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SUM '20 - Pharm II > Week 4 - Endocrine > Flashcards

Week 4 - Endocrine Flashcards

1
Q

insert image pituitary 1

A

know hormones from pituitary gland and hypothalamus

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2
Q
A

EXAM* ID: -anterior pituitary -Sella turcica of SPHENOID BONE -Hypothalamus - posterior pituitary

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3
Q

Hypothalamus is located at the

A

base of the brain and above the pituitary gland.

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4
Q

Environmental factors that stimulate the hypothalamus to secrete hypothalamic releasing and hypothalamic inhibitory hormones are:

A

Light Temperature Adrenergic and dopaminergic receptors Pain signals Emotions, and Olfactory sensations

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5
Q

the collecting and coordinating center for information and links the central nervous system and endocrine system to the environment

A

Hypothalamus

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6
Q

** EXAM Hypothalamic hormones (releasing or inhibiting) originate in the ______ and control secretions from the _______.

A

originate in the: hypothalamus control secretions from the: anterior pituitary

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7
Q

These hormones travel via hypothalamic hypophyseal portal vessels (undiluted by peripheral blood) to interact with cell membrane receptors in the

A

anterior pituitary.

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8
Q

This increases the intracellular concentrations of calcium ions and ____

A

cyclic adenosine monophosphate (cAMP)

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9
Q

Pituitary Gland: Lies in the

A

sella turcica

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10
Q

sella turcica is at the base of

A

at the base of the brain and is connected to the hypothalamus by the pituitary stalk.

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11
Q

Pituitary gland lies inside or outside the BBB?

A

outside

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12
Q

the pituitary gland is divided into:

A

Divided into 1. anterior pituitary (adenohypophysis) and 2. posterior pituitary (neurohypophysis)

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13
Q

Hypothalamic and pituitary secretion is pulsatile rather than tonic and these pulses are superimposed on broader biologic rhythms such as the:

A
  1. circadian (which releases adrenocorticotrophic hormone (ACTH), 2. HGH -the sleep entrained release of human growth hormone (HGH) 3. Gonadotropins for the monthly cycle of females
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14
Q

anterior pituitary AKA

A

adenohypophysis

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15
Q

posterior pituitary AKA:

A

neurohypophysis

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16
Q

adenohypophysis

A

anterior pituitary

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17
Q

neurohypophysis

A

posterior pituitary

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18
Q

hormone released by circadian rhythm:

A

ACTH (adrenocoritcotrophic hormone)

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19
Q

hormone released during sleep:

A

HGH human growth hormone

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20
Q

hormones released that regulates female mensuration

A

gonadotropins

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21
Q

Anterior Pituitary: Synthesizes, stores, and secretes tropic hormones: (6)

A
  1. ACTH: polypeptide 2. Prolactin: polypeptide 3. HGH: polypeptide 4. (TSH) Thyroid Stimulating Hormone: glycoprotein 5. (LH) Luteinizing Hormone: glycoprotein 6. (FSH) Follicle stimulating hormone : glycoprotein
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22
Q

Anterior pituitary also secretes beta-lipotropin containing the amino acid sequences of several endorphins

A

that bind to opioid receptors.

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23
Q

Posterior Pituitary: Stores and secretes two hormones:

A
  1. Arginine vasopressin (AVP): Formally known as antidiuretic hormone (ADH) 2. Oxytocin
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24
Q

AVP/ADH and Oxytocin are initially synthesized in the _____ and subsequently transported (via axons) to the ___________.

A

-hypothalamus -posterior pituitary

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25
Q

HGH - cell type and principal action Tbl 37-2

A

somatotropes -accelerates body growth; insulin antagonism

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26
Q

Prolactin - cell type and principal action Tbl 37-2

A

Lactotropes -stimulates secretion of milk and maternal behavior inhibits ovulation

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27
Q

LH - cell type and principal action Tbl 37-2

A

gonadotropes stimulates ovulation in females testosterone secretion in males

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28
Q

FSH - cell type and principal action Tbl 37-2

A

gonadotropes - stimulates ovarian follicle growth in females and spermatogenesis in males

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29
Q

ACTH - cell type and principal action Tbl 37-2

A

Adrenocorticotrophic hormone -corticotropes -stimulates adrenal cortex secretion and growth; steroid production

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30
Q

TSH - cell type and principal action Tbl 37-2

A

thyrotropes -stimulates thyroid secretion and growth

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31
Q

Beta-lipopropin - cell type and principal action Tbl 37-2

A

corticotropes -precursor of endorphins

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32
Q

Arginine Vasopressin (AVP) - cell type and principal action Tbl 37-2

A

supraoptic nuclei -promotes water retention and regulates`

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33
Q

oxytocin - cell type and principal action Tbl 37-2

A

paraventricular nuclei -causes ejection of milk and uterine contraction

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34
Q

the Most abundant anterior pituitary hormone:

A

Growth hormone (Somatotropin):

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35
Q

this Stimulates growth of all tissues in the body.

A

GH

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36
Q

GH’s specific effect is stimulation of

A

linear bone growth –resulting from GH action on the epiphyseal cartilage plates of long bones.

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37
Q

Specific effect is stimulation of linear bone growth resulting from GH action on the

A

epiphyseal cartilage plates of long bones.

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38
Q

Excess secretion of GH before epiphyseal closure occurs becomes

A

gigantism

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39
Q

Excess secretion of GH after epiphyseal closure long bones

A

-increase in thickness, not length and -called acromegaly

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40
Q

Metabolic Effect of GH:

A

-Increase rates of protein synthesis (anabolic effect) -Increased mobilization of free fatty acids (ketogenic effect) -Antagonism of insulin action (diabetogenic effect) -Na+ and water retention

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41
Q

STIMULATION of GH results from: Table 37-3

A
  1. stress 2. physiologic sleep 3. hypoglycemia 4. decreased free fatty acid 5. increased amino acid 6. fasting 7. estrogens 8. dopamine 9. Alpha adrenergic agonists
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42
Q

INHIBITION of GH results from: table 37-3

A
  1. Pregnancy 2. Hyperglycemia 3. Increased free fatty acid 4. Cortisol 5. Obesity 6. Insulin-like growth factor 1 (IGF-1)
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43
Q

PERIOP stress and anxiety evokes the release

A

of GH

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44
Q

Plasma concentrations of GH characteristically increase during

A

physiologic sleep

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45
Q

Pregnancy stimulates the release of and

A

prolactin

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46
Q

dopamine inhibits its release

A

prolactin

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47
Q

Drugs may influence the secretion of GH, presumably via effects on the

A

hypothalamus

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48
Q

Large doses of corticosteroids suppress secretion of

A

GH

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49
Q

Dopaminergic agonists acutely increase the secretion of

A

GH

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50
Q

Preop anxiety increases plasma level of

A

prolactin

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51
Q

Prolactin secretion inhibits ovarian function thus may have

A

lack of ovulation and resulting in infertility

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52
Q

LH and FSH responsible for

A

pubertal maturation and secretion of steroid sex hormones by gonads of either sex.

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53
Q

ACTH regulates secretions of cortisol and stimulates formation of cholesterol in the

A

adrenal cortex.

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54
Q

**** the initial building block for corticosteroid synthesis:

A

Cholesterol

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55
Q

****Corticotropin-releasing hormone and ACTH are high in

A

am (~ 20 mcg/dL)

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56
Q

****Corticotropin-releasing hormone and ACTH are low in

A

low (~ 5 mcg/dL) in pm

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57
Q

Surgical incision, reversal of anesthesia, and postop pain stimulate .

A

ACTH release

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58
Q

Secretion of ACTH responds dramatically to stress under the control of corticotropin-releasing hormone from the: (2)

A
  1. hypothalamus, 2. negative feedback mechanism from circulating cortisol
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59
Q

ACTH Absence: The adrenal cortex undergoes

A

atrophy *Zona glomerulosa where aldosterone is secreted is least affected

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60
Q

***the hallmark of hypopituitarism.

A

Pallor is

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61
Q

Hyperpigmentation in presence of adrenal insufficiency from primary adrenal gland disease reflects

A

high concentrations of ACTH in plasma (as the anterior pituitary attempts to stimulate corticosteroid secretion)

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62
Q

high concentrations of ACTH in plasma as the anterior pituitary attempts to stimulate corticosteroid secretion presents as:

A

Hyperpigmentation from primary adrenal gland disease

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63
Q

Chronic administration of corticosteroids suppresses corticotropin-releasing hormone and leads to

A

atrophy of the hypothalamic-pituitary axis

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64
Q

**** Stressful events during the periop might evoke life threatening

A

hypotension

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65
Q

*** to pts considered at risk for suppression of the hypothalamic pituitary axis, what do we need to ensure we do?

A

administer supplemental exogenous corticosteroids

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66
Q

SNS stimulation and corticosteroids suppresses secretion of ____ and diminish _________.

