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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the lipid soluble hormones?

A

steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the water soluble hormones?

A

amines
proteins
peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

synthesis
secretion
transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is peptide hormone synthesis controlled?

A

modulating transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is amine and steroid hormone synthesis controlled?

A

regulating enzymes and substrate availability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

True or false: precursors to hormones are typically active

A

false
precursors are typically inactive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

free-form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the key hormones?

A

thyroid
cortisol
parathyroid
vasopressin
mineralocorticoid
insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do feedback loops allow for?

A

fine control of hormone levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Explain negative feedback.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Explain positive feedback.

A

action of hormone causes more of the hormone to be released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where is the pineal gland and what does it produce?

A

epithalamus
melatonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

inhibits puberty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Describe regulation of human growth hormone.
low blood sugar-->release of GHRH (secrets HGH=glycogen breakdown) high blood sugar-->release of GHIH (reduces HGH=decreases glycogen breakdown)
26
Which hormones released from the hypothalamus are inhibitory signals?
somatostatin (inhibits HGH and thyroid stimulating hormone) dopamine (inhibits prolactin)
27
Describe the thyroid gland.
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
28
What are the cells of the thyroid gland?
colloid (synthesis and storage of T3 and T4) follicular (synthesize calcitonin, help secrete T3 and T4) parafollicular (no thyroid function)
29
What is required for the creation of T3 and T4?
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
30
What are the actions of T3 and T4?
heart: chronotropic and inotropic adipose: catabolic muscle: catabolic bone: developmental nervous system: developmental gut: metabolic others: calorigenic
31
Describe the control of T3 and T4 secretion.
a negative feedback loop low levels-->stimulates hypothalamus-->pituitary-->thyroid lithium (-) iodide (deficiency= +, excess= -)
32
Where is the parathyroid gland and what does it produce?
posterior surfaces of the lateral lobes of the thyroid parathyroid hormone (PTH)
33
What are the actions of PTH?
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
34
How are the actions of PTH opposed?
calcitonin -inhibits osteoclasts -decreases reabsorption of Ca from urine calcium acts on parathyroid gland to reduce PTH
35
Describe the thymus.
in front of heart behind sternum T cell development
36
Where are the adrenal glands located?
on top of the kidneys
37
Name each section of the adrenal cortex and what it is responsible for secreting.
zona glomerulosa: secretes mineralocorticoids (aldosterone) zona fasiculata: secretes glucocorticoids (cortisol) zona reticularis: secretes sex hormones (DHEA and DHEA-S) medulla: secretes epinephrine and norepinephrine
38
What is the role of aldosterone?
helps regulate blood pressure and electrolyes sends signal to kidneys to promote Na reabsorption and K excretion
39
What are the roles of cortisol?
widespread effects on the body regulates the bodys stress response fat, protein, and carb metabolism helps regulate the inflammatory response and immune system
40
What is the role of dehydro-epi-androsterone (DHEA) and DHEA-S?
protein anabolism and growth main source of androgens in females (testes are main source for men)
41
What are the roles of norepinephrine and epinephrine?
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
How is the adrenal cortex regulated?
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
What would happen to the inner zones of the cortex in the absence of anterior pituitary and ACTH stimulation?
atrophy
44
How is the adrenal medulla regulated?
release stimulated by fight or flight response
45
What is the HPA axis?
hypothalamic-pituitary-adrenal axis feedback interaction of the hypothalamus, pituitary, and adrenal glands
46
What are some bodily processes regulated by the HPA-axis?
stress response digestion immune system mood and emotions energy storage and expenditure
47
List off some facts regarding the HPA-axis.
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
Describe the steps in the HPA-axis.
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
Explain how corticosteroids cause negative feedback of CRH and ACTH.
exogenous corticosteroids mimic cortisol the HPA-axis is under negative feedback control by cortisol thus, corticosteroids suppress the HPA-axis
50
What is the acronym to remember the commercially available corticosteroids?
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
What are the factors that can predict HPA-axis suppression from corticosteroids?
dose duration timing of steroid use
52
When is HPA-axis suppression from corticosteroids more likely?
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
When is HPA-axis suppression from corticosteroids less likely?
using less than <2 weeks alternate-day dosing <10mg of prednisone equiv/day
54
How do you taper off of corticosteroids?
decrease by set amounts every few days/weeks decrease by set percentages every few days/weeks
55
