Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PAM Semester 4 > Pharm GI Exam 1 > Flashcards

Pharm GI Exam 1 Flashcards

1
Q

Treatment for acute cholecystitis

A 
Initial treatment is supportive care
IV fluids
Electrolyte correction
pain meds (NSAIDS) (can use opioids)
Ketorolac (NSAID)
Morphine, diluadid, Demerol
(no longer meperidine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Acute calculous cholecystitis Tx

A 
Admit
Initial treatment is supportive care
IV fluids
Electrolyte correction
pain meds
IV ABX
Fasting
NG tube if vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acute cholecystitis IV ABX

A

Continue IV ABX until gallbladder removed

or cholecystitis resolves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Empiric abx for Acute cholecystitis

A

Cover most pathogens of
Enterobacteriaceae family
including gram negative rods
and anaerobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The most frequent isolates from the gall bladder and common bile duct are…

A

Ecoli 41%
Enterococcus 12%
Klebsiella 11%
Enterobacter 9%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Single agent regimens of low risk, and hospital-acquired intra-abdominal infections

A

Ertapenem 1 G IV QD

Piper Taz 3.375 G IV Q6h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Single agent regimens of high risk, and hospital-acquired intra-abdominal infections

A

Imipenem 550mg IV Q6h

Meropenem 1 G IV Q8h

Doripenem 500mg IV Q8H

Piper Taz 4.5 G IV Q6H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Health care acquired intra abdominal infections

A 
Empiric therapy coverage for
Streptococci
Enterococci
Enterobacteriaceae resistant to 3rd gen cef
Pseudomonas
Anaerobes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cholangitis S/S Charcot

A

Charcot’s triad
Fever
Jaundice
RUQ pain

50-75% of patients have all 3

Most common is fever and abdominal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cholangitis S/S Reynolds

A

Reynolds
Fever
Jaundice
RUQ pain

Plus

Hypotension
AMS

Other misc symptoms can include: Hepatic abscess, MSOD, shock, sepsis,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Acute cholangitis in elderly on glucocorticoids

A

Hypotension may be only symptom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Charcot’s triad

A

Fever
Abdominal pain
Jaundice

Should suspect Acute cholangitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Acute cholangitis treatment

A

Biliary drainage is required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Infectious Esophagitis CMV

treatment

A

Ganciclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Infectious Esophagitis HSV

treatment

A

Acyclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Infectious Esophagitis Candida

treatment

A

Fluconazole or ketoconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Medication induce esophagitis

meds that can cause it

A 
ABX eg tetracycline
Aspirin
NSAIDS
potassium chloride
quinidine 
iron
bisphosphonates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Medication induce esophagitis

factors that affect it

A 
size of med
position of patient
amount of fluid ingested with it
rate of esophageal transit
prolonged caustic contact
altered esophagus anatomy
increased age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

GERD treatment criteria

A

frequency
severity
presence or absence of erosive esophagus
or Barrett’s esophagus on upper gi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

GERD Tx

mild/intermittent
with no previous treatments
and no evidence of Barrett’s or erosion

A

lifestyle and diet changes

low dose histamine 2 receptor antagonists
(H2 blockers)
Antacids or sodium alginate
(for symptoms less than once a week)

If more than once a week
Increase to standard dose H2blockers
BID for minimum of 2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

GERD Tx

Persistent GERD

A

lifestyle and diet changes

Stop H2 blockers

Start PPI once a day at low dose
increase to standard dose if symptoms persist

once controlled,
should be continued for minimum of 8 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

GERD tx

with erosive esophagitis

A

lifestyle and diet changes

Initial acid suppression therapy with

Standard dose PPI

Once a day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

GERD in Pregnancy

A

lifestyle and diet changes

TX with
antacids
sucralfate

Avoid antacids with sodium bicarb
and
mag trisilicate

move on to H2 blockers
and PPI’s
if antacids don’t work

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Systemic antacids

A

Sodium bicarbonate

sodium citrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Non systemic antacids

