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Pathophysiology > Endocrine Disorders (Exam 3) > Flashcards

Endocrine Disorders (Exam 3) Flashcards

1
Q

How doe endocrine glands get their jobs done?

A

by secreting or releasing hormones into the blood

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2
Q

hormone

A

molecule that acts as a message to convey information

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3
Q

what kind of responses do hormones give off?

A

slower, long acting responses

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4
Q

do hormones affect all cells/tissues?

why?

A

NO!

they reach all parts of the body, but only target certain cells that have receptors to the hormone

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5
Q

where are receptors for water soluble hormones found?

A

on the surface of the target cell, on the plasma membrane

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6
Q

water soluble hormone examples

A

polypeptides
catchecholamines

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7
Q

lipid soluble hormones examples

A

steroids
thyroids

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8
Q

where are lipid soluble hormones found?

A

in the nucleus

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9
Q

water soluble hormone receptors are coupled to

A

various second messenger systems which mediate the action of the hormone in the cell

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10
Q

changes evoked by the actions of secondary messengers are

A

usually rapid

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11
Q

three levels of integration for hormones

A

hypothalamus hormones
anterior pituitary hormones
endocrine targets and the hormones they secrete

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12
Q

hypothalamic hormones

A

regulate anterior pituitary trophic hormones that determine target gland secretion

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13
Q

What does the endocrine system regulate/control?

A

growth and development
male/female reproductive system
energy
level of salts/sugars in the blood

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14
Q

what are the organs that regulate the endocrine system (10)

A

pineal gland
hypothalamus
parathyroid glands
adrenal glands
kidneys
testes/ovaries
pancreas
thyroid gland
pituitary gland

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15
Q

the endocrine glands are located

A

all over the body

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16
Q

pituitary gland

A

master gland
regulates other endocrine glands

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17
Q

thyroid gland

A

metabolism, body heat, bone growth

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18
Q

parathyroids

A

use of calcium and phosphorus

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19
Q

hypothalamus

A

links NS to endocrine system

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20
Q

adrenal gland

A

responses to stress, metabolism, BP, salt balance

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21
Q

pancreas

A

blood sugar

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22
Q

ovaries

testes

A

eggs and female characteristics

sperm and male characteristics

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23
Q

a molecule is only a _____________ when described in the context of its role in an ________________ system

A

hormone

endocrine communication

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24
Q

GH solubility

and hypothalamic releasing factor

A

lipid soluble

GHRH (stimulates)
somatostatin (inhibits)

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25
Q

ACTH solubility

and hypothalamic releasing factor

A

water soluble

CRH (stimulates)

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26
Q

FSH solubility

and hypothalamic releasing factor

A

lipid soluble

GnRH (stimulates)

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27
Q

LH solubility

and hypothalamic releasing factor

A

water soluble

GnRH (stimulates)

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28
Q

TSH solubility

and hypothalamic releasing factor

A

lipid soluble

TRH (stimulates)

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29
Q

PRL solubility

and hypothalamic releasing factor

A

water soluble

DA (inhibits)
TRH (stimulates)

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30
Q

hormones in the hypothalamus

A

PRH
PIH (dopamine)
TRH
CRH
GHRH
GHIH
GnRH

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31
Q

hormones in the anterior pituitary

A

prolactin
TSH
ACTH
GH
FSH
LH

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32
Q

what regulates hypothalamic and pituitary hormones?

A

peripheral hormones feedback

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33
Q

adrenal cortex

A

responsible for secretion of mineralocorticoids, glucocorticoids and androgens

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34
Q

mineralcorticoids

A

aldosterone
maintains sodium and fluid balance

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35
Q

glucocorticoids

A

cortisol
provide the body with the materials needed for energy

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36
Q

androgens

A

testosterone
hyper secretion can cause masculinizing characteristics

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37
Q

regulation of the adrenal hormones is accomplished through

A

adrenocorticotropic hormone (ACTH)

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38
Q

aldosterone secretion is primarily accomplished through

A

RAAS

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39
Q

11 beta hydroxylase defect

A

second most common enzyme defect

excessive production of 11-deoxycorticosterone which in high concentrations in an effective mineralcorticosteroid
aldosterone and cortisol production is greatly decreased

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40
Q

administration of glucocorticoids shuts down _____________ production by inhibiting ______________

A

androgen

ACTH secretion

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41
Q

Congenital Adrenal Hyperplasia

A

genital abnormalities due to deficiencies of the adrenal gland and caused by 21-hydroxylase defects

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42
Q

complications of chronic exogenous corticosteroid use

A

suppressed or quiescent HPA axis
Zona fasciculata atrophy
decreased CRH and ACTH secretion

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43
Q

full recovery of endogenous cortisol secretion may require up to ___________

why?

