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GSSE pshysiology > Endocrine and reproductie physiology > Flashcards

Endocrine and reproductie physiology Flashcards

1
Q

are steroid hormones bound to plasma proteins?

A

no

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2
Q

where in the cell are protein hormones stored?

A

in cytoplasmic granules

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3
Q

how are protein hormones released from the cell?

A

exocytosis

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4
Q

what type of hormone class are adrenal medulla and thyroid hormones?

A

amino acid tyrosine derivatives (water soluable)

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5
Q

increasing or decreasing adenylate cyclase will increase or decrease the production of what?

A

cAMP

by changing the conversion of ATP to cAMP via G proteins

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6
Q

catecholamines acting via Beta-1 receptors
and
ctecholamines acting via alpha receptors will each respectively do what to cAMP levels?

A

beta 1= increased cAMP

beta 2= decreased cAMP

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7
Q

which part of the brain regulates thirst?

A

the anterior hypothalamus senses the osmolarity of blood throught the osmoreceptors

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8
Q

which part of the brain regulates thirst?

A

the anterior hypothalamus senses the osmolarity of blood throught the osmoreceptors

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9
Q

the posterior pituitary makes which hormeones?

A

ADH and oxytocin

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10
Q

how are oxytocin and ADT stored and released from the posterior pituitary?

A

stored in vesicles and released following nervous stimuli

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11
Q

what is the main role of ADH?

A

to concentrate urine thus preventing the loss of water from the kidneys

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12
Q

how does ADH work to increase water resprption?

A

acts on renal colecting ducts to increase the permeability to water passing from medullary fluid.

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13
Q

what hormonal mediators allow ADH to resorb water?

A

vasopressin 2 - cAMP - increases water channels from endososmes

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14
Q

does ADH increase urea resorption?

A

yes, increase surea permeability int he collecting ducts inthe inner medulla of the kidney

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15
Q

how does ADH increase vasoconstriction?

A

via V1a - G protein - ca2+ = blood vessel constriction.

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16
Q

Does ADH increase glycogen breakdown in the blood?

A

no it stimulate glycogen breakdown in the liver

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17
Q

what are the effects of oxytocin (2)

A

Contraction of myoepithelial cells in the breast → milk ejection
Contraction of smooth muscle of uterus

Also has an ADH effect in high concentrations.

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18
Q

what will an increase in plasma osmotic pressure do to the ADH levels?

A

sensed in the anterior pituitary

increase levels of ADH release

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19
Q

what does angiotensin 2 do to ADH levels

A

stimulates release

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20
Q

what 3 things will reduce the release of ADH?

A

alcohol
decrease in plasma osmolality
increase in plasma volume

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21
Q

what stimulate GH release?

A

stress, starvation, ketosis

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22
Q

what is somatostatin and what does it do?

A

inhibits the release to GH in the hypothalamus

also known as growth hormone inhibting hormone

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23
Q

what are the functions of growth hormone?

A

increasing protein and carb stores which reducing fat stores.

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24
Q

how does GH stimulate lypolyis?

A

from adipose tissue into fatty acids into acetyl co a

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25
Q

how does GH increase proetin storage?

A

increases aa uptake, increase RNA translocation, decrease the catabolism of aa.

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26
Q

what is the inhibiting hormone of prolactin?

A

dopamine

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27
Q

what is the half life of GH?

A

20 mins

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28
Q

what inhibits GH release?

A

presence of fuel and somatostain

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29
Q

high concentrations of prolactin will decrease the release of what?

A

LH and FSH

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30
Q

what are catecholamines derived from?

A

the amino acid tyrosine.

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31
Q

what converts noradrenaline to adrenaline? where is it found?

A

PNMT

in the brain and medulla

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32
Q

What hormone is secreted in the largest quantity from the adrenal medulla?

A

adrenaline

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33
Q

What effect does adrenaline have on the heart?

A

It exerts its effects via beta 1 receptors and increases intracellular cAMP.
It is an inotrope (↑ contractility) and chronotrope (↑ HR), therefore ↑ SBP and results in
a wider pulse pressure.

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34
Q

How are catecholamines metabolised?

A

They can be degraded either by methylation via catechol-O-methyltransferases
(COMT) or by deamination via monoamine oxidases (MAO).

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35
Q

the adrenal medulla is derived from which cells?

A

neural crest cells

modified sympathetic ganglion.

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36
Q

cromaffin cells are innervated by what mechanism?

A

durect preganglionic nervous stimulation then secrete directly into the blood stream.

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37
Q

the neurotransmitter secreted by the preganglionic axon into the medulla is?

A

achetylcholine

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38
Q

chromaffin cells secrete what proportions fo catechlamines?

A

80% adrenaline
15% noradrenaline
small amounts dopamine

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39
Q

effector sites of catecholamines are?

A

(α1 and 2, β1 and 2)

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40
Q

the half life of catecholamines are?

A

2 mins

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41
Q

what Alpha subunit is responsible for pupillary dilation?

A

alhoa 1

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42
Q

what alpha subunit is responsible for platelt aggregation?

A

alpha 2

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43
Q

what beta subulit is responsible for cardiac contractility?

A

beta 1

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44
Q

which beta subulit is responaible for bronchodilation?

A

beta 2

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45
Q

do a1 and a2 have any affects on cerebral and coronary vasculatue?

A

no

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46
Q

the b2 subulin will do what to skeletal muscle?

A

vasodilation

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47
Q

the subunit responsible for excessive sweating in catecholamine release is?

A

alpha 1

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48
Q

what is the difference in effects on skeletal muscle between adrenaline and noadrenaline?

A

adrenaline causes vasodilation and NA causes vasoconstriction

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49
Q

What are the layers of the adrenal cortex and what do they release?

A

From out to in; “GFR”
15% Glomerulosa – Aldosterone (mineralocorticoid)
75% Fasciculata – Cortisol (glucocorticoids) and androgens
10% Reticularis – Cortisol (glucocorticoids) and androgens

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50
Q

What are adrenal cortex hormones synthesised from?

A

Cholesterol (80% of which comes from LDL, some ability to synthesise de novo)

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51
Q

What controls secretion of aldosterone?

A

Angiotensin II, ACTH, [K+] and [Na+]

Angiotensin II and K+ are the most important factors.

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52
Q

How is cortisol transported in the blood?

A

Bound to CBG (corticosteroid-binding globulin/transcortin) (~75%),
albumin (~15%)
and free (10%).

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53
Q

What are the effects of adrenal insufficiency?

A

The term for this is ‘Addisons disease’ and results in ↓ ECF, hyponatraemia, hyperkalaemia, mild acidosis, hypoglycaemia, ↑ melanin production leading to characteristic pigmentation (due to ACTH stimulation of melanocytes).

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54
Q

aldosterone is regulated by which mechanism? (3)

A

RAAS: reduced ECF - JG cells - renin release - lysis on angiotensinogen to angiotensis 2 = stimulates the adrenal cortex to produce aldosterone
hyperkalaemia
ACTH adn AN+ also have small effects on aldosterone secretion

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55
Q

the ion flow in the kidney from aldosterone is what?

A

Na+ retention and K+/H+ loss

56
Q

what happens if there is an excess in aldosterone?

A

In aldosterone excess there is an increase in ECF, however sodium [Na+] stays relatively constant.
There is hypokalaemia and metabolic alkalosis

57
Q

what is the result of severe aldoserone deficiency?

A

Severe renal sodium wasting and hyperkalaemia. Total loss causes
death in as little as 3 days.

58
Q

what are the functional cells of the adrenal medulla?

A

chrommafin cells

59
Q

What influences the release of TSH from the anterior pituitary?

A
  • TRH from the hypothalamus
  • T4 and T3
  • Temperature
  • Stress
  • Dopamine
  • Glucocorticosteroids
60
Q

Which thyroid hormone is released in the greatest quantity?

A

93% of the thyroid hormone released from the thyroid is T4, with the remaining
amount being T3 with a small amount of rT3.
However it is T3 that is more potent (4×) and in the periphery 50% of T4 is converted to T3.

61
Q

What is needed for iodide concentration in the thyroid gland?

A

Na+/I− symporter in the basolateral membrane of thyroid cells. It works by secondary active transport. Energy is provided by the electrochemical gradient of
Na+ which is maintained by Na+/K+ ATPase. It has the ability to concentrate
iodide to 40× that found in plasma.