A

TSH activity of thyroid gland

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67
Q

Secretion of TSH from the anterior pituitary is under control of ? from?

A

-thyrotropin-releasing hormone -from the hypothalamus **negative feedback mechanism (depending on the concentration of thyroid hormone circulating in the plasma).

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68
Q

What hormone? Widely distributed in the CNS Potent analeptic (stimulate characteristics) Stimulates respiratory rate Induces tremor Reduces sleep time.

A

thyrotropin-releasing hormone

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69
Q

Thyrotropin-releasing hormone does:

A

(STIMULATES) 1.Widely distributed in the CNS 2. Potent analeptic (stimulate characteristics) 3. Stimulates respiratory rate 4. Induces tremor 5. Reduces sleep time.

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70
Q

***Immunoglobulin A binds to

A

receptor sites on thyroid cells

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71
Q

*** IgA binding mimics effects of

A

TSH and accounts for hyperthyroidism

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72
Q

patients with hyperthyroidism often have detectable circulating concentrations of:

A

IgA proteins bound to thyroid cells

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73
Q

***primary hypothyroidism is

A
  • increased [plasma] TSH -indicative of primary defect at the thyroid gland. - In response, the ANTERIOR PITUITARY stimulates release TSH
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74
Q

*** secondary hypothyroidism is:

A
  • low levels of BOTH TSH and Thyroid Hormones -defect at the hypothalamus or anterior pituitary
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75
Q

**Hypothyroidism with increased plasma concentrations of TSH indicates a primary defect at the thyroid gland and an attempt by the anterior pituitary to stimulate hormonal output by releasing TSH. This is known as

A

primary hypothyroidism

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76
Q

***A defect at the hypothalamus or anterior pituitary is indicated by low concentrations of both TSH and thyroid hormones circulating in plasma and is known as

A

secondary hypothyroidism

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77
Q

Posterior pituitary supports terminal nerve endings of supraoptic and paraventricular nuclei of hypothalamus. Name Hormones of Posterior pituitary:

A
  1. AVP 2. Oxytocin
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78
Q

Arginine Vasopressin (AVP): synthesized in the

A

in the supraoptic nuclei

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79
Q

Oxytocin synthesized in the

A

paraventricular nuclei

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80
Q

Both hormones (AVP/oxytocin) are transported in secretory granules along axons from corresponding nuclei in the hypothalamus to the

A

posterior pituitary -for release when appropriate stimuli arise

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81
Q

Arginine Vasopressin (AVP): Functions include:

A

1-corticotropin secretion 2-vasoconstriction, 3-water retention

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82
Q

Three subtypes of AVP receptors:

A

V1, V2, V3

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83
Q

**V1 : Location - Job - Use -

A
  • vascular smooth muscle - stimulation causes vasoconstriction - vasopressor (hypotension, sepsis, cpr) *DDAVP
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84
Q

**** KNOW V2 : Location - Job - Use -

A

-located on collecting duct cells in kidney - increases REabsorption of water by attaching to receptors on capillary side of epithelial cells lining the: 1.) distal convoluted renal tubules 2.) collecting ducts of the renal medulla

85
Q

V3 : Location - Job - Use -

A
  • AVP binds to these receptors in the adenohypophysis (anterior pituitary) -release corticotropin, -suggesting that this hormone affects the stress response.
86
Q

*** Destructions of neurons in or near the supraoptic and paraventricular nuclei of the hypothalamus from pituitary surgery, cerebral ischemia, or malignancy may decrease vasopressin release to

A

cause central diabetes insipidus **PEE!!!** very dilute

87
Q

If posterior pituitary alone is damaged, will there still be any secretion of AVP?

