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20 Cards in this Set

  • Front
  • Back
Treatment strategy for type 1 DM
low sugar diet, insulin replacement
Treatment strategy for type 2 DM
dietary modification and exercise for weight loss; oral hypoglycemics and insulin replacement
Insulin:

lispro (short acting)
aspart (short acting)
regular (short acting)
NPH (intermediate)
glargine (long acting)
detemir (long acting)
Binds insulin receptor; increased tyrosine kinase activity.

liver: increased glucose stored as glycogen
muscle: increased glycogen and protein synthesis, K uptake (taken up with glucose)
Fat: aids TG storage

use: Type I and II DM, life threating hyperkalemia and stress induced hyperglycemia

toxicity: hypoglycemia, hypersensitivity reaction
Sulfonylureas:

1st gen:
Tolbutamide
Chlorpropamide
close K channel on B cell membrane to depolarize cell --> triggers insulin release via increased Ca influx

use: type II DM

toxicity: disulfiram like reaction
Sulfonylureas:

2nd gen:
Glyburide
Glimepiride
Glipizide
close K channel on B cell membrane to depolarize cell --> triggers insulin release via increased Ca influx

use: type II DM

toxicity: hypoglycemia
Biguanides:

Metformin
unknown mechanism: possibly decreased gluconeogenesis, increased glycolysis, decreased serum glucose levels. Overall insulin sensitizer.

use: oral hypoglycemic. can be used in patients wo islet function.

toxicity: lactic acidosis, contraindicated in renal failure.
Glitazones/thiazolidinediones:

pioglitazone
rosiglitazone
increased insulin sensitivity in peripheral tissue.

use: monotherapy in type II or combined with other agents.

toxicity: weight gain, edema, hepatotoxicity, CV toxicity
a-glucosidase inhibitors:

acarbose
miglitol
inhibit intestinal brush border a-glucosides. delayed sugar hydrolysis and glucose absorption lead to decreased postprandial hyperglycemia.

use: monotherapy in type II or combined with other agents.

toxicity: FART (gi disturbance)
Mimetics:

Pramlintide
decrease glucagon

use: Type II

toxicity: hypoglycemia, nausea, diarrhea
GLP-1 (glucagon like peptide) mimetics:

Exenatide
increase insulin, decrease glucagon release

use: type II

toxicity: n/v, pancreatitis
orlistat
alters fat metabolism by inhibiting pancreatic lipases.

use: long term obesity management with modified diet.

toxicity: steatorrhea, GI discomfort, reduced vit. KADE absorption, HA

orliSTAT gets rid of FAT
sibutramine
indirect sympathomimetic serotonin and norepinephrine reuptake inhibitor

use: short and long term obesity management by reducing appetite

toxicity: hypertension and tachycardia
propylthiouracil, methimazole
inhibit organification and coupling of iodide for thyroid hormone synthesis. propylthiouracil also decreases peripheral conversion of T4 to T3.

use: hyperthyroidism

toxicity: skin rash, agranulocytosis (rare), aplastic anemia.
levothyroxine, triiodothyronine
thyroxine replacement

use: hypothyroidism, myxedema

toxicity: tachycardia, heat intolerance, tremors, arrhythmias (general symptoms seen in hyperthyroidism)
hypothalamic/pituitary drugs

GH
GH deficiency, Turner's syndrome
hypothalamic/pituitary drugs

Somatostatin (octreotide)
Acromegaly, carcinoid, gastrinoma, glucagonoma
hypothalamic/pituitary drugs

oxytocin
stimulate labor, uterine contraction, milk let-down; controls uterine hemorrhage
hypothalamic/pituitary drugs

ADH (desmopressin)
central diabetes insipidus
demeclocycline
ADH antagonist (its a tetracycline)

use: SIADH

toxicity: nephrogenic DI, photosensitivity, abnormalities of bone and teeth
Glucocorticoids:

hydrocortisone, prednisone, triamcinolone, dexmethasone, beclomethasone
decreases the production of LT and PG by inhibition of PLA2; also inhibit COX-2 expression.

use: addison's disease, inflammation, immune suppression, asthma

toxicity: iatrogenic cushing's syndrome (MCC) - buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic)