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Endocrinology > introduction > Flashcards

introduction Flashcards

1
Q

where does the anterior pituitary develop from?

A

from epithelium in the roof of the mouth before the bony palate closes

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2
Q

where does the posