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2-Pharm Final > Insulin and & Oral Hypoglycemics > Flashcards

Insulin and & Oral Hypoglycemics Flashcards

1
Q

Where is insulin synthesized?

A

β cells islets of Langerhans in pancreas

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2
Q

Why is insulin needed?

A

Insulin needed for glucose transport across cell membranes

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3
Q

What does insulin increase?

A

Insulin increases glucose uptake & use in fat and muscle

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4
Q

What does insulin inhibit?

A

Insulin inhibits gluconeogenesis & glycogenolysis

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5
Q

What happens in the state of Insulin deficiency & peripheral insulin resistance?

A

hyperglycemia results from impaired glucose utilization, increased glycogenolysis, & increased gluconeogenesis

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6
Q

What happens in the absence of insulin?

A
  • Absence of insulin
    • increased lipolysis & circulating free fatty acids
    • ketone production in liver
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7
Q

What does hyperglycemia impair?

A
  • vasodilation, proinflammatory, prothrombotic, and proatherogenic
  • predisposes to vascular complications
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8
Q

Define Type I DM.

A

Autoimmune mediated destruction of pancreatic β cells

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9
Q

Define characteristiccs of Type I DM?

A
  • Onset usually younger age
  • sensitivity to insulin normal – require exogenous insulin administration
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10
Q

Lack of insulin may precipitate ________

A

ketoacidosis

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11
Q

Define components of Type II DM.

A

Failure to secrete insulin due to pancreatic β cells dysfunction coupled w/ peripheral insulin resistance

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12
Q

What is the treatment of DM II?

A

Treatment w/ oral hypoglycemic agents or insulin

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13
Q

What are the goals of DM tx?

A

prevent adverse consequences of hyperglycemia & hypoglycemia

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14
Q

What is the components of HbA1c?

A
  • Long-term glucose control best monitored with HbA1c levels
  • glucose levels over 2-3 months
  • <6-7% less associated w/ fewer microvascular complications
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15
Q

Goal targeted for blood glucose ______

A

< 200 mg/dL intraoperatively

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16
Q

What is the treatment of DM1?

A

DM require exogenous administration of insulin for survival

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17
Q

What is the tx for DM2?

A

insulin also used in type 2 DM patients if oral hypoglycemics don’t achieve adequate glucose control

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18
Q

What are the components of the insulin receptor?

A

Insulin receptors are tyrosine kinase receptors (2nd messenger receptors that work mainly via phosphorylation)

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19
Q

What allows glucose into the cell?

A

upregulation of Glut 4

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20
Q

What is the normal secretion of basal insulin?

A

Under normal condition, basal insulin is secreted into portal venous system at rate 1unit/hour

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21
Q

total daily secretion of insulin is ________

A

approx. 40 units

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22
Q

What stimulates a decrease in basal secretion insulin?

A

Sympathetic nervous system innervates islet cells of pancreas: α-adrenergic stim decreases basal secretion insulin

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23
Q

What increases basal insulin secretion?

A

β-adrenergic stim & parasympathetic nervous system stim increases basal insulin secretion

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24
Q

What is the pharmacological effects of insulin? Why?

A

Despite elimination ½ time of 5-10 min, pharmacologic effects last 30-60 min d/t insulin being tightly bound to tissue receptors

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25
Q

What is the administration of insulin?

A

SQ route produces a slower, sustained delivery

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26
Q

What is the prinicple of insulin replacement?

A

provide a slow, long-acting, continuous supply of insulin that mimics the nocturnal and between-meal basal secretion of normal pancreatic β cells

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27
Q

What are examples of principle of insulin replacement?

A

NPH, insulin glargine, insulin detemir, insulin degludec

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28
Q

What is rapid short acting insulin?

A

A rapid short-acting insulin administered before meals mimics normal meal-stimulated (prandial) release of insulin

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29
Q

What are examples of rapid short acting?

A

Insulin aspart, lispro, glulisine

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30
Q

What is the total exogenous insuling dose for type 1 DM?

A

Total daily exogenous insulin dose for tx of type 1 DM usually in range of 0.5 to 1 U/kg/day

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31
Q

What is true about the insulin requirements for DM 1?

A

this requirement may be increased by stress asso/w sepsis or trauma

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32
Q

Review components of insulin

A
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33
Q

What is the major side effect of diabetic medications?

A
  • most serious side effect
  • patients most susceptible if receive exogenous insulin administration in absence of carbohydrate intake (i.e., perioperative fasting period before surgery)
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34
Q

What are the first symptoms of hypoglycemia?

A

d/t increased epinephrine secretion to raise the blood glucose level (diaphoresis, tachycardia, HTN)

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35
Q

What is the somogyi effect?

A
  • rebound hyperglycemia caused by sympathetic nervous system activity response to hypoglycemia
  • can mask actual diagnosis of hypoglycemia
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36
Q

What are the CNS effects of hypoglycemia?

