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FOM sem 1 > endocrine system > Flashcards

endocrine system Flashcards

1
Q

What is the overall ‘goal’ of the endocrine system

A

secrete chemicals that affect different parts of the body to maintain bodily functions and homeostasis

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2
Q

what are the 3 types of signalling in the endocrine system

A

autocrine = self
paracrine = neighbouring cell (close)
endocrine = target cell through blood stream (distant)

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3
Q

what are some major functions of the endocrine system

A

growth and dev
pregnancy
sleep and wake cycles
temp regulation
muscle and strength dev

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4
Q

what are the two diff types of glands in the endocrine system

A

endocrine (ductless > secretes into surrounding fluids)

exocrine (ducted > travel through these)

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5
Q

what are the two types of endocrine glands

A

classical and nonclassical

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6
Q

give examples of non classical glands and one eg of their chemicals

A

heart - ANP
skin - vitamin D
stomach - gastrin
kidney - renin
placenta - oestrogens
liver - thrombopoietin

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7
Q

give examples of classical glands (MAJOR GLANDS)

A

pineal gland, hypothalamus, pituitary gland > CENTRAL

thyroid gland
parathyroid glands
adrenal glands
pancreas
ovary
testes
thymus > PERIPHERAL

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8
Q

what are the three types of hormones

A

peptide, steroid, amine

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9
Q

describe peptide based hormones

A

amino acids, varying lengths, hydrophilic, short life span, stored in secretory vesicles, released via exocytosis

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10
Q

describe steroid based hormones

A

derived from cholesterol, extended life span due to being bound to carrier proteins, synthesised when needed, activate genes for protein synthesis

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11
Q

describe amine hormones

A

from tyrosine (catecholamines, thyroid hormones) + tryptophan (melatonin)

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12
Q

what are the two types of tyrosine derived amine hormones

A

catecholamines - tyrosine derived, hydrophilic, extracellular receptors, e.g noradrenaline, adrenaline and dopamine > MORE LIKE PEPTIDES

thyroid hormones - iodinated tyrosine derived, hydrophobic, intracellular receptors > MORE LIKE STEROIDS

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13
Q

what are the two types of receptors

A

intracellular (for steroid hormones) and cell surface (for peptide hormones)

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14
Q

what are the two cell surface receptors

A

g coupled protein (ligand bind > ion channel open)

receptor enzyme (ligand bind >enzyme activate)

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15
Q

what are intracellular receptors

A

found in nucleus and cytoplasm

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16
Q

what is signal transduction

A

receptor enzyme > amplifying enzymes activated > many secondary messengers > series of reactions > SIGNAL TRANSDUCTION

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17
Q

what determines the extent of hormone activity

A

number of receptors (down regulation/up regulation)

amount of hormone circulating

bond affinity

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18
Q

what is up regulation

A

target cells form more receptor cells usually in response to increased hormone

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19
Q

what is down regulation

A

target cells lose receptor cells usually in response to decreased hormone

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20
Q

what are the 4 factors of timing of hormones

A

onset
duration
clearance
half life

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21
Q

what are the types of hormonal stimulation

A

humoral = level of substance in the blood

neural = nerve fibres

hormonal (TROPIC) = stimulated by another hormone

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22
Q

what are the three types of hormone combinations

A

permissiveness = one hormone permits the action of another

antagonist = one hormone reduces the effect of another

synergism = ‘summation’ of action of multiple hormones

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23
Q

negative feedback eg of endocrine system

A

TRH from hypothalamus > TSH from pituitary gland > T4 and T3 from thyroid gland > system metabolic effects > homeostasis

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24
Q

factors which affect hormone concentration

A

rate of secretion (most commonly regulated)

rate of binding (to carrier proteins)

rate of metabolism (activation/degradation)

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25
Q

what is a primary disorder

A

abnormality in the gland

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26
Q

what is a secondary disorder

A

normal gland, but too much/little stimulation

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27
Q

what is hyposecretion and what disease can it lead to

A

too little hormone secreted e.g diabetes

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28
Q

what is hypersecretion and what disease can it lead to

A

too much hormone secreted e.g tumour/cancer

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29
Q

causes of endocrine dysfunction

A

problems in the signal transduction pathways

down regulation

loss of stimulus

autoimmune destruction of gland

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30
Q

how can endocrine dysfunction be treated

A

hormone supplements

drugs to promote/decrease release of hormones

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31
Q

what are the structures in the pancreas

A

pancreatic islets
exocrine cells
endocrine cells (beta cells, alpha cells, D cells, pp cells)
bile duct
pancreatic duct

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32
Q

explain how glucose stimulates insulin secretion

A

glucose enters cell
oxidative metabolism occurs
increased ATP
closed potassium ATP channels
depolarisation
opening of voltage gated Ca2+ channels
increase Ca2+
insulin secretion

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33
Q

explain how insulin promotes glucose entry into skeletal muscles and adipose tissue

A

insulin binds to receptor
signal transduction cascade occurs
exocytosis of GLUT 4
increase glucose entry into cells

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34
Q

explain how insulin promotes glucose utilisation

A

insulin binds to receptor
activates secondary messengers
secondary messenger pathways are initiated
increase in transcription factors and enzymes
changes in metabolism

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35
Q

what cells release insulin

A

beta

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36
Q

what cells release glucagon

A

alpha

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37
Q

explain how liver and skeletal muscles store excess glucose as glycogen

A

high insulin
GLUT 2 helps move glucose into liver cell
signal cascade occurs
ATP used in the process of converting glucose into glycogen via glycogen synthase

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38
Q

explain the regulation of insulin secretion in the case of low plasma glucose

A

sympathetic stimulation (adrenaline)
low free fatty acids
somatostatin

> inhibits insulin secretion

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39
Q

explain the regulation of insulin secretion in the case of high plasma glucose

A

GI hormones
high free amino acids
parasympathetic stimulation

> stimulates insulin secretion

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40
Q

what is GLUT 4

A

glucose transporter into skeletal muscle and adipose cells

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41
Q

explain glucagon regulation in the case of high plasma glucose

A

insulin
high free fatty acids and ketoacids

> inhibits glucagon secretion

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42
Q

explain glucagon regulation in the case of low plasma glucose

A

sympathetic stimulation (catecholamines)
high free amino acids
low free fatty acids

> stimulates glucagon secretion

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43
Q

what are the actions of glucagon

A

decrease glycogen synthesis/increase breakdown of stored glycogen
stimulate gluconeogenesis
promotes fat breakdown and inhibits triglyceride synthesis and increases ketogenesis > increase in blood levels of fatty acids and ketones

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44
Q

what is type 1 diabetes mellitus

A

no insulin secretion (autoimmune destruction of beta cells)

ketoacidosis, polyuria, glucosuria, polydipsia

coma + death

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45
Q

what is type 2 diabetes mellitus

A

not as much insulin produced post feeding

genetic component

down regulation > progressive development of insulin resistance

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46
Q

what are micro- macrovascular complications of diabetes

A

increased risk of heart attack, stroke, blindness and ischemia

hypetension

atherosclerosis

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47
Q

what are peripheral/ANS complications of diabetes

A

impaired bladder control

impaired CV reflexes

distal sensory neuropathy

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48
Q

where is the hypothalamus located

A

in the diencephalon, surrounded by the limbic lobe

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49
Q

what systems does the hypthalamus link

A

endocrine + nervous

‘post office’ > receive info, sort info, relay info

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50
Q

what tissue is the anterior pituitary gland made of

A

glandular epithelial

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51
Q

what tissue is the posterior pituitary gland made of

A

nervous tissue

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52
Q

how are the two parts of the pituitary gland developed

A

anterior pituitary = up growth from oral cavity > vascular connection with hypothalamus

posterior pituitary = down growth from brain > neural connection with hypothalamus

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53
Q

what does the posterior pituitary gland do

A

stores + secretes hormones that were formed in the hypothalamic neurons (ADH and oxytocin)

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54
Q

where are ADH and oxytocin synthesised

A

cell bodies of neurons located in hypothalamic paraventricular and supraoptic nuclei