A

18 months following steroid withdrawal

ACTH has to act for an extended time to restore normal synthetic capacity of adrenal cortex
Cortisol production lags behind restoration of ACTH secretion

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44
Q

posterior pituitary

A

composed mainly of cells called “pituicytes” which act as packing and supporting cells
stores and releases hormones into the close capillaries. Hormones produced in the hypothalamus

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45
Q

where are posterior pituitary hormones produced?

A

in the hypothalamic nuclei

ADH - supraoptic nucleus, 1/6 in PV nuclei
Oxytocin - paraventricular nucleus, 1/6 in S nuclei

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46
Q

which hormones does the posterior pituitary release?

A

antidiuretic hormone/arginine vasopressin

oxytocin

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47
Q

anti diuretic hormone

A

decreases the amount of water lost at the kidneys and elevates BP

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48
Q

increased blood osmolarity or decreased blood volume are sensed in the _________________ and increase ___________ secretion

A

brain or cortex

vasopressin

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49
Q

diabetes insipidus

A

hypo-osmotic polyuria secondary to abnormal synthesis, regulation or renal action of antidiuretic hormone
blocked ADH production

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50
Q

central diabetes insipidus vs nephrogenic diabetes insipidus

A

central - vasopressin deficiency

nephrogenic - vasopressin resistance

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51
Q

oxytocin

A

stimulates contractile cells in mammary glands
stimulates smooth muscle cells in uterus
stimulates myoepithelial cells of breast to contract

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52
Q

oxytocin is responsible for the _________ of milk

A

ejection

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53
Q

factors inhibiting release of oxytocin

A

emotions - stress, fright
drugs and alcohol

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54
Q

factors stimulating release of oxytocin

A

suckling
emotions - sight/sound of a baby’s cry
dilation of cervix

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55
Q

myometrial sensitivity to OT increased by ____________ concentration of which is high in _____________

A

estrogen

pregnancy at the end of pregnancy

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56
Q

what hormone stimulates prolactin secretion?

which one inhibits it?

A

stimulates - thyrotropin releasing hormone

inhibits - dopamine

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57
Q

hyperprolactinemia

A

abnormally high levels of prolactin in the blood
caused by a benign tumor in the pituitary gland

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58
Q

OT/PRL axis

A

PRL stimulates development/growth of mammary glands and milk production during pregnancy

OT causes muscle contraction to expel milk in the breast

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59
Q

secondary hyper secretion due to hypothalamic problem

A

CRH levels - high
ACTH levels - high
Cortisol levels - high

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60
Q

secondary hyper secretion due tov pituitary problem

A

CRH levels - low
ACTH levels - high
cortisol levels - high

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61
Q

primary hyper secretion due to problem with adrenal cortex

A

CRH levels - low
ACTH levels - low
cortisol levels - high

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62
Q

adrenocortical primary insufficiency

A

Addisons disease
autoimmune destruction of the adrenal cortex –> acute adrenal crisis

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63
Q

characteristics of Addisons disease

A

low glucocorticoids, androgen, and mineralocorticoids
low cortisol - hypoglycemia
low aldosterone - hypotension, hyperkalemia
high ACTH secretion

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64
Q

adrenocortical secondary insufficiency

A

caused by deficiency of ACTH

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65
Q

Cushing’s syndrome/disease characteristics

A

high cortisol - hyperglycemia, poor wound healing, central obesity, HTN
high androgen - virilization of women

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66
Q

aldosterone-secreting tumor (Conn’s syndrome) characteristics

A

high sodium reabsorption - HTN
high potassium secretion - hypokalemia

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67
Q

adrenocortical excess examples

A

Cushings syndrome/disease

Aldosterone secreting hormone (Conn’s syndrome)

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68
Q

Addison’s disease leads to ________________ due to uninhibited ________________ from anterior pituitary

A

hyperpigmentation

ACTH release

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69
Q

symptoms of Addison’s disease

A

muscle weakness and fatigue
hypotension
n/v, weight loss, diarrhea
hair loss
hypoglycemia

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70
Q

addison’s disease occurs when a person is exposed to

A

major stresses such as trauma, infection, surgery or major illness

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71
Q

waterhouse-friderichesen syndrome

A

one or both adrenal glands stop working from severe infection
stop producing cortisol

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72
Q

Cushings syndrome

A

hyper secretion of cortisol from adrenal cortex

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73
Q

Cushings Disease

A

hyper secretion of ACTH –> increased release of both cortisol and androgenic hormones

