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Block 4a: GI > Week 3: Celiac Disease, GI Infections, & snow day GI drugs! > Flashcards

Week 3: Celiac Disease, GI Infections, & snow day GI drugs! Flashcards

1
Q

What is the drug class that can be both a laxative and an anti-diarrheal?

A

Bulk Forming

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2
Q

What is the MOA of bulk forming drugs?
What 2 classes of GI drugs can they fall under?

A

*Mechanical Laxative or Anti-Diarrheal*

Absorbs H2O and forms gels in intestine that can either induce peristalsis or slow passage through intestine

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3
Q

What are contraindications of bulk forming drugs (though these are also shared by many laxatives)?

A

GI obstruction, perforation, gastric retention, undiagnosed abdominal pain, vomiting, signs of appendicitis, toxic colitis, ileus, megacolon

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4
Q

What interactions can bulk forming drugs have?

A

Impact absorption of other drugs (requiring separate administration by at least 1 hour)

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5
Q

What are some other considerations w/ bulk forming agents as laxatives?

A

As unmetabolized plant fibers, avoid giving to patients w/ difficulty swallowing

severely slow colon

diverticulitis

watch Na [CHF]/ K [kidney failure]/Aspartame content

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6
Q

What are 2 ex’s of bulk forming laxatives that can also be anti-diarrheals?

A

Psyllium “silly plant” *swipes leaf*

Carboxymethycellulose

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7
Q

What is the class & indications of osmotic laxatives?

A

*Mechanical Laxatives*
Constipation

Colon prep for GI procedures

Toxin Removal

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8
Q

In addition to the usual contraindications of laxatives, what are some that are unique to osmotic laxatives?

What is a major AE?

A

UC

Diverticulitis

Colostomy/Ileotomy

Renal Insufficiency

Heart Block

Rectal Bleeding

AE: electrolyte abnormalities

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9
Q

What are 2 possible interactions for osmotic laxatives?

A

1) Link between oral sodium phosphates (OSP) & acute phosphate nephropathy, also to be avoided in kidney disease or decreased renal function; caution in patients taking diuretics, ACE I, ARB, NSAIDs
2) Drugs given before colon prep can be flushed out before they’re absorbed

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10
Q

What are some examples of osmotic laxatives? What are some significant AE’s w/ 1 in particular?

A

Magnesium Hydroxide: (-) ↓ ab absorption
(-) early release of enteric coated drugs

Magnesium Citrate, Sodium Phosphates, Polyethylene Glycol & Electrolytes, Lactulose, Sorbitol, Glycerin

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11
Q 
What is the MOA & drug class of *Surfactant*?
When is it indicated?
A

*Mechanical Laxative*

MOA: anionic detergent, stool softener

Indication: Hemorrhoids*

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12
Q

When is surfactant contraindicated?

A

Fecal impaction, obstruction, acute surgical abdomen
(X) mineral oil toxicity: w/ Lubricant

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13
Q

What is something to consider with Surfactant?

A

NOT useful once constipation has occured

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14
Q

What are some ex’s of Surfactants?

A

Detergents: docusate diocytyl
sodium sulfoceinate [Ca] [K]

*Docusate: weak contact laxative*

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15
Q

What is the class & MOA of Lubricants?

When is it indicated?

A

*Mechanical Laxative*

MOA: penetrates feces for easier passage, prevents H2O absorption

Fecal impaction [CI w/ Surfactant], post MI, surgery, partum

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16
Q

What are 2 things that can result from chronic use of Lubricants?

A

1) Malabsorption of fat soluble minerals
2) Chronic intestinal hypomotility

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17
Q

What is the class & MOA of stimulant/irritant/contact laxatives?

A

*Mechanical Laxative*

MOA: irritant effects on enterocytes, enteric neurons & muscle; cause H2O & electrolyte accumulation & stimulate intestinal motility via pathways (Prostaglandin, cAMP, NO, cGMP, inhibition of Na, K-ATPase)

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18
Q

What are stimulant laxatives contraindicated & 2 other considerations?

A

CI: Rectal bleeding; N/V, Acute Abdomen, Bowel Obstruction, Appendicitis, Gastroenteritis

*Not for chronic use

*Do not chew enteric coated tablets

*All prodrugs must be metabolized in stomach into active forms

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19
Q

What are the AE’s of stimulant laxatives?