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55
Q

what stimulates the release of ADH

A

increase osmolarity
decrease BP
increase stressors

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56
Q

how does ADH work

A

V2 receptors on kidney tubules > increase in cAMP > increase insertion of aqua-poring in collecting ducts > INCREASE H2O REABSORPTION

V1 receptors on blood vessels > INCREASE VASOCONSTRICTION

V1b receptors on anterior pituitary corticotrophs > increase ACTH > increase aldosterone > INCREASE NA2+ AND H2O REABSORPTION

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57
Q

what is the positive feedback loop associated with oxytocin

A

childbirth

fetus drops lower in uterus > cervical stretch > oxytocin from posterior pituitary / prostalglandins from uterine wall > uterine contractions > cervical stretch > repeat

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58
Q

what does oxytocin do

A

promotes ejection of milk in mammary glands

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59
Q

oxytocin vs ADH chemically

A

very similar chemically (both peptides that are 9 amino acids long) but DIFF FUNCTIONS

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60
Q

what are the pituitary cells, hormones, targets and functions

A

thyrotrophs - THS - thyroid - t3 and t4 secretion

corticotrophs - ACTH - adrenal cortex - cortisol secretion

gonadotrophs - FSH and LH - ovaries and testes - reproduction

lactotrophs - prolactin - mammary glands - milk production

somatotrophs - GH - bone, tissues, liver - growth

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61
Q

how does hormone release in the anterior pituitary work

A

short axon neurones synthesise hypophysiotropic hormones >

release into capillary bed of hypothalamic-hypophyseal portal system >

portal vessels carry hormones to anterior pituitary >

endocrine cells of anterior pituitary controlled by hypophysiotropic hormones >

secrete anterior pituitary hormones into blood

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62
Q

what are hypophysiotropic hormones

A

peptide neurohormones
releasing hormones/inhibiting hormones
neuroendocrine system (fast + specific)

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63
Q

what are the hypophysiotropic hormones associated w anterior pituitary

A

thyrotropin releasing hormone (TRH) > release of TSH

corticotropin releasing hormone (CRH) > release of ACTH

gonadotropin releasing hormone (GnRH) > release of FSH and LH

growth hormone releasing (GHRH) > release of growth hormone

growth hormone inhibiting hormone (GHIH) > inhibits release of GH and TSH

prolactin releasing hormone (PRH) > release of prolactin

prolactin inhibiting hormone (PIH) > inhibits release of prolactin

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64
Q

what is growth

A

progressive increase in size of an organism
elongation of bone
increase in size and number of cells in soft tissue
requires net synthesis of protein

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65
Q

what factors influence growth

A

genetics
growth influencing hormones
nutrition
stress/disease

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66
Q

what factors affect fetal growth

A

uterine environment
genetics
placental hormones

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67
Q

what factors affect post natal growth

A

growth hormones
increase GH during puberty
increase androgens (sex steroids)

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68
Q

what hormones influence growth

A

excess insulin > excess growth
androgens > pubertal growth spurt and protein synthesis

hypothyroidism can stunt growth, BUT this doesn’t mean that excess thyroid hormones lead to excess growth

69
Q

what is a growth hormone

A

peptide hormonem, synthesised by somatotrophs in anterior pituitary (secretion regulated by GHRH and GHIH)

stimulates growth

70
Q

what is the overall purpose of a growth hormone

A

protein synthesis, increase use of fat storage, increase hyperglycaemia

71
Q

what are the GH secretion patterns

A

larger bursts during sleep
irregular pulses
during puberty then declines

72
Q

what are the positive stimuli that release GH

A

major:
exercise
circadian rhythm
stress
hypoglycaemia
fasting

minor:
increase amino acids
decrease fatty acids

73
Q

what decreases GH and through what mechanism does this occur

A

IGF inhibits somatotrophs > decrease GH

IGF stimulates GHIH

GH inhibits GHRH > increases GHIH

these occur through a negative feedback loop

74
Q

what does GH stimulate in liver

A

somatomedins

75
Q

what are somatomedins

A

peptide hormone w strong mitogenic properties
produced mainly in the liver
two types (IGF1 and IGF2)