A
  • mental confusion progressing to seizures & coma
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37
Q

Prolonged hypoglycemia can result in _________

A

irreversible brain damage

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38
Q

What is the components of hypoglycemia and GA?

A

difficult b/c anesthetic drugs mask classic signs of sympathetic nervous system stimulation

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39
Q

What can hypoglycemia cause hemodynamically?

A

changes in HR & BP – likely to be confused w/evoked responses to painful surgical stimulation in anesthetized pt

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40
Q

What can also mask symptoms of hypoglycemia?

A

Nonselective β-adrenergic antagonists

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41
Q

What is the treatment of severe hypoglycemia?

A
  • 50-100mL 50% glucose solution IV; glucagon 0.5-1mg IV or SC
  • if no CNS depression, carbohydrate PO
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42
Q

What are allergic reaction components of insulin?

A

less common w/human insulins (no longer use animal-derived pork or beef)

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43
Q

What are the prinicple components of allergic reactions?

A

less common w/human insulins (no longer use animal-derived pork or beef)

44
Q

Chronic exposure to low doses of protamine in NPH insulin may stimulate production of ______

A

antibodies against protamine

45
Q

Patients who receive a large dose of protamine IV to antagonize anticoagulant effect of heparin may have ___________

A

allergic reaction

46
Q

Define lipodystrophy.

A

fat atrophy at site of SC injections

47
Q

What are hormone drugs that can interact with insulin?

A

Hormones (admin as drugs) that counter insulin hypoglycemic effect: ACTH, estrogens, glucagon

48
Q

What are epinephrine’s interact with insulin?

A

inhibits insulin secretion & stim glycogenolysis

49
Q

What drugs can increase insulin hypoglycemic effect?

A

tetracycline, chloramphenicol, salicylates, phenylbutazone, MAO inhibitors

50
Q

Review oral hypoglyemics table.

A
51
Q

What is the first line of tx for type 2 DM?

A

Metformin

52
Q

What is the MOA of Metformin?

A
  • suppresses hepatic glucose production
  • decreases GI glucose absorption
  • increases insulin sensitivity in peripheral tissues
53
Q

What is not a risk with Metformin?

A

Hypoglycemia not a risk (as solo tx agent)

54
Q

What can Metformin be used in combo with?

A
  • Can be used in combination w/ insulin & sulfonylureas
  • + risk of hypoglycemia in combo w/insulin and/or sulfonylureas
55
Q

What are other uses of Metformin?

A

weight loss, polycystic ovarian disease, nonalcoholic fatty liver disease, & premature puberty

56
Q

What is a possible side effect of Metformin?

A

Lactic acidosis

57
Q

What is the recommendation of Metformin and surgery?

A

DC metformin 48 hours or longer before elective surgery

58
Q

What needs to be done if metformin can’t be d/c before surgery?

A

must closely monitor patient for development of lactic acidosis

  • ABG/pH
  • serum lactate
  • renal fnx
59
Q

When should Metformin not be used?

A
  • lactic acidosis
  • acute kidney injury
  • GI intolerance
  • acute hepatic disease
60
Q

What is tx of metformin-induced lactic acidosis?

A
  • bicarbonate
  • hemodialysis
  • largely supportive
61
Q

What is the MOA of metformin-induced lactic acidosis?

A
  • b/c underlying pathologic change is blockade of mitrochondrial respiratory chain
  • Metformin inhibits mitochondrial enzyme to suppress glucose production in liver
62
Q

What is the use of Sulfonylureas?

A

Successful use in type 2 DM management requires some β cell function

63
Q

What is Sulfonylureas ineffective in?

A

tx type 1 DM

64
Q

Who should Sulfonylureas not be administered?

A

Should not be administered in patients w/sulfa drug allergy

65
Q

What is the MOA of Sulfonylureas?

A
  • exert their action on pancreatic sulfonylurea receptors by inhibiting ATP-sensitive K ion channels which cause influx of Ca
  • release of insulin storage granules
66
Q

What drugs are Sulfonylureas?

A

glyburide, glipizide, glimepiride

67
Q

What is the most severe complication of Sulfonylureas?

A

Hypoglycemia

68
Q

What are risk factors for sulfonylurea-induced hypoglycemia?

A
  • Impaired nutrition
  • age > 60
  • impaired renal function
  • concomitant drug therapy that potentiates sulfonylureas (phenylbutazone, sulfonamide antibiotics, warfarin)
  • interaction w/alcohol or salicylates
69
Q

What is the greatest risk of for sulfonylurea-induced hypoglycemia?

A

drugs w/long elimination half-life (glyburide, chlorpropamide)

70
Q

What is true about the hypoglycemia associated with Sulfonylureas?

A

Hypoglycemia often more prolonged & more dangerous than hypoglycemia from insulin

71
Q

Where are Sulfonylureas metabolites excreted?

A

renally excreted

72
Q

What are the short acting Sulfonylureas? When are these prefered?

