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Guyton > Unit 14 > Flashcards

Unit 14 Flashcards

1
Q

What 2 classes of hormone are derived from tyrosine?

A

Thyroid and adrenal medullary

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2
Q

Where are receptors for protein hormones typically found?

A

Cell membrane

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3
Q

Where are receptors for steroid hormones typically found?

A

Cytoplasm

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4
Q

Where are receptors for catecholamine hormones typically found?

A

Cell membrane

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5
Q

Where are receptors for thyroid hormones typically found?

A

Nucleus

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6
Q

What hormones are synthesised from cholesterol?

A

Steroid and thyroid

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7
Q

Which hormones are secreted from the anterior pituitary?

A

GH
TSH
ACTH
Prolactin
FSH/LH

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8
Q

Which hormones are secreted from the posterior pituitary?

A

ADH
Oxytocin

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9
Q

What hormones are secreted from the hypothalamus?

A

GHRH
CRH
TRH
GnRH
Somatostatin (growth hormone-inhibitory protein)
Dopamine (prolactin-inhibitory hormone)

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10
Q

What are the metabolic effects of GH?

A

Increased protein synthesis
Increased fatty acid mobilisation
Decreased glucose utilisation

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11
Q

What factors stimulate GH release?

A

Decreased BG
Decreased blood FFA
Increased blood amino acids
Starvation
Exercise
Testosterone
Sleep
GHRH
Ghrelin

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12
Q

What factors inhibit GH release?

A

Increased BG
Increased FFA
Aging
Obesity
Somatostatin
Exogenous GH
Insulin-like growth factors

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13
Q

Describe the structure of the thyroid gland

A

Composed of follicles filled with colloid
Lined with cuboidal epithelial cells

C cells - secrete calcitonin

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14
Q

What is the main constituent of colloid?

A

Thyroglobulin

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15
Q

What is the main influencer of iodine trapping in the thyroid?

A

TSH

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16
Q

How is iodide transported out of the cell across the apical membrane into the follicle?

A

Via iodine/chloride transporter - Pendrin

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17
Q

Briefly describe the steps of thyroid hormone formation

A

Thyroglobulin produced in thyroid cells, transported into follicle
Iodide transported into follicle via pendrin
Iodide oxidised by peroxidase and H2O2
Iodide binds with thyroglobulin - produces T4
Stored in follicle
Reabsorbed back into cell by pinocytosis

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18
Q

How do T3/T4 circulate in blood?

A

Small free fraction
Bound to thyroxine-binding globulin, thyroxine-binding prealbumin and albumin

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19
Q

What layer of the adrenal gland secretes aldosterone?

A

Zona glomerulosa

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20
Q

What stimulates aldosterone secretion?

A

AngII and potassium

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21
Q

Where is the majority of cholesterol for synthesis of adrenocortical hormones from?

A

LDLs

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22
Q

In which organelles are adrenal steroids synthesised?

A

Mitochondria and endoplasmic reticulum

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23
Q

Why doesn’t cortisol activate the renal mineralocorticoid receptor?

A

11B-hydroxysteroid dehydrogenase converts cortisol => less potent cortisone

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24
Q

Where is the main site of aldosterone action?

A

Principal cells in collecting tubules

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25
Q

What acid base disturbance is seen with aldosterone excess?

A

Metabolic alkalosis
H+ secreted in exchange for K+ in intercalated cells of collecting ducts

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26
Q

Where in the cell does aldosterone act?

A

Cytoplasm - mineralocorticoid receptor

27
Q

What factors increase aldosterone secretion?

A

^K+
^AngII

28
Q

What factors decrease aldosterone secretion?

A

^Na
^ANP

29
Q

What effect does ACTH have on the rate of aldosterone secretion?

A

Very little, however, is necessary for secretion

30
Q

How does cortisol affect CHO metabolism?

A

Stimulates gluconeogenesis - increases enzymes required for aa => glucose, mobilises amino acids, antagonises insulin’s antagonist effects on gluconeogenesis
Reduces cellular glucose utilisation - reduces GLUT4 translocation

31
Q

How does ACTH stimulate steroid synthesis?

A

Activates adenyl cyclase, which activates cAMP
Activates protein kinase A - converts cholesterol to pregnenolone - rate-limiting step of steroid synthesis

32
Q

What are the 3 cell types of the endocrine pancreas and what are their secretions?

A

Alpha cells - glucagon
Beta cells - insulin
Delta cells - somatostatin
PP cells - pancreatic polypeptide

33
Q

Insulin half life

A

6 minutes

34
Q

How is insulin degraded?

A

Insulinase (liver)

35
Q

What is the main energy source for muscle, how does this change in different states?

A

Rest - fatty acids
Exercise - muscle contraction increases translocation of GLUT4 to membrane - glucose
Following meal - insulin allows transport of glucose into cells - glucose

36
Q

How does insulin affect glucose handling in the liver?

