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N926 Pharmacology > insulins > Flashcards

insulins Flashcards

1
Q

Lispro (Humalog)

____-acting insulin

Closely parallels ____ insulin secretion and needs

Onset:within___minutes

Peak of action:__-___minutes

Duration: _-_hours

Must b eadministered ___-___ minutes before meal to limit postprandial hyperglycemia

A

Lispro (Humalog)

Short-acting insulin

Closely parallels physiologic insulin secretion and needs

Onset:within 15 minutes

Peak of action: 30-90 minutes

Duration:3-5hours

Must be administered 30-60 minutes before meal to limit postprandial hyperglycemia

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2
Q

Lispro has a lysine/proline switch that prevents hexamer formation and the ______ is rapidly absorbed

Administration just before eating provides similar profile to normal insulin secretion

**Benefit:decrease in ____ hyperglycemia and less risk of ____

___ may not decrease unless basal(NPH, detemir, glargine) doses are increased

A

Lispro has a lysine/proline switch that prevents hexamer formation and the monomer is rapidly absorbed

Administration just before eating provides similar profile to normal insulin secretion

**Benefit:decrease in postprandial hyperglycemia and less risk of hypoglycemia

HbA1c may not decrease unless basal(NPH, detemir, glargine) doses are increased

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3
Q

Insulin Aspart and Glulisine

Aspart (___), Glulisine (____)

___ ____-acting analogues

Profile of action and therapeutic benefits similar to ___

Onset: __-___ minutes

Peak: ___-___ minutes

Duration: __-__ hours

A

Insulin Aspart and Glulisine

Aspart (Novolog), Glulisine (Apidra)

Synthetic rapid-acting analogues

Profile of action and therapeutic benefits similar to lispro

Onset: 10-15 minutes

Peak: 45-75 minutes

Duration: 2-4 hours

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4
Q

Regular Insulin

___, ____, ____

_____ zinc insulin

___-acting preparation

ONLY preparation that can be given ___ and___

Can be mixed in ___ syringe as other insulin if ___ is similar

Preferred for treatment of ___ onset of ____ or ____

A

Regular Insulin

HumulinR, NovolinR, ReliOnR

Crystalline zinc insulin

Fast-acting preparation

ONLY preparation that can be given IV and SQ

Can be mixed in same syringe as other insulin if pH is similar

Preferred for treatment of abrupt onset of hyperglycemia or ketoacidosis

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5
Q

Regular Insulin

Perioperative: Single dose (___-_____ U) or infusion (___- ____ U/hr)

Onset: ____ minutes

Peak: __-____ hours after SQ injection because of inulin ____

Duration: ___-_____hours

Maximal effect when given ___-____ minutes before a meal

A

Regular Insulin

Perioperative: Single dose (1-5U) or infusion (0.5- 2.0 U/hr)

Onset: 30 minutes

Peak: 2-4 hours after SQ injection because of inulin hexamers

Duration: 6-8hours

Maximal effect when given 30-60 minutes before a meal

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6
Q

Neutral Protamine Hagedorn (NPH)

_____-acting

Absorption from SQ site is delayed due to ___ with ____

Preparation contains _____ protamine/U of insulin

Onset:___hour

Peak: ____ hours

Duration:_____ hours

A

Neutral Protamine Hagedorn (NPH)

Intermediate-acting

Absorption from SQ site is delayed due to conjugation with protamine

Preparation contains 0.005mg protamine/U of insulin

Onset:2 hour

Peak: 4-12 hours

Duration:18-28 hours

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7
Q

Detemir (Levemir)

_____-acting insulin: analogue for ____ replacement

Onset: ___hours

Peak: ___-____ hours

Duration: __-_____ hours

Can be administered as single ___ time injection to provide ___ insulin for ____ hours with less nocturnal _____

____ be mixed with ____-acting insulins

A

Detemir (Levemir)

Long-acting insulin: analogue for basal replacement

Onset: 2 hours

Peak: 3-9 hours

Duration: 6-24 hours

Can be administered as single bed time injection to provide basal insulin for 24 hours with less nocturnal hypoglycemia