A

the transected fibers of the pituitary stalk can still continue to secrete AVP

88
Q

Excessive secretion of AVP with subsequent retention of water and dilutional hyponatremia may result from:

A

1.Head injuries 2.Intracranial tumors 3.Meningitis *** 4.Pulmonary infections

89
Q

***** Aberrant production of AVP is observed most commonly in pts with what form of cancer ?

A
  • oat cell carcinoma –> in which the tumor itself produces AVP
90
Q

Secretion of this is stimulated by breast feeding, cervical and vaginal dilation

A

oxytocin

91
Q

oxytocin Binds to G proteins on surface of uterine myocytes to trigger the release

A

of calcium from the sarcoplasmic reticulum, exerting a contracting effect on the pregnant uterus. ** keep in mind this is similar to MOA for MH**

92
Q

Augments the action potential of the uterine smooth muscle?

A

oxytocin

93
Q

Large amounts of oxytocin cause sustained uterine contraction necessary for postpartum

A

hemostasis

94
Q

oxytocin has only 0.5% - 1.0% the antidiuretic activity of ___ and can be released __________.

A

-AVP -abruptly and independently of AVP

95
Q

pitocin availability and mixing

A

10units/ml ~ usually mixing 20u/1000ml for C/S

96
Q
A

Note the 3 lobes “butterfly”: 1. Pyramidal lobe 2. Left lobe 3. right lobe

97
Q

thyroid gland Principal hormone secretions are:

A
  • thyroxine (T4) and triiodothyronine (T3).
98
Q

T4 a prohormone synthesized from

A

tyrosine —> represents 80% of body’s thyroid hormone production

99
Q

T3 is 5 times more active than

A

T4

100
Q

metabolism of T4 and T3 to inactive compounds is done by? where?

A
  • Two distinct deiodases (an enzyme catalyst) - in the liver, kidneys, and CNS
101
Q

T3 is produced directly from:

A
  1. tyrosine metabolism or from 2. conversion of T4 in peripheral tissues
102
Q

Half life of T3 and T4 is:

A

T3 = 1.5 days T4 = 7 days

103
Q

**Both T3 and T4 are highly bound to

A

albumin

104
Q

Thyroid gland also secretes

A

calcitonin which is important for calcium ion use

105
Q

**** Thyroid hormones increase O2 consumption in all tissues except for ? What does this mean?

A

-the brain. -Thus there are minimal changes in anesthetic requirements (MAC) for pts with hyper/hypo thyroid

106
Q

although thyroid hormones may not impact anesthetic needs, what might it impact?

A

cardiac O2 consumption

107
Q

***Earliest clinical manifestations of abnormal thyroid hormone levels are often:

A

Cardiac changes

108
Q

***Absent thyroid hormone decreases O2 consumption

A

40%;

109
Q

*** Excess of thyroid hormones can expand O2 consumption

A

as much as 100%

110
Q

The thyroid receives innervation from the

A

autonomic nervous system

111
Q

The thyroid is two lobes connected by

A

thyroid isthmus

112
Q

the thyroid is highly _____.

A

vascular!! *think of bleeding

113
Q

*** T4 serves principally as a prohormone

A

for T3

114
Q

Thyroid hormones exert most if not all of its effects through

A

control of protein synthesis.

115
Q

Thyroid hormones activate

A

DNA transcription process in the cell nucleus to form new cell proteins and enzymes

116
Q

Been proposed that thyroid hormones modulate conversion of

A

alpha-adrenergic to beta-adrenergic receptors

117
Q

Cardiac cholinergic receptors numbers are decreased by thyroid hormones which is consistent with an increase in HR that is out of proportion to .

A

the increase in C.O

118
Q

Thyroid hormones accelerate metabolism thus tissues vasodilate and as a result CO often increases. There is no increase in ? why?

A

SBP because peripheral vasodilation offsets the impact of more blood flow. **think thyroid storm**

119
Q

calcitonin is a polypeptide hormone secreted by the? it does what? *book

A

thyroid gland - decreases calcium ion concentration in plasma by weakening activity of osteoclasts and strengthening the actiit of osteoblasts.

