GI DISEASES Flashcards

1
Q

ANTACID MECHANISM

A

weak bases that react with gastric HCl to form salt and water. The end result is an INCREASED pH. Provide QUICK RELIEF OF SYMPTOMS

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2
Q

COMMONLY USED ANTACIDS

A

1) MAGNESIUM HYDROXIDE (Milk of Magnesia)
2) ALUMINUM HYDROXIDE
3) CALCIUM CARBONATE (TUMS)

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3
Q

ADVERSE EFFECT of

1) MAGNESIUM HYDROXIDE
2) ALUMINUM HYDROXIDE
3) CALCIUM CARBONATE (TUMS)

A

1) Magnesium hydroxide produces Mg salt, which is very poorly absorbed and causes DIARRHEA
2) ALUMINUM HYDROXIDE: reacts with HCl to form Aluminum chloride, which is insolube and causes CONSTIPATION + HYPOPHOSPHATEMIA
3) CALCIUM CARBONATE: hypercalcemia, nephrolithiasis, and constipation (fecal compaction) -

NOTE FOR ALL 3: note that Ca, Mg, and Al can all CHELATE TETRACYCLINE

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4
Q

FACTORS that ENHANCE GASTIC ACID SECRETION

A

3 AGONISTS:

1) HISTAMINE
2) ACETYLCHOLINE
3) GASTRIN
- the final pathway of these compounds is activation of the H+/K+ ATPase pump

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5
Q

H2 RECEPTOR BLOCKERS

Names + function

A

1st Gen: CIMETIDINE =

–> shorter acting and inhibit CYP450

2nd Gen: =

–> longer acting and do not inhibit CYP450

–> anything that ends in “TIDINE” that’s not Lora Fux

1) Famotidine
2) Ranitidine
3) Famotidine
4) Nizatidine

FUNCTION: blocks the Gs mediated increase in cAMP that activates the H+/K+ pump

–> are capable of decreasing nearly 60-90% of basal secretion of gastric acid following a single dose

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6
Q

INDICATION for ANTACIDS

A

1) GERD
2) GASTRITIS
3) PUD
- provide quick releif for these symptoms

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7
Q

Drug used to treat ACUTE STRESS ULCERS (associated with major trauma and in high-risk patients in intensive car units)

A

H2 BLOCKERS –> are usually given IV injection

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8
Q

Drus used PREOPERATIVELY to PREVENT ASPIRATION PNEUMONIA

A

H2 blocker

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9
Q

ADVERSE EFFECTS of H2 BLOCKERS

A

-H2 second gen: normally all tolerated well

H2 blocker: first gen = CIMETIDINE: presents unwanted endocrinal adverse effects including

1) GYNECOMASTIA, (“Ci-me-tiddies”)
2) ELEVATED SERUM PROLACTIN LEVELS,
3) CONFUSION in ELDERLY

Big tittied confused lady at dinner that’s lactating

CIMETIDINE is also a STRONG INHIBITOR of cytochrome P450

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10
Q

PROTON PUMP INHIBITORS (names)

A

1) OMEPRAZOLE
2) LANSOPRAZOLE
3) PANTOPRAZOLE
4) ESOMEPRAZOLE
5) RABEPRAZOLE

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11
Q

PPI MECHANISM OF ACTION

A

-is a PRODRUG that after transporation into the parietal cell canaliculus, is converted to the active form, which reacts with a CYSTEINE RESIDUE of the H+/K+ ATPase, forming a stable COVALENT BOND leading to IRREVERSIBLE INACTIVATION OF ENZYME

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12
Q

PPI INDICATIONS

A

1) GERD
2) DUODENAL/GASTRIC ULCERS
3) MEN-1/ZOLLINGER-ELLISON SYNDROME
4) Contribute in combo with antibotics to eradicate H. Pylori
5) NSAID INDUCED ULCERS –> they support platelet aggregation and maintain clot integrity –> used in hemorrhagic ulcers

