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Pharmacotherapeutics

Total questions: 262

Worksheet time: 2hrs 11mins

Name
Class
Date
1.

Insulin is secreted by?

a)

Beta cells on islet of langerhans

b)

Alpha Cells on islet of langerhans

c)

Thyroid Gland

d)

Pituitary Gland

2.

DM 1 is a ?

a)

deficiency of insulin secretion

b)

insulin resistance

c)

insulin hyperactivity

3.

Beta cell destruction can occur due to?

a)

Viruses, Cox B, CMV

b)

XX

c)

XX

d)

XX

4.

DM 1 is most prevalent in?

a)

Hispanic

b)

African Americans and Asian Americans

c)

Caucasians

d)

XX

5.

DM 2 is most prevalent in?

a)

African Americans

b)

Native Americans and Hispanics

c)

XX

d)

XX

6.

Sulfonylureas should not be used in combination with?

a)

SGLT-2 Inhibitors

b)

GLP-1 Agonists

c)

Meglitinides

d)

Dipeptidyl Peptidase- 4 Inhibitors

7.

True/False: Sulfonylureas can be used as Monotherapy.

a)

True

b)

False

8.

What are the 3 sulfonylureas?

a)

GlipizIDE

b)

GlimepirIDE

c)

GlyburIDE

d)

Metformin

9.

MOA for sulfonylureas?

a)

INCREASES Blood Glucose by increasing insulin secretion from Beta cells (Decreases A1c by 1-2%)

b)

XX

c)

Lowers Blood Glucose by increasing insulin secretion from Beta cells (Decreases A1c by 1-2%)

d)

XX

10.

Skin reaction of sulfonylureas?

a)

SJS

b)

TEN

c)

Atopic Dermatitis

d)

Photosensitivity

11.

If patient ingests alcohol while on sulfonylureas?

a)

Disulfiram Like Rxn

b)

TEN

c)

SJS

d)

Atopic Derm

12.

Hematological reaction of sulfonylureas?

a)

Aplastic Anemia

b)

Hemolytic Anemia

c)

Decreased Bone Marrow Activity

d)

Thrombocytopenia and Agranulocytosis

13.

What medications will cause increased effect of sulfonylureas?

a)

XX

b)

MAOIs, Digoxin

c)

Azoles, NSAIDs, Sulfonamides, TCA

d)

XX

14.

What medications will cause decreased effect of sulfonylureas?

a)

Phenobarbital, Beta Blockers, Hydantoins

b)

ACE Inhibitors

c)

Statis

d)

ARB's

15.

Sulfonylureas have a cross sensitivity with sulfonamides and _____?

a)

Lasix

b)

Furosemide

c)

Thiazides

d)

ACEi

16.

When should metformin be discontinued?

a)

Prior to Surgery and Procedures requiring IV contrast

b)

When Plavix is given

c)

When simvastatin is given

d)

xx

17.

Only Biguanide medication available? (freebie)

a)

Glipizide (Sulfonylureas)

b)

Metformin (Biguanide)

c)

Sitagliptin (DPP-4i) (-Gliptin family)

d)

Liraglutide (GLP-1 agonist) (-Glutide and -Tide family)

18.

MOA for metformin?

a)

Increased Hepatic Glucose Prod.

b)

Increased Thiamine Prod.

c)

Decreased Thiamine Prod.

d)

Decreased Hepatic Glucose Prod.

19.

Where is metformin absorbed?

a)

50-60% absorption in stomach (Peak Effect in 2 weeks)

b)

20% absorption in stomach (Peak Effect in 2 weeks)

c)

100% absorption in stomach (Peak Effect in 2 weeks)

d)

5% absorption in stomach (Peak Effect in 2 weeks)

20.

Metformin partititons/enter into?

a)

WBC's

b)

Platelets

c)

RBC's

21.

Where is metformin metabolized?

a)

It is not

b)

in the lung

c)

in the stomach

d)

in the kidney

22.

Adverse Gastrointestinal reactions of metformin?

a)

GI Upset

b)

Unpleasant Metallic Taste

c)

Migraines

d)

Deafness

23.

With metformin, there is increased risk of lactic acidosis with?

a)

Renal dysfunction

b)

Age

c)

Heart Failure

24.

What medications may increase metformin levels?

a)

Furosemide

b)

Nifedipine

c)

Digoxin

d)

H2RA(Ranitidine, Cimetidine)

e)

Morphine, Trimethoprim

25.

Alcohol with metformin can cause?

a)

Hyperglycemia

b)

Urinary Retention

c)

Hypoglycemia

26.

What patients should not receive metformin?

a)

Those with increased Risk for Lactic Acidosis because of Renal Impairment, Heart Failure, Hepatic Dysfunction, and Alcoholism

b)

XX

c)

XX

d)

XX

27.

Mitiglinides have shorter half lives so they must be administered more frequently and are most useful in?

a)

Preprandial Hyperglycemia

b)

Postprandial Hyperglycemia

28.

MOA for mitiglinides?

a)

Same as sulfonylureas but different binding site

b)

Same as sulfonylureas including same binding site

29.

Mitiglinides are mostly (a)   Bound.

30.

Where are mitiglinides metabolized?

a)

Liver P-450 system

b)

Lung Alveoli

c)

Nephrons

d)

Urine

31.

How are meglitinides excreted?

a)

Repaglinide = Bile

b)

Nateglinide = Urine

c)

Repaglinide = Urine

d)

Nateglinide = Bile

32.

Meglitinides can cause what adverse reactions?

a)

Ischemia

b)

GU infections

c)

Upper Resp Infections

d)

None of the choices

33.

What medications can cause increased effect of meglitinides?

a)

Beta Lactams

b)

Gemfibrozil

c)

Macrolides

d)

Cephalosporins

34.

What natural herbs/remedies can caue increased effect of meglitinides?

a)

St John's Wart

b)

EtOH

c)

Garlic

d)

XX

35.

What patients should not receive meglitinides as a treatment?

a)

Renal Impaired

b)

With one lung only

c)

Hepatic Impaired

d)

Males

36.

Thiazolidinediones (TZDs) family includes?

a)

-gliptin (DPP-4)

b)

-tide (GLP-1)

c)

-zone

d)

-gliflozin (SGLT-2) (Some Girls Like To/2 Flo)

37.

TZDs do not produce?

a)

Hyperglycemia

b)

Hypoglycemia

38.

TZD's mechanism of action?

a)

increase sensitivity of muscle, fat and liver to insulin + insulin sensitivity as well

b)

XX

c)

XX

d)

XX

39.

TZD most common adverse effects?

a)

Weight gain, fluid retention

b)

Weight Loss

c)

Hyperparathyroidism

d)

Hypoparathyroidism

40.

Why has rosiglitazone use decreased?

a)

Risk of CV events

b)

Risk of DM

c)

Risk of Thyroid cancer

41.

TZD is dependent on the production of?

a)

T3

b)

T4

c)

T5

d)

Insulin

42.

TZD bioavailability percentage?

a)

20%

b)

30%

c)

99%

d)

10%

43.

How long do TZDs take to see peak effect?

a)

30 Weeks

b)

12 Weeks

c)

4 Weeks

d)

3 Weeks

44.

TZDs adverse effects?

a)

Edema/CV Events

b)

Increased Lipid Panel Levels (Across the board)

c)

Anemia

d)

URI's

45.

Where are TZDs metabolized?

a)

Liver P450

b)

Kidney

c)

Heart

d)

Brain

46.

Do not use TZD's in patients with ____.

a)

Congestive Heart Failure

b)

Hepatic Impairment

c)

XX

47.

Pioglitazone alters the levels of medications metabolized in the P450 isomer CYP3A4 such as?

a)

Carbamazepine

b)

Cyclosporine

c)

Oral Contraceptives

d)

XX

48.

What are the two Alpha Glucosidase Inhibitors available?

a)

Acarbose

b)

Rosiglitazone

c)

Miglitol

d)

Sitagliptin

49.

What do Alpha Glucosidase inhibitors do?

a)

Decrease rate of digestion of polysaccharides in proximal small intestine (less effective than biguanide/sulfonylureas)

b)

XX

c)

XX

d)

XX

50.

Alpha Glucosidase inhibtors do not cause (a)   or weight loss often.

51.

AGI's are not recommended in renal impairment and in patients with SrCr > ?

a)

SrCr >2mg/dL

b)

SrCr >1mg/dL

c)

SrCr >4mg/dL

52.

What may reduce AGI effect?

a)

Charcoal

b)

Amylase

c)

Pancreatin

d)

XX

53.

Where does absorption and metabolism of Alpha Glucosidase Inhibitors occur?

a)

GI Bacteria and their Enzymes (metabolized by)

b)

Less than 2% is absorbed (acts in GI Tract)

54.

Adverse effects of AGIs?

a)

Rash

b)

GI Upset

c)

XX

d)

XX

55.

AGI Acarbose has what interactions?

a)

Decreases effect of digoxin

b)

Decreases effect of Thiazides

c)

Deceases effect of Thyroid Meds

d)

Decreases Effect of Estrogens and Calcium Channel Blockers

56.

When are AGI's contraindicated?

a)

GI Obstruction

b)

Malabsorption Syndrome

c)

XX

d)

XX

57.

Amylin Analogue Pramlintide (Symlin) is a synthetic analogue of?

a)

Human Amylin

b)

Human Lipase

c)

Human Chorionic Gonatotropin Hormone

d)

Thyroxine

58.

Symlin should be used as a?

a)

Addon with insulin glargine (Lantus, Toujeo Solostar etc)

b)

Monotherapy

c)

Single one time use

59.

How are amylin analogues administered?

a)

SC before meals

b)

IM before meals

c)

ID post meals

d)

Lumbar Puncture

60.

Amylin analogues inhibit?

a)

Glucagon production and decrease postprandial glucose excursions

b)

XX

c)

XX

d)

XX

61.

What is the most common adverse effect of amylin analogues?

a)

Nausea

b)

XX

c)

XX

d)

XX

62.

