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Endo & Repro block > Drugs > Flashcards

Drugs Flashcards

1
Q

How does the body prevent cortisol from activating the MR receptor?

A

11BHSD converts cortisol to cortisone, which will not bind

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2
Q

What is cross-coupling?

A

Hormone A makes the cell sensitive to hormone B.

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3
Q

Target tissue specificity depends on ___

A

The type and number or receptors in tissues

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4
Q

Hormone receptor specificity refers to

A

ability of a hormone to interact with its receptor but not others

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5
Q

What is spillover?

A

High concentrations of a promiscuous hormone activate another receptor and non-physiologic effects are seen

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6
Q

These hormones are made as preprohormones

A

Peptide class

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7
Q

These hormones circulate free (not bound to plasma proteins)

A

Peptide

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8
Q

These hormones cannot cross the plasma membrane

A

Peptide

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9
Q

These hormones are mainly degraded int he kidney (some liver and lung)

A

Peptide

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10
Q

Where are peptide hormones degraded?

A

Kidney (some liver and lung)

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11
Q

Where are steroid hormones degraded?

A

Liver by cytochrome p450s

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12
Q

These hormones criculate bond to plasma proteins, activity depends on free (not total) concentration

A

Steroid

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13
Q

These hormones are released as soon as they are synthesized

A

Steroid

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14
Q

Steroid hormone that is not released as soon as it is synthesized

A

Thyroid hormone stored as precursor in lumen gland

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15
Q

Why is IGF-1 an exception to its hormone class?

A

It is a peptide hormone that is bound to plasma proteins

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16
Q

Which hormones share an alpha chain?

A

LH, FSH, TSH, hCG

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17
Q

What is the mechanism for pseudohypoparathyroidism type 1b?

A

PTH resistance because of a mutated Gs (no increase in cAMP)

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18
Q

Why do diabetics need more insulin during times of stress?

A

Hormones and cytokines released inhibit secretion and action of insulin

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19
Q

Why will patients with kidney disease develop hyperparathyroidism?

A

Impaired Vit D metabolism (no conversion of 25OHD3 to 1,25OHD3)

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20
Q

Why does aspirin cause hyperthyroid?

A

It displaces the thyroid hormone from its binding protein, increasing free concentration

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21
Q

Why does pregnancy cause hypothyroid?

A

Increased serum globulin proteins cause lower levels of free thryroid hormone

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22
Q

Why do post-menopausal women secrete FSH and LH in their urine?

A

They don’t produce estrogen to generate a negative feedback on FSH and LH production

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23
Q

Explain estrogen’s role in cross-coupling

A

Estrogen increases oxytocin receptors on uterine muscle during late pregnancy (better contractions). Estrogen also activates expression of progesterone receptor.

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24
Q

Glucose transporter in ____ is insulin-independent

A

Liver

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25
Q

Somatotropin

A

GH (human recombinant) SQ
GHD, Turner’s, CKD, AIDS, short
X: malignancy, ICU
SE: SCFE in heavy boys, HTN & headache; edema, arthalgia & carpal tunnel in adults

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26
Q

Octreotide

A

Somatostatin analog (long-lasting) SQ
Acromeg, P-HTN, carcinoid, VIPomas, hyperisulin
SE: gallstones & sludge, GI

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27
Q

Pedvisomant

A

GH variant (pegylated), blocks GHR SQ
Acromegaly
SE: hepatitis, tumor
*cross-reacts with GH is assays (use IGF-1)

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28
Q

Bromocriptine

A

D2 receptor agonist PO
Hyperprolactin, acromegaly, Parkinson’s
SE: GI, orthostasis & syncope, less efficient antipsychotics

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29
Q

Cabergoline

A

D2 receptor agonist PO
Hyperprolactin, acromegaly, PArkinson’s
SE: cardiac valvular lesion @ highdose
*more specific & expensive than bromocriptine

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30
Q

hCG

A

stimulate ovluation, cryptochordism (undescended testes) SQ/IM
acts as LH substitute
Evaluate pregnancy (beta-subunit)
SE: multiples, Ovarian hyperstimulation syndrome (OHSS): hypotension, ascites, pleural effusions, coag abnormalities (risk: high E & >3 big follicles)