A

Senna: Melanosis Coli,
Castor Oil & Diphenylmethanes: mucosal damage
Cathartic Colon, Cramps, Severe diarrhea, Dependency

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20
Q

What are some ex’s of stimulant laxatives?

A

Anthraquinones: Cascara Sagrada, Senna/Sennosides, Cassia Plant, Aloe, Castor Oil, Diphenylmethane, Bisacodyl

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21
Q

What is the class, MOA & PK of Methylnaltrexone & Alvimopan?

A

*Receptor Mediated Laxatives*

MOA: opioid receptor antagonist

PK: slow dissociation from receptor
higher affinity for peripheral receptors
poor systemic availability
metabolized by intestinal flora, not hepatic P450

Substrate for P Glycoprotein

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22
Q

What are the receptors affected in receptor mediated laxatives?

A

Mu opioid receptors

ClC-2 Cl Channels

Guanylate Cyclase (GC-C) Receptors

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23
Q

When are the opioid anatagonists (receptor mediated laxatives) Methylnaltrexone & Alvimopan indicated?

When are they contraindicated?

A

Post-op ileus
Short-term in hospital use (X >15 doses post op)

CI: therapeutic doses of opioids used for >7 consecutive days

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24
Q

When are the AE’s & interactions that opioid anatagonists (receptor mediated laxatives) Methylnaltrexone & Alvimopan can have?