A 
Magnesium hydroxide
Mag trisilicate
aluminum hydroxide gel
magaldrate
calcium carbonate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Antacid MOA

A

Usually contain combination of
Magnesium hydroxide
Mag trisilicate
calcium carbonate

this neutralizes gastric pH

This decreases exposure of esophageal mucosa to acid during reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Antacid onset/duration

A

Usually work within 5 minutes

short duration of
30-60 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Calcium carbonate

A

Tums

Warning
Hypoparathyroidism

interactions
Calcium blocks absorption of tetracyclines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Antacid misc info

A

NSAIDS should be taken with antacids

MOA - neutralizes gastric HCL

should not lower pH below 5 due to rebound hyperacidity

Foam is produce which can result in esophageal burning
give with simethicone (anti foam)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

sucralfate

A

Carafate (aluminum sucrose sulfate)

for short term tx of active duodenal ulcers and maintenance of healed ulcers
up to 8 weeks (tabs only)

Interactions
avoid antacids with 30 mins of taking
may reduce absorption
(cimetidine, ranitidine)

A surface agent that promotes healing protects form injury and adheres to mucosal surface

limited to GERD in pregnancy due to short acting compared to PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

sucralfate MOA

A

thought to form ulcer adherent complex at the ulcer site protecting it from further injury from stomach acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

sodium alginate

A

a poly saccharide derived from seaweed that forms a viscous gum that floats in the stomach and neutralizes the post prandial acid pocket in the proximal stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Histamine 2 receptor antagonists

A

decrease the secretion of acid by inhibiting the histamine 2 receptor on the gastric parietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Cimetidine

A

Tagamet (H2 blocker)

Warnings
impaired renal/hepatic function, elderly, debilitated, immunocompromised,

Preg Cat B,
not recommended for nursing mothers

interactions
Antacids within 1 hour of taking

Adverse
HA, diarrhea, dizziness, somnolence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Proton pump inhibitors

A

To be used in patients who fail twice daily H2 blockers

Patients with erosive esophagitis

frequent or sever GERD (2 or more times per week)

PPIs are the most potent inhibitors of gastric acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium (H-K) ATPase pump

PPIs should be administered daily rather than on-demand because continuous therapy provided better symptom control, quality of life, and higher endoscopic remission rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

PPI Onset

A

PPIs are most effective when taken 30 minutes before the first meal of the day because the amount of H-K-ATPase present in the parietal cell is greatest after a prolonged fast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Omeprazole indications

A

Prilosec

Used in triple therapy or dual therapy for H. Pylori
in duodenal ulcer disease
Short term active benign gastric ulcer
active duodenal ulcer
erosive esophagitis
maintenance of erosive esophagitis
Symptomatic GERD
pathologic hypersecretory conditions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Omeprazole

A

Prilosec
PPI

Warnings
Gastric malignancy

Adverse
HA, abdominal pain, N/V/D, flatulence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q 
Omeprazole dosage
(low)
A

10mg QD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q 
Cimetidine dosage
(low)
A

200mg BID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Foods that worsen GERD by lowering LES pressure

A 
Fatty meals
Mints
Chocolate
coffee
tea
garlic
onions
chili peppers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Meds that worsen GERD by lowering LES pressure

A 
Anticholinergics
Barbs
Caffeine
Dihydropyridine CCB
Dopamine
Estrogen
Ethanol
Nicotine
Nitrates
Progesterone
Tetracycline
Theophylline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Foods that worsen GERD by direct irritation

A

Spicy foods
Juices (tomato, orange)
Coffee

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Meds that worsen GERD by direct irritation

A 
Alendronate
Aspirin
NSAIDS
Iron
Quinidine
Potassium chloride
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Mallory Weiss syndrome tx

A

IV PPI BID (initial)
(for all patients suspected of upper GI bleed)
prior to endoscopy

Continue standard therapy for 2 weeks
Omeprazole 20mg QD
after endoscopy

These promote hemostasis by neutralizing gastric acid and stabilizing blood clots

PPI and antiemetics

Antiemetics are for persistent nausea and vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

