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Pharm Flashcards

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1
Q

What are the receptors targeted for NV?

A 
5-HT3 R antagonists
NK1 R antagonists
H1R antagonists
D2R antagonists
M1R antagonists
Cannabinoid R agonists
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2
Q

What are the 5-HT3R antagonists used for NV and what is their strength? (5) (remember the family name)

A

Dolasetron, granisetron, palonosetron, ondansetron, and alosetron (used for treatment R IBS-D exclusively)

Strong anti-emetic agents

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3
Q

What is the MOA of 5-HT3 R antagonists (setrons)

A

Block vagal n terminal 5-HT3R in CTZ (chemo trigger zone)

Block serotonin released from enterochromaffin cells from binding receptors

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4
Q

What are the clinical uses of 5-HT3R antagonists (setrons) and what are the major SE?

A

Uses- CINV, RINV, PONV, and NVP

SE- QT prolongation and torsade arrhythmias (for this reason dolasetron is not used as prophylaxis for CINV)

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5
Q

What are the kinetics of 5-HT3R (specifically at granisetron and palonosetron)

A

Setrons have short halflifes except for granisetron and palonosetron which have long half lives and are given as a single dose for delayed CINV

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6
Q

What are the drug interactions who have to pay attention to if you are using 5-HT3R antagonist (setrons)?

A

QT prolonging anti-arrhythmics

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7
Q

What are the NK1R antagonists used for NV? (4- think about family name)What is the strength?

A

Aprepitant, fosaprepitant, netupitant (given in combo w/ palonosetron), and rolapitant

Moderate anti-emetic agents

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8
Q

What is the MOA of NK1 R antagonists? (Pitants)

What are the therapeutic uses?

A

MOA- block NK1 (substance P) R in CZT, VC (vomit center), and vagal terminals in the gut

Uses- CINV (given in combo w/ glucocorticosteroids and setrons) and aprepitant and fosaprepitant are used as prophylaxis for PONV

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9
Q

What are the SE of NK1 R antagonists (pitants)? Think about dcd dfd

A

SE- dyspepsia, constipation, diarrhea, drowsy, fatigue, dizzy

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10
Q

What are the kinetics of NK1R antagonists and what drug interactions should you pay attention to?

A

Kinetics- netupitant and rolapitant have long half lives b/c they are metabolized into active compounds

Interactions- pitants are mild cyp450 inhibitors

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11
Q

What are the H1R antagonists used for NV? (7) what is their strength?

A

Diphenhydramine, dimenhydrinate, hydroxyzine, promethizine, meclizine, cyclizine, doxylamine (given w/ B6)

Weak anti-emetic agents

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12
Q

What is the MOA of H1R antagonists used for NV? What are their SE?

A

MOA- block H1R in VC and vestibular system and have anti-cholingergic effects in CTZ

SE- drowsy, dry mouth, constipation, urinary retention, blurred vision, and dec BP

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13
Q

What are the therapeutic uses of H1R antagonists? What are the kinetics of hydroxyzine and promethazine?

A

Uses- mild NV, PONV, motionsickness (dimenhydrinate, meclizine, cyclinzine), add ons for CINV and RINV

Hydroxyzine has long half life; promethazine has intermediate half life and low F (dec dose if switch from PO to IV)

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14
Q

What are the drug interactions to pay attention to for H1R antagonists?

A

Cumulative effect w/ other anti-cholinergic agents

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15
Q

What are the D2R antagonists used for NV? (4)What is their strength?

A

Phenothiazines- chlorpromazine, prochlorperazine, and perphenazine
Metoclopramide

Weak-mod anti-emetic agents

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16
Q

What is the MOA of D2R antagonists used for NV? What are the SE?

A

MOA- block D2R in CTZ w/ anticholinergic effects
Metaclopramide stim Ach activity in gut to inc GI motility and LES tone

SE- drowsy, dry mouth, constipation, urinary retention, blurred vision, dec BP, (arrhythmia and extra-pyramidal SE at high doses)

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17
Q

What is the kinetics of prochlorperazine?

What are the interactions to watch for w/ D2R antagonists?

A

Prochlorperazine has low F (dec dose if PO to IV)

Cumulative effect w/ other anti-cholinergic agents and QT prolonging anti-arrhythmic

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18
Q

What is the M1R antagonists used for NV? (1) What is its strength and clinical uses

A

Scopalamine

Weak anti-emetic used exclusively for motion sickness

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19
Q

What are the clinical uses of D2R antagonists?

A

Mild NV, diabetic gastroparesis (metoclopramide), add on for CINV, RINV, and PONV

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20
Q

What is the MOA of M1R antagonists? What are the SE? What are the interactions to pay attention to?

A

MOA- block Ach from stim MR between vestibular nuclei and brainstem and between RF and VC
SE- drowsy, dry mouth, constipation, urinary retention, blurred vision
Interactions- cumulative effect w/ other anticholinergics

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21
Q

What are the cannabinoids used for NV? (2)What is their strength and clinical uses

A

Dronabinol and nabilone

Strong-antiemetics used exclusively for treatment resistant CINV and for appetite stimulation

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22
Q

What is the MOA of cannabinoids for NV?

A

MOA- stim central CB1 and peripheral CB2 in VC and CTZ to inc signal transduction via GPCR to dec neuron excitability and dec serotonin release

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23
Q

What are the adverse effects of cannabinoids? What are the interactions to pay attention to?

A

SE- euphoria, irritation, vertigo, sedation, impaired cognition, altered perception, inc HR/BP, dry mouth, and hunger

Interactions- CNS depressants, CV agents, and sympathomimetics

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24
Q

What are the kinetics of cannabinoids?

A

Dronabinol is metabolized into one active compound
Nabilone is metabolized into many active compounds

