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Pharm Exam V > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q

Signs and Symptoms of Diabetes?

A

Signs and symptoms of diabetes:

a. Polyuria (frequent urination)
b. Polydipsia (increased thirst)
c. Polyphagia (increased hunger)
d. Weight loss (type 1)
e. Blurred vision
f. Extreme fatigue and slow healing

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2
Q

Acute complications in diabetes?

A

Acute diabetic complications:

  1. Diabetic ketoacidosis (DM1) - N/V, dehydration, abdominal pain, acetone breath, kassmaul breathing (deep), and decreased consciousness/coma
  2. Nonketotic hyperosmolar state__ (DM2) - severe dehydration, increase in osmolarity, coma, and death
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3
Q

Long term diabetic complications?

A

Long term complications

a. Microvascular - nephropathy and retinopathy
b. Macrovascular - cerebrovascular/peripheral vascular disease and coronary artery disease
c. Neuropathic - sensory, motor, and autonomic neuropathy
d. Associated often with dyslipidemia and hypertension

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4
Q

Diagnoses of diabetes?

A

Diagnosis:

a. HbA1c test: measures average glucose for the past 2-3 months
b. Fasting plasma glucose
c. Oral glucose tolerance test: checks blood glucose levels before and 2 hours after drinking a glucose solution

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5
Q

What is prediabetes?

A

Prediabetes:

a. blood glucose higher than normal but not high enough to be diabetes
b. increased risk for DM2 and CVD
c. No clear signs/symptoms
d. Impaired glucose tolerance
e. Diet/exercise can lower risk of DM2

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6
Q

What is metabolic syndrome?

A

Metabolic syndrome:

a. similar to prediabetes
b. increased risk for coronary heart disease, stroke, and DM2
c. Risk factors: high fasting blood glucose, abdominal obesity, high triglycerides, low HDL, and increased BP (diagnosis = 3/5 risk factors)

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7
Q

Insulin:

Steps in the first phase of insulin?

A

Insulin:

Glucose enters beta cells through GLUT2 –> glycolysis/TCA with increased ratio of ATP:ADP –> this leads to closure of ATP-sensitive K+ channel –> leads to depolarization of the cell surface membrane –> Ca++ channels open and Ca++ influx –> activation of PLPC which cleaves membrane phospholipid to IP3 –> binds to receptors on ER allowing Ca++ efflux and increased intracellular Ca++ –> triggers release of insulin from storage vesicles

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8
Q

Insulin:

  1. Second phase?
  2. Release of insulin is strongly inhibited by?
A

Insulin:

  1. Second phase: sustained, slow release of newly formed vesicles triggered independently of sugar
  2. Release is strongly inhibited by NE
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9
Q

Parts of the insulin receptor?

A

Insulin receptor

a. Cell surface receptor
b. Alpha subunit on outside to bind insulin
c. Beta subunit on the inside has tyrosine kinase activity

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10
Q

Signal transduction pathway via insulin binding?

A

Insulin binds alpha subunit –> conformational change in receptor –> activation of beta subunit –> tyrosine residues on C-terminus of receptor (and residues on the IRS-1 protein) are autophosphorylated –> activation of PI3K, PKB, and glycogen synthase kinase –> increase in glycogen and GLUT4 transporters in plasma membrane

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11
Q

Insulin preparations?

Use?

A

Insulin preparations:

a. Rapid acting insulin
b. Regular or short acting insulin
c. Intermediate-acting insulin
d. Long acting insulin

For DM1

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12
Q

Insulin preparations:

  1. Rate limiting step?
  2. Rapidly acting insulin drugs?
  3. Regular/short acting insulin drugs?
A

Insulin preps:

  1. Rate limiting step: subcutaneous dissociation into dimers and then monomers
  2. Rapid acting insulin: Lispro, Aspart, Glulsine
  3. Regular/short acting insulin: regular insulin
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13
Q

Insulin:

  1. Intermediate acting insulin drugs?
  2. Long-acting insulin drugs?
  3. Insulin delivery options?
A

Insulin:

  1. Intermediate acting: NPH = neutral protamin Hagedorn - only give subcutaneously
  2. Long acting: glargine and detemir (strongly binds albumin and slows release)
  3. Insulin pen or pump
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14
Q

Side effects of insulin?

A

Side effects:

a. Lipodystrophy: localized loss of fat at injection site interferring with insulin absorption
b. Allergic reactions to additives
c. Hypoglycemia leading to insulin shock

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15
Q

Insulin shock:

  1. symptoms?
  2. Treat?
A

Insulin shock:

  1. Symptoms: impaired neurologic function, inability to concentrate, slurred speech, lack of coordination, and staggering. This is often mistaken for being drunk
  2. Treat - give glucose
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16
Q

Types of oral antihyperglycemics?

What does this treat?

