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Pharmacology > Insulin and Diabetes > Flashcards

Insulin and Diabetes Flashcards

1
Q

Describe the age, onset, primary cause and nature of insulin defect for DM1

A

Age: childhood or adolescence

Onset: abrupt

Cause: autoimmune destruction of pancreatic B cells

Insulin defect: insulin dependent, lack absolute insulin

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2
Q

Describe the age, onset, primary cause and nature of insulin defect for DM2

A

Age: 40+

Onset: Gradual

Cause: insulin resistance in tissue, B cell dysfunction w/ impaired insulin secretion, increased HGP

Insulin defect: non-insulin dependent, low normal or high insulin levels

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3
Q

Describe the symptoms, proneness to ketosis of DM1

A

Sx: thin, hyperglycemia, polydipsia, polyuria, nocturia

Proneness to ketosis: PRONE!

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4
Q

Describe the symptoms, proneness to ketosis of DM2

A

Sx: 90% obese, asymptomatic

Proneness to ketosis: uncommon

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5
Q

Describe the tx of DM1

A
  1. Eucaloric diet
  2. Preprandial rapid-acting insulin
  3. Basal insulin replacement
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6
Q

Describe the pathogenesis of hyperglycemia with DM2

A
  1. Beta cell dysfunction: impaired basal and stimulated insulin secretion
  2. Insulin resistance in tissue: increased rate of hepatic glucose production + inefficient peripheral tissue utilization
  3. increased hepatic glucose production
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7
Q

Describe the tx of DM2

A
  1. lifestyle interventions
  2. weight reduction
  3. hypocaloric diet
  4. oral agents +/- insulin
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8
Q

what are acute diabetic complications

A

10% of diabetes related deaths from ketoacidosis and hypoglycemia

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9
Q

What are long range complications of diabetes

A
  1. Microvascular (nephropathy, retinopathy, neuropathy)
  2. Macrovascular (altered LDL, MI, stroke, HTN)
  3. Hyperglycemia w/ suspectibilty to infections
  4. cavities and gum disease
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10
Q

What stimulates insulin secretion

A
  1. Elevated plasma glucose
  2. nutrient breakdown products
  3. vagal stimulation
  4. B2 agonists
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11
Q

Describe the PK of insulin including t1/2 and elimination

A

t1/2: 3-5min (can be increased by keeping it away from the liver)

Elimination: liver 60%, kidney 40%

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12
Q

Describe the target cell metabolic effects of insulin

A

Liver: promotes glucose storage (glycogen) –> inhibits gluconeogenesis and ketogenesis

Muscle: increase AA transport–> protein synthesis and glycogen synthesis

Fat cells: inhibit intracellular lipolysis, increased TG storage and FA synthesis

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13
Q

Describe the target cell metabolic effects w/o insulin

A
  1. Decrease glucose transport into muscle–> hyperglycemia
  2. Decrease conversion of glucose to glycogen–> hyperglycemia
  3. Increase protein to glucose via gluconeogensis in liver–> hyperglycemia, muscle wasting
  4. Increase mobilization of peripheral fat–> increase FFA and ketone bodies–> DKA
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14
Q

Insulin’s actions include:
A.  Increased conversion of amino acids into glucose
B.  Increased gluconeogenesis
C.  Increased glucose transport into cells
D.  Inhibition of lipoprotein lipase
E.  Increased lipogenesis
F.   Stimulation of glycogenolysis

A

C.  Increased glucose transport into cells

E.  Increased lipogenesis

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15
Q

A 24-year-old woman with type 1 diabetes wishes to try tight control of her diabetes to improve her long-term prognosis. Which of the following insulin regimens would be most appropriate?
A.  Morning injections of insulin lispro mixed with insulin aspart
B.  Evening injections of regular insulin mixed with insulin glargine
C.  Morning and evening injections of regular insulin supplemented by small amounts of NPH insulin at mealtimes
D.  Morning injections of insulin glargine, supplemented by small amounts of insulin lispro at mealtimes
E.  Morning injections of NPH insulin and evening injections of regular insulin

A

D.  Morning injections of insulin glargine, supplemented by small amounts of insulin lispro at mealtimes

(basal + release around meals)