120
Q

Calcitonin works in the early moments after *flood p 739

A

ingestion of high calcium meals

121
Q

Total thyroidectomy and subsequent absence of calcintonin does not measurably influence the plasma concentration of calcium, b/c of the *flood p 739

A

predominance of parathyroid hormone.

122
Q

PTH and Ca have what kind of relationship?

A

inverse increase of one , decreases the other

123
Q

how many parathyroid glands secrete parathyroid hormone (PTH) that regulate plasma concentration of calcium ions?

A

4

124
Q

Secretion of PTH is inversely related to

A

plasma ionized calcium concentration

125
Q

Small declines in the plasma concentrations of calcium ions stimulate

A

the release of PTH.

126
Q

PTH promotes mobilization of bone calcium (osteoclast) by:

A
  • enhances conversion of vitamin D to its active form to increase GI absorption of Ca (active form of vit d 1,25-dihydroxycholecalciferol)
127
Q

PTH increases renal tubular Ca absorption by:

A

-inhibiting renal reabsorption of phosphate -to increase Ca and to decrease phosphate concentrations in plasma.

128
Q

PTH has targeted effects on:

A

Bones Renal tubules GI

129
Q

Adrenal cortex: Secretes 3 major classes of corticosteroids

A
  1. Mineralocorticoids (aldosterone) 2. Glucocorticoids (cortisol) 3. Androgens
130
Q

**** the precursor of all corticosteroids:

A

Cholesterol is

131
Q

2 important corticosteroids:

A

Aldosterone (mineralocorticoid) Cortisol (principal glucocorticoid)

132
Q

Adrenal cortex has 3 zones:

A

Zona glormerulosa: Zona fasiculata: Zona reticulari **Zona “G.F.R.”

133
Q

** Zona glormerulosa: secretes

A

mineralocorticoids

134
Q

Zona fasiculata: secretes

A

glucocorticoids

135
Q

Zona reticularis: secrete

A

s androgens and estrogens

136
Q

According to the ADA and WHO diabetes is classified by the underlying disease etiology (types 1 or 2)…. how is DM NOT classified?

A

-Not classified by age-of-onset (juvenile vs. adult) -not classified by treatment modality (IDM vs NIDM)

137
Q

Type 1 Diabetes FYI’s:

A

-Onset younger age than type 2 -Sensitivity to insulin is normal -Lack of insulin may precipitate diabetic ketoacidosis

138
Q

Pancreatic beta cell dysfunction leads to

A

type 2 diabetes

139
Q

Type 2 DM distinguishing features:

A
  • peripheral insulin resistance - pancreatic beta cell dysfunction –> failure to secrete insulin
140
Q

ratio of type 1 vs type 2 diabetics

A

1:9

141
Q

Diabetes can be caused by: including table 38-1 *ppt

A

-*Gestation -*Exocrine defects in insulin action and beta cell function (pancreatitis, cystic fibrosis) -*Infections (rubella, CMV) -*Uncommon immune-mediated disorders (“stiff man” syndrom, anti insulin receptor antibodies) - Drug induced (glucocorticoids, thyroid hormone, beta-adrenergic agonists) -Genetic defects in pancreatic Beta cell fxn -Genetic defects in insulin action (resistance)

142
Q

****Most protein used for glucose formation comes from

A

skeletal muscles

143
Q

Liver which is insulin deficient uses fatty acids to produce ketones which can serve as an energy source

A

for skeletal muscle and cardiac muscle.

144
Q

Production of ketones can lead to

A

ketoacidosis;

145
Q

urinary excretion of ketones contributes to

A

electrolyte depletion especially K+. This hypokalemia may go unnoticed d/t intracellular K+ ions are exchanged for extracellular ions to compensate for the acidosis

146
Q

Impacts of Hyperglycemia:

A

-Impairs vasodilation -Induces a chronic proinflammatory, prothrombotic, and proatherogenic state leading to vascular complications -Atherosclerotic vascular, renal and nervous system effects with peripheral vascular disease renal insufficiency and cerebrovascular disease

147
Q

of the hyperglycemia impairments, the greatest relevance for anesthesia are:

A

atherosclerotic vascular, renal and nervous system effects w/PVD, renal insufficiency, and cerebrovascular disease.

