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endocrine Flashcards

1
Q

what are hormones?

A

they are chemical messengers produced by endocrine glands and they regulate metabolic function of the cells in our body

elicits a specific response in distant target tissues

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2
Q

how are hormones transported to target cells?

A

by the circulation or blood at a very low concentration

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3
Q

how does hormone work on target cells?

A

the hormone enters the blood stream and is distributed throughout the entire body and there are receptors on tissues for example on skeletal muscle tissue then when the hormones get there binding occurs and hormonal effects appear

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4
Q

what are the 4 major chemical classes of hormones?

A

amines

peptides

glycoproteins

steroids

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5
Q

what are amine hormones?

A

they include:

catecholamines (dopamine, epi and norepi)

thyroid hormones(T3 & T4) and melatonin

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6
Q

amine hormones are derived from?

A

amino acid called tyrosine and tryptophan

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7
Q

amine hormones are secreted by?

A

adrenal medulla, thyroid and pineal glands( melatonin)

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8
Q

____are the largest group of hormones?

A

peptide hormones

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9
Q

where are peptide hormones synthesized in?

A

in the rough endoplasmic reticulum of endocrine cells as an inactive preprohormones

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10
Q

list peptide hormones

A

hypothalamus: all releasing hormones

pituitary gland: ACTH, GH, MSH, ADH, prolactin and oxytocin

pancreas: insulin and glucagon

parathyroid gland: parathyroid hormone

C cells of the thyroid gland: calcitonin

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11
Q

what are glycoprotein hormones?

A

they contain long polypeptide bound to one or more carbohydrate groups

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12
Q

list glycoprotein hormones

A

TSH

FSH

LH

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13
Q

where does steroid hormones come from?

A

they are synthesized from cholesterol

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14
Q

list steroid hormones

A

cortisol

aldosterone

testosterone

estrogen

progesterone

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15
Q

features of steroid hormones?

A

they are not stored in vesicles and rapidly diffuse out of the cell once they are synthesized due to their high lipid solubility

they require carrier proteins in the blood due to their low water solubility

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16
Q

what are other organs that produce hormones?

A

placenta: HCG or human chorionic gonadotropin

heart: ANP or atrial natriuretic peptide

stomach: gastrin

small intestine: CCK, secretin

kidney: renin, 1-25-dihydroxycholecalciferol and erythropoietin

fat cells/ adipose tissue: leptin or adipokines

GIT: ghrelin

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17
Q

what does hCG do?

A

it maintains corpus luteum early in pregnancy

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18
Q

what does atrial natriuretic peptide do?

A

it reduces blood pressure, blood volume and blood sodium concentration
it also increases renal Na+ excretion

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19
Q

what does gastrin do?

A

it stimulates HCl secretion by parietal cells of gastric mucosa

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20
Q

what does CCK do?

A

it stimulates release of pancreatic enzymes
contracts gallbladder
relaxes sphincter of oddi
inhibits stomach motility or delay gastric emptying

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21
Q

what does secretin do?

A

increases fluid and HCO3 secretion by pancreatic duct
feedback inhibition of gastric H+ secretion

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22
Q

what does renin do?

A

it cleaves circulating angiotensinogen to angiotensin I

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23
Q

what does 1-25-Dihydroxycholecalciferol do?

A

it stimulates gastrointestinal Ca2+ and phosphate absorption

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24
Q

what does erythropoietin do?

A

it stimulates RBC production

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25
Q

what does leptin do?

A

it activates satiety center of hypothalamus which suppresses appetite

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26
Q

what does ghrelin do?

A

it activates hunger center of the hypothalamus which stimulates appetite

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27
Q

where is the receptors for steroids hormone located?

A

in cytoplasm

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28
Q

where is the receptor for thyroid hormones located?

A

on the nucleus

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29
Q

where is the receptor for protein, peptide and catecholamines hormones located?

A

on the surface of cell membrane

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30
Q

true or false: hormones can act directly on target cells

A

false, hormones never act directly they need to combine with specific receptors

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31
Q

what are receptors?