A
  • Shorter-acting sulfonylureas (glipizide, glimepiride) have short half-lives & inactive metabolites
  • are preferable to use in patients w/renal insufficiency to those w/longer duration of action (glyburide)
73
Q

What Sulfonylureas has longer duration of action?

A

glyburide or Chlorpropamide

74
Q

When are Sulfonylureas not recommended?

A

patients w/ hepatic dysfunction (prolongs elim half-life & enhances hypoglycemic effect)

75
Q

What is associated with Chlorpropamide?

A

Sulfonylureas

  • disulfiram-like reaction & inapprop secretion of arginine vasopressin hormone resulting in hyponatremia
76
Q

What drugs are Thiazolidinediones
(TZDs)?

A

rosiglitazone, pioglitazone

77
Q

Where do Thiazolidinediones (TZDs) act?

A

rosiglitazone, pioglitazone

Act at skeletal muscle, liver, & adipose tissue to decrease insulin resistance & hepatic glucose production, increase glucose use by the liver

78
Q

What do Thiazolidinediones (TZDs) result in?

A

decrease in HgbA1c

79
Q

When are Thiazolidinediones (TZDs) contraindicated?

A

These drugs contraindicated in patients w/liver failure

80
Q

What should be monitored with Thiazolidinediones (TZDs)?

A

Must monitor plasma hepatic transaminases d/t possibility of drug-induced liver dysfunction

81
Q

What are Glucagon-Like Peptide-1 Receptor Agonists (GLP-1) drugs?

A

liraglutide, semaglutide

82
Q

What are the characteristics of GLP-1 agonists?

A

are injectable agents that bind to receptors in pancreas, GI tract, & brain

83
Q

What does binding of GLP-1 agonists result in?

A

increased insulin secretion from β cells, decreasing glucagon production from α cells in pancreas

84
Q

What is the result of GLP-1 agonists?

A

These drugs result in slowing of gastric emptying, reducing appetite, weight loss

85
Q

What is the relationship between hypoglyecmia and GLP-1 agonists?

A

Do not cause hypoglycemia unless combined w/other medications known to cause hypoglycemia (sulfonylureas & insulin)

86
Q

Where is Sodium-Glucose Cotransporter 2 Inhibitors (SGLT2) present?

A

SGLT2 is a transport protein present in proximal tubule

87
Q

What is SGLT2 responsible for?

A

responsible for approx. 90% glucose reabsorption in the kidneys

88
Q

What do SGLT2 inhibitors cause?

A

These drugs lower serum glucose levels by increasing glucose excretion in the kidneys via osmotic diuresis

89
Q

What are examples of Sodium-Glucose Cotransporter 2 Inhibitors (SGLT2)?

A

empagliflozin, canagliflozin, dapagliflozin, ertugliflozin

90
Q

What is the side effects of Sodium-Glucose Cotransporter 2 Inhibitors (SGLT2)?

A
  • volume loss d/t osmotic diuresis may cause hypotension or acute kidney injury (esp in patients taking diuretics, ACE-I or ARB drugs)
  • renal function assessment recommended
91
Q

What is the PO Dipeptidyl-Peptidase-4 (DPP-4) Inhibitors?

A

saxagliptin, sitagliptin, linagliptin, alogliptin, vildagliptin

92
Q

What is the effect of Dipeptidyl-Peptidase-4 (DPP-4) Inhibitors?

A

Lower blood glucose by increasing insulin secretion from β pancreatic cells & reduce α pancreatic cell secretion of glucagon

93
Q

What is the side effects of Dipeptidyl-Peptidase-4 (DPP-4) Inhibitors?

A

musculoskeletal pain, pancreatitis

94
Q

What is the recommendation for herbal medications?

A

General recommendation is two stop 2-3 weeks before surgery

95
Q

Review herbal medications.

A
96
Q

How many people use St. John’s Wart?

A

7.5 million Americans take regularly

97
Q

What is the use for St. John’s Wart?

A

Used for anxiety, depression, sleep disorders

98
Q

What effect can St. John’s Wart have on anesthesia?

A

May intensify or prolong the effects of opioids and thus the anesthetic

99
Q

How many individuals take Ginkgo Biloba?

A

11 million Americans take regularly

100
Q

What is the use for Ginkgo Biloba?

A

Used to improve memory, enhance blood circulation

101
Q

What is the effect of Ginkgo Biloba on anesthesic?

A
  • May reduce platelet function and clotting formation
  • Acts as an anticoagulant
102
Q

What are 4G’s are increased bleeding risk?

A

garlic, ginseng, gingko, ginger (and Vit E)

103
Q

What is the most popular herbal preparation?

A

Ginseng

104
Q

What is the use of Ginseng?

A

Used for vitality, fatigue, and cancer prevention

105
Q

What are the properities of Ginseng?

A
  • May cause episodes of tachycardia and hypertension
  • May have anticoagulant properties

2-Pharm Final (10 decks)

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