vancomycin

229
Q

What is the MOA and Use of Loperamide

A

Mu opioid agonist/Meperidine derivative, inhibits Ach and decreases peristalsis w/out crossing BBB

MIld-Mod non-invasive diarrhea Sxs
First line choice anti-diarrheal for acute diarrhea
Less sedating/addicting than Diphenoxylate

230
Q

What are the adverse and contras for Loperamide?

A

PTs w/ severe colitis

231
Q

When is Diphenoxylate w/ Atropine used for diarrhea?

What are the adverse effects and times it shouldn’t be used?

A

Mod-Severe non-invasive diarrhea
Refractory diarrhea

Suboptimal to Loperamide or Bismuth
No analgesia
Higher/longer use can cause dependence

Not for children
PTs w/ severe colitis

232
Q

What miscellaneous agents are used for diarrhea?

A

Bismuth Subsalicylate- Traveler’s Diarr.
Octerotide- inhibs GH, Tx tumor/HIV associated diarrhea
Lactase enzyme- lactase deficiency/intoelrance
Probiotics- bacteria overgrowth in sm. int., C Diff treatment

233
Q

What is the MOA of Osmotic Laxatives

What is it used for?

A

Moves water into distal small bowel/colon causing high volume liquid stool

Acute/intermittent constipation
Pre-op/procedure prep

234
Q

What are the adverse effects of osmotic laxatives?

A

Na Phosphate- may cause hypoE+, hypernatremia, nephropathy

MgSulfate- caution w/ renal impairment, will cause Mg intoxication, E+ abnormalities

235
Q

What is the MOA of non-absorbable osmotic laxatives?

What is it used for?

A

Metabolized by bacteria to increase osmotic pressure, causing increased fluids/cramps

Acute, intermittent, chronic constipation

236
Q

When is Lactulose use preferred?

A

Chronic liver dz
Prevention of hepatic/portal encephalopathy
Reduce ammonia levels

237
Q

When is Polyethylene glycol solution used?

A

Endoscopic/radiology pre-op prep
Ingested 2-4L over 2-4hrs
Safe for Liver Dz and Pregnancy

238
Q

When is PEG 3350 powder use for constipation preferred?

A

Chronic constipation
IBS constipation w/ less cramping/gas
Safe for Liver/Renal Dz and Pregnancy

239
Q

When is Glycerin Suppository use preferred for constipation?

When is Mineral Oils used?

A

Acute to intermittent constipation in Peds Pts

Mild constipation and need for intestinal lube
Avoid aspiration
Potential for lipoid pneumonia (lipids in lungs)

252
Q

What triptan for short term relief of menstrual related migraines

A

Nara

253
Q 
Where do the following DMARDs work?
Abatacept
Methotrexate
Lefunomide
Tocilizumab
Anakinra
A

Abatecept- stimulation of dendrite to T cell
Meth/Leflu- CD4 to B or Macrophage
Ana- IL-1
Tocil- IL-6

254
Q

Where do Etanercept/ I/A/G/Cmabs work?

A

TNF-a

255
Q

Use and adverse facts of Infliximab

A

Combo w/ Meth, not for monotherapy
Ankylosing spond.

Infusion reaction
Activation of latent TB

256
Q

Use and adverse facts of Etanercept

A

Meth failures, JRA

Infection and CA risk

257
Q

Facts of Non-TNF Co-Stim Adatacept, , and

A

Aba- used for severe RA in PTs w/ incomplete response to DMARDs or TNF-a antagonists
Binds to CD80 and CD86 to inhibits T cells
Can be used w/ Meth of non-bio DMARD

258
Q

Facts of Non-TNF Co-Stim Rituximab

A

Combo w/ Meth
Doesn’t activate TB
Binds to CD-20
Used in leukemia, hodgkin and Plyangiitis PTs

Don’t give as bolus/push
Reaction to first infusion, give w/ corticosteroids
Heb B reactivation

259
Q

Facts of Non-TNF Co-Stim Rituximab

A

Combo w/ Meth
Doesn’t activate TB
Binds to CD-20
Used in leukemia, hodkin and Plyangiitis PTs

260
Q

Facts of Non-TNF Co-Stim Tocilzumab

A

For PTs not responded to TNF-a

IL-6 antagonist

261
Q

Facts of Non-TNF Co-Stim Tofacitnib

A

JAK inhibitor

262
Q

Adverse effects of Abatecept

A

HA, URI

Hypersensitivity

263
Q

What triptans can be administered ODT, MLT, SubQ and Intransal?