Cannot be mixed with rapid-acting insulins

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8
Q

Glargine (Lantus)

_____-acting insulin analogue for ____ insulin replacement

____ onset of action and ____ peaks

Can bea dministered as a single ____ injection to provide ___ insulin for ___ hours with less nocturnal ____

Onset: ___ minutes

Peak: ___

Duration: _____ hours

A

Glargine (Lantus)

Long-acting insulin analogue for basal insulin replacement

Later onset of action and less pronounced peaks

Can bea dministered as a single bedtime injection to provide basal insulin for 24 hours with less nocturnal hypoglycemia

Onset: 90 minutes

Peak: None

Duration: 20-24+ hours

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9
Q

Degludec (Tresiba)

____-acting insulin analogue for ____ insulin replacement

____ be mixed with rapid-acting insulins

Onset: ___ hours

Peak: ___

Duration: ___hours

SQ ___ daily administration

Can use in __/___ impairment

A

Degludec (Tresiba)

Long-acting insulin analogue for basal insulin replacement

Can be mixed with rapid-acting insulins

Onset: 2 hours

Peak: None

Duration: >40 hours

SQ once daily administration

Can use in hepatic/renal impairment

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10
Q
  1. Hypoglycemia

Most ____ side effect

At risk: Receiving exogenous insulin without ____ intake, ___ period (especially ____)

First symptoms are ____ effects of increased ____ secretion: ___, ____, ____, rebound ____ caused by SNS ___ may ____ diagnosis (___ effect)

CNS symptoms of hypoglycemia: mental ___, ___, ____ (severe effects because brain depends on glucose as a selective substrate for ____ metabolism)

A

Five Main Side Effects

  1. Hypoglycemia

Most serious side effect

At risk: Receiving exogenous insulin without carbohydrate intake, perioperative period (especially preop)

First symptoms are compensatory effects of increased epinephrine secretion: diaphoresis, tachycardia, HTN, rebound hyperglycemia caused by SNS activation may mask diagnosis (Somogyi effect)

CNS symptoms of hypoglycemia: mental confusion, seizures, coma (severe effects because brain depends on glucose as a selective substrate for oxidative metabolism)

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11
Q

Prolonged hypoglycemia==>___ brain damage

Difficult to diagnose under __ ____(____ symptoms are masked by anesthetic drugs)

Severe hypoglycemia treatment: ____ mL of ___% ____ IV

Glucagon_____mg IV/SQ

• (Side effect: ____)

A

Prolonged hypoglycemia==>irreversible brain damage

Difficult to diagnose under general anesthesia(SNS symptoms are masked by anesthetic drugs)

Severe hypoglycemia treatment: 50-100 mL of 50% glucose IV

Glucagon 0.5 – 1.0 mg IV/SQ

• (Side effect: N/V)

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12
Q

Five Main Side Effects

  1. Allergic Reactions

– ___ allergic rxns __x more frequent than ____ rxns

  • Type I hypersensitivity rxn most frequent

– Chronic ____ exposure in NPH may stimulate production of ___ against ____->if large dose of ____ is administered IV to antagonize anticoagulant effects of heparin-> allergic reactions to ____

A

Five Main Side Effects

  1. Allergic Reactions

– Local allergic rxns 10X more frequent than systemic rxns

  • Type I hypersensitivity rxn most frequent

– Chronic protamine exposure in NPH may stimulate production of antibodies against protamine->if large dose of protamine is administered IV to antagonize anticoagulant effects of heparin-> allergic reactions to protamine

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13
Q

Five Main Side Effects

  1. Lipodystrophy - fat ___ at site of ___ injection
A

Five Main Side Effects

  1. Lipodystrophy - fat atrophies at site of SQ injection
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14
Q

Five Main Side Effects

  1. Insulin Resistance
    - If patient requires > _)___ U insulin daily = “insulin resistance”
    - Acute insulin resistance is associated with ___ from ___/____
  2. Drug Interactions
    - Hormones (administered as drugs) that ___ hypoglycemic effects of insulin: ___ hormone, ___ and ____
    - ____ inhibits insulin secretion and stimulates ____
    - ___, ___ and ____ increase duration of action of insulin (may have hypoglycemic effect)
    - Hypoglycemia may be potentiated by____
A