62
Q

What percentage of T4 and T3 are bound to plasma proteins?

A

T4 and T3 are highly protein bound, 99.98% and 99.8% respectively.

63
Q

What are the clinical features of hypothyroidism and what are some causes?
Clinical features include:

A
  • General slowness
  • Husky voice
  • ↑ Cholesterol
  • Sparse dry hair
  • ↓ Reflexes
  • Weight gain
64
Q

which part of the thyroid secretes thyroid hormone and which part secreted calcitonin ?

A

Secretes thyroid hormones from thyroid follicles (and calcitonin from parafollicular C cells)

65
Q

what type of cells are thyroid follicles lined with?

A

cuboidal epithelial cells

66
Q

what are thyroid follicles mainly filled with?

A

colloid (mainly thyroglobulin)

67
Q

what influsences the rate of uptake of ioidine into the the thyroid follicle?

A

TSH

68
Q

what are the three elements of a thyroid hormone?

A

iodine
thyroglobulin
tyrosine

69
Q

when thyroid hormones leave the thyroid does thyroglobulin get released from the cell and into circulation as well?

A

no
T4 and T3 are cleaved from the thyroglobulin molecule
– Apical surface of the thyroid cell creates a pseudopod that causes pinocytosis
of colloid
– Fuse with lysosomes in the cytoplasm and proteases release T4 and T3
– T4 and T3 diffuse out into the bloodstream
– 93% T4 and 7% T3, however in the periphery 50% of T4 is converted to T3

70
Q

what proteins in circulation can thyroid hormones attach to?

A

Protein binding includes albumin,
transthyretin
and thyroxine-binding globulin (TBG)

71
Q

TBG levels ↑ when?

A

↑ with oestrogen and pregnancy, and ↓ with androgens

72
Q

how are thyroid hormones metabolised?

A

Metabolism results from deiodination in the liver, kidneys and other organs

73
Q

where is the thyroid receptor?

A

Thyroid hormone receptor (T3 > T4) are either attached to DNA strands or in
close proximity

74
Q

what is the main role of thyroid hormone?

which tissues does thyroid hormone not affect?

A

Calorigenic mechanism → ↑ O2 consumption in almost all metabolically active
tissues (except brain, testes, uterus, anterior pituitary)

75
Q

how does thyroid hormone exert its effects to increase 02 consumption in the cell?

A

Effect due to ↑ fatty acid metabolism and ↑ in Na+/K+ ATP-ase activity

76
Q

What percentage of calcium is in the ECF?

A

.1%

77
Q

What are the effects of hypo and hyper-calcaemia?

A

Hypocalcaemia causes increased neuronal excitability (e.g. tetany).
Hypercalcaemia causes CNS depression, shortens QTc, renal stones, constipation. (Moans, groans, stones, psych overtones)

78
Q

What are the effects of PTH on Ca2+ and PO4 levels in the blood?

A

PTH: ↑ plasma Ca2+, ↓plasma PO4

79
Q

what are the three ways that PTH increases calcium ?

A

Bone, kidney, GI tract

  • Bone- ↑ bone reabsorption → ↑ Ca2+
  • Kidney- ↑ reabsorption of Ca2+ in the renal tubule → ↑ Ca2+ (although if Ca2+ concentration is too high this system may be overwhelmed and renal secretion may increase)
  • GI tract- PTH also increases formation of 1,25 DHCC → ↑ GI Ca2+ reabsorption
80
Q

what are the three ways PTH can decrease P04?

A

Bone, kidney and gI tract

Bone- ↑ bone reabsorption → ↑ PO4
• Kidney- ↑ PO4 excretion in the urine, due to ↓ reabsorption of PO4 in the proximal tubules
• GI tract- ↑ absorption from the GIT by increasing formation of 1,25 DHCC in the kidneys.

81
Q

What cells of the thyroid release calcitonin?

A

The parafollicular C cells which make up only 0.1% of the human thyroid gland
and are remnants of the ultimobranchial body.

82
Q

What level does Ca2+ need to be to stimulate release of calcitonin?