A

they are large protein molecules and they are present either on the surface of cells or inside a cell like the cytoplasm or in nucleus

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32
Q

cells give a response to a particular hormone if only there’s—?

A

if only there’s specific receptors for that hormone

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33
Q

what are first messengers?

A

are extracellular factors, often hormones or neurotransmitters, such as epinephrine, growth hormone, and serotonin

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34
Q

the binding of a hormone to it’s receptor causes the generation of intracellular signaling molecules called___

A

second messengers

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35
Q

what are second messengers

A

are intracellular signaling molecules released by the cell in response to exposure to extracellular signaling molecules—the first messengers.

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36
Q

what does second messengers do?

A

they amplify the hormonal signal within the target cells

-> they trigger physiological changes at cellular level such as proliferation, differentiation, migration, survival, apoptosis and depolarization.

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37
Q

second messengers use___ to bring changes in cellular activity

A

the stimulation of kinases

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38
Q

what are kinases?

A

they are enzymes that phosphorylate target proteins

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39
Q

list common second messengers

A

cAMP
DAG and IP3
cGMP
Ca2+

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40
Q

explain how cAMP is a second messenger

A
  1. the hormone receptor complex associates with intracellular heterotrimeric G proteins
  2. this combination activates adenylyl cyclase protein enzyme which is also located in the membrane also but a large portion of it protrudes in the cytoplasm
  3. the activated adenylyl cyclase convert ATP into cAMP
  4. cyclic AMP activates cytoplasmic protein kinases
  5. activated protein kinases which affects cellular activity through phosphorylation of the effector proteins

the cAMP signal is terminated when cAMP is broken down by the action of a phosphodiesterase enzyme

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41
Q

what does hypothalamus do?

A

->it receives signals from almost all sources in NS
->it acts as a collecting center for internal body
informations
->it control secretion of pituitary gland hormones

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42
Q

what controls the pituitary gland?

A

by releasing hormones of the hypothalamus
and by target hormones which is negative FB system

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43
Q

why is the pituitary called the master gland

A

because it control different peripheral target glands

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44
Q

what is the hypothalamic pituitary axis?

A

is an intricate pathway with a central role in maintaining homeostasis by integrating complex physiological and endocrine inputs, and neuronal and hormonal output

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45
Q

___is a well studied interface between the nervous system and endocrine system

A

hypothalamic pituitary axis

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46
Q

what are the organs that are directly or indirectly affected by the axis?

A

reproduction
growth
lactation
stress response
metabolism
water balance
immune system

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47
Q
A
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48
Q

what are the 2 connections of the hypophyseal pituitary axis?

A

vascular connection and neural connection

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49
Q

which has organ has vascular connection?

A

the anterior pituitary lobe

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50
Q

which organ has a neural connection?

A

the posterior pituitary lobe

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51
Q

the vascular connection is between?

A

the hypothalamic and the hypophyseal portal circulation

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52
Q

what does the vascular connection in anterior pituitary lobe do?

A

hormonal regulation by releasing hormones of the hypothalamus and by feedback from the target gland hormones

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53
Q

the neural connection is between?

A

the hypothalamic and the hypophyseal tract

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54
Q

the neural connection is regulated by?

A

the neuroendocrine reflex

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55
Q

the hormones secreted by the anterior pituitary are called?

A

trophic hormones

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56
Q

high anterior pituitary hormones cause their target organs to be___

A

hypertrophy

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57
Q

low concentration of anterior pituitary hormones cause their target organs to be___

A

atrophy

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58
Q

GH is released from?

A

somatotroph cells of the anterior pituitary glands

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59
Q

what does GH control of release?

A

GHRH+ and GHIH- of the hypothalamus

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60
Q

what is the target organ of GH?

A

most tissues

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61
Q

what are the actions of GH?

A

-> it stimulates protein synthesis and cell growth via somatomedins or IGF-1 released from liver
-> lipolysis and increased blood glucose
-> it causes growth of all tissues
-> it promotes hypertrophy and hyperplasia

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62
Q

how does GH promotes overall tissues and organ growth?