A

Riza- sublingual
Suma- SubQ, Nasal
Zolmi- sublingual, Nasal

Alma- sulfa allergy

264
Q

Acronym for Tension HA management

Acronym for Cluster HA management

A

T: AcNRA

C: OSZEVL/PD

265
Q

Acronym for Tension HA management

Acronym for Cluster HA management

A

T: AcNRA

C: OSZEVL/PD

266
Q

What is the treatment for RA

A 
NSAID- Meloxicam, Ibuprofen, Nabumetone, Naproxen
Steroid- Prednison
DMARD- M L S H
Biologics- T N B (ICAGE)
Duloxetine- FDA Tx for MSK pain
267
Q

Sequence for gout treatment

A

Flare- N C G

ULT- XOI (AF), UA (Pro, Lesi), Uricase (Peglo, Rasbur)

268
Q

H Pylori ulcer treatment

A

PPI, Clarithromycin, Amoxicillin (Triple Therapy) (substitute amoxicilin w/ metron if PT penicillin allergic)

Retreatment/no clarithromycin/areas of high clarithromycin resistance= Tetracycline, Metronidazole, Bismuth Salicylate (Quad therapy)

269
Q

NSAID ulcer treatment

A

Reduce/switch to APAP or non-acetylated salicylate
Celecoxib- last line
PPI or Misoprostol

270
Q

Stress ulcer treatment

A

Recommended for ICU PTs

PPI and H2RA
IV PPI equivalent to IV H2RA
PT w/ feeding tube gets enteric formulation of either

271
Q

Rifaxamin usage and facts

A

MOA: alters bacterial content in GI

Use: IBS-D for global Sx relief; E Coli induced traveler’s diarrhea in PTs w/ Hepatic
Encephalopathy

Adverse: Nausea, ALT increase, C Diff eval if no improvement

Caution: liver impairment

272
Q

Eluxadoline MOA, Use, Adverse and C/C

A

MOA: Mu/K agonist, D antagonist that lessen bowel contractions in IBS-D
Use: Adults w/ IBS-D
Adverse: Spincter of Odi spasms, Pancreatitis
Contra: Bile obstruction, Pancreatitis, +3 drinks/day

273
Q

5HT3 Antagonist MOA, Use, Adverse and Warning

A

MOA: affect visceral pain, increase motility and GI secretions
Use: women w/ IBS-D
Adverse: only avail through Prometheus Rx program
Warning: Ischemic Colitis, Constipation

274
Q

5HT3 Antagonist

A

MOA: affect visceral pain, increase motility and GI secretions
Use: women w/ IBS-D
Adverse: only avail through Prometheus Rx program
Warning: Ischemic Colitis, Constipation

275
Q

IBS-C female older than 18=
IBS-C in women=
IBS-C=
IBS-D in women:=

A

Lubiprostone
Tegaserod
Linaclotide
Alosetron

276
Q

Drugs for IBS-C

A

Laxative
Cl activator: Lubiprostone
5ht4 agonist: Tegaserod

277
Q

Drugs for IBS Pain/Bloating

A

Antispasmodic: Dicyclomine, Hyoscyamine
MOA: block Ach in PNS
Use: adjunct to IBS med for PRN pain relief

278
Q

Drugs for IBS Pain/Bloating

A

Antispasmodic: Dicyclomine, Hyoscyamine
MOA: block Ach in PNS
Use: adjunct to IBS med for PRN pain relief

279
Q

TCAs for IBS-C

SSRIs for IBS-D and IBS-C:

A

Amitriptyline, Nortriptyline, Imipramine

Fluoxetine, Setraline, Citalopram, Paroxetine

280
Q

What medications are used as adjuncts for IBD/o

A

Loperamide- proctitis, diarrhea

Anti-Achl- Dicyclomine, Hyoscyamine

281
Q

Aminosalicylates for IBD/o

A

First line for IBD
Anti-inflammatory w/ little systemic absorption
Sulfasalazine metabolized to active mesalamine
Crohns and UC
Mesalamine- fewer allergic reactions