A

It needs to be above 2.4 mmol/L. It acts to lower Ca2+ level by inhibiting bone
reabsorption, ↓ absorbtion and ↑ urinary excretion.

83
Q

where is calcium stored in the body and in what percentages?

A

Total body stores = 1.3 kg
(99% skeleton, 1% intracellular, 0.1% ECF).

‘Exchangeable calcium’ is about 0.4–1% of total body calcium (TBC).

84
Q

where is calcium absorbed?

A

Active absorption in duodenum and upper jejunum (calcitriol dependent)
– Small amount further down GI tract, which is passiv

85
Q

what impairs calcium absorption

A

Impaired by phosphates, oxalates, fatty acids → form insoluble Ca2+
compounds

86
Q

what is calcium bound to in blood?

A

albumin 45%

87
Q

what does increase and decrease pH in calcium do to calcium levels in the blood?

A

pH dependent: Acidosis → ↓ binding → more free Ca2+.

Alkalosis → ↑ binding → less free Ca2+→ tetany

88
Q

how much calcium filtered in the kidney is resorbed?

A

99%

89
Q

which areas in the kidney is calcium resorbed ?

A

60% in proximal tubule

40% in the ascending limb of loop of Henle and distal tubule

90
Q

where does PTH exert its effects in the kidney?

A

PTH stimulates reabsorption in the distal tubule, increased reabsorption
with ↓ plasma [Ca2+].

91
Q

what stimulates phosphate absorption int he GIT?

A

calcitriol

92
Q

where is P04 resorbed in the kidney?

A

85–90% of filtered PO4 is reabsorbed in the proximal tubule.

93
Q

what inhibits P04 resorption?

A

PTH

94
Q

what are the main stages in bone production?

A

Osteoblasts secrete collagen and ground substance to make osteoid.
Some of the osteoblasts get caught in osteoid → osteocytes.
Calcium precipitates onto osteoid → hydroxyapatite.

95
Q

what resorbes bone?

A

Bone resorption by osteoclasts which secrete proteolytic enzymes and acid.

96
Q

what are the two types of cells in the PTH glands?

A

– Chief cells – majority, contain a prominent golgi apparatus, ER and secretory granules → PTH
– Oxyphil cells – minority, but larger, unknown function

97
Q

what triggers PTH release?

A

– Low Ca2+, low Mg2+, high PO4

98
Q

what reduces PTH?

A

– High Ca2+, high Mg2+, calcitriol

99
Q

What is the main effect of insulin?

A

It is secreted primarily in response to hyperglycaemia and acts to increase muscle cell uptake of glucose, as without insulin they are relatively impermeable to glucose and use fatty acids as their primary fuel.

100
Q

How is insulin released from the pancreas?

A

Raised glucose levels → Glut-2 → Enters β cells→ ↑ ATP → closes K+ channels
→ depolarisation → opens Ca2+ channels → Ca2+ enters the cells → triggers exocytosis of insulin

101
Q

What effect does insulin have on fat metabolism?

A

Activation of lipoprotein lipase in the capillary walls of the adipose tissue,
inhibition of hormone-sensitive lipase.

102
Q

What is the consequence of insulin deficiency?

A
  • Glucose- reduced entry of glucose into peripheral cells and ↑ plasma glucose
  • Protein- ↑ rate at which amino acids are catabolised → protein deficiency
  • Fatty acids- Fat breakdown → ketosis → acidosis → coma
  • Poor resistance to infections
103
Q

Name 4 stimuli for the release of glucagon?

A 
Any of the following:
• Hypoglycaemia
• Amino acids
• Cholecystokinin (CCK)
• Gastrin
• Cortisol
• Exercise
• Stress
• Infection
• Theophylline
104
Q

What is the action of glucagon?

A

• Primarily on the liver by stimulating glycogen breakdown via glycogenolysis
and glucose production via gluconeogenesis
• In fat and liver, stimulates lipolysis via action of hormone-sensitive lipase
(adipose and liver), ketosis, inotropic effect on the heart, ↑ insulin secretion
• Has NO effect on muscle

105
Q

What is the most important hormone in the defense of acute hypoglycaemia?

A

Adrenaline.