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31
Q

Leuprolide

A 
GnRH agonist (long-acting synthetic)  IM
central precocious puberty (no LH/FSH release after single dose), endometriosis (E-dependent), fibroids (E-dependent), prostate cancer (chemical castration)
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32
Q

FSH

A

fertility treatment SQ/IM

Evaluate precocious or delayed pubery

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33
Q

Cosyntropin

A 
ACTH analog (synthetic)
Diagnose 1 vs 2 adrenal insufficiency
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34
Q

GH direct effects

A

Lipolysis, anti-hypoglycemia

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35
Q

GHR is in a family that also includes the

A

EPO and IL receptors (cytokines receptor family)

NO kinase activity

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36
Q

GH-GHR pathway

A

GHR recruites JAK2 kinase, STAT5 phosphorylated, transcription of IGF-1

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37
Q

What is the problem in Laron’s? How are they treated?

A

GHR mutation.

Treat with IGF-1

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38
Q

GH indirect effects (IGF-1)

A

Activation of insulin receptor (high concentrations), lower glucose concentrations

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39
Q

Why dodes IGF-1 have a long half-life?

A

It is associated with IGFBP-3 and ALS

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40
Q

Positive stimulator of GH release?

A

GHRH (+synthesis), protein, hypoglycemia, stress (catelcholamines), sleep, excercise, a-adrenergic (block SST)

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41
Q

Where is GHRH produced?

A

Arcuate nucleus

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42
Q

Negative regulator of GH release?

A

Somatostatin, glucose, FA, b-adrenergics

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43
Q

Where is somatostatin produced?

A

Hypothalamus (widely dispersed)

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44
Q

What is the most common anterior pituitary deficiency?

A

GH

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45
Q

How is the GH feedback loop completed?

A

IGF-1 feeds back to hypothalamus and anterior pituitary to prevent release of GH

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46
Q

Genes implicated in GH defficiency

A

HESx1m PIT1, PROP1 (all needed for pituitary development)

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47
Q

What are some causes of acquired GH deficiency?

A

Brain trauma, GBHS infancy, iatrogenic (after surgery to remove craniopharyngioma)

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48
Q

3 ways to diagnose GH deficiency

A

Arginine: protein (+GH)
Clonidine: a-adrenergic (+GH)
Insulin: hypoglycemia (+GH)

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49
Q

Diagnosing GH excess

A
  • Elevated IGF-1
  • Failure of glucose load to suppress GH
  • MRI for pituitary adenoma
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50
Q

Mechanism of PRL action

A

Similar to GH

Cytokine receptor family, JAK2/STAT5 pathway

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51
Q

Major regulator of PRL

A

Dopamine via D2R (inhibit secretion), secreted by hypothalamus

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52
Q

Why do patients with hypothyroid have excess PRL?

A

TRH activates the PRL receptor at high concentrations and causes lactotroph hypertrophy

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53
Q

Common etiologies for hyperPRL (4)

A
  • Pituitary adenoma
  • antipsychotics (D2R antagonists)
  • 1ry hypothyroid (TRH spillover to PRL-R)
  • PCOS
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54
Q

Which hormones share a very similar beta subunit?

A

LH and hCG

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55
Q

Gonadotrope mechanism of action

A

Gs, AC, cAMP

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56
Q

Which gonadotropins share a receptor?

A

LH and hCG both bind to the LH receptor

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57
Q

FSH function in males and females

A

F: follicle growth, +inhibin, +estrogen
M: Spermatogenesis, +inhibin

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58
Q

FSH targets in males and females

A

F: granulosa cells
M: sertoli cells

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59
Q

LH targets in males and females

A

F: theca, corpus luteum, follicles
M: leydig cells

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60
Q

LH effects in males and females

A

F: +estrogen & progesterone
M: +testosterone

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61
Q

hCG targets & effects in females

A

T: corpus luteum
E: +progesterone

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62
Q

How does FSH stimulate estrogen production in females?