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13
Q

PPI SIDE EFFECTS

A
  • are well tolerated, but can produce nausea/diarrhea
  • long term administration of Omeprazole, in ANIMALS, is associated with gastric carcinoid tumors (not seen in humans)
  • Omeprazole INHIBITS the metabolism of warfarin, clopidogrel, phenytoin, diazepam, and cyclosporin
  • reports of small increase in resp and GI infections; decrease in serum Mg2+ and Hip fractures with long term use of PPI
  • rarely pancreatiits, hepatotoxicity, and interstitial nephritis
  • prolonged therapeutic use of PPI + H2 blockers may DECREASE BIOAVAILABILITY of
    1) VITAMIN
    2) DIGOXIN
    3) KETOCONAZOLE

this is because the acid is required for their absorption

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14
Q

ANTIMICROBIALS used for H. Pylori eradication

A

1) CLARITHROMYCIN (crows in sketchy
2) AMOXICILLIN (amo box in sketchy)
3) METRONIDAZOLE
4) TERACYCLINE
- to document infection with H. Pylori –> do
1) endoscopic biopsy of the ulcer margin,
2) serolgic tests OR
3) Urea breath tests:
- eradication of H. pylori results in rapid healing of active peptic ulcers and low recurrence rates

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15
Q

UREASE BREATH BEST

A
  • used to diagnose Helicobacter Pylori infection
    1. Subjects are given urea labelled with 13C orally
    2. H. pylori produces UREASE, which hydrolyses the labelled urea to 13CO2 and ammonia
    3. 13CO2 is dissolved in the blood and transported to the lungs
    4. Exhaled 13CO2 is analyzed –> the presence of H. pylori results in an increase in the ratio of 13CO2: 12CO2 in expired breath
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16
Q

FIRST + SECOND LINE REGIMEN for eradication of H. Pylori

A

FIRST LINE: TRIPLE THERAPY, regimen for at least 4 WEEKS

1) 2 ANTIBIOTICS
2) PPI
- clathithromycin + amoxicillin, or clarithromycin + metronidazole both = 70=85% eradication rate

SECOND LINE THERAPY: QUADRUPLE THERAPY for 4 weeks

1) BISMUTH (a mucosal protective agent)
2) 2 ABX (Metro + tetracycline)
3) PPI OR RANITIDINE
- second line therapy has a 75-90% eradication rate

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17
Q

MUCOSAL PROTECTIVE AGENTS

A

1) SUCRALFATE
2) BISMUTH SUBSALICYLATE
3) MISOPROSTOL

“Sugar Latte’s By Mouth and Miso Soup” all help with mucosal protection

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18
Q

SUCRALFATE MOA

A

“sugar-late” –> binds all the shitty girls = the necrotic tissue –> needs to be ACIDIC (hot) or else they won’t like them (ie can’t be given with an H2 blocker or PPI)

is a mucosal protecting agent that undergoes polymerization and selective binding to NECROTIC TISUE where it acts as a barrier to acid

-it also stimulates PROSTAGLANDIN SYNTHESIS

Note: sucralfate is INEFFECTIVE with action of H2 receptor blockers or PPI

–> it req_uires acidic pH to be activated_ therefore it should NOT be administered simultaneously with H2 blockers, PPI, or other antacids

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19
Q

BISMUTH THERAPEUTIC ACTIONS

A

-appears to have some antimicrobial effect on H Pylori

–> when it is admisisterd along with metronidazole and tetracycline, ulcer healing rate increases to 90%

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20
Q

MISOPROSTOL

A

MISO SOUP of PROSTaglandins for Every1

–> AEs include DIARRHEA + ABORTIONS –> soup makes everything come out AND irritates bowel!!!

  • a muucosal protective agent that is a PROSTAGLANDIN E1 ANALOGUE that
    1) DECREASES ACID SECRETION
    2) STIMULATES MUCIN + BICARB PRODUCTION

Clinical Uses: approved for PREVENTION OF GASTRIC ULCERS induced by NSAIDS, but it is L_E_SS EFFECTIVE than H2 blockers or PPI in acute cases

ADVERSE EFFECTS:

1) DIARRHEA in up to 30% of patients
2) ABORTIONS –> d/t induction of uterine contractions during pregnancy, therefore it is contraindicated in pregnancy
3) Exacerbations of inflammatory bowel disease

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21
Q

GERD TREATMENT

A

NON-PHARMACOLOGICAL:

-small meals, weigh loss, avoid bed-time acid rich drinks, elevate head of the bed to 6-8 inches and lifestyle modifications (smoking, alcohol)

DRUGS:

1) PPI +/- H2 blocker

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22
Q

PROKINETIC DRUGS USED IN GI DISORDERS

A

1) NEOSTIGMINE/BETHANECHOL
2) METOCLOPRAMIDE
3) CISAPRIDE
4) ERYTHROMYCIN

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23
Q

METOCLOPRAMIDE

A

“Metro-cop Ride” –> Serotonin3 and Dopamine receptor blocker (blocks the good things b/c is a cop), but allows the “4” to be an agonist

AE: they always PARK, SLEEP, and POOP in the wrong places (parkinsons, sedation, and diarrhea all d/t dopamine

  • is a PROKINETIC DRUG that performs as a 5-HT3 and D2 receptor blocker
  • The prokinetic activity of metoclopramide is mediated by muscarinic activity via 5-HT4 receptor agonist activity.

