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ENDO > 181 Pharmacology > Flashcards

181 Pharmacology Flashcards

1
Q

What drug is a synthetic long acting analog of vasopressin?

A

desmopressin

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2
Q

What is the mechanism of vasopressin?

A

binds to GPCR –> V1/Gq activates phospholipase C, V2/Gs activates cAMP

phospholipase C causes calcium influx, leading to vasoconstriction

cAMP leads to increased water permeability and water resorption in the collecting duct

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3
Q

How are vasopression and its analogs metabolized?

A

metabolized through hepatic and renal metabolism

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4
Q

What are the major therapeutic uses of vasopressin and desmopressin?

A

treat central diabetes insipidus and to stop bleeding (vasopressin for esophageal varices, desmopressin for hemophilia and von willebrand’s disease)

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5
Q

What are the major adverse effects of vasopressin and analogs?

A

uterine rupture and fetal distress at high doses

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6
Q

Growth hormone secretion is stimulated by _________ and inhibited by _________.

A

Growth hormone secretion is stimulated by GNRH and inhibited by somatostatin.

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7
Q

What analogs of growth hormone are used pharmacologically?

A

somatotropin and somatatrem

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8
Q

What is the mechanism of growth hormone?

A

acts on a tyrosine kinase membrane receptor –> activates JAK and STAT

also works through IGF-1

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9
Q

What are the therapeutic uses of growth hormone analogs?

A

growth hormone deficiency in children, short stature in children, Turner syndrome, Prader Willi syndrome, chronic renal insufficiency, idiopathic short stature, AIDS-associated wasting, malabsorption (due to short bowel)

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10
Q

What are the adverse effects of growth hormone analogs?

A

arthralgias, myalgias, carpal tunnel syndrome, slipped epiphyses, scoliosis progression, intracranial hypertension

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11
Q

What are clinically used IGF-1 analogs? What is it used for?

A

mecasermin –> promotes growth and normalizes metabolism in cases of IGF-1 deficiency

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12
Q

What are the adverse effects of mecasermin?

A

hypoglycemia, lipohypertrophy

mecasermin = IGF-1 recombinant form

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13
Q

What are clinically used growth hormone antagonists?

A

octreotide –> analog of somatostatin (inhibitor of growth hormone secretion)

pegvisomant –> growth hormone receptor antagonist

bromocriptine and cabergoline –> mimics of dopamine with D2 selectivity

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14
Q

What hormones have secretion inhibited by somatostatin?

A

growth hormone, thyroid stimulating hormone, glucagon, gastrin, insulin

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15
Q

What are the adverse effects of octreotide?

A

nausea, bloating, bradycardia

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16
Q

What is pegvisomant used for?

A

used to treat acromegaly

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17
Q

What are the adverse effects of pegvisomant?

A

increase in LFTs, worsening of growth hormone secreting adenomas, compulsive behaviors

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18
Q

What are the adverse effects of bromocriptine and cabergoline?

A

nausea and vomiting, headache, orthostatic hypotension, headache, nasal congestion, vasospasm, hallucinations, psychoses, nightmares, insomnia

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19
Q

What is the mechanism of thyroid hormones?

A

nuclear receptors and phosphatidylinositol-3-kinase receptors

nuclear –> activate transcription factors and gene expression

also provide feedback inhibition at the hypothalamus and pituitary

20
Q

How are thyroid hormones metabolized?

A

metabolized in the liver by deamination, decarboxylation, glucuronide/sulfate conjugation

21
Q

What are the therapeutic uses of thyroid hormone?

A

to treat hypothyroidism (ex. Hashimotos)

22
Q

What are the adverse effects of therapeutic thyroid hormone?

A

headaches, weight loss, diarrhea, anxiety, palpitations, angina, coronary and cerebral thromboses

basically hyperthyroidism

23
Q

What agents are used to treat hyperthyroidism?

A

radioactive iodine, thionamides (ex. propylthiouracil and methimazole), sympatholytic agents (like beta blockers), iodides (ex. potassium iodide)

24
Q

What is the mechanism of thionamides?

A

enzymes preferentially iodinate the drugs, reducing the amount of activated thyroid hormone

25
Q

What are side effects of thionamides?

A

dermatits, hepatitis, arthralgias, lymph node enlargement, agranulocytosis

26
Q

What is the mechanism of glucocorticoids?

A

they interact with receptors in the cytoplasm, leadign to release of heat shock protein –> leads to translocation of ligand bound receptors to the nucleus

27
Q

What are the metabolic actions of glucocorticoids?

A

liver –> production and conservation of glucose through increased gluconeogenesis (insulin antagonist) and increased glycogen synthesis

connective tissue –> decreased synthesis and increased breakdown of proteins

adipose tissue –> fat redistribution, truncal obesity

28
Q

What are the actions of glucocorticoids on the kidneys, immune system, GI, CNS, and stress response?

A

kidney –> Na retention, K excretion, H excretion, Ca excretion

Immune –> decreased antibodies, antigen processing, lymphocytes, and inflammatory reaction

GI –> thinning mucosa, increased acid/pepsin, decreased Ca absorption

CNS –> euphoria, depression, sleep disturbances, psychoses

stress response –> increased CO, increased GFR

29
Q

What is the mechanism of mineralocorticoids?

