Gi Pharmacology+Pancreaticobiliary

Front 1

4 Strategies to treat ulcers

Back 1

1. Reduce Acid secretion from parietals
2. Neutralize acid in lumen
3. Protect mucosa from acid
4. Eradicate H.Pylori

Front 2

3 pathways for parietal control

Back 2

1. Vagus Nerve
2. Gastrin (endocrine)
3. Histamine (paracrine)

Front 3

Cons to Cimetidine (tagamet)

Back 3

Inhibits cytochrome P450 activity
Anti-androgen activity

Front 4

why is ranitidine better?

Back 4

less side effects

Front 5

what is the most potent H2RA?

Back 5

famotidine (pepcid)

Front 6

what is another H2RA that is more or less equipotent to ranitidine?

Back 6

Nizatidine (axid)

Front 7

what is the most widely used genre of drugs worldwide?

Back 7

PPI'S!

Front 8

Mechanism of PPI's

Back 8

Irreversibly block H/K ATPase of the parietal cells
Only works on ACTIVE pumps
Given in inactive form, protonated and activated near parietals

Front 9

How long does a single dose of a PPI work?

Back 9

2-3 days

Front 10

who are the agents for enhanced mucosal protection?

Back 10

Bismuth cmpds
Sucralfate (Carafate)
Prostaglandin analogs (misoprostol, cytotec)

Front 11

Uniqueness of Omeprazole and importance.

Back 11

Omeprazole is a racemate (R and S). S is active. So S-only drug (esomeprazole=nexium) is available in market even though people with CYP 2C19 convert R to S. Sold b/c not everyone has 2C19

Front 12

Destruction of PPI's and prevention

Back 12

Destroyed at low pH (stomach), so they're encapsulated

Front 13

Main con to omep/esomep?

Back 13

not for immediate relief

Front 14

Bismuth Cmpds
1. mechanism

Back 14

Not exactly known
Maybe bacteriostatic against H.pylori
Maybe increases prostaglandins

Front 15

Contraindications of H2 blockers

Back 15

hypersensitive pts
impaired renal fxn
impaired liver fxn
elderly or debilitated
CPD
DM
immunocompromised

Front 16

Bismuth Cmpds
2. Side effects

Back 16

black poo
dark tongue

Front 17

Contraindications of PPI's

Back 17

Hypersensitive pts
impaired liver fxn
high dose toxic
long term use
>50yo

Front 18

Causes of ulcers

Back 18

1. H.pylori
2. NSAIDs
3. Malignancy

not stress

Front 19

2 Rx plans for Ulcers

Back 19

1. Clarithromycin Triple Therapy
PPI + Clarithromycin + amoxicillin/metronidazole

2. Bismuth Quadruple Therapy (pcn allergies)
PPI/H2RA + Bismuth + metronidazole + tetracycline

Front 20

Sucralfate
1. mech

Back 20

not exactly known
may bind the surface of ulcers to protect
maybe decrease pepsin and bile salts
maybe increases prostaglandins

Front 21

When do you attack H. pylori?

Back 21

when an ulcer (d or p) is present or when MALT is present. Not for asymptomatic or just dyspepsia

Front 22

Sucralfate
2. side effects

Back 22

constipation sometimes

Front 23

Biggest Problem with antacids

Back 23

Their Acid-Neutralizing Capacity would require us to take well over recommended dose-->SIDE EFFECTS

Front 24

Types of Antacids and their side effects

Back 24

ALUMINUM-absorb/chelate many drugs
MAGNESIUM-laxative action
CALCIUM-acid rebound, increase Ca in urine may lead to stones, constipation
SODIUM-avoid this one. complicates CHF and diuretic therapy for HBP, short duration, acid rebound

Front 25

Prostaglandin Analogs
1. indicated for

Back 25

NSAID-induced gastric ulcers
Labor-induction
Abortion-induction

Front 26

Prostaglandin Analogs
2. mech

Back 26

All about mucosa protection:
-decreases acid secretion through PG receptors
-reduces pepsin levels
-increases mucus and bicarb secretion

Front 27

Prostaglandin Analogs
3. Side Effects

Back 27

Abortions
Diarrhea
Other GI stuff

Front 28

Lifestyle factors contributing to ulcers

Back 28

Caffeine
Alcohol
Cigarettes
Stress
Surgery (as Rx)