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74
Q

symptoms of adrenocortical excess

A

purple striae
moon face with upper body obesity

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75
Q

growth hormone is produced in the

A

anterior pituitary

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76
Q

Liver can synthesize __________________ to help regulate growth

A

Insulin-like GF-1

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77
Q

growth hormone increases

A

lean growth by increasing rates of muscle protein synthesis and decreasing degredation

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78
Q

GH increases _____________ of fatty acids from _____________

A

lipolysis

adipocytes

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79
Q

using IGF-1, GH increases

A

chondrocyte proliferation and osteoblast activity in bone

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80
Q

the plasma concentration of GH

A

changes with age

(decreases exponentially)

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81
Q

why is plasma measurement of GH problematic?

A

pulsatile release and short half life of GH

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82
Q

GH is highest during

A

strenuous exercise and during sleep

83
Q

dwarfism

A

due to panhypopituitarism during childhood

correct proportions but development is slow

84
Q

does someone with dwarfism go through puberty?

A

No

85
Q

if there is only growth hormone deficiency in dwarfism then

A

sexual maturity occurs

86
Q

african pygmy

A

form of dwarfism

rate of growth hormone secretion is normal/high
inability to form IGF-1

87
Q

giantism cause

A

acidophilic tumors of anterior pituitary before puberty

88
Q

giantism

A

body tissue grow rapidly
hyperglycemia

89
Q

acromegaly cause

A

acidophilic tumor after puberty

90
Q

acromegaly

A

bones, soft tissues become thicker
enlargement of organs
kyphosis

91
Q

metabolic effects of GH on protein metabolism

A

increase protein synthesis
reduces breakdown of cell proteins by decreasing catabolism of protein

92
Q

metabolic effects of GH on fat metabolism

A

increases the concentration of fatty acids

93
Q

metabolic effects of GH on glucose metabolism

A

increase of the blood glucose concentration

(dec uptake of glucose and glucose utilization)

94
Q

low glucose stimulates the release of

A

GHRH (growth hormone releasing hormone)

95
Q

GHRH ________ release of GH which works to ______________

A

increases

raise blood glucose levels to normal

96
Q

high blood glucose stimulates the release of

A

GHIH (growth hormone inhibiting hormone)

97
Q

GHIH __________ release of GH which works to ______________

A

inhibits

lower blood glucose levels to normal

98
Q

high protein intake leads to

A

increased GH, somatomedin and insulin –> no change in caloric storage

99
Q

high carbohydrate intake leads to

A

decreased GH, inc insulin, no change somatomedin –> inc caloric storage

100
Q

fasting leads to

A

inc GH, dec somatomedin and insulin –> inc caloric mobilization

101
Q

if there is an increase in somatomedin, there is

A

an increase in protein synthesis and growth

(direct relationship)

102
Q

two important thyroid hormones

A

thyroxine (T4)
triiodothyronine (T3)

103
Q

the difference between T3 and T4 is that

A

T3 has 3 iodines and T4 has 4 iodines

104
Q

Thyroid hormone is synthesized by

A

tyrosine

105
Q

enzyme that helps in TH synthesis

A

thyroid peroxidase

106
Q

TH synthesis

A

tyrosine –> MIT or DIT –> T3 or T4

107
Q

T4 is converted to T3 by

A

deiodinase

108
Q

which isoform of deiodinase converts T4 to reverse T3?

A

D3 (sometimes D1)

109
Q

which isoform of deiodinase converts T4 to T3?

A

D1 and D2

110
Q

major actions of thyroid hormones

A

increase basal metabolic rates
maintenance of body temp
stimulates rate of cellular respiration
necessary for normal growth and maturation

111
Q

when T3/T4 are decreased, the basal metabolic rate ______________ and carbohydrate metabolism __________

A

decreases

decreases (gluconeogenesis/glycogenolysis)

112
Q

when T3/T4 are increased, the basal metabolic rate ______________ and carbohydrate metabolism __________

A

increases

increases (gluconeogenesis/glycogenolysis)

113
Q

where are thyroid hormones made

A

the thyroid gland duh!

114
Q

size of the thyroid gland depends on

A

age
sex
physiological condition (pregnancy/lactation)

115
Q

which TH is secreted more?

A

T4 (100 mcg/day) —- T3 is only 6!