A

Via effects on aromatase (test-est)

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63
Q

Which gonadotropin can exert positive feedback? When?

A

Estrogen during ovulation

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64
Q

Where is GnRH made?

A

Arcuate nucleus of the hypothalamus

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65
Q

How does GnRH stimulate production of LH and FSH?

A

Through GPCRs

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66
Q

What happens if GnRH delivery is constant?

A

The GnRH receptor is down-regulated, less gonadotropin secretion (how long-acting GnHR agonists prevent precocious puberty)

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67
Q

What are negative feedback molecules for gonadotropins?

A

Estrogen, progesterone, testosterone, inhibin

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68
Q

What phase?

Gn stimulate follicles, + estrogen, + endometrium. Gn has small, frequent pulses.

A

Follicular

69
Q

Follicular phase

A

Gn stimulates follicles to make estrogen, which builds up endometrium. Pulses are small and frequent.

70
Q

Ovulation phase

A

Estrogen rises and exerts positive feedback, LH surge causes ovulation, follicle produces corpus luteum, which makes E&P

71
Q

Luteal Phase

A

Progesterone causes vascularization & mucus production in endometrium, feedback causes bigger but less frequent pulses.

72
Q

Fertilization

A

Trophoblasts secrete hCG, +P&E by corpus luteum, >9 wks P&E by placenta

73
Q

Menstration

A

Corpus luteum progresses, no more endometrial support

74
Q

Ganirelix

A

GnRH receptor antagonist
IVF, prostate & breast cancer
Shut off Gn release with no flares seen in GnRH long-term agonists

75
Q

Which are the most common insulin types in pumps?

A

Rapid acting

76
Q

What type of insulin is lispro?

A

Rapid-acting

77
Q

What type of insulin is aspart?

A

Rapid-acting

78
Q

Wahat type of insulin is glulisine?

A

Rapid-acting

79
Q

What type of insulin is regular?

A

Short-acting

80
Q

What type of insulin is NHP?

A

Intermediate-acting (basal)

81
Q

Which is the only insulin that is cloudy?

A

NPH

82
Q

What type of insulin is glargine?

A

Long-acting

83
Q

What type of insulin is Levemir?

A

Long-acting

84
Q

What do gamma or F-cells secrete?

A

pancreatic polypeptide

85
Q

What enzyme processes the preprohormone of insulin itnto disulfide-linked alpha and beta chains?

A

carboxypeptidase

86
Q

What percentage of insulin is released at unproteolyzed proinsulin?

A

6%

87
Q

What is the insulin concentration in the portal blood? In peripheral blood?

A

50-100 uU/mL vs 12 uU/mL

Differential not achieved with insulin therapy

88
Q

What is the earliest defect in T2D?

A

Priming phase of insulin secretion

89
Q

How many units of insulin are released daily from a normal pancreas?

A

20-30

90
Q

Which insulin cannot be combined with any others in a single injection?

A

Glargine and Determir (long-acting basal insulins)

91
Q

When should regular insulin be taken?

A

30 min before a meal

92
Q

When are long-acting insulins given?

A

Once a day, usually at bedtime

93
Q

Why is glargine long-acting?

A

Mutation causes polypeptide soluble at pH 4 but precipitates at physiological

94
Q

Why is determir long-acting?

A

Myristolated which increases self-association and binding to albumin.

95
Q

What is the rule of 15 for correcting hypoglycemia?

A

Injest 15 g of glucose, wait 15 min, repeat.

96
Q

What are the side effects of using insulin therapy?

A

Hypoglycemia, allergic rxns (uncommon), lipoatrophy (immune response), lipohypertrophy (insulin), weight gain, worse retinopathy

97
Q

What is the mechanism of action of sulfonylureas?

A

Stimulate b cell secretion by inhibiting ATP-sensitive K channel. Delivery independent of glucose levels.

98
Q

What are the disadvantages of sulfonylureas?

A

Hypoglycemia, weight gain, sulfa allergies, fail when beta cells fail

99
Q

Glyburide class

A

Sulfonylurea

100
Q

Glipzide class

A

Sulfonylurea

101
Q

Glimepiride class

A

Sulfonylurea

102
Q

Pioglitazone class

A

Thozolidinediones (TZD)

103
Q

How does pioglitazione work?