A

by promoting the movement of amino acids into cells and the incorporation of these amino acids into proteins

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63
Q

linear growth occurs indirectly through the stimulation of?

A

insulin like growth factor or IGF-1 secretion

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64
Q

___is the most important endocrine regulator of final body size

A

GH

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65
Q

how does GH exerts effect on bones?

A

it causes liver to form somatomedins or IGF that strongly increases all aspects of bone growth

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66
Q

how does somatomedins increase bone growth?

A

->by stimulating osteoblasts
->increased protein deposition by chondrocytic and osteogenic cells

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67
Q

what are the metabolic effects of GH?

A

effects on protein metabolism
effects on fats
effects on CHO

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68
Q

list the effects on GH in protein metabolism

A

increases transport of a.a through cell membrane
increase protein synthesis by ribosome
decreases protein catabolism
it stimulates nucleus for formation of RNA

so GH increases protein synthesis

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69
Q
A
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70
Q

how does GH have effect on fats?

A

it has a lipolytic effect or gives energy

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71
Q

effects of GH on CHO?

A

it has diabetogenic effect, which means its anti insulin action and it increases blood glucose

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72
Q

list the effect of GH on CHO

A

decrease glucose utilization in muscle
decrease number of insulin receptor
decrease glucose uptake by the cells
enhance gluconeogenesis in the liver

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73
Q

what are defects in GH secretion in childhood?

A

gigantism and dwarfism

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74
Q

what are defects in GH secretion in adulthood?

A

acromegaly

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75
Q

what is gigantism?

A

it is caused by GH excess

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76
Q
A
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77
Q

what does gigantism result in?

A

it increase linear height because the epiphyseal growth plates in the long bones are open

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78
Q

what’s the cause for gigantism?

A

a GH secreting pituitary tumor

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79
Q

what is dwarfism?

A

it is GH deficiency

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80
Q

what does dwarfism result in?

A

short stature and growth retardation

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81
Q

what is acromegaly

A

it’s GH excess in adults

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82
Q

what causes acromegaly?

A

excess secretion of GH after puberty

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83
Q

what are the characteristics of acromegaly

A

linear height is fixed due to closure of the growth plates in long bones
the hands, feet, jaw, forehead and nose continue to grow giving patients a characteristic appearance

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84
Q

why is GH excess associated with hyperglycemia?

A

its likely to cause DM due to the anti insulin actions of GH

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85
Q

from where is the thyroid stimulating hormone released?

A

from thyrotroph cells of anterior pituitary

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86
Q

what is the control of release of TSH?

A

TRH of the hypothalamus and coldness+
T3 and T4- and negative FB

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87
Q

what is the target organ of TSH?

A

thyroid gland

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88
Q

what is the action of TSH?

A

->it stimulates the thyroid gland to produce and secrete thyroxine T4 or triiodothyronine T3
->it maintain the structural integrity of the thyroid gland

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89
Q

from where is the adrenocorticotropic released?

A

the corticotroph cells of the anterior pituitary gland

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90
Q

what is the control of release of ACTH?

A

CRH of the hypothalamus +
glucocorticoids - and negative FB

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91
Q

what is the target organ of ACTH?

A

adrenal cortex

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92
Q

what is the action of ACTH?

A

->it stimulates the adrenal cortex to secrete glucocorticoids like hydrocortisone or cortisol
->it promotes structural integrity of the adrenal cortex

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93
Q

where is follicle stimulating hormone released from?

A

from gonadotroph cells of the anterior pituitary glands

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94
Q

what is the control of release of the FSH?

A

GnRH of the hypothalamus+
prolactin, estradiol and inhibin-, negative FB+ prolactin

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95
Q

what is the target organ of the FSH?

A

gonads

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96
Q

what is the action of the FSH?

A

->it acts on testicular Sertoli cells in the male and follicular granulosa cells in the female
->stimulates the growth of ovarian follicles + production of estrogen in females
-> stimulates the production of sperm cells which is spermatogenesis via Sertoli cells of the testis of males

97
Q

from where is luteinizing hormone released from?

A

released from gonadotroph cells of the anterior pituitary glands

98
Q

what is the control of release of LH?

A

GnRH of the hypothalamus+
prolactin, testosterones and negative FB
before ovulation+ and after ovulation- it releases estradiol

99
Q

what is the target organ of LH?

A

gonads

100
Q

what is the action of LH?

A

-> it stimulates ovulation and the conversation of the ovulated ovarian follicle into an endocrine structure called a corpus luteum in females
-> stimulates the secretion of male sex hormones mainly testosterones from the interstitial cells or Leydig cells in the testes

101
Q

from where is the prolactin released?

A

from lactotroph cells of the anterior pituitary glands

102
Q

what is the control of release of PRL?

A

-> inhibited by PIH, prolactin inhibiting hormone dopamine
->secretion increases during pregnancy and peaking near the time of parturition
-> sucking and tactile stimulation of the nipples increase the secretion
->negative FB mechanism facilitates the secretion of dopamine and regulate it’s own secretion

103
Q

___inhibits the effects of gonadotropins and prevent ovulation in lactating women

A

PRL

104
Q

what is the action of PRL?

A

-> stimulation of milk production by the mammary glands of women after the birth of a baby and mammary gland development
-> negative FB regulation of gonadotropins which are FSH and LH
->acts on the kidneys to help regulate water and electrolyte balance

105
Q

clinical correlates to PRL?

A

hyperprolactinemia and hypoprolactinemia

106
Q

hyperprolactinemia can occur form?

A

overproduction or loss of the dopamine inhibitory effect

107
Q

the overproduction of PRL can be from?

A

a prolactin secreting pituitary adenoma

108
Q

in hyperprolactinemia the loss the dopamine inhibitory effect can be from?

A

use of antipsychotic drugs or damage to the pituitary stalk

109
Q

what is the key clinical indicator of hyperprolactinemia?

A

galactorrhea or milky nipple discharge

110
Q

hypoprolactinemia can occur due to?

A

with other adenohypophysial deficiencies

111
Q

the clinical effect of hypoprolactinemia is?

A

inhibition of lactation

112
Q

what is the other name of GH?

A

somatotropin

113
Q

what is the other name for TSH?

A

thyrotropin

114
Q

what is the other name for ACTH?

A

corticotropin

115
Q

what is the other name for FSH?

A

folliculotropin

116
Q

what is the other name for LH?

A

luteotropin

117
Q

which hormones are released from the gonadotroph cells of anterior pituitary?

A

FSH and LH

118
Q
A
119
Q

say something about hormones of neurohypophysis

A

Antidiuretic hormone and oxytocin are mainly synthesized in neuros cell bodies that originate in the supraoptic nucleus and paraventricular nucleus of the hypothalamus and then they are stored in the posterior pituitary

120
Q

what is the control of release of ADH

A

neuroendocrine reflex
->ADH+ released in low levels of water like dehydration and decrease blood volume and pressure and it increase osmolar pressure detected by hypothalamus
->ADH- released to increase blood volume and BP to normal level

121
Q

what is the target organ of ADH?

A

kidney tubules and blood vessels

122
Q

what is the other name of ADH?

A

vasopressin

123
Q

what is the action of ADH?

A

-> it has constricting effect on afferent arterioles so when it decreased GFR the urine output will also decreases
-> it increases the reabsorption of water at the collecting duct and collecting tubules
->it promotes aldosterone production from adrenal cortex

124
Q

how does ADH promotes aldosterone production from adrenal cortex?

A

by Na+ retention and K+ excretion

125
Q

how does ADH respond to decrease blood volume and pressure?

A

by increasing fluid retention at the kidney
and by increasing blood pressure through vasoconstriction

126
Q

what happens when someone has ADH deficiency?

A

it results in the formation of dilute urine in which urine osmolarity will be less than that of plasma

127
Q

the condition in which urine osmolarity will be less than that of plasma is called?

A

central diabetes insipidus

128
Q

ADH deficiency will cause

A

dilute urine output

129
Q

what is the control of release of oxytocin?