Amylin analogues should be used by patients who use?

a)

Mealtime insulin Tx

b)

XX

c)

XX

d)

XX

63.

Absorption percentage of Amylin analogues?

a)

100 % due to SC administration

b)

50 % due to SC administration

c)

25% due to SC administration

d)

10%due to SC administration

64.

Amylin analogues are primarily excreted by?

a)

Liver

b)

Kidneys

c)

Feces

65.

Adverse neurological effects of amylin analogues?

a)

Fatigue

b)

Dizziness

c)

Chorea

d)

Parkinsonism

66.

Severe hypoglycemia due to Amylin Analogues usually occurs within?

a)

12 hours

b)

24 hours

c)

3 hours

67.

Blackbox warning for Amylin Analogues?

a)

Use with insulin

b)

Will cause hemorrhage

c)

You'll get pregnant easier

68.

Contraindications to prescribing amylin analogues?

a)

Hypoglycemia Unawareness

b)

Diagnosis of Gastroparesis

c)

XX

d)

XX

69.

What should you not use in conjunction with Amylin analogues?

a)

Agents that alter GI Motility and analgesics or other agents that REQUIRE rapid onset

b)

xx

c)

Xx

d)

XxX

70.

GLP-1 agonists stimulate? (Has GI Upset Side effects)

a)

Increased Insulin production

b)

Increased response to elevated blood glucose

c)

Increased satiety

d)

xx

71.

GLP-1 Agonists have a high frequency of which side effects?

a)

GI Side effects

b)

Convulsions

72.

GLP-1 Agonists are an analogue of?

a)

Secretin

b)

Gastrin

c)

Incretin

73.

GLP-1 Agonists also have an inhibition portion that?

a)

inhibits release of glucagon after meals and slows rate in which nutrients are absorbed

b)

xx

c)

xx

d)

xx

74.

GLP-1 agonists are recommended in conjunction with?

a)

Sulfonylureas AND Metformin

b)

Sulfonyluears OR Metformin

c)

Thiazolidinediones

75.

GLP-1 agonists absorption percentage?

a)

MINIMAL, acts in the GI tract (Intestine)

b)

XX

c)

Xx

d)

xx

76.

Where are GLP-1 agonists excreted?

a)

Feces

b)

Urine

c)

Saliva

77.

GLP-1 agonists and sulfonylureas may cause?

a)

Increased incidence of hypoglycemia

b)

Increased incidence of Hyperglycemia

c)

XX

d)

XX

78.

Adverse neurological effects of GLP-1 Agonists?

a)

Somnolence

b)

Fat

c)

Hyperglycemia

d)

Makes you want to exercise

79.

When using GLP-1 agonists, drugs with threshold concentrations should be taken ?

a)

4 hours before

b)

6 hours before

c)

1 hour before

80.

When using GLP-1 agonists (liraGLUTIDE, TIDE), what may happen to the patients coagulation studies?

a)

Increased INR/Bleeding Time

b)

XX

c)

XX

d)

Destruction of factor VIII

81.

Contraindications to using GLP-1 Agonists?

a)

T1DM

b)

Renal Impairment

c)

Severe GI Disease

82.

Dipeptidyl-Peptidase 4 inhibitors are the the ___ family.

a)

GLiptin

b)

Flozin

c)

Glutide/Tide

d)

TZD's

83.

DPP4 inhibitors inactivate and ____ incretin hormones.

a)

Decrease

b)

Destroy

c)

Prolong

84.

DPP4 inhibitors increase ____ productivity and decrease amount of glucose produced by liver.

a)

Secretin

b)

Gastrin

c)

Insulin

85.

Where are DPP4 inhibitors metabolized?

a)

Liver

b)

Kidney

c)

Heart

d)

Brain

86.

DPP4 inhibitors may be used in combination with?

a)

Metformin

b)

Thiazolidinediones

c)

Macrobid

d)

Sulfonylureas

87.

MOA for DPP4 inhibitors?

a)

Slows inactivation of incretin hormones, such as GLP1 and Glucose dependent insulinotropic polypeptide

b)

XX

c)

X

d)

X

88.

Adverse effects of DPP4 Inhibitors?

a)

Nasopharyngitis

b)

Upper Resp Infections

c)

XX

d)

XX

89.

DPP4 drug interactions?

a)

Increased Digoxin levels, need to use lower doses of sulfonylureas (if being used) due to risk of hypoglycemia

b)

xx

c)

x

d)

xx

90.

Glucagon is secreted by?

a)

Alpha cells

b)

Beta cells

c)

Gamma Cells

91.

Glucagon is used to increase blood glucose and is administered?

a)

IM

b)

IV

c)

SC

92.

Indication for glucagon?

a)

Severe hypoglycemia and diagnostic aid

b)

XX

c)

XX

d)

XX

93.

MOA for glucagon?

a)

Accelerates glycogenolysis converting glycogen stores to glucose

b)

Relaxes smooth muscles of GI tract

c)

xx

d)

xx

94.

Where is glucagon metabolized? (degraded in plasma)

a)

Liver

b)

Kidney

c)

Liver + Kidney (degraded in plasma)

95.