Five Main Side Effects

  1. Insulin Resistance
    - If patient requires > 100 U insulin daily = “insulin resistance”
    - Acute insulin resistance is associated with trauma from infection/surgery
  2. Drug Interactions
    - Hormones (administered as drugs) that counter hypoglycemic effects of insulin: andrenocorticotrophic hormone, estrogen and glucagon
    - Epinephrine inhibits insulin secretion and stimulates glycogenolysis
    - Tetracycline, salicylates and phenylbutazone increase duration of action of insulin (may have hypoglycemic effect)
    - Hypoglycemia may be potentiated by monoamine oxidase inhibitors
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15
Q

Oral Antidiabetic Drugs

Four major classes:

– Sec___gues (___ and ___) - increase ___ availability

• _____ are usually the treatment for ____

– Bi____ides (____) – suppress excessive ____ glucose release

– Thia___diones or glitazones (___, ___) - improve insulin ___

– Alpha-____ inhibitors (___, ____): delay ___ glucose ___ (used to maintain ___ control)

A

Oral Antidiabetic Drugs

Four major classes:

– Secretagogues (sulfonylureas and meglitinides) - increase insulin availability

• Sulfonylureas are usually the treatment for T2DM

– Biguanides (metformin) – suppress excessive hepatic glucose release

– Thiazolidinediones or glitazones (rosiglitazone, pioglitazone) - improve insulin sensitivity

– Alpha-glucosidase inhibitors (acarose, miglitol): delay GI glucose absorption (used to maintain glucose control)

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16
Q

Metformin

Oral ____

Often prescribed as ____ agent for T2DM

Decreases blood glucose concentrations in both ___ and ____ state

Rarely causes ___

Can be used in combination with ___ and ____

A

Metformin

Oral biguanide

Often prescribed as initial agent for T2DM

Decreases blood glucose concentrations in both fasting and postprandial state

Rarely causes hypoglycemia

Can be used in combination with insulin and sulfonylureas

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17
Q

Metformin

Contraindications: ____, ____, ____, acute ____ disease

Improves lipid profiles and fibrinolysis ,promotes mild to moderate weight loss

Other uses: ___ , ____ fatty liver, premature ____

Not bound to plasma proteins

Does not undergo _____

A

Metformin

Contraindications: lactic acidosis, AKI, GI intolerance, acute hepatic disease

Improves lipid profiles and fibrinolysis ,promotes mild to moderate weight loss

Other uses: PCOS (polycyptic ovary syndrome)__ , nonalcoholic fatty liver, premature puberty

Not bound to plasma proteins

Does not undergo metabolism

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18
Q

Metformin

Elimination via ____

90% oral dose is excreted in ___hours

Peak plasma concentration:___hours

Elimination half-time: __to ___ hours

Prescribed: __ID (____) with ___

Due to dependence on ___ clearance, caution in patients with renal dysfunction

A

Metformin

Elimination via kidneys

90% oral dose is excreted in12 hours

Peak plasma concentration:2 hours

Elimination half-time: 2 to 4 hours

Prescribed: TID (500-1000mg) with meals

Due to dependence on renal clearance, caution in patients with renal dysfunction

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19
Q

Metformin

MOA: blood glucose-lowering effect is ___ mediated through stimulation of endogenous ___ secretion

Activates ___ ___-activated ___ ___ase to suppress hepatic glucose production by decreasing ___ and ____ and to enhance postprandial insulin suppression of ___ glucose production

Also regulates glucose by decreasing GI absorption, increasing insulin sensitivity in peripheral tissues and enhancing synthesis of glucagon-like peptide-1 in ileum

A

Metformin

MOA: blood glucose-lowering effect is NOT mediated through stimulation of endogenous insulin secretion

Activates adenosine monophosphate-activated protein kinase to suppress hepatic glucose production by decreasing gluconeogenesis and glycogenolysis and to enhance postprandial insulin suppression of hepatic glucose production

Also regulates glucose by decreasing GI absorption, increasing insulin sensitivity in peripheral tissues and enhancing synthesis of glucagon-like peptide-1 in ileum