A

it also has neuroendocrine reflex
->during late pregnancy or trimester period and tactile stimulation of the mammary gland and sex organs
in nursing mothers the mechanical stimulus of sucking acts it will stimulate the reflex secretion of oxytocin via sensory nerve impulses to the hypothalamus

130
Q

what is the target organ of oxytocin?

A

uterus and mammary gland

131
Q

what is the action of oxytocin?

A

->it stimulates uterine contraction, it acts on the target cells by increasing the intracellular Ca+ content which leads to muscle contraction
-> it stimulates milk ejection from the lactating breast
->it promotes maternal behavior toward the neonate

132
Q

how is oxytocin used clinically?

A

used for induction of labor if they pregnancy is prolonged
or in the case of severe pregnancy induced hypertension or preeclampsia

133
Q

explain the mechanism of action of oxytocin on uterine smooth muscle contraction

A

-> oxytocin increases late in pregnancy causing a powerful uterine contraction response during labor
->distention of the uterine cervix stimulates the release of oxytocin via the neuronal pathway
->the uterine contractions that result further cervical distension
-> a cycle of positive feedback develops during the later stages of labor in which progressive cervical distention stimulates more oxytocin release
-> this cycle terminates with the birth of the infant

134
Q

what are the 2 cells of thyroid gland?

A

follicular and para follicular cells

135
Q

what’s the function of follicular cells of thyroid gland?

A

it synthesizes and secretes the principal thyroid hormones T4 and T3

136
Q

what is the ratio of T4 and T3?

A

4:1

137
Q

which thyroid hormone is the most biologically active?

A

T3

138
Q

what is the function of para follicular cells?

A

it synthesizes and secretes calcitonin

139
Q

why does the thyroid hormones have wide spread effect?

A

because it has calorigenic action which is stimulating oxygen consumption

140
Q

through the activation of genes thyroid hormones stimulate…?

A

-> protein synthesis
->promote maturation of the nervous system
-> increase the rate of cell respiration in most tissues
->they are need for proper growth and development

141
Q

what are the metabolic functions of thyroid hormones?

A

->are primarily responsible for determining the BMR, it either increase the BMR and oxygen consumption of most of tissues of the body
-> they increase synthesis of many intracellular enzymes and increase activity of Na+ K+ and ATPase which increase the rate of transport of both Na+ and K+ through the cell membrane, this process utilized energy and increase heat production

142
Q

what’s the action of thyroid hormones on mitochondria?

A

they increase the size, number and activity of mitochondria which will increase the rate of formation of ATP to enhance cellular function

143
Q

what’s the action of thyroid hormones on ribosomes?

A

->they increase the rate of formations of proteins by the ribosomes via mRNA

->they increase mRNA synthesis by the genes which leads to a generalized increase in synthesis of many types of protein within the cells

-> large amount of thyroid hormone lead to excess catabolism of muscle protein

144
Q

what’s the action of thyroid hormones on carbohydrate metabolism?

A

-> it increases the rate of absorption of carbohydrate from the GIT

-> they enhance glucogenesis and glycolysis

-> they increase enzymes acting on carbohydrates metabolism

145
Q

what happens after carbohydrate meals and what’s thyroid association here?

A

blood glucose level increases but it normally falls again rapidly because of the rate of glucose utilization is also increased

146
Q

the effects of thyroid on carbohydrate results from?

A

increases in the activity of enzymes

147
Q

what’s the action of thyroid hormones on fat metabolism?

A

-> all aspects of fat metabolism are increased including synthesis, mobilization and utilization

-> it accelerates the oxidation of fatty acids by the cells

->it lowers the level of cholesterol, phospholipids and triglycerides in the blood

148
Q

as thyroid hormone accelerates the oxidation of fatty acids by the cells so this means?

A

more lipolytic effect than lipogenic effect

149
Q

what’s the action of thyroid hormones on skeletal growth and development?

A

->due to its protein synthesis by ribosomes its important for normal growth of soft tissues and skeleton
-> its required for production and action of GH and insulin like growth factors on skeleton growth and development

150
Q

what’s the action of thyroid hormones on fetal and neonatal nervous system?

