• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/53

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

53 Cards in this Set

  • Front
  • Back
What kind of insulin are these: Insulin lispro, insulin aspart, insulin glulisine
Regular insulin
What is the onset, peak, duration of regular insulin
30-60 mins
1-2 hrs
4-5 hrs
Lente & NPH - what kind of insulin
Intermediate insulin
Onset, peak duration of intermediate insulin
2-4 hrs
4-10 hrs
10-16 hrs
Ultralente, Insulin glargine, PZI, Insulin detemir - what kind of insulin
Long acting insulin
Onset, peak, duration of long acting insulin
2-4 hr
No peak
~24 hr duration
First line medication for Type II DM
Metformin
MOA Metformin
Inhibits glucose absorption from gut
Decreases glucose output by liver
Increases glucose uptake in adipose tissue & sk. m.
When should you avoid/stop Metformin
Stop - prior to IV contrast, re-start >48 hrs after
Avoid - Alcoholic, Severe CHF, Liver & renal failure
MOA Acarbose
Alpha-glucosidase inhibitor
(inhibits GI tracts ability to degrade carbohydrates)

Works to limit post-prandial hyperglycemia
Common SE Acarbose
Flatulence
MOA "glitazones"
(thiazolidinediones)
Sensitize sk. m. & fat tissue to insulin
(increase # insulin R & glucose transporters)
What are the glitazones
Rosiglitazone
Pioglitazone
SE glitazones
Edema
Wt gain
New onset HF
Exacerbation of pre-existing CHF
Hepatotoxic
Avoid glitazones in who?
Liver dz
If on nitrates or insulin
A/w increased risk myocardial ischemia
MOA "glitinides"
Increase insulin release by beta-islet cells

(No decrease in effect if used long term)
MOA Sulfonylureas
Promote insulin release from beta-islet cells

(Decreased effect after long term tx)
What are the sulfonylureas
-1st generation -
Tolbutamide
Chlorpropamide
Tolazamide
-2nd generation -
Glimepiride
Glyburide
Glipizide
MOA Pramlintide
Amylin analogue
Who is pramlintide contraindicated in
Pt hypoglycemic unaware
On alpha-glucosidase inhibitors
Decreased GI motility
HbA1C > 9%
Compliance problems
What are the incretins? How do they work?
GLP-1
GIP

Release from GI cell after meal
(increase insulin release, decrease gastric emptying, inhibit glucagon release)
What is exenatide? Use?
GLP-1 analogue
Adjunct for DM type II
SE Exenatide
GI distrubance
Increased risk pancreatitis
Promotes wt loss
What is Liraglutide?
GLP-1 analogue
SE Liraglutide
Medullary cell CA thyroid
(increased serum calcitonin)
Liraglutide is contraindicated in
Personal or FMHx medullary thyroid CA or MEN Type II
Exenatide is contraindicated in
Renal failure
Conditions w/ decreased GI motility
Type I DM
What is Sitagliptan? Use?
DDP-4 inhibitor
(DDP-4 catalyzes destruction of incretins)
Adj in Type II DM
SE Sitagliptan
Pancreatitis
Increased risk of CA
What is Saxagliptan? SE?
DDP-4 inhibitor
URI
UTI
Pharyngitis
GI disturbance
MOA Niacin
Decreased hepatic uptake of released FFA
Inhibits lipolysis in fat cells

(Increase HDL, efficacy of resins, CM & VLDL clearance decrease LDL,TG)
SE Niacin
SEVERE cutaneous flushing & pruritis
Use Niacin
Prophylactic
Adjunct

(Never as monotherapy)
MOA Clofibrate, Fenofibrate, Gemfibrozil
Increase lipoprotein lipase
(decrease CM & VLDL)
Increase apoprotein R recognition sites
(increase lipoprotein uptake by liver)
SE fibric acid agents
Gallstones
Cardiac dysrhythmias
Increase malignancy
Risk of myopathy (rhabdomyolysis)
Use fibric acid agents
DOC Hypertriglyceridemia
MOA Cholestyramine, Colestipol, Colsevelam
(bile acid sequestrant)
Binds CH in gut--> Increased hepatic CH synthesis --> increases hepatic LDL uptake
(LDL decreased, VLDL & TG increased)
Contraindication for bile acid sequestrant
Hypertriglyceridemia
What are the HMG CoA reductase inhibitors
"statins"
Lovestatin
Atorvastatin
Fluvastatin
Pravastatin
Rosuvastatin
Simvastatin
SE "statins"
Hepatotoxic
Myopathy --> Rhabdo
Effect of "statins"
Increased LDL uptake by liver --> decreased CH in blood
Reduce mevalonate levels (normally mevalonate upregulates ACE)
What are the H2 blockers
Cimetidine
Ranitidine
Nizatidine
Famotidine
MOA H2 blockers
Competitiively bind H2 R on parietal cells --> No histamine can act

(45 mins onset)
SE Cimetidine
Anti-androgenic
(galactorrhea, gynecomastia, decreased sperm count)
MOA Misoprostol
PGE2 analogue

(PG cytoprotective to stomach, increase mucus & bicarb, decrease HCl)
Misoprostol contraindication
Pregnancy
(uterine contractions)
What are the PPI
Omeprazole
Esomeprazole
Lansoprazole
Pantoprazole
Rabeprazole
SE PPIs
Increased gastric carcinoids
Use of antimuscarinics in a/w peptic ulcers
Zollinger-Ellison
MOA Pirenzepine
M1 R blocker
(affects the stomach w/o affecting heart, eye, salivary glands)
MOA Sucralfate
Binds to positively charged grps of exposed mucosa --> forms gel over mucosa
Why is sucralfate CI in taking H2 blocker, PPIs, Antacids
Requires low pH for activation
MOA and Use Bismuth
Inhibits pepsin
Toxic to H.pylori