What is Cushings Syndrome?
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
What is the treatment for Cushings Syndrome?
surgery is the treatment of choice drug therapy is less effective -ketoconazole -metyrapone -mitotane -pasireotide
57
What is Addisons Disease?
primary adrenal insufficiency autoimmune destruction of all 3 zones of the adrenal cortex
58
What is the treatment of Addisons Disease?
daily glucocorticoid and mineralocorticoid replacement may require stress dosing perhaps DHEA for women
59
What are the components of the pancreas?
acini (secretes digestive enzymes and water) islets of Langerhans (a cells=glucagon, B cells=insulin, D=somatostatin)
60
Describe insulin regulation.
release stimulated by: glucose, amino acids, fatty acids, GLP-1, ketone bodies, glucagon release inhibited by: somatostatin, a2 stimulation
61
Describe glucagon regulation.
release stimulated by: cortisol, exercise, infections, stressors, gastrin, insulin release inhibited by: glucose, somatostatin
62
Describe the roles of the ovaries in the endocrine system.
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
Describe the roles of the testes in the endocrine system.
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
What are some characteristics of hyperthyroidism?
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
What are the common causes of hyperthyroidism?
toxic diffuse goiter (Graves disease) toxic multi-nodular goiter (Plummers disease) acute phase of thyroiditis toxic adenoma
66
Describe toxic diffuse goiter (Graves disease).
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
Describe toxic multi-nodular goiter (Plummers disease).
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
Describe what happens with iodine deficiency in Plummers disease.
iodine deficiency-->less T4-->thyroid cells grow larger (multi-nodular goiter)-->TSH receptors mutate-->continually active
69
Describe toxic adenoma.
benign tumors growing on thyroid gland secreting T3 and T4 but not responding to -ve feedback
70
Describe acute phase of thyroiditis.
inflammation and damage to the thyroid gland damage causes excess hormone to be released eventually leads to hypothyroidism
71
What are some symptoms of hyperthyroidism?
tremor in hands diarrhea weight loss tachycardia hypertension anxiety
72
What are the signs and symptoms of toxic diffuse goiter?
exophthalmos (proptosis) peri-orbital edema diplopia diffuse goiter pre-tibial myxedema
73
What are the thioamides?
propylthiouracil methimazole
74
What is the main use of thioamides?
reduce severity of hyperthyroidism to prepare a patient for curative therapy
75
What is the MOA of thioamides?
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
What is the additional action of PTU?
inhibits conversion of T4 to T3 by inhibiting 5-deiodinase
77
What is the dosing of thioamides?
begin with high initial dose, followed by lower maint doses titrate every 4-6 weeks decrease gradually once target reached
78
What are the common adverse effects of thioamides?
GI upset rash arthralgia
79
What are the serious side effects of thioamides?
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
How are thioamides handleded during pregnancy?
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
What role do beta-blockers play in hyperthyroidism?
reduces symptoms related to cardiac over-stimulation -palpitations -tremors -tachycardias -anxiety -heat intolerance
82
Which beta-blockers should be avoided in hyperthyroidism?
beta blockers with intrinsic sympathomimetic activity -pindolol and acebutolol
83
What are the downfalls of the curative options for hyperthyroidism?
surgery: permanent hypothyroidism radioactive iodine: temporary thyroiditis, worsening hyperthyroidism, followed by hypothyroidism
84
What is a thyroid storm?
rare, life-threatening condition severe manifestations of hyperthyroidism patients with untreated hyperthyroidism triggered by many acute events (surgery, radioactive iodine, trauma, birth, infection)
85
What are some characteristics of hypothyroidism?
thyroid hormone deficiency caused by a defect anywhere on the hypothalamic-pituitary-thyroid axis most via autoimmune thyroiditis (Hashimotos disease)
86
What is Hashimotos disease?
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
What are some symptoms of hypothyroidism?
fatigue weight gain bradycardia constipation hypoglycemia
88
What are the treatment options for hypothyroidism?
desiccated thyroid liothyronine levothyroxine combined T3/T4
89
Describe desiccated thyroid.
first agent available from thyroid glands of animals contains T3 and T4 high peak of T3 not well standardized batch to batch
90
Describe liothyronine.
contains T3, no effect on T4 wide fluctuations costly not routinely recommended
91
Describe levothyroxine.
analogue of T4 standard 1st line therapy half life of 7 days conversion to T3 regulated by the body
92
What is the dosing for levothyroxine?
average dose is 1.6mcg/kg/day often give 100mcg empirically starting dose ranges from 12.5mcg/day to max wt based
93
When is it recommended to start low and titrate up for levothyroxine?
any CVD rhythm disturbances >50 years long-standing hypothyroidism *titrate up 12.5-25mcg q4-6 wks*
94
How should levothyroxine be administered?
empty stomach, 30 min before meals or 1 hour after best in AM
95
What are the side effects of levothyroxine?
minimal if dosed properly -hyperthyroidism symptoms -cardiac risk increases -aggravate existing CVD -BMD reduction
96
What are the drug interactions with levothyroxine? How can we manage these interactions?
antacids/H2 blockers/PPIs iron calcium/mineral supps cholestyramine raloxifene managed by taking levothyroxine 2h before or 4h after the above