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16
Q

What are rapid acting insulins and their DOA and onset

A
  1. Gluisine
  2. Aspart
  3. Lispro
  4. (inhaled Afrezza ~3 hrs)

DOA:~4 hrs, onset 5-15min

*short and rapid acting are prandial insulins

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17
Q

What are short acting insulins and their DOA and onset

A
  1. regular insulin

DOA 5-7 hrs
onset: 30-60min

*short and rapid acting are prandial insulins

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18
Q

What are intermediate acting insulins and their DOA, onset, and peak

A
  1. NPH insulin

DOA: 10-20hrs
Onset: 2-4 hrs
Peak: 8-10hrs
**Given BID

*intermediate and long acting are basal insulins

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19
Q

What are long acting insulins are their administration

A
  1. Glargine (Lantus)- SC QD *peakless
  2. Detemir (Levemir)- SC BID
  3. Degludec (Tresiba) SC QD

*intermediate and long acting are basal insulins

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20
Q

What insulin is relatively peakless?

A

Glargine (Lantus)

*Peakless =LESS risk of hypoglycemia

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21
Q

What insulin can you administer IV or infusion pump for managing DKA

A

Regular insulin

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22
Q

Compare the absorption of Insulin lispro vs regular insulin

A

Rapid dissociation of lispro hexamer to monomer following SC injection results in more rapid absorption.

*NOTE: NO difference in onset of action if given by the IV route.

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23
Q

Which of the following statements is correct regarding insulin glargine?
A.  It is primarily used to control postprandial hyperglycemia
B.  It is considered a “peakless” insulin
C.  The prolonged duration of action is due to slow dissociation from albumin
D.  It is commonly used in a regimen with insulin lispro or insulin aspart
E.  It may be administered intravenously in emergency cases

A

B.  It is considered a “peakless” insulin

D.  It is commonly used in a regimen with insulin lispro or insulin aspart

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24
Q 
WD is a 40-year-old patient with type 2 diabetes who has a blood glucose of 400 mg/dL today at his office visit. The PA would like to give some insulin to bring the glucose down before he leaves the office. Which of the following would lower the glucose in the quickest manner in WD? 
A.  Insulin aspart 
B.  Insulin glargine 
C.  NPH insulin 
D.  Regular insulin 
E.  Insulin lispro 
F.   Insulin detemir
A

A.  Insulin aspart

E.  Insulin lispro

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25
Q

NPH insulin has a delayed onset by combing insulin with ___

A

promatine

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26
Q

Describe the dosing of insulin in type1 compared to type2

A

type1: lower dose typically, multiple dose therapy/basal-bolus

type 2: higher dose, less urgency for starting aggressive therapy due to less like DKA

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27
Q

What factors can alter blood glucose control?

A
  1. Diet (alcohol, overeating, irregular meals)
  2. Physical activity (improve insulin sensitivity)
  3. Stress (increase GC levels)
  4. Puberty
  5. Menstrual cycle (glucose higher premenstrually)
  6. Drugs
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28
Q

Drugs that can increase blood glucose

A
  1. GCs

2. Sympathomimeticss

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29
Q

Drugs that can decrease blood glucose

A
  1. BB

2. Ethanol

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30
Q

Complications of insulin therapy

A
  1. Hypoglycemia (MC)
  2. Impaired CNS fxn
  3. Autonomic system hyperactivity
  4. weight gain
  5. DKA
  6. Hyperglycemia
  7. Immunologic rxns
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31
Q

Hypoglycemia is more common in who

A
  • older diabetes or diabetics taking long-acting insulins (goes down slowly and don’t see the SNS effects/no warning signs)
  • rapid onset of sx w/ short acting insulins
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32
Q

Signs of hypoglycemia

A
  1. impaired CNS fxn
  2. night sweats
  3. HA
  4. visual disturbance
  5. bizarre behavior
  6. Increased SNS and PNS (hunger)
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33
Q 
An unconscious patient wearing a diabetes alert bracelet is admitted to the ED. Blood sugar as measured by a glucometer was found to be very low, and the patient has skin turgor suggestive of dehydration. Before receiving stat lab results which of the following is most likely to be immediately administered? 
A.  Bicarbonate solution 
B.  Dextrose solution 5% 
C.  Hypotonic saline 
D.  Normal (isotonic saline) 
E.  Potassium chloride solution
A

B.  Dextrose solution 5%

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34
Q

Why are diabetes who are hypoglycemic also usually dehydrated?