Front 29

Rx of GERD

Back 29

1. PPIs
2. Coating Agents
3. Promotility/Prokinetic agents (tighten LES and promote emptying)- usually for progressive treatment

Front 30

PROKINETIC/PROMOTILITY DRUGS

Back 30

Metoclopramide
Bethanechol
Cisapride

Front 31

Prokinetic Agents
1. example
2. mech

Back 31

METOCLOPRAMIDE
-increases SI peristalsis
-increases tone and amplitude of stomach contractions
-tightens LES
-relaxes pyloric sphincter

Front 32

METOCLOPRAMIDE
1. Side Effects

Back 32

Similar to dopamine antagonists:
-hyperprolactemia
-parkinsonian effects

Front 33

Bethanechol
1. mech

Back 33

BETHANECHOL
Parasympathetic choline ester that stimulates specific muscarinic receptors-->inc motiity

Front 34

Bethanechol
1. contraindications
2. side effects

Back 34

1. asthma, PU's, incontinence
2. GI stuff, sweating, flushing

Front 35

CISAPRIDE
mechanism

Back 35

Parasympathomimetic that acts on 5-HT receptors
Increases muscle tone of LES

Front 36

CISAPRIDE
problem

Back 36

can lead to heart rhythm abnormalities and so its not prescribed anymore

Front 37

what is zollinger-ellison syndrome?

Back 37

Non-beta cell tumor of pancreatic islets
Produces gastrin in butt loads
Rx with PPI

Front 38

common role of all laxatives

Back 38

convert colon from primarily absorbing to secreting

Front 39

Laxative Classifications

Back 39

1. Bulk-forming
2. Stool Softeners
3. Lubricants
4. Stimulants
5. Osmotic

Front 40

BULK-FORMING AGENTS
1. popular examples
2. mech

Back 40

1. metamucil, bran, fiber, citrucel
2. cause poo to be bulkier and retain more water

Front 41

BULK-FORMING AGENTS
3. pros
4. time to work?

Back 41

3. gentlest laxative, minimal SE's
4. 1-3 days

Front 42

STOOL SOFTENERS
1. mech

Back 42

1. detergents/surfactants that act as poo-wetters, i.e. mix poo with water, lipids, etc.
-increases water and electrolyte secretion into intestines

Front 43

STOOL SOFTENERS
2. time till they work

Back 43

2. 1-3 days

Front 44

STOOL SOFTENERS
3. side effects

Back 44

3. Tolerance can develop quickly.
specific agents can screw with absorption of vitamins and other drugs

Front 45

LUBRICANTS
1. site of action
2. onset of action

Back 45

1. colon
2. 6-8 hours

Front 46

LUBRICANTS
3. example and mech

Back 46

3. mineral oil; it makes it slippery (malapsorption of KADE)

Front 47

STIMULANTS
1. mech

Back 47

1. stimulate motility
-promote accumulation of water and electrolytes in lumen

Front 48

STIMULANTS
2. SE'S

Back 48

2. N&V
abd cramps
rectal burning
SERIOUS: electrolyte imbalance
cathartic colon
(long term use)
MOST SEVERE LAXATIVE

Front 49

STIMULANTS
3. onset of action

Back 49

3. as short as 15 minutes to an hour

Front 50

OSMOTIC/HYRDRATING LAXATIVES
1. mech

Back 50

1. poorly and slowly absorbed --> more water in lumen

Front 51

OSMOTIC/HYRDRATING LAXATIVES
2. types

Back 51

Saline

Hyperosmotic

Front 52

OSMOTIC/HYRDRATING LAXATIVES
Saline
1. site of action
2. onset

Back 52

1. small and large intestine
2. 0.5-6 hours

Front 53

OSMOTIC/HYRDRATING LAXATIVES
1. examples

Back 53

milk of magnesia
epsom salt

Front 54

OSMOTIC/HYRDRATING LAXATIVES
1. side effects

Back 54

-can alter fluid and electrolyte balance
-can accumulate and screw with kidneys

Front 55

OSMOTIC/HYRDRATING LAXATIVES
HYPEROSMOTIC!
1. site of action
2. onset

Back 55

1. colon
2. 30 min - 3hrs

Front 56

OSMOTIC/HYRDRATING LAXATIVES
hyperosmotic
1. example
2. use

Back 56

1. lactulose
2. whole bowel irrigation

Front 57

OSMOTIC/HYRDRATING LAXATIVES
hyperosmotic
1. side effects

Back 57

1. cramps, gas, borborygmus

Front 58

Types of Diarrhea

Back 58

secretory
osmotic
motility-related
inflammatory

Front 59

mech for secretory diarrhea

Back 59

increased active secretion or decrease in absorption (cholera) --> water ends up in colon