A

Oral antihyperglycemics:

a. Insulin sensitizers
b. Insulin secretagogues
c. Inhibitors of carbohydrate absorption
d. Intestinal/pancreatic peptides

This is for DM2 (along with diet and exercise)

17
Q

Insulin sensitizers:

Biguanides:

  1. Drugs?
  2. MOA and result?
  3. Adverse effects?
  4. Contraindications?
A

Insulin sensitizers:

Biguanides:

  1. Metformin
  2. MOA: Inhibits hepatic gluconeogenesis and G6P activity –> increased insulin receptor activity, decreased insulin resistance, decreased gut absorption of glucose, increased uptake in muscle and hepatocytes by activation AMPPK, decreases triglycerides/total cholesterol/LDL, and increases HDL
  3. SE:GI disturbances, rarely lactic acidosis, weight loss, and some decrease in blood pressure **NOT hypoglycemic even at high doses
  4. Contra: renal/hepatic dysfunction and alcoholism. Also, cimetidine can inhibit drug metabolism
18
Q

Insulin sensitizers:

Thiazolidinediones:

  1. Drugs?
  2. MOA?
A

Insulin sensitizers:

Thiazolidinediones:

  1. Rosiglitazone and Pioglitazone
  2. MOA: PPARgamma agonists, increase insulin sensitivity, increase GLUT4 receptor density, reduce hepatic glucose output, and DOES NOT increase insulin secretion
19
Q

Insulin sensitizers:

Thiazolidinediones:

  1. Rosiglatazone black box warning?
  2. Pioglitazone: excretion? Warning?
  3. For both - time till effective?
  4. Contraindications?
A

Insulin sensitizers:

Thiazolidinediones:

  1. Rosiglatazone: Increased risk of MI
  2. Pioglitazone: feces excretion; warning - use >1 year may have association with Bladder cancer risk (no evidence of hepatotoxicity)
  3. Maximal effect in 4-6 weeks
  4. Contra: acute liver disease and heart failure – can cause edema and increase plasma volume
20
Q

Insulin secretagogues:

  1. Sulfonylurea drugs?
  2. Meglitinide drugs?
A

Insulin secretagogues:

  1. Sulfonylureas: Glimepiride, Glipizide, Glyburide, and chlorpropamide
  2. Meglitinide: Repaglinide and Nateglinide
21
Q

Insulin secretagogues:

Sulfonylureas:

  1. MOA?
  2. Uses?
A

Insulin secretagogues:

Sulfonylureas:

  1. MOA: bind ATP-dependent K+ channel on B cells –> inhibit K+ efflux and causing electric potential to become more positive –> voltage gated Ca++ channels open –> increased intracellular Ca++ and stimulates fusion of insulin granule with cell membrane –> increased secretion of (pro)insulin
  2. Uses: second line when metformin is contraindicated/not efficient, not for type one, more effective when beta cell function hasnt been severely compromized, most appropriate in non/mildly obese
22
Q

Insulin secretagogues:

Sulfonylureas:

  1. Adverse effects?
  2. Contraindications?
A

Insulin secretagogues:

Sulfonylureas:

  1. AE: severe hypoglycemia (5x higher than metformin), increased weight, erythema, hematological reactions, hepatic dysfunction, and GI. Interactions with alcohol can lead to severe hypoglycemia
  2. Contra: pregnancy, surgery, severe infection, severe stress/trauma, and severe hepatic/renal failure. Use insulin instead in these cases
23
Q

Insulin secretagogues:

Meglitinides:

  1. MOA?
  2. Drug interactions?
A

Insulin secretagogues:

Meglitinides:

  1. MOA: Similar to sulfonylureas but bind elsewhere. Insulin release is rapid and brief. Should be taken with meals.
  2. Interactions: Decreased effectiveness of: thiazide diuretics/corticosteroids/estrogens/thyroid hormones/phenytoin; Increased effectiveness of: ACEI/sulfonamides/NSAIDs/Gemfibrozil (lipid regulator)/alcohol
24
Q

Inhibitors of carbohydrate absorption:

Class of drug and drugs?

A

Inhibitors of carbohydrate absorption:

Alpha-Glucosidase inhibitors:

a. Acarbose
b. Miglitol

25
Q

Inhibitors of carbohydrate absorption:

  1. MOA?
  2. Use? Doesnt cause?
  3. Adverse effects?
  4. Contraindications?
A

Inhibitors of carbohydrate absorption:

  1. MOA: competitive, reversible inhibitors of alpha glucosidase –> delay CHO digestion/absorption –> prevent postprandial glucose peaks
  2. Use: mild to mod fasting hyperglycemia and significant postprandial hyperglycemia; DOES NOT produce hypoglycemia, lactic acidosis, or weight gain
  3. AE: GI (N/D, flatulence, and bloating), if hypoglycemic - give glucose and NOT sucrose
  4. Contra: inflammatory and obstructive bowel disease and colonic ulcers
26
Q

Intestinal/Pancreatic peptidases:

2 classes and their drugs?