A

low glucose causes dehydration because ketone bodies are excreted and not absorbed, acts as an osmotic diuretic and fluid is excreted to that way

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35
Q

How do you tx hypoglycemia

A
  1. Glucose (oral)
  2. +/- glucagon
  3. Dextros 50% IV if severe
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36
Q

How can you distinguish hypoglycemia from DKA

A
  1. DKA is generally gradual onset (hrs-days)
  2. acetone/sweet breath from ketone bodies
  3. dry
  4. flushed skin
  5. thirst
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37
Q 
An unconscious patient wearing a diabetes alert bracelet is admitted to the ED. Blood sugar as measured by a glucometer was found to be very high, and the patient has skin turgor suggestive of dehydration. Before receiving stat lab results and in addition to IV administration of rapid-acting insulin which of the following is most likely to be immediately administered? 
A.  Bicarbonate solution 
B.  Dextrose solution 5% 
C.  Hypotonic saline 
D.  Normal (isotonic saline) 
E.  Potassium chloride solution
A

D.  Normal (isotonic saline)

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38
Q

tx of DKA

A
  1. Normal saline IV
  2. regular insulin (iv boluse then low dose infusion)
  3. +/- K and PO4 replacement
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39
Q

Diabetic ketoacidosis rare in Type 2 diabetics BUT dehydration in untreated, poorly controlled individuals can lead to potential life-threatening ___ coma

A

non-ketotic hyperosmolar

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40
Q

What Immunologic reactions can be seen with insulin therapy

A
  1. Insulin allergy (rare w/ human insulin)
  2. Insulin resistance
  3. Lipodystrophy (SC atrophy at injection site or hypertrophy)
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41
Q

What are targets for DM2

A
  1. pancreas
  2. Liver
  3. GI tract
  4. muscle
  5. fat
  6. kidney
42
Q

Which of the following statements is characteristic of metformin?
A.  Metformin is inappropriate for initial management of type 2 diabetes
B.  Metformin decreases hepatic glucose production
C.  Metformin undergoes significant metabolism by the CYP450 system
D.  Metformin should not be combined with sulfonylureas or insulin
E.  Most common adverse effects are gastrointestinal in nature

A

B.  Metformin decreases hepatic glucose production

E.  Most common adverse effects are gastrointestinal in nature

43
Q

Actions of Metformin

A
  1. decrease HPG in liver/gluconeogensis
  2. increase glucose uptake into muscle
  3. slow glucose absorption
  4. Decrease VLDL synthesis
  5. Decrease platelet aggregation
  6. increase fibrinolysis
44
Q

Benefits of Metformin

A
  1. decrease A1c by 1-1.5%
  2. No hypoglycemia
  3. no wt. gain
45
Q

Describe the PK of metformin including absorption and elimination

A
  1. orally absorbed

2. excreted unchanged by kidneys

46
Q

Adverse reactions of Metformin

A
  1. GI effects (N/V, bloating, diarrhea)
  2. Lactic acidosis
  3. CI renal impairment EGFR = 30ml/min and CHF
47
Q 
A 54-year-old obese patient with type 2 diabetes has a history of alcoholism. In this patient, metformin should be avoided or used with extreme caution because the combination of ethanol and metformin increases the risk of which of the following? 
A.  An antabuse-like reaction 
B.  Excessive weight gain 
C.  Hypoglycemia 
D.  Lactic acidosis 
E.  Serious hepatotoxicity
A

D.  Lactic acidosis

48
Q 
Which of the following agents promotes the release of endogenous insulin? 
A.  Acarbose 
B.  Canagliflozin 
C.  Glipizide 
D.  Metformin 
E.  Pioglitazone
A

C.  Glipizide (Sulfonylurea- acts on pancreas)

49
Q

Examples of sulfonylureas

A
  1. Glipizide

2. Glyburide

50
Q

MOA of Sulfonylureas (glipidzide)

A
  1. increased insulin release in response to glucose via depolarization of blocking K channels (before B cells lose fxn)
    * blocks ATP-sensitive Kchannel–> depolarization–> Ca entry–> increase insulin release
51
Q

How do thiazide diuretics affect glucose levels

A

Open K channels–> hyperpolarize cell–> decrease insulin release–> hyperglycemia

**Opposite action of Sulfonylureas

52
Q

Adverse effects of Sulfonylureas

A
  1. Hypoglycemia– esp. w/ glyburide (do NOT use in elderly)
  2. Weight gain (due to increase in insulin)
  3. GI
  4. require hepatic-renal dysfunction dose reductions
53
Q

Describe the PK of Sulfonylureas including adminstration and elimination

A

administration: PO QD
elimination: metabolized by liver then renally excreted

54
Q

What is the MOA of thiazolidinediones

A
  1. increase target sensitivity to insulin (liver, fat cells, and muscle) via increase gene transcription (PPAR-gamma)
    * slow onset of effect (6-14 weeks to maximum effect)
55
Q

The PPAR-γ receptor that is activated by thiazolidinediones (pioglitazone) increases tissue sensitivity to insulin by which of the following mechanisms?
A.  Activating adenylyl cyclase and increasing the intracellular concentration of cAMP
B.  Inactivating a cellular inhibitor of the GLUT2 glucose transporter
C.  Inhibiting acid glucosidase, a key enzyme in glycogen breakdown pathways
D.  Regulating transcription of genes involved in glucose utilization
E.  Stimulating the activity of a tyrosine kinase that phosphorylates the insulin receptor

A

D.  Regulating transcription of genes involved in glucose utilization

56
Q

Describe the PK of thiazolidinediones including absorption, administration, and elimination

A

Absorption/administration: oral QD or BID

Elimination: hepatic CYP450 metabolism

57
Q

Adverse effects of Thiazolideiones

A
  1. Fluid retention edema
  2. exacerbation of HF

*anithyperglycemia so LOW risk of hypoglycemia

58
Q

Thiazolideiones should be avoided in who

A
  1. active liver dz
  2. mod-sever CHF
  3. CV risk
59
Q

Examples of thiazolideiones

A

Pigolitazone

60
Q

Incretin mimetics preferred over DDP-4 inhibitors because

A

better reductions in postpradial glucose and weight

61
Q

MOA of GLP-1 Agonists

A

GLP-1 receptor agonist

  • increase insulin in response to high BG and inhibition of glucagon release after meals
  • slow gastric emptying- reduce food intake
62
Q

Examples of incretin enhancers

A

MIMETICS: GLP-1 agonist: Exenatide

DDP-4 Inhibitors: Sitagliptin (Junuvia)

63
Q

Adverse reactions of incretins mimetics

A
  1. Hypoglycemia when used with SUs
  2. HA
  3. N/V/D–GI
  4. Pancreatitis
  5. DDI: delay absorption of oral meds
64
Q

Describe the PK of incretin mimetics including administration and elimination

A

administration: SC BID w/ meal

Elimination: renal–> avoid in pts w/ severe renal dz

65
Q

MOA of DDP-4 inhibitors

A

enhance the actions of endogenous incretins by blocking their degradation

66
Q

Describe the PK of DPP-4 inhibitors including administration and elimination

A

Administration: PO QD w/ or w/o food

Elimination: renal – need dose adjustments with renal dz

67
Q

Adverse effects of DPP-4 inhibitors

A
  1. Nasopharyngitis
  2. URI
  3. Ha

**NOT associated w/ wt. gain

68
Q

MOA of SGLT-2 inhibitors

A

-inhibits PCT transporter reabsorption of glucose and therefore more is renally excreted

69
Q

Benefits of SGLT-2 inhibitors

A
  1. wt. loss

2. slight BP reduction

70
Q

Adverse effects of SGLT-2 inhibitors

A
  1. Dehydration/hypovolemia
  2. Mycotic UTIs
  3. hypotension
  4. expensive
  5. renal dysfunction in elderly if taking loop diuretic
71
Q

