Pharm Block 7

Front 1

METRONIDAZOLE MOA

Back 1

Nitro group serves as an electron acceptor (reduced) → forms ROS → cell death

Front 2

METRONIDAZOLE SPECTRUM / USE

Back 2

GGETBaC
DOC:
Entamoeba histolytica
Giardia lamblia
Trichomonas vaginalis

Front 3

METRONIDAZOLE IS USUALLY GIVEN WITH THIS LUMINAL AMEBICIDE DRUG. --> WHY?

Back 3

Diloxanide furoate 90% cure rate

Front 4

BECAUSE OF ITS METABOLISM BE CAUTIOUS IF GIVING METRONIDAZOLE TO PTS WITH ________ BECAUSE THE DRUG ACCUMULATES THERE

Back 4

LIVER DISEASE

Front 5

METRONIDAZOLE SE

Back 5

*DISULFIRAM- LIKE RXN
*METALLIC TASTE IN MOUTH

Front 6

Diloxanide furoate can only be obtained by _______ WHAT IS ITS ONLY INDICATION?

Back 6

can only get it from CDC. ONLY USED TO TREAT INTESTINAL AMEBIASIS

Front 7

Diloxanide furoate S.E.

Back 7

MILD - FLATULENCE

Front 8

name 1 Systemic amebicide

Back 8

Chloroquine

Front 9

Primaquine WHAT TYPE OF DRUG, IS ONLY EFFECTIVE AGAINST THIS FORM ___

Back 9

MALARIA DRUG EXOERYTHROCYTIC FORMS (malaria not inside RBC = tissue schizont)

Front 10

Primaquine MOA

Back 10

ACTS AS AN OXIDANT WHICH MAY CAUSE ITS SIDE EFFECTS

Front 11

Primaquine SE WHICH OCCURS MOST COMMONLY IN THESE PTS

Back 11

DRUG INDUCED HEMOLYTIC ANEMIA, IN PTS WITH LOW LEVELS OF G6PD (glucose-6-phosphate dehydrogenase).

Front 12

Chloroquine GIVE ALL 4 MOA

Back 12

1) In RBC, interferes with heme polymerase → soluble heme (TOXIC) kills parasite.
2) Binds ferriprotoporphyrin 9→ damages RBC membrane →RBC & parasite lysis.
3) Alkalinization of food vacuole→ prevents parasite heme digestion
4) ↓ DNA synthesis

Front 13

Chloroquine TYPE / USE (2)

Back 13

Blood schizonticide
DOC FOR PLASMODIUM FALCIPARUM & Systemic amebicide

Front 14

Chloroquine SE

Back 14

QUINIDINE EFFECT (ECG changes), chronic Tx = discolor nail beds, and visual disturbances

Front 15

Quinine TYPE / USE

Back 15

(Cinchona alkaloid) - Blood schizonticide; Chloroquine-resistant acute malaria

Front 16

Quinine GIVE ALL 3 MOA

Back 16

1) Inhibits heme polymerase
2) Damages membrane
3) Affects DNA synthesis

Front 17

Quinine SE

Back 17

Cinchonism: nausea, vomiting, tinnitus, vertigo (reversible). Potentiation of neuromuscular blocking agents

Front 18

Mefloquine TYPE

Back 18

Blood Schizonticide

Front 19

Mefloquine MOA / BEST ADVANTAGE

Back 19

Damages parasite→ membrane
T1/2 = 17 DAYS (GIVEN ONCE WEEKLY)

Front 20

Mefloquine
-SE
-CAUTION IN THESE PTS

Back 20

CNS: dizziness, disorientation, hallucinations
(caution to scuba divers).

Front 21

WHAT DO YOU GIVE FOR MALARIA PROPHYLAXIS?

Back 21

Chloroquine

Front 22

Melarsoprol

MOA

Back 22

Reacts with sulfhydryl group of enzymes in organism & host

Front 23

Melarsoprol

USE

Back 23

DOC: late-stage T. brucei gambiense & rhodesiense with CNS involvement.

Front 24

Melarsoprol

SE

Back 24

CNS: encephalopathy

Front 25

Pentamidine isethionate

MOA

Back 25

Binds to parasite’s DNA
→ interferes with synthesis of DNA, RNA proteins.

Front 26

Pentamidine isethionate

USE / NOT EFFECTIVE AGAINST _____

Back 26

T. brucei gambiense during hematological stage & Pneumocystis carinii

NOT effective against T. cruzi.