Absorption of glucagon time?

a)

IV = 5-20 mins

b)

IM = 30 mins

c)

SC = 30-45 mins

96.

Where is glucagon is excreted?

a)

In Urine

b)

In feces

c)

In blood

97.

Glucagon drug interactions?

a)

Oral anticoagulant effect may be INCREASED

b)

XX

c)

xx

d)

xX

98.

Side effect/adverse effects of glucagon?

a)

Hypotension

b)

Resp Distress

c)

XX

d)

XX

99.

Contraindications to Glucagon?

a)

Pheochromocytoma

b)

Pituitary Adenoma

c)

Thymoma

100.

What is the most effective treatment for lowering glycemia?

a)

Glucagon

b)

Cake

c)

Insulin

d)

Pheochromocytoma

101.

Insulin does what?

a)

Promote storage of fat + glucose

b)

Increase Cell Growth + Metabolism

c)

Lowers BGL

d)

Inhibits hepatic glucose prod.

102.

Pork insulin often results in ____ doses and ____ allergies.

a)

Lower; Less

b)

Higher: More

103.

How should insulin be given?

a)

0.6 to 1 unit / kg / day

b)

xx

c)

xx

d)

xx

104.

Insulin MOA?

a)

Acts on glucose cell membrane transporters, in liver causes increase in glycogen by preventing glycogenolysis, promotes triglyceride storage, acts on muscle cells to promote protein synthesis.

b)

XX

105.

Can insulin be given Orally?

a)

No, stomach acids/enzymes destroy the insulin

b)

Yes, stomach acids/enzymes destroy the insulin

c)

Yes, stomach acids/enzymes will not destroy the insulin

106.

What type of insulin has fastest onset?

a)

Human>Pork>Beef

b)

Pork>Human>Beef

107.

In the event of hypoglycemia, what can be done?

a)

IM or IV dextrose/glucagon

b)

IM or IV Insulin

108.

Injection sites that are better for absorption of insulin?

a)

Abdomen>Thighs>Buttocks

b)

Thighs>Buttocks>Buttocks

109.

DIabetic ketoacidosis may be caused in T1DM due to ____ dose of insulin.

a)

ONE MISSED DOSE

b)

5 MISSED DOSES

c)

4 MISSED DOSES

110.

Treatment of diabetic ketoacidosis requires?

a)

At home insulin

b)

At office insulin

c)

Hospitalization! (MEDICAL EMERGENCY)

111.

Drug of choice for hypothyroidism?

a)

Levothyroxine

b)

Levothyronine

c)

Propylthiouracil

d)

Methimazole

112.

MOA for levothyroxine?

a)

Central metabolic processes ; believed to play role in DNA/Protein synthesis

b)

DD

c)

XX

d)

DDA

113.

Levothyroxine absorption percentage?

a)

50 - 80% (increases when fasting)

b)

10% only

c)

4%

114.

Levothyroxine is metabolized by?

a)

Kidney

b)

Lung

c)

Liver

115.

Levothyroxine adverse reactions? (TTRH)

a)

Tachycardia

b)

Tremors

c)

Heat intolerance

d)

Rash

116.

What can cause DECREASED absorption of levothyroxine?

a)

Antacids

b)

Oxycodone

c)

Aspirin

117.

What reduces the body's response to levothyroxine?

a)

Estrogen

b)

Oxygen

c)

Water

118.

Contraindications to levothyroxine?

a)

Recent MI

b)

Thyrotoxicosis

119.

Liothyronine mechanosm of action?

a)

INCREASED O2 consumption by most tissues, basal metabolic rate, carbohydrate metabolism, lipid and protein metabolism

b)

x

c)

xx

d)

xX

120.

Liothyronine absorption percentage?

a)

95% in 4 hours (Very short half life)

b)

x

121.

Liothyronine is metabolized by?

a)

Liver

b)

Kidney

122.

Adverse reactions of liothyronine?

a)

Arrhythmias

b)

Hair Loss

c)

GI Upset

123.

Contraindications of liothyronine?

a)

Thyrotoxicosis

b)

Adrenal Insufficiency

c)

XX

d)

XX

124.

Drug interactions with liothyronine?

a)

Anticoagulants, Insulin

b)

Decreases Digoxin dosage

125.

Liothyronine/Levothyroxine combo MOA?

a)

Increases gluconeogenesis, utilization of glycogen stores, protein synthesis, cell growth and CNS development

b)

sx

c)

xx

126.

Liothyronine/Levothyroxine onset time?

a)

Rapid (few hours) (95% absorbed in 4 hours)

b)

Slow (few months) (95% absorbed in 3 weeks)

127.

Adverse reactions of levothyronine/levothyroxine?

a)

CV Collapse, Accelerates Bone Maturation

b)

Arrhythmias, Increased BP, Irritability, Anxiety

c)

Hyperthyroid, Wt Loss, Heat Intolerance

128.

Contraindications for levothyronine/levothyroxine combo?

a)

Thyrotoxicosis

b)

Recent MI (Or Elderly w/Cardiac Problems)

129.