A

they act on epihelial tissues involved in electrolyte transport, leading to increased trans-epithelial NaCl transport and increased lumen-negative trans-epithelial voltage –> driving force for potassium and hydrogen ion movement into the tubular lumen

30
Q

What are the major uses of glucocorticoids for replacement therapy?

A

chronic hypoadrenalcorticism (Addison’s disease) - with mineralocorticoids

loss of adrenal function - with salt and water replacement

treatment of congenital adrenal hyperplasias

31
Q

_____________ deficiency is treated by mineralocorticoid and glucocorticoid replacement, ____________ deficiency is treated with only glucocorticoids.

A

21-hydroxylase deficiency is treated by mineralocorticoid and glucocorticoid replacement, 11-hydroxylase deficiency is treated with only glucocorticoids.

32
Q

What is the mechanism of mifepristone?

A

it blocks glucocorticoid receptors and is a progestin antagonist

used to treat hyperglycemia in patients with hypercortisolism and type 2 diabetes

33
Q

Which drugs are glucocorticoids synthesis inhibitors?

A

metyrapone - inhibits 11-hydroxylase

ketoconazole - blocks several steps of pathway

aminoglutethimide - blocks cholesterol side chain cleavage

Mitotane

used to treat adrenal hyperfunction (ex. adrenocorticol carcinoma)

34
Q

What are the possible outcomes of an ACTH test?

A

positive –> suggests that the deficiency is from inadequate ACTH from the pituitary

negative –> suggests that the deficiency is from primary adrenal insufficiency

35
Q

What is the utility of a metyrapone test?

A

it assesses the extent to which the pituitary can be stimulated in the case of pituitary stimulation problems

36
Q

How can dexamethasone be used to assess adrenal hyperfunction?

A

it is a glucocorticoid that elicits feedback inhibition of pituitary ACTH - used to determine if high cortisol/metabolites derive from a supressible or non-supressible source

37
Q

What is the mechanism of the anti-inflammatory and immunosuppressive activity of glucocorticoids?

A

inhibition of synthesis of prostaglandins and proinflammatory cytokines

also decrease the numbers of immune cells

38
Q

What are the major side effects of glucocorticoids?

A

hypokalemic alkalosis, glycosuria (diabetogenic), susceptibility to infection, ulcers, myopathy, osteoporosis, hypercoagulability, psychoses, glaucoma, reproductive disturbances, adrenal insufficiency

39
Q

Octreotide:

a) inhibits secretion of growth hormone
b) is an antagonist peptide analog of growth hormone
c) is a dopamine receptor analog that inhibits secretion of hypothalamic hormones
d) acts through tyrosine kinase-linked receptors
e) side effects include stimulation of secretion of glucagon and gastrin

A

a) inhibits secretion of growth hormone

octreotide is an analog of somatostatin

40
Q

All of the following are symptoms of excessive thyroid hormone except:

a) elevated heart rate
b) decreased TSH
c) increased glycogenolysis
d) increased basal metabolic rate
e) increased cholesterol

A

e) increased cholesterol

thyroid hormone lowers cholesterol

41
Q

Prednisone has the advantage over hydrocortisone that prednisone:

a) is less likely to increase blood glucose
b) doesn’t suppress the immune response
c) has a longer duration of action
d) is orally effective
e) has greater glucocorticoid/mineralocorticoid activity

A

e) has greater glucocorticoid/mineralocorticoid activity

the glucocorticoid/mineralocorticoid ratio for prednisone is 5X that for hydrocortisone

42
Q

Which of the following is true?

a) vasopressin decreases the fluid volume in the circulation
b) thiazide diuretics are used to treat central diabetes insipidus
c) desmopressin activates V1 receptors more potently than V2 receptors
d) both oxytocin and vasopressin are polypeptides with 9 amino acid residues

A

d) both oxytocin and vasopressin are polypeptides with 9 amino acid residues

43
Q

Which of the following is true?

a) GH stimulates metabolism of IGF-1 in the liver
b) Mecasermin is an IGF-1 antagonist
c) Somatostatin is a physiological inhibitor of GH secretion
d) Cabergoline inhibits GH production via somatostatin receptor

A

c) Somatostatin is a physiological inhibitor of GH secretion

44
Q

Which of the following is true about therapy for hyperthyroidism?

a) Methimazole inhibits peripheral conversion of T4 to T3
b) 131-I kills follicular cells by beta emission
c) Dose of methimazole should be increased when treating pregnant hyperthyroid patients
d) KI suppresses thyroid function by inhibiting peripheral conversion from T4 to T3

A

b) 131-I kills follicular cells by beta emission

45
Q

Which of the following is true?

a) Addison’s disease is treated with glucocorticoids only
b) 11-hydroxylase deficiency is treated with mineralocorticoids
c) dexamethasone test is used to determine etiology of adrenal hyperfunction
d) steroid withdrawal syndrome results from chronic excess of ACTH synthesis

A

c) dexamethasone test is used to determine etiology of adrenal hyperfunction

ENDO (19 decks)

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