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

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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)

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3
Q

What is a major regulator of insulin release?

A

Glucose

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4
Q

Describe the physiological processes involved in insulin release after a meal

A
  1. Glucose enters B cells & contribute to ATP via glucose metabolism
  2. K+ channels close & the B cell membrane depolarizes
  3. Voltage-gated Ca2+ channels open causing an influx and stimulation of insulin exocytosis
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5
Q

What is the peak time of short acting insulins? How long do they last?

A

Peak = 2.5hrs
Lasts = 4-6hrs

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6
Q

What is the peak time of intermediate acting insulins? How long do they last?

A

Peak = 8hrs
Lasts = 8-16hrs

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7
Q

What is the peak time of Long acting insulins? How long do they last?

A

No peak
Lasts = 24hrs

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8
Q

Which line represents a rapid acting insulin?

A

A

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9
Q

Which line represents the effects of Lispro?

A

A

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10
Q

Which line represents the effects of Aspart?

A

A

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11
Q

Which line represents the effects of Glulisine ?

A

A

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12
Q

Which line represents the effects of short acting insulin?

A

B

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13
Q

Which line represents the effects of regular insulin?

A

B

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14
Q

Which line represents the effects of Intermediate?

A

C

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15
Q

Which line represents the effects of NPH?

A

C

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16
Q

Which lines represent the effects of Long insulins?

A

D&E

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17
Q

Which line represents the effects of Glargine?

A

E

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18
Q

Which line represents the effects of Detemir?

A

D

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19
Q

List the rapid acting insulins

A

Lipspro
Aspart
Glulisine

“rapid doesn’t LAG”

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20
Q

List the short acting insulin

A

Regular insulin

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21
Q

List the Intermediate insulin

A

NPH

“Int is Not Particularly Hasty”

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22
Q

List the Long acting insulins

A

Detemir
Glargine

“God Dam 24hrs is long)

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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

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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

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25
Q

Describe the side effects of Metformin

A
  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”

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26
Q

Which patients should be a red flag for using metformin (i.e avoid or be cautious)

A

Renal & heart failure or chronic hypoxic lung disease

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27
Q

What is the MOA of combining metformin/biguanide with thiazolidinediones?

A

They increase insulin sensitivity in muscle/fat (GLUT 4) & decrease glucose production in the liver

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28
Q
  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?

A

Metformin

“MET= metabolic lactic acidosis”

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29
Q

A diabetic patient is scheduled for a CT scan, what should be done prior to the scan & why?

A

Discontinue their Metformin (if they’re on it) because the contrast required for a CT can cause contrast-induced nephropathy

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30
Q

Describe the MOA of Sulfonylureas

A

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

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31
Q

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?

A

MOA of Sulfonylureas

32
Q

Chlorpropamide, Tolbutamide, Tolazamide describe which type of drug?

A

Sulfonylureas

33
Q

Describe the side effects of Sulfonylurea

A

Hypoglycemia & Disulfiram-like reaction (1st gen)

34
Q

Hypoglycemia & Disulfiram-like reaction (1st gen) are side effects of which diabetes-specific drug?

A

Sulfonylureas

35
Q

Which sulfonylurea is best used for elderly diabetic patients?

A

Tolbutamide

36
Q

How do you manage hypoglycemia, which drugs do you use, what are the clinical uses?

A

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
Q

List the Sulfonylurea drugs

A

GlimipirIDE
GlipizIDE
GlyburIDE
ChlorpropramIDE
TolbutamIDE

“IDE take your sulfonylureas”

38
Q

What are the 1st gen Sulfonylureas that can cause a Disulfiram-like reaction?

A

Chlorpropamide & Tolbutamide

39
Q

Describe the MOA of Meglitinides

A

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
Q

List the Meglitinides

A

NateglinIDE
RepaglinIDE

“IDE take your Meglitinides”

41
Q

What is the side effect of taking Meglitinides?

A

Only Hypoglycemia

42
Q

Describe the MOA of DDP-4 inhibitors

A

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
Q

List the DPP-4 inhibitors

A

Linagliptin
Saxagliptin
Sitagliptin

44
Q

What are the side effects of DPP-4 inhibitors?

A

Urinary & Respiratory infections
&
Satiety

45
Q

Urinary & Respiratory infections
&
Satiety

Which diabetic-specific drugs causes these side-effects?

A

DPP-4 Inhibitors

46
Q

Describe the MOA of GLP-1 Agonists/Analogs

A

They increase the potency of GLP-1 enzyme increasing insulin & decreasing glucagon

47
Q

What are the side effects of GLP-1 Agonist/analogs?

A

Pancreatitis**
nasopharyngitis
Upper respiratory tract infection
Headache
Weight loss
Satiety

48
Q

Pancreatitis**
Nausea/vomiting
Weight loss
Satiety

Are side effects of which diabetes-specific drug?

A

GLP-1 agonist/analogues

49
Q

List the GLP-1 agonist/analogues

A

ExanTIDE
LiragliTIDE
SemagluTIDE

50
Q

Describe the MOA of SGCT-2 inhibitors

A

They inhibit SGCT-2 in the PCT of kidneys causing more glucose to be peed out (food for bacteria)

51
Q

List the SGCT-2 drugs

A

CanagliFLOZIN
DapagliFLOZIN
EmpagliFLOZIN

“FLOZIN through the urine”

52
Q

Describe the side effects of SGCT-2 inhibitors

A
  1. Glucosuria (more glucose in pee)
  2. UTI’s & Yeast infections (glucose is food!)
  3. Hyperkalemia
  4. Dehydration
  5. Weight loss
53
Q
  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?

A

SGCT-2 inhibitors

54
Q
A
55
Q

SGCT-2 inhibitors should be cautioned with which condition?

A

Renal insufficiency because they’re less efficacious due to the reduced GFR

56
Q

Describe the MOA of Alpha-glucosidase inhibitors

A

They inhibit Alpha-glucosidase in the intestinal brush border to prevent the conversion of oligosaccharides into glucose so it can’t be absorbed

57
Q

What are the side effects of Alpha-glucosidase inhibitors?

A

The increase in intestinal oligosaccharides causes Gi upset & gas/bloating

58
Q

List the Alpha-glucosidase inhibitors

A

Acarbose
Miglitol

59
Q

What process do Alpha-glucosidase inhibitors prevent in the intestines

A

Carbohydrate hydrolysis & glucose absorption

60
Q

What is the MOA of alpha-glucuronidase inhibitors? & what are the side effects?

A

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
Q

Describe the MOA of Thiazolidinediones (pioglitazone)

A

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
Q

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?

A

Thiazolidinediones (pioglitazone)

63
Q

What are the side effects of Thiazolidinediones?

A

Heart failure (edema)
High fracture risk
MI risk (cardiac death risk)
Weight gain
Liver dysfunction
Contraception failure

64
Q

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?

A

Thiazolidinediones

65
Q

List the Thiazolidinediones

A

PioGLITAzone
RosiGLITAzone

66
Q

Describe the MOA of Amylin analogs

A

Synthetic amylin works alongside insulin to help it do its job

67
Q

What are the side effects of Amylin analogs?

A

Hypoglycemia

68
Q

What is the only Amylin analog you might need to know?

A

Pramlintide

69
Q

Describe the following for a Hyperglycemic Hyperosmolar syndrome:

What is it?

What are the symptoms?

What is the treatment?

A

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
Q

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?

A

Hyperglycemic Hyperosmolar syndrome

71
Q

Describe the following for SGCT-2 inhibitors:

What is the MOA?

What are the adverse effects?

A

MOA:
They reduce glucose reabsorption in the PCT

SE:
1) Mild weight loss
2) Hypertension

72
Q

MOA:
They reduce glucose reabsorption in the PCT

SE:
1) Mild weight loss
2) Hypertension

Describes which type of drug?

A

SGCT-2 (Canagliflozin & Dapagliflozin)

73
Q

Describe the following for insulin:

What is the MOA?

What are the side effects?

What are the clinical uses?

A

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
Q

Describe the following for diabetic ketoacidosis:

What are the symptoms?

What are the lab findings?

What is the treatment?

A

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
Q

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?

A

Diabetic ketoacidosis

76
Q
A