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78 Cards in this Set
- Front
- Back
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what three peptide hormones is the pancreas responsible for synthesizing?
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1. insulin
2. glucagon 3. somatostatin |
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what are two ways that diabetes can be managed?
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1. with parenterall insulin
2 with oral hypoglycemic agents |
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what is Type I DM characterized by?
whatlife threatening conditions can this lead to? |
*Beta cells destruction from autoimmune antibodies
*total abscence of insulin with increased glucagon levels can cause life threatening ketoacidosis |
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what are syptoms of Type I
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*polyuria, polydipsia , weight loss.
*long term neuropathy, nephropahty retinoathy and vascular dz from thickening blood vessels |
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what is tx?
what is only oral antidiabetic agent effectice in type I |
need insulin or will die
Metformin is only antidiabetic agent effective |
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what type of dm is more prevalent?
what is the problem with this Diabetic? |
type 2 Non insuline dependent
insulin levels are insufficient due to developed tissue insensitivity and/or weakened B cell response |
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what are symptoms of Type II?
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obestity, polyuria
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WHAT is tx of type II?
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*dietary tx and exercise
*oral hyoglycemic *insulin for more severe cases |
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why can't insulin be given orally?
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*b/c peptide hormones are metabolized too quickly
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what is the mechanism of insulin release?
what drugs has its site of action on the K channels in B cell membranes? |
high blood surgar levels cause increase that are dependent upon active transport o glucose in B cells
drug is sulfonylureas |
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what are the three target tissues of insulin?
where is the insulin receptor? |
liver, muscle and adipose
receptor is in the plasma membrane and is composed of an alpha and beta subunit |
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where is the alpha subunit and what does it contain?
where is the beta subunit and what does it contain? |
alph is totally extracellular
-alpha contains binding site beta is a transmembrane protein -beta contains a tyrosine kinase |
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what is the physiological effects of insulin on cell membranes?
what is relocated into plasma membrane of muscle and adiose cells by insulin? |
*facilitates glucose transport across cell membranes
GLUT 4(the most impt quantitative transporter for decreasing circulating lglucose levels) |
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what physiologic effect does insulin have on liver?
is the hepatic permeability to glucose affected? |
it increases glucose storage as glycogen (glycogen synthase is stimulated)
NO, hepatic permeability is not |
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what is physiologic effect of glucose on muscle?
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stimualtes both glycogen synthesis (through glut 4) and PRO synthesis
*lack of insulin can lead to muscle wasting |
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what is physiologic effect of insulin on adipose tissue?
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facilitates TG storage and decreases free fatty acids in adipocytes
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what are the different insulin preps available?
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Human
2. Ultra rapid and very short 3. Rapid onset and short action4. Intermediate onset and action 4. Slow onset and extended action 5. Combination(short and long acting) |
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how is human insulin manufactured?
what preparation release the hormone slowly? |
recombinant DNA
Depot suspension |
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what do all insulin preps contain?
what does this do? |
all contain zinc
ratio of zinc to insulin determines both the rate of insulin release from site of administration and the duration of action |
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what are the Ultra rapid and very short action insulins?
when are these taken? |
1. Lispro(Huamlog)#2
2. Aspart (Novolog) 3. Glulisin(Apidra) (for use immeditely prior to meals) 5-10 min onset and 3-5 hour duration |
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what are rapid onset and short action?
when are these taken? what is duration? which insulin is used in the buffered pump? |
Crystallilne zinc(regular)
*anything with R in it is Regular insulin *this insulin is required 30-60 minutes before each meal *lasts 5-7 hours velosulin BR is used in the buffered pump |
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why are Rapid onset regular insulins (crystalline zinc) used in IV emergencies?
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b/c are cheaper than ultra rapid
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what are the intermediate onset and action insulins?
what is crystalline zinc combined with to increase onset? is this suitable for IV use? |
Isophane insulin suspension
*anything with "N" in the name means intermediate (Novolin N, RElion N, Humulin N etc.) mix is a suspension of crystalline zinc with PROTAMINE b/c it reduces solubility and absorption *this maintains FASTING levels *is NOT suitable for IV use |
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what is slow onset and extended action drugs?
what are clinical uses? |
*Insulin glarfine (lantus)#1)
*Insulin detemir(Levemir)new ~provide a peakless basal insulin level that lasts more than 24 hours ~is administered once a day |
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what are the combination drugs?