Front 27

Pentamidine isethionate CANNOT BE GIVEN ___ BECAUSE ____

Back 27

DO NOT give IV
causes tachycardia, ↓↓↓ BP

Front 28

Pentamidine isethionate

SE

Back 28

**Toxicity to β cells of pancreas
Renal dysfunction (reversible).
Hypotension

Front 29

Pentamidine isethionate

KINETICS

Back 29

DOES NOT ENTER CNS

Front 30

Nifurtimox

MOA

Back 30

Nitroaromatic compound that’s reduced→ forms ROS → cell death

Front 31

Nifurtimox

USE

Back 31

ONLY acute T. cruzi infections
(effective against organisms that lack catalase)

Front 32

Nifurtimox

SE

Back 32

Anaphylaxis, (Delayed hypersensitivity)
Peripheral neuropathy

Front 33

Sodium stibogluconate

MOA

Back 33

Inhibits phosphofructokinase → inhibits glycolysis.

Front 34

Sodium stibogluconate

USE

Back 34

3 types of leishmaniasis
Cutaneous
Mucocutaneous
Visceral

Front 35

Sodium stibogluconate

SE

Back 35

Cardiac arrhythmias

Front 36

Pyrimethamine

MOA

Back 36

Inhibits DHFR (dihydrofolate reductase)
→ ↓ tetrahydrofolate
→ ↓ purines, pyrimidines.

Front 37

Pyrimethamine

USE

Back 37

Drug of choice for T. gondii.

Front 38

Pyrimethamine

SE / ANTIDOTE

Back 38

Megaloblastic anemia

reversible with leucovorin (antidote)

Front 39

Ondansetron

MOA

Back 39

Blocks 5-HT3 receptors, which contribute to emesis via vagal afferents & area postrema (chemoreceptor trigger zone [CTZ]).

Front 40

Ondansetron

USE

Back 40

Chemotherapy-induced nausea
Pregnancy-induced hyperemesis
Postoperative nausea

Front 41

Prochlorperazine & Chlorpromazine & Promethazine

CLASS / MOA

Back 41

Dopamine receptor antagonists
Blocks D2 receptor at CTZ
*Also antihistamine & anticholinergic effects

Front 42

Prochlorperazine & Chlorpromazine & Promethazine

USE

Back 42

General purpose antinauseants, antiemetics

Front 43

Prochlorperazine & Chlorpromazine & Promethazine

SE

Back 43

Drowsiness

Front 44

Droperidol

CLASS / MOA

Back 44

Dopamine receptor antagonists
Blocks D2 receptor at CTZ

Front 45

Droperidol

USE

Back 45

Antiemetic in surgical, diagnostic procedures

Front 46

Droperidol

SE

Back 46

HIGH INCIDENCE OF ALTERING CARDIAC CONDUCTION

Front 47

Metoclopramide

MOA AND EFFECTS FOR ANTINAUSEA

Back 47

Blocks D2 receptor at CTZ

Also a prokinetic (promotility) agent.
↑ ACh release from enteric neurons by:
1) Suppressing 5-HT3 inhibitory neurons
2) Activating 5-HT4 excitatory neurons

Front 48

Metoclopramide

USE

Back 48

Chemotherapy-induced nausea
GERD (promotility)

Front 49

Metoclopramide

SE

Back 49

Extrapyramidal effects
*Acute dystonia
**Tardive dyskinesia-like condition (reversible)

Front 50

Meclizine & Diphenhydramine

CLASS / MOA

Back 50

Antihistamines

Block H1 receptors on vestibular afferents (motion sickness) and in the brain stem

Front 51

Meclizine & Diphenhydramine

AS A WHOLE THEY ARE USED FOR____
GIVE USE FOR EACH SPECIFICALLY

Back 51

Antinauseant
Meclizine = DOC Pregnancy-induced nausea

Diphenhydramine = Chemotherapy-induced nausea

Front 52

Scopolamine

CLASS &
USE

Back 52

Anticholinergic

MOTION SICKNESS

Front 53

AS A GENERAL RULE, ANTICHOLINERGIC AGENTS ARE NOT USED FOR THIS TYPE OF NAUSEA

Back 53

NOT FOR CHEMO INDUCED NAUSEA

Front 54

Dronabinol

MOA

Back 54

δ-9-tetrahydrocannabinol (THC)
CB1 cannabinoid receptors in vomiting center

Front 55

Dronabinol

USE

Back 55

Chemotherapy-induced nausea (prophylaxis)
Stimulates munchies in AIDS patients

Front 56

Dronabinol

SE

Back 56

Central sympathomimetic activity
Tachycardia, marijuana-like highs

Front 57

Dronabinol IS THIS TYPE OF DRUG

Back 57

MARIJUANA (CANNABIS)

Front 58

NAME 2 DRUGS USED IN IRRITABLE BOWEL SYNDROME WHICH IS:
Constipation-predominate

Back 58

Dietary fiber
Psyllium

Front 59

NAME 2 DRUGS USED IN IRRITABLE BOWEL SYNDROME WHICH IS:
Diarrhea-predominate

Back 59

Psyllium
Loperamide

Front 60

NAME 2 CLASSES AND 2 DRUGS IN EACH CLASS USED IN IRRITABLE BOWEL SYNDROME WHICH MOSLTY CAUSES:
Abdominal pain & bloating

Back 60

-Antispasmodic Agents
*Dicyclomine
*Atropine + Hyoscyamine
+ Phenobarbital + Scopolamine

-Antidepressants
*TCA: Amitriptyline
*SSRI: Paroxetine

Front 61

what are the physiological effects of bile acid

Back 61

induce bile flow
feedback inhibition of CE synthesis
elimination of CE
dispersion/absorption of lipids and fat soluble vitamins

Front 62

Ursodeoxycholic acid

CLASS

Back 62

Bile acid

Front 63

Ursodeoxycholic acid

USE

Back 63

cholesterol monohydrate gallstone (< 15 mm) dissolution, cholestatic liver disease
works in 40-60% of patients

Front 64

Uncoated Lipase & Protease

USE

Back 64

malabsorption & pain

Front 65

Enteric-coated Lipase and Protease

USE / ADVANTAGE

Back 65

malabsorption

dissolves farther down in the intestines

Front 66

name 4 Intraluminal agents to treat diarrhea

Back 66

-Psyllium
-Kaolin
-Cholestyramine
-Bismuth subsalicylate

Front 67

Psyllium

MOA

Back 67

bulking agent, absorbs water and increases stool bulk

Front 68

Psyllium

USE

Back 68

constipation,
mild chronic diarrhea

Front 69

Kaolin

MOA

Back 69

Clay that binds water avidly
Also may bind enterotoxins

Front 70

Kaolin

USE

Back 70

Mild diarrhea (symptomatic relief)

Front 71

Cholestyramine

MOA

Back 71

Anion-exchange resin that binds bile acids, some bacterial toxins

Front 72

Cholestyramine

USE

Back 72

-Patients with resected distal ileum (< 100 cm) who develop bile salt-induced diarrhea.
-Clindamycin-associated diarrhea
-C. difficile-induced mild colitis

Front 73

why should Cholestyramine not be given in bowel resection greater than 100 cm?

Back 73

will aggravate diarrhea because of bile-salt depletion → steatorrhea.

Front 74

Bismuth subsalicylate

MOA / EFFECTS OF EACH COMPONENT

Back 74

Reacts with HCl in stomach to form bismuth oxychloride and salicylic acid.
Salicylic acid is absorbed in stomach,
Bismuth has antisecretory,
anti-inflammatory, antimicrobial effects.

Front 75

Bismuth subsalicylate

USE

Back 75

Traveler’s diarrhea
H. pylori eradication adjunct

Front 76

Bismuth subsalicylate

SE / WHY

Back 76

Dark, black stools; darkening of tongue
(reaction between drug and sulfides produced by bacteria in mouth).

Front 77

name 2 opioids to treat diarrhea

Back 77

-Loperamide
-Diphenoxylate + Atropine

Front 78

how do opioids affect diarrhea by acting on the specific receptors

Back 78

-intestinal motility (μ receptors),
-intestinal secretion (δ receptors),
-absorption (μ, δ)

Front 79

Loperamide

effects compared to morphine

Back 79

40 to 50 times more potent than morphine as antidiarrheal agent.

Front 80

Loperamide

advantage

Back 80

DOES NOT penetrate CNS (NO abuse potential),

Front 81

Diphenoxylate is structurally related to _____

Back 81

structurally related to meperidine

Front 82

Diphenoxylate

effects compared to morphine

Back 82

Slightly more potent than morphine as antidiarrheal agent.

Front 83

Diphenoxylate

disadvantage

Back 83

produce CNS effects (high potential for abuse or addiction)

Front 84

this drug is added to Diphenoxylate when treated for diarrhea, WHY?

Back 84

Atropine is added to diphenoxylate to discourage abuse.

Front 85

Loperamide

USE

Back 85

chronic diarrhea
travelers diarrhea
occasional "bouts" of diarrhea

Front 86

Octreotide

related to ______

Back 86

analog of somatostatin

Front 87

Octreotide

USE

Back 87

Severe secretory diarrhea caused by metastatic carcinoid tumors that secrete VIP

Front 88

VIP secreting tumors found in the:
GI tract are called _______
PANCREASE are called _____

Back 88

GI tract: carcinoid syndrome

Pancreas: Verner-Morrison syndrome or pancreatic cholera

Front 89

this is defined as the part of food that is resistant to enzymatic digestion (fermentation). this attracts water and increases stool bulk

Back 89

Dietary Fiber

Front 90

Psyllium husk

MOA

Back 90

undergoes significant fermentation in colon
→ ↑ colonic bacterial mass

Front 91

Psyllium husk

USE

Back 91

Constipation

Front 92

Psyllium husk is contraindicated in these pts

Back 92

Contraindicated in patients with obstructive symptoms.

Front 93

Methylcellulose & Polycarbophil

MOA

Back 93

Poorly fermentable compounds that are able to absorb water and ↑ fecal bulk.