A

->it promote growth and development of the brain during fetal life and for the first few years of life
-> essential for normal myelination and development of the NS in infant

151
Q

if there’s thyroid hormone deficiency what is its effect on infants?

A

-> growth and maturation of the brain s retarded

-> myelination is defective

-> the reflex time prolonged

152
Q

if there’s thyroid hormone excess what is its effect on adults?

A

-> it causes an increased response of the brain to catecholamines and increases activation of reticular activating system
-> restlessness and hyper excitability

153
Q

what’s the action of thyroid hormones on the cardiovascular system?

A

-> increase the number and affinity of beta-1 adrenergic receptors in the heart

-> it increases the heart sensitivity to catecholamine and catecholamine increases all properties of the heart

->increased metabolism in the tissues causes more rapid utilization of oxygen and causes greater metabolic end products to be released from the tissues

->these effects cause vasodilation thus increasing the rate of blood flow in the skin for heat elimination

->increase blood flow leads to increase venous return leading to increase in CO and systolic blood pressure

154
Q

what’s the action of thyroid hormones on respiration?

A

->increase respiration due to increase rate of metabolism which increase the utilization of oxygen and formation of carbon dioxide

-> helps in dissociation of oxygen from hemoglobin by increasing the amount of 2,3 diphosphoglyceride in the RBC

155
Q

what’s the action of thyroid hormones on GIT?

A

-> they increase the rate of secretion of the digestive juice and motility which leads to increased appetite and food intake

156
Q

what’s the action of thyroid hormones on sexual functions?

A

-> normal amount is important for normal sexual function

-> essential for normal menstrual cycle and fertility

-> increase milk secretion in lactating women

157
Q

thyroid malfunction is very common in which gender?

A

more prevalent in females

158
Q
A
159
Q

hyperthyroidism results from?

A

a secretory tumor of the thyroid gland or from an autoimmune condition as in graves diseases

160
Q

what happens in graves diseases?

A

thyroid stimulating immunoglobulin are produced by the immune system
and these are agonists at the TSH receptor causing both hypersecretion and growth of the gland causing a goiter

161
Q

what causes hypothyrodism?

A

inadequate production of thyroid hormones due to sufficient dietary iodine

162
Q

inadequate amounts of T4 and T3 causes?

A

abnormally high levels of TSH secretion with lack of negative feedback inhibition which in turn stimulates the abnormal growth of the thyroid

163
Q

hypothyroidism is usually a problem in?

A

a problem in thyroid gland and not with pituitary production of TSH

164
Q

list the causes for goiter

A

-> iodine deficiency

-> anti thyroid drugs

-> thyroidal enzyme defects

all these cause decrease in T3, T4 synthesis and secretion and increase in TRH and plasma TSH

165
Q

what is the other name for para follicular cells?

A

C cells

166
Q

where are C cells found?

A

scattered outside of follicle epithelium

167
Q

what is the function of calcitonin?

A

->lowers blood Ca+ levels
->inhibits osteoclasts cells of bones+
->stimulates osteoblast cells of bone
->increases urinary calcium loss

168
Q

the secretion of calcitonin is triggered by?

A

high blood Ca+ level

169
Q

what is parathyroid gland?

A

they are 4 glands embedded on posterior side of thyroid gland

170
Q

___cells produce parathyroid hormone

A

chief cells

171
Q

what is the control of secretion of PTH?

A

-> lowers blood Ca+ level
-> it act on bones osteoclast cells for bone resorption
->acts on GIT dietary absorption of Ca+
->act on kidneys to decrease Ca+ loss via renal excretion

172
Q

what is PTH action?

A

it raises blood Ca+ to normal level

173
Q

where is the adrenal glands located anatomically?

A

situated on superior border of each kidney surrounded by fibrous capsule

174
Q

what are the 2 parts of adrenal gland?

A

the outer adrenal cortex and the inner adrenal medulla

175
Q

the outer glandular region has__ layers

A

3 layers and the cells of the last 2 act as a single unit

176
Q

what does the glandular region of outer adrenal cortex secretes?

