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WorksheetsEndo Exam 2 - Gupta
Total questions: 150
Worksheet time: 1hrs 15mins
Name
Class
Date
1.
When glucose enters the liver & brain, what takes place
a)
no regulation by insulin
b)
secondary active transport (Na+/glucose sypmporters)
c)
facilitated diffusion regulated by insulin
d)
GLUT (glucose transporters)
2.
When glucose enters the GI tract & kidneys, what takes place
a)
no regulation by insulin
b)
secondary active transport (Na+/glucose sypmporters)
c)
facilitated diffusion regulated by insulin
d)
GLUT (glucose transporters)
3.
When glucose enters MOST cells, what takes place
a)
no regulation by insulin
b)
secondary active transport (Na+/glucose sypmporters)
c)
facilitated diffusion regulated by insulin
d)
GLUT (glucose transporters)
4.
What do cells utilize glucose for
a)
ATP production
b)
amino acid (non-essential synthesis)
c)
glycogenesis
d)
lipogenesis
e)
urinary excretion
5.
Where does glycogenesis occur
a)
liver
b)
mitochondria
c)
adipose tissue
d)
kidneys
e)
cells
6.
What occurs in lipogenesis
a)
formation of glycerol
b)
formation of fatty acids
c)
glycerol + fatty acids = triglycerides
d)
increased expression of lipoprotein lipases
e)
adipose tissue deposits
7.
When glucose levels are too high in the blood, how is it excreted
a)
sweat
b)
urine
c)
tears<br />
8.
Where is insulin produced
a)
pancreatic beta cells
b)
pancreatic alpha cells
c)
pancreatic delta cells
9.
What is the mid region of proinsulin that is removed
a)
insulin
b)
A-chain
c)
B-chain
d)
C peptide
10.
Which are coupled together to form insulin
a)
preproinsulin
b)
A-chain
c)
B-chain
d)
C peptide
11.
In the absence of glucose, in resting beta cells
a)
ATP is high
b)
ATP is low
c)
ADP is high
d)
ADP is low
12.
In the absence of glucose,
a)
keeps ATP-dependent K+ channel open
b)
keeps ATP-dependent K+ channel closed
c)
K+ diffuses out through K+/ATP channel
d)
K+ diffuses in through the K+/ATP channel
e)
intracellular potential is hyperpolarized (-)
13.
In the presence of glucose
a)
glucose enters via Glut 2 transporter
b)
glucose metabolism raises ATP concentration
c)
ATP inhibits the K+/ATP channel; decrease K+ conductance causing depolarization
d)
voltage-gated Ca2+ channel activated
e)
Ca2+ mediates insulin secretion
14.
What does insulin bind to
a)
IR/IGF-1 receptors
b)
IRS-1
c)
PIP3
d)
GLUT 2
15.
When insulin binds to IR/IGF-1, what is activated
a)
growth promotiing genes
b)
protein synthesis (muscles)
c)
glycogen synthesis (liver)
d)
fatty acid synthesis (adipose); lipase inactivation (triglycerides)
e)
cell survival (antiapoptosis); Glut4 translocation to membrane
16.
GLUT4 promotes glucose intake in
a)
muscles
b)
adipose
c)
brain
d)
liver
17.
Where is glucagon produced
a)
pancreatic beta cells
b)
pancreatic alpha cells
c)
pancreatic delta cells
18.
Glucagon is
a)
catabolic
b)
anabolic
19.
When is glucagon released
a)
when glucose levels are low
b)
when glucose levels are high
c)
stress
d)
exercise
e)
sleep
20.
What does glucagon do
a)
mobilizes glucose, fat, and protein synthesis
b)
gluconeogenesis
c)
glycogenolysis
d)
lipolysis
21.
What incretins are released after a meal
a)
GLP-1
b)
GIP
c)
DPP-4
d)
DPP-4 Inhibitors
22.
What are some characteristics about incretins
a)
produced in the GI tract
b)
increases insulin secretion
c)
suppresses glucagon secretion
d)
delays gastric emptying
e)
suppresses appetite
23.
Which type of diabetes mellitus is considered juvenile onsent or insulin-dependent (IDDM)
a)
Type 1
b)
Type 2
24.
