Block 1 Drugs for diabetes Flashcards
1
Q
What is the peak time of rapid acting insulins? How long do they last? What are the side effects?
A
Peak time = 1-1.5hrs
last = 3-4hrs
Usually used after meals or to quickly control high blood sugars (DM1)
SE:
Hypoglycemia
Lipodystrophy
Hypersensitivity reactions
Weight loss
2
Q
Peak time = 1-1.5hrs
last = 3-4hrs
Usually used after meals or to quickly control high blood sugars (DM1)
SE:
Hypoglycemia
Lipodystrophy
Hypersensitivity reactions
Weight loss
Describes which type of insulin
A
Rapid acting insulins (Lispro, Aspart, Glulisine)
3
Q
What is a major regulator of insulin release?
A
Glucose
4
Q
Describe the physiological processes involved in insulin release after a meal
A
- Glucose enters B cells & contribute to ATP via glucose metabolism
- K+ channels close & the B cell membrane depolarizes
- Voltage-gated Ca2+ channels open causing an influx and stimulation of insulin exocytosis
5
Q
What is the peak time of short acting insulins? How long do they last?
A
Peak = 2.5hrs
Lasts = 4-6hrs
6
Q
What is the peak time of intermediate acting insulins? How long do they last?
A
Peak = 8hrs
Lasts = 8-16hrs
7
Q
What is the peak time of Long acting insulins? How long do they last?
A
No peak
Lasts = 24hrs
8
Q
Which line represents a rapid acting insulin?
A
A
9
Q
Which line represents the effects of Lispro?
A
A
10
Q
Which line represents the effects of Aspart?
A
A
11
Q
Which line represents the effects of Glulisine ?
A
A
12
Q
Which line represents the effects of short acting insulin?
A
B
13
Q
Which line represents the effects of regular insulin?
A
B
14
Q
Which line represents the effects of Intermediate?
A
C
15
Q
Which line represents the effects of NPH?
A
C
16
Q
Which lines represent the effects of Long insulins?
A
D&E
17
Q
Which line represents the effects of Glargine?
A
E
18
Q
Which line represents the effects of Detemir?
A
D
19
Q
List the rapid acting insulins
A
Lipspro
Aspart
Glulisine
“rapid doesn’t LAG”
20
Q
List the short acting insulin
A
Regular insulin
21
Q
List the Intermediate insulin
A
NPH
“Int is Not Particularly Hasty”
22
Q
List the Long acting insulins
A
Detemir
Glargine
“God Dam 24hrs is long)
23
Q
Describe the MOA of Metformin/Biguanide
A
It decreases insulin resistance by Inhibiting mitochondrial glycerol phosphate (mGDP):
1) Reduced hepatic glucogenesis
2) reduced glucose absorption from intestines
3) Increased peripheral glucose uptake (fat/muscle via GLUT 4)
4) Increase glycolysis
Overall it lowers blood glucose
24
Q
It decreases insulin resistance by Inhibiting mitochondrial glycerol phosphate (mGDP):
1) Reduced hepatic glucogenesis
2) reduced glucose absorption from intestines
3) Increased peripheral glucose uptake (fat/muscle via GLUT 4)
4) Increase glycolysis
Overall it lowers blood glucose
Describes the MOA of which drug?
A
Metformin/Biguanide
25
Describe the side effects of Metformin
1. Can cause lactic acidosis (especially in people with renal insuff)
2. B12 & folate deficiency
3. Gi upset (diarrhea & abd pain)
4. Weight loss
"METformin = METabolic acidosis"
26
Which patients should be a red flag for using metformin (i.e avoid or be cautious)
Renal & heart failure or chronic hypoxic lung disease
27
What is the MOA of combining metformin/biguanide with thiazolidinediones?
They increase insulin sensitivity in muscle/fat (GLUT 4) & decrease glucose production in the liver
28
1. Can cause lactic acidosis (especially in people with renal insuff)
2. B12 deficiency
3. Gi upset
4. Weight loss
Are side effects of which diabetes specific drug?
Metformin
| "MET= metabolic lactic acidosis"
29
A diabetic patient is scheduled for a CT scan, what should be done prior to the scan & why?
Discontinue their Metformin (if they're on it) because the contrast required for a CT can cause contrast-induced nephropathy
30
Describe the MOA of Sulfonylureas
It increases insulin release from pancreatic a-cells via depolarization by blocking K channels (close K+ & open Ca2+ channels). This causes a Ca2+ influx & release of preformed insulin
31
It increases insulin release from pancreatic a-cells via depolarization by blocking K channels (close K+ & open Ca2+ channels). This causes a Ca2+ influx & release of preformed insulin
Describes the MOA of which type of drug?