Both are fast acting and long lasting

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25
Acute CINV= Chronic CINV= Anticipatory CINV=
Acute- NV <24hr after treatment Chronic- NV >24hr after treatment Anticipatory- NV before treatment
26
What is the strong emetogenic regmine for CINV?
3 drugs- 5-HT3R and NK1 antagonists w/ dexamethasone (corticosteroid) Given prior to and for 3 days after If not effective, add cannabinoid Provide therapy for breakthrough/anticipatory NV
27
What is the moderate emetogenic regime for CINV?
2 drugs- 5-HT3R antagonist and dexamethazone (corticosteroid) Given prior to and for 2 days after If not effective add NK1 R antagonist then cannabinoid Provide therapy for breakthrough/anticipatory NV
28
What is the weak emetogenic regime for CINV?
Dexamethazone or 5-HT3R or metoclopramide or prochlorperazine Given prior to Provide therapy for breakthrough/anticipatory NV
29
Explain the 3 stepped therapy for NVP?
1- B6 plus 5-HT3R or H1R antagonists 2- D2R antagonists 3- steroid or different D2R antagonists
30
What are antacids used for? what are the classes and the examples for each?
Short term relief of GERD/PUD symptoms Low systemic (Al, Mg, Ca) High systemic (Na) Supplemental (simethicone- surfactant to aid in gas expulsion)
31
What is the MOA of antacids?
MOA- bind H and create H2O, CO2, Cl salts (do not dec gastric acid secretion/production); at high doses inc LES tone
32
What are the properties of antacids?
Mg and Ca- fast acting, long lasting, good neutralizer Na- fast acting, short lasting, ok neutralizer Al- slow acting, short lasting, bad neutralizer
33
What are the SE of the different antacids?
Al- constipation and hypophosphatemia Ca- constipation, hypophosphatemia, hypercalcemia, kidney sttone Mg- diarrhea and hypermagnesemia Na- gas, hypernatremia, and metabolic alkalosis
34
What are the interactions w/ antacids aka how should you take them?
1-2 hr before other meds or 2-4 hr after taking other meds
35
What are the drug classes used as anti-ulcers? (5)
H2R antagonists, PPI, surface acting agents, PGE analog, and bismuth compounds
36
What are the H2R antagonists used for anti-ulcers (tidines-4)
Cimetidine, ranitidine, famotidine, nizatidine
37
``` What is the MOA of H2R antagonists? What fast do you see the effects How fast do ulcers heal How much gastric acid production does it stop How often do you take ```
``` MOA- block H2R on parietal cells Prompt onset and relief of symptoms Ulcers heal in 4-8 weeks Moderately dec (20-50%) gastric acid production Take 1 or 2 a day ```
38
What are the adverse effects of H2R blockers? What are the interactions and CI?
SE- nausea, constipation, diarrhea, HA, drowsy Interactions- cimetidine inhibits lots of cyp450 enzymes; ranitidine inhibits fewer CI- pregnancy; use ranitidine if necessary
39
What are the PPIs? (6-Prazole); what is the MOA
Omeprazole, esomeprazole, lansoprazole, dexlansoprazole, pantoprazole, and rabeprazole MOA- irreversibly inhibit H-K ATPase on parietal cells by bind sulfhydryl group
40
``` PPIs How quickly do you see the effects How fast do ulcers heal How much gastric acid is prevented What is the dosing frequency ```
See effects in a few days Ulcers heal 4-8 weeks Prevent majority (50-90%) gastric acid production Take 1 a day
41
What are the adverse effects of PPI | What are the interactions and CI
SE- HA, dizzy, clostridium difficile assoc diarrhea (stop treatment immediately) Interactions- omeprazole is cyp450 inhibitor CI- pregnancy- use lansoprazole if necessary, never use omeprazole
42
What is the surface acting agent used to treat ulcers? What are its clinical uses?
Sucralfate DU, apthous ulcers, radiation ulcers, bile reflux, and mucositis
43
What is the MOA of sucralfate? (2 major actions)
MOA- forms adhesive polymer that adheres to mucosal epi and covers ulcer preventing acid from entering; involved in cytoprotection by inc mucus and PG production
44
What are the SE of sucralfate? CI? What are the interactions aka how do you take it and how often?
SE- constipation due to Al CI- renal dysfunction due to Al Take 2 hr after other meds-4 times a day
45
What is the PGE analog used to treat ulcers? what type of ulcer and what are the off label uses?
Misoprostol is used to treat NSAID induced ulcer | Off-label- pregnancy termination, cervical ripening, and treat postpartum hemorrhage
46
What is misoprostols MOA
MOA- PGE analog that inc HCO3 and mucus production, mucosal blood flow, and dec gastric acid secretion- aka cytoprotection
47
What are the SE and CI of misoprostol
SE- diarrhea, HA,dizzy | CI- pregnancy and IBD
48
What are bismuth compounds activitys?