Which type of diabetes mellitus is considered adult onset or non-insulin-dependent (NIDDM)
a)
Type 1
b)
Type 2
25.
What are some components of Type 1 DM
a)
destruction of beta cells (several months to years)
b)
autoimmune
c)
HLA-DR antigens
d)
~50% concordance rate in identical twins
e)
destruction of alpha cells
26.
In Type 1 DM, low insulin levels cause
a)
reduction in glucose intake by cells
b)
net catabolism
c)
increase glucose synthesis
d)
increase glycogen, protein, and fatty acid breakdowns
e)
increase of glucose intake by cells
27.
What is created when the liver oxidizes fatty acids
a)
ketone bodies (keto acids)
b)
glycogen
c)
protein
d)
insulin
28.
Having an excess amount of ketone bodies (keto acids) leads to
a)
hyperglycemia
b)
hypoglycemia
c)
diabetic ketoacidosis
29.
What are some characteristics about type 2 DM
a)
makes up >90% of diabetic cases
b)
onset usually after age 40
c)
onset usually during teenage years
d)
makes up <50% of cases
e)
about 20% of the US population over 65 years old has type 2 DM
30.
What are some characteristics about type 2 DM
a)
obesity is a major risk factor
b)
chronic disease
c)
strong inheritable genetic connection
d)
not genetic
e)
increased risk of CV disease
31.
What are some characteristics of Stage I Type 2 DM
a)
insulin resistance in tissues
b)
tissues require higher levels of insulin
c)
beta cells compensate by producing more
d)
major causes: obesity, sedentary lifestyle, aging
e)
hyperglycemia
32.
What are some characteristics of Stage II Type 2 DM
a)
some decline in pancreatic beta cells due to decreased rate of beta cell renewal
b)
apoptosis of beta cells
c)
beta cells cannot keep up with increased insulin demand
d)
beta cells are "exhausted"
e)
hyperglycemia
33.
What are some microvascular complications of diabetes
a)
glaucoma
b)
nephropathy
c)
neuropathy
d)
CAD
34.
What are some macrovascular complications of diabetes
a)
glaucoma
b)
nephropathy
c)
stroke/cerebrovascular disease
d)
CAD
e)
peripheral vascular disease
35.
What are characteristics of diabetic ketoacidosis
a)
decreased blood pH
b)
increased blood pH
c)
occurs in the absense of insulin
d)
release of free fatty acids by liver
e)
occurs in the presence of insulin
36.
What are diagnostic characteristics of diabetic ketoacidosis
a)
high glucose (>250mg/dL)
b)
elevated ketones
c)
arterial pH <7.2
d)
plasma bicarbonate <15 mEq/L
e)
hyperventilation (to decrease CO2)
37.
What are some pharmacological approaches for DM
a)
insulin replacement
b)
insulin secretagogues
c)
insulin sensitizers
d)
GLP-1 agonists
e)
inhibitors of instestinal glucose absorption or renal glucose absorption
38.
What non-insulin based drugs can be used to decrease insulin absorption in the gastrointestinal tract
a)
incretins
b)
alpha-glucosidase inhibitors
c)
amylin
d)
bile acid sequestrant
e)
sulfonyureas
39.
What non-insulin based drugs can be used to increase insulin secretion
a)
incretins
b)
meglitinides
c)
amylin
d)
bile acid sequestrant
e)
sulfonyureas
40.
What non-insulin based drugs can be used to decrease glucagon secretion
a)
incretins
b)
meglitinides
c)
amylin
d)
bile acid sequestrant
e)
sulfonyureas
41.
What non-insulin based drugs can help with appetite control
a)
incretins
b)
meglitinides
c)
amylin
d)
bile acid sequestrant
e)
sulfonyureas
42.
What non-insulin drugs reduce glucose reabsorption in the kidneys
a)
incretins
b)
SGLT2 inhibitors
c)
metformin
d)
thiazolidinediones<br />
e)
salicylates
43.
What non-insulin drugs increase glucose uptake and utilization in muscle cells
a)
incretins
b)
SGLT2 inhibitors
c)
metformin
d)
thiazolidinediones<br />
e)
salicylates
44.