A

Binds PPARs in fatty tissue and increases insulin sensitivity.Promote differentiation of adipocytes, so fat is stored subq instead of in organs. Also increase iver & muscle sensitivity

104
Q

Advantages of pioglytazione

A

Increases HDL, lower TG, no hypo, may improve fatty liver

105
Q

Disadvantages of pioglytazione

A

Takes weeks, weight gain, worse HF, worse osteo, increases LDL, bladder cancer, p450’s

106
Q

How does metformin work?

A

Improves insulin sensitivity, mainly in liver. Lower glucose output, improve uptake. Slows glucose absorption from gut

107
Q

Advantages of metformin

A

Rapid, no weight gain, no hypo, better lipids

108
Q

Disadvantages of metformin

A

lactic acidosis in renal/liver fail, GI effects when starting, B12 deficiency

109
Q

Metformin class

A

biguanide

110
Q

Liraglutide class

A

GLP-1 analog

111
Q

How does liraglutide work?

A

GLP-1 analog. Incretin effect.Stimulates insulin release and beta cell growth. Suppresses gastric emptying, glucagon secretion & appetite.

112
Q

Liraglutide advantages

A

Only works if glucose is high, increase beta cell mass, weight loss

113
Q

Liraglutide disadvantages

A

Injected, nausea, acute pancreatitis, nto for those with MEN muts of medullary carcinoma of thyroid

114
Q

Sitagliptin mdoe of action

A

DPP-IV inhibitor (less degrade of GLP-1 and GIP)

115
Q

Difference in GLP-1 levels between liraglutide and sitagliptin.

A

Liraglutide has pharmacological concentrations (analog) and sitagliptin had phyisiological concentrations (DPP-IV inhibitor)

116
Q

Sitagliptin advatages

A

Oral, no hypo unless with sulfonylureas, less nausea than liraglutide

117
Q

Sitagliptin disadvantages

A

Not as potent as liraglutide, no weight loss

118
Q

How does canaglifozin work?

A

SGLT2 inhibitor. Lowers renal threshold for glucose=urine glucose loss & osmotic diuresis

119
Q

Advantages of canagliflozin

A

Weight loss, rare hypo, oral, independent of islet cells, improve BP

120
Q

Diadvantages of canagliflozin

A

Need renal function, more genital infections, hypotension, increased LDL

121
Q

Cosyntropin

A

Synthetic ACTH, screening for adrenocortical insufficiency

122
Q

Dexamethasone

A

Gluccocorticoid w/o mineralocorticoid (long-acting)

123
Q

Fludrocortisone

A

Mineralocorticoid (Aldo analog)

124
Q

Hydrocortisone

A

Glucco/mineralocorticoid (short-acting)

125
Q

Fluticasone

A

Gluccocorticoid (nasal spray)

126
Q

Methylprednisolone

A

Gluccocorticoid (intermediate)

127
Q

Prednisone

A

Gluccocorticoid (converted to prednisolone in vivo by HSD11B1, doesn’t work with liver disease, use during pregnancy, intermediate)

128
Q

Prednisolone

A

Gluccocorticoid (use instead of prednisone in liver disease, intermediate)

129
Q

Triamcinolone

A

Gluccocorticoid w/no mineralocorticoid, causes muscle weakness.(intermediate)

130
Q

Long-acting gluccocorticoid with no mineralocoirticoid activity

A

Dexamethasone

131
Q

Intermediate-acting gluccocorticoid with no mineralocorticoid activity

A

Triamcinolone

132
Q

Which zone of the adrenal cortex is not stimulated chronically by ACTH?

A

Zona glomerulosa

  • *ACTH does activate Ald production acutely
  • *region is regulated by AngII & K+
133
Q

Treu androgens are formed in the

A

Periphery. Zona fasciculata makes precursors (DHEA & androstenedione)

134
Q

Will zona glomerulosa aterophy with HP axis failure?

