ENDO Flashcards

1
Q

what are the general functions of hormones?

A

-homeostasis
-growth & differentiation
-reproduction

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2
Q

which types of proteins are made and then stored?

A

-proteins and polyptide
-amine

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3
Q

which hormones are synthesized on demand?

A

steriod

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4
Q

when do cortisol levels peak?

A

am

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5
Q

when do GH hormone levels peak?

A

at night

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6
Q

which proteins bind to plasma membrane receptors?

A

-polypeptide & protein
-amine

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7
Q

which hormones have tyrosine kinase receptors?

A

insulin and GH

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8
Q

which hormones have GPCRs?

A

beta adrenergic
glucagon
vasopressin
angiotensin II

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9
Q

which hormone types bind to nuclear receptors?

A

steroid & thyroid

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10
Q

which hormones tend to circulate freely (no binding protein)?

A

-amine
-protein and polypeptide

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11
Q

which hormones tend to circulate bound to binding protein?

A

steroid & thyroid

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12
Q

what hormones come from anterior pituitary

A

growth hormone
adrenocorticotropin (ACTH)
thyroid-stimulating hormone
follicle-stimulating hormone
lutenizing hormone
prolactin

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13
Q

what hormones come from posterior pituitary

A

antidiuretic hormone/ vasopressin
oxytocin

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14
Q

where do hypothalamic hormones release?

A

primary capillary plexus in median eminence

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15
Q

what carries hypothalamic hormones to the anterior pituitary

A

hypothalamic-hypophyseal portal blood vessels

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16
Q

what hormones come from hypothalamus

A

thryotropin releasing hormone
gonadotropin releasing hormone
corticotropin releasing hormone
somatostatin
growth hormone releasing hormone
dopamine
prolactin releasing hormone

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17
Q

what stimulates GH release

A

sleep
hypoglycemia
stress (catecholamines)
GHRH
dopamine
excitatory AAs
thyroid hormone
exercise

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18
Q

what inhibits GH release

A

somatostatin
IGF-1
glucose
FFAs
aging

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19
Q

where is the major site of synthesis of IGF-1?

A

liver

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20
Q

actions of GH and IGF-1

A

growth in all tissues
AA uptake
protein synthesis
lipolysis

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21
Q

symptoms of GH excess

A

course facial features
coronary heart disease
diabetes mellitus
thickened skin
kyphosis

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22
Q

oral manifestations of GH excess

A

thick rubbery skin, big nose, thick lips
macrocephaly
macrognathia
disproportionate mandibular growth (prognathism and diastema)
anterior open bite & malocclusion
macroglossia
dyspnea
dysphagia
dysphonia
sialorrhea (excess saliva)
sleep apnea (hypertrophy of pharyngeal and laryngeal tissues)

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23
Q

clinical manifestations of GH deficiency

A

slow linear growth rates
normal skeletal proportions
pudgy, youthful appearance
hypoglycemia (in setting of cortisol deficiency)

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24
Q

oral manifestations of growth hormone

A

small facial appearance
tooth crowding & malocclusion
increased tendency for plaque accumulation
difficulty maintaining oral hygeine
prone to gingivitis & perio disease
solitary median maxillary central incisor
delayed tooth eruption (primary and permanent)