For patients with disorders of esophageal hyperperistalsis and GERD symptoms

A

PPI BID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

For patients with no GERD (or well controlled GERD) but have dysphagia
tx

A 
Peppermint oil
(2 altoids taken sublingually before each meal)

if no improvement, CCB (diltiazem 60-90 mg QID

If CCB not effective, low dose TCA
(imipramine 25mg at bed time)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Esophageal strictures

tx

A

After esophageal dilation
PPI
Omeprazole 20mg BID x 1 year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Esophageal varices

vasoactive meds tx

A

Med to be started at time of presentation and not held pending diagnosis

Vasoactive meds decrease portal blood flow and have shown to decrease mortality and improve hemostasis with acute variceal bleeding
(octreotide, terlipressin, somatostatin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Esophageal varices

BB Tx

A

Goal of treatment is to decrease portal venous inflow

Non selective beta blockers block the adrenergic dilatory tone in mesenteric arterioles

This results in unopposed alpha adrenergic mediated vasoconstriction and therefore decrease venous inflow

Propranolol and nadolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Esophageal varices

Acute management

A 
Hemodynamic resuscitation
Octreotide
Banding
Sclerotherapy
Prophylactic ABX (ceftriaxone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Esophageal varices

Chronic management

A

Beta blockers

Endoscopic variceal ligation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Hep A vaccine

A

Havrix (inactivated)

Contraindications
Neomycin allergy

Interactions
immunosuppressives may reduce efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Hep B Diagnoses

A

Based on detection of Hep B surface antigen (HBsAG)
and IgM antibody to hepatitis B core antigen

Treatment is mainly supportive

The decision to start treatment is based on presence of cirrhosis, ALT and HBV DNA level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Hep B Tx

A

Treatment is mainly supportive

The decision to start treatment is based on presence of cirrhosis, ALT and HBV DNA level

for treatment naïve patients
nucleotide analogue
we recommend tenofir or entecavir

Tenofovir alafenamide 25mg QD
tenofovir disoproxil fumarate 300mg QD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

tenofovir alafenamide

A

Vemlidy 25mg

Nucleoside analogue (reverse transcriptase inhibitor)

Chronic Hep B Virus in patients with compensated liver disease

Warning
Post treatment severe acute exacerbation of Hep B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

tenofovir MOA

A

Nucleotide analogue of AMP

Inhibits HBV polymerase

First approved for treatment of HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

emtricitabine MOA

A

Nucleoside analog of cytosine active against HIV and ABV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Hep B Vaccine

A

Recombivax HB

Contra
yeast hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

HCV infected patient education

A

HCV-infected patients should be counseled on measures to decrease the risk of transmission and correcting factors associated with accelerated liver disease, including alcohol use, obesity and insulin resistance, and marijuana use.

Substance use treatment is also an important element of care in patients who have ongoing illicit drug use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Protease inhibitors Meds

A 
Telaprevir
boceprevir
asunaprevir
simeprevir
faldaprevir
MK-5172r

Translation and polyprotein processing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

NNPI Meds

A 
Deleobuvir
filibuvir
setrobuvir
tegobuvir
VX-222

RNA replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Hep D tx

A

Optimal treatment is uncertain

Treatment of choice for chronic Hep D is
interferon Alfa (IFNa)

Mainstay of treatment for Hep D is vaccination against Hep B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Hep E Tx

A

12 week course of ribavirin monotherapy to certain non pregnant patients with chronic Hep E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Ribavirin

A

Copegus (nucleoside analogue)

Contraindications:

Hemoglobinopathies
(thalassemia, sickle cell)

Preg Cat X

Male partners of pregnant women

66
Q

Lactulose

A

Cephulac (colonic acidifier)

Prevention and treatment of portal systemic encephalopathy
including stages of hepatic pre-coma and coma

Contra
Patients who require a low galactose diet

Adverse
Gas, cramping, diarrhea, nausea, vomiting

67
Q

Lactulose MOA

A

Synthetic disaccharide of galactose and fructose

Resists intestinal disaccharidase activity

MOA
Hydrolyzed in the colon to short chain fatty acids
Stimulate colonic propulsive motility

68
Q

Which of the below is the most common low dosage of omeprazole?