What non-insulin drugs decrease lipotoxicity allowing more utilization of glucose in adipose tissues
a)
incretins
b)
SGLT2 inhibitors
c)
metformin
d)
thiazolidinediones<br />
e)
salicylates
45.
What non-insulin drugs decrease hepatic glucose output
a)
incretins
b)
SGLT2 inhibitors
c)
metformin
d)
thiazolidinediones<br />
e)
salicylates
46.
What are the classes of anti-diabetic drugs
a)
peptides
b)
non-peptides
c)
steroid
d)
thyroid<br />
47.
What are the anti-diabetic drugs that are parenterally active (peptides)
a)
insulin products
b)
amylin agonists (pramlintide)
c)
GLP-1 agonist (exenatide)
d)
dipeptidyl peptidase-4 inhibitor (DPP4Is or gliptins)
e)
sulfonyl ureas (SUs)
48.
What are the anti-diabetic drugs that are orally active (non-peptides)
a)
substituted benzoic acids (glinides); thiazolidinediones (glitazones)
b)
SGLT2 inhibitors (gliflozins); biguanides
c)
alpha-glucosidase inhibitors
d)
dipeptidyl peptidase-4 inhibitor (DPP4Is or gliptins)
e)
sulfonyl ureas (SUs)
49.
What amino acid can be modified on the A-chain without significant loss of activity
a)
AsnA21
b)
GlyB23
c)
PheB24
d)
PheB25
e)
TyrB26<br />
50.
What amino acid residues are important for insulin activity
a)
AsnA21
b)
GlyB23
c)
PheB24
d)
PheB25
e)
TyrB26<br />
51.
What amino acid residues can be modified on the B chain
a)
ProB28
b)
LysB29
c)
ThrB30
d)
AsnA21
e)
GlyB23
52.
What can be added to insulin products to create intermediate-acting insulin
a)
protamine
b)
zinc
c)
aspart
d)
lispro
e)
glulisine
53.
If insulin products are unchanged, what characteristics will it have
a)
it will have a greater propensity to convert to monomers
b)
faster onset and shorter duration
c)
slower onset and longer duration
d)
no significant change in immunogenicity
e)
significant change in immunogenicity
54.
Which insulin products are fast acting
a)
fiasp
b)
lispro-aabc
c)
aspart
d)
lispro
e)
glulisine
55.
What is modified on insulin to make Lispro
a)
B28 Pro to Lys
b)
B29 Lys to Pro
c)
B28 Pro to Asp
d)
B29 Lys to Glu
e)
B3 Asn to Lys
56.
What is added to lispro to make lispro-aabc
a)
treprostinil (vasodilator)
b)
citrate
c)
niacinamide (vit b)
d)
L-ariginine
57.
What is modified on insulin to make Aspart
a)
B28 Pro to Lys
b)
B29 Lys to Pro
c)
B28 Pro to Asp
d)
B29 Lys to Glu
e)
B3 Asn to Lys
58.
What is added to aspart to make fiasp
a)
treprostinil (vasodilator)
b)
citrate
c)
niacinamide (vit b)
d)
L-ariginine
59.
What is modified on insulin to make glulisine
a)
B28 Pro to Lys
b)
B29 Lys to Pro
c)
B28 Pro to Asp
d)
B29 Lys to Glu
e)
B3 Asn to Lys
60.
What modifications are made to create glargine
a)
A21 Asn to Gly
b)
Add ArgB31
c)
Add ArgB32
d)
Remove B30 Thr
e)
Add myristic acid to B29 Lys
61.
What does adding ArgB31 and ArgB32 do for glargine
a)
helps interact with polar environment
b)
more positively charged (neutral pKa)
c)
absorbed slowly
d)
absorbed quickly
e)
precipitates at physiological pH
62.
What modifications are made to create detemir
a)
A21 Asn to Gly
b)
Add ArgB31
c)
Add ArgB32
d)
Remove B30 Thr
e)
Add myristic acid (C14 FA) to B29 Lys
63.
