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PHAR123 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the endocrine system responsible for?

A

maintaining homeostasis through the actions of hormones
-release of hormones controlled by nervous system
-nervous system and hormones influence each other by
feedback loops

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2
Q

What are the lipid soluble hormones?

A

steroids

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3
Q

What are the water soluble hormones?

A

amines
proteins
peptides

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4
Q

What are the three factors that determine circulating levels of hormones?

A

synthesis
secretion
transport

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5
Q

How is peptide hormone synthesis controlled?

A

modulating transcription

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6
Q

How is amine and steroid hormone synthesis controlled?

A

regulating enzymes and substrate availability

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7
Q

True or false: precursors to hormones are typically active

A

false
precursors are typically inactive

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8
Q

What is the final step of hormone synthesis?

A

most hormones are created as a larger polypeptide and are converted to a final hormone via an enzyme

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9
Q

What are the manners in which hormones are secreted?

A

exocytosis (when cell receives a specific signal)
diffusion (changed by modification to enzymes or proteins)
pulsatile manner (concentration matters)

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10
Q

What is hormone transport dependent on?

A

affinity of hormone for plasma protein carriers
hormone degradation (all hormones have a T1/2)
availability of receptors (up/down regulation)
receptor binding (hormone must bind for effect)
hormone uptake

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11
Q

In what form will a hormone be able to exert its effect?

A

free-form

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12
Q

What are the functions of hormones binding to proteins?

A

protects hormone from degradation or uptake
allows for fine control over circulating levels
prevents hormone from binding to unintended sites
allows transport of lipid soluble hormones

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13
Q

What are the key hormones?

A

thyroid
cortisol
parathyroid
vasopressin
mineralocorticoid
insulin

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14
Q

What could happen when a hormone binds to cell surface or nuclei?

A

the cell could:
-synthesize new molecules
-change permeability of the membrane
-alter rate of reactions

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15
Q

What are the three types of actions that a hormone can have?

A

permissive: binding allows a different hormone to have its full
effect
synergistic: two hormones act together to achieve a greater
effect
antagonistic: two hormones produce an opposite effect

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16
Q

What do feedback loops allow for?

A

fine control of hormone levels

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17
Q

Explain negative feedback.

A

high level of hormone–>signal to reduce secretion/production
low level of hormone–>signal to increase secretion/production

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18
Q

Explain positive feedback.

A

action of hormone causes more of the hormone to be released

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19
Q

Where is the pineal gland and what does it produce?

A

epithalamus
melatonin

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20
Q

What are the actions of melatonin?

A

produces anti-excitatory effects
peaks at 1-2 yrs of age, stable until puberty then declines
regulates sleep patterns
stimulated by darkness; inhibited by light

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21
Q

What happens if you have high levels of melatonin during childhood?

A

inhibits puberty

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22
Q

What is the role of the hypothalamus?

A

major integrating link between nervous and endocrine system
receives input from cortex, thalamus, limbic system, and other organs
communicates with the pituitary gland to control homeostasis
regulates almost all aspects of growth, development, metabolism, and homeostasis

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23
Q

List off the all the hypothalamus-pituitary gland interactions.

A

growth hormone-releasing hormone–>human growth hormone
thyrotropin-releasing hormone–>thyroid stimulating hormone
gonadotropin-releasing hormone–> FSH and LH
corticotropin-releasing hormone–>adrenocorticotrophic hormone
dopamine–>prolactin (inhibitory)
somatostatin–>TSH and HGH (inhibitory)

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24
Q

Describe human growth hormone.

A

most plentiful anterior pituitary hormone
promotes synthesis of insulin-like growth factor (IGFs)
pulsatile secretion peaks during puberty then declines

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25
Q

Describe regulation of human growth hormone.

A

low blood sugar–>release of GHRH (secrets HGH=glycogen breakdown)
high blood sugar–>release of GHIH (reduces HGH=decreases glycogen breakdown)

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26
Q

Which hormones released from the hypothalamus are inhibitory signals?

A

somatostatin (inhibits HGH and thyroid stimulating hormone)
dopamine (inhibits prolactin)

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27
Q

Describe the thyroid gland.

A

butterfly-shaped in the front of the neck
synthesis, storage, and release of T3 and T4 controlled by TSH
-T3 more potent than T4
-T4 can be converted to T3

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28
Q

What are the cells of the thyroid gland?