10 mg once a day by mouth
20 mg once a day by mouth
30 mg once a day by mouth
40 mg once a day by mouth

A

10 mg once a day by mouth

69
Q

Which of the following medications is would be used for the pharmacologic treatment is to decrease portal venous inflow secondary to esophageal varices?

atenolol
propranolol
acetabutol
metoprolol

A

propranolol

70
Q

Which of the below medications is considered a histamine-2 antagonist?

Sucralfate
Omeprazole
Cimetidine
Calcium carbonate

A

Cimetidine

71
Q

Which of the below medications is considered a proton pump inhibitor?

Sucralfate
Omeprazole
Cimetidine
Calcium carbonate

A

Omeprazole

72
Q

Which of the following is not one of the most frequent isolates from the gallbladder or common bile duct

Escherichia coli
Enterococcus
Klebsiella
Streptococci

A

Streptococci

73
Q

Antacid

Gastric acid neutralizers

A

Systemic
Sodium bicarbonate
Sodium citrate

Nonsystemic
Magnesium hydroxide
Magnesium trisilicate
Aluminum hydroxide gel
magaldrate
calcium carbonate
74
Q

GI anticholinergics

A

Chloridiazepoxide / clidinnium (Librax)
for IBS and PUD

Dicyclomine (Bentyl) for IBS

75
Q

Gastrointestinal drugs

Antispasmodics

A

Used to treat symptoms such as pain and spasm in irritable bowel syndrome

Antimuscarinics and anticholinergics
Hyoscine
Butylbromide
Atropine
Dicyclomine
Propantheline
Smooth muscle relaxants
Drotaverine
Alverine
Mebeverine
Peppermint oil
76
Q

Causes of gastritis

A 
autoimmune
pernicious anemia
H Pylori
NSAIDS
ETOH
Stress from 
CNS injury, burns, sepsis, surgery
77
Q

Peptic ulcer disease

A

A defect in the gastric or duodenal wall that extends through the muscularis mucosa into the deeper layers of the wall

Tx is based on etiology, ulcer characteristics and anticipated natural history

78
Q

PUD and H. Pylori

A

Patients with peptic ulcer disease should be tested forHelicobacter pylori(H. pylori).

Patients withH. pylorishould be treated with a goal of eradication ofH. pyloriinfection.

In patients treated forH. pylori,eradication of infection should be confirmed four or more weeks after the completion of eradication therapy.

79
Q

PUD and NSAIDS

A

Patients with peptic ulcers should be advised to avoid nonsteroidal anti-inflammatory drugs (NSAIDs).

Contributing factors should be addressed and treated (eg, treating medical comorbidities, poor nutritional status, ischemia).

80
Q

PUD anti-secretory therapy

A

All patients with peptic ulcer disease should receive anti-secretory therapy to facilitate ulcer healing.

The choice and duration of therapy varies based on the etiology, ulcer location (eg, gastric or duodenal), and the presence of ulcer complications (eg, bleeding, perforation, penetration, or gastric outlet obstruction).

All patients with peptic ulcers should receive anti-secretory therapy with a proton pump inhibitor (PPI) (eg,omeprazole20 to 40 mg daily or equivalent) to facilitate ulcer healing

81
Q

PUD and duodenal ulcers

A

Patients with duodenal ulcers who have been treated do not need further endoscopy unless symptoms persist at four weeks or recur.

82
Q

PUD and PPI

A

PPI use results in faster control of peptic ulcer disease symptoms and higher ulcer healing rates as compared with H2RA (eg, famotidine) as a consequence of stronger acid suppression.

PPIs also heal NSAID-related ulcers more effectively as compared with H2RAs

83
Q

PUD and H2 blockers with PPI

A

Combining PPIs and H2RAs adds to cost without enhancing healing.

Although antacids andsucralfatecan heal duodenal ulcers, they are not routinely recommended to treat peptic ulcers as PPIs heal ulcers more rapidly and to a greater extent.