What modifications are made to create degludec (Tresiba)
a)
remove B30 Thr
b)
add hexadecandioic acid (C16 FA) to B29 Lys
c)
forms hexamer with zinc in the preparation
d)
binds to albumin
e)
released slowly
64.
What are characteristics of inhaled insulin
a)
ultra rapid acting
b)
slow acting
c)
improves postprandial glycemic control
d)
recombinant human insulin
e)
improves basal glycemic control
65.
When making an insulin product, what considerations must be taken
a)
stability
b)
formulation
c)
pharmacokinetics
d)
amount
e)
cost
66.
At a pH of 2-3, what happens to insulin
a)
deamidation of AsnA21
b)
deamidation of AsnB3
67.
At a neutral pH, what happens to insulin
a)
deamidation of AsnA21
b)
deamidation of AsnB3
68.
What happens to insulin that is exposed to high temperatures in a hydrophobic environment
a)
forms fibrils
b)
forms hexamers
c)
increases solubility
d)
deamidation of AsnA21
e)
deamidation of AsnB3
69.
What are solutions to increase the stability of an insulin product
a)
avoid unfavorable conditions
b)
adding zinc ions due to zinc promoting the formation of hexamers
c)
forming fibrils
d)
deamidation of AsnA21
e)
deamidation of AsnB3
70.
What are adverse reactions that can occur from insulin products
a)
hypoglycemia
b)
allergic reactions
c)
lipodystrophy
d)
hyperglycemia
71.
What occurs during a hypoglycemia episode
a)
release of epinephrine, glucagon, and cortisol to try and compensate
b)
sweating, hunger, palpitations, tremor, anxiety
c)
may lead to convulsions & coma
d)
feeling full, sleepy
72.
Amylin agonists work only for Type 1 DM patients
a)
true
b)
false
73.
Amylin, insulin, and glucagon work together in interrelated fasion to maintain normal blood glucose
a)
true
b)
false
74.
The synthetic analogue of amylin (pramlintide) contains a Pro at<br />
a)
25
b)
28
c)
29
d)
30
75.
The group of gastric hormones stimulating insulin release are commonly called<br />
a)
insulin
b)
incretins
c)
glucagon
76.
What does the incretin GLP-1 do<br />
a)
increase insulin
b)
decrease insulin
c)
increase glucagon
d)
decrease glucagon
77.
What does the incretin GIP do<br />
a)
increase insulin
b)
decrease insulin
c)
increase glucagon
d)
decrease glucagon
78.
GLP-1 agonists are preferred over GIP agonists
a)
true
b)
false
79.
GLP-1 agonists (peptides) help lower elevated blood glucose levels by
a)
mimicing incretins (GLP-1)
b)
inhibiting DPP-4 enzyme
c)
inactivating metabolites
80.
DPP4 inhibitors or "gliptins" help lower elevated blood glucose levels by
a)
mimicing incretins (GLP-1)
b)
inhibiting DPP-4 enzyme
c)
inactivating metabolites
81.
What are the preferred GLP-1 analog drugs
a)
natide
b)
glutide
c)
gliptin
d)
glithazones
82.
What are some characteristics of Exenatide (Byetta)
a)
isolated from the saliva of the gila monster
b)
39 a.a. polypeptide (53% same AA as GLP-1)
c)
t1/2 = 2-4 hrs
d)
taken bid
e)
taken Q7d
83.
What are some characteristics of Liraglutide (Victoza)
a)
fatty acid molecule at one position of GLP-1
b)
t1/2 = 11-15 hrs
c)
taken once daily
d)
taken bid
e)
taken Q7d
84.
What are some characteristics of Dulaglutide (Trulicity)
a)
GLP-1 analog with amino acid substitution
b)
t1/2 = 4 days
c)
taken once daily
d)
taken bid
e)
taken Q7d
85.
What are some characteristics of Semaglutide (Ozempic)
a)
GLP-1 analog with stearic diacid substitution at Lys26 & introduction of amino alpha-aminobutyric at position 8 acid for DPP4-stability
b)
t1/2 = ~1 wk
c)
taken once daily
d)
taken bid
e)
taken Q7d
86.