A

No

135
Q

Will zona fasciculata atropy under HP axis failure?

A

yes

136
Q

Steroid synthesis is regulated by trophic hormones via ___, which controls ____

A

cAMP controls flux of cholesterol into mitochondria

137
Q

How does ACTH acutely stimulate aldo production?

A

Via cholesterol delivery

138
Q

How does ACTH stimulate the adrenal gland?

A

Binds to Gs, AC, cAMP (increase P450 SCC and StAR)

139
Q

Which enzyme is responsible for the transfer of cholesterol fom the outer mitochondrial membrane into the inner mitochondrial membrane/

A

StAR

140
Q

Low dose cosyntropin can be used to

A

Secondary adrenal insufficiency

141
Q

High dose cosyntropin test is used to

A

Differentiate enzymatic defects that cause primary adrenal insufficiency

142
Q

What is a good measure of adrenal function because it is only made in the adrenals?

A

DHEA

143
Q

Coricosteroids have __ carbons

A

21

144
Q

Androgens have __ carbons

A

19

145
Q

Only the ___ can feed back on the anterior pituitary to repress ACTH secretion

A

Gluccocorticoids

146
Q

Will changes is plasma proteisna ffect adlo or cortisol levels?

A

Cortisol. Aldo is not mainly bound to proteins.

147
Q

Gluccocorticoids are inactivated in

A

liver

148
Q

What is the function of renin?

A

Converts angiotensinogen to ANGI

149
Q

What is the function of ACE?

A

Converts AngI to AngII

150
Q

Prior to binding, corticosteroid receptors are ina complex with

A

HSP70, HSP90, immunoophilins

151
Q

What receptor family do corticosteroid receptors belong to?

A

Nuclear hormone receptors

152
Q

Aldosterone increases the expression of ___ and ___ in the distal tubule

A

ENaC adnd SGK1 (acitvates ENaC)

153
Q

Name 2 ways that aldo affects K homeostasis.

A
  • Activates Na/K ATPase

- SGK1 activates ROMK

154
Q

Where is the MR found?

A

kidney, sweat glands, salivary glands, exocrine pancreas, GI mucosa

155
Q

What are the effects of gluccos on protein and carb metaolism?

A
  • gluconeogenesis (PEPK in liver)
  • protein catabolism
  • reduce peripheral gluc uptake
  • ## glycogen synthesis (only anabolic effect)
156
Q

effects of gluccos on fat

A
  • lipolysis & fat distribution
  • steroids increase number of enzymes and stimulate FA relase
  • catecholamines increase enzyme activity
157
Q

Effects of gluccos on immune system

A
  • lympho/monocytopenia (distribute from vascular into spleen, lymph and BM)
  • prevent neutrophil adeherence, demargination
  • inhibit chemotactic factors
158
Q

Which is a side effect of triamcinolone?

A

Muscle weakness

159
Q

Which glucco shoudl eb used during pregnancy?

A

prednisone (fetal liver can convert it to active form)

160
Q

Spirinolactone

A

Mineralocorticoid antagonist, treats HTN due to CHF. Also antagonizes angroen and progesterone receptor (hirtuism).

161
Q

Eplerenone

A

More selective mineralocorticoid antagonist.

162
Q

How do antacids affect corticosteroid use?

A

Inhibit oral absorption

163
Q

What are some symptoms of Addisonian crisis?

A

hypoglycemia, hyponatremia, hypotension, weakness, Gi stress, hyperkalemia (late), hyperpigmentation (chronic)

164
Q

What is the treatment for an Addisonian crisis?

A

Fluids and stress-dose gluccocorticoids (will spill over and have mineralo effects)

165
Q

Steroid used for RA

A

Prednisone, triamcinolone in acute cases

166
Q

Steroid used for asthma

A

Fluticasone, methyl-prednisolone for severe

167
Q

Steroid used for cerebral edema

A

dexamethasone

168
Q

Steroid used for ocular disease

A

dexamethasone, or prednisone

169
Q

Steroid used for rashes

A

hydrocortisone, triamcinolone

Endo & Repro block (2 decks)

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