A

colloid (synthesis and storage of T3 and T4)
follicular (synthesize calcitonin, help secrete T3 and T4)
parafollicular (no thyroid function)

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29
Q

What is required for the creation of T3 and T4?

A

iodide, thyroglobulin, tyrosine
1. iodide binds with tyrosine attached to thyroglobulin=MIT or
DIT
2. MIT+DIT=T3 or DIT+DIT=T4
3. secreted into circulation

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30
Q

What are the actions of T3 and T4?

A

heart: chronotropic and inotropic
adipose: catabolic
muscle: catabolic
bone: developmental
nervous system: developmental
gut: metabolic
others: calorigenic

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31
Q

Describe the control of T3 and T4 secretion.

A

a negative feedback loop
low levels–>stimulates hypothalamus–>pituitary–>thyroid
lithium (-)
iodide (deficiency= +, excess= -)

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32
Q

Where is the parathyroid gland and what does it produce?

A

posterior surfaces of the lateral lobes of the thyroid
parathyroid hormone (PTH)

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33
Q

What are the actions of PTH?

A

increases blood calcium
-stimulates # + activity of osteoclasts
-increases Ca and Mg reabsorption from urine
-increases calcitriol (increases Ca and Mg absorption)
decreases blood phosphate
-increases excretion

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34
Q

How are the actions of PTH opposed?

A

calcitonin
-inhibits osteoclasts
-decreases reabsorption of Ca from urine
calcium acts on parathyroid gland to reduce PTH

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35
Q

Describe the thymus.

A

in front of heart behind sternum
T cell development

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36
Q

Where are the adrenal glands located?

A

on top of the kidneys

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37
Q

Name each section of the adrenal cortex and what it is responsible for secreting.

A

zona glomerulosa: secretes mineralocorticoids (aldosterone)
zona fasiculata: secretes glucocorticoids (cortisol)
zona reticularis: secretes sex hormones (DHEA and DHEA-S)
medulla: secretes epinephrine and norepinephrine

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38
Q

What is the role of aldosterone?

A

helps regulate blood pressure and electrolyes
sends signal to kidneys to promote Na reabsorption and K excretion

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39
Q

What are the roles of cortisol?

A

widespread effects on the body
regulates the bodys stress response
fat, protein, and carb metabolism
helps regulate the inflammatory response and immune system

40
Q

What is the role of dehydro-epi-androsterone (DHEA) and DHEA-S?

A

protein anabolism and growth
main source of androgens in females (testes are main source for men)

41
Q

What are the roles of norepinephrine and epinephrine?

A

epinephrine:
-increases blood flow to muscles and brain
-conversion of glycogen to glucose
-stimulation of metabolic rate
norepinephrine:
-less potent effect as epinephrine
-main action is vasoconstriction to increase bp

42
Q

How is the adrenal cortex regulated?

A

adrenocorticotrophic hormone stimulates adrenal cortex to release its hormones
-mineralocorticoid secretion is independently controlled by
other factors
all secreted hormones exhibit negative feedback to hypothalamus and pituitary gland

43
Q

What would happen to the inner zones of the cortex in the absence of anterior pituitary and ACTH stimulation?

A

atrophy

44
Q

How is the adrenal medulla regulated?

A

release stimulated by fight or flight response

45
Q

What is the HPA axis?

A

hypothalamic-pituitary-adrenal axis
feedback interaction of the hypothalamus, pituitary, and adrenal glands

46
Q

What are some bodily processes regulated by the HPA-axis?

A

stress response
digestion
immune system
mood and emotions
energy storage and expenditure

47
Q

List off some facts regarding the HPA-axis.

A

normally secretes 10-20mg/d of cortisol
secretions highest in am, decreases throughout day
secretion increases during times of stress
maintains appropriate amounts of glucocorticoids

48
Q

Describe the steps in the HPA-axis.

A

hypothalamus secretes CRH which acts on pituitary
pituitary secretes ACTH which acts on adrenal glands
adrenal glands secrete glucocorticoids (cortisol) or catecholamines
cortisol can have negative feedback on hypothalamus or pituitary

49
Q

Explain how corticosteroids cause negative feedback of CRH and ACTH.

A

exogenous corticosteroids mimic cortisol
the HPA-axis is under negative feedback control by cortisol
thus, corticosteroids suppress the HPA-axis

50
Q

What is the acronym to remember the commercially available corticosteroids?