A

AE: Dyspepsia, Hypokalemia, Urinary Retention

Interactions: Drugs that inhibit P Glycoprotein

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25
What is the class & MOA of **Lubiprostone**?
\*Receptor mediated Laxative\* MOA: Agonist at GI ClC-2 Cl channels, activates channels in apical membrane of intestine leading to incr production of Cl-rich intestinal fluids w/o affecting serum Na+ or K+ levels Essentially an osmotic laxative PG derivative
26
What is the PK of Lubiprostone?
Poor systemic absorption (plasma serum levels not even detectable w/ therapeutic doses)
27
What are 2 unique considerations of Lubiprostone?
No restriction on length use No evidence of tolerance, dependence, or rebound effects
28
What is a shared indication among the receptor mediated laxative drugs: **Lubriprostone**, **Linaclotide** & **Plecanatide**?
Chronic idiopathic constipation IBS w/ constipation \*Lubiprostone: fems 18+ y/o\*
29
What is a CI shared by **Lubiprostone** & **Linaclotide**?
CI: known or suspected mechanical GI obstruction
30
Does Lubiprostone have drug interactions?
No, based on structure, protein binding, in vivo studies
31
What is the shared MOA of **Linaclotide & Plecanatide**?
MOA: 14 aa (L) and 16 aa oligopeptide (P) GC-C receptor agonists that increases cGMP levs PK: acts locally, once daily dosing
32
What is **Linaclotide**'s boxed warning? How does it compare w/ **Plecanatide**'s CI?
Both share extreme dehydration L: avoid in patients 6-17 y/o (up to 6 yrs) P: avoid in \<6 y/o
33
Does **Linaclotide** have drug interactions? What is a unique consideration?\*
No bc neither drug nor metabolite occurs at measurable levs No interaction via P450/P Glycoprotein \*Anti-hyperalgesic; more SN to pain, reducing IBS GI discomfort
34
What are 3 "other" anti-diarrheal drugs? What is the MOA & Indications for the plant-derived one?
1) GI Serotonin (5-HT4) Receptor agonists (though, not used for general diarrhea Tx) 2) Anticholinergics 3) **Crofelemer**: plant derivative 'goalie "fell" & subsequently blocked Cl ' MOA: blocks _CFTR_ & _A**noc**tamin I_, & thereby Cl currents "it k**noc**ked him hard" Indication: Non-infectious diarrhea in adult HIV/AIDs patient
35
Give an ex of an anti-diarrheal bulk forming drug
Kaolin-Pectin
36
When are narcotic analogues (ie: opiate agonists) vs. diarrhea contraindicated?
Infectious diarrhea: E Coli, Salmonella, Shigella
37
What are 2 AE's and 3 possible interactions that narcotic analogues can have?
AE: 1) Constipation 2) Toxic Megacolon CI's: 1) Other anticholinergic drugs (ie: Atropine) 2) Sedative drugs 3) Monoamine Oxidase Inhibitors (MAO Inhibitors) "No MAO"
38
What are ex's of narcotic analogues?
Phenylpiperidine analgesic analogues Loperamide Diphenyloxylate-Atropine
39
What is the MOA of non-specific anti-diarrheals? When are they indicated?
MOA: may bind bacterial toxins anti-secretory effects, non-SP anti-inflammatory effects Traveller's Diarrhea: ETEC-non-inflammatory gastroenteritis
40
When are non-specific anti-diarrheals CI & what are their AE's?
CI: Hypersensitive to ASA/salicylates Not for \<16 y/o w/ viral infections (Reye's Syndrome: progressive encephalopathy) Chronic use in renal failure patients AE: Temporary black tongue & stools, salicylate toxicity at high doses
41
What interactions can non-specific anti-diarrheals have? What is one consideration & ex?
W/ tetracyclines & other salicylates (additive effects) Consider if tablets used: ensure they are chewed! Ex: Bismuth **_Sub_**salicylate "under the radar and non-SP"
42
What is the class, MOA and indications for Bile Acid Binders?
\*Anti-diarrheal\* MOA: binds bile acids, anion exchange resins Indications: Secretory Diarrhea & Post-Op
43
What are the CI's, AE's, and interactions of Bile Acid Binders?
CI: Pts sensitive to constipation bc AE: constipation and bloating Interactions: can bind other drugs (req sep admin times) & interferes w/ some dx tests
44
What are 3 ex's of Bile Acid Binders? Which is not absorbed or metabolized, leading to fewer drug interactions?
1) Cholestyramine 2) Colestipol 3) Colesevelam\*
45
What is the MOA and indications for the anti-diarrheal anti-secretory agents?
MOA: Somatostatin receptors; hyperpolarizes gut neurons, decreases Ach and slows peristalsis Indications: AIDS-related diarrhea Refractory endocrine tumor related diarrhea
46
What are the AE's and interactions of anti-secretory agents? Give an ex:
AE: gallbladder stasis, inhibition of pancreatic secretions Interacts w/ Cyclosporine Ex: **Octreotide**: somatostatin analogue, w/ a longer T1/2 is more potent at inhibiting gastric & pancreatic secretions