20
Q

Metformin

Side Effects: anorexia, nausea, diarrhea

Does not cause ___\_

Associated with vitamin B12 deficiency

Lactic Acidosis

– Possible side effect of metformin therapy

– Discontinue ____hours before elective surgery

– Monitor for lactic acidosis (ABG, serum lactate, renal function)

– Anaerobic metabolism results in pyruvate==>reduced to lactate

– Do not administer in patients with ___ dysfunction, ____ insufficiency (creatinine > ___ mg/dL), IV ___, acute___, ___, arterial ___, ___\_

– Treatment: hemodialysis, bicarbonate administration

A

Metformin

Side Effects: anorexia, nausea, diarrhea

Does not cause hypoglycemia

Associated with vitamin B12 deficiency

Lactic Acidosis

– Possible side effect of metformin therapy

– Discontinue 48 hours before elective surgery

– Monitor for lactic acidosis (ABG, serum lactate, renal function)

– Anaerobic metabolism results in pyruvate==>reduced to lactate

– Do not administer in patients with hepatic dysfunction, renal insufficiency (creatinine > 1.5 mg/dL), IV contrast dye, acute MI, CHF, arterial hypoxemia, sepsis

– Treatment: hemodialysis, bicarbonate administration

21
Q

Sulfonylureas

Can lower glucose levels to hypoglycemic levels

Improved blood glucose control, decreased hepatic production of very low-density lipoproteins, improved hypertriglyceridemia

Up to___% of patients do not have adequate _____response to maximal doses (primary failures) and another _____% of patients who initially respond will ______ to therapy each year (secondary failure)

Successful treatment requires some _____ function

Do not administer to patients with ____ allergy

A

Sulfonylureas

Can lower glucose levels to hypoglycemic levels

Improved blood glucose control, decreased hepatic production of very low-density lipoproteins, improved hypertriglyceridemia

Up to 20% of patients do not have adequate hypoglycemic response to maximal doses (primary failures) and another 10-15% of patients who initially respond will fail to respond to therapy each year (secondary failure)

Successful treatment requires some beta cell function

Do not administer to patients with sulfa allergy

22
Q

Sulfonylurea Oral Hypoglycemics

MOA: act on ___ receptors on ___ and ____ cells; inhibit ___ ___ sensitive ____channels on pancreatic ___ cells resulting in ____ influx and simulation of ____ release

Decrease insulin resistance

Minor effect in decreasing blood glucose concentrations

Biological effects may be longer than plasma half-lives because of formation of ______metabolites

Weak____, circulate bound to protein (______%) and are eliminated by renal tubular secretion and in feces

A

Sulfonylurea Oral Hypoglycemics

MOA: act on sulfonylurea receptors on pancreatic and cardia cells; inhibit adenosine triphosphate sensitive K+ channels on pancreatic beta cells resulting in Ca2+ influx and simulation of insulin release

Decrease insulin resistance

Minor effect in decreasing blood glucose concentrations

Biological effects may be longer than plasma half-lives because of formation of active metabolites

Weak acids, circulate bound to protein (90-98%) and are eliminated by renal tubular secretion and in feces

23
Q

Sulfonylurea Oral Hypoglycemics

____, while infrequent, is more often ___ and more ____ than hypoglycemia from insulin

Treat hypoglycemia with prolonged infusions of glucose- containing solutions

Renal disease decreases elimination of sulfonylureas and their active metabolites (greater risk for hypoglycemia)

Cross _____ (risk for ____ hypoglycemia)

Close _____ channels and inhibit ____ preconditioning (_____ mechanism)

May discontinue _____ hr preop for high-risk patients

A

Sulfonylurea Oral Hypoglycemics

Hypoglycemia, while infrequent, is more often prolonged and more dangerous than hypoglycemia from insulin

Treat hypoglycemia with prolonged infusions of glucose- containing solutions

Renal disease decreases elimination of sulfonylureas and their active metabolites (greater risk for hypoglycemia)

Cross placenta (risk for fetal hypoglycemia)

Close K-ATPase channels and inhibit ischemic preconditioning (cardioprotective mechanism)