148
Q

Symptoms of adverse consequences usually resolve with blood glucose levels less than

A

200 mg/dL

149
Q

A1C measures:

A

long term control of diabetes - 3 month avg -less than 7% are associated with fewer microvascular complications

150
Q

Type 1 Diabetes: Do not produce

A

insulin

151
Q

*** Type 2 Diabetes: Rx insulin when oral glucose regulators fail. Auto antibodies have developed or WHAT have been dysfunctional?

A

Pancreatic beta cells

152
Q

Larger doses of insulin last longer and exert a greater net effect than small doses. The number of insulin receptors seems to be inversely r/t

A

the plasma concentration of insulin

153
Q

Obesity and type 1 diabetes mellitus are associated with fewer

A

insulin receptors

154
Q

Insulin is metabolized in? by?

A
  • kidney and liver -by a proteolytic enzyme
155
Q

**** what % of insulin reaches the liver through the portal vein and is metabolized in a single passage – FIRST PASS

A

~ 50%

156
Q

what effects clearance rate of circulating insulin more ? renal or liver disease?

A

Renal dysfunction effects clearance rate of circulating insulin more so than liver dysfunction/disease

157
Q

in renal disease, what do you what to do to your insulin dosing?

A

decrease it

158
Q

*** Although it has rapid clearance , IV insulin has a pharmacologic effect that lasts for .

A

30-60 minutes - because insulin is tightly bound to tissue receptors

159
Q

***Total units of insulin secretion per day

A

is ~ 40 units

160
Q

***Rate of insulin secretion increases ___ after food intake

A

5-10 fold

161
Q

***Insulin secreted into the portal venous system in the basal state at a rate

A

of ~ 1 unit/hour

162
Q

***SNS and PNS innervate the insulin-producing islet cells to influence : (2)

A

1.basal rate of hormone secretion as well as 2. response to stress.

163
Q

***Alpha adrenergic stimulation to insulin basal secretion

A

decreases basal secretion of insulin

164
Q

***Beta adrenergic or PNS stimulation to insulin basal secretion:

A

increases basal secretion of insulin

165
Q

insulin response to IV Insulin vs oral ingestion - which is greater response to glucose?

A

Oral -b/c glucose dependent insulinotropic polypeptide is released after oral ingestion of glucose and the pancreatic beta cell response is augmented.

166
Q

Type 1 diabetes: usually requires 2 daily SQ injections of

A

intermediate or long acting insulin combined with a rapid acting insulin .

167
Q

manufactured insulin using recombinant DNA to replace beef and pork insulin resulted in decrease in :

A

allergies

168
Q

potency of insulin:

A

22-26U/mg U-100 (100U/mL) is most common commercial preparation

169
Q

Sulfonylureas - FYI’s

A
  • can lower BG to hypogylcemic levels - require some beta cell function - not effective in DM1 - Do not give w/know slufa allergy - m/c : Metformin
170
Q

known for causing vit b12 deficiency:

A

metformin

171
Q

*** ~ 20% of pts with Type 2 DM who begin sulfonylurea therapy do not have an adequate hypoglycemic response to maximal doses - this is known as:

A

(Primary Failure)

172
Q

***Each year an additional 10 – 15% who responded initially , fail to respond to sulfonylurea therapy

A

Secondary Failure)

173
Q

sulfonylurea receptors are found on

A

pancreatic and cardiac cells

174
Q

sulfonylureas inhibit adenosine triphosphate sensitive potassium ion channels (sulfonylurea receptor-1) on

A

pancreatic beta cells

175
Q

after binding to the pancreatic beta cells, what causes the stimulation of exocytosis/ release of insulin storage granules?

A

the an influx of Ca+

176
Q

Oral hypoglycemic are readily absorbed from the

A

GI tract

177
Q

Weakly acidic sulfonylureas circulate bound to ____? what %?

A

protein (primarily albumin) 90-98%.

178
Q

sulfonylureas are metabolized extensively in the

A

liver

179
Q

*** ~ 50% of glyburide is excreted

A

in feces

180
Q

***Most common severe complication of sulfonylureas is

A

hypoglycemia

181
Q

Greatest risk of hypoglycemia occurs with: why?