Anti-diarrheal Anti-microbial- prevent H pylori from attaching to mucosa Stim PG and mucosa production
49
What are the uses of bismuth compounds? What are the drug interactions aka when do you take?
Heartburn, indigestion, diarrhea, treat H pylori SE- constipation and dark black stools interactions- take 2 hrs after other meds
50
What are the CI and absolute CI for bismuth compounds
CI- anti-coagulants and renal dysfunction | Absolute CI- siacylate sensitivity (aspirin) or GI bleed
51
Explain H pylori treatment: Combo therapy Triple therapy Quad therapy
Combo- always take 2 antibiotics and a HCl inhibitor Triple (14 days BID)- PPI + clarithromycin + amoxycilin/metronidazole Quad (10-14 days)- PPI (BID) + tetracycline + metronidazole + bismuth compound (rest QID) Continue PPI after therapy until ulcers heal
52
Treating H pylori- What if amoxicillin allergy? R to metronidazole R to clarithromycin
Amoxicillin allergy- use metronidazole Metro R?- use tetra or quad of amoxy and clarithro Clarithro R?- use tetra or amoxy
53
What are the treatment classes for UC? | What are the treatment classes for CD?
UC- 5-ASA, corticosteroids, TNFa inhibitors, a4 integrin inhib CD- Il-12/23 I, corticosteroid, TNFa inhibitor, a4 integrin inhib
54
What are the 5-ASAs used for UC? (4-sala); what is their MOA
Sulfasalazine, mesalamine, olsalazine, balsalazine MOA- inhibit COX and LIPOX to dec PG and leukotriene production; dec PMN and macrophage chemotaxis by inhibiting NFKB pathway
55
What are the SE of 5-ASA? What are the CI?
SE- general neuro and GI SE (not as bad if you dont take sulfasalazine) CI- ASA or sulfa allergy
56
What are the therapeutic uses of the different 5-ASAs
Sulfasalazine/mesalamine- mild to mod UC- active/maintenance Olsalazine- maintenance Balsalazine- active
57
What are the TNF-a inhibitors used for IBD? (4) MOA?
Adalimumab, infliximab, golimumab, certolizumab MOA- neutralize TNFa signaling to prevent expression of pro-inflammatory genes
58
What are the SE of TNFa inhibitors (5)
Infections- test for TB prior- stop if pt develops infection or sepsis Liver dysfunction, arthralgia, headache, fatigue
59
What are the therapeutic uses for the individual TNFa inhibitors; what is the dosing frequency/form
Adalimumab- mod to severe UC/CD- SQ every other week Infliximab- mod to severe UC/CD- IV every 8 wks Golimumab- mod to severe UC- SQ every 4 wks Certolizumab- mod to severe CD- SQ every 4 wks
60
What are the a4 integrin inhibitors used to treat IBD? (2) MOA
Natalizumab and vedolizumab MOA- prevent cell adhesions, transmigration, and activation of immune cells
61
What are the SE of a4 integrin inhibitors (specifically just one of them)
Natalizumab is assoc w/ JCV infections -> progressive multifocal leukoencephalopathy (inc risk of if med for 2 years, have history of immunosuppressant use, or if anti-JCV Ab)
62
What are the uses of the a4 integrin inhibitors? Dosing frequency/form
Natalizumab- mod to severe treatment R CD- IV every 4wk | Vedolizumab- mod to severe treatment R CD/UC- IV every 8wk
63
What is the IL-12/23 inhibitor used to treat CD? MOA and therapeutic use
Ustekinumab MOA- inhibit IL-12/23 R- prevent TH1/TH17 differentiation Uses- mod to severe treatment resistant CD (active IV, maintenance SQ every 8wk)
64
What are the SE of ustekinumab (IL12-23 inhibitor for CD)
SE- infections-test for TB prior, infusion rxn, arthralgia, headache, fatigue
65
Explain glucocorticosteroid use for IBD? When is it used? What is the dosing? MOA? SE?
Used to treat active severe acute IBD uncontrolled by other therapies; give smallest dose for shortest period of time MOA- bind cytoplasmic R to dec leukocyte infiltration, humoral suppression, and intefere w/ inflammatory mediators SE- inc BP, lipids, glucose, fluid retention (monitor Na and K for renal or heart failure), bone/psychiatric/GI defects
66
What are the 3 opioid agonists used to treat diarrhea?
Loperamide, diphenoxylate, eluxadoline
67
Explain Loperamide MOA and SE
No analgesic properties MOA- interfere w/ peristalsis via direct action on circular and longitudinal smooth m SE- drowsy, dizzy, urinary retention
68
Diphenoxylate properties, MOA, and SE
Analgesic properties at high dose- mixed w/ atropine to prevent OD and abuse MOA- acts on GI smooth m cells to dec GI motility SE- more prominent drowsy, dizzy, and urinary retention
69
Eluxadoline used for? MOA SE CI
Used for IBS-D MOA- mu and kappa agonists- slow peristalsis MOA- delta antagonist- dec stomach, pancreatic, and GB secretions SE- liver and pancreatic toxicity, pancreatitis if pt lacks GB CI- biliary obstruction, sphincter of oddi obstruction, liver/pancreatic dysfunction, and alcoholics