282
Q

Aminosalicylates for IBD/o

A

First line for IBD
Anti-inflammatory w/ little systemic absorption
Sulfasalazine metabolized to active mesalamine
Crohns and UC
Mesalamine- fewer allergic reactions

283
Q

Naloxegol OIC

A

Substrate for PEG and Naloxone derivative

Adult PTs w/ OIC w/ chronic non-CA pain

284
Q

Naloxegol OIC

A

Substrate for PGlycoprotein transport

Adult PTs w/ OIC w/ chronic non-CA pain

285
Q

Guanylate cyclase C Agonist

A

Lincaclotide
induces Cl and BiCarb secretion and decrease visceral pain
IBS-C; CIC
Diarrhea
Contraindicated for <17, dehydration risk

286
Q

Cl Channel Activators

A

Activates CIC-2 to stimulate Cl secreation
Female >18y/o w/ IBS-C, CIC, OIC w/ non-CA
R/o pregnancy prior
N/Diarrhea/Dyspnea

287
Q

Cl Channel Activators

A

Activates CIC-2 to stimulate Cl secreation
Female >18y/o w/ IBS-C, CIC, OIC w/ non-CA R/o pregnancy prior
N/Diarrhea/Dyspnea

288
Q

Stimulant Laxatives

A

Misacodyl
Acts on nerves of colon
Constipation, pre-op prep in conjunctino w/ PEG solution

Castor Oil
Reduced to ricinoleic acid to stimulate peristalsis
Don’t use in pregnancy

Senna
Causes water/E+ secretion
Combo w/ Docusate for Constipation/OIC
Cramping, E+ disturbance

289
Q

What is a gluten free bulk laxative?

Which one can be used w/ Celiac Dz?

A

Wheat Dextrin

Synthetic fiber Methylcellulose`

290
Q

What can be used for antacid AND for laxative?

A

Magnesium Hydroxide

291
Q

What can be used for antacid AND for laxative?

A

Magnesium Hydroxide

292
Q

Contraindications for giving triptans?

A

Hx ischemic heart dz (angina, previous MI)
Uncontrolled HTN
CV dz (stroke)
Hemiplegic/Basilar migraine

293
Q

How many aura for PTs to Dx w/ migraine?

A

2 auras= Dx w/ migraine

294
Q

What is contained in Bismuth

A

Metronidazole

Tetracycline

295
Q

Use of Octerotide

A

HIV diarrhea

Tumor diarrhea

296
Q

Use of Octerotide

A

HIV diarrhea

Tumor diarrhea

297
Q

What are the adverse effects of using Cimetidine

A

Gynecomastia
Inhibits CYP 450
Competes w/ meds and creatinine for secretion

Dont give to PTs on several drugs

298
Q

What are the adverse effects of using Cimetidine

A

Gynecomastia
Inhibits CYP 450
Competes w/ meds and creatinine for secretion

Dont give to PTs on several drugs

299
Q

When to start Senna

Don’t give PT Meperidine if they’ve taken ? drug?

A

Long term prevention of OIC by causing water and E+ to secrete into bowel

MAOI

300
Q

When to start Senna

A

Long term prevention of OIC by causing water and E+ to secrete into bowel

301
Q

How quickly are pharmacologic initiated for initial gout treatment?

A

Within 24hrs

302
Q

Use of Lubiprostone

A

Stims Cl secretions into intestine for IBS-C females +18y/o
CIC
OIC w/ non CA pain

303
Q

How long should PTs that have been on long term opioids tapered off?

A

10%/wk or 5-20%/mon

Not addicted= 20-50%/wk

304
Q

What drug is used for life saving constipation and required FDA approval for use?

When is Alosetron use preferred?

A

Tegaserod

Female IBS-D

305
Q

What drugs can’t be taken while taking uricosuric agents?

How frequently can Naloxone be given?

A

Salicylates

Q2-5min

306
Q

What has Ondansetron use been popular with?

What is the first line choice for anti-diarrheal for acute diarrhea

A

Anti-emetic for peds w/ gastroenteritis
Adult/Post-op N/V

Loperamide

307
Q

Which XOI is more likely to achieve target uric acid levels when levels are <6mg/dl

What drug can be used for OIC and given SubQ?

A

Febuxostat

Methynaltrexone

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