Liothyronine/Levothyroxine should not be given with?

a)

Mineral Supplements

b)

Water

c)

Oxygen

130.

Propylthiouracil MOA?

a)

inhibits oxidation of iodine = inhibits production of both T3, T4

b)

xx

131.

Propylthiouracil should be taken with?

a)

Meals Everyday

b)

Empty stomach always

c)

With Margaritas

132.

PTU is metabolized by?

a)

Kidney

b)

lung

c)

Liver

133.

PTU time that it takes to be effective?

a)

24-36 hours but absorption takes place fully within 1 hour

b)

XX

c)

XX

d)

XX

134.

PTU adverse reactions?

a)

Skin changes, Lupus Like Syndrome

b)

Agranulocytosis

135.

PTU increases the effect of ?

a)

Warfarin

b)

Cocaine

136.

PTU is contraindicated in ? (REMEMBER THIS IS PHARMACOLOGY!!! ALTHOUGH IT IS PREFERRED IN PREGNANCY FOR ENDOCRINOLOGY, IT IS CONTRAINDICATED

a)

Pregnancy

b)

ZZ

c)

ZZZ

d)

ZZZZ

137.

Why is methimazole preferred over PTU?

a)

Better adherence

b)

Poor adherence

c)

Provides sexual arousal

138.

Methimazole mechanism of action?

a)

inhibits the synthesis of thyroid hormone

b)

blocks oxidation of iodine

c)

interferes with iodine coupling to tyrosine

139.

Where is methimazole concentrated ?

a)

Thyroid Gland

b)

X

c)

XX

d)

xX

140.

Adverse reactions of methimazole?

a)

Agranulocytosis

b)

UTIs

141.

What is methimazole metabolized by?

a)

Kidney

b)

Liver

142.

Cinacalcet increases sensitivity of? (use for hyperparathyroid)

a)

Ca2+ sensing receptors on parathyroid gland

b)

XX

143.

Cinacalcet belongs to a group of medications called?

a)

Calcimimetics

b)

CC

c)

Thyroid analogues

144.

Cinacalcet signals to?

a)

produce LESS PTH, LESS CA2+

b)

produce MORE PTH, LESS CA2+

145.

What lowers the absorption of Cinacalcet?

a)

High Fat Meals

b)

Low Fat Meals

146.

How is Cinacalcet metabolized?

a)

Kidney

b)

Liver

147.

Adverse reactions of Cinacalcet?

a)

Arrhythmias

b)

Muscle Aches, Paresthesias

148.

What medications will increase levels of Cinacalcet?

a)

Amitriptyline/ Notriptyline (TCAs)

b)

XX

c)

xx

149.

Treatment of hypoparathyroidism>

a)

Calcitriol

b)

Cincacalcet

150.

According to FDA, cinacalcet is not approved for?

a)

Secondary Hypoparathyroidism

b)

Primary Hypoparathhyroidism

151.

Calcitriol mechanism of action?

a)

Stimulates Ca2+ and PO42 absorption, increases Ca2+release from bone, increases reabsorption from renal tubule, increases skeletal growth, Inhibits parathyroid gland.x

b)

xx

152.

Where is calcitriol absorbed?

a)

Small Intestine

b)

Lung

153.

Where is calcitriol metabolized?

a)

Kidney

b)

Liver

154.

Adverse reaction of calcitriol?

a)

Arrhythmias

b)

Constipation

c)

Hypercalcimea

155.

Vasopressin MOA?

a)

Increases reabsorption of H2O in kidneys, stimulates smooth muscle receptors in GI tract and arterioles (peristalsis and vasoconstriction)

b)

x

156.

Subcutaneous onset post-absorption of vasopressin?

a)

1 - 2 hours (2 to 8hr duration)

b)

x

157.

Vasopressin adverse reaction?

a)

Myocardial infarction

b)

Rash

c)

Water Intoxication

158.

Drug interactions with vasopressin?

a)

None

b)

XX

159.

IV Onset post absorption of Vasopressin?

a)

Immediate (With 1/2 to 1 hr duration)

b)

XX

160.

Oxytocin IM produces?

a)

Uterine Contractions within 3-5 mins (lasts 2 to 3 hours)

b)

XX

161.

Oxytocin adverse reactions?

a)

Tachy, Arrhythmias

b)

Hypotension, Hemorrhage Post Partum

c)

Neonatal Retinal Hemorrhage, Water Intox

162.

What drug can increase the effect oxytocin?

a)

Dinoprostone (Used for Cervix Dilation)

b)

Misoprostol (used to reduce gatric acid secretion and directly acts on parietal cells but also increase Uterine Contraction)

163.

MOA for desmopressin?

a)

Increased reabsorption of water+ plasminogen activator which increases factor VIII

b)

xx

164.

Contraindications to oxytocin?

a)

Anticipation of NON VAGINAL delivery

b)

XX

165.

Drawback to desmopressin?

a)

Poorly absorbed in all routes

b)

XX

166.

Adverse reactions of desmopressin?

a)

Myocardial Infarction

b)

Thrombosis

c)

GI Upset, Rhinorrhea

d)

Decreased Urination, Water Intox

167.

Drugs that increase the effect of desmopressin?

a)

Chlorpropamide (Sulfonylureas) (IDES)

b)

Ethanol

168.

Contraindication to using desmopressin?

a)

Renal Impairment

b)

Liver Dysfunction

169.

Drugs that decrease the effect of desmopressin?

a)

Demeclocycline (Tetracycline Abx, Also used in SIADH)

b)

Lithium

170.

Lypressin MOA? (IT IS ONLY INTRANASAL!!)

a)

Promotes reabsorption of H2O

b)

Increases Permeability of collecting ducts, Increases Urine Osmolality

c)

Decreases Urinary Output

171.

Lypressin is administered?

a)

Intranasally only

b)

IM only

c)

IV only

172.

How is Lypressin excreted?

a)

Urine

b)

Feces

173.

Lypressin drug interactions (increase the effect)?

a)

Carbamazepine (Anticonvulsant) [Increases antidiuretic effect]

b)

Chlorpropamide ((Sulfonylureas) [Increases antidiuretic effect]

c)

Clofibrate (Triglyceride lowering, Fibrate)

[Increases antidiuretic effect]

174.

Lypressin drug interactions (drugs that decrease the effect)?

a)

Demeclocycline

b)

Lithium

c)

Norepinephrine

175.

Recombinant somatotropin /somatrem MOA? All choices are correct, read thoroughly

a)

Increases metabolism of connective tissue by stimulating synthesis of Chondroitin sulfate and collagen by urinary excretion of hydroxyproline

b)

Increases number and size of skeletal muscle cells, and size of organs, red blood cell mass by EPO stimulation.

c)

Increased metabolism of carbohydrates by decreasing insulin sensitivity

d)

Increased protein metabolism by increased synthesis + Increased Nitrogen retention

176.

Recombinant somatotropin/Somatrem is highly absorbed and metabolized by?

a)

Kidneys

b)

Liver

177.

Recombinant Somatotropin/Somatrem has interactions with?

a)

Anabolic Steroids

b)

Thyroid Hormones (acceleration of epiphyseal plate closure)

178.

Adverse reactions of Recombinant Somatotropin/Somatrem?

a)

Edema, Hypoglycemia

b)

Hypothyroidism, Insulin Resistance

179.

Octreotide is an analogue of?

a)

Somatostatin

b)

Somatropin

c)

T3

d)

T4

180.

How fast is a SC injection of octreotide take to be absorbed?

a)

30 mins

b)

3 hours

181.

Where is octreotide metabolized?

a)

Lung

b)

Liver

c)

Kidney

182.

Adverse reaction from Octreotide?

a)

Arrhythmia

b)

GI Upset, Gallstones, GB Abnormalities

c)

Hypothyroid, Hypo/Hyperglycemia

183.

Where is octreotide excreted?

a)

Feces

b)

Urine

184.

Glucocorticoid mechanism of action?

a)

Stimulate gluconeogenesis in liver, mobilizes amino acids products for gluconeogenesis, stimulates fat breakdown.

b)

XX

185.

Glucocorticoid mechanism of action in inflammation?

a)

Potent antiinflammatorie properties and immunosuppressive properties

b)

xx

186.

Glucocorticoids inhibit glucose uptake where?

a)

In adipose tissue and muscle tissue

b)

In Stomach

c)

In Gallbladder

187.

Glucocorticoid role in fetal development?

a)

Promote Lung Maturation

b)

Kill Fetus

188.

Glucocorticoids are best absorbed ?

a)

IM = widely distributed to all tissues

b)

Oral

189.

Glucocorticoid metabolism takes place where? (READ ALL 2 OPTIONS and SELECT ALL THREE FOR CORRECT)

a)

Liver, they get broken down into (see other options)

b)

Cortisone = Hydrocortisone

c)

Prednisone = Prednisolone

190.

Excessive glucocorticoid use can lead to?

a)

Inhibition of bone formation

b)

Suppress Ca++ deposition

c)

Delay Wound Healing

191.

Short Acting Glucocorticoids (2 of them)

a)

Cortisone

b)

Hydrocortisone

c)

Dexamethasone

192.

Intermediate acting glucocorticoids? (4 of them)

a)

Methylprednisolone

b)

Prednisone

c)

Prednisolone

d)

Triamcinolone

e)

Nystatin

193.

Long acting glucocorticoids? (3 of them)

a)

Betamethasone

b)

Budesonide

c)

Dexamethasone

d)

prednisone

194.

Adverse effects of glucocorticoids?

a)

Tachy, Cushings

b)

GI Upset + bleeds

195.

Glucocorticoids should not be used with?

a)

Fungal Infections

b)

Heart Failure

c)

Renal Impairment

d)

Infection resistant to Abx

196.

Glucocorticoids interactions/effects?

a)

Increases Bleeding Time

b)

Increases Hypokalemia with K+ Depleting diuretics

c)

Increased RIsk of Arrhythmia

197.

Fludrocortisone is used as replacement of?

a)

Glucocorticoids

b)

Aldosterone

198.