76
Q

what does IGF1 do

A

it is in most cells of the body > increase cell growth, multiplication and decrease apoptosis

77
Q

what does IGF2 do

A

growth promoting hormone during gestation

78
Q

what growth hormone receptor is GH associated w

A

JAK/STAT signal transduction > surface membrane receptors > turns on transcription to synthesise protein > increase GH

79
Q

what are the GH influences on metabolism

A

increase protein synthesis

increase lipolysis

increase glucose output from liver (hepatic gluconeogenesis)

decrease insulin sensitivity in muscle (decrease glucose uptake by muscles so they use free fatty acids which increase blood glucose)

80
Q

what are GH influences on growth

A

increased protein synthesis

decreased protein degradation

increase hyperplasia

increase hypertrophy

stimulates proliferation of epiphyseal cartilage

increase proliferation of periosteal osteoblasts

81
Q

what are gonadotropins

A

luteinising hormones (LH) and follicle-stimulating hormone (FSH)

acts on gonads by activating cAMP

increase in GnRH activity > puberty

82
Q

what does FSH and LH stimulate in males

A

FSH = spermatogenesis
LH = testosterone secretion

83
Q

what does FSH stimulate in females

A

follicle dev
induces LH receptors on dominant follicle
stimulates estrogen secretion from follicles

84
Q

what does LH stimulate in females

A

ovulation
maintains corpus luteum

85
Q

what happens during the early to mid follicular phase

A

FSH stimulates growth of ovarian follicles + oocyte maturation > follicles secrete more oestrogen

rising levels of oestrogen > selectively inhibits FSH sections from gonadotrophs / inhibits GnRH secretion / promotes proliferation of endometrium

86
Q

what happens during follicle development

A

granulosa cells proliferate > surrounding CT differentiates into thecal cells > thecal cells produce androgens which are converted into estrogen in granulosa cells > oocyte in each follicle enlarges

follicles grow + secrete increasing amounts of estrogen > single dominant follicle develops

follicle ruptures > ova released

87
Q

how are FSH and LH linked

A

LH stimulates thecal cells which convert cholesterol into androgen which diffuses from thecal cells into granulosa cells

FSH stimulates granulosa cells which convert androgen into estrogen

estrogen from LH stimulation and estrogen from FSH stimulation is then secreted into blood, remains in the follicle, or stimulates proliferation of granulosa cells

88
Q

what happens during late follicular phase

A

inhibin inhibits FSH secretion from pituitary

high levels of estrogen trigger LH surge > reinitiation of oocyte meiosis / luteinisation of follicular cells to luteal cells

89
Q

what happens during early to mid luteal phase

A

LH causes differential of both thecal and granulosa cells into luteal cells of the corpus luteum > corpus luteum secretes progesterone, estrogen and inhibin

90
Q

what does progesterone do

A

-ve feedback on hypothalamus and anterior pituitary

secretory changes in endometrium

thickens cervical mucus

exerts thermogenic activity

91
Q

what happens during late luteal phase

A

no pregnancy > corpus luteum deteriorates > decrease in progesterone > endometrial necrosis > progesterone decrease means FSH can increase again to start new cycle

pregnancy > maintain increased progesterone, estrogen and inhibin

92
Q

what are the phases of the uterine cycle

A

proliferative phase (endometrium repair + proliferation under influence of estrogen)

secretory phase (endometrial glands secrete glycogen and mucus)

menstrual phase (uterine prostaglandins > vasoconstriction, contractions and cramping, discharge of blood

93
Q

what does hyper secretion of GH lead to

A

children (body stays in proportion) = gigantism

adults (bone doesn’t length) = acromegaly

94
Q

what are the cause, effect and treatments of gigantism

A

causes = pituitary adenoma / pituitary hyperplasia

effects = rapid growth of all tissues / hyperglycaemia

treatment = surgery / somatostatin analogs

95
Q

what are the cause, effect and treatments of acromegaly

A

causes = pituitary tumour

effect = increase width of bone > enlargement of hands and feet, ribs and tongue

treatment = surgery / somatostatin analogs

96
Q

how does reduced growth occur

A

social/psychological factors > decreased stimulation of hypothalamus > lack of GHRH/increased GHIH > no growth hormone > down regulation > decreased IGF

97
Q

where is the thyroid gland located

A

directly below the larynx
on either side of and anterior to the trachea

98
Q

what are the two lobes of the thyroid gland connected by

A

isthmus

99
Q

what does the thyroid gland consist of

A

follicular cells > secrete thyroid hormones

c cells > secrete calcitonin

capillaries

thyroid follicles > functional units

colloid (lumen within follicular cells) > contain thyroglobulin

100
Q

what are thyroid hormones

A

amine based hormones that affect almost all cell types

101
Q

what are the two pathways that thyroid hormones have to impact the body

A

effects on metabolic pathways
effects on cellular development and differentiation

102
Q

elaborate on the impact of thyroid hormones on metabolic pathways

A

they boost energy metabolism in mitochondria which increase basal metabolic rate and influences body temp

103
Q

elaborate on the impact of thyroid hormones on the cellular development and differentiation pathways

A

they promote development and differentiation of many cells

104
Q

how is secretion from the thyroid gland regulated

A

TRH > TSH > T3 and T4 (free and unbound ones are biologically active)

-ve feedback loop = maintains relatively constant supply of thyroid hormones

105
Q

what are the two types of impacts that TSH has

A

genomic and non genomic

106
Q

what are genomic impacts of TSH

A

iodide pump, thyroglobulin, T3/T4 synthesis

increase blood flow through vasodilation

hyperplasia and hypertrophy of gland

107
Q

what nongenomic impacts does TSH have

A

increased iodide trapping
increased T3 and T4 synthesis
increased pleased of T3 and T4

108
Q

what effects do thyroid hormones have

A

oxygen delivery (up regulates beta adrenergic receptors > increase HR, SV and RBC mass)

metabolism (increase mito number and size, increase lipolysis and glycogenesis)

neural activity (increase alertness, memory, learning)

reproduction and growth (required for reproductive capabilities / enhances effect of GH)

109
Q

what mechanism causes thyroid disorder

A

hypothyroidism (iodine deficiency):
decrease iodine > no t3 and t4 > no negative feedback

hyperthyroidism (graves disease):
autoantibodies (TSI) > too much negative feedback

110
Q

what three factors can lead to hyperthyroidism

A

grave’s disease
excess hypothalamic/anterior pituitary secretion
hyper secreting thyroid tumour

111
Q

what three factors can lead to hypothyroidism

A

iodine deficiency
failure of anterior pituitary or hypothalamus
failure of thyroid gland

112
Q

how is thyroid functions assessed

A

use radio iodide > scans or urinary excretion

113
Q

what are some pathological causes of hypothyroidism

A

primary = antibodies against thyroimmunoglobulins and TSH receptors (hasimoto’s disease)

secondary = pituitary deficit

tertiary = hypothalamic deficit

latrogenic = treatments for hyperthyroidism

114
Q

what are signs and symptoms of hypothyroidism

A

fatigue, decreased HR, decreased Q, weight gain, decreased growth

115
Q

what are pathological causes of hyperthyroidism

A

grave’s disease > TSI > overstimulates thyroid

116
Q

what are signs and symptoms of hyperthyroidism

A

protrusion of eyeballs (exophthalmos)

tachycardia

decreased weight despite no loss of appetite

fatigue due to muscular atrophy

117
Q

why must Ca2+ be tightly regulated

A

free Ca2+ in ECf is biologically active
> NT release
> Hormone secretion
> blood clotting
> muscle contractility

118
Q

what hormones are involved in the endocrine regulation of Ca2+

A

parathyroid hormone (PTH)

activated vitamin D

calcitonin

119
Q

where are the parathyroid glands located

A

posterior surface of thyroid

120
Q

what are the 3 main actions PTH has

A

increase PTH in kidneys > increase renal Ca2+ reabsorption > less urinary excretion of Ca2+ > increase plasma Ca2+

increase PTH in kidneys > increase activation of vitamin D > increase absorption of Ca2+ in intestine > increase plasma Ca2+

increase PTH in bone > mobilisation of Ca2+ from bone > increase plasma Ca2+

121
Q

what is vitamin D

A

synthesised from cholesterol
must be activated into calcitriol by liver and kidneys before having effect on intestines