47
How are antacids viewed in treating peptic disorders?
Largely replaced by H2 receptor blockers & PPI's But they are inexpensive & widely used for self-Tx
48
Describe the rates of reaction for the various metal hydroxides in antacids
Al: slow Mg: slow/moderate Na & Ca bicarbonates: fast
49
What are two examples of non-acid neutralizing compounds?
1) Simethicone (gas sx) 2) Alginic acid
50
How do tablet vs. liquid antacid formulas compare?
Tablets neutralize less acid/dose & have a longer onset of action than Liqs
51
Describe the CI's, AE's, and interactions of antacids
CI: renal function AE: minimal (constipation/diarrhea) Many interactions
52
What is the MOA & PK of topical mucosal protectants?
MOA: Complexes w/ protein exudates at ulcer sites, acting as protecting barrier PK: minimal absorption w/ minor AE's
53
What are the interactions & CI's of topical mucosal protectants?
Interactions: may bind to other medications, so reqs separate doses CI: renal failure; do not give w/ antacids, H2 blockers, PPI's
54
What is an example of a non-specific anti-diarrheal with mucosal protective properties?
Bismuth subsalicylate
55
What is the MOA & indications of systemic mucosal protectants?
MOA: As PG E1 analogue, inhibits gastric acid secretions and promotes mucosal protective properties Indications: prevent NSAID induced gastric ulcers
56
What are the drug interactions and CI's of systemic mucosal protectants?
Interactions: NO effect on P450 system (despite hepatic metabolism), aspirin or NSAID PK CI's: **Pregnancy Category X**; miscarriages possible bc of induced labor
57
What is an ex of a systemic mucosal protectant?
Misoprostol
58
Compare and contrast the presentations, GI areas affected and treatments of invasive & non-invasive gastroenteritis
Invasive: fever, bloody diarrhea [dysentery], fecal leukocytes present, involves colon more involved Tx Non-invasive: non-inflammatory, toxin producing, usually watery diarrhea, affects upper GI; self-limiting
59
What is the #1 cause of gastroenteritis in the US?
Norovirus
60
What is an ex of an agent that can induce non-inflammatory gastroenteritis & cause villus blunting on histology? Why is there a 30% secondary attack rate for contacts?
Norovirus: "winter vomiting disease" Many genotypes, high recurrence
61
What is an agent that can induce non-inflammatory gastroenteritis but can still cause fever?
Rotavirus
62
Describe the sources of these agents that can cause non-inflammatory gastroenteritis: a) Staph Aureus b) Bacillus Cereus: 2 forms c) Clostridium Perfringens d) Entertoxigenic E Coli
a) Food: ham, potato salad, cream filled pastries b) Emetic form: contaminated fried rice Diarrheal form: meat & vegs c) Catered evts w/ reheated food d) Food & H2O
63
Why is Clostridium Perfringens' toxin unique compared to that of other non-inflammatory gastroenteritis agents?
Clostridium Perfringen's entertoxin is released from the organism during sporulation in small intestine, whereas Staph Aureus' toxin is preformed & Bacillus Cereus' entertoxin is also preformed
64
What condition is Entertoxigenic E Coli (ETEC) most responsible for? What is the MOA of its two toxins? What is unique about its Tx?
Traveler's Diarrhea Heat Stable Toxin (ST) and Heat Labile Toxin (LT) increase cAMP Tx: Ab's can shorten duration: Cipro or TMP-Sulfa
65
What is unique about Nontyphoidal Salmonella diarrhea even though it is an agent that induces inflammatory gastroenteritis?
Watery rather than expected bloody
66
Although it is self-limiting (no 1st or alternative ab choices), when would ab's be administered in Nontyphoidal Salmonella?
Risk for metastatic complications: newborns, elderly, lymphoproliferative disorders, prosthetic joints, HIV +, valvular heart disease, hemoglobinopathies
67
What is an oxidase + agent that can induce inflammatory gastroenteritis?
Campylobacter
68
Which agent of inflammatory gastroenteritis can lead to terminal ileitis, mesenteric lymphadenitis & appendicitis-like sx?
Yersinia Enterocolitica
69
What are the sources of Enterohemorrhagic E Coli & characteristics of its toxin?
Sources: poorly cooked meat, unpasteurized foods, municipal water, petting zoos Shiga Toxin Producing E Coli (STEC) w/ O157:H7 strain Shiga toxin detected in stool: preferred dx method
70
What are potential complications of EHEC?
Toxic megacolon, intussusception, HUS
71
Would you administer ab's in EHEC?
Abx **_contraindicated_** bc can increase risk of HUS
72
What gross pathology might you sometimes find in C Diff induced inflammatory gastroenteritis? How would you Tx C Diff?