What are some adverse effects of GLP-1 agonist drugs
a)
fullness
b)
nausea/vomiting
c)
GERD
d)
decreased appetite
e)
edema
87.
Which GLP-1 agonist has an oral form, Rybelsus
a)
Exenatide (Byetta)
b)
Liraglutide (Victoza)
c)
Dulaglutide (Trulicity)
d)
Semaglutide (Ozempic)
88.
Which of the following GLP-1 agonist is fused to a fatty molecule to increase its half life
a)
dulaglutide
b)
liraglutide
c)
detemir
d)
pramlintide
e)
semaglutide
89.
What do DPP4I drugs do to help lower blood glucose levels
a)
increase endogenous incretin levels
b)
decrease endogenous incretin levels
c)
decreases plasma glucose
d)
increases plasma glucose
90.
What are some adverse effects of DPP4I drugs
a)
nausea
b)
nasopharyngitis
c)
tonsilitis
d)
edema
91.
Which drugs are DPP-4 Inhibitors
a)
sitagliptin
b)
saxagliptin
c)
linagliptin
d)
alogliptin
e)
liraglutide
92.
What are some characteristics of DPP4I drgus
a)
rapid absorption with good bioavailability
b)
extensive distribution and DOA = 12-24 hrs
c)
not much metabolized (except saxa-)
d)
mainly eliminated by urine (except lina-)
e)
slower absorption with good bioavailability
93.
What are characteristics of saxagliptin's metabolism
a)
CYP3A4/5 to 5-hydroxy saxagliptin
b)
active
c)
~50% potency of the parent compound
d)
not extensive
94.
What is the duration of action for saxagliptin
a)
12 hours
b)
24 hours
c)
21 hours
95.
Saxagliptin is a slow reversible (pseudoirreversible) inhibitor
a)
true
b)
false
96.
What is the main mechanism of elimination of linagliptide
a)
urine
b)
feces
c)
sweat
d)
it is not eliminated
97.
What is the T1/2 of alogliptin
a)
12 hours
b)
24 hours
c)
21 hours
98.
What functional group is responsible for the longer duration of action for Saxagliptin (Onglyza) and Alogliptin (Nesine)
a)
OH
b)
COOH
c)
CN
99.
Sitagliptin (Januvia) comes in what size oral tabs
a)
25 mg
b)
50 mg
c)
100 mg
d)
200 mg
e)
10 mg
100.
How much Saxagliptin (Onglyza) should be given when switching from Sitagliptin (Januvia)
a)
1/10th the dose of Sitagliptin
b)
10x the dose of Sitagliptin
c)
1/2 the dose of Sitagliptin
d)
2x the dose of Sitagliptin
101.
What strength tablets are available for Saxagliptin (Onglyza) and Alogliptin (Nesine)
a)
2.5 mg
b)
5 mg
c)
10 mg
d)
15 mg
e)
20 mg
102.
Which functional group is responsible for Saxagliptin's pseudoirreversible nature
a)
hydroxyl
b)
amine of beta-amino acid
c)
peptide/amide (-CO-NH)
d)
cyano
103.
What is a first generation sulfonylurea
a)
small substituion
b)
bulky substituion
104.
What is the second generation sulfonylurea
a)
small substituion
b)
bulky substituion
105.
Bulkier substitutents at ___ increases molecular affinity for SUR1 receptors
a)
R1
b)
R2
106.
Sulfonylureas cause beta cells to
a)
secrete insulin
b)
inhibit glucagon
107.
What are some characteristics of first generation sulfonylureas
a)
R1: small substitution
b)
R2: cyclic or acyclic
c)
less potent
d)
Short half-life
e)
has a chance of hypoglycemia
108.
What are some characteristics of second generation sulfonylureas
a)
R1: bulky substitution
b)
R2: cyclic only
c)
increased potency
d)
increased DOA
e)
lesser chances of hypoglycemia compared to first generation
109.
2nd generation sulfonylureas are ___ times more potent than 1st generation
a)
10
b)
20
c)
50
d)
100
110.
Which sulfonylurea carries a lesser chance of hypoglycemia
a)
1st
b)
2nd
111.