Describe the PK of SGLT-2 inhibitors including administration and eliminatoin

A
  1. PO QD
  2. fecal-renal elimination via glucuronidation

Canaglifozin (40% fecal, 30% renal)

72
Q

Examples of SGLT-2 Inhibitors

A

“-gliflozin” class

  • Canaglifozin
  • Dapagloifozin
73
Q

Do not use Canaglifozin if GFR is

A

less than 45

74
Q

Examples of alpha-glucosidase inhibitors

A

Acarbose (Precose)

75
Q

MOA of alpha-glucosidase inhibitors

A

inhibition of alpha-glucosidase break down of complex starches which reduces postprandial glucose levels–> digestion of starches delayed from supper SI to distal SI

*decrease intestinal glucose absorption

76
Q

Describe the PK of alpha-glucosidase inhibitors including administration and elimination

A

adminstration: orally, (low F)

metabolized by gut

77
Q

Adverse effects of alpha-glucosidase inhibitors

A
  1. GI effects (gas, cramps, diarrhea)
  2. abdominal distention
  3. Hepatotoxicity– caution w/ liver dz
  4. don’t work that well (but less SE)

*GI effects due to unabsorbed carbohydrates undergoing fermentation

78
Q 
A 55-year-old menopausal woman was recently diagnosed with type 2 diabetes based on her fasting blood glucose levels. Her HbA1c levels average >7% so that diet exercise, and a single drug (monotherapy) may be sufficient to regulate her fasting glucose levels. Which of the following should be prescribed? 
A.  Acarbose 
B.  Dapagliflozin 
C.  Insulin lispro 
D.  Metformin 
E.  Glyburide 
F.   Glipizide
A

D.  Metformin

79
Q 
Which of the following drugs is most likely to cause hypoglycemia when used as monotherapy in the treatment of type 2 diabetes? 
A.  Acarbose 
B.  Canagliflozin 
C.  Glyburide 
D.  Insulin lispro 
E.  Metformin 
F.   Rosiglitazon
A

D.  Insulin lispro

80
Q

Which of the following antidiabetic agents is INCORRECTLY paired with its primary mechanism of action?
A.  Sitagliptin –> prolongs activity of glucagon-like peptide-1
B.  Glipizide–> stimulates insulin release
C.  Exenatide–> increases glucose-dependent insulin release
D.  Pioglitazone –> decreases hepatic glucose production
E.  Canagliflozin –> increases urinary excretion of glucose

A

D.  Pioglitazone –> decreases hepatic glucose production

81
Q 
The target of drug therapy for type 2 diabetes is generally an A1C of less than: 
A.  6.8% 
B.  7.0% 
C.  7.2% 
D.  7.4%
A

B.  7.0%

82
Q 
Metformin: 
A.  Reduces A1C by 1-1.5% 
B.  May decrease both microvascular and macrovascular complications of diabetes 
C.  Does not cause weight gain 
D.  All of the above
A

D.  All of the above

83
Q 
GLP-1 receptor agonists (-tides): 
A.  Reduce A1C by 0.5% 
B.  Cause more gain than insulin 
C.  Have been shown to increase the risk of myocardial infarction 
D.  Must be injected
A

D.  Must be injected

84
Q 
DPP-4 inhibitors (-gliptins): 
A.  Are taken orally
B.  Do not cause weight gain 
C.  Produce small reductions in A1C 
D.  All of the above
A

D.  All of the above

85
Q 
Which of the following can cause hypovolemia, dehydration and cause acute renal injury?
A.  Sulfonylureas 
B.  DPP-4 inhibitors 
C.  SGLT2 inhibitors 
D.  GLP1 receptor agonists
A

C.  SGLT2 inhibitors

86
Q

68-year-old woman with a BMI of 36, systolic hypertension, and type 2 diabetes has not achieved an A1C < 8% on maximum doses of metformin and exenatide. You are considering whether to start her on insulin or an SGLT2 inhibitor. Factors that you might consider could include which of the following?
A.  SGLT2 inhibitors cause weight loss
B.  SGLT2 inhibitors reduce systolic blood pressure
C.  Empagliflozin has been found to reduce the risk of cardiovascular events
D.  All of the above