70
Alosetron MOA Use SE (including black box label)
MOA- 5-HT3R antagonist Use- chronic severe treatment resistant IBS-D SE- constipation, GERD, and ischemic colitis (blackbox- doc must take IBS training, enroll in Rx program, pt must have followup before refill, and doc/pt must sign statement to adhere to treatment plan)
71
Crofelemer MOA Use SE
MOA- inhibit cAMP from opening CFTR and Ca from stim CaCC (Cl channel inhibitor) Use- non-infectious diarrhea in immunocompromised pt SE- URI and inc ALT/AST/bilirubin
72
What are the 3 (4) anti-muscarinics used for IBS? What is the MOA and specific use of them? SE
Hyoscyamine, dicyclomine, clidinium/chlordiazepoxide MOA- inhibit post-synaptic MR in GI to dec GI motility/spasms assoc w/ IBS SE- drowsy, dry mouth, constipation, urinary retention, and blurred vision
73
Linaclotide Use MOA SE
Linaclotide- used for chronic idiopathic constipation and IBS-C MOA- stim GCC to inc cGMP and stim CFTR SE- GERD
74
Lubiprostone Use MOA SE
Lubiprostone- used for CIC, IBS-C, and opioid-induced C MOA- stim CIC-2 Cl channel SE- nausea, dyspepsia, dizzy
75
What are the 2 opioid antagonists used to treat opioid induce constipation? MOA?
Methylnaltrexone and naloxegol | MOA- mu antagonists
76
``` What are the bulk forming agents (4) MOA When are effects seen SE Interactions aka when do you take ```
Dietary fiber, psyllium, cellulose, and polycarbophil MOA- inc bulk vol and water vol to stim GI motility Effective in 2 days SE- bloating Take 2 hr after other meds
77
What are the stool softeners (2) MOA How long to be effective SE
Docusate and mineral oil MOA- surfactates that lubricate feces, inc GI secretion, and directly soften the stools Effective in 1-3 days SE- bloating and gas
78
``` What are the stimulants for constipation (5) MOA When effective? SE (just one of the stimulants) CI Which is used for colonoscopy ```
Senna, bisacodyl, castor oil, glycerol, and picosulfate MOA- stim peristalsis via irritation by inhibiting NaK ATPase and inc PG production Effective in 12-36 hr SE- senna (discolored urine) CI- GI obstruction Picosulfate is used pre colonoscopy
79
What are the 2 saline agents used for constipation MOA Interactions to pay attention to
Mg salt, and Na phosphate MOA- inc osmotic pull Interactions- diuretics, renal dysfunction, CHF, or HTN
80
What are the osmotic agents (3) MOA When to they take effect What is special about the last one and how fast does it work
Lactulose and sorbitol MOA- inc GI fluid secretion Effects in 1-2 days PEG3350 (polyethylene glycol) used for surgery and colonscopy-effects in 1-3 hr
81
What are the two general classes of drug treatments available for HBV infection?
IFNa and nucleoside/nucleotides
82
What are the (3) IFNa treatments for HBV?
IFNa-2b, PEG IFNa-2a/b
83
What are the pros and cons of IFNa treatments for HBV?
Pros- short course, effective, rare to develop R, dec HBV DNA and HBeAg Cons- parenteral, expensive, SE are very common, and can not give to decompensated pt
84
What is the MOA of IFNa treatments
IFNa binds R, activates JAK and TYK, phosphorylate R, recruit phosphorylate and activate STAT, STAT translocates to nucleus and results in transcription/translation of ISGs ISGs inhibit viral protein synthesis and replication
85
Why can you not give IFNa to decompensated pt?
IFNa causes a transient inc in ALT leading to inflammation and fibrosis
86
What are the pros of using nucleoside/nucleotide treatment for HBV? What is the MOA
Better tolerated, better response, and can give to decomp pt MOA- encode NRTI (reverse transcriptase inhibitor) that prevents viral replication; nucleosides must be converted to nucleotides by kinases to become active compounds
87
What causes resistance to nucleosides? Does it affect nucleotides?
Dec kinase activity (still responsive to nucleotides but can't convert nucleosides to active form) Mutant DNA polymerase
88
What are the two nucleotides, which is preferred, and what is an adverse rxn? (Class- fovir)
Tenofovir (1st choice, given if resistance develops to nucleosides, but can cause proximal renal tubule toxicity) Adefovir
89
What are the 2 nucleosides, which is the preferred treatment and why, why is the other not used as often
Entecavir- 1st choice if pt has renal dysfunction "Vudine"- resistance inc with use
90
What HCV treatment is a nucleoside given w/ PEG-IFNa
PEG-IFNa and ribavirin- low cure rate, ribavirin is a nucleoside that potentiates the affects of PEG-IFNa
91
What are the NS3 protease inhibitors used to treat HCV? How are they given?
"Previrs" are given either in combo with PEG-IFNa and ribavirin or in combo w/ ribavirin and sofobuvir