Front 60

mech for osmotic diarrhea

Back 60

loss of water due to heavy osmotic load, like with malabsorption and nutrients remain in lumen

Front 61

mech for motility-related diarrhea

Back 61

motility is high-->not enough time to absorb water

Front 62

mech for inflammatory pooing

Back 62

damage to BB or mucosal lining leads to decreased absorption. Factors in the other 3 kinds can be seen with this one.

Front 63

Antidiarrheals

Back 63

Opiates
Adsorbents

Front 64

Opiates
1. 2 examples
2. side effects

Back 64

1. Loperamide (imodium) and Piphenoxylate
2. Dependence, constipation, mild euphoria, mild stimulationf

Front 65

Adsorbents
1. mech

Back 65

1. coat lining of GI tractto adsorb bacterial and toxin products

Front 66

Adsorbents
1. ex's

Back 66

1. bismuth subsalicylate and cholestyramine

Front 67

What is cholelithiasis

Back 67

the presence of gallstones

Front 68

composition of gallstones

Back 68

80% are cholesterol
rest are billirubin pigmented stones

Front 69

What are the 5 F's

Back 69

Female, Fat, Flatulence, Fertile, Fifty

Front 70

Acute Cholecystitis
1. types

Back 70

Calculous
Acalculous

Calculous means a stone is blocking, acalculous = no stones

Front 71

when does Acute Acalculous Cholecystitis typically occur?

Back 71

Post-Op, trauma, sepsis, burns

Front 72

ACUTE CHOLECYSTITIS
1. presents with

Back 72

-Acute onset of colicky pain after a fatty meal
-N&V of bilious material
-Pain becomes constant later
-RUQ-point tender, guarding, rebound
-Radiates to scapula
-Murphy's Sign

Front 73

Which is more common?
calc or acalc
acute or chronic

Back 73

Calculous is more common
Chronic is more common

Front 74

CHRONIC CHOLECYSTITIS
1. Presents with?

Back 74

-recurrent colicky post-fatty meal pain

Front 75

CHRONIC CHOLECYSTITIS
2. dx

Back 75

ultrasound

Front 76

CHRONIC CHOLECYSTITIS
3. Rx

Back 76

Surgery
Ursodiol-dissolves stones
Lithotripsy - not good cause fragments get stuck elsewhere

Front 77

What the crap is Choledocholithiasis?

Back 77

COMMON DUCT STONES!

Front 78

Pathogenesis of Choledocholithiasis?

Back 78

1. Cholangitis-gram neg infection, high fever, sepsis
2. Hepatic abscess
3. Chronic liver disease - secondary biliary cirrhosis

Can also cause pancreatitis

Front 79

Cholangiocarcinoma!
1. pathogenesis

Back 79

1. arises from intra and extra-hepatic billiary tree

Front 80

Cholangiocarcinoma
2. types?

Back 80

Gallbladder (most common)
Klatskin
Common duct????

Front 81

Cholangiocarcinoma
Gallbladder
1. demo's

Back 81

1. older women with H/O chronic cholelithiasis or liver parasites

Front 82

What's up with the Klatskin Tumor?

Back 82

1. Arises at the bifurcation of the right and left common hepatic ducts

Front 83

Cholangiocarcinoma
1. prognosis

Back 83

1. DISMAL, <1% mean 5yr survival

Front 84

ACUTE PANCREATITIS
1. what it is

Back 84

enzymatic necrosis of pancreatic parenchyma

Front 85

ACUTE PANCREATITIS
2. common cause

Back 85

protolytic destruction of pancreas via activated trypsin!

Front 86

ACUTE PANCREATITIS
3. destruction leads to?