A

Intestinal/Pancreatic peptidases:

a. Incretin mimetics: Exenatide, Liraglutide, Sitagliptin, and Saxagliptin
b. Amylin analogue: Pramlintide

27
Q

Intestinal/Pancreatic peptidases:

Incretin mimetics:

MOA?

A

Intestinal/Pancreatic peptidases:

Incretin mimetics:

MOA: Increase insulin secretion, decrease glucagon release, slow gastric emptying, increase satiety, decrease food intake, & intake intake of glucose in muscle and adipose

28
Q

Intestinal/Pancreatic peptides:

Exenatide and Liraglutide:

  1. What are these?
  2. Adverse events?
  3. Contraindications?
  4. Combination?
A

Intestinal/Pancreatic peptides:

Exenatide and Liraglutide:

  1. GLP-1 mimetics
  2. AE: mild to moderate nausea
  3. Contra: hypertriglyceridemia or gall stones – may cause pancreatitis
  4. Combination: When used with sulfonylureas or metformin or both – better HbA1c levels
29
Q

Insulin/Pancreatic Peptides:

Sitagliptin and Saxagliptin

  1. What is this?
  2. Combinations?
  3. Contraindications?
A

Insulin/Pancreatic Peptides:

Sitagliptin and Saxagliptin

  1. DDP4 - inhibits GLP-1 breakdown
  2. Used as monotherapy or with metformin or thiozolinediones; no increase in weight
  3. Contraindications - hypertriglyceridemia or gallstones
30
Q

Insulin/Pancreatic Peptides:

Amylin Analog:

  1. MOA?
  2. Adverse effects?
  3. Uses?
A

Insulin/Pancreatic Peptides:

Amylin Analog

  1. MOA: amylin-like effect - prevents post prandial blood glucose spikes but overal no change in absorption of CHO, slows gastric emptying, suppresses glucagon secretion, and decreases hepatic glucose output.
  2. Adverse: N/V/HA, anorexia, hypoglycemia (discontinue if recurrent hypoglycemic events occur)
  3. For DM1 and DM2 in patients treated with insulin, must be given subcutaneously
31
Q

Combination therapy:

Why is this good?

Combinations?

A

Combination therapy is good because you can reduce the dose of each drug and thus reduce side effects:

a. insulin sensitizer + insulin
b. insulin sensitizer + insulin secretagogue
c. TZDs + metformin (both sensitizers but diff. MOA)
d. insulin or secretagogue + acarbose
e. secretagogue or sensitizer + incretin mimetics
f. insulin + amylin analogue

32
Q
A
33
Q

Gestational diabetes:

  1. How do women get insulin resistance?
  2. Affect on baby?
  3. treat?
  4. Later risk?
A

Gestational diabetes:

  1. Insulin resistance from hormones in the placenta; up to 3x more insulin is needed
  2. Child: birth defects, macrosomia (big sized), increased insulin production, and increased risk for obesity/DM2
  3. Treat: diet, physical activity, oral antihyperglicemics, or insulin
  4. Later risk in future pregnancies and DM2 in the future
34
Q

Hypoglycemia:

  1. Causes?
  2. Signs and symptoms?
  3. Drugs?
A

Hypoglycemia:

  1. Causes: diabetic hypoglycemia, insulinoma (tumor), and hyperinsulinemia
  2. S/S: shakiness, nervousness, anxiety, dysphoria, neuroglycopenia (not enough glucose to the brain), seizures, unconsciousness, and death
  3. Diazoxide and Glucagon
35
Q

Diazoxide:

  1. MOA?
  2. Adverse effects?
A

Diazoxide:

  1. MOA: increases the open time of the K+ channel, inhibits insulin secretion, but DOESNT inhibit insulin synthesis, increases hepatic gluconeogenesis, and decreases peripheral utilization of insulin
  2. AE: N/V, heart failure, bowel obstruction, fluid retention, pancreatitis, neutropenia, and thrombocytopenia
36
Q

Glucagon:

  1. Secretion inhibited by?
  2. Secretion stimulated by?
  3. MOA?
A

Glucagon:

  1. Secretion inhibited by insulin, glucose, and somatostatin
  2. Stimulated by amino acids, catecholamines, and glucocorticoids
  3. Binds to G-protein coupled receptors –> increased cAMP –> production of IP3 –> Increased intracellular Ca++.
37
Q

Glucagon:

  1. Effects?
  2. Uses?
A

Glucagon:

  1. Inhibits glycogen synthesis/lipogenesis, stimulates glycogenolysis/ketogenesis/gluconeogenesis, positive inotrope and chronotrope to the heart, and relaxation of intestinal smooth muscle
  2. For severe hypoglycemia, complication of DM (diabetic hypoglycemia), meds, poisons, alcohol, and prolonged starvation, insulinoma, and congenital hyperinsulinemia

Pharm Exam V (6 decks)

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