116
Q

almost all of T4 is

A

converted to T3 in tissues

117
Q

colloid

A

pink staining proteinaceous material in thyroid follicle

118
Q

thyroglobulin (TBG)

A

stores thyroid hormones

119
Q

when the thyroid gland is inactive

A

follicles are large

120
Q

when the thyroid gland is active

A

follicles are small

121
Q

thyroid homeostasis

A

release of TRH -> release of TSH –> release T3 and T4 in follicles –> normal body temperature

122
Q

the half life of TRH is ___________
the half life of TSH is ______________
the thyroid hormone half life is ____________

A

5 min

1 hour

1-7 days

123
Q

thyroid stimulating hormone is a __________ while thyrotropin releasing hormone is a _____________

A

glycoprotein

tripeptide

124
Q

untreated hypothyroidism can contribute to

A

hypertension
dyslipidemia
infertility
cognitive impairment
neuromuscular dysfuntion

125
Q

two most common causes of hypothyroidism

A

hashimotos thyroiditis (developed)
iodine deficiency (developing countries)

126
Q

who is more affected in hypothyroidism?

A

women

127
Q

symptoms of hypothyroidism

A

SLUGGISH
sleepiness
loss of memory
unusually dry skin
goiter
gradual personality
increase in weight
sensitivity to cold
hair loss

128
Q

endemic goiter

A

in iodine insufficient area

129
Q

sporadic goiter

A

in iodine sufficient area

130
Q

how is hypothyroidism related to goiters?

A

dec TH –> inc TSH –> TSH acts on thyroid –> increases blood flow -> stimulates follicular cells and inc colloid production

131
Q

Wolff-Chaikoff effect

A

plasma iodide levels are extremely high (15-20X)

132
Q

Primary hypothyroidism

A

insufficient functioning of thyroid gland
impaired TH synthesis

133
Q

drug mediated inhibition of TH production involved

A

thionamide
amiodarone
lithium

134
Q

severe conditions of primary hypothyroidism is called __________

extreme?

A

myxedema

myxedema coma

135
Q

Hashimoto’s Thyroiditis

A

immune system attacks the thyroid gland causing inflammation
autoimmune

136
Q

secondary hypothyroidism

A

insufficient secretion of TSH

137
Q

tertiary hypothyroidism

A

insufficient secretion of TRH

138
Q

thyroid resistant syndrome

A

organs not responding to T4 and T3
reduced binding affinity for T3 at TR beta

139
Q

diagnostic test for checking thyroid hormones

A

anti-TPO antibody test

140
Q

Allan Herndon Dudley Syndrome

A

X linked mental retardation
manifest with truncal hypotonia, poor head control
mutation in MCT8 (transports TH to neurons)

141
Q

Allan Herndon Dudley syndrome results in

A

high levels of serum T3, low levels of T4 and normal levels of TSH

142
Q

Hyperthyroidism key symptoms

A

apparent bulging of the eyes
rapid heartbeat
nervous excitability

143
Q

primary hyperthyroidism

A

graves disease (autoimmune - mimics effect of TSH)

144
Q

graves disease

A

excessive production of TH
enlarged thyroid gland
exophthalmic goiter

145
Q

99% of calcium is in

A

the bone and teeth

146
Q

after the 3rd decade of life,

A

bone resorption exceeds bone accretion/formation

147
Q

can calcium be synthesized

A

nope

148
Q

calcium balance

A

intake = output

149
Q

positive calcium balance

A

intake > output
occurs during growth

150
Q

negative calcium balance

A

intake < output
leads to osteoporosis

151
Q

nondiffusable plasma calcium

A

40%
bound to albumin

152
Q

diffusible plasma calcium

A

60%
salt form (50% - ionized, 9% complexed)

153
Q

what form of calcium is active

A

ionized calcium

154
Q

acidosis decreases protein binding resulting in

A

increased free calcium levels

155
Q

alkalosis promotes increased protein binding which

A

decreases free calcium levels

156
Q

bone

A

67% - inorganic hydroxyapatite
33% - organic osteoid

157
Q

majority of organic calcium in the bone is

A

type I collagen

158
Q

if free calcium is too low it can lead to

A

neural hyper excitability

159
Q

if free calcium is too high it can lead to

A

neuronal depression

160
Q

control points for calcium

A

absorption in intestines
excretion in urine
temp storage in bone

161
Q

active control of calcium

A

vitamin d3
PTH
calcitonin
skeletal loading

162
Q

phosphate metabolism

A

majority is in the bone
kidneys and bones are primary sites of regulation

163
Q

two forms of inorganic phosphate

A

ECF
ICF

164
Q

calcium phosphate has

A

limited solubility

165
Q

solubility product for calcium phosphate

A

ion calcium x phosphate ion concentration
(constant = 1.36 x 10^-26)

166
Q

if the product of the two ions is greater than SP,

A

you would expect precipitation of calcium phosphate

167
Q

the regulation of plasma calcium levels are critical for

A

normal cell function
neural transmission
membrane stability
bone structure
blood coagulation
intracellular signaling

168
Q

the regulation of plasma calcium relies on

A

interactions with PTH
dietary vitamin D
calcitonin synthesized in the C cells of thyroid gland

169
Q

major sites of regulation for calcium

A

bone
kidney
intestine

170
Q

how is calcium regulated in the bone?