A

Care (cortisone)
Health (hydrocortisone)
Professionals (prednisone)
Put (prednisolone)
Money (methylprednisolone)
in TD (triamcinolone, dexamethasone)
Bank (betamethasone)
glucocorticoid potency increases as you go down the list, thus greater HPA-axis suppression

51
Q

What are the factors that can predict HPA-axis suppression from corticosteroids?

A

dose
duration
timing of steroid use

52
Q

When is HPA-axis suppression from corticosteroids more likely?

A

maintenance dosing
-equiv dose of 5-15mg of prednisone/day: variable
-equiv dose of >15mg of prednisone/day
when using for >2 weeks
cushingoid appearance

53
Q

When is HPA-axis suppression from corticosteroids less likely?

A

using less than <2 weeks
alternate-day dosing <10mg of prednisone equiv/day

54
Q

How do you taper off of corticosteroids?

A

decrease by set amounts every few days/weeks
decrease by set percentages every few days/weeks

55
Q

What is Cushings Syndrome?

A

a condition characterized by hypercortisolemia due to:
-ACTH-producing pituitary tumor
-ACTH secretion by non-pituitary tumor
-cortisol secretion by adrenal adenoma or carcinoma
-excess glucocorticoid use

56
Q

What is the treatment for Cushings Syndrome?

A

surgery is the treatment of choice
drug therapy is less effective
-ketoconazole
-metyrapone
-mitotane
-pasireotide

57
Q

What is Addisons Disease?

A

primary adrenal insufficiency
autoimmune destruction of all 3 zones of the adrenal cortex

58
Q

What is the treatment of Addisons Disease?

A

daily glucocorticoid and mineralocorticoid replacement
may require stress dosing
perhaps DHEA for women

59
Q

What are the components of the pancreas?

A

acini (secretes digestive enzymes and water)
islets of Langerhans (a cells=glucagon, B cells=insulin, D=somatostatin)

60
Q

Describe insulin regulation.

A

release stimulated by: glucose, amino acids, fatty acids, GLP-1,
ketone bodies, glucagon
release inhibited by: somatostatin, a2 stimulation

61
Q

Describe glucagon regulation.

A

release stimulated by: cortisol, exercise, infections, stressors,
gastrin, insulin
release inhibited by: glucose, somatostatin

62
Q

Describe the roles of the ovaries in the endocrine system.

A

produce+secrete estrogen, testosterone, and progesterone
release stimulated by LH and FSH from pituitary
release inhibited by estrogen during follicular+luteal phase
released inhibited by progesterone during luteal phase
sexual development and reproductive characteristics

63
Q

Describe the roles of the testes in the endocrine system.

A

produce+secrete androgens (mainly testosterone)
release stimulated by LH and FSH from pituitary
release inhibited by testosterone and inhibin
sexual development and reproductive characteristics

64
Q

What are some characteristics of hyperthyroidism?

A

caused by excess synthesis and secretion of thyroid
ranges from mild symptoms to life-threatening
no curative pharmacotherapy available
definitive treatment is radioactive iodine or surgery

65
Q

What are the common causes of hyperthyroidism?

A

toxic diffuse goiter (Graves disease)
toxic multi-nodular goiter (Plummers disease)
acute phase of thyroiditis
toxic adenoma

66
Q

Describe toxic diffuse goiter (Graves disease).

A

more common in younger, female patients (20-50)
most common cause of hyperthyroidism
autoimmune
immune system creates antibodies against TSH receptor
can result in hyperplasia of thyroid gland, leading to a goiter

67
Q

Describe toxic multi-nodular goiter (Plummers disease).

A

most common in older, female patients (>50)
second most common cause of hyperthyroidism
iodine deficiency most common trigger for nodules to grow
develops slowly

68
Q

Describe what happens with iodine deficiency in Plummers disease.

A

iodine deficiency–>less T4–>thyroid cells grow larger (multi-nodular goiter)–>TSH receptors mutate–>continually active

69
Q

Describe toxic adenoma.

A

benign tumors growing on thyroid gland
secreting T3 and T4 but not responding to -ve feedback

70
Q

Describe acute phase of thyroiditis.

A

inflammation and damage to the thyroid gland
damage causes excess hormone to be released
eventually leads to hypothyroidism

71
Q

What are some symptoms of hyperthyroidism?

A

tremor in hands
diarrhea
weight loss
tachycardia
hypertension
anxiety

72
Q

What are the signs and symptoms of toxic diffuse goiter?

A

exophthalmos (proptosis)
peri-orbital edema
diplopia
diffuse goiter
pre-tibial myxedema

73
Q

What are the thioamides?

A

propylthiouracil
methimazole

74
Q

What is the main use of thioamides?

A

reduce severity of hyperthyroidism to prepare a patient for curative therapy

75
Q

What is the MOA of thioamides?

A

inhibits production of T3 and T4 by preventing iodine from incorporating with tyrosine residue on thyroglobulin
inhibits coupling of MIT and DIT
achieved through inhibition of thyroid peroxidase

76
Q

What is the additional action of PTU?

A

inhibits conversion of T4 to T3 by inhibiting 5-deiodinase

77
Q

What is the dosing of thioamides?

A

begin with high initial dose, followed by lower maint doses
titrate every 4-6 weeks
decrease gradually once target reached

78
Q

What are the common adverse effects of thioamides?

A

GI upset
rash
arthralgia

79
Q

What are the serious side effects of thioamides?

A

agranulocytosis (WBC falls to <0.5x10 to the 9)
neutropenia (neutrophil count declines)
hepatoxicity and cholestatic jaundice (resolves once drug is dc)
vasculitis (autoimmune)
polyarthritis (dc drug)

80
Q

How are thioamides handleded during pregnancy?

A

1st trimester–>PTU (low teratogenicity, higher hepatoxicity)
2nd and 3rd trimester–> methimazole (some teratogenicity in 1st trimester, lower hepatoxicity)
either can be used while breastfeeding if doses are low

81
Q

What role do beta-blockers play in hyperthyroidism?

A

reduces symptoms related to cardiac over-stimulation
-palpitations
-tremors
-tachycardias
-anxiety
-heat intolerance

82
Q

Which beta-blockers should be avoided in hyperthyroidism?

A

beta blockers with intrinsic sympathomimetic activity
-pindolol and acebutolol

83
Q

What are the downfalls of the curative options for hyperthyroidism?

A

surgery: permanent hypothyroidism
radioactive iodine: temporary thyroiditis, worsening
hyperthyroidism, followed by
hypothyroidism

84
Q

What is a thyroid storm?

A

rare, life-threatening condition
severe manifestations of hyperthyroidism
patients with untreated hyperthyroidism
triggered by many acute events (surgery, radioactive iodine, trauma, birth, infection)

85
Q

What are some characteristics of hypothyroidism?

A

thyroid hormone deficiency caused by a defect anywhere on the hypothalamic-pituitary-thyroid axis
most via autoimmune thyroiditis (Hashimotos disease)

86
Q

What is Hashimotos disease?

A

most common cause of hypothyroidism
autoimmune disorder where antibodies form and bind to TSH receptors and destroy thyroid cells
antibodies may interfere with T3 and T4 production

87
Q

What are some symptoms of hypothyroidism?

A

fatigue
weight gain
bradycardia
constipation
hypoglycemia

88
Q

What are the treatment options for hypothyroidism?

A

desiccated thyroid
liothyronine
levothyroxine
combined T3/T4

89
Q

Describe desiccated thyroid.

A

first agent available
from thyroid glands of animals
contains T3 and T4
high peak of T3
not well standardized batch to batch

90
Q

Describe liothyronine.

A

contains T3, no effect on T4
wide fluctuations
costly
not routinely recommended

91
Q

Describe levothyroxine.

A

analogue of T4
standard 1st line therapy
half life of 7 days
conversion to T3 regulated by the body

92
Q

What is the dosing for levothyroxine?

A

average dose is 1.6mcg/kg/day
often give 100mcg empirically
starting dose ranges from 12.5mcg/day to max wt based

93
Q

When is it recommended to start low and titrate up for levothyroxine?

A

any CVD
rhythm disturbances
>50 years
long-standing hypothyroidism
titrate up 12.5-25mcg q4-6 wks

94
Q

How should levothyroxine be administered?

A

empty stomach, 30 min before meals or 1 hour after
best in AM

95
Q

What are the side effects of levothyroxine?

A

minimal if dosed properly
-hyperthyroidism symptoms
-cardiac risk increases
-aggravate existing CVD
-BMD reduction

96
Q

What are the drug interactions with levothyroxine? How can we manage these interactions?

A

antacids/H2 blockers/PPIs
iron
calcium/mineral supps
cholestyramine
raloxifene
managed by taking levothyroxine 2h before or 4h after the above

PHAR123 (15 decks)

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