106
Q

what is the formation of insulin pathway

A

Preproinsulin → proinsulin (stored in granules) → insulin in 𝛽-pancreatic islet cells
• Secretion occurs by exocytosis in response to ↑ intracellular Ca2+

107
Q

what BSL will trigger the release of insulin?

A

> 5

108
Q

what other things apart from glucose stimulate insulin release?

A

– Arginine, leucine and other amino acids
– Cyclic AMP, note that Adrenaline lowers cAMP → inhibits insulin release
– Glucagon and theophylline via cAMP
– Autonomic stimulation via acetylcholine
– GI hormones (GIP, + enteroglucagon, secretin, CCK)
– Oral hypoglycaemic drugs → close ATP sensitive K+ channels

109
Q

what inhibits insulin release?

A

– Somatostatin, beta blockers, K+ depletion, thiazide diuretics [negative feedback]

110
Q

which tissues in the body do not respond to insulin?

A

brain, gut, RBC, pancreatic β -cells

111
Q

Which cells of the ovary secrete oestrogen?

A

Granulosa and theca interna cells.

112
Q

Explain the effects of LH and FSH.

A

FSH causes growth of follicles and LH surge stimulates ovulation.

113
Q

. Can theca cells convert androgens to oestrogens?

A

No, as they lack the enzyme aromatase.

114
Q

Why does osteoporosis occur after menopause?

A

Oestrogen inhibits osteoclastic activity. After menopause, no oestrogen is secreted by the ovaries, hence there is an increase in bone turnover.

115
Q

What mechanisms increase oxygen carriage in the fetus in the setting of low
placental PaO2?

A
  1. HbF causes left shift of the oxygen dissociation curve

2. Higher Hb concentration in fetus

116
Q

What effect does oestrogen and progesterone have on the breast?

A

Oestrogens are primarily responsible for duct development and progesterone for
lobular development in the breast

117
Q

granulosa cells have different receptors at different times of the month, what are they?

A

FSH then LH

118
Q

theca interna cells have which receptors?

A

LH receptors not FSH

119
Q

when do estrogen levels peak?

A

24 to 48 hours pre ovulation

120
Q

progesterone is peak when in the cycle?

A

day 21

121
Q

which cells form antregens?

A

theca cells make androstenodione and testosterone

122
Q

after how many weeks is the placenta making its own hormones independent from the ovary?

A

6 weeks

123
Q

HCG can be measured in blood how many days after ovulation? with fertilised ovum?

A

8-9 days

124
Q

what is responsible for the initiation of lactation and milk letdown?

A

oestrogen and prolactin

125
Q

Which hormones are involved in spermatogenesis?

A

Testosterone, LH, FSH, oestrogen and GH

126
Q

What is the most potent androgen?

A

DHEA

127
Q

At which age do males secrete testosterone?

A

The Leydig cells, which secrete testosterone, are under control of LH from the
anterior pituitary and are active for the first few months of life and after puberty.
Virtually no testosterone is produced between the ages of 2–3 months to puberty.

128
Q

What hormones do Leydig and Sertoli cells release?

A

Leydig – testosterone

Sertoli – inhibin

129
Q

which chromosome determines the male sex?

A

the Y chromosome

130
Q

in the embryo when does the embryo begin to differentiate into sex?

A

after 6 weeks differentiation starts

131
Q

the wollfian duct becomes what?

A

Male: Wolffian duct plus mesonephros becomes the epididymis, the vas deferens, and the seminal vesicle.

132
Q

the mullarian ligament becomes?

A

Female: Mullerian ligament forms the uterine tubes, uterus, cervix, and the
upper two third of the vagina.

133
Q

which cells synthesise testosterone?

A

leydig cells form testosterone from cholesterol when stimulated by leutenising hormone from the anterior pituitary

134
Q

what cells make stermatogenesis?

A

sertoli cells make sperm with stimulation from FSH

135
Q

how is estrogen created in the teste?

A

estrogen is created in the sertoli cell from testosterone

136
Q

what hormones does the sertoli cell secrete

A

inhibin and androgen binding blobulin

137
Q

negative feedback cycles in the feedback loop feed back to where?

A

hypothalamus and pituitrary

GSSE pshysiology (5 decks)

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