92
What is the NS5B inhibitor used to treat HCV? What is general MOA? What are the NS5A inhibitors used to treat HCV? General MOA and how they are given
NS5B- sofosbuvir, nucleotide inhibits viral replication, given in combo NS5A-"asvirs", inhibit viral assembly, often given in combo w/ PEG-IFNa and ribavirin
93
Explain Clostridium difficile (gram stain, when it infects, what it causes, and via what toxins) what are the general treatments given (do not include the meds given)
Gram positive, opportunistic, causes pseudomembranous colitis (toxin B), and diarrhea (toxin A) Treat- remove causative antibiotic, give fluids, and give fecal transplant
94
What are the 3 treatments for c diff and explain each and under what circumstances they are given
Vancomycin- for severe c diff, inhibits CW, PO, can cause red man syndrome Metronadizole- for mild c diff or if pt cant take oral vancomycin, incorps toxic metabolites into bacterial genome, IV, can cause peripheral neuropathy/metallic taste/disulfiram rxn Fidaxomicin- recurrent c diff, spares normal flora, targets sigma unit of RNA poly, given orally
95
Entemoeba histolytica (life cycle and invasion of host)
Trophozoite ->bicyst ->tetracyst Trophozoite can invade mucosa (RBC in cytosol on stool sample) Flask shaped ulcers-bloody diarrhea
96
Explain the 2 part treatment of e histolytica
Eliminate trophozoite- metronidazole (primary choice) or tinidazole Eliminate luminal organism- paromomycin (luminal amebocide)
97
Giardia (life cycle, invasion, and major characteristic of disease)
Trophozoite -> cyst (does not invade mucosa-no bloody diarrhea) Fatty, smelly, frothy diarrhea
98
Explain the treatment for giardia; explain the second choice treatments MOA and special SE
Tinidazole (fist choice) | Nitazoxanide (inhibits oxidoreductase involved in nrg metabolism- cause bright yellow eyes and urine)
99
Cryptosporidium | Life cycle and what the infections are commonly assoc w/
Cyst -> 4 sporozoites | Contaminated water, day care, travel, immunocompromised diarrhea
100
Explain the 2 part treatment of cryptosporidum; what about if pt is immunocompromised
Anti-diarrheal such as loperamide Anti-microbial- nitazoxanide (1st choice) or paromomycin HIV- anti-retroviral and nitazoxanide
101
N americanus and A duodenale How they infect S/S Treatment (MOA and CI)
Penetrate skin -> eggs in stool Diarrhea, abdominal pain, wt loss, iron deficient anemia, and intense itchiness at site of penetration Treatment- albendazole/mebendazole (inhibit microtubule synthesis leading to paralysis, 1st pass effect, CI in pregnancy or cirrhosis)
102
Ascaris lumbricoides General life cycle S/S (2) treatment
Contaminated food -> eggs in stool Malnutrition and cramps Albendazole or mebendazole
103
Strongyloides sterc general life cycle S/s Treatment/MOA/CI
Penetrate skin-> larvae in stool Diarrhea, abdominal pain, wt loss, anemia, itchiness, eosinophilia, lung involvement, autoinfection if on immunosuppressant like prednisone (asthma) Treatment- ivermectin (gaba enhancer leads to paralysis, CI if pregnant or on other gaba enhancer)
104
Trich Life cycle S/s (hey arnold) Treatment
Eggs in food -> lay 100s of eggs but no larvae no invasion, eosinophilia, lung involvment, or autoinfection Diarrhea w/ football shaped eggs Treat- mebendazole
105
Enterobius vermicularis Special things about the infection Eosinophilia? Treatment 3 (include last ones MOA and CI)
Ingest eggs, itchy anus, scotch tape test No eosinophilia Albendazole, mebendazole, pyranfel (stim Ach, inhibit AchE, paralysis, CI w/ liver dysfunction)
106
``` Schistosoma blood fluke How it invades and where it is found How it evades host immune system 3 steps of disease Diagnosis- where are eggs and what clinical feature Treat- MOA, immune response, CI ```
Eggs found in fresh water (where they hatch), enter venous sytem via open wound No immune response due to molecular mimicry Dermatitis -> katayama fever -> chronic fibrosis Eggs in stool/urine and eosinophilia Treatment- praziquantel (Ca influx and paralysis, causes an immune response due to the dead fluke, CI in pregnancy
107
Taenia solium and sagigata Food and how they invade Special clinical feature of one of them Treatment
Solium (pork-hooks) and sagigata (beef-suckers) Solium is assoc w/ cysts in brain, seizure, meningitis, and hydrocephalus Treat- albendazole and praziquantel
108
Diphyll latum
Fresh water fish -> eggs and epiglottids in stool | Treat- niclosamide inhibits oxphos
109
E granulosus
Hydatid cysts | Treatment- albendazole and praziquantel

GI2 Final (1 decks)

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