May discontinue 24-48 hr preop for high-risk patients

24
Q

Glyburide

Stimulates insulin secretion over___hrperiod

Dose: _____ daily (__D/___ID)

Peak plasma levels: __ hours

DOA:___-___ hours

Elimination half-time: ___-___hours

MOA:increases insulin ____ and inhibits liver production of ____

A

Glyburide

Stimulates insulin secretion over 24-hrperiod

Dose: 2.5–20mg daily (QD/BID)

Peak plasma levels: 3 hours

DOA:18-24 hours

Elimination half-time: 4.6-12 hours

MOA: increases insulin sensitivity and inhibits liver production of glucose

25
Q

Glyburide

Metabolism: ____

Metabolite excretion: Urine/feces

One metabolite has ___% activity of parent compound

Mild ___ effect

Plasma clearance in ___ hours after discontinuation

A

Glyburide

Metabolism:Liver

Metabolite excretion: Urine/feces

One metabolite has 15% activity of parent compound

Mild diuretic effect

Plasma clearance in 36 hours after discontinuation

26
Q

Glipizide

Dose: ____mg daily

QD/BID dosing

DOA: ____ hours

Elimination half-time: ___ hours

Peak plasma levels: 1 hour after PO administration

Stimulates insulin secretion over 12-hour period

MOA: increases glucose uptake and suppresses liver glucose output – effects persist for prolonged periods without tolerance

Metabolism: Liver -> ___ substances (urine)

____ plasma clearance minimizes risk for ___

A

Glipizide

Dose: 5-40 mg daily

QD/BID dosing

DOA: 12-24 hours

Elimination half-time: 4-7 hours

Peak plasma levels: 1 hour after PO administration

Stimulates insulin secretion over 12-hour period

MOA: increases glucose uptake and suppresses liver glucose output – effects persist for prolonged periods without tolerance

Metabolism: Liver -> inactive substances (urine)

Rapid plasma clearance minimizes risk for hypoglycemia

27
Q

Glimepiride

Dose:____mg daily

QD/BID dosing

DOA:___hours

Elimination half-time: ____hour

MOA:Decreases blood glucose by ___ release of __ from ___ and may decrease ___ glucose production

Combined with insulin therapy when ____ are not effective

A

Glimepiride

Dose: 2-4mg daily

QD/BID dosing

DOA:24+ hours

Elimination half-time: 5-8 hour

MOA:Decreases blood glucose by stimulating release of insulin from pancreas and may decrease hepatic glucose production

Combined with insulin therapy when sulfonylureas are not effective

28
Q

Meglitinides

____ and ____

Exert effects on beta cells (similar to sulfonylurea)

Peak effect in 1 hour

DOA about 4 hours

Beta cell stimulation lowers HbA1c by 1%

Administer 15-30 minutes before meal

Never ingest while ___

____ DOA in the presence of glucose should lower risk of prolonged ___

Metabolism: Liver

A

Meglitinides

Repaglinide and Nateglinide

Exert effects on beta cells (similar to sulfonylurea)

Peak effect in 1 hour

DOA about 4 hours

Beta cell stimulation lowers HbA1c by 1%

Administer 15-30 minutes before meal

Never ingest while fasting

Short DOA in the presence of glucose should lower risk of prolonged hypoglycemia

Metabolism: Liver

29
Q

Repaglinide (Prandin)

class ____

MOA: stimulates release of ___ from beta islet cells of pancreas

Protein binding > 98%

Excretion by kidneys is ____ – no need to dose adjust for renal insufficiency

Metabolism: Liver oxidation and glucuronidation (CYP3A4)

Elimination half-life: 1 hour

Excretion: Fecal, urine

A

Repaglinide (Prandin)

Meglitinide

MOA: stimulates release of insulin from beta islet cells of pancreas

Protein binding > 98%

Excretion by kidneys is minimal – no need to dose adjust for renal insufficiency

Metabolism: Liver oxidation and glucuronidation (CYP3A4)