what is clinical use of combination? |
*Humalog Mix 75/25 and 50/50
(mix of isophane(NPH) and Lispro respectively) *Novolog Mix 70/30#6 (Isophane(NPH) insulin aspartw *Humulin 70/30 #4 *Novolin 70/30#5 *RElion 70/30 *Humulin 50/50 comb is used to cover both fasting and postprandial glucose levels whe |
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how many times is combination injected?
is combination containing more of the slow or fast? |
twice daily (before morning and evening meal)
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what is standard mode of therapy delivery?
what are others? |
subq injection
*pen sized injectors *insulin pumps |
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which method of delivery is an open loop system?
what is increased risk with insulin pumps? |
Open loop sys is continuous pump
increased risk of hypoglycemia |
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what is standard insulin therapy tx?
what is intensive? |
stand=two sc insulin injections/day
intensive is TIGHT control. ~stabilize blood glucose levels by more frequent insulin injections ~60% decrease in long term diabetic comp but increased frequency of hypglycemic episode |
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what is the most common and severe side effect of insulin therapy?
what are symptoms of this? |
hypoglycemia
SX: -Sympathetic symp(palpitations, tachycardia, sweating and tremulousness) -CNS (confusion, bizare behavior, convulsions and coma |
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what are drugs that increase risk of hypoglycemia?
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*B blockers (b/c reduce action of catecholamines)
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what can happen if repeated injections are made at the same site?
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hypertrophy, move injection site around
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what are oral hypoglycemic agents indicated for?
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management of patients with Type II diabetes whose hyperglycemia is uncontrolled by diet alone
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what are the six groups of drugs clinically employed as oral antidiabetics?
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1. insulin secretagogues
2. Biguanide 3. Thiazolidinediones 4. Alpha Glucosidease inhibitor 5. Incretin miment 6. Incretin potentiator |
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what does the insulin secretegagogues require?
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functional beta
b/c stimulates release of ENDOGENOUS insulin |
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what is mech of action?
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stim release of endogenous insulin from B cells by binding to membrane receptors that close K channels to cause membrane depolarization and trigger insulin release
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what are First generation Secretagogues?
what are clinical indications? |
1. Tolbutaminde(ORinase)
2. Chlorpropamid(Diabines) manages both fasting and postprandial hyperglycemia |
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which first generation is longer?
which first generation is safest for use in elderly?why? |
chlorpropamide is longer(Diabinese)
Tolbutamide(orinas) is still used in ELDERLY patients b/c less potential to casue hypoglycemia |
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what are second generation secretagogues?
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1. Glyburide(Diabeta, Micronase, GLynae PresTab)#4
2. GLipizide(Glucotrol #8, and GLucotrol XL #5) 3. GLimepiride (Amaryl) #6 |
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how do the second generatios compare to first?
what patient population should these be used with caution |
more potent than first
use with caution in elderly and CVD b/c of hypoglycemia |
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what are the MEglitinides
what is their action similar to? what is difference? |
newer insulin secretagogues
similar to sulfonylureas but faster |
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what is clincal use of meglitinides?
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priot to meals to control Postprandial glucose levels
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what are the adverse effects of insulin secretagogues?
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Hypoglycemia due to OD
*more common wih second gen sulfonylureas and first gen chlorpropramide |
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what can enahnce hypoglycemic effects?
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*ASA
*Clofibrate *Sulfonamides *phylbutazone |
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what are the two impt physiologic effects of BIGUANIDES
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1. reduce gluconeogenesis
2. reduce GI glucose absorption |
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what is the only Biguanide available in US?
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Metformin
(Glucophage XR #1 and Glucophage #7) |
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what is good about the biguanides?
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does not induce hypoglycemia (EUGLYCEMIA)
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what is clinical use of biguanides?
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manage both fasting and post prandial hyperglycemia in TYPE 1 AND 2 DM
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what are adverse effects of biguanides?
what are c/i? |
effects:
-GI distress -lactic acidosis -B12 defic c/i in liver dz patients |
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what is mech of action o THIAZOLIDINEDIONES
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activate peroxisome proliferator activatedreceptro gamma
(PPAR-y receptor) |
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what are effects of this drug?
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*increased insulin sensitivity
*reduce insulin resistance enhance effect w/o increasing release |
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what are the thiazolidinediones?
