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GI2 Final > Pharm > Flashcards

Pharm Flashcards

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
Q

Acute CINV=
Chronic CINV=
Anticipatory CINV=

A

Acute- NV <24hr after treatment
Chronic- NV >24hr after treatment
Anticipatory- NV before treatment

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26
Q

What is the strong emetogenic regmine for CINV?

A

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

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27
Q

What is the moderate emetogenic regime for CINV?

A

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

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28
Q

What is the weak emetogenic regime for CINV?

A

Dexamethazone or 5-HT3R or metoclopramide or prochlorperazine
Given prior to
Provide therapy for breakthrough/anticipatory NV

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29
Q

Explain the 3 stepped therapy for NVP?

A

1- B6 plus 5-HT3R or H1R antagonists
2- D2R antagonists
3- steroid or different D2R antagonists

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30
Q

What are antacids used for? what are the classes and the examples for each?

A

Short term relief of GERD/PUD symptoms
Low systemic (Al, Mg, Ca)
High systemic (Na)
Supplemental (simethicone- surfactant to aid in gas expulsion)

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31
Q

What is the MOA of antacids?

A

MOA- bind H and create H2O, CO2, Cl salts (do not dec gastric acid secretion/production); at high doses inc LES tone

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32
Q

What are the properties of antacids?

A

Mg and Ca- fast acting, long lasting, good neutralizer
Na- fast acting, short lasting, ok neutralizer
Al- slow acting, short lasting, bad neutralizer

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33
Q

What are the SE of the different antacids?

A

Al- constipation and hypophosphatemia
Ca- constipation, hypophosphatemia, hypercalcemia, kidney sttone
Mg- diarrhea and hypermagnesemia
Na- gas, hypernatremia, and metabolic alkalosis

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34
Q

What are the interactions w/ antacids aka how should you take them?

A

1-2 hr before other meds or 2-4 hr after taking other meds

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35
Q

What are the drug classes used as anti-ulcers? (5)

A

H2R antagonists, PPI, surface acting agents, PGE analog, and bismuth compounds

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36
Q

What are the H2R antagonists used for anti-ulcers (tidines-4)

A

Cimetidine, ranitidine, famotidine, nizatidine

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37
Q 
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
A 
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
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38
Q

What are the adverse effects of H2R blockers? What are the interactions and CI?

A

SE- nausea, constipation, diarrhea, HA, drowsy
Interactions- cimetidine inhibits lots of cyp450 enzymes; ranitidine inhibits fewer
CI- pregnancy; use ranitidine if necessary

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39
Q

What are the PPIs? (6-Prazole); what is the MOA

A

Omeprazole, esomeprazole, lansoprazole, dexlansoprazole, pantoprazole, and rabeprazole

MOA- irreversibly inhibit H-K ATPase on parietal cells by bind sulfhydryl group

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40
Q 
PPIs
How quickly do you see the effects
How fast do ulcers heal
How much gastric acid is prevented
What is the dosing frequency
A

See effects in a few days
Ulcers heal 4-8 weeks
Prevent majority (50-90%) gastric acid production
Take 1 a day

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41
Q

What are the adverse effects of PPI

What are the interactions and CI

A

SE- HA, dizzy, clostridium difficile assoc diarrhea (stop treatment immediately)
Interactions- omeprazole is cyp450 inhibitor
CI- pregnancy- use lansoprazole if necessary, never use omeprazole

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42
Q

What is the surface acting agent used to treat ulcers? What are its clinical uses?

A

Sucralfate

DU, apthous ulcers, radiation ulcers, bile reflux, and mucositis

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43
Q

What is the MOA of sucralfate? (2 major actions)

A

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

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44
Q

What are the SE of sucralfate? CI? What are the interactions aka how do you take it and how often?

A

SE- constipation due to Al
CI- renal dysfunction due to Al
Take 2 hr after other meds-4 times a day

45
Q

What is the PGE analog used to treat ulcers? what type of ulcer and what are the off label uses?

A

Misoprostol is used to treat NSAID induced ulcer

Off-label- pregnancy termination, cervical ripening, and treat postpartum hemorrhage

46
Q

What is misoprostols MOA

A

MOA- PGE analog that inc HCO3 and mucus production, mucosal blood flow, and dec gastric acid secretion- aka cytoprotection

47
Q

What are the SE and CI of misoprostol

A

SE- diarrhea, HA,dizzy

CI- pregnancy and IBD

48
Q

What are bismuth compounds activitys?

A

Anti-diarrheal
Anti-microbial- prevent H pylori from attaching to mucosa
Stim PG and mucosa production

49
Q

What are the uses of bismuth compounds? What are the drug interactions aka when do you take?