Elimination half-life: 1 hour

Excretion: Fecal, urine

30
Q

Nateglinide (Starlix)

class: _____

MOA: lowers blood glucose by stimulating release of insulin from pancreas

Metabolism: Liver

Metabolites excreted by kidney

Protein binding: 98%

Elimination half-life: 1.5 hours

Accumulation of ___ metabolites may cause ___

A

Nateglinide (Starlix)

Meglitinide

MOA: lowers blood glucose by stimulating release of insulin from pancreas

Metabolism: Liver

Metabolites excreted by kidney

Protein binding: 98%

Elimination half-life: 1.5 hours

Accumulation of active metabolites may cause hypoglycemia

31
Q

Alpha-Glucosidase Inhibitors

• ___ and ___

• Decrease ____ digestion and absorption of ___ by interfering with intestinal ___ activity

  • Slower release of glucose from food anda bsorption from GI tract
  • HbA1c decreases _____
A

Alpha-Glucosidase Inhibitors

• Acarbose and Miglitol

• Decrease carbohydrate digestion and absorption of disaccharides by interfering with intestinal glucosidase activity

  • Slower release of glucose from food anda bsorption from GI tract
  • HbA1c decreases 0.5-0.8%
32
Q

Alpha-Glucosidase Inhibitors

Useful as _____ when ____ hyperglycemia is the problem

Side effects:flatulence, abdominal __ and ___, increases in liver ___

– Due to undigested ___ that reach ___ in the lower colon

No __ with monotherapy

A

Alpha-Glucosidase Inhibitors

Useful as monotherapy when postprandial hyperglycemia is the problem

Side effects:flatulence, abdominal cramping and diarrhea, increases in liver transaminases

– Due to undigested carbohydrates that reach bacteria in the lower colon

No hypoglycemia with monotherapy

33
Q

Thiazolidinediones (TZDs)

____ and _____

Act at ___ muscle, ___ and ___ tissue via _____ proliferator activator receptor-gamma to decrease insulin ____ and hepatic glucose ___, and to increase use of ____ by liver

Insulin ____

Decrease insulin ___

Act in the _____ of insulin

A

Thiazolidinediones (TZDs)

Rosiglitazone and Pioglitazone

Act at skeletal muscle, liver and adipose tissue via peroxisome proliferator activator receptor-gamma to decrease insulin resistance and hepatic glucose production, and to increase use of glucose by liver

Insulin sensitizers

Decrease insulin resistance

Act in the presence of insulin

34
Q

Thiazolidinediones (TZDs)

Especially effective in ___ patients

Decrease HbA1c by _____%

Clinical effect takes ___-____ weeks

Can cause _____ (partly ECF - ____)

Contraindicated: ___, ____ failure

A

Thiazolidinediones (TZDs)

Especially effective in obese patients

Decrease HbA1c by 1-1.5%

Clinical effect takes 4-12 weeks

Can cause weight gain (partly ECF - ____)

Contraindicated: CHF, liver failure

35
Q

Glucagon-like Peptide-1 Receptor Agonists

GLP-1 receptor agonists

Long-acting and short-acting

[list of drugs]

Injectable agents that bind to receptors in pancreas, GI tract and brain to increase ___ secretion from ____ cells (glucose dependent), decrease ____ production from ____ cells and reduce gastric ___

Reduced ___ and ____ loss

Side effects:nausea/vomiting

Risk of hypoglycemia increases if combined w/ sulfonylurea

Exenatide – short and long-acting formulations, ____ weekly injections

Liraglutide – half life 8-14 hours; injected QD

A

Glucagon-like Peptide-1 Receptor Agonists

GLP-1 receptor agonists

Long-acting and short-acting

Exenatide, Lixisenatide, Liraglutide, Dulaglutide, Semaglutide

Injectable agents that bind to receptors in pancreas, GI tract and brain to increase insulin secretion from beta cells (glucose dependent), decrease glucagon production from alpha cells and reduce gastric emptying

Reduced appetite and weight loss

Side effects:nausea/vomiting

Risk of hypoglycemia increases if combined w/ sulfonylurea

Exenatide – short and long-acting formulations, once weekly injections

Liraglutide – half life 8-14 hours; injected QD

36
Q

Dipeptidyl-Peptidase-4 Inhibitors

DDP-4 Inhibitors enhance the ___ effect via inhibition of native GLP-1 degradation