Back 86

3. necrosis of blood vessels with hemorrhage
-necrosis of fat: saponification
-inflammation rxn-->fluid loss

Front 87

ACUTE PANCREATITIS
1. clinical etiologies

Back 87

1. Booze and gallstones (80%)
Hyperlipidemia, hypercalcemia
drugs
genetics
shock
infectious diseases

Front 88

ACUTE PANCREATITIS
1. theories of etiology

Back 88

1. WRONG: channel/ductal obstruction
MAYBE RIGHT: Primary Acinar Cell Injury-->
-abnormal trypsinogen activation
-defective intracellular transport of proenzymes

Front 89

ACUTE PANCREATITIS
1. presentation

Back 89

1. acute epigastric pain, N&V
if really bad: shock, sepsis, ARDS, multi-organ failure

Front 90

ACUTE PANCREATITIS
1. differential dx

Back 90

rule out perf ulcer, acute cholecystitis, bowel infarct

Front 91

ACUTE PANCREATITIS
1. dx

Back 91

-Amylase and Lipase should be INCREASED?
-In severe AP: hypocalcemia, elevated bili, hyperglycemia

Front 92

Which isoenzyme of amylase is important for AP?

Back 92

ALPHA-Amylase

Front 93

ACUTE PANCREATITIS
Rx for Mild AP

Back 93

NPO
Fluid Support

Front 94

ACUTE PANCREATITIS
Rx for severe Ap

Back 94

ICU
Antibiotics
Surgical Debridement

Front 95

CHRONIC PANCREATITIS
1. etiology

Back 95

Booze
Hypercalcemia
hyperlipidemia
malnutrition
idiopathic (50%)

Front 96

CHRONIC PANCREATITIS
2. pathogenesis

Back 96

2. Hypersecretion of concentrated proteins (CFTR mutation)
-ductal plugs, dilation and stones
-Calcium Carbonate precipitates
Parenchymal Fibrosis and Atrophy

Front 97

CHRONIC PANCREATITIS
1. Clinical Presentation

Back 97

1. Repetitive moderate abd pain-->endstage is unrelenting
-diabetes
-fat malabsorption
-cystic dilation of pancreatic duct-->chain of lakes
-pseudocysts

Front 98

CHRONIC PANCREATITIS
1. Dx

Back 98

1. Pain
Jaundice
Stool Eval
Bentiromide Test
Imaging

Front 99

What is the bentiromide test?

Back 99

deals with PABA and the renal secretion of converted bentiromide?

Front 100

CHRONIC PANCREATITIS
Rx?

Back 100

very little, give enzymes PO

Front 101

Benign Exocrine Neoplasms

Back 101

Microcystic Serous Cystadenoma
Mucinous Cystadenoma
Intraductal Papillary Mucinous Neoplasm

Front 102

Malignant Exocrine Neoplams

Back 102

Adenocarcinoma (only one on test)
Serous/Mucinous cystadenocarcinoma
Acinar Cell Carcinoma
Papillary and Solid epithelial neoplasms

Front 103

ADENOCARCINOMA
Etiology and Pathogenesis

Back 103

Arises from ductal epithelium
Smoking inc risk
Older pts
Hereditary pancreatitis (40-fold inc)
Genetic Aberrations (k-ras, p53, HER2, etc)

Front 104

ADENOCARCINOMA
Location

Back 104

60% head-->painless jaundice
20% body
5% tail

Front 105

ADENOCARCINOMA
Differentiation

Back 105

Gray-white scirrhous tumor w/ interspersed malignant glands

Front 106

ADENOCARCINOMA
spread?

Back 106

surrounding structures and nodes
Hepatic metastases

Front 107

Three tumors that cause painless jaundice?

Back 107

1. Pancreatic Adenocarcinoma
2. Cholangiocarcinoma of common duct
3. Ampullary carcinoma of vater

Front 108

ADENOCARCINOMA
dx

Back 108

Pain
Painless Jaundice
Labs: bilirubin and CA19-9
Imaging

Front 109

ADENOCARCINOMA
Rx

Back 109

Surgical: better for tail
Whipple procedure
+/- for rad/chemo

Front 110

What's a whipple surgery?

Back 110

take out part of stomach, duodenum, etc. and pancreas

high surgical mortality