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25
stimuli for ADH
increased blood volume increased osmolarity decreased blood pressure
26
what is the problem with neurogenic diabetes insipidus
low ADH secretion
27
what is the problem with nephrogenic diabetes insipidus
lack of kidney response to ADH
28
what is hypodipsia
decreased or absent feeling of thirst which results in decreased water intake causes hypernatremia (increased ECF NA+)
29
what is syndrome of inappropriate ADH
increased & uncontrolled secretion of ADH causes hyponatremia (decreased ECF Na+)
30
what is the function of pendrin
Cl-/I- ion exchanger (for thyroid hormone production)
31
what is needed to make thyroid hormone
peroxidase and iodine
32
what cleaves T3 and T4 from thyroglobulin for secretion?
proteases
33
how do cells convert T4 to T3 for use
deiodinases (iodinases)
34
what are the broad effects of thyroid hormones
-growth -CNS development -cardiovascular (permissive effect on beta adrenergic receptors) -large effect on metabolism
35
when does TSH secretion peak?
midnight
36
effects of TH on metabolism
-stimulates O2 consumption -increased BMR -stimulate carb metabolism (uptake of glucose, enhances glycolysis & gluconeogenesis, increase rate of carb absorption) -stimulates protein catabolism & synthesis (protein turnover) -stimulates fat metabolism (increased lipid mobilization & oxidation of FA)
37
what is important about the fat metabolism effect of TH
required to convert beta carotene into vitamin A -important for wound healing -hypothyroid pt could appear orange
38
effects of TH on nervous system
-normal development of NS -impacts reflex time
39
effects of TH on cardiovascular system
-increased expression of beta adrenergic receptors -increased blood flow, HR and contractility
40
effects of TH on endocrine system
activation of bone formation --> need for increased PTH secretion
41
effects of TH on GI system
-increased appetite & food intake (BMR) -increased rate of secretion & motility of GI tract
42
what is Grave's disease
*hyperthyroidism* autoimmune disease where antibodies to TSH receptor (thyroid stimulating immunoglobulins) stimulate thyroid gland to excess (causes low TRH and TSH levels)
43
what are the symptoms of hyperthyroidism
-exopthalmos -nervousness, restlessness, insomnia -goiter -tachycardia, palpitations -weight loss & increased appetite -tremor -pretibial myxedema (redness & swelling in pretibial region)
44
what are the oral symptoms of hyperthyroidism
-burning mouth syndrome -gum disease -increased salivation -weakening of mandible -increased caries risk
45
what is Hashimotos thyroiditis
*hypothyroidism* autoimmune rxn against thyroid gland
46
what are symptoms of hypothyroidism
-iodine deficiency=goiter -TSH deficiency= NO goiter -weight gain -lethargy/impaired memory -slow pulse -course/dry brittle hair -loss of lateral eyebrows
47
what is myxedema
seen in severely hypothyroid patients -increased hyaluronic acid and chondroitin sulfate bound with protein and water accumulate in skin
48
what are symptoms of myxedema
-dull, expressionless face -skin appears swollen and pale with increased creases
49
what is cretinism
*hypothyroidism* can be congenital or due to iodine deficient diet -causes physical and mental retardation of neonates -skeletal growth more inhibited than soft tissue
50
what are the oral manifestations of hypothyroidism
-macroglossia -dysgeusia -delayed tooth eruption -poor wound healing -increased risk of infection -increased periodontal disease -salivary gland enlargement
51
what are patients with hypothyroidism sensitive to
CNS depressants ad barbituates
52
what are treatments for osteoporosis
-exercise -estrogen -calcium -vitamin D -bisphosphonates
53
what do chief cells secrete
parathyroid hormone
54
what causes increased PTH secretion
-pregnancy -rickets -lactation
55
what causes decreased PTH secretion
-increased vitD3 intakes -excess quantities of Ca2+ in the diet -bone resorption caused by factors other than PTH
56
what are the functions of PTH to increase plasma calcium
-bone resorption -reabsorption of calcium by renal tubules which reduces excretion -convert precursor into active vitD3, which causes increased intestinal calcium absorption
57
what are the functions of PTH to decrease plasma phosphate
decreased reabsorption by renal tubules leading to increased urinary excretion
58
what 3 organs are necessary for calcitrol (vitD3) activation
-skin -liver -kidneys
59
what are the signs/symptoms of primary hyperparathyroidism
-extreme osteoclastic activity in bones causes cystic bone disease -hypercalcemia leads to polyuria and calcuria -low phosphate due to increased renal excretion -muscle weakness & easy fatigability (due to increased excitability) -high secretion of alkaline phosphatase
60
what does vitD deficiency lead to in children
rickets
61
what does vitD deficiency lead to in adults
osteomalacia (and high PTH)
62
what are the signs/symptoms of primary hypoparathyroidism
-neuromuscular excitability, muscle spasms, and tetany -spasm of laryngeal muscles obstructs respiration
63
what does the adrenal cortex secrete
-corticosteroids -mineralocorticoids -sex hormones