___liptin, ____liptin, ___liptin, ___liptin, ___liptin

Increase insulin ___ from ___ cells(glucose dependent) and reduce pancreatic alpha cell secretion of ___

DOA:12-24 hours

Reduce dose for renal ____

A

Dipeptidyl-Peptidase-4 Inhibitors

DDP-4 Inhibitors enhance the incretin effect via inhibition of native GLP-1 degradation

Saxagliptin, Sitagliptin, Linagliptin,Alogliptin, Vildagliptin

Increase insulin secretion from beta cells(glucose dependent) and reduce pancreatic alpha cell secretion of glucagon

DOA:12-24 hours

Reduce dose for renal insufficiency

37
Q

Amylin Agonists

• ______which drug?

• _______ alter insulin levels

  • Suppress gastric emptying, inhibit glucagon release and reduce HbA1c levels
  • Side effects:nausea/vomiting
A

Amylin Agonists

• Pramlintide

• Do not alter insulin levels

  • Suppress gastric emptying, inhibit glucagon release and reduce HbA1c levels
  • Side effects:nausea/vomiting
38
Q

Other Medications

  • Colesevalam (____sequestrant) and bromocriptine mesylate (___ receptor agonist) lower glucose levels and decrease HbA1c (mechanism ____)
  • Not associated with hypoglycemia
  • May cause GI intolerance
A

Other Medications

  • Colesevalam (bile acid sequestrant) and bromocriptine mesylate (dopamine receptor agonist) lower glucose levels and decrease HbA1c (mechanism unclear)
  • Not associated with hypoglycemia
  • May cause GI intolerance
39
Q

Combination Therapy

Target two or more causes of hyperglycemia simultaneously

Metformin (decrease ____ in liver)+ sulfonylurea (increased insulin ___)

Exogenous insulin may also be apartof combination therapy

Primary aim:decrease ___

Secondary aim:decrease in ____dose

A

Combination Therapy

Target two or more causes of hyperglycemia simultaneously

Metformin (decrease insulin resistance in liver)+ sulfonylurea (increased insulin secretion)

Exogenous insulin may also be apartof combination therapy

Primary aim:decrease HbA1c

Secondary aim:decrease in daily insulin dose

40
Q

Anesthetic Implications

• DM+HTN=___% likelihood of diabetic ___ ___ (decreased ability to compensate/risk of CV ___/sudden cardiac death)

Incidence of periop CV instability is increased by concomitant use of ____ inhibitors or angiotensin receptor blockers

Autonomic dysfunction->delayed gastric emptying (gastroparesis)->premed with nonparticulate ___ and ____

A

Anesthetic Implications

• DM+HTN=50% likelihood of diabetic autonomic neuropathy (decreased ability to compensate/risk of CV instability/sudden cardiac death)

Incidence of periop CV instability is increased by concomitant use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers

Autonomic dysfunction->delayed gastric emptying (gastroparesis)->premed with nonparticulate antacid and metoclopramide

41
Q

Anesthetic Implications

Diabetic renal dysfunction – elevated serum creatinine – Most T1DM have kidney disease by ___years of age

Glycosylation of tissue proteins and limited mobility of joints

– ___ joint and ___ spine mobility should be assessed preoperatively in diabetic patients to assess for risk for ____

– Difficult intubation ~ ____% of T1DM

Intraoperative blood glucose management to avoid hypoglycemia

– Keep glucose < ____mg/dL

A

Anesthetic Implications

Diabetic renal dysfunction – elevated serum creatinine – Most T1DM have kidney disease by 30 years of age

Glycosylation of tissue proteins and limited mobility of joints

– Temporomandibular joint and cervical spine mobility should be assessed preoperatively in diabetic patients to assess for risk for difficult intubation

– Difficult intubation ~ 30% of T1DM

Intraoperative blood glucose management to avoid hypoglycemia

– Keep glucose < 180 mg/dL

42
Q

Anesthetic Implications

Hyperglycemia associated with:hyperosmolarity, ____, poor wound ___, increased mortality

Sever hyperglycemia->worse ___ outcomes following ischemia (CV surgery/acute MI)

Keep glucose

Control blood glucose levels important in ___ diabetic patients to improve ___ outcomes

A

Anesthetic Implications

Hyperglycemia associated with:hyperosmolarity, infection, poor wound healing, increased mortality

Sever hyperglycemia->worse neurological outcomes following ischemia (CV surgery/acute MI)

Keep glucose<180mg/dL during CPB

Control blood glucose levels important in pregnant diabetic patients to improve fetal outcomes

43
Q

Anesthesia Management

“Time-honored” approach– patient takes 2/3 nighttime insulin (NPH/regular) and 1⁄2 total morning insulin dose in form of intermediate- acting insulin (NPH)

AM dose of regulari nsulin should _____

• For pump: decrease overnight rate by ____% and keep at basal rate for ____

• If patient takes glargine and lispro/aspart daily,t ake2/3 glargine dose and entire lispro/aspart the night before; hold all ___ dosing

A

Anesthesia Management

“Time-honored” approach– patient takes 2/3 nighttime insulin (NPH/regular) and 1⁄2 total morning insulin dose in form of intermediate- acting insulin (NPH)

AM dose of regulari nsulin should be held

• For pump: decrease overnight rate by 30% and keep at basal rate for DOS

• If patient takes glargine and lispro/aspart daily,t ake2/3 glargine dose and entire lispro/aspart the night before; hold all AM dosing

44
Q

Anesthesia Management

Insulin is then administered after IV access and blood glucose level checked

Alternatively, administer regular insulin via infusion

Add regular insulin to NS in concentration of ____ and begin at ___(wt based dose) (Target: glucose < ___ mg/dL)

Regular insulin – Units per hour = plasma glucose/____

One unit of regular insulin usually lowers plasma glucose by ___-____ mg/dL

A

Anesthesia Management

Insulin is then administered after IV access and blood glucose level checked

Alternatively, administer regular insulin via infusion

Add regular insulin to NS in concentration of 1 unit/mL and begin at 0.02 -0.1 unit/kg/hr (Target: glucose < 180 mg/dL)

Regular insulin – Units per hour = plasma glucose/150

One unit of regular insulin usually lowers plasma glucose by 25-30 mg/dL

45
Q

Anesthesia Management

Oral medications – can continue drugs until ____

Sulfonylureas and metformin have long half-lives, discontinue ____hours before surgery

Can restart postop when patient resumes PO intake

Stress causes increased catecholamines, glucocorticoids and growth hormones->stress hyperglycemia and ___ insulin requirements

Monitor plasma glucose levels frequently (insulin infusions – monitor ___ minutes or ____)

Pumps: continue ____ infusion settings

A

Anesthesia Management

Oral medications – can continue drugs until day of surgery

Sulfonylureas and metformin have long half-lives, discontinue 24-48 hours before surgery

Can restart postop when patient resumes PO intake

Stress causes increased catecholamines, glucocorticoids and growth hormones->stress hyperglycemia and increased insulin requirements

Monitor plasma glucose levels frequently (insulin infusions – monitor q30 minutes or hourly)

Pumps: continue basal infusion settings

46
Q

Sodium-Glucose Cotransporter 2 Inhibitors

____2 – transport protein in proximal tubule responsible for 90% of _____ in kidneys

Gliflozins – orally administered agents

Empagli____ and Canagli____

MOA: rely on normal renal function to lower serum glucose levels by increasing glucose excretion in kidneys

Weight loss and reduced blood pressure

Side effects: hypotension, AKI, urinary tract infection, reduced bone mineral density

A

Sodium-Glucose Cotransporter 2 Inhibitors

SGLT2 – transport protein in proximal tubule responsible for 90% of glucose reabsorption in kidneys

Gliflozins – orally administered agents

Empagliflozin and Canagliflozin

MOA: rely on normal renal function to lower serum glucose levels by increasing glucose excretion in kidneys

Weight loss and reduced blood pressure

Side effects: hypotension, AKI, urinary tract infection, reduced bone mineral density

N926 Pharmacology (16 decks)

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