Front 94

Methylcellulose & Polycarbophil

USE

Back 94

Constipation

Front 95

Methylcellulose & Polycarbophil is contraindicated in these pts

Back 95

Contraindicated in patients with obstructive symptoms.

Front 96

Docusate (-sodium or -calcium)

MOA

Back 96

Anionic surfactants that ↓ surface tension of stool to allow mixing of aqueous & fatty substances → softens stool (easier defecation).

Front 97

Docusate (-sodium or -calcium)

USE

Back 97

Constipation (low efficacy despite widespread use)

Front 98

Mineral oil

EFFECTS

Back 98

Softens stool

Front 99

Mineral oil is rarely used anymore due to THESE SE

Back 99

↓ Absorption of fat-soluble vitamins
Foreign-body reactions in intestinal mucosa
Leakage of oil

Front 100

GIVE 2 EXAMLES OF SALINE LAXATIVES (osmotically active agent)

Back 100

Magnesium Sulfate
Magnesium Citrate

Front 101

SALINE LAXATIVES

MOA

Back 101

Osmotically-mediated water retention
→ stimulates peristalsis

Front 102

SALINE LAXATIVES

USE

Back 102

Acute evacuation of bowel before diagnostic exams
Parasite elimination adjunct

Front 103

DO NOT USE SALINE LAXATIVES WITH:

Back 103

Renal insufficiency
Cardiac disease
Preexisting electrolyte abnormalities
Patients on diuretic therapy

Front 104

Glycerin

CLASS / MOA

Back 104

Nondigestible Alcohols

Hygroscopic agent (rectal lubricant)

Front 105

Glycerin

USE

Back 105

Constipation

Front 106

Lactulose

CLASS / MOA

Back 106

Nonabsorbable sugar
hydrolyzed in intestine to organic acids → acidify luminal contents→ osmotically draw water into lumen → ↑ colonic propulsive motility

Front 107

Lactulose

2- USE (also for IM)

Back 107

Constipation
Hepatic encephalopathy

Front 108

Polyethylene glycol
(PEG)-electrolyte solutions

MOA

Back 108

Long-chain PEGs are poorly absorbed→ osmotically draw water into lumen.

Front 109

Polyethylene glycol
(PEG)-electrolyte solutions

USE

Back 109

Widely used as a cathartic prior to bowel procedures (4 liters over 3-4 hours).

Front 110

Bisacodyl

EFFECT

Back 110

Induce low-grade inflammation in intestines to ↑ water & electrolyte secretion, ↑ intestinal motility

Front 111

Bisacodyl

KINETICS

Back 111

Enteric-coated
requires hydrolysis in bowel for activation

Front 112

Anthraquinones (Cascara & Senna)

MOA / EFFECTS

Back 112

Bacterial action in colon activates agents → produce giant migrating colonic contractions, ↑ water & electrolyte secretion

Front 113

Ricinoleic Acid (Castor Oil)

MOA

Back 113

Castor oil is hydrolyzed in small bowel by lipases into glycerol & ricinoleic acid,
→ ↑ fluid & electrolyte secretion, speeds intestinal transit.

Front 114

Ricinoleic Acid (Castor Oil) is not used much anymore because ___

Back 114

ricin is a toxic metabolite that has effects on intestinal epithelium, enteric neurons.

Front 115

Mesalamine

MOA

Back 115

Inhibits cyclooxygenase pathway.
VERY POTENT Scavenger of ROS (especially OH-)

Front 116

Mesalamine

USE

Back 116

Acute mild to moderate ulcerative colitis or Crohn’s disease.
Prophylaxis during remission

Front 117

Mesalamine

SE

Back 117

Nephrotoxicity (serious but very rare)

Front 118

Sulfasalazine

KINETICS / MOA

Back 118

Mesalamine is main active metabolite, which is linked to sulfapyridine by diazo bond (prevents early absorption of mesalamine). Diazo bond is split by bacterial azoreductases in colon.

Front 119

Sulfasalazine

USE

Back 119

Acute mild to moderate ulcerative colitis
(NOT Crohn’s disease).
Prophylaxis during remission.

Front 120

Sulfasalazine

SE OF WHICH COMPONENT

Back 120

Sulfapyridine component:
Megaloblastic anemia (give folate)
Agranulocytosis
Drug-induced lupus
Steven-Johnson syndrome

Front 121

Mesalamine & Sulfasalazine

which is better for the treatment of SEVERE IBD?

Back 121

NEITHER IS USED IN SEVERE IBD

Front 122

name 2 glucocorticoids used in the treatment of SEVER IBD

Back 122

Prednisone
Hydrocortisone

Front 123

Prednisone & Hydrocortisone

USE

Back 123

Severe ulcerative colitis
Severe Crohn’s disease

Front 124

Cyclosporine

MOA

Back 124

Calcineurin inhibitor
Causes pronounced suppression of proinflammatory transcription factors

Front 125

Cyclosporine

USE

Back 125

Acute IBD not responsive to glucocorticoids
(NOT effective for maintenance therapy)

Front 126

Azathioprine

MOA

Back 126

*Converted to 6-mercaptopurine*
Has *several anti-inflammatory properties**
(↓ lymphocyte proliferation).