–> It accelerates gastric emptying and intestinal motility.

USES:

1) DIABETIC + POST-OP GASTROPARESIS

2) ANTIEMETIC (reduces nausea and vomiting associated with chemo agents)

3) RELIEF OF SX OF GERD

-At HIGHER DOSES, 5-HT3 antagonist activity may also contribute to the anti-emetic effect.

ADVERSE EFFECTS: are d/t ANTI-DOPAMINERGIC effects = sedation, diarrhea, and Parkinsonian effects which limit its high-doses and long-term use

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24
Q

CISAPRIDE

A

“CIS PRIDE” –> like metro cop ride but is the CIS, so can drive fast (4 wheels for HT4 agonist) –> stimulates ACh secretion etc… but because CIS agents work so hard, their adverse effect = arrhythmia

-5-HT4 AGONIST –> stimulates ACh secretion

USES:

1) GASTROPARESIS
2) GERD
3) CONSTIPITION

AEs: ARRYTHMIAS

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25
Q

NEOSTIGMINE

A

-is a CHOLINOMIMETIC

USES:

1) COLONIC PSEUDO-OBSTRUCTION in hospitalized patients

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26
Q

BETHANECHOL

A
  • a CHOLINOMIMETIC
  • is resistant to cholinesterdase, has a long duration of action

USES:

1) POST-OP BOWEL + BLADDER atony

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27
Q

ERYTHROMYCIN

A

-is a MACROLIDE antibiotic that acts as a PROKINETIC AGENT

–> is a MOTLIN RECEPTOR AGONIST

USES:

1) GASTRIC EMPTYING before upper GI endoscopic procedures

Tolerance may develop in gastroparesis

28
Q

ANTIEMETIC AGENTS

A

a) 5-HT3 inhibitors – Ondansetron (Zofran)

b) H1 antihistamines & antimuscarinics

Diphenhydramine & Scopolamine

  • *c) Corticosteroids** – Dexamethasone
  • *d) NK1–receptor blocker** – Aprepitant
  • *e) D2 Receptor antagonist** – Prochlorperazine f) Benzamide – Metoclopramide
  • *g) Marijuana** – Dronabinol (Marinol)
29
Q

ONDANSETRON

A

“little chemo girl on the “jumbo-tron” dancing… dancing on 2 legs and has 1 arm up = serotonin 3 receptor

5-HT3 INHIBITOR/ANTAGONIST in the GUT + CNS

USES:

1) CHEMOTHERAPY INDUCED moderate-severe emesis or post-op nausea/vomiting
- usually given IV, for prophylaxis given orally

Note: CORTICOSTEROIDS can be combined with ondansetron to provide a GREATER ANTI-EMETIC EFFECT

30
Q

DIPHENHYDRAMINE

CYCLIZINE

MECLIZINE

A

H1 ANTIHISTAMINES

-are moderately effective in motion sickness + chemotherapy induced nausea/vomiting

31
Q

SCOPOLAMINE

A

“SCOPE LA MINE” –> as in come scope the mine but it’s shitty travel there so may need some scopolamine for the motion sickness

-anti-emetic that is an ANTIMUSCARINIC

–> is the DOC for emesis d/t MOTION SICKNESS

32
Q

APREPITANT

FOSAPREPITANT

A

“A Prepitant” of that New Killer 1 shit –> makes you not feel nautious during chemo brooooo”

-anti-emetic that is an NK1-receptor blocker in the CNS (NK = NeuroKinin)