84
Q

H. pylori tx

A

Bismuth quad therapy
Bismuth, metronidazole, tetracycline, PPI

Clarithromycin Triple therapy
Amoxicillin, clarithromycin, PPI

Clarithromycin/metronidazole triple therapy

Clarithromycin, metronidazole, PPI

85
Q

bismuth subsalicylate

A

Pepto bismol OTC (262mg)
Antidiarrheal

Contra
Varicella or influenza in peds and teenagers

Warnings
Coagulation disorders, diabetes, reyes, pregnancy, nursing mothers (not recommended)

Interactions
Potentiates anticoagulants

Adverse
Darkened tongue and stool

86
Q

Antidiarrheal MOA

A

Adsorbents

Coats the walls of the GI tract

Bind to the causative bacteria or toxin which are then eliminated through stool

Pepto bismol
Kaopectate

87
Q

Prophylactic treatment with PPI

A

Should be considered in patients with a history of ulcer who require daily NSAIDs use,

as well a history of complications like bleeds, need for chronic steroid use or anticoagulant use.

88
Q

Pyloric stenosis

A

IHPS is typically treated with surgical pyloromyotomy.

If the child is well hydrated with normal electrolytes, and if surgeons with expertise in the procedure are available, surgery may take place on the day of diagnosis.

Surgery should be delayed in the setting of dehydration and/or electrolyte derangements until these abnormalities are corrected with appropriate fluid and electrolyte therapy.

Mild regurgitation after pyloromyotomy is common and should not delay the initiation of feeding.

89
Q

Acute pancreatitis types

A

Edematous

Necrotizing

90
Q

Causes of pancreatitis

A

Heavy alcohol use 40%

Gallstones 40%

Other 20%
Trauma
meds
infection, tumor
High calcium
High TGL
Genetic
91
Q

Acute pancreatitis treatment

A

Supportive care
Lots of fluids in first 24 hours
pain control
Electrolyte and metabolic corrections

The majority of patients with mild pancreatitis require no further therapy, and recover within three to seven days.

Patients with moderately severe and severe pancreatitis require more intensive monitoring as they have transient (<48 hours) or persistent (>48 hours) organ failure and local or systemic complications.

92
Q

Acute pancreatitis most common symptom

A

Abdominal pain is often the predominant symptom in patients with acute pancreatitis.

Adequate pain control requires the use of intravenous opiates, such asmorphineandfentanyl, usually in the form of a patient-controlled analgesia pump.

93
Q

Chronic pancreatitis

A

Presents with chronic unrelenting pain with episodic flares

94
Q

The goal of treatment in chronic pancreatitis

A

The goals of treatment include pain management, correction of pancreatic insufficiency, and management of complications.

95
Q

Pain management in chronic pancreatitis

A

Pain management should proceed in a stepwise approach.

Initial treatment begins with recommendations to stop alcohol and tobacco and to eat small meals that are low in fat.

We suggest the use of pancreatic enzyme supplements in patients with pain persisting after the above interventions. These relieve pain in some patients and are generally safe.

Treatment with acid suppression (either with an H2 receptor blocker or a proton pump inhibitor) should be given along with pancreatic enzyme supplements to reduce inactivation from gastric acid.

Analgesics with opiates and/or nonsteroidal anti-inflammatory agents can be considered if pancreatic enzyme therapy fails to control pain.

Adjuvant therapy withpregabalincan be considered in patients whose pain is not adequately controlled with opiates and/or nonsteroidal anti-inflammatory agents.

96
Q

Chronic pancreatitis and diet

A

Steatorrhea (fat malabsorption) may develop in patients with severe pancreatic exocrine dysfunction. Treatment depends upon the severity of disease.

Dietary modification should begin with restriction of fat intake (to less than 20 g per day).

For patients who do not respond to dietary restriction, we suggest lipase supplementation.