MOA of Sulfonylureas
32
Chlorpropamide, Tolbutamide, Tolazamide describe which type of drug?
Sulfonylureas
33
Describe the side effects of Sulfonylurea
Hypoglycemia & Disulfiram-like reaction (1st gen)
34
Hypoglycemia & Disulfiram-like reaction (1st gen) are side effects of which diabetes-specific drug?
Sulfonylureas
35
Which sulfonylurea is best used for elderly diabetic patients?
Tolbutamide
36
How do you manage hypoglycemia, which drugs do you use, what are the clinical uses?
Use IV/IM Glucagon & Dextrose
MOA:
They act through a G-protein coupled receptors in the heart, SM, & liver via cAMP to increase hepatic glycogenolysis & gluconeogenesis (increases heart contractility)
Clinical uses:
Used to treat B-blocker overdose to increase myocyte Ca2+ & Hr
37
List the Sulfonylurea drugs
GlimipirIDE
GlipizIDE
GlyburIDE
ChlorpropramIDE
TolbutamIDE
"IDE take your sulfonylureas"
38
What are the 1st gen Sulfonylureas that can cause a Disulfiram-like reaction?
Chlorpropamide & Tolbutamide
39
Describe the MOA of Meglitinides
Same as Sulfonylureas i.e it increases insulin release by depolarizing pancreatic B cells (close K+ & open Ca2+ channels) except they bind to a different site (don't really need to know)
40
List the Meglitinides
NateglinIDE
RepaglinIDE
"IDE take your Meglitinides"
41
What is the side effect of taking Meglitinides?
Only Hypoglycemia
42
Describe the MOA of DDP-4 inhibitors
They inhibit DDP-4 (obviously) which in turn increases the potency of GLP-1 ending in more insulin & less glucagon release following a meal
43
List the DPP-4 inhibitors
Linagliptin
Saxagliptin
Sitagliptin
44
What are the side effects of DPP-4 inhibitors?
Urinary & Respiratory infections
&
Satiety
45
Urinary & Respiratory infections
&
Satiety
Which diabetic-specific drugs causes these side-effects?
DPP-4 Inhibitors
46
Describe the MOA of GLP-1 Agonists/Analogs
They increase the potency of GLP-1 enzyme increasing insulin & decreasing glucagon
47
What are the side effects of GLP-1 Agonist/analogs?
Pancreatitis**
nasopharyngitis
Upper respiratory tract infection
Headache
Weight loss
Satiety
48
Pancreatitis**
Nausea/vomiting
Weight loss
Satiety
Are side effects of which diabetes-specific drug?
GLP-1 agonist/analogues
49
List the GLP-1 agonist/analogues
ExanTIDE
LiragliTIDE
SemagluTIDE
50
Describe the MOA of SGCT-2 inhibitors
They inhibit SGCT-2 in the PCT of kidneys causing more glucose to be peed out (food for bacteria)
51
List the SGCT-2 drugs
CanagliFLOZIN
DapagliFLOZIN
EmpagliFLOZIN
"FLOZIN through the urine"
52
Describe the side effects of SGCT-2 inhibitors
1. Glucosuria (more glucose in pee)
2. UTI's & Yeast infections (glucose is food!)
3. Hyperkalemia
4. Dehydration
5. Weight loss
53
1. Glucosuria (more glucose in pee)
2. UTI's & Yeast infections (glucose is food!)
3. Hyperkalemia
4. Dehydration
5. Weight loss
Are side effects of which diabetic-specific drugs?
SGCT-2 inhibitors
54
55
SGCT-2 inhibitors should be cautioned with which condition?
Renal insufficiency because they're less efficacious due to the reduced GFR
56
Describe the MOA of Alpha-glucosidase inhibitors
They inhibit Alpha-glucosidase in the intestinal brush border to prevent the conversion of oligosaccharides into glucose so it can't be absorbed
57
What are the side effects of Alpha-glucosidase inhibitors?
The increase in intestinal oligosaccharides causes Gi upset & gas/bloating
58
List the Alpha-glucosidase inhibitors
Acarbose
Miglitol
59
What process do Alpha-glucosidase inhibitors prevent in the intestines
Carbohydrate hydrolysis & glucose absorption
60
What is the MOA of alpha-glucuronidase inhibitors? & what are the side effects?
Aka Acarbose, miglitol, & Voglibose
MOA:
They target surface membrane-bound alpha-glucuronidase from converting oligosaccharides/disaccharides & into glucose/monosaccharide so it can't be absorbed by the intestines
Side effects:
1) GAS/BLOATING
2) Flatutence
3) Malabsorption
4) Abdominal pain
5) Rash
61
Describe the MOA of Thiazolidinediones (pioglitazone)
1) They bind Peroxisome-Proliferator activated receptors (PPAR-gamma aka a nuclear receptor)
2) increases adipokines to store more free fatty acids & reduce fat metabolism forcing the liver to use up its glucose (increased insulin sensitivity) & produce less of it
They have a delayed onset of about several weeks & don't use in patients with heart failure
62
1) They bind Peroxisome-Proliferator activated receptors (PPAR-gamma aka a nuclear receptor)
2) increases adipokines to store more free fatty acids & reduce fat metabolism forcing the liver to use up its glucose (increased insulin sensitivity) & produce less of it
They have a delayed onset of about several weeks & don't use in patients with heart failure
Describes the MOA OF WHICH DRUG?
Thiazolidinediones (pioglitazone)
63
What are the side effects of Thiazolidinediones?
Heart failure (edema)
High fracture risk
MI risk (cardiac death risk)
Weight gain
Liver dysfunction
Contraception failure
64
Heart failure (edema)
High fracture risk
MI risk (cardiac death risk)
Weight gain
Liver dysfunction
Contraception failure
Are side effects of which diabetes-specific drug?
Thiazolidinediones
65
List the Thiazolidinediones
PioGLITAzone
RosiGLITAzone
66
Describe the MOA of Amylin analogs
Synthetic amylin works alongside insulin to help it do its job
67
What are the side effects of Amylin analogs?
Hypoglycemia
68
What is the only Amylin analog you might need to know?
Pramlintide
69
Describe the following for a Hyperglycemic Hyperosmolar syndrome:
What is it?
What are the symptoms?
What is the treatment?
Patho:
A life threatening complication of diabetes (type 2) often with a serum glucose of over 1000!!!
Symptoms:
1) Severe dehydration
2) Polyuria & polydipsia
3) Mental status changes (coma/confusio)
Rx. IV Insulin & IVF
70
Patho:
A life threatening complication of diabetes (type 2) often with a serum glucose of over 1000!!!
Symptoms:
1) Severe dehydration
2) Polyuria & polydipsia
3) Mental status changes (coma/confusio)
Rx. IV Insulin & IVF
Describes which condition?
Hyperglycemic Hyperosmolar syndrome
71
Describe the following for SGCT-2 inhibitors:
What is the MOA?
What are the adverse effects?
MOA:
They reduce glucose reabsorption in the PCT
SE:
1) Mild weight loss
2) Hypertension
72
MOA:
They reduce glucose reabsorption in the PCT
SE:
1) Mild weight loss
2) Hypertension
Describes which type of drug?
SGCT-2 (Canagliflozin & Dapagliflozin)
73
Describe the following for insulin:
What is the MOA?
What are the side effects?
What are the clinical uses?
MOA:
iNSULIN BIND THE tkr CAUSING AUTOPHOSPHORYLATION OF THE TYROSINE RESIDUES:
1) PIK3 PATHWAY CAUSES ACTIVATION OF GLUT4 RECEPTORS ON SKELETAL MUSCLE/FAT TO INCREASE UPTAKE OF PERIPHERAL GLUCOSE
2) RAS/MAP PATHWAY INCREASES GROWTH & GENE TRANSCRIPTION
Side effects:
1) Hypoglycemia
2) Lipodystrophy
3) Allergy
4) Weight gain
Clinical uses:
Diabetes mellitus
Diabetic keto acidosis
Preggo/gestational diabetes
Emergency treatment of hyperkalemia
74
Describe the following for diabetic ketoacidosis:
What are the symptoms?
What are the lab findings?
What is the treatment?
Symptoms:
1) Kussmaul sign (deep/labored breathing)
2) Abdominal pain
3) Dehydration
4) Fruity breath ***
5) Hyperventilation (to lose Co2 & raise pH)
Labs:
Hyperglycemia
Hyperkalemia
Increased plasma/urine ketones & glucose
Anion gap metabolic acidosis
Rx: IV Insulin & IVF
75
Symptoms:
1) Kussmaul sign (deep/labored breathing)
2) Abdominal pain
3) Dehydration
4) Fruity breath ***
5) Hyperventilation (to lose Co2 & raise pH)
Labs:
Hyperglycemia
Hyperkalemia
Increased plasma/urine ketones & glucose
Anion gap metabolic acidosis
Rx: IV Insulin & IVF
dESCRIBES WHICH CONDITION?
Diabetic ketoacidosis
76