What is the mechanism of sulfonylureas
a)
binds to SUR1 subunit of K+/ATP channel
b)
Inhibit K+ conductance
c)
promote depolarization
d)
Ca2+ influx = insulin release
e)
inhibit hepatic clearance of insulin
112.
Hypoglycemia when taking sulfonylureas
a)
is more likely to occur in elderly patients with decreased renal or hepatic function
b)
with chloropropamide having the highest incidence
c)
occurs when there is a failure to inhibit insulin secretion during decreased glucose
d)
is least likely to occur in glimepiride
e)
is more likely to occur in 1st generation sulfonylureas
113.
Sulfonamide in sulfonylureas cause
a)
facial flushing reaction (disulfiram effect when administered with alcohol)
b)
sun sensitivity
c)
hypersensitivity
114.
What adverse effects can occur when taking sulfonylureas
a)
hypoglycemia
b)
sulfonamide reactions
c)
weight gain
d)
drug interactions
115.
Which of the following drugs can produce a much longer hypoglycemic side effect as seen with sulfonylureas and therefore contraindicated in elderly patients?
a)
chlorpropamide
b)
glipizide
c)
glyburide
d)
glimepiride
e)
acetohexamide
116.
Substiuted benzoic acids ("glinides")
a)
are non-sulonylurea derivatives (binds to SUR1)
b)
have a short duration of action
c)
have less problematic hypoglycemia
d)
bind to different site than SU
e)
have structural and functional similarities to Sus
117.
Which of the following drugs is the most potent
a)
chlorpropamide
b)
glipizide
c)
glyburide
d)
glimepiride
e)
acetohexamide
118.
What drugs have the chance of hypoglycemia
a)
insulin
b)
amylin
c)
sulfonylureas
d)
glinides
e)
all of them
119.
Which drugs are Non-SU hypoglycemics
a)
Repaglinide (Prandin)
b)
Nateglinide (Starlix)
c)
Rosiglitazone (Avandia)
d)
Pioglitazone (Actos)
120.
What are thiazolidinediones (glitazones) considered
a)
insulin sensitizer
b)
non-SU hypoglycemic
c)
sulfonylureas
d)
SGLT2 inhibitors
e)
Biguanides
121.
Thiazolidinediones bind to peroxisome proliferator-activated receptor (PPAR-gamma) receptors in
a)
brain cells
b)
muscle cells
c)
liver cells
d)
fat cells
122.
Thiazolidinediones make cells more
a)
responsive to insulin
b)
resistant to insulin
c)
responsive to amylin
d)
resistant to amylin
123.
Which thiazolidinediones are required to be purchased through specified pharamcies and can only be prescribed by certified physicians
a)
Rosiglitazone (Avandia)
b)
Pioglitazone (Actos)
124.
What are adverse effects of thiazolidinediones (glitazones)
a)
increase liver transaminases
b)
weight gain
c)
fluid retention
d)
edema
e)
palpitations
125.
SGLT2 inhibitors (gliflozins)
a)
reduce glucose reabsorption into the body from the proximal tubule
b)
increase glucose in urinary excretion
c)
are glucose derivatives-antagonists
d)
have a low hypoglycemic risk
126.
SGLT1 reabsorbs 10% of the glucose in the kidneys while SGLT2 reabsorbs 90% of the glucose in the kidneys
a)
true
b)
false
127.
SGLT2 inhibitors (gliflozins) include
a)
Canagliflozin (Invokana)
b)
Dapaglifozin (Farxiga)
c)
Empagliflozin (Jardiance)
d)
Ertugliflozin (Steglatro)
e)
Repaglinide (Prandin)
128.
Which SGLT2 inhibitor is the newest in its class
a)
Canagliflozin (Invokana)
b)
Dapaglifozin (Farxiga)
c)
Empagliflozin (Jardiance)
d)
Ertugliflozin (Steglatro)
129.
Which drug combination has been FDA approved
a)
sitagliptin + ertugliflozin
b)
metformin + ertugliflozin
c)
metformin + sitagliptin
130.
Ertugliflozin (Steglatro) has a half-life of
a)
10.6 hrs
b)
12.9 hrs
c)
12.4 hrs
d)
16.6 hrs
131.
Biguanides are
a)
highly polar, basic drug
b)
almost 100% eliminated by kidneys through active tubular secretion through organic cation transporter
c)
insulin sensitizers
d)
has no effect on insulin levels
e)
does not cause hypoglycemia
132.
Biguanides have multiple mechanisms of action including
a)
decreasing gluconeogenesis and glycogenlysis in the liver
b)
increasing glucose uptake in the muscles
c)
increasing glucose uptake and decreasing lypolysis in fat
d)
increase gluconeogenesis and glycogenlysis in liver
e)
decrease glucose uptake and increase lipolysis in fat
133.
What drug is a biguanide
a)
Metformin (Glucophage)
b)
Canagliflozin (Invokana)
c)
Dapaglifozin (Farxiga)
d)
Empagliflozin (Jardiance)
e)
Pioglitazone (Actos)
134.
What are some side effects of biguanides
a)
GI upset (nausea, discomfort, diarrhea, metallic taste)
b)
lactic acidosis (rare)
c)
Macrocytic anemia
d)
decreased B12 absorption
135.
What patients should avoid taking biguanides
a)
patients with liver or kidney failure
b)
respiratory disease
c)
cardiac disease
d)
during procedures involving contrast media
136.
Alpha-glucosidase
a)
releases glucose from larger carbohydrates
b)
is required for digestion of complex carbohydrates
c)
has no effect on absorption of monosaccharides
d)
inhibitors can decrease carbohydrate metabolism
137.
What are some alpha-glucosidase inhibitors
a)
Acarbose (Precose)
b)
Miglitol (Glyset)
c)
Dapaglifozin (Farxiga)
d)
Empagliflozin (Jardiance)
e)
Pioglitazone (Actos)
138.
Acarbose (Precose)
a)
replaces an -O- with a -NH-
b)
the sugar ring changed to cyclohexene
c)
is a transition state analogue
d)
has extensive metabolism by GI bacteria (51% of the drug is excreted in feces and metabolites are excreted in urine)
139.
Miglitol (Glyset)
a)
is a sugar monomer like structure
b)
is highly absorbed
c)
has no metabolism and is excreted unchanged in urine
d)
gets absorbed and removed from kidneys
e)
can cause systemic side effects
140.
Where is the site of action for alpha-glucosidase inhibitors
a)
liver
b)
kidney
c)
intestine
d)
muscles
141.
Alpha-glucosidase inhibitors have a risk for hypoglycemia
a)
true
b)
false
142.
Alpha-glucosidase inhibitors increase carbohydrate absorption
a)
true
b)
false
143.
A patient on alpha-glucosidase inhibitor is experiencing hypoglycemia. What should be given
a)
fruit juice (fructose)
b)
glucose tabs
c)
lactose (milk)
d)
complex carbohydrates
144.
Which drug class carry a risk of hypoglycemia
a)
GLP-1 agonist
b)
DPP4 inhibitor
c)
alpha-glucosidase inhibitors
d)
SGLT2 inhibitors
e)
Glinides
145.
Which drug classes assist in weight loss
a)
amylin
b)
GLP-1 agonist
c)
Metformin
d)
DPP-4 Inhibitors
e)
sulfonyl ureas (SUs)
146.
Which drug classes are considered weight neutral
a)
Metformin
b)
DPP4 inhibitor
c)
sulfonylureas
d)
Meglinitides
e)
Thiazolodinediones
147.
Which drug classes cause weight gain
a)
Metformin
b)
DPP4 inhibitor
c)
sulfonylureas
d)
Meglinitides
e)
Thiazolodinediones
148.
Miglitol (Glyset) is an example of
a)
alpha-glucosidase inhibitor
b)
DPP4 inhibitor
c)
Amylin analogue
d)
GLP-1 agonists
149.
Metformin belongs to which class of anti-diabetics
a)
biguanides
b)
sulfonylureas
c)
glitazones
d)
gliptins
150.
Which of the following statements is not applicable to metformin
a)
insulin sensitizer
b)
not hypoglycemic
c)
can cause weight gain
d)
no effect on insulin levels
e)
anti-hyperglycemic
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