As a general rule, 30,000 international units (IU) of pancreatic lipase (90,000 United States Pharmacopeia units [USP]) swallowed during each meal should suffice in reducing steatorrhea and preventing weight loss. Fat soluble vitamin replacement may be required.

Medium chain triglycerides(MCTs) can provide extra calories in patients with weight loss and a poor response to diet and pancreatic enzyme therapy.

97
Q

lipase

A

Ku-zyme (digestive enzyme)
supplement in digestive enzyme deficiency

Contra
Acute pancreatic exacerbations, pork allergy

Interactions
Avoid antacids

Adverse
diarrhea

98
Q

Digestive enzymes

Amylase

A

Breaks down carbohydrates to sugars

99
Q

Digestive enzymes

protease

A

Breaks down proteins to amino acids

100
Q

Digestive enzymes

lipase

A

Breaks down fats to fatty acids

101
Q

Anorectal abscess treatment

A

Surgical drainage is primary treatment

should be drained promptly;

lack of fluctuance should not be a reason to delay treatment.

Any undrained anorectal abscess can continue to expand into adjacent spaces as well as progress to generalized systemic infection.

Give empiric abx
4-5 days of Augmentin or cipro + flagyl

102
Q

Anorectal abscess wound culture

A

Not necessary unless suspicion or immunosuppression

103
Q

Anorectal abscess WASH

A

Warm water sitz bath
Analgesics
Stool softener
High fiber diet

104
Q

Stool Softners

A

Docusate sodium

Docusate calcium

105
Q

Docusate sodium

A

Colace (stool softener)

interactions
may increase systemic absorption of mineral oil

MOA
Increases penetration of fluid into stool
Softens stool to facilitate passage

106
Q

Anal fissure treatment

A

initial therapy with a combination of supportive measures
(fiber, stool softener, sitz bath, topical analgesic)
and one of the topical vasodilators (nifedipineornitroglycerin) for one month,
rather than surgery.

For patients who have access to a compounding pharmacy, we suggestnifedipineointment rather thannitroglycerinointment as the topical vasodilator.

Nifedipine ointment has fewer side effects and potential drug interactions compared with nitroglycerin and may be more effective.

107
Q

Constipation
Chronic
Tx

A 
Patient education
Lifestyle modifications
Diet 
Laxatives
Enema
108
Q

Constipation in patients over 70

A

Warm water enema
rather than sodium phosphate

Sodium phosphate complications in elderly

associated with complications including hypotension and volume depletion, hyperphosphatemia, hypo- or hyperkalemia, metabolic acidosis, severe hypocalcemia, renal failure, and electrocardiogram changes (prolonged QT interval).

109
Q

Idiopathic constipation

tx

A

dietary fiber
bulk-forming laxatives such aspsylliumormethylcellulose,

together with adequate fluids.

110
Q

Constipation

cant tolerate fiber or bulk laxatives

A

Osmotic laxatives
Stool, softeners
Stimulant laxatives
Secretory laxatives

111
Q

Constipation drugs

Bulk forming laxatives

A

Psyllium
Methylcellulose

Side effects
Impaction above strictures
Fluid overload
Gas and bloating

112
Q

Psyllium

A

Metmucil (OTC)

Contra
S/S of appendicitis
Obstruction, impaction, dysphagia

Warnings
Rectal bleeding, esophageal narrowing, Diabetes

Adverse
Obstruction

113
Q

Constipation drugs

Surfactants (softeners)

A

Docusate sodium
Docusate calcium

Adverse
Well tolerated
use lower dos if given with another laxative
contact dermatitis

114
Q

Constipation drugs

Osmotic laxatives

A 
Lactulose
Sorbitol
Glycerin
Magnesium sulfate
Magnesium citrate
Polyethylene glycol
115
Q

polyethylene glycol

A

Miralax (OTC) (osmotic laxative)

Contra
Obstruction

Adverse
Loose watery frequent stools

116
Q

Constipation drugs

Stimulant laxatives

A

Bisacodyl

Senna

117
Q

Bisacodyl

A

Dulcolax 10mg (Stimulant laxative)

Interactions
Do not take within 1 hour after antacids or milk (TABS)