122
Q

what does vitamin D do

A

activation increased by PTH > increases Ca2+ absorption from intestine

123
Q

how does vitamin D increase Ca2+ absorption in intestines

A

increase expression of calcium channels

increase expression of calbindin

increases expression of Ca-ATPase pumps

124
Q

what is calcitonin

A

produced by c-cells of thyroid

125
Q

what does calcitonin do

A

protective against hypercalcemia
protecting skeletal integrity

126
Q

how does calcitonin maintain homeostasis

A

decreases the mvmt of Ca2+ from labile pool and inhibits osteoclast activity

decreases reabsorption of Ca2+ from kidney tubules

increase plasma Ca2+ > thyroid C cells stimulated > increase calcitonin > decrease plasma Ca2+

127
Q

where are the adrenal glands (suprarenal glands) located

A

on top of each kidney

128
Q

what is the structure of adrenal glands

A

outer = adrenal cortex (release steroids)
inner = adrenal medulla (release catecholamines)

129
Q

what are the 3 layers of the adrenal cortex

A

zona reticularis
zona fasciculata
zona glomerulosa

130
Q

outline the release of hormones from the zona reticularis

A

releases androgens in the form of DHEA

secretion is increased by ACTH

main function is ‘male’ sex hormone

131
Q

outline the release of hormones from the zona fasciculata

A

release glucocorticoids in the form of cortisol

secretion is increased by ACTH

main function is to help resist stress / metabolism

132
Q

outline the release of hormones from the zona glomerulosa

A

release mineralocorticoids in the form of Aldosterone

secretion is increased by plasma K+ and angiotensin II

main function is to maintain electrolyte balance and blood pressure

133
Q

outline the release of hormones from the adrenal medulla

A

release catecholamines in the form of adrenaline

secretion is increased by sympathetic NS

main function is to resist stress

134
Q

what are the adrenal sex hormones

A

estrogen and androgens, which are regulated by ACTH

DHEA = only sex hormone of biological importance (in males, it is overpowered by testosterone and in females, it promotes pubic and axillary hair growth and maintains sex drive)

135
Q

what is stress

A

body’s non specific response to any demand made on it

136
Q

what are examples of stressors

A

physical e.g trauma
psychological e.g fear
physiological e.g pain
social e.g change in lifestyle
chemical e.g toxins

137
Q

what type of reactions can stressors have

A

specific and non specific

138
Q

what comprises the General Adaptation Syndrome (non specific response)

A

alarm reaction - fight or flight/acute/varies bases on sex and severity of stressor

resistance stage - adaptation and defence

allostatic overload - protective and damaging effects > long term damage due to prolonged impact of stressors e.g depression

139
Q

what happens during the alarm reaction

A

hypothalamic activation of the sympathetic NS
> release of noradrenaline from nerve terminals
> secretion of noradrenaline and adrenaline from adrenal medulla

140
Q

how does the adrenal medulla release catecholamines

A

sympathetic stimulation of post ganglionic neurons (chromaffin cells) using ACTH > chromaffin cells release NA and A (in a 1:5 ratio) into the bloodstream

141
Q

how are catecholamines made

A

L tyrosine > L dopa > dopamine > NA > using PNMT (only in adrenal medulla) > A

142
Q

what do catecholamines do

A

heart > increase HR and contraction (beta 1 receptors

kidney > vasoconstriction (alpha receptors) and increase renin release (beta receptors)

liver > glycogenolysis (beta receptors) and gluconeogenesis (alpha receptors)

pancreas > increase glucagon and decrease insulin (alpha and beta cells)

143
Q

what are acute response to stress

A

increased HR
increased metabolic rate
change in blood flow pattern
dilation of bronchioles
increase BP
increase glycogenolysis

144
Q

what are the impacts of aldosterone in longer term stress response

A

increase retention of sodium and water

increase blood volume and BP

145
Q

what are the impacts of cortisol in longer term stress response

A

increase gluconeogenesis

increase proteolysis

increase lipolysis

decrease immune system

146
Q

how is release of mineralocorticoids and glucocorticoids regulated

A

CRH from hypothalamus > ACTH from anterior pituitary > acts of zona fasciculata > cortisol release