Low dose fludrocortisone MOA?

a)

Distal tubules causes increased K+ & H+ excretion = increased Na+ retention

b)

Proximal tubules causes increased K+ & H+ retention= increased Na+ excretion

199.

Metabolism of fludrocortisone?

a)

Kidney + Liver (Excreted in Urine)

b)

Lung only

200.

High dose fludrocortisone MOA?

a)

inhibits exogenous adrenal cortical secretion, thymic activity, and secretion of corticotropin

b)

Promotes exogenous adrenal cortical secretion, thymic activity, and secretion of corticotropin

201.

Adverse drug reactions of fludrocortisone?

a)

Acne, Ulcers

b)

GI Upset, Unusual Hair Growth

c)

Decreases Inflamm/Immune Response, Mild Neuro ADR

202.

Fludrocortisone decreases the effect of?

a)

Rifampin

b)

Barbiturates(phenobarbital)

c)

Hydantoins (Phenytoin)

203.

Fludrocortisone mixed with amphotericin, loop diuretics, thiazides,?

a)

Causes excessive K+ Depletion

b)

Causes excessive K+ Retention

204.

Aminoglutethimide MOA?

a)

Adrenal androgen blocker; Blocks Corticosteroids from being made; Stops signals that tell body to produce androgens/estrogens

b)

XX

205.

Aminoglutethimide 35-45% is excreted in?

a)

Urine, unchanged

b)

Feces. Unchanged

206.

Adverse reactions from Aminoglutethimide

a)

GI Upset

b)

Mild Neuro Issues

207.

Aminoglutethimide interactions?

a)

Corticosteroids

b)

Carbamazepine

208.

Aminoglutethimide is contraindicated in?

a)

Pregnancy

b)

Hammertoe

209.

Anastrozole MOA?

a)

selective aromatase inhibitor; decreases tumor mass/delay progression by decreasing estrogen levels

b)

xx

210.

Anastrozole is metabolized by?

a)

Liver

b)

Lung

c)

Kidney

211.

Adverse drug reactions of Anastrozole?

a)

Edema, Vaginal Bleeds

b)

Flu Syndrome, Fractures

c)

Mood Alteration

212.

Obesity is a complex?

a)

unifactorial complementary application

b)

Multifactorial chronic disoder

213.

Tool for initial obesity screening

a)

BMI

b)

Waist Circumference

214.

Step Up Approach to obesity care? (Know it!)

a)

Counseling and Intervention, Lifestyle changes, Pharmacotherapy, Surgery

b)

XX

215.

BMI for obesity Class I?

a)

30-34.99

b)

35-39.99

c)

>40

216.

BMI for obesity Class II?

a)

35.0 - 39.99

b)

30.0-34.99

c)

>40

217.

BMI for Obese class III?

a)

35.0-39.99

b)

30.0-34.99

c)

>40

218.

What can reduce risk factors due to obesity?

a)

10% reduction in body weight (lost 1-2 lbs/week)

b)

20% reduction in body weight (lose 5-10lbs/week)

219.

Obesity lifestyle interventions? (1st line Treatment!!!)

a)

Reduction of caloric intake

b)

Increased Physical Activity

c)

Bahavior Mod.

220.

Initial goal of weight loss is?

a)

5-10% weight loss in 6 months

b)

50% weight loss in 1 month

221.

When is pharmacologic therapy indicated for obesity?

a)

BMI >27 with comorbidites

b)

BMI >30 without comorbidities

222.

When is bariatric surgery indicated for obesity?

a)

BMI >35 with comorbidites

b)

BMI >40 without comorbidities

223.

1st line SHORT TERM management intervention medications for obesity?

a)

Phentermine (Lomaira)

b)

Xenical, Alli (Orlistat)

224.

1st line LONG TERM management intervention meds for Obesity?

a)

Orlistat

b)

Lorcaserin

c)

Phentermine-Topiramate

d)

Naltrexone-Bupropion

e)

Liraglutide

225.

All obesity medications target appetite mechanisms except?

a)

Phentermine

b)

Naltrexone-Bupropion

c)

Orlistat (Xenical, Alli)

226.

Medications for obesity work where?

a)

Arcuate Nucleus and Stimulate POMC neurons = Increased Satiety

b)

xx

227.

How long should phentermine be used for? (short term remember)

a)

3 months

b)

12 months

228.

Phentermine is a (a)   releasing agent.

229.

Adverse effects of Phentermine?

a)

Tachy, Increased BP, Overstimulation, Insomnia

b)

Psychosis, Unpleasant taste

c)

Impotence/ Libido Change

230.

Contraindications to phentermine?

a)

Anxiety Disorders, Seizures

b)

MAOIs, Glaucoma, Drug abuse Hx

231.

Orlistat is offered in two forms?

a)

Alli = 60 mg (OTC)

b)

Xenical = 120 (Rx)

232.

MOA for orlistat?

a)

Pancreatic and Gastric Lipase Inhibitor

b)

Blocks 25-30% of fat calories

233.