–> effective in both decreasing the EARLY + DELAYED EMESIS in CANCER CHEMO

APREPITANT = ORAL

FOSAPREPITANT = IV

ADVERSE EFFECTS: dizziness, fatigue, diarrhea, and CYP interaction may occur

33
Q

CHEMOTHERAPY INDUCED NAUSEA + VOMITING TX

A

A) Solo DEXAMETHASONE

–> Dex DOES it by itself

OR

B) Combo of

  • METHYLPREDNISOLONE +
  • ONDANSETRON/APREPITANT
34
Q

PROCHLORPERAZINE

A

an ANTI-EMETIC that is a “pro” for “chlorine” vomiting… makes you not vomit –> antagonizes those dopamine receptors and the muscles)

a PHENOTHIAZINE –> an ANTAGONIST at

  • D2 RECEPTORS
  • MUSCARINIC RECEPTORS

SIDE EFFECTS:

  • EXTRAPYRAMIDAL SYMPTOMS,
  • HYPOTENSION,
  • SEDATION
35
Q

METOCLOPRAMIDE (MCP)

A
  • PHENOTHIAZINE
  • is a PRO-MOTILITY agent and an ANTI-EMETIC

–> Antagonist at D2 receptors and muscarinic receptors

-effective at HIGH DOSES against the highly emetogenic CISPLATIN

AEs: has ANTIDOPAMINERGIC SIDE EFFECTS

–> TARDIVE DYSKINESIA

–> sedation, diarrhea, extrapyramidal symptoms, limit its high-dose use

36
Q

LORAZEPAM

ALPRAZOLAM

DIAZEPAM

A
  • are BENZO’S
  • the antiemetic potency of lorazepam, alprazolam, and diazepam is low
  • their beneficial effects may be d/t their sedative, anxiolytic, and amnesic properties
  • useful in ANTICIPATORY NAUSEA/VOMITING
37
Q

INFLAMMATORY BOWEL DISEASE DRUGS

A

1) Sulfasalzine,
2) glucocorticoids (Budesonide),
3) azathioprine,
4) Methotrexate,
5) Cyclosporine,
6) Infliximab and
7) Natalizumab

38
Q

SULFASALAZINE

MESALAMINE (5-ASA)

  • BALSALAZIDE
  • SULFASALAZINE
A

DRUG FOR IBD

  • MOA: inhibits the pro-inflammatory mediators –IL1, and TNF-α
  • It is a sulfa derivative. So, it should be avoided in patients with sulfa allergy.
  • In the GIT,
  1. sulfapyridine (antibacterial) and
  2. 5- Aminosalicylic acid (5-ASA) (anti-inflammatory) released from sulfasalazine by colonic bacteria.

• It is used in mild to moderate Crohn’s disease or ulcerative colitis

ADVERSE EFFECTS: Nausea, vomiting, diarrhea, _hypersensitivity, and *reversible oligospermia*. Bone morrow suppression_ is related to the sulfapyridine release from sulfasalazine.

NOTE: MESALAMINE (5-ASA) = “metabolite”

• Balsalazide: releases mesalamine (5-ASA) in the large intestine at the active site of ulcerative colitis.

–> B for BIG BOWEL –> LARGE INTESTINE –> more for UC (the LARGE INTESTINE)

• Sulfasalazine: Proximal, distal colon and rectum.

39
Q

6-mercaptopurine(6-MP)

Methotrexate (MTX)

A

-IMMUNOMODULATORS

  • 6-MP may promote apoptosis of immune response. –> Me-Cap’d (ie getting shot… promoting apoptosis)
  • MTX blocks dihydrofolate reductase (DHFR)

They cause generalized immune suppression

They are used in moderately severe to severe Crohn’s disease and ulcerative colitis.

AE:

6-MP: mucositis, myelosupression.

–> Hepatotoxicity can occur with 6-MP.

-MTX: Toxicities are rare at low doses.

40
Q

INFLIXIMAB

ADALIMUMAB

A

MAB –> can think monoclonal antibody –> MAB the MOBSTER that helps with ACUTE FISTS(ULA’s) and FLARES –> fight That New Fuck ALPHA (TNF-alpha) in town. Test these mobsters for TB before you give them the MAB

MOA: is a MONOCLONAL ANTIBODY that targets TNF-alpha, a principal mediator in Crohns disease

-used in conditions associated with FLARE UP of IBD; particularly in Crohn’s related FISTULAS + ACUTE FLARES

Note: it is also used in RHEUMATOID ARTHRITIS

AEs: reactivationof latent tuberculosis and other infections. It is given IV – fever, chills, urticarial reaction, hypotension may occur. Antibodies to infliximab may develop.

