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PHRM 844 Therapeutics > Exam 2 - Random Multiple Choice > Flashcards

Exam 2 - Random Multiple Choice Flashcards

1
Q

Which is NOT a consequence of lack of insulin?
a. Hyperglycemia
b. Glucosuria
c. Hypolipidemia
d. Uninhibited glucagon

A

c. Hypolipidemia

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2
Q

The acute increase in insulin secretion observed with GLP-1 is:
a. Result of direct and persistent activation of Katp channel
b. Result of activation of the ERK1/2 pathway
c. Glucose dependent
d. Glucose independent

A

c. Glucose dependent

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3
Q

What is the only orally available GLP-1 agonist?
a. Tirzepatide
b. Semaglutide
c. Exenatide
d. Liraglutide

A

b. Semaglutide

(Rybelsus)

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4
Q

Glucose-stimulated insulin secretion from pancreatic beta cells would be inhibited by all of the following EXCEPT:
a. Activation of glucokinase
b. Inhibition of GLUT2
c. Blockade of voltage-dependent Ca2+ channels
d. Opening of K/ATP channels

A

a. Activation of glucokinase

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5
Q

The hormone released from the small intestine that potentiates insulin secretion in a glucose dependent manner is:
a. Glucagon-like peptide 1
b. Somatostatin
c. Glucagon
d. Amylin

A

a. Glucagon-like peptide 1

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6
Q

A common technique used to increase the duration of action of insulin derivatives as well as GLP-1 derivatives is to ___________________.
a. Insert amino acid substitutions that decrease dimerization.
b. Covalently attach them to human serum albumin.
c. Covalently attach a long-chain fatty acid or dicarboxylic acid.
d. Create chimeric peptides by inserting amino acids from other, related hormones.

A

c. Covalently attach a long-chain fatty acid or dicarboxylic acid.

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7
Q

Gestational Diabetes usually appears:
a. In the early, developmental phase of pregnancy
b. With no discernable temporal pattern
c. After 40 weeks, when the birth is overdue
d. In the later, rapid fetal growth phase of pregnancy

A

d. In the later, rapid fetal growth phase of pregnancy

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8
Q

Ketoacidosis is primarily the result of:
a. Excessive oxidation of fatty acids
b. Glucosuria
c. Excessive oxidation of carbohydrates
d. Hyperglycemia

A

a. Excessive oxidation of fatty acids

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9
Q

Prolonged hyperglycemia is toxic because:
a. B and C
b. High blood glucose levels can reduce activation of the Polyol pathway.
c. High blood glucose levels can decrease activation of the Hexosamine pathway.
d. Glucose can covalently derivatize proteins and alter their function.

A

d. Glucose can covalently derivatize proteins and alter their function.

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10
Q

The target tissue of insulin that’s responsible for the largest percentage of glucose uptake after a meal is:
a. Liver
b. White Fat
c. Skeletal Muscle
d. Pancreas

A

c. Skeletal Muscle

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11
Q

Insulin is __________ and typically causes weight _________ in type 2 diabetes patients who use it.
a. Catabolic; gain
b. Anabolic; gain
c. Anabolic; loss
d. Catabolic; loss

A

b. Anabolic; gain

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12
Q

The insulin listed below that has been engineered to minimize dimerization in solution and be rapidly absorbed from the site of injection is:
a. Aspart (Novolog)
b. Detemir (Levemir)
c. Degludec (Tresiba)
d. NPH

A

a. Aspart (Novolog)

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13
Q

The following are true of type 2 diabetes except:
a. Insulin resistance is a component of the disease
b. Diminished first phase insulin secretion is a component of the disease
c. It results from the autoimmune destruction of beta cells early in life
d. It is predominantly coupled with obesity

A

c. It results from the autoimmune destruction of beta cells early in life

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14
Q

MOA of glyburide
a. Activation of Katp channels
b. Prolonged block of Katp channels
c. Activation of GLP-1 channels
d. Insulin analogue

