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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
Q

What is the class & MOA of Lubiprostone?

A

*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

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26
Q

What is the PK of Lubiprostone?

A

Poor systemic absorption (plasma serum levels not even detectable w/ therapeutic doses)

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27
Q

What are 2 unique considerations of Lubiprostone?

A

No restriction on length use

No evidence of tolerance, dependence, or rebound effects

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28
Q

What is a shared indication among the receptor mediated laxative drugs: Lubriprostone, Linaclotide & Plecanatide?

A

Chronic idiopathic constipation
IBS w/ constipation

*Lubiprostone: fems 18+ y/o*

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29
Q

What is a CI shared by Lubiprostone & Linaclotide?

A

CI: known or suspected mechanical GI obstruction

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30
Q

Does Lubiprostone have drug interactions?

A

No, based on structure, protein binding, in vivo studies

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31
Q

What is the shared MOA of Linaclotide & Plecanatide?

A

MOA: 14 aa (L) and 16 aa oligopeptide (P)
GC-C receptor agonists that increases cGMP levs

PK: acts locally, once daily dosing

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32
Q

What is Linaclotide’s boxed warning? How does it compare w/ Plecanatide’s CI?

A

Both share extreme dehydration

L: avoid in patients 6-17 y/o (up to 6 yrs)

P: avoid in <6 y/o

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33
Q

Does Linaclotide have drug interactions?

What is a unique consideration?*

A

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

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34
Q

What are 3 “other” anti-diarrheal drugs?
What is the MOA & Indications for the plant-derived one?

A

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 & Anoctamin I, & thereby Cl currents
“it knocked him hard”
Indication: Non-infectious diarrhea in adult HIV/AIDs patient

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35
Q

Give an ex of an anti-diarrheal bulk forming drug

A

Kaolin-Pectin

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36
Q

When are narcotic analogues (ie: opiate agonists) vs. diarrhea contraindicated?

A

Infectious diarrhea: E Coli, Salmonella, Shigella

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37
Q

What are 2 AE’s and 3 possible interactions that narcotic analogues can have?

A

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”

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38
Q

What are ex’s of narcotic analogues?

A

Phenylpiperidine analgesic analogues
Loperamide
Diphenyloxylate-Atropine

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39
Q

What is the MOA of non-specific anti-diarrheals?
When are they indicated?

A

MOA: may bind bacterial toxins
anti-secretory effects, non-SP anti-inflammatory effects

Traveller’s Diarrhea: ETEC-non-inflammatory gastroenteritis

40
Q

When are non-specific anti-diarrheals CI & what are their AE’s?

A

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
Q

What interactions can non-specific anti-diarrheals have?
What is one consideration & ex?

A

W/ tetracyclines & other salicylates (additive effects)

Consider if tablets used: ensure they are chewed!

Ex: Bismuth Subsalicylate
“under the radar and non-SP”

42
Q

What is the class, MOA and indications for Bile Acid Binders?

A

*Anti-diarrheal*
MOA: binds bile acids, anion exchange resins

Indications: Secretory Diarrhea & Post-Op

43
Q

What are the CI’s, AE’s, and interactions of Bile Acid Binders?

A

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
Q

What are 3 ex’s of Bile Acid Binders?

Which is not absorbed or metabolized, leading to fewer drug interactions?

A

1) Cholestyramine
2) Colestipol
3) Colesevelam*

45
Q

What is the MOA and indications for the anti-diarrheal anti-secretory agents?

A

MOA: Somatostatin receptors; hyperpolarizes gut neurons, decreases Ach and slows peristalsis

Indications: AIDS-related diarrhea
Refractory endocrine tumor related diarrhea

46
Q

What are the AE’s and interactions of anti-secretory agents?
Give an ex:

A

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
Q

How are antacids viewed in treating peptic disorders?

A

Largely replaced by H2 receptor blockers & PPI’s
But they are inexpensive & widely used for self-Tx

48
Q

Describe the rates of reaction for the various metal hydroxides in antacids

A

Al: slow
Mg: slow/moderate
Na & Ca bicarbonates: fast

49
Q

What are two examples of non-acid neutralizing compounds?

