Diabetes Medication Flashcards
(31 cards)
1
Q
what fasting plasma glucose and HbAIC levels consistute
- pre-diabetes?
- diabetes?
A
- fasting plasma glucose
- prediabetes: 100-125
- diabetes: 126 +
- HbA1C:
- prediabetes: 5.7-6.4%
- diabetes: 6.5% +
2
Q
what “random” blood sugar levels are indicative of
- pre-diabetes?
- diabetes?
how are these levels obtained?
A
- pre-diabetic = 140 mg/dL
- diabetic = 200 mg/dL +
measured by oral glucose tolerance test (OGTT)
3
Q
the treatment target for diabetes is a HbA1c of?
A
< 7%
4
Q
discuss the mechanism by which glucose stimulate insulin secretion
A
- glucose enters beta cells on pancreas via GLUT-2 transporters
- it is phosphorylated to G-1-P by glucokinase, which traps it in the cell
- enters the glycolitic pathway to become ATP
- elevation in ATP/ATP ratio blcks ATP-sensitive K+ channel, trapping K+ in the cell
- the cells depolarizes, which opens voltage gated Ca++ channels
- increased cytosolic Ca++ triggers exocytosis of insulin granules
5
Q
once released, how does insulin induce gucose uptake?
A
by inducing translalocation of GLUT-4, the glucose receptor on adipose & muscle cells, to he membrane
6
Q
insulin replacement therapy - includes
- what classes of drugs?
- what are the drugs in each class?
- in which formulation is each drug?
- what are the drugs in each class?
- when is each class used?
A
- short duration - used to manage postprandial (post-meal) glucose
-
rapid acting short duration:
- lispro / aspart - injected
- afrezza - inhaled
-
slower acting short duration
- human insulin
-
rapid acting short duration:
- long duration - used for basal control of glucose
- glargine - injected
7
Q
glargine
- what kind of drug?
- how is it given?
A
- long duration insulin replacement
-
injected sub-Q
- given once daily - manages glucose for 24 hrs
8
Q
what are the major adverse effects of insulin replacement use?
how are each of these AEs managed?
A
- insulin overdose - can cause
-
hypoglycemia
- tx:
- dextrose
- glucagon
- tx:
-
hypokalemia
- tx
- K+ supplements
- tx
-
hypoglycemia
- insufficient insulin - can cause
-
ketoatcidosis (d/t prolonged hyperglycemia)
- this can lead to coma/death
- tx
- inc insulin dose (monitor K+)
- water / Na+ replacement
-
ketoatcidosis (d/t prolonged hyperglycemia)
9
Q
pramlintide
- what kind of drug?
- MOA?
- clinical uses?
- AEs?
- drug-drug interaction?
A
- is an amylin mimetic
- clinical uses: management of post-prandial glucose levels in of Type I &Type II diabetes
- MOA:
- delays gastric emptying
- suppresses glucagon secretion
- AEs
- nausea
- hypoglycemia
10
Q
what are the ways of treating pre-diabetes?
what is the goal of treaing pre-diabetes?
A
goal is to prevent/delay entry into Type II diabetes
- treatments
- lifestyle
- weight (calorie restriction)
- exercise: aerobic and resistant training both improve insulikn sensitivity
- pharmaceutical
- metformin - is the best available choice, tho technically not FDA approved
- lifestyle
11
Q
ideal diet for tx of type II diabetes
A
–Carbohydrates 60-70%
–Protein 15-20%
–Polyunsaturated fat 10%
–Saturated fat less than 10%
–Cholesterol- less than 300 mg/day
12
Q
metformin
- MOA
- indications
- AEs/CIs
- drug-drug interactions
A
- MOA: suppresses gluconeogeneis
- indication:
- type 2 diabetes
- can be used for pre-diabetes, but not technically FDA approved
- AEs:
- common: GI - nausea/flutulence/diarrhea, subside over time
- rare: lactic acidosis
- CI: in pts with GRF < 30 mL/min
- drug-drug interactions:
- nephrotoxic contrast agents
- acarbose
13
Q
which patients must temporarily discontinue metformin?
A
those needing imaging that requires nephrotoxic contrast agents
14
Q
sulfonuyreas
- include what drugs?
- MOA?
- AEs?
- drug-drug interactions?
A
- tolbutamide, glyburide
- MOA:
-
induce insulin release:
- bind ATP sensitive K+ channels in beta cells –> membrane depolarizes –> Ca++ influx induces insulin release
-
induce insulin release:
- AEs:
- hypoglycemia
- drug-drug interactions
- ethanol - facial flushing
- beta-blockers: b-blockers blunt drug effects
15
Q
repaglinide
- what kind of drug?
- MOA?
- AEs/CIs?
- drug drug interactions?
A
- a meglitide
- MOA:
-
induces insulin release:
- bind ATP sensitive K+ channels in beta cells –> membrane depolarizes –> Ca++ influx induces insulin release
-
induces insulin release:
- AE
- hypoglycemia
- drug-drug interactions:
- gemfibrozil (a trigclyeride lowering drug): is a potent CYP2C8 inhibitor, which metabolizes repaglinide
16
Q
what drugs interact with gemfibrozil?
what should pts on gemfibrozil be given instead?
A
- repaglinide:
- - glitazones: rosiglitazone, pioglitazone
these pts should be switched to fenofibrate
17
Q
which diabetes drugs induce insulin secretion by blocking ATP sensitive K+ channels?
A
- sulfonylureas: tolbatamide, glyburide
- repaglinide
18
Q
thiozolidinediones
- includes what drugs?
- MOA?
- AEs/CIs?
- drug drug interactions?
A
- -glitazones: rosiglitazone, pioglitazone
- MOA:
- an insulin sensitizer:
- __activates PPAR gamma, which turns on genes that inc cellular repsonse to insulin
- an insulin sensitizer:
- AEs:
- fluid retention: edema / congestive HF
- possible MI risk
- drug-drug interactions:
- gemfibrozil (trigclyceride lowering drug) inhibits CYP-2C8, which metabolizes rosiglitazone
19
Q
acarbose
- MOA
- AES
- drug drug interactions
A
- alpha-glucosidase inhibitors
- MOA:
- delays absorption of carbohydates from the intestine
- inhibits alpha-glucosidase (breaks down carbs)
- delays absorption of carbohydates from the intestine
- AE:
- GI: flatulence / cramps / abdominal distension / diarrhea
- drug-drug interactions:
- metformin: GI effects compound
20
Q
glucagon-like peptide (GLP-1) agonists
- includes what drugs
- MOA
- indications
- AEs?
A
- - glutides: liraglutide, dulagutide & exantide
- MOA: stimulates glucose dependent insulin release
- indications:
- liraglutide
- used for weight loss
- may reduce the risk of cardiac events
- liraglutide
- AE:
- hypoglycemia
21
Q
DDP-4 inhibitors
- what drugs?
- MOA?
- indications?
- AEs?
A
- - gliptin: saxagliptin, alogliptin, linagliptin
- MOA: maintains high level of incretin hormones
- inhibits dipeptidyl peptidase-4 (DPP-4), the metabolizer of incretin hormones (GLP-1, CCK, secretin, gastrin, B-agonists), which increase insulin secretion
- indications:
- Type 2 diabetes
- AE
- hypoglycemia
- renal problems
22
Q
SLGT-2 inhibitors
- which drugs?
- MOA?
- indications?
- AEs/CIs?
- drug drug interactions
A
- glifozin - canaglifozin, dapaglifozin, empafligozin
- MOA:
- inhibit glucose reabsorption at gut / kidney by inhibitng Na/glucose symporters
- indications
- type 2 diabetes
- may reduce CV risk
- AEs: urinary tract infections
- drug drug interactions: rifampicin (with canaglifozin)
23
Q
which diabetes drugs reduce CV risk?
A
- Metformin
- GLP-1 agonists (liraglutide)
- SGLT-2 inhibitors (glifozin)
24
Q
which two diabetes drugs cause significant GI AEs?
A
- metformin
- acarbose
25
what are the sulfonyureas?
* tolbutamide
* glyburide
26
**- gliptins:** saxagliptin, alogliptin, linagliptin
are in what drug class?
DDP-4 (incretin metabolizer) inhibitors
27
which diabetes drugs can cause hypoglycemia?
high risk
* insulin supplements - lispro, alezza, glargine
* drugs that induce insulin release
* sulfonuryeas - tolbutamide, glyburide
* regalinitide
low risk (high when combined with other drugs)
* DDP-4 inhibitors (-gliptins)
* GLP-1 agonists (- glutides)
28
**glitazones**: rosiglitazone, pioglitazone
are what drugs?
have what AEs?
* thiazolidinediones
* AEs
* **fluid congestion / edema / CHF**
* possible MI risk
29
which diabetes drug can interact with alcohol?
sulfonylureas - tolbutamide, glyburide
30
what is the general progression treatment of type II diabetes?
start of with
* lifestyle change + **metformin** + _two_ hypoglycemic drugs
if not controlled,
* three hypoglycemic drugs
if still not controlled
* hypoglycemic drugs + _insulin_
31
what is the general treatment plan for type I diabetes?
* lifestyle control
* **insulin**