A

D.  All of the above

87
Q 
Compared to NPH insulin, the main advantage of the recombinant insulin analogs glargine, detemir, and degludec is that they: 
A.  Do not cause weight gain 
B.  Cause less nocturnal hypoglycemia 
C.  Have a more rapid peak effect 
D.  All of the above
A

B.  Cause less nocturnal hypoglycemia

88
Q 
A 58-year-old man with type 2 diabetes had a myocardial infarction 12 years ago and is concerned about the effect of diabetes treatment on his heart disease. You could tell him that a number of the drugs used to treat diabetes have been associated with a lower risk of cardiovascular disease. These include:
A.  Metformin
B.  Liraglutide
C.  Empagliflozin
D.  All of the above
A

D.  All of the above

89
Q

The inhaled form of insulin (Afrezza®):
A.  Has an earlier maximal effect than injected insulin lispro
B.  Has a longer duration of action than injected insulin lispro
C.  Does not cause hypoglycemia
D.  All of the above

A

A.  Has an earlier maximal effect than injected insulin lispro

90
Q 
Describe what diabetes med target the following tissues:
Liver
Fat
Muscle
Pancreas
Intestines
Kidney
A
  1. Liver- Metformin (decrease HGP)
  2. Fat- Thiazolidinediones (increase glucose uptake)
  3. Muscle- Thiazolidinediones (increase glucose uptake)
  4. Pancreas- insulin and sulfonyureas
  5. Intestines- incretins mimetics/GLP-4 inhibitors and DPP-4 inhibitors
  6. Kidney- SGLT-2 inhibitors
91
Q

For Metformin describe the:

  1. Hypoglycemia risk:
  2. Wt effect:
  3. Main SE:
A
  1. Hypoglycemia risk: LOW
  2. Wt effect: neural
  3. Main SE: GI/ lactic acidosis
92
Q

For Sulfonyurleas describe the:

  1. Hypoglycemia risk:
  2. Wt effect:
  3. Main SE:
A
  1. Hypoglycemia risk: YES-mod
  2. Wt effect: GAIN
  3. Main SE: hypoglycemia, wt gain
93
Q

For Thiazolidinedione describe the:

  1. Hypoglycemia risk:
  2. Wt effect:
  3. Main SE:
A
  1. Hypoglycemia risk: ANTI- (Low)
  2. Wt effect: GAIN
  3. Main SE: edema, HF, fx
94
Q

For DDP-4 inhibitor describe the:

  1. Hypoglycemia risk:
  2. Wt effect:
  3. Main SE:
A
  1. Hypoglycemia risk: low
  2. Wt effect: NEUTRAL
  3. Main SE: rare
95
Q

For SGLT-2 inhibitor describe the:

  1. Hypoglycemia risk:
  2. Wt effect:
  3. Main SE:
A
  1. Hypoglycemia risk: low
  2. Wt effect: LOSS
  3. Main SE: UTI, dehydration
96
Q

For GLP-1 agonist describe the:

  1. Hypoglycemia risk:
  2. Wt effect:
  3. Main SE:
A
  1. Hypoglycemia risk: low
  2. Wt effect: LOSS
  3. Main SE: GI, pancreatitis
97
Q

For insulin describe the:

  1. Hypoglycemia risk:
  2. Wt effect:
  3. Main SE:
A

For Metformin describe the:

  1. Hypoglycemia risk: HIGH
  2. Wt effect: GAIN
  3. Main SE: hypoglycemia
98
Q

What diabetes med cause weight gain and weight loss

A

Gain:

  1. Sulfonylurea
  2. Thiazolidinedione
  3. Insulin

Loss:

  1. SGLT-2 inhibitor
  2. GLP-1 agonist
  3. Metformin (or neutral)

DPP-4 inhibitors (neutral)
Meglitinides (neutral)

99
Q

Examples of insulin secretagogues

A
  1. sulfonylureas (glipizide)

2. meglitinides (Repaglinide)

100
Q

Adverse effect of Meglitinides

A
  1. Bloating/gas
  2. abdominal cramps
  3. diarrhea

*wt neutral

101
Q

benefits of meglitinides over sulfonylureas for choice of insulin secretagogues

A
  1. more dosing flexibility

2. less hypoglycemia

Pharmacology (31 decks)

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