Front 127

Azathioprine

USE

Back 127

IBD long-term maintenance therapy
(↓ requirement for steroids)

Front 128

Azathioprine

DISADVANTAGE

Back 128

limited by slow onset of action

Front 129

Methotrexate

EFFECTS

Back 129

Cytotoxic agent with pronounced immunosuppressive and anti-inflammatory properties.

Front 130

Methotrexate

USE

Back 130

Steroid-dependent Crohn’s disease
(NOT ulcerative colitis).

Front 131

Infliximab

MOA

Back 131

Monoclonal Antibody against TNF
(neutralizes TNF activity).

Front 132

Infliximab

USE / ADVANTAGE

Back 132

Severe Crohn’s disease.
(promotes healing of fistulae)

Front 133

what are the 2 major causes of GI ulcer formation, which is more important

Back 133

decreased mucous (* most imp)

increased acid production

Front 134

cells of the stomach
what 2 things are produced by parietal cells

Back 134

HCL and intrinsic factor

Front 135

cells of the stomach
chief cells secrete _____

Back 135

pepsinogen

Front 136

secretion of acid requires this type of pump specifically

Back 136

Hydrogen/Potassium ATPase Proton pump

Front 137

**GASTRIC ACID SECRETION OCCURS DUE TO THESE 3 ENDOGENOUS SUBSTANCES**

Back 137

*************
ACTEYLCHOLINE
GASTRIN
HISTAMINE

Front 138

pepsinogen is a proenzyme that will form _______ in this type of environment. that will combine with acid to form a ______ complex

Back 138

pepsinogen → PEPSIN
in an ACID environment
pepsin + acid → PROTEOLYTIC COMPLEX

Front 139

what 2 features of gastric epithelium helps it to avoid injury from the gastric acid

Back 139

mucous production
rapid and continual cell turnover

Front 140

what are the 2 mechanisms by which PROSTAGLANDINS protect the GI mucosa

Back 140

inhibits gastric acid production (by parietal cells)
stimulating mucous and bicarb production (in mucous secreting cells)

Front 141

this causes an inflammatory gastritis and is a MAJOR CONTRIBUTOR TO PEPTIC ULCER DZ

Back 141

H pylori

Front 142

this syndrome is manifested as a condition of excessive GASTRIN PRODUCTION WHICH INCREASES HISTAMINE RELEASE AND ESSENTIALLY INCREASED acid production
**GIVE DOC FOR Tx

Back 142

Zollinger- Ellison syndrome

DOC = OMEPRAZOLE (-PRAZOLE's)

Front 143

how is the pain of ulcers typically described

Back 143

burning "Gnawing"

Front 144

WHAT IS THE PRIMARY DEFECT IN GERD?

Back 144

DECREASED LOWER ESOPHAGEAL SPHINCTER (LES) PRESSURE

Front 145

CIMETIDINE (& ALL -TIDINE's)

CLASS

Back 145

Histamine H2 receptor antagonists

Front 146

CIMETIDINE (& ALL -TIDINE's)

MOA / EFFECT

Back 146

H2 block → ↓ gastric acid secretion (from parietal cells)

Front 147

CIMETIDINE (& ALL -TIDINE's)

USE

Back 147

Peptic ulcers
GERD

Front 148

CIMETIDINE

SE

Back 148

POTENT P450 INHIBITOR

Maybe antiandrogenic effects
→ gynecomastia

Front 149

Omeprazole & Esomeprazole (ALL THE -PRAZOLES)

CLASS

Back 149

H+/K+-ATPase Proton pump inhibitors (PPIs)

Front 150

Omeprazole & Esomeprazole (ALL THE -PRAZOLES)

MOA / EFFECT

Back 150

irreversibly Block proton pump
→ ↓↓↓ gastric acid secretion
(effects last long after drug elimination)

Front 151

Omeprazole & Esomeprazole (ALL THE -PRAZOLES)

USE

Back 151

Active ulcers
GERD
Zollinger-Ellison syndrome (DOC)
H. pylori eradication adjunct

Front 152

of all the -PRAZOLES which is the only one with significant kinetics?
--> what is it

Back 152

Omeprazole is P450 inhibitor

Front 153

name 2 ULCER DRUGS WHICH INHIBIT P450

Back 153

CIMETIDINE
OMEPRAZOLE

Front 154

WHAT IS THE TREATMENT STRATEGY TO ERADICATE H. PYLORI?

Back 154

PPI + 2 ANTIBIOTICS FROM THIS SELECTION: MCAT
metronidazole
clarithromycin
amoxicillin
tetracycline

Front 155

Misoprostol

CLASS

Back 155

Prostaglandin ANALOG

Front 156

Misoprostol

MOA / EFFECT

Back 156

Prostaglandin E2, I2 receptor agonist.
↓ cAMP → ↓ acid secretion.