A

glyburide and chlorpropamide drugs with the longest elimination half times

182
Q

Sulfonylureas can act up to

A

7 days

183
Q

**Hypoglycemia from sulfonylureas may be infrequent, it is often more

A

-prolonged and -more dangerous than hypoglycemia from insulin

184
Q

how do you tx sulfonylurea induced hypoglycemia?

A

prolonged infusion of glucose solution

185
Q

**Risk factors for sulfonylurea induced hypoglycemia:

A

-Impaired nutrition as in periop period -Older that 60 years -Impaired renal function -Concomitant drug therapy that potentiates sulfonylureas (warfarin, and sulfonamide abx) or those that DECREASE blood glucose such as ETOH and salicylates -Renal dz decreases elimination and active metabolites thus increases chance of hypoglycemia

186
Q

Renal dz decreases elimination and active metabolites of sulfonylureas thus

A

increases chance of hypoglycemia

187
Q

-Concomitant drug therapy of what drugs potentiates sulfonylureas ? or Those that DECREASE blood glucose ?

A
  • warfarin, and sulfonamide abx - such as ETOH and salicylates (decrease blood sugar)

Flood. pg 754-potentiates- phenylbutazone, sulfonamide abx, warfarin.

188
Q

Sulfonylureas cross the placenta and can produce

A

fetal hypoglycemia.

189
Q

can sulfonylureas cross the placenta?

A

yes

190
Q

Sulfonylureas close the K-ATP channels and

A

inhibit ischemic preconditioning, a cardioprotective mechanism.

191
Q

for renal patients, what oral drugs are preferable? why?

A

Tolbutamide and Glipizide - only small amounts of drug are excreted unchanged in the urine

192
Q

what event (type?) has been associate with sulfonylureas,

A

CV mortality especially those with prior MI

193
Q

***Sulfonylureas not recommended for pts with liver dysfunction d/t prolongs elimination half time and enhances chance of hypoglycemia except for

A

acetohexamide

194
Q

** acetohexamide is the only sulfonylurea recommended for:

A

for pts with liver dysfunction *it does not increase r/o hypoglycemia

195
Q

Disulfiram-like reactions and inappropriate secretion of arginine vasopressin hormone that results in hyponatremia are…

A

are unique side effects of chlorpropamide

196
Q

** A unique side effect of chlorpropamides

A

-disulfiram like reactions -inappropriate secretion of AVH —> hyponatremia

197
Q

Disulfiram (Antabuse) like reactions:

A

Flushing of skin Tachy Sob n/v Throbbing head ache Visual disturbances Confusion Syncope Circulatory collapse

198
Q

glucagon is a catabolic hormone acting to mobilize

A

glucose fatty acids amino acids into the systemic cirulation

199
Q

principal stimulus for secretion of glucagon is

A

hypoglycemia

200
Q

glucagon abruptly increases the blood glucose concentration by stimulating

A

glycogenolysis in the liver

201
Q

glucagon activates adenylate cyclase for the subsequent fromation of

A

cAMP

202
Q

glucagon undergoes enzymatic degradation to inactive metabolites in the

A

liver and kidneys and at receptor sites in cell membranes

203
Q

**the elimination half time of glucagon is

A

brief: only 3-6 minutes

204
Q

**the longest acting sulfonylurea is

A

chlorpropamide ~ 72hr doa

205
Q

***shortest acting and least potent sulfonylurea is

A

tolbutamide

206
Q

**what sulfonylurea is appropriate for a diabetic patient with gout?

A

actohexamide

207
Q

while taking chlorpropamide-risk factors for development of hyponatremia include: if all these RF are present, the frequency of hyponatremia increases how much?

A
  • > 60 yrs - female gender - concomitant admin of thiazide diuretics ** THREEfold
208
Q

like metformin, this type of drug, act in the presnce of insulin and are especially effective in Obese patients

A

TZDs = thiazolidinediones - tzds tend to decrease triglycerides and increase HDL and LDL levels

209
Q

Amylin agonists (pancreatic beta cells secrete insulin and amylin) do not alter insulin levels they do

A

-suppress gastric emptying -inhibit glucagon release -reduce HbA1C levels

SUM '20 - Pharm II (30 decks)

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