147
Q

what is the HPA axis

A

hypothalamic-pituitary-adrenal axis

148
Q

what is the cortisol secretion pattern

A

high during early morning and lower during night to prevent hypoglycaemia over overnight fast&raquo_space;» circadian diurnal rhythm

149
Q

what are the actions of cortisol on metabolism

A

increase BG

stimulate hepatic gluconeogenesis

inhibit glucose uptake

inhibit protein synthesis/promote protein degradation

facilitates lipolysis

150
Q

cortisol acts in…to actions of insulin

A

opposition

151
Q

why does cortisol act in opposition to insulin

A

life threatening situation > protect brain from malnutrition during extended fasting period

152
Q

what are the actions of cortisol on CV function

A

increases sensitivity of heart to adrenaline, noradrenaline and angiotensin II > maintains cardiac contractility, vascular tone and BP

153
Q

how does cortisol affect CV function

A

increases synthesis of hormone receptors

increases synthesis of catecholamines and Na/K ATPase pumps

decreases synthesis of nitric oxide

154
Q

what are the actions of cortisol on immune responses

A

decreases formation of prostaglandins and leukotrienes > decrease vasodilation, decrease capillary permeability

inhibit accumulation of macrophages

decreases production of T cells and B cell proliferation

reduces fever

155
Q

what are the actions of cortisol on bones, blood, memory

A

inhibits bone formation

alters mood and behaviour

affects memory and learning

stimulates RBC production

stimulates gastric acid secretion

156
Q

what does aldosterone do

A

increases reabsorption of sodium while increasing excretion of potassium

157
Q

how does aldosterone have its impact

A

renin-angiotensin-aldosterone system (RAAS)

> decrease Na+ > increase renin > increase angiotensin I > increase angiotensin II > combine with impact of increase plasma K+ and increase ACTH > increase aldosterone > increase tubular Na+ reabsorption and K+ secretion > increase urinary K+ excretion and decrease urinary Na+ excretion

158
Q

what are diseases linked to adrenal hyper secretion

A

phaeochromocytoma (adrenal medulla tumour)

conn’s syndrome

cushing’s syndrome

159
Q

what results from phaeochromocytoma

A

catecholamine excess > increase HR, systemic hypertension, anxiety, pallor, sweating, hyperglycaemia

160
Q

what are primary causes of conn’s syndrome

A

small, aldosterone secreting tumour of zona glomerulosa

161
Q

what are secondary causes of conn’s syndrome

A

RAAS too active due to low renal blood flow

162
Q

what does conn’s syndrome lead to

A

mineralocorticoid excess > hypokalaemia, hypertension due to hypervolaemia, ANP secretion from heart

163
Q

what are primary causes of cushing’s syndrome

A

adrenal cortex adenomas

164
Q

what are secondary causes of cushing’s syndrome

A

increase ACTH from pituitary tumour

165
Q

what does cushing’s syndrome lead to

A

glucocorticoid excess
> increase gluconeogenesis > increase hyperglycaemia > decrease sensitivity to insulin > adrenal diabetes
increase fat mobilisation from lower body to thorax and abdomen
facial oedema
protein loss

DHEA excess
acne, excess growth of facial hair
results from tumour within z.reticularis or congenital adrenal hyperplasia

166
Q

what are primary causes of adrenal insufficiency

A

anatomic destruction of adrenal glands due to autoimmune attack (addisons disease)

167
Q

what are secondary causes of adrenal insufficiency

A

negative feedback suppression of HPA axis due to steroid medications

168
Q

what does adrenal insufficiency lead to

A

glucocorticoid deficiency
> decrease gluconeogenesis > hypoglycaemia, weight loss, weakness
> decrease normal feedback by cortisol > increase melanocyte stimulating hormone > hyperpigmentation

mineralocorticoid deficiency
> increase K+ and H+ > tachycardia, chills, sweating, mild acidosis, hyperkalaemia

FOM sem 1 (10 decks)

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