Note: Adalimumab: (HUMIRA) - TNF-α inhibitor

41
Q

NATALIZUMAB

A

“nat” LIZ “MAB” –> blocks that integration

blocks leukocyte integrins

  • can produce multifocal leukoencephalopathy.
42
Q

HYDROCORTISONE

PREDNISONE

PREDNISOLONE

A

CORTICOSTEROIDS

  • are gneralized anti-inflammatory drugs used in acute cases
  • Inhibit TNF-α, IL-1, IL-8

Age you can start “corting” at is 18 (IL1, IL-8… can be the ALPHA male for TNF-alpha)

43
Q

BUDESONIDE

A

CORTICOSTEROID

-controlled release formation in the distal ileum and colon

44
Q

IBS (Irritable Bowel Syndrome)

A

IBS Characterized by

  • diarrhea (D) or
  • constipation (C) or
  • alternating (A)

Chronic symptoms with no structural abnormalities

Frequent abdominal pain correlated with following:

  • Altered stool frequency
  • Pain gets better with defecation
  • Alteration in stool appearance

Treatment: symptomatic

45
Q

ALOSETRON

A

5-HT3 BLOCKER

Al! Set (up) RON for the 3!

  • 5-HT3 antagonist with long duration of action, has high potency

MOA: Reduces smooth muscle activity in the gut (For IBS-D).

USES: Recommended for severe diarrhea associated IBS.

AE: Rare, serious constipation; ischemic colitis and infarction may occur.

46
Q

DICYCLOMINE

HYOSCYAMINE

GLYCOPYRROLATE

METHSCOPALAMINE

A

ANTICHOLINERGICS

non-selective action on the gut (IBS-D)

USES: IBS: diarrhea

-Chronic symptoms with no structural abnormality

47
Q

LUBIPROSTONE

A

CHLORIDE CHANNEL ACTIVATOR in IBS

“lubey up my prostone” bro, i need to shit”

-used in CONSTIPATION-associated IBS (IBS-C)

48
Q

LOPERAMIDE

DIPHENOXYLATE

A

ANTI-DIARRHEAL, OPIOID AGONISTS

-are both opiate derivatives that SLOW GUT MOTILITY with NEGLIGABLE CNS EFFECTS

–> acts via GI mu-opioid receptors

  • INHIBITS ACH release + decreases perstalsis!!

DIPHENOXYLATE: is formulated with ATROPINE to REDUCE ABUSE POTENTIAL –> High doses can cause CNS EFFECTS

AE: risk of TOXIC MEGACOLON in children or patients with severe colitis

49
Q

CHOLESTYRAMINE

COLESTIPOL

COLESEVELAM

A

-prevent diarrhea of IBS + IBS by blocking osmotic and irriating actions of bile salts (ie PREVENT SECRETORY DIARRHEA)

–> BILE SALTS stimulate Cl- secretion in the colon (cAMP) –> Resins form insoluble complexes with bile acids that are no longer able to stimulate this excess secretion

  • they form INSOLUBLE COMPLEXES with BILE ACIDS in the intestine
  • also used in LOWERING CHOLESTEROL
50
Q

LAXATIVES

A
  • classified by mechanism of action as
    1) STIMULANTS
    2) OSMOTIC AGENT
    3) BULK FOMRING AGENTS
    4) STOOL SOFTENERS
51
Q

SENNA

BISACODYL

CASTOR OIL

A

LAXATIVE STIMULANT

–> can thing SENNA for STIMULANT, and that CODYL which kind of soudns like CASTOR OIL which casts off the poop (b/c is a laxative)

  • may cause cramping
  • chronic use may lead to habit of perceived need for laxitives

Note: Senna is used with docusate for opioid induced constipation

52
Q

METHYCELLULOSE

PSYLLIUM

BRAN

A

BULK FORMING AGENT LAXITIVES

  • if pack cells full of methyl will get bulky, as well if you go to a psyllium, you get bulky as well, and we all know bran makes bulk occur too
  • these are insolube indigestible derivatives form fruits and vegetables (are hydrophilic colloids)
  • they are NON-ABSORBABLE —> increase water retention and stool becomes BULKY
  • the distention of bowel leads to peristaltic stimulation of the gut
53
Q

MAGNESIUM CITRATE

MAGNESIUM HYDROXIDE

LACTULOSE

POLYETHYLENE GLYCOL

A

OSMOTIC AGENTS used as LAXATIVES

  • the magnesium ones are “magnetic” –> help draw the water out (as does the lactose)
  • Magnesium citrate, Magnesium hydroxide = SALINE CATHARTICS
  • Lactulose + Sorbitol = NON-DIGESTIBLE SUGARS
  • they OSMOTICALLY DRAW WATER into the lumen of GIT, which then stimulate motility