A

1) Simethicone (gas sx)
2) Alginic acid

50
Q

How do tablet vs. liquid antacid formulas compare?

A

Tablets neutralize less acid/dose & have a longer onset of action than Liqs

51
Q

Describe the CI’s, AE’s, and interactions of antacids

A

CI: renal function

AE: minimal (constipation/diarrhea)

Many interactions

52
Q

What is the MOA & PK of topical mucosal protectants?

A

MOA: Complexes w/ protein exudates at ulcer sites, acting as protecting barrier

PK: minimal absorption w/ minor AE’s

53
Q

What are the interactions & CI’s of topical mucosal protectants?

A

Interactions: may bind to other medications, so reqs separate doses

CI: renal failure; do not give w/ antacids, H2 blockers, PPI’s

54
Q

What is an example of a non-specific anti-diarrheal with mucosal protective properties?

A

Bismuth subsalicylate

55
Q

What is the MOA & indications of systemic mucosal protectants?

A

MOA: As PG E1 analogue, inhibits gastric acid secretions and promotes mucosal protective properties

Indications: prevent NSAID induced gastric ulcers

56
Q

What are the drug interactions and CI’s of systemic mucosal protectants?

A

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
Q

What is an ex of a systemic mucosal protectant?

A

Misoprostol

58
Q

Compare and contrast the presentations, GI areas affected and treatments of invasive & non-invasive gastroenteritis

A

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
Q

What is the #1 cause of gastroenteritis in the US?

A

Norovirus

60
Q

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?

A

Norovirus: “winter vomiting disease”

Many genotypes, high recurrence

61
Q

What is an agent that can induce non-inflammatory gastroenteritis but can still cause fever?

A

Rotavirus

62
Q

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

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
Q

Why is Clostridium Perfringens’ toxin unique compared to that of other non-inflammatory gastroenteritis agents?

A

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
Q

What condition is Entertoxigenic E Coli (ETEC) most responsible for?

What is the MOA of its two toxins?

What is unique about its Tx?

A

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
Q

What is unique about Nontyphoidal Salmonella diarrhea even though it is an agent that induces inflammatory gastroenteritis?

A

Watery rather than expected bloody

66
Q

Although it is self-limiting (no 1st or alternative ab choices), when would ab’s be administered in Nontyphoidal Salmonella?

A

Risk for metastatic complications: newborns, elderly, lymphoproliferative disorders, prosthetic joints, HIV +, valvular heart disease, hemoglobinopathies

67
Q

What is an oxidase + agent that can induce inflammatory gastroenteritis?

A

Campylobacter

68
Q

Which agent of inflammatory gastroenteritis can lead to terminal ileitis, mesenteric lymphadenitis & appendicitis-like sx?

A

Yersinia Enterocolitica

69
Q

What are the sources of Enterohemorrhagic E Coli & characteristics of its toxin?

A

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
Q

What are potential complications of EHEC?

A

Toxic megacolon, intussusception, HUS

71
Q

Would you administer ab’s in EHEC?

A

Abx contraindicated bc can increase risk of HUS

72
Q

What gross pathology might you sometimes find in C Diff induced inflammatory gastroenteritis?

How would you Tx C Diff?

A

“Pseudomembranous Colitis:” plaques from Toxins A & B

Tx: eliminate inciting agent (ab’s)
Metronidazole, Vancomycin (PO), Fidaxomycin

73
Q

What is the 1st choice & alternative ab Tx for Campylobacter?

A

1st: Azithromycin “zip the camp”

Alt: Ciprofloxacin “roll back the revolver”

74
Q

What is the 1st choice & alternative ab Tx for C Diff?

A

1st: Vancomycin
2nd: Fidaxomicin *not rec for <18 y/o, so Metronidazole “play nice for the kids”

75
Q

What is the 1st choice & alternative ab Tx for Salmonella enterica Typhi?

A

1st: Ceftriaxone/Ciprofloxacin

Alt: Ampicillin/TMP-SMX or Azithromycin

“bringing the forgotten A game, round II”

76
Q

What is the 1st choice & alternative ab Tx for Paratyphi Shigella? Exception?