"Pseudomembranous Colitis:" plaques from Toxins A & B Tx: eliminate inciting agent (ab's) Metronidazole, Vancomycin (PO), Fidaxomycin
73
What is the 1st choice & alternative ab Tx for **Campylobacter**?
1st: Azithromycin "zip the camp" Alt: Ciprofloxacin "roll back the revolver"
74
What is the 1st choice & alternative ab Tx for **C Diff**?
1st: Vancomycin 2nd: Fidaxomicin \*not rec for \<18 y/o, so Metro**ni**dazole "play **ni**ce for the kids"
75
What is the 1st choice & alternative ab Tx for **Salmonella enterica Typhi**?
1st: Ceftriaxone/Ciprofloxacin Alt: Ampicillin/TMP-SMX or Azithromycin "bringing the forgotten A game, round II"
76
What is the 1st choice & alternative ab Tx for **Paratyphi Shigella**? Exception?
1st: Azithromycin, Ciprofloxacin, Ceftriaxone Alt: Ampicillin, TMP-SMX \*Shigellois: fluoroquinolones shouldn't be prescribed if ciprofloxacin MIC is 0.12 ug/mL or incr even if lab report says isolate susceptible
77
What is the 1st choice & alternative ab Tx for **Vibrio Cholerae**?
1st: **D**oxycycline: incr **c**AMP remediated w/ **D** Alt: Ciprofloxacin, Azithromycin, Ceftriaxone
78
What is the 1st choice & alternative ab Tx for non-Vibrio Cholerae?
Usually not indicated for non-invasive disease or single agent Tx for non-invasive disease 1st: Ceftriaxone + Doxycycline (invasive case) Alt: TMP-SMX + Aminoglycoside
79
What is the 1st choice & alternative ab Tx for **Yersinia Enterocolitica**?
1st: TMP-SMX Alt: Cefotaxime or Ciprofloxacin
80
What is the type of inheritance and the most severe form in Alpha1 Antitrypsin Deficiency? Describe its pathogenesis
Autosomal Codominant; PiZZ AA substitution in SERPINA1 gene, protein misfolding and polymerization, stuck in ER and causes hepatocyte apoptosis
81
What is the type of inheritance and mutations in Hereditary Hemochromatosis? Describe its pathogenesis
Autosomal recessive, low penetrance Mutations in HFE: C282Y (N Eur) and H63D (worldwide) HFE mutation ↓ Hepcidin, ↑ Ferroportin & Plasma Fe (overload in tissues)
82
What are 2 significant clinical features in Hereditary Hemochromatosis?
Cardiac dysfunction and Bronze Diabetes
83
What is the inheritance of Wilson's Disease and the associated mutation? Describe its pathogenesis
Autosomal recessive; ATP7B mutation Mutaton in CU transport ATPase-\>impaired Cu excretion in bile and failure to incorporate Cu into ceruloplasmin
84
What are three ways to treat Wilson's Disease?
1) Cu Chelators 2) Zn (induces methallothionein to bind Cu in enterocyte) 3) Avoid Cu rich foods (shellfish, liver, chocolate, whole grains)
85
What is the EPI, inheritance and mutation in Cystic Fibrosis?
EPI: most common AR disorder in Caucasians Mutation in CFTR, deltaF508: most common
86
What are three ways to treat Cystic Fibrosis?
1) Pancreatic enzyme replacement 2) Vit/mineral supplementation 3) Pancreas-liver-lung transplant
87
What are two possible inheritance patterns in Hereditary Pancreatitis?
AD: PRSS1 mutation in cationic trypsinogen gene, alters site for inactivation of trypsin by itself; inappropriate trypsin activation AR: SPINK1 mutation in trypsin inhibitor
88
Describe the pathogenesis, Tx & cancer risk in FAP
Germline mutation in APC Tx: Prophylactic total colectomy 100% CRC risk by 40 y/o
89
Describe the pathogenesis of MUTYH Associated Polyposis
AR mutation in MUTYH: BER enzymes that prevents oxidative damage mutations
90
Describe the pathogenesis of Polymerase Proofreading Associated Polyposis (PPAP) Apart from CRC, what are other possible cancer risks?
AD mutation in exonuclease domain of POLE or POLD1 (polymerase) Other: endometrial, brain
91
Describe the pathogenesis of Peutz Jeghers Syndrome
AD mutation in LKB1/STK11 (tumor suppressor gene)
92
Describe the histologic characteristics of MSI
Crohn's like reaction Tumor infiltrating lymphocytes Pushing border Poor differentiation
93
Describe the pathogenesis of Lynch Syndrome
Mutation in DNA mismatch repair genes (MLH1 [major], PMS2 [minor], MSH2 [major], MSH6 [minor])
94
Describe the main diagnostic feature of Lynch-like Syndrome
IHC shows loss of DNA MMR proteins but mutation testing shows no mutations in genes \*Somatic Mutation\*
95
What condition accounts for 85% of all CRC's?
Sporadic CRC
96
How can you categorize Familial CRC Type X (FCCTX)?
HNPCC w/o MSI & w/ strong family history of CRC meeting clinical criteria for Lynch Syndrome but also w/o germline DNA MMR gene mutations
97
What inherited GI condition can occur in a background of polyposis & also be a HNPCC w/o MSI?
Polymerase Proofreading Associated Polyposis (PPAP)

Block 4a: GI (5 decks)

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