A

b. Prolonged block of Katp channels

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15
Q

Which insulins have the longest duration of action?
a. Glargine
b. Lispro
c. Aspart
d. Glulisine

A

a. Glargine

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16
Q

Which insulin preparation is NOT genetically modified?
a. NPH
b. Lispro
c. Aspart
d. Glulisine

A

a. NPH

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17
Q

the toxicity of hyperglycemia results from

a. the chemical reactivity of glucose
b. shunting of excess glucose into the polyol and hexosamine pathway
c. formation of AGEs and activation of receptors for AGEs
d. all of the above

A

d. all of the above

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18
Q

glucose-stimulated insulin secretion from pancreatic beta cells would be inhibited by all of the following EXCEPT

a. blockage of voltage gated Ca2+ channels
b. blockade of Katp channels
c. inhib of glucokinase
d. inhib of GLUT2

A

b. blockade of Katp channels

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19
Q

insulin resistance in type 2 pts normally results from

a. inc activation of mTOR in target tissues
b. inc activation of AMPK in target tissues
c. inc rate of insulin clearance
d. inactivation of insulin by antibodies

A

a. inc activation of mTOR in target tissues

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20
Q

the drug used to treat type 2 that works primarily in adipose tissue to dec FFA, stimulate adipocyte differentiation, and reduced transcription of resistin and TNF alpha is

a. metformin
b. pioglitazone
c. glyburide
d. pramlintide

A

b. pioglitazone

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21
Q

differences between GLP-1 receptor agonist and sulfonylureas include:

a. GLP-1RA’s amplify glucose-stimulated insulin secretion, while SU’s persistently stimulate insulin secretion regardless of blood glucose levels
b. SU’s uniquely slow gastric emptying while GLP-1RA’s have no effect on gastric emptying
c. SU’s stimulate glucagon secretion and prevent hypoglycemia, while GLP-1RA’s have no effect on glucagon secretion
d. SU’s tend to be weight neutral, while GLP-1RA’s tend to induce weight gain

A

a. GLP-1RA’s amplify glucose-stimulated insulin secretion, while SU’s persistently stimulate insulin secretion regardless of blood glucose levels

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22
Q

gestational diabetes is result of

a. inc metabolic demand of the fetus
b. placenta-induced insulin resistance that is not compensated by increased insulin secretion
c. an unhealthy diet during pregnancy
d. previously diagnosed type 2 diabetes in the mother

A

b. placenta-induced insulin resistance that is not compensated by increased insulin secretion

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23
Q

which is true regarding the action of insulin?

a. enhances ketone production
b. stimulates glucose uptake in the periphery
c. it activates PPAR-gamma
d. increases amylin production

A

b. stimulates glucose uptake in the periphery

(a. insulin inhibits ketone production; c. this is what thiazolidinediones do)

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24
Q

which drug therapy may mask the signs of hypoglycemia?

a. hydrochlorothiazide
b. pioglitazone
c. atenolol
d. valsartan

A

c. atenolol

(beta blocker)

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25
Q

which of the following regimens should be avoided in older pts with type 2 diabetes?

a. metformin
b. semaglutide
c. insulin glargine
d. glyburide

A

d. glyburide

(it has increased risk of hypoglycemia)

26
Q

which of the following is relevant for Xultophy?

a. ketoacidosis
b. bone fracture
c. genital mycotic infections
d. thyroid C-cell tumors

A

d. thyroid C-cell tumors

(Xultophy = degludec and liraglutide; liraglutide has risk of thyroid tumors)

27
Q

commercially available Symlin should be administered by which route?

a. IV
b. IM
c. SubQ
d. via insulin pump

A

c. SubQ

28
Q

lipodystrophy

a. loss of fat in SubQ tissue
b. accumulation of fat in SubQ tissue
c. changes in fat at over used injection site

A

c. changes in fat at over used injection site

29
Q

lipoatrophy

a. loss of fat in SubQ tissue
b. accumulation of fat in SubQ tissue
c. changes in fat at over used injection site

A

a. loss of fat in SubQ tissue

30
Q

lipohypertrophy

a. loss of fat in SubQ tissue
b. accumulation of fat in SubQ tissue
c. changes in fat at over used injection site

A

b. accumulation of fat in SubQ tissue

31
Q

which insulin is made by reversing the positions of proline 28 and lysine 29 on B-chain?

a. Glulisine
b. Glargine
c. Lispro
d. Aspart

A

c. Lispro

32
Q

which insulin is made by switching proline 28 to aspartate?

a. Glulisine
b. Aspart
c. Glargine
d. Detemir

A

b. Aspart

33
Q

which insulin is made by switching Asn 3 and Lys 29 to Lys and Glu?

a. Degludec
b. Detemir
c. Aspart
d. Glulisine
e. Lispro

A

d. Glulisine

34
Q

which insulin is made by switching Asn 21 of A-chain to Gly and adding 2 arginine residues to the end of the b-chain?

a. Lispro
b. Aspart
c. Glulisine
d. Glargine
e. Detemir
f. Degludec

A

d. Glargine

35
Q

which insulin is made by deleting Thr 30 of the b-chain and myristylating Lys 29?

a. Degludec
b. Lispro
c. Glulisine
d. Detemir

A

d. Detemir

36
Q

which insulin is made by replacing Thr 30 of the b-chain with a gamma-Glu/C16 fatty acid?

a. Detemir
b. Degludec
c. Glargine
d. Aspart
e. Lispro

A

b. Degludec

37
Q

Pioglitazone is associated with an increased risk of _____ cancer

a. lung
b. prostate
c. bladder
d. skin

A

c. bladder

38
Q

which is not elevated in type 2 diabetics?

a. resistin
b. adiponectin
c. TNF alpha

A

b. adiponectin

39
Q

which insulin has these modifications?

2-aminoisobutyrate inserted
Hydrophilic spacer and fatty acid added to lysine

a. exenatide
b. dulaglutide
c. liraglutide
d. semaglutide
e. lixisenatide

A

d. semaglutide

(Ozempic)

40
Q

which insulin is made by adding Glu and Arg, and adding a fatty acid to the Glu linker?

a. dulaglutide
b. liraglutide
c. semaglutide

A

b. liraglutide

41
Q

Which is false regarding SGLT2 inhibitors?

a. they increase risk of genital/UT infections
b. they increase risk of DKA
c. they decrease urine flow/volume depletion/hypotension
d. they increase risk of lower limb amputation

A

c. they decrease urine flow/volume depletion/hypotension

(increase urine flow)

42
Q

which hormone is one of the main contributors to insulin resistance?

a. CRH- cortisol
b. placental GH (GH-V)
c. progesterone
d. placental lactogens (PL)

A

d. placental lactogens (PL)

43
Q

gestational diabetes: what is the gold standard drug?

a. metformin
b. glyburide
c. insulin
d. thiazoladinediones

A

c. insulin

(doesn’t cross placenta)

44
Q

gestational diabetes: which drug works, but may harm the fetus?

a. insulin
b. glyburide
c. metformin
d. TzDs

A

b. glyburide

(crosses placenta)

45
Q

gestational diabetes: which drug works and crosses the placenta, but does not harm the fetus?

a. TzDs
b. metformin
c. glyburide
d. insulin

A

b. metformin

46
Q

mutations in which receptors are associated with gestational diabetes mellitus?

a. GH
b. RAGE
c. GLP-1 receptor
d. PRL (prolactin receptor)

A

d. PRL (prolactin receptor)

47
Q

What is the difference between Type 1 and Type 2 diabetes?

a) Type 1 is more common than Type 2 diabetes.
b) Type 1 often has previous family history and Type 2 is not associated with family history.
c) In Type 1 beta cells are non-functioning and require exogenous insulin
d) In Type 2 diabetes, obesity is not a contributing factor

A

c) In Type 1 beta cells are non-functioning and require exogenous insulin

(due to autoimmune rxn)

48
Q

Which of the following is NOT a consequence due to a lack of insulin?

a) Glucosuria
b) Hypoglycemia
c) Hyperlipidemia
d) Uninhibited glucagon

A

b. hypoglycemia

49
Q

Which of the following signals an increased risk for developing Type 1 Diabetes?

a) Family history of DM.
b) Antibodies to one or more Beta cell proteins.
c) Increasing age.
d) A high C-peptide level.

A

b) Antibodies to one or more Beta cell proteins.

50
Q

match the following insulin effects to the tissue type: liver, skeletal muscle, adipose tissue

a. stimulates glucose amino acid transport
b. stimulates triglyceride transport and glucose storage
c. stimulates glycogen and triglyceride synthesis

A

Liver - C
Skeletal Muscle - A
Adipose Tissue - B

51
Q

Put these steps in order for insulin receptor signaling in liver, muscle, and fat cells

a) Rapid translocation of Glut4 to the cell surface
b) IRS is phosphorylated
c) PI3K is recruited and phosphorylated
d) Insulin binds to its receptor
e) Recruitment and phosphorylation of PDK1 and PKB to the cell surface

A

d, b, c, e, a

52
Q

True or False: reversing the positions of proline and lysine at positions 28 and 29 on the insulin B chain prevents dimer and hexamer formation and decreases self-association risk.

A

true

53
Q

true or false: GLP-1RA’s can cause hypoglycemia

A

false (GLP1-RA stimulation of insulin secretion is glucose dependent, therefore the medication has very low risk of hypoglycemia)

54
Q

Which of the following is NOT a common side effect of dulaglutide?
a) Nausea/vomiting
b) Hypothyroidism
c) Risk of thyroid C-cell tumors
d) Contraindicated in patients with a family history of medullary thyroid cancer

A

b) Hypothyroidism

55
Q

Which of the following is not a drug that can lead to increased hyperglycemia?
a) Hydrochlorothiazide
b) Oral contraceptives
c) Corticosteroids
d) High dose salicylates

A

d) High dose salicylates

56
Q

Which of the following statements best describes the role of adipokines in the development of T2DM.
a) Adipokines promote insulin resistance, contributing to the development of T2DM.
b) Adipokines have no influence on T2DM development.
c) They can directly stimulate insulin production, reducing the risk of T2DM development.
d) Adipokines only have an effect on Type 1 diabetes, not Type 2.

A

a) Adipokines promote insulin resistance, contributing to the development of T2DM.

57
Q

Why can sulfonylureas cause obesity?

a) Sulfonylureas decrease the release of insulin, increasing the amount of liver glucose output
b) Sulfonylureas increase the release of insulin, which stimulates triglyceride storage
c) Sulfonylureas decrease the release of insulin, which increase glucose transport
d) Sulfonylureas increase the release of insulin, which stimulates triglyceride synthesis in the skeletal muscle

A

b) Sulfonylureas increase the release of insulin, which stimulates triglyceride storage

58
Q

How does obesity lead to insulin resistance?

a) Fatty acids deactivate the insulin receptor
b) Excessive nutrients lead to the insulin receptors being phosphorylated with a serine, which leads to degradation
c) Excessive nutrients cause inflammation, which activate the mTOR protein to prevent IRS1/2 degradation
d) p85/p110 are overactive in obesity, and reduce glucose transport

A

b) Excessive nutrients lead to the insulin receptors being phosphorylated with a serine, which leads to degradation

59
Q

Which of the following is not a sign and symptom of diabetes?
a. Polyuria
b. Fatigue
c. Weight gain
d. Ketoacidosis

A

c. Weight gain

(it is weight loss instead)

60
Q

Which of the following is NOT a diagnostic criteria of diabetes?
a. A1C ≥ 7.0%
b. Random glucose ≥ 200 mg/dL
c. FBG ≥ 126 mg/dL
d. 2 hr postprandial glucose ≥ 200 mg/dL

A

a. A1C ≥ 7.0%

(should be 6.5% or more)

PHRM 844 Therapeutics (28 decks)

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