A

->aldosterone

->cortisol

->sex hormones like androgen and estrogen

177
Q

what does the neural tissues of an inner medulla secretes?

A

release catecholamines, 80% epi and 20% norepi

178
Q

what are the 3 layer of adrenal cortex?

A

->zona glomerulosa, yehe outermost nw

-> zona fasiculata, middle

->zona reticularies, inner most

179
Q

what does the zona reticularies of adrenal cortex secretes?

A

secretes glucocorticoids mainly cortisol and androgens

180
Q

which adrenal gland doesn’t have nerve supply?

A

adrenal cortex

181
Q

what does the zona glomerulosa produce?

A

the principal physiological mineralocorticoid hormone aldosterone

182
Q

what the function of aldosterone?

A

->promotes the renal tubular reabsorption or retention of Na+

->secretion or excretion of K+ and H+

->it has major role in the maintenance of electrolyte and fluid balance and regulate mineral content in blood volume, water and electrolyte balance

183
Q

the stimulation of aldosterone is triggered by?

A

decreased Na+
increased K+
decreased blood volume
BP and stress

184
Q

the secretion of aldosterone is regulated by?

A

by renin, ADH and ACTH

185
Q

what is the target organ of aldosterone?

A

renal tubules

186
Q

aldosterone control of secretion is?

A

->high K+ of ECF detected by JGA and activated renin

-> low Na+ of ECF detected by hypothalamus and activate CRH and then ACTH which will release aldosterone and cortisol

-> dehydration which is detected by hypothalamus and activates ADH

187
Q

what does the zona fasiculata produce?

A

glucocorticoids like cortisone and cortisol

188
Q

glucocorticoids are released due to?

A

in response to ACTH

189
Q

what’s the function of glucocorticoids?

A

->helps to resist long term stressors

->promote normal cell metabolism

190
Q

prolonged ACTH secretion results in?

A

hypertrophy and hyperplasia of the adrenal cortex

191
Q

what are actions of glucocorticoids?

A

-> are essential to give relief from prolonged stressors

-> increase gluconeogenesis

-> increase protein catabolism in muscle and decrease protein synthesis by providing more a.a to the liver for gluconeogenesis

->decrease glucose utilization and insulin sensitivity of adipose tissue

-> increase lipolysis which provide more glycerol to the liver gluconeogenesis

192
Q

what are the anti inflammatory effects of glucocorticoids?

A

-> induce the synthesis of lipocortin which is an inhibitor phospholipase A

->inhibit the production of interleukin 2 and inhibit the proliferation of T- lymphocyte

->inhibit the release of histamine, serotonin from mast cells and platelets

it suppresses immune response

193
Q

what is Cushing’s syndrome?

A

it’s excess of glucocorticoids

194
Q

hypercortisolism is characterized by?

A

-> hyperglycemia due to enhanced gluconeogenesis

->muscle wasting and weakness due to protein catabolism

->truncal obesity and rounding of the face or moon face

->hypertension is common due to mineralocorticoid effects of excess glucocorticoids

195
Q

what is Addison’s diseases?

A

caused by hyposecretion of corticosteroids especially glucocorticoids

196
Q

what causes the pigment in Addison’s diseases?

A

results from stimulation of melanocytes by ACTH which is structurally similar to MSH

197
Q

zona fasiculata is more or less similar to___

A

zona reticularies

198
Q

what is the function of zona reticularies?

A

-> to form glucocorticoids cortisol and corticosterone

->and form lesser extent of androgens and estrogens

199
Q

adrenal medulla is innervated by?

A

preganglionic nerve fibers of sympathetic NS and axons stimulate hormone secretion

200
Q

what’s the function of adrenal medulla hormones?

A

-> increase heart rate and force releases glucose and fatty acids into blood and opens airways

they prepare the body to deal with short term stress

201
Q

the release of catecholamines by adrenal medulla is controlled by?

A

preganglionic sympathetic neurons
Ach is released and acts at the nAchR of the chromaffin cells

202
Q

what happens during the stress response?

A

it is sensed in the hypothalamic pituitary adrenocortical axis sustains epi secretion by the adrenal medulla

203
Q

what is the target cell for adrenal medulla hormones?

A

most cells

204
Q

what are the effects of adrenal medulla hormones?

A

->increase cardiac activity, blood pressure, glycogen breakdown, and blood glucose level and release of lipids by adipose tissue

205
Q

where is the pancreas located?

A

behind stomach and beneath liver

206
Q

pancreas has both ___ and ___
cells

A

exocrine and endocrine cells

207
Q

endocrine cells of the pancreas are organized into__

A

islets of langerhans

208
Q

what does islets of Langerhans secretes?

A

insulin and glucagon

209
Q

insulin is produced by which cells of the islets?

A

beta cells

210
Q

glucagon is produced by which cell of the islets?

A

alpha cells

211
Q

exocrine cells of the pancreas secrete?

A

pancreatic juice and digestive enzyme

212
Q

what is the action of insulin?

A

-> lowers blood glucose concentration

-> increased glucose uptake, storage and use by target cells

213
Q

what is the target cell for insulin?

A

liver, muscle and fat cells

214
Q

what is the action of glucagon?

A

-> it raises blood glucose concentration

->increases glycogen breakdown and glucose synthesis

215
Q

what is the target cell of glucagon?

A

liver cells

216
Q

what is the role of glucagon in carbohydrate metabolism?

A

->it stimulates hepatic glycogeneolysis which increases blood glucose

217
Q

what is the role of glucagon in lipid metabolism?

A

->stimulates lipolysis which increases the release of free fatty acid and glycerol from adipose tissue

->increase hepatic ketogenesis and facilitates the conversion of fatty acids to keton bodes

218
Q

what is the role of glucagon in protein metabolism?

A

-.has catabolic effect on hepatic protein and inhibit the incorporation of amino acids into hepatic protein

219
Q

what is the role of insulin in carbohydrate metabolism?

A

-> lowers the level of blood glucose by increasing the transport and peripheral utilization of glucose

->increases muscle and liver glycogen

220
Q

what is the role of insulin in protein metabolism?

A

-> strongly anabolic effect alew, it synthesizes protein and inhibit protein catabolism

-> increase the incorporation of a.a into protein by accelerating the entry of a.a into cells

221
Q

what is the role of insulin in lipid metabolism?

A

-> inhibit the breakdown of triglycerides and stimulates the formation of triglycerides

->accelerates synthesis of fatty acids and glycerol phosphate and leading into increased deposition of triglycerides in adipose tissue

222
Q

____is insulin excess

A

insulinoma

223
Q

insulinoma results from?

A

adenoma of the islets

224
Q

what is the treatment of insulinoma?

A

surgical removal of the tumor

225
Q

____is deficiency of insulin

A

diabetes mellitus

226
Q

define DM

A

a chronic disorder of carbohydrate, fat and protein metabolism

227
Q

DM is characterized by?

A

hyperglycemia and commonly glycosuria which is sugar in urine

228
Q

what’s the cause of DM?

A

relative or absolute deficiency of insulin

229
Q

what is known as the most endocrine abnormality?

A

DM, it has 4% of incidence

230
Q

type 1 and 2 DM onset

A

sudden
gradual

231
Q

type 1 and 2 DM age at onset

A

any age
mostly in adults

232
Q

type 1 and 2 DM body habitus

A

thin or normal
often obese

233
Q

type 1 and 2 DM ketoacidosis

A

common
rare

234
Q

type 1 and 2 DM autoantibodies

A

usually present
absent

235
Q

type 1 and 2 DM endogenous insulin

A

low or absent
normal which is increased or decreased

236
Q

type 1 and 2 DM concordance in identical twins

A

50%
90%

237
Q

type 1 and 2 DM prevalence

A

less prevalent
more

238
Q

what are the clinical signs of DM?

A

->polyuria which is huge urine output

->polydipsia which is excessive thirst

->polyphagia which is excessive hunger and food consumption

239
Q

____is excessive insulin secretion

A

hyperinsulinemia which results in hypoglycemia

physiology 2 (4 decks)

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