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1. Rosiglitazone(Avandia) #2
2. Pioglitazone (actos) #3 |
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what is clinical indication of thiazolidinediones?
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manage both fasting and post prandial hyperglycemia w/o increased risk of hypoglycemia
*can be used as combination therapy with insulin (EUGLYCEMIC) |
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what is adverse effect of avandia
what is adverse effet of pioglitazone? |
*increased risk of heart failure and nonfatal MI
*pioglitazone induces cytochrome P450 enzymes and decreases levels of drugs metabolized such as oral contraceptives and thyroids |
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what are alpha glucosidase inhibitors? mech of action
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inhibit intestinal alpha glucosidase
*alpha glucosidase is enzyme required to convert starches and disaccharides i nto monosacc's |
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what are effects of alpha glucosidase inhibitors?
do these drugs have any effect on fastin blood sugar? |
decreased carb absorption LIMITS POST PRANDIAL HYPERGLYCEMIA
*insulin sparing action *NO Effect on fasting blood sugar |
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what are the alpha glucosidase inhibitor drugs?
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*acarbose(Precose,GLucobay)
*Midlitol(GLyset) |
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what are the clinical uses of alpha glucosidase inhibitors?
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manage postprandial hyperglycemia
*can be used as combination therapy |
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what are adverse effects of alpha glucosidase inhibs?
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GI disturbance
Hypoglycemia mangaged with dextrose b/c sucrose is prolonged |
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what are INCRETIN MIMETIC mech of action
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*actiabtes glucagon like polypep (GLP1) recep in hypothalamus
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what are effects of Incretin mimetics?
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increase insulin secretion and decrease glucagon
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what is the only Incretin mimetic?
what is clinical use? what are adverse effects? |
Exenatide (Byetta) #10
clinical use is Postprandial hyperglycemia IN COMBO with other antidiabetic agent adverse effect is HYPOGLYCEMIA, N/V/D |
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what is unique abou the incretin (Byetta)
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give sub cut
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what is mechanism and effect of incretin Potentiators?
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they potentiate the effects of incretins(GLP1) to :
*increase insulin secretion *decrease glucagon |
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what is the incretin potentiator drug?
what is inhibited that makes this drug work? what is the only time that these drugs are active? |
Sitagliptin(Januvia)
DPP-4 is inhibited(DPP-4 metabolizes incretin) ONLY ACTIVE DURING HYPERGLYCEMIC STATE |
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what is clinical use of this?
what are adverse effects? |
used to manage fasting and postprandial hypeglyceis
can be used alone or in combo adverse effect: -HA |
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what are the comination oral hypoglycmic agents?
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*Glucovance(Glburide/Meformin)#9)
fixed dose combinations that usually contain metformin |
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what is clinical use of combination oral antidiabetics?
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treat both fasting and postprandial
provides improved glycemic control when neither agent alone is effective |
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what determines DM clinically?
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two or more fasting blood sugar levels above 126 mg/dL
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what is tx of Type I dm?
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*diet restriction
*parneteral insulin *TIghtr management of blood glucose -decreased risk of vas com -increased risk of hypoglycemia |
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what is tx of type II?
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initial therapy is :
*second gen sulfonylura (GLyuride, glipizide or glimpiride) *Metformin *Thiazolidenedione combo therapy |
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what are the long acting agents?
what blood glucose levels are maintain? |
sulfonylureas
metformin thiazolidinediones long ating insulines maintain both fasting and postprandial blood glucose levels |
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what are short acting agents?
what blood glucose levels are maintained |
short are
*meglitinides, *alpha glucosdase inhibitors, *regular insulin *insulin lispro and *insulin aspart used to conrol postprandial levels |
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what is used to treat hyperglycemia?
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glucagon
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where is glucagon produced in the body?
what is mech of action |
pancraetic alpha cells
mech: -activates G protein coupled receptors in heart, smooth muscle and liver ~stim adenylyl cyclse and increase intracellular cAMP |
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what are the physiologic effects of glucagon?
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*increaes blood glucose levels
*relaxation of smooth muscle iin GI tract (oppose effects of glucagon) |
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what are clinical uses of glucagon?
how is it administered? |
*Emergency mangement of severe hypoglycemia
*managment of Beta blocker OD *given IM or IV |
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why is glucagon the most effective method for stimulating the depressed heart?
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increases cAMP w/o activated beta receptors
(has a similar effect on smooth muscle relaxation as a beta agonist) |
