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180 Cards in this Set
- Front
- Back
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HCl secretion: lowest rates occur ___ and highest occur ____
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in the morning
at night |
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both the cephalic phase of HCl secretion and the basal circadian rhythm are mediated through _____
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vagal nerve activity
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what is the principal stimulus for HCl secretion during the gastric phase
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gastrin
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pepsin is secreted by ___
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chief cells
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PGE2 directly inhibits ____
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HCl secretion
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5 cytoprotective effects of PGs
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inhibit HCl secretion
stimulate mucus and bicarb secretion enhance mucosal capillary blood flow reduce back-diffusion of H ions enhance cell turnover |
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most common cause of PUD? 2nd most?
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H. pylori
chronic use of NSAIDs |
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antral gastritis due to H. pylori infx is found in a high number of patients with _______
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gastric and duodenal ulcers
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what are 4 things that H. pylori secretes
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urease - generates free ammonia
protease - decreases mucus viscosity platelet-activ factor - promotes thrombotic occlusion of surface capillaries LPS - recruits inflamm cells |
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action of myeloperoxidase
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results in production of HOCl and monochloramine
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NSAID users with signif risk factors for PUD should receive ____
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ulcer prophylaxis (PPIs or misoprostol)
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corticosteroids + NSAIDs = good or bad
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bad
increases risk of gastric injury |
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relation of acute alcohol ingestion and PUD
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no conclusive evidence as a risk factor for PUD
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noninvasive lab test for H. pylori
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urea breath test
identifies presence of active infx and confirms eradication at >1 month after antimicrobial therapy |
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what triple therapy regimen is best for H. pylori-induced PUD
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PPI
amoxicillin clarithromycin 7-14 days |
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if triple therapy does not work for PUD, what is recommended
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quadruple therapy:
PPI bismuth metronidazole tetracycline |
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most reliable way to assess successful eradication of PUD
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urea breath test
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prevention of NSAID-induced PUD
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PPI
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should antacids be taken on an empty stomach or after a meal
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after a meal (1 hour after)
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Magnesium hydroxide: ADRs
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diarrhea
CNS depression |
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aluminum hydroxide: ADRs
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constipation
hyperphosphatemia in chronic kidney disease |
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calcium carbonate: ADR
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acid rebound - increased gastric acid secretion after doses of 4-8g
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sodium bicarb should only be used for ___
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short term relief of indigestion
contraindicated for chronic use |
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milk-alkali syndrome
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metabolic alkalosis occurs when high calcium intake is combined with any factor that produces alkalosis
results in hypercalcemia, metabolic alk, neuro symptoms, and renal impairment |
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sodium bicarb: 2 major ADRs
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milk alkali syndrome
sodium overload - caution in HTN, CHF, CKD, and cirrhosis |
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what are some DIs of aluminum and magnesium hydroxides
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fluoroquinolones
tetracyclines H2 antagonists |
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sucralfate
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nonabsorbed, locally-acting agent that protects ulcerated tissue from acid, pepsin, and bile salts
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how does sucralfate compare with H2-antagonists in tx of acute ulcers
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equally safe and effective
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mechanism of H2-antagonists
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competitively inhibit actions of histamine at H2 receptors
inhibit fasting secretions |
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approved H2-antagonists
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cimetidine
ranitidine famotidine nizatidine |
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which H2-antagonist has highest potency
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famotidine
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what H2-antagonists inhibit P450? which ones do not?
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cimetidine
famotidine and nizatidine |
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cimetidine slows the dissolution of _____ and reduces its absorption
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ketoconazole
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what is the most imp factor for DU healing
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suppression of nocturnal acid
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PPIs: mechanism
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irreversibly binds to H-K ATPase and inhibits basal and stimulated gastric acid secretion
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where does PPI absorption occur
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GI mucosa into the portal circulation and then into systemic blood
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oral dosage forms of PPIs must be ____
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enteric coated
to protect the drug molecules from gastric acid |
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what class is the most potent of the acid suppressive agents
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PPIs
due to noncompetitive and irreversible inhibition |
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maximal acid suppression occurs when PPI is taken when
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30 min to an hour before a meal
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DOC (class) for PUD, GERD, and ZES
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PPIs
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what are the 6 PPIs we need to know
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omeprazole (Prilosec)
lansoprazole (Prevacid) rabeprazole pantoprazole esomeprazole |
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indicated to decrease risk of gastric ulcers associated w/use of NSAIDs in pts in whom a GU has been previously documented and who must use an NSAID to tx signs and symptoms of RA, OA, or AS
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lansoprazole DR capsule/naproxen tablets
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what is the S-isomer of omeprazole
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esomeprazole
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esomeprazole vs. omeprazole
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metabolized slower, producing higher and more prolonged plasma levels
increased bioavailability |
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lansoprazole and P450
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no clinically significant examples reported
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omeprazole and P450
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inhibits it
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clopidogrel and omeprazole: DI
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antiplatelet effects of clopidogrel are reduced
esomeprazole should also not be used |
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sucralfate compared to H2RAs in preventing recurrences of healed duodenal ulcers
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as effective or more effective
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what is the DOC (class) for NSAID-associated ulcer bleeding
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PPI
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misoprostol
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synthetic prostaglandin used for prevention of NSAID-induced ulcers
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what symptoms are present in >50% of ZES
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diarrhea
steatorrhea |
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what are ulcers mostly found in ZES
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1st portion of duodenum
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what are some findings that suggest ZES
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PUD refractory to standard therapy
recurrent ulcers diarrhea in ulcer pts PUD with complications |
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what lab test is used to diagnose ZES
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secretin provocation test
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treatment of ZES
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PPIs (omeprazole)
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GERD: factors that relax the LES
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pregnancy
drugs with smooth muscle relaxant properties alcohol cigarettes |
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douching is ___
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BAD
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pathogenesis of GERD
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dysfunction of LES
increased intra-abd pressure failure of mechanisms to clear acid |
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what are 2 conditions that can impair acid-clearing mechanisms
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scleroderma - loss of esophageal peristalsis
Sjogrens syndrome - salivary hyposecretion |
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atypical sxs of extraesophageal presentations of GERD
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laryngitis, pharyngitis, eroded dental enamel
reflex bronchospasm and exacerbation of asthma |
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"alarm" symptoms of GERD
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dysphagia
bleeding wt loss anemia |
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drug classes for treatment of GERD
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antacids
alginic acid PPIs prokinetic agents |
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alginic acid
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reacts with sodium bicarb and water to form a viscous solution
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superior to any other class for relief of GERD
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PPIs
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when should PPIs be taken for tx of GERD
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30-60 min before meals, usually breakfast
divide into 2 doses, with the 2nd given with the evening meal |
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prokinetic agents: mech of action
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stimulate motility of the upper GIT by enhancing actions of ACh
increases tone/amplitude of gastric contractions relaxes pyloric sphincter increases peristalsis |
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metoclopramide: ADRs
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extrapyramidal symptoms: acute dystonias, tardive dyskinesia
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metoclopramide is contraindicated in what dz
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Parkinson's (antagonizes levodopa)
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DOC for maintenance therapy of esophagitis
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PPIs
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stress ulcers are usually associated with what 3 things
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major trauma
burns sepsis |
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pathogenesis of stress ulcers
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alteration of defensive factors resulting in impaired host defense mechanisms
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risk factors for stress ulcers
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critical illness/injury
resp failure and coagulopathy |
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an intragastric pH higher than ____ lowers the frequency of bleeding in pts at risk for stress related mucosal dz
what drugs maintain this |
3.5
antacids |
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what drug is approved for prevention of upper GI bleeding due to stress ulcers
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cimetidine
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what drug is used for replacement therapy in hypothyroidism and myxedema coma
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levothyroxine sodium (synthetic T4)
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when do you take levothyroxine sodium
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30 min before breakfast, with water
take at same time every day |
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high doses of levothyroxine causes
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CV stimulation
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after taking levothyroxine sodium, wait ___ before eating and 4 hrs before taking ________
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30 min
calcium, iron, magnesium, aluminum, orlistat |
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what drugs may reduce absorption of levothyroxine
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acid-suppressive agents
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no interaction bt sucralfate and levothyroxine when dosing separated by ____
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8 hrs
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levothyroxine plus warfarin
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increases anticoagulant effect
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liothyronine sodium
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synthetic T3
DOC if peripheral conversion is deficient |
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thyroid USP
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desiccated thyroid derived from pork glands
contains both T4 and T3 should be avoided in hypothyroid pts |
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tx for myxedema coma
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medical emergency
immediate, aggressive thyroid replacement |
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tx for hyperthyroid
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thioamides - propythiouracil, methimazole
iodides - suppress TH secretion glandular ablation with radiation/surgery |
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propylthiouracil - 4 main actions
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blocks oxidation of iodine to active iodide
blocks organification of iodide blocks coupling rxns that form T3 and T4 inhibits conversion of T4 to T3 |
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methimazole: effect on peripheral conversion
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does NOT inhibit peripheral conversion
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propylthiouracil: boxed warning
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risk of acute liver failure
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potential serious toxicities of thioamides
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agranulocytosis
hepatotoxicity |
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iodides: mechanism
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suppress TH release
decreases size and vasularity of the hyperplastic gland used preoperatively for thyroid gland surgery |
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iodides: disadvantages
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increased iodide uptake and storage within gland
prevents uptake of radioactive iodine |
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iodides: safe or contraindicated in pregnancy?
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contraindicated
produces fetal goiter |
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iodides: DIs
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lithium: potentiation of hypothyroidism
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what must you treat pts with before undergoing thyroidectomy
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preoperative conversion to euthyroid state with thioamides to avoid thyroid storm, and iodides prior to surgery to decrease vascularity
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RAI is treatment of choice for what 2 diseases
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Graves'
toxic multinodular goiters |
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adjunct therapy for hyperthyroidism
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beta blockers (propranolol)
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treatment for thyroid storm
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thioamides - block TH synth
iodides - block TH release propranolol - decrease sxs of sympa overactivity hydrocortisone - suppress peripheral conversion |
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DOC for thyrotoxicosis during pregnancy
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PTU during the 1st tri
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regular insulin: features
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clear
labeled for SC use short acting only form that can be administered IV |
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regular insulin exists primarily as ____ complexes; after SC injection they dissociate into ________
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hexameric
monomeric forms that can be absorbed |
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NPH stands for what
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neutral protamine Hagedorn
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NPH features
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opaque suspension
SC use only intermediate acting |
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describe human insulin analogs
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recombinant DNA products using inserted genes that code for altered insulin structures
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insulin lispro
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human insulin analog
lowered propensity to form hexameric complexes ultrashort acting clear solution SC use |
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insulin aspart
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human insulin analog
hexameric complexes less likely to form, resulting in faster absorption clear solution SC use |
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insulin glulisine
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human insulin analog
clear solution SC use |
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insulin glargine
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human insulin analog
clear solution long acting basal insulin SC use only |
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insulin detemir
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human insulin analog
long acting basal insulin clear solution SC use only |
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where is insulin absorption fastest?
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abdomen
decreases in order from the arm, hip, and thigh (alphabetical order) |
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which insulin analog is ultrashort-acting
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insulin lispro
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Humulin N, Novolin N: duration of action
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18-24 hrs
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which 2 insulins are long-acting
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glargine and detemir
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virtually all patients using insulin are injecting ______
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U-100 insulin (100 units/mL)
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U-500 insulin
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not for IV use
available when exceptionally high doses are required |
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how long do fast onset insulins last
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up to 12 hrs
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which insulin analogs require Rx
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all of them
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high dose insulin syringes hold up to ___
low dose ___ |
1mL (100 units)
.5mL (50 units) |
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insulin vials currently in use may be stored at room temp for ___
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28 days
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what can you mix insulin glargine or detemir with
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must NOT be mixed or diluted with any other insulin or solution
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what can you mix insulin aspart or glulisine with
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may be mixed only with NPH human insulin
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what can you mix insulin lispro with
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Humulin N
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mixtures containing NPH or other protamine forms are ____ and must be ____
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cloudy suspensions
agitated before withdrawal, by rolling between the palms |
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what does IIT stand for
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intensive insulin therapy
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IIT is contraindicated in ____
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children < 7 years, bc the developing brain is extremely susceptible to hypoglycemia
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bt meals and during the night, small basal amts of insulin are secreted to _________
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suppress lipolysis and hepatic glucose synthesis
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basal insulin requirements are approx ___ of total daily dose of insulin required
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50%
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Somogyi effect
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reactive hyperglycemia in response to a nocturnal hypoglycemic episode
bedtime normoglycemia, nighttime hypo, and rebound hyper at breakfast |
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dawn phenomenon
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rise in blood glucose bt 5-8am due to reduced tissue sensitivity to insulin
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causes of midmorning hyperglycemia
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insufficient dose of rapid or short-acting insulin before breakfast
poor timing bt meal intake and insulin action excess carb consumption at breakfast |
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solution of midmorning hyperglycemia
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increase prebreakfast dose of insulin
correct timing of premeal insulin dose alter carb content |
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insulin requirements are ____ in presence of infx or illness
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increased
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with moderate exercise, decrease preceding dose of regular insulin by ____
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30-50%
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risk factors of hypoglycemia
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long hx of type 1 DM
intensive insulin therapy extremes of age inappropriate timing of meals and insulin dose*** |
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major cause of drug-induced hypoglycemia
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sulfonylureas
others: insulin, ethanol, pentamidine |
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treatment of unconscious hypoglycemic patient
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parenteral glucagon
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glucagon stimulates ____
what are some other pharm actions |
hepatic glycogenolysis to raise blood glucose
smooth muscle relaxant in GIT enhances warfarin coagulant effect |
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treatment of hospitalized hypoglycemic adults
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give IV 50 mL of D50W
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clinical presentation of DKA
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high serum glucose concentrations
increased serum osmolality glycosuria dehydration ketone production (odor of acetone on breath) metabolic acidosis |
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treatment of DKA (5 things)
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fluids - normal saline for hypotension
sodium - replaced with normal saline potassium - total body K is always depleted, but serum K may be high/nl/low insulin - loading dose, continuous IV infusion sodium bicarb - for severe acidosis or shock |
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5 causes of drug-induced hyperglycemia
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diazoxide
thiazide/loop diuretics glucocorticoids pentamidine protease inhibitors |
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actions of pentamidine
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beta cell toxin, causes a cytolytic-induced release of insulin, resulting initially in hypoglycemia
followed by a beta-cell destruction and insulin deficiency, resulting in drug-induced DM |
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what oral agents stimulate insulin secretion? these are also called?
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sulfonylureas
repaglinide secretagogues |
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what oral agents stimulate insulin action? also called?
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metformin
thiazolidinediones sensitizers |
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sulfonylureas: contraindications
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type 1 DM
pregnant/lactating severe, acute, concurrent illness, surgery |
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sulfonylureas: mech of action
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bind to a beta cell receptor linked to the K ion channel, preventing its efflux
causes depolarization which opens Ca channels, Ca influx stimulates insulin release |
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sulfonylureas are completely ineffective in _____
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pancreatectomized or type I diabetics who have no pancreatic fxn
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2nd gen sulfonylureas compared to 1st
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greater potency, shorter half life, longer duration of action
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glyburide
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2nd gen sulfonylurea
most effective in pts with fasting hyperglycemia high incidence of severe, prolonged hypoglycemia less effective in pts with postprandial hyperglycemia |
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glimeperide compared to glyburide
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more potent
more effective for postprandial hyperglycemia, with lesser incidence of hypoglycemia |
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most common and severe ADR of sulfonylureas? 2nd most?
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hypoglycemia
weight gain |
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repaglinide: mech of action
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binds to sites on beta cell membranes and closes ATP-dependent K channels; depolarizes cell which opens Ca channels; Ca influx induces insulin secretion
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unlike sulfonylureas, insulin release by repaglinide is _____
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glucose-dependent and diminishes at low glucose concentrations
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repaglinide is contraindicated in ____
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type 1 DM or DKA
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most common ADR of repaglinide
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hypoglycemia
weight gain |
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metformin is an insulin ______
mech of action? |
sensitizer
direct stimulation of tissue glycolysis, with increased glucose removal from the blood and uptake into peripheral tissues inhibits gluconeogenesis decreases GI glucose absorption |
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____ is essentially unreported with metformin
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hypoglycemia and wt gain
|
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metformin: contraindications
|
renal dysfunction
temporarily withhold in pts undergoing radiologic studies involving parenteral iodinated contrast agents pts prone to metabolic acidosis or hypoxic states |
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metformin boxed warning
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very rarely associated with lactic acidosis
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thiazolidinediones: mech of action (4 things)
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increase tissue insulin sensitivity through activation of the peroxisome proliferator-activated receptor gamma
improves insulin sensitivity decreases insulin resistance decreases gluconeogenesis |
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what do you do when diet, exercise, or rosiglitazone alone do not control blood glucose
|
use rosig in combination with a sulfonylurea or metformin
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rosiglitazone: brand name? contraindications? black box warning?
|
Avandia
do not initiate in hepatocellular dz may be associated with angina or MI |
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pioglitazone: indications
|
for type II, to improve glycemic control for:
use alone as monotherapy use in combination with sulfonylureas, metformin, or insulin |
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pioglitazone and rosiglitazone: ADRs
|
wt gain when used as monotherapy
increased CV risk due to fluid retention/edema risk of MI |
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what drug is no longer recommended for management of type II DM
|
rosiglitazone (Avandia)
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what type II drug class has increased risk of fractures in women
|
TZDs
|
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acarbose: drug class? brand name?
|
alpha-glucosidase inhibitor
Precose |
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acarbose: mech of action
|
complex oligosaccharide
competitive, reversible inhibition of alpha-glucosidase, pancreatic A-amylase, and sucrase prevents digestion of complex carbs to glucose |
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DOC for elderly type II patient with postprandial hyperglycemia
|
acarbose
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acarbose: ADRs
|
abdominal pain
diarrhea flatulence |
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actions of endogenous incretins and exogenous GLP-1
|
normalize fasting and postprandial glucose
suppress glucagon secretion (except during hypoglycemia) reduce appetite and food intake |
|
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exenatide: class? actions?
|
incretin-mimetic
lowers serum glucagon during hyperglycemia slows gastric emptying and reduces rate of glucose absorption reduces food intake |
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exenatide: administer before or after meals?
|
60 min before breakfast and supper
|
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exenatide: warnings
|
not for use in type I, pts using insulin, pts experiencing DKA, or pts with ESRD
|
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sitagliptin: warnings
|
risk of anaphylaxis, angioedema, and exfoliative skin conditions
|
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amylinomimetics: actions
|
reduces postprandial glucose levels
slows/delays gastric emptying induces satiety and regulates food intake |
|
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pramlintide: class? action?
|
amylinomimetic
slows gastric emptying which decreases postprandial elevation in blood glucose prevents postprandial increase in glucagon secretion decreased appetite |
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with pramlintide, insulin dosages should be reduced by ___
|
50%
|
|
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when do you d/c pramlintide therapy
|
recurrent unexplained hypoglycemia requiring medical assistance
persistent clinically significant nausea patient noncompliance |
|
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what patients should not be considered for pramlintide therapy
|
recurrent severe hypoglycemia
confirmed gastroparesis pediatric patients |
|
|
first and only med with FDA approval to lower both A1c and LDL
|
colesevelam (WelChol)
|