USES:

1) SIMPLE CONSTIPATION
2) BOWEL PREP FOR ENDOSCOPE

54
Q

LACTULOSE

A

OSMOTIC LAXATIVE

  • is a semi-synthetic disaccharid sugar that acts as an OSMOTIC LAXITIVE
  • large doses are degraded by colonic bacteria to form lactic, formic, and acetic acid –> this increases osmotic effect too
  • is also used in HEPATIC ENCEPHALOPATHY: it helps to “draw out” ammonia (NH3) from the body and is useful for PREVENTING HYPERAMMONIA
55
Q

PEG (Polyethylene glycol)

A

OSMOTIC LAXATIVE

  • “draws you out” like a “PIG” (for peg)
  • used for COLONIC LAVAGE for ENDOSCOPIC and RADIOLOGICAL PROCEDURES
56
Q

MINERAL OIL

DOCUSATE SODIUM

A

STOOL SOFTENERS

-mineral oil + docusate sodium –> together they EMULSIFY STOOL and SOFTEN IT –> lubricate it and make it wasy to pass

SENNA –> is used in combo with a DOCUSATE (make stools softer and easier to pass) –> used to treat cases of OPIOID-INDUCED CONSTIPATION

57
Q

LUBIPROSTONE

A

CL- CHANNEL ACTIVATOR LAXATIVE

  • prostanoic acid derivative
  • stimulate chloride secretion into GI –> increases fluid content
58
Q

ALVIMOPAN

METHYLNATREXONE

A

-blocks GI mu-receptors but do not enter CNS

–> useful in OPIOID INDUCED CONSTIPATION

59
Q

PANCRELIPASE

A

DRUGS FOR IBS: PANCREATIC ENZYME

  • a replacement enzyme from animal pancreatic extract
  • improve the digestion of dietary fat, protein, and carbs (increases A, D, E, K vit absorption)

USE:

1) Patients with CHRONIC PANCREATITIS
2) AFTER PANCREATECTOMY
3) STEATORRHEA
4) CYSTIC FIBROSIS associated insufficiences

60
Q

URSODIOL

A

BILE ACID THERAPY FOR GALLSTONES

  • has enterohepatic circulation
  • it reduces cholesterol absorption by breaking up micelles containing cholesterol
  • used in patient who refuses or not eligible for surgery

AE: DIARRHEA

61
Q

OCTREOTIDE

A

SOMATOSTATIN ANALOGUE

-is a LONG ACTING somatostatin analogue

USE:

1) CARCINOID TUMORS: note if tumor is in GIT there are no symptoms noticed at 5-HT is metabolized in the liver
2) VIPoma
3) ACUTE VARICEAL BLEEDING
4) ACROMEGALY

AE: abdominal cramps, nausea, steatorrhea, gallstones

62
Q

TREATMENT OF CARCINOID TUMOR

A

OCTREOTIDE (somatostatin analogue)

63
Q

TREATMENT OF VIPoma (Vasoactive Intestinal Polypeptide)

A

A non α and β islet cell pancreatic tumor that secretes VIP, produce copious diarrhea.

  • Source: PANS in sphincters, gall bladder & small intestine
  • Increase water and electrolyte secretion, relax intestinal smooth muscle and sphincters
  • Treatment with Somatostatin analog: octreotide
64
Q

TX OF VARICEAL HEMORRHAGE

A

1) Octreotide: I.V.

A somatostatin derivative with uncertain MOA

Alter portal blood flow and variceal pressure.

Uses: bleeding varices or high risk of repeat bleeding.

Adverse effect: reduce endocrine and exocrine pancreatic activity.

2) NON-SELECTIVE B-BLOCKERS –> Propanolol + Nadolol)

–> are effective in reducing portal pressures

–> β1 & β2 blockade result in ↓CO &↑VC Improves GI blood vessel tone↑systemic vasoconstriction & ↓vasodilation

65
Q

TX OF REYE’S SYNDROME

A
  • Reye’s syndrome is associated with fatty liver, hypoglycemia, and coma – childhood hepatic- encephalopathy.

This is linked to viral infection treated with aspirin.

Therefore, acetaminophen may be advised in place of aspirin.