A

Heartburn, indigestion, diarrhea, treat H pylori

SE- constipation and dark black stools

interactions- take 2 hrs after other meds

50
Q

What are the CI and absolute CI for bismuth compounds

A

CI- anti-coagulants and renal dysfunction

Absolute CI- siacylate sensitivity (aspirin) or GI bleed

51
Q

Explain H pylori treatment:
Combo therapy
Triple therapy
Quad therapy

A

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
Q

Treating H pylori-
What if amoxicillin allergy?
R to metronidazole
R to clarithromycin

A

Amoxicillin allergy- use metronidazole
Metro R?- use tetra or quad of amoxy and clarithro
Clarithro R?- use tetra or amoxy

53
Q

What are the treatment classes for UC?

What are the treatment classes for CD?

A

UC- 5-ASA, corticosteroids, TNFa inhibitors, a4 integrin inhib
CD- Il-12/23 I, corticosteroid, TNFa inhibitor, a4 integrin inhib

54
Q

What are the 5-ASAs used for UC? (4-sala); what is their MOA

A

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
Q

What are the SE of 5-ASA? What are the CI?

A

SE- general neuro and GI SE (not as bad if you dont take sulfasalazine)

CI- ASA or sulfa allergy

56
Q

What are the therapeutic uses of the different 5-ASAs

A

Sulfasalazine/mesalamine- mild to mod UC- active/maintenance

Olsalazine- maintenance
Balsalazine- active

57
Q

What are the TNF-a inhibitors used for IBD? (4) MOA?

A

Adalimumab, infliximab, golimumab, certolizumab

MOA- neutralize TNFa signaling to prevent expression of pro-inflammatory genes

58
Q

What are the SE of TNFa inhibitors (5)

A

Infections- test for TB prior- stop if pt develops infection or sepsis

Liver dysfunction, arthralgia, headache, fatigue

59
Q

What are the therapeutic uses for the individual TNFa inhibitors; what is the dosing frequency/form

A

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
Q

What are the a4 integrin inhibitors used to treat IBD? (2) MOA

A

Natalizumab and vedolizumab

MOA- prevent cell adhesions, transmigration, and activation of immune cells

61
Q

What are the SE of a4 integrin inhibitors (specifically just one of them)

A

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
Q

What are the uses of the a4 integrin inhibitors? Dosing frequency/form

A

Natalizumab- mod to severe treatment R CD- IV every 4wk

Vedolizumab- mod to severe treatment R CD/UC- IV every 8wk

63
Q

What is the IL-12/23 inhibitor used to treat CD? MOA and therapeutic use

A

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
Q

What are the SE of ustekinumab (IL12-23 inhibitor for CD)

A

SE- infections-test for TB prior, infusion rxn, arthralgia, headache, fatigue

65
Q

Explain glucocorticosteroid use for IBD? When is it used? What is the dosing? MOA? SE?

A

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
Q

What are the 3 opioid agonists used to treat diarrhea?

A

Loperamide, diphenoxylate, eluxadoline

67
Q

Explain Loperamide MOA and SE

A

No analgesic properties
MOA- interfere w/ peristalsis via direct action on circular and longitudinal smooth m
SE- drowsy, dizzy, urinary retention

68
Q

Diphenoxylate properties, MOA, and SE

A

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
Q

Eluxadoline used for?
MOA
SE
CI

A

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
Q

Alosetron
MOA
Use
SE (including black box label)

A

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
Q

Crofelemer
MOA
Use
SE

A

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
Q

What are the 3 (4) anti-muscarinics used for IBS? What is the MOA and specific use of them? SE

A

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
Q

Linaclotide
Use
MOA
SE

A

Linaclotide- used for chronic idiopathic constipation and IBS-C

MOA- stim GCC to inc cGMP and stim CFTR

SE- GERD

74
Q

Lubiprostone
Use
MOA
SE

A

Lubiprostone- used for CIC, IBS-C, and opioid-induced C
MOA- stim CIC-2 Cl channel
SE- nausea, dyspepsia, dizzy

75
Q

What are the 2 opioid antagonists used to treat opioid induce constipation? MOA?

A

Methylnaltrexone and naloxegol

MOA- mu antagonists

76
Q 
What are the bulk forming agents (4)
MOA
When are effects seen
SE
Interactions aka when do you take
A

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
Q

What are the stool softeners (2)
MOA
How long to be effective
SE

A

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
Q 
What are the stimulants for constipation (5)
MOA
When effective?
SE (just one of the stimulants)
CI
Which is used for colonoscopy
A

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
Q

What are the 2 saline agents used for constipation
MOA
Interactions to pay attention to

A

Mg salt, and Na phosphate
MOA- inc osmotic pull
Interactions- diuretics, renal dysfunction, CHF, or HTN

80
Q

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

A

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
Q

What are the two general classes of drug treatments available for HBV infection?

A

IFNa and nucleoside/nucleotides

82
Q

What are the (3) IFNa treatments for HBV?

A

IFNa-2b, PEG IFNa-2a/b

83
Q

What are the pros and cons of IFNa treatments for HBV?

A

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
Q

What is the MOA of IFNa treatments

A

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
Q

Why can you not give IFNa to decompensated pt?

A

IFNa causes a transient inc in ALT leading to inflammation and fibrosis

86
Q

What are the pros of using nucleoside/nucleotide treatment for HBV? What is the MOA

A

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
Q

What causes resistance to nucleosides? Does it affect nucleotides?

A

Dec kinase activity (still responsive to nucleotides but can’t convert nucleosides to active form)

Mutant DNA polymerase

88
Q

What are the two nucleotides, which is preferred, and what is an adverse rxn? (Class- fovir)

A

Tenofovir (1st choice, given if resistance develops to nucleosides, but can cause proximal renal tubule toxicity)

Adefovir

89
Q

What are the 2 nucleosides, which is the preferred treatment and why, why is the other not used as often

A

Entecavir- 1st choice if pt has renal dysfunction

“Vudine”- resistance inc with use

90
Q

What HCV treatment is a nucleoside given w/ PEG-IFNa

A

PEG-IFNa and ribavirin- low cure rate, ribavirin is a nucleoside that potentiates the affects of PEG-IFNa

91
Q

What are the NS3 protease inhibitors used to treat HCV? How are they given?

A

“Previrs” are given either in combo with PEG-IFNa and ribavirin or in combo w/ ribavirin and sofobuvir

92
Q

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

A

NS5B- sofosbuvir, nucleotide inhibits viral replication, given in combo

NS5A-“asvirs”, inhibit viral assembly, often given in combo w/ PEG-IFNa and ribavirin

93
Q

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)

A

Gram positive, opportunistic, causes pseudomembranous colitis (toxin B), and diarrhea (toxin A)

Treat- remove causative antibiotic, give fluids, and give fecal transplant

94
Q

What are the 3 treatments for c diff and explain each and under what circumstances they are given

A

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
Q

Entemoeba histolytica (life cycle and invasion of host)

A

Trophozoite ->bicyst ->tetracyst
Trophozoite can invade mucosa (RBC in cytosol on stool sample)
Flask shaped ulcers-bloody diarrhea

96
Q

Explain the 2 part treatment of e histolytica

A

Eliminate trophozoite- metronidazole (primary choice) or tinidazole

Eliminate luminal organism- paromomycin (luminal amebocide)

97
Q

Giardia (life cycle, invasion, and major characteristic of disease)

A

Trophozoite -> cyst (does not invade mucosa-no bloody diarrhea)

Fatty, smelly, frothy diarrhea

98
Q

Explain the treatment for giardia; explain the second choice treatments MOA and special SE

A

Tinidazole (fist choice)

Nitazoxanide (inhibits oxidoreductase involved in nrg metabolism- cause bright yellow eyes and urine)

99
Q

Cryptosporidium

Life cycle and what the infections are commonly assoc w/

A

Cyst -> 4 sporozoites

Contaminated water, day care, travel, immunocompromised diarrhea

100
Q

Explain the 2 part treatment of cryptosporidum; what about if pt is immunocompromised

A

Anti-diarrheal such as loperamide
Anti-microbial- nitazoxanide (1st choice) or paromomycin
HIV- anti-retroviral and nitazoxanide

101
Q

N americanus and A duodenale
How they infect
S/S
Treatment (MOA and CI)

A

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
Q

Ascaris lumbricoides
General life cycle
S/S (2)
treatment

A

Contaminated food -> eggs in stool
Malnutrition and cramps
Albendazole or mebendazole

103
Q

Strongyloides sterc
general life cycle
S/s
Treatment/MOA/CI

A

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
Q

Trich
Life cycle
S/s (hey arnold)
Treatment

A

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
Q

Enterobius vermicularis
Special things about the infection
Eosinophilia?
Treatment 3 (include last ones MOA and CI)

A

Ingest eggs, itchy anus, scotch tape test
No eosinophilia
Albendazole, mebendazole, pyranfel (stim Ach, inhibit AchE, paralysis, CI w/ liver dysfunction)

106
Q 
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
A

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
Q

Taenia solium and sagigata
Food and how they invade
Special clinical feature of one of them
Treatment

A

Solium (pork-hooks) and sagigata (beef-suckers)
Solium is assoc w/ cysts in brain, seizure, meningitis, and hydrocephalus
Treat- albendazole and praziquantel

108
Q

Diphyll latum

A

Fresh water fish -> eggs and epiglottids in stool

Treat- niclosamide inhibits oxphos

109
Q

E granulosus

A

Hydatid cysts

Treatment- albendazole and praziquantel

GI2 Final (1 decks)

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