A

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
Q

What is the 1st choice & alternative ab Tx for Vibrio Cholerae?

A

1st: Doxycycline: incr cAMP remediated w/ D

Alt: Ciprofloxacin, Azithromycin, Ceftriaxone

78
Q

What is the 1st choice & alternative ab Tx for non-Vibrio Cholerae?

A

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
Q

What is the 1st choice & alternative ab Tx for Yersinia Enterocolitica?

A

1st: TMP-SMX

Alt: Cefotaxime or Ciprofloxacin

80
Q

What is the type of inheritance and the most severe form in Alpha1 Antitrypsin Deficiency?

Describe its pathogenesis

A

Autosomal Codominant; PiZZ

AA substitution in SERPINA1 gene, protein misfolding and polymerization, stuck in ER and causes hepatocyte apoptosis

81
Q

What is the type of inheritance and mutations in Hereditary Hemochromatosis?

Describe its pathogenesis

A

Autosomal recessive, low penetrance

Mutations in HFE: C282Y (N Eur) and H63D (worldwide)

HFE mutation ↓ Hepcidin, ↑ Ferroportin & Plasma Fe (overload in tissues)

82
Q

What are 2 significant clinical features in Hereditary Hemochromatosis?

A

Cardiac dysfunction and Bronze Diabetes

83
Q

What is the inheritance of Wilson’s Disease and the associated mutation?

Describe its pathogenesis

A

Autosomal recessive; ATP7B mutation

Mutaton in CU transport ATPase->impaired Cu excretion in bile and failure to incorporate Cu into ceruloplasmin

84
Q

What are three ways to treat Wilson’s Disease?

A

1) Cu Chelators
2) Zn (induces methallothionein to bind Cu in enterocyte)
3) Avoid Cu rich foods (shellfish, liver, chocolate, whole grains)

85
Q

What is the EPI, inheritance and mutation in Cystic Fibrosis?

A

EPI: most common AR disorder in Caucasians
Mutation in CFTR, deltaF508: most common

86
Q

What are three ways to treat Cystic Fibrosis?

A

1) Pancreatic enzyme replacement
2) Vit/mineral supplementation
3) Pancreas-liver-lung transplant

87
Q

What are two possible inheritance patterns in Hereditary Pancreatitis?

A

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
Q

Describe the pathogenesis, Tx & cancer risk in FAP

A

Germline mutation in APC

Tx: Prophylactic total colectomy

100% CRC risk by 40 y/o

89
Q

Describe the pathogenesis of MUTYH Associated Polyposis

A

AR mutation in MUTYH: BER enzymes that prevents oxidative damage mutations

90
Q

Describe the pathogenesis of Polymerase Proofreading Associated Polyposis (PPAP)

Apart from CRC, what are other possible cancer risks?

A

AD mutation in exonuclease domain of POLE or POLD1 (polymerase)

Other: endometrial, brain

91
Q

Describe the pathogenesis of Peutz Jeghers Syndrome

A

AD mutation in LKB1/STK11 (tumor suppressor gene)

92
Q

Describe the histologic characteristics of MSI

A

Crohn’s like reaction

Tumor infiltrating lymphocytes

Pushing border

Poor differentiation

93
Q

Describe the pathogenesis of Lynch Syndrome

A

Mutation in DNA mismatch repair genes (MLH1 [major], PMS2 [minor], MSH2 [major], MSH6 [minor])

94
Q

Describe the main diagnostic feature of Lynch-like Syndrome

A

IHC shows loss of DNA MMR proteins but mutation testing shows no mutations in genes

*Somatic Mutation*

95
Q

What condition accounts for 85% of all CRC’s?

A

Sporadic CRC

96
Q

How can you categorize Familial CRC Type X (FCCTX)?

A

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
Q

What inherited GI condition can occur in a background of polyposis & also be a HNPCC w/o MSI?

A

Polymerase Proofreading Associated Polyposis (PPAP)

Block 4a: GI (5 decks)

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