A

vitamin D increases bone reabsorption with a resulting increase of calcium into circulation

171
Q

how is calcium regulated in the kidney?

A

PTH promotes calcium reabsorption and phosphate excretion

172
Q

PTH stimulates the formation of

A

active form of vitamin D

173
Q

how is calcium regulated in the intestine?

A

vitamin D increases absorption of dietary calcium and facilitates renal reabsorption of filtered calcium

174
Q

three ways homeostatic regulation returns blood calcium to normal when it is low

A

kidney saves calcium
digestive tract absorbs calcium (inc PTH)
bones release calcium (dec calcitonin)

175
Q

three ways homeostatic regulation returns blood calcium to normal when it is high

A

kidneys excrete more calcium
digestive tract absorbs less calcium (dec PTH)
bones take up calcium (inc calcitonin)

176
Q

vitamin D

A

steroid hormone when active
has both dietary and endogenous precursors

177
Q

vitamin D2

A

ergocalciferol
from plants from ergosterol

178
Q

vitamin D3

A

cholecalciferol
UV rays from precursor 7-dehydrocholesterol in skin

179
Q

vitamin D promotes

A

intestinal absorption of calcium

180
Q

vitamin D causes synthesis of

A

calcium binding and related facilitated transport

181
Q

it takes ____________ to get a fully developed response from vitamin D

A

a couple of days

182
Q

vitamin D works with

A

PTH to cause calcium absorption from bone

183
Q

principal target of vitamin D and what happens there

A

intestine

stimulates calcium and phosphorus absorption

184
Q

second major target of vitamin D and what happens there

A

bone

provides calcium and phosphate to initiate crystallization of bone osteoid

185
Q

does vitamin D effects the immune system?

if so, how?

A

yes

promotes differentiation of monocyte precursors to monocytes and macrophages

186
Q

what happens in the kidney due to vitamin D?

A

increases renal tubular reabsorption of both calcium and phosphate

187
Q

vitamin D deficiencies due to

A

insufficient dietary intake of vitamin D
inadequate exposure to light
renal and liver disease
severe bone dimineralization

188
Q

vitamin D deficiency due to renal and liver disease

A

inadequate conversion to 25-cholecalciferol and 1,25 - dihydroxycholecalciferol

189
Q

vitamin D deficiency due to severe bone demineralization

A

osteomalacia
rickets

190
Q

PTH release is increased by

A

hypocalcemia
hyperphosphatemia
catecholamines

191
Q

PTH release is suppressed by

A

hypercalcemia
vitamin D
severe hypomangesemia

192
Q

primary hyperparathyroidism

A

excessive production and release of PTH by PT glands

193
Q

secondary hyperparathyroidism

A

defect is outside the PT

194
Q

primary hyperparathyroidism examples

A

chief cell adenoma
PT hyperplasia
PT carcinoma

195
Q

secondary hyperparathyroidism examples

A

severe calcium and vitamin D deficiency
CKD

196
Q

primary hypoparathyroidism

A

too little PTH secretion

197
Q

secondary hypoparathyroidism

A

decreased end organ responsiveness to PTH

198
Q

digeorge syndrome

A

genetic disorder, low PTH
low blood calcium and high phosphorus

199
Q

endocrine disorders result from

A

hormone deficiency
hormone excess
hormone resistance

200
Q

endocrine disruptors

A

exogenous substance that changes endocrine function and causes adverse effects at the level of the organism, its progeny, or population

201
Q

diethylstilbestrol (DES)

A

endocrine disruptor
interrupts the estrogen pathway
used to prevent miscarriages, but would lead to daughters of mothers that took this having them instead

202
Q

why would the same hormone have different effects on target cells?

A

different receptors for the same hormone
different hormones for the same receptor

203
Q

different hormones may have the same effects on target cells if

A

the same receptors for different hormones, leading to target gene expression

204
Q

why would the same hormone have different effects on target cells?

A

different receptors for the same hormone
different signal transduction pathways

Pathophysiology (18 decks)

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