Adverse drug reactions of Orlistat?

a)

Steatorrhea, Oily Spotting, Oily Evacuation

b)

Flatulence with Discharge

c)

Focal Urgency, Loss of ADEK vitamins(fat soluble)

d)

Increased Defecation, fecal incontinence

234.

How to avoid depleted levels of ADEK?

a)

Multivitamin

b)

Probiotic

235.

Orlistat interactions systemically?

a)

Not absorbed systemically

b)

XX

236.

Contraindications to Orlistat?

a)

Cyclosporine Use, Malabsorption syndrome

b)

Levothyroxine

c)

Warfarin, and Antiepileptic drugs

237.

Lorcaserin MOA?

a)

Selective Serotonin Agonist that acts on hypothalamus to increased satiety

b)

XX

238.

Adverse effects of lorcaserin?

a)

Dizziness, Fatigue

b)

Nausea, Dry Mouth, Constipation

c)

In diabetics, can cause hypoglycemia

239.

LorcaSERin has an increased risk of (a)   syndrome. (Look at medication name)

240.

Lorcasein is contraindicated in?

a)

Pregnancy

b)

Hammertoe

241.

Phentermine-Topiramate weight loss after 1 year at recommended and HIgh DOse?

a)

14.5 lb at recommended dose

b)

18.9 lb at high dose

242.

Phentermine-Topiramate MOA?

a)

Norepinephrine releasing agent =Phentermine = decrease appetite

b)

GABA receptor modulator to decrease appetite + increase satiety

243.

Adverse effects of phentermine/topiramate?

a)

Mild Neuro SE

b)

Constipation

c)

Teratogenic

d)

Seizures (Decrease gradually to avoid)

244.

Contraindications to Phentermine/Topiramate?

a)

Pregnancy, Hypothyroid

b)

Glaucoma, MAOIs

245.

Naltrexone-Bupropion MOA?

a)

Naltrexone is opioid antagonist (protect against DOPE!!)

b)

Bupropion is reuptake inhibitor of dopamine and NE which stimulates POMC neurons= Increased Satiety

246.

Contraindication to Naltrexone/Bupropion?

a)

Uncontrolled Hypertension, Seizures

b)

Anorexia, Drug-Alcohol Withdrawal

247.

Liraglutide is offered/administered as?

a)

Injection

b)

Tablet

248.

MOA of Liraglutide? (TIDE!!!!) (Select both, and READ!)

a)

GLP-1 Receptor Agonist; Stimulates insulin secretion, supression of glucagon,

b)

Decreased gastric emptying, and decreased food intake

249.

Adverse effects of liraglutide?

a)

Dyspepsia, Fatigue

b)

Pancreatitis, Hypoglycemia

c)

Risk of Medullary Thyroid Carcinoma

d)

Symptoms of Thyroid Cancer

250.

Canagliflozin(Invokana) Mechanism of Action?

a)

SLT-2 inhibitor, promotes weight loss by preventing glucose reabsorption, but no effect on appetite

b)

XX

251.

Contraindications to Liraglutide?

a)

Hx of med thyroid carcinoma

b)

MEN-2

c)

Renal Failure

252.

Average weight loss of in 1 year of Orlistat?

a)

2.9-3.4kg/year

b)

XX

253.

Average weight loss of in 1 year of Lorcaserin?

a)

3.6kg/year

b)

XX

254.

Average weight loss of in 1 year of phentermine-topiramate?

a)

6.6-8.6 kg/year

b)

xx

255.

Average weight loss of in 1 year of Naltrexone-Bupropion

a)

2.4 kg/year

b)

xx

256.

Average weight loss of in 1 year of Liraglutide ?

a)

5.8 kg/year

b)

xx

257.

NOT BUYING OBESITY, LETS LOOK PHYSICALLY TRAINED (NBOLLPT)

LISTED FROM LEAST WEIGHT LOSS TO MOST WEIGHT LOSS

a)

NALTREXONE BUPROPION (2.4)

b)

ORLISTAT (2.9-3.4), LORCASERIN (3.6), LIRAGLUTIDE(5.8),

c)

PHENTERMINE-TOPIRAMATE (6.6-8.6)

258.

Rapid acting and Short acting insulin are given?

a)

Before meals

b)

After meals

259.

Insulin Lispro (Humalog), Insulin Aspartate (Novolog), and Insulin Glulisine (Apidra) are all forms of

a)

rapid acting insulin

b)

long acting insulin

260.

Short acting insulins are used when meals have been eaten. What are the two kinds?

a)

Velosulin (typically used with insulin pumps)

b)

regular (Humulin)

c)

Novolog

261.

Intermediate acting insulins are used to cover half the day or overnight and are used in conjunction with rapid and short acting insulins. What are the types?

a)

NPH

b)

Lente

c)

Humulin

d)

Novolog

262.

Long acting insulin is the daily dose of insulin a person takes, basal rate for maintenence. They are used with meals as needed. What are the names?

a)

Insulin Glargine (Lantus)

b)

Protamine Zinc

c)

Detemir (Levemir) (Modified human recombinant)

d)

Ultralente

e)

Humulin(short) and Novolog(rapid)/ NPH and Lente(intermed)

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