Adverse
Abdominal discomfort, faintness, cramps
Suppositories: Rectal burning

118
Q

Bulk forming laxatives (fiber)

MOA

A

Retention of water in the stool

must be taken with adequate fluid intake

119
Q

Stool softeners

MOA

A

Detergent, traps water in the stool

120
Q

Osmotic laxatives

A

osmotically pulls water into the stool

121
Q

Stimulant laxatives

A

increases contraction of intestinal muscle and increase peristalsis

122
Q

Fecal impaction tx

A

Digital disimpaction

warm water enema with mineral oil to soften and assist passage

123
Q

Mineral oil enema

A

Fleet enema

Lubricant laxative

124
Q

Hydorcortisone acetate 25mg

A

Anusol (steroid)

Adverse
Dermal and epidermal atrophy
poor wound healing
local irritation

125
Q

IBD

Crohn’s

A

Choice of therapy depends on location of disease, severity of disease and whether goal is to induce remission or maintain remission

5-ASA (sufasalazine, mesalamine)

Glucocorticoids (prednisone, budesonide)

Immunomodulators (azathioprine, methotrexate)

Biologics (-mabs, certolizuma, pegol , etc)

126
Q

5 types of meds used to treat IBD

A

Amino salicylates (anti-inflammatory)

Corticosteroids (anti-inflammatory)

Immunomodulators (suppress the immune system)

ABX (infection)

Biologics (blocks protein Tumor necrosis factor)

127
Q

Oral 5 -amino salicylates MOA

A

Mesalamine
Sulfasalazine
Balsalazide

MOA
interfere with the production of arachidonic acid by affecting the thromboxane and lipoxygenase synthesis pathway

Used mainly for UC and less for Crohn’s

128
Q

Oral 5-amino salicylates-sulfasalazine

A

Azulfidine

For moderate to severe UC
Adjunct in severe UC
Prolong remission between attacks

Contra
intestinal or urinary obstruction, porphyria

Interactions
Reduces absorption of digoxin and folic acid

129
Q

Sulfasalazine MOA

A

Reaches the colon intact
Then metabolized into 5-ASA and sulfa-pyridine

Used for UC and Crohn’s as initial therapy or to maintain remission

0.5g PO BID
increase to 0.5-1.055g PO QID if tolerated

Remission 1g PO BID-QID

130
Q

mesalamine

A

Lialda (amino salicylate)

Interactions
Increased toxicity with nephrotoxic drugs (ie NSAID)

Adverse
UC, HA, flatulence, LFT’s, Abdominal pain, acute intolerance syndrome

131
Q

Glucocorticoids MOA

A

Treats inflammation

132
Q

Immunomodulators

A

Azathioprine
6 mercaptopurine
methotrexate

Purine analogues (prodrugs)

MOA
impair purine biosynthesis and inhibit cell proliferation

Treatment of steroid dependent/resistant disease

UC, Crohn’s
Recurrence
Fistulas

133
Q

infliximab

A

Remicade (tumor necrosis factor blocker)

Contra
Moderate or sever heart failure (dose over 5mg)
allergy to murine proteins

Warning
Serious infections
Malignancy

134
Q

IBS

A

Lifestyle mods
Diet (limit gas producing foods FODMAPS)
Limit lactose and gluten

Trial of psyllium in patients with IBS constipation

If Psyllium fails, polyethylene glycol

If laxatives fail
Trial of lubiprostone or linaclotide

135
Q

FODMAPS

A 
Fermentable 
oligosaccharides
disaccharides
monosaccharides
and 
polyols
136
Q

Constipation meds

Non Laxatives

A

Lubiprostone

Linaclotide

Plecanatide

137
Q

lubiprostone

A

Amitiza

IBS with constipation in women

Contra
Obstruction

Adverse
NVD, abdominal pain, hypotension, dyspnea

138
Q

lubiprostone MOA

A

opening of chloride channels locally in the GI luminal epithelium, which stimulates chloride rich intestinal fluid secretion and shortens GI transit times