A

Inactivate phosphorylase - prevents glycogen breakdown
Activates glucokinase - increases glucose uptake
Activates glycogen synthase - increases glycogen synthesis

37
Q

How is glucose handling in the liver affected by lack of low glucose (and insulin) levels)

A

Phosphorylase activated - glycogen breakdown
Glucose phosphatase activated - allows release of free glucose

38
Q

Briefly describe the mechanism of insulin secretion by the pancreatic beta cells

A

Glucose entters via GLUT-2 channel
Phosphorylated to glucose-6-phosphate (glucokinase)
Oxidised to ATP
Inhibits ATP K channels
Depolarises cell
Opens voltage-gated calcium channels
Exocytosis of insulin-containing vesicles

39
Q

Other than glucose, what factors increase insulin secretion?

A

Amino acids (small effect when BG normal, when BG high potentiate glucose stimulation)
GI hormones - GLP-1 and GIP most potent (also gastrin, secretin and CCK)
Other hormones - glucagon, GH, cortisol, progesterone/oestrogen

40
Q

What are the effects of glucagon on metabolism?

A

Increased glycogenolysis
Increased gluconeogenesis
Increases amino acid uptake by liver
Activates adipose cell lipase - increases fatty acids
Inhibits storage of triglycerides

41
Q

What stimulates glucagon release?

A

Increased BG
Increased blood amino acids
Exercise

42
Q

How does hypocalcaemia affect the nervous system and why?

A

Increased excitability
Increased neuronal permeability to sodium

43
Q

How is calcium handled in the kidneys?

A

Protein-bound not filtered in glomerulus, rest is
99% reabsorbed
90% in PT, LOH and DT
10% in CD - more variable

44
Q

What is bone composed of?

A

Organic matrix and calcium salts

45
Q

What is the composition of organic matrix of bone?

A

90-95% collagen fibres
Remained ground substance - extracellular fluid, proteoglycans (chrondroiton sulphate and hyaluronic acid)

46
Q

What ions are present in bone salts?

A

Calcium, phosphate, magnesium, sodium, potassium, carbonate

47
Q

What prevents precipitation of hydroxyapatite in extracellular fluid?

A

Inhibitors - eg pyrophosphate

48
Q

How is calcium salt deposition in osteoid regulated?

A

Inhibited by pyrophosphate
Levels regulated by tissue-nonspecific alkaline phosphatase, secreted by osteoblasts

49
Q

What 3 substances are secreted by osteoblasts?

A

Tissue-nonspecific alkaline phosphatase - inhibits pyrophosphate
Nucleotide pyrophosphate phosphodiesterase 1 - produces pyrophosphate outside the cells
Ankylosis protein - transports pyrophosphate from inside to surface of cell

50
Q

What is the main regulator of osteoclast activity? How does the regulation take place?

A

PTH
Indirectly - osteoblasts signal osteoclast precursors to mature - RANKL and macrophage colony-stimulating factor

51
Q

How to osteoblasts prevent bone respiration?

A

Secrete osteoprotegerin (OPG) - binds RANKL and prevents binding to osteoclasts

52
Q

How to PTH and Vit D affect osteoclast signalling?

A

Inhibit OPG production
Stimulate RANKL production

53
Q

What regulates the rate of conversion of cholecalciferol to 25-hydroxycholecalciferol and where does conversion occur?

A

Liver
Feedback inhibition

54
Q

What regulates the rate of conversion of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol and where does conversion occur?

A

PTH
Proximal tubule of kidney

55
Q

Where in the cell are vitamin D receptors found?

A

Nuclei

56
Q

What are the effects of vitamin D?

A

Increases intestinal absorption of calcium and phosphorus
Decreases renal excretion of potassium and phosphorus
Promotes bone calcification in small quantities
Increases bone resorption in extreme quantities

57
Q

How does vitamin D increase intestinal absorption of calcium?

A

Increasing formation of calbindin in intestinal epithelial cells

58
Q

How does PTH affect the kidneys?

A

Increased calcium reabsorption
Reduced phosphate reabsorption
Increases reabsorption of magnesium and hydrogen ions
Decreases reabsorption of sodium, potassium and amino acids

Increased formation of 1.25-dihydroxycholecalciferol

59
Q

Where does renal calcium reabsorption increase in response to PTH?

A

Thick ascending LOH
Distal tubules

60
Q

How is PTH secretion regulated?

A

Calcium-sensing receptor
G-protein-coupled receptor
Stimulated by calcium - activates phospholipase C - increases inositol triphosphate and DAG formation => stimulates calcium release from intracellular stores => PTH secretion decreased

61
Q

Where is calcitonin secreted?

A

Thyroid gland
Parafollicular (C) cells

62
Q

How does calcitonin act?

A

Decreases osteoclast activity
Decreases osteoclast formation

63
Q

What is the first line of defence against hypocalcaemia?

A

Buffer function of exchangeable calcium - predominantly in bones but also mitochondria especially of liver and intestine

Guyton (10 decks)

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