Also ↑ mucous, bicarbonate production.

Front 157

Misoprostol

ONLY USED FOR ______

Back 157

NSAID-induced gastric ulcers ONLY

Front 158

Misoprostol

MAIN SE

Back 158

ABORTION

Front 159

Dicyclomine

CLASS / SIMILAR TO _____

Back 159

Antimuscarinic agent

atropine like

Front 160

Dicyclomine

MOA / EFFECT

Back 160

Block muscarinic receptors
→ ↓ gastric acid secretion

Front 161

Dicyclomine

USE

Back 161

Adjunct in peptic ulcer treatment
(rarely used)

Front 162

Dicyclomine

SE

Back 162

Atropine-like adverse effects

Front 163

Antacids

ADVANTAGE / DISADVANTAGE

Back 163

FASTEST TO RELIEVE PAIN

BUT SHORT ACTING

Front 164

what are the 4 main metals used in antacids?

Back 164

Al - (OH)3,
Mg - (OH)2
Ca - CO3,
Na - HCO3

Front 165

antacids

MOA

Back 165

react with gastric acid to produce water and salt.
Also reduce pepsin activity by ↑ pH.

Front 166

ANTACIDS

USE

Back 166

Promote healing of gastric ulcers

Relieve symptoms of GERD

Front 167

ANTACIDS

KEY KINETICS

Back 167

SINCE THEY ↑pH THEY WILL
↓ ABSORPTION OF WEAK ACIDS
AND ↑ ABSORPTION OF WEAK BASES

Front 168

WHAT TIMING SHOULD YOU NOTIFY YOUR PATIENTS TALKING ANTACIDS WITH ANY OTHER DRUG?

Back 168

Take antacids 2 hours before or after other drugs

Front 169

WHICH 2 METALS HAVE THE MOST SIGNIFICANT SE POTENTIAL OF THE ANTACIDS
--> GIVE EFFECT

Back 169

Al(OH)3: constipation

Mg(OH)2: diarrhea

Front 170

Sucralfate

MOA / EFFECT

Back 170

(sulfated sucrose) creates gel barrier that impairs acid diffusion

coats ulcer surface and enhances healing

Front 171

Sucralfate

requires ____ for activation
do not use with _____

Back 171

Requires acid to be activated

CAN NOT be taken with antacid

Front 172

Colloidal bismuth

MOA

Back 172

neutralizes acid, ↑ mucous, bicarbonate production

Front 173

Colloidal bismuth

SE

Back 173

BLACK TONGUE
BLACK STOOL
INCREASED BLEEDING TIME

Front 174

Metoclopramide

CLASS

Back 174

Promotility agent

Front 175

Metoclopramide

MOA / EFFECT for GERD

Back 175

↑ ACH release from enteric neurons =↑ GI motility and INCREASES LES PRESSURE
(also blocks D2 receptors)

Front 176

Metoclopramide

USE

Back 176

GERD
(alternative to PPIs, H2 blockers)
Also antiemetic

Front 177

why has the use of Metoclopramide been drastically reduced?

Back 177

because of the D2 antagonism (similar to typical antipsychotics)
TARDIVE DYSKINESIA HAS BEEN NOTED IN THEIR SE

Front 178

HOW ARE NSAIDS AND CORTICOSTEROIDS INVOLVED WITH ACID PRODUCTION?

Back 178

NSAIDS AND CORTICOSTEROIDS
block phospholipase A2 so less PG's produced allowing for increased acid production

Front 179

how does the efficacy of PPI compare to H2 receptor blockers (cimetidine)?
--> why

Back 179

PPI's are much more efficacious

they block acid production from all 3 inputs ACH, Histamine and Gastrin

Front 180

define:
p
pc
PO
PR
prn

Back 180

p= after
pc= after meals
PO= by mouth
PR= per rectum
prn= when needed

Front 181

define:
q
qam, om
qh, q1h
q2h, q3h

Back 181

q = every
qam, om = every morning
qh, q1h = every hour
q2h, q3h =every 2 hrs, every 3 hrs

Front 182

define:
qid
qod
qs

Back 182

qid = 4 times per day
qod = every other day
qs = sufficient quantity

Front 183

who can prescribe medications?

Back 183

all DO's and MD's, and in some states:
pharmacists, NP, PA, optometrists, dentists
(usu they are limited to what classes can be written)

Front 184

what should be written after the sig: notation on a script

Back 184

how to take the medication (ie take 1 tab twice daily) and the use of the medicine (for blood pressure control)

Front 185

WHAT IS THE POTENTIAL HEALTH BENEFIT IN HUMANS OF:
Black cohosh root

Back 185

↓ Menopausal symptoms

Front 186

WHAT IS THE POTENTIAL HEALTH BENEFIT IN HUMANS OF:
Echinacea

Back 186

↑ Immune function (colds)

Front 187

WHAT IS THE POTENTIAL HEALTH BENEFIT IN HUMANS OF:
Garlic

Back 187

↓ Cholesterol & lipids, ↓ HTN

Front 188

WHAT IS THE POTENTIAL HEALTH BENEFIT IN HUMANS OF:
Ginko biloba leaf

Back 188

Improve cognition (studies with Alzheimer’s)

Front 189

WHAT IS THE POTENTIAL HEALTH BENEFIT IN HUMANS OF:
Ginseng root

Back 189

↓ Fatigue

Front 190

WHAT IS THE POTENTIAL HEALTH BENEFIT IN HUMANS OF:
Saw palmetto berry

Back 190

↓ BPH symptoms

Front 191

WHAT IS THE POTENTIAL HEALTH BENEFIT IN HUMANS OF:
St. John’s wort

Back 191

Antidepressant (common use in Europe)

Front 192

WHAT IS THE POTENTIAL HEALTH BENEFIT IN HUMANS OF:
Valerian root

Back 192

Improves sleep quality

Front 193

WHAT IS THE POTENTIAL HEALTH BENEFIT IN HUMANS OF:
Soy

Back 193

↓ Cholesterol & lipids

Front 194

WHAT IS THE POTENTIAL HEALTH BENEFIT IN HUMANS OF:
Glucosamine
& Chondroitin

Back 194

Attenuates osteoarthritis

Front 195

WHAT IS THE POTENTIAL HEALTH BENEFIT IN HUMANS OF:
Creatine

Back 195

↑ Muscle mass, strength, performance during short bouts of intense exercise

Front 196

Saw palmetto berry

MOA / SIMILAR ACTION OF ____

Back 196

Anti-androgenic
inhibits 5α-reductase

ACTS like FINESTERIDE

Front 197

St. John’s wort

MOA / SIMILAR ACTION OF ___

Back 197

Proposed to ↑ 5-HT

SIMILAR TO AN SSRI

Front 198

the DSHEA was created by FDA what actions did they create for herbal products

Back 198

DSHEA requires:
-no proof of efficacy,
-no proof of safety,
-no sets for quality control
-products may not promise a specific cure, but they can make statements of benefits to use

Front 199

what are the 5 main signs of chronic lead poisoning?

Back 199

lead colic
lead palsy
wrist drop
foot drop
lead encephalopathy

Front 200

what classic sign is seen on xray of lead poisoning

Back 200

lead lines

Front 201

hematologic signs of lead poisoning

Back 201

basophillic stippling
sideroblastic (hypochromic, microcytic) anemia

Front 202

lead inhibits heme synthesis:
which 2 enzymes are actually inhibited in the pathway, and GIVE THE MOLECULE WHICH ACCUMULATES FOR EACH

Back 202

AMINOLEVULINATE DEHYDRATASE
→ increase Delta-ALA

FEROCHELATASE
→PROPOPORPHYRIN

Front 203

WHAT IS THE TX OF LEAD POISONING

Back 203

DIMERCAPROL

SUCCIMER (for children)

Front 204

give the MOST COMMON SOURCE FOR:
METHYLMERCURY (organic Hg)
&
MERCURY VAPOR

Back 204

methylmercury
→FISH

mercury vapor
→Dental amalgams

Front 205

because of the reaction with _____ Arsenic is found here in HIGH concentrations

Back 205

rxn with sulfhydryls in keratin
accumulate in skin and nails

Front 206

what is the major target of chronic cadmium poisoning

Back 206

kidney

Front 207

how are most pts exposed to iron?

Back 207

Acute exposure from accidental poisoning with ferrous salts

Front 208

Symptoms of Iron toxicity:
when is it seen
s/sx
when does death occur?

Back 208

seen w/in 30 minutes
Severe GI upset: BLOODY VOMIT AND BLOODY DIARRHEA, ABD PAIN
death w/in 6hrs OR 12-24 hrs

Front 209

what is Tx for Iron toxicity

Back 209

DEFEROXAMINE

Front 210

WHAT IS USE OF HEAVY METAL ANTAGONIST (CHELATOR):

Dimercaprol

Back 210

MANY MANY DIFFERENT TOXINS
is a good 1st choice

Front 211

WHAT IS USE OF HEAVY METAL ANTAGONIST (CHELATOR):

Succimer

Back 211

Lead poisoning in children

Front 212

WHAT IS USE OF HEAVY METAL ANTAGONIST (CHELATOR):

Penicillamine

Back 212

Copper poisoning (Wilson’s disease)

Front 213

WHAT IS USE OF HEAVY METAL ANTAGONIST (CHELATOR):

Deferoxamine

Back 213

Iron poisoning

Front 214

** WHICH TOPICAL VEHICLE IS:

MOST HYDRATING

MOST DRYING

Back 214

Ointments: most hydrating

Soaks: least hydrating (most drying)

Front 215

Neosporin
(Triple antibotic ointment [TAO])

OTC or Rx
COMPOSITION
USE

Back 215

OTC
Neomycin + Bacitracin + Polymyxin B.
Use: minor cuts, scrapes, burns

Front 216

Neosporin G

OTC or Rx
COMPOSITION
USE

Back 216

Rx
Neomycin + Gramicidin
Use: minor cuts, scrapes, burns

Front 217

Mupirocin

OTC or Rx
USE

Back 217

Rx.

Use: S. pyogenes impetigo

Front 218

Povidone-iodine

OTC or Rx
USE

Back 218

OTC
Use: wound cleansing

Front 219

Hexachlorophene

OTC or Rx
USE

Back 219

Rx solution.

Use: wound cleansing

Front 220

Hexachlorophene

Adverse effect:

Back 220

CNS toxicity

Front 221

Chlorhexidine

OTC or Rx
USE

Back 221

OTC solution

Use: wound cleansing

Front 222

Name 1 of each:
High
Intermediate
Low
-Potency topical glucocorticoids

Back 222

H -Betamethasone dipropionate
I - Triamcinolone acetate
L- Hydrocortisone

Front 223

WHAT ARE THE
LOCAL &
SYSTEMIC
ADVERSE EFFECTS OF topical glucocorticoids

Back 223

Local: Skin atrophy, acneiform eruptions, hypopigmentation.

Systemic: Suppression of HPA axis, growth retardation in small children.

Front 224

Retinoids: basically _____ compounds

give the major effects

Back 224

Vit A compounds

influence cellular proliferation, differentiation, inflammation, sebum production; mediated through nuclear acid receptors (RARs) → enhance transcription

Front 225

Tretinoin

MOA

Back 225

↓ Hyperkeratinization → ↓ microcomedone formation (initial acne lesion).

Front 226

Tretinoin

USE

Back 226

Topical use: Acne

Front 227

Tretinoin

SE / CI IN THESE PTS

Back 227

Erythema & Photosensitivity (greater risk of sunburn)

NEVER USE IN A PREGNANT PT!!!

Front 228

Isotretinoin

MOA

Back 228

decreases:
1) Sebum synthesis,
2) Propionibacterium acnes (causes acne inflammation),
3) Microcomedone formation

Front 229

Isotretinoin

USE

Back 229

Oral use: Severe nodular acne & acne unresponsive to oral antibiotics

Front 230

Isotretinoin

TOXICITY (SE)

Back 230

VERY VERY TERATOGENIC
Mucous membrane dryness, dry eyes, conjunctivitis
Photosensitivity
Hyperlipidemia
Depressive episodes, suicidal tendencies

Front 231

Retinoic acid

IS USED FOR THESE PROCEDURES

Back 231

Skin peels (removes the top layer of skin)

Front 232

Etretinate

MOA

Back 232

Normalizes expression of keratins

Front 233

Etretinate

USE / T 1/2

Back 233

ORALLY FOR Inflammatory psoriasis

T 1/2 = 100 DAYS

Front 234

Etretinate

SE

Back 234

Hair loss, sticky skin, easy bruising, liver function abnormalities
TERATOGENIC

Front 235

Methoxsalen

COMPONENT OF ____ THERAPY
MOA

Back 235

PUVA THERAPY

MOA: ↑ melanogenesis in normal skin.

Front 236

Methoxsalen

SE EARLY & WITH CHRONIC USE

Back 236

EARLY: blistering, painful erythema, cataract formation, liver dysfunction

Chronic effects within skin: photo-aging, non-melanoma skin cancer (10x incidence of squamous cell carcinoma)

Front 237

Calcipotriene

MOA

Back 237

Vitamin D analog (modulates transcription in epidermal keratinocytes)

Front 238

Calcipotriene

USE

Back 238

Psoriasis topical therapies

Front 239

Anthralin

MOA

Back 239

MOA: ↓ DNA synthesis (intercalation), ↓ mitochondrial activity, ↓ ROS formation

Front 240

Anthralin

USE / SE

Back 240

Psoriasis topical therapies

Black staining & irritation of skin

Front 241

Coal Tar

MOA / USE

Back 241

MOA: ↓ DNA synthesis

Psoriasis topical therapies

Front 242

Lactic acid, Glycolic acid & Salicylic acid

MOA / USE

Back 242

MOA: eats away at the skin

Use: hyperkeratosis, scaling cutaneous eruptions

Front 243

Podophyllin resin

USE / SE

Back 243

Use: genital warts.

SE: Serious neuropathy & death from use of large amounts on multiple lesions (take warts off one at a time).

Front 244

Lindane

MOA / USE

Back 244

Stimulates nervous system → death of arthropods
head lice, crab lice & their ova (scabies)

Front 245

Calamine

COMPOSED OF

Back 245

Zinc oxide + ferric oxide

Front 246

Domeboro

COMPOSED OF

Back 246

Aluminum sulfate + calcium acetate