139
Q

Diarrhea meds with IBS

A

Lopermide

diphenoxylate / atropine (Lomotil)

140
Q

Lopermide

A

Imodium (antidiarrheal)

Warnings
Acute UC or pseudo colitis, discontinue if distention, If taking too much, serious cardiac events or death, abnormal heart rhythm, Hepatic dysfunction, CNS Toxicity

Adverse
Abdominal pain, distention, constipation, dry mouth, nausea, drowsiness, dizziness, fatigue, rash

141
Q

diphenoxylate / atropine

A

Lomotil 2.5mg/0.025mg (Opioid anticholinergic)
Diarrhea

Contra
<6yrs resp/CNS depression, Sepsis, jaundice, pseudomembranous colitis, bacteria

Warnings
Dehydration, electrolyte imbalance, acute UC
Hepatic/renal impairment, drug users

Interactions
ETOH

Adverse
NVD, Abdominal pain, paralytic ileus, toxic mega colon

142
Q

diphenoxylate / atropine
Lomotil
controlled substance category

A

Category 5

143
Q

Intestinal ischemia

A

Abdominal pain is most common symptom of intestinal ischemia

Pain out of proportion to exam

144
Q

Colonic ischemia

A

Colonoscopy or sigmoidoscopy

used to diagnose colonic ischemia

145
Q

Goal of treatment for acute intestinal ischemia

A

restore blood flow as rapidly as possible after initial supportive management

146
Q

Ischemic bowel

Initial management

A 
GI decompression
Fluid resuscitation
hemodynamic support
electrolytes
pain control
anti coagulation
Broad spectrum ABX
147
Q

Ischemic bowel

Pain control

A

Judiciously controlled

use parenteral opioids

148
Q

Ischemic bowel

Anticoagulation

A

systemic anticoagulation to prevent thrombus formation
unless patients are actively bleeding
If abdominal exploration is required, continue anticoagulant after surgery

149
Q

Ischemic bowel

ABX

A

Broad spectrum ABX

150
Q

Obstruction Tx

A 
NPO
NG suction / decompression
IV fluids
Pain meds
Surgery
151
Q

Toxic megacolon

A

Contraindicated:
Bowel prep
barium enema
colonoscopy

Due to risk of perforation

152
Q

122

A

122

153
Q

Vancomycin

non-severe C Diff

A

WBC <15,000 / serum Cr <1.5

125mg PO QID x 10 days

154
Q

Fidaxomicin

non-severe C Diff

A

WBC <15,000 / serum Cr <1.5

200mg PO BID x 10 days

155
Q

Vancomycin

severe C Diff

A

WBC >15,000 / serum Cr >1.5

125mg PO QID x 10 days

156
Q

Fidaxomicin

severe C Diff

A

WBC >15,000 / serum Cr >1.5

200mg PO BID x 10 days

157
Q

Fidaxomicin

A

Dificid (macrolide)

N/D, Abdominal pain, GI hemorrhage, anemia, neutropenia

158
Q

Diverticulitis tx

Outpatient

A

Found on CT, can be out patient

Outpatient tx is ABX for 7 to 10 days

reassess 2-3 days after ABX started

Patients who fail outpatient should be admitted

159
Q

Diverticulitis

Inpatient

A

Inpatient treatment of acute colonic diverticulitis typically begins with administration of intravenous antibiotics, intravenous fluids, and parenteral pain medications.

Patients can be made nil per os (NPO) to allow for bowel rest or be offered a clear liquid diet depending upon their clinical status.

Patients without complications typically show clinical response within two to three days, at which point their diet can be further advanced.

Patients who continue to improve are discharged with oral antibiotics to complete a total of 10 to 14 days of antibiotic therapy.

Patients who fail inpatient treatment require surgery.

160
Q

Anti emetics for Mallory Weiss

A

Metoclopramide

Prochlorperazine

161
Q

Smooth muscle relaxants

A

-verine

peppermint oil

162
Q

anticholinergic / antimuscarinic

A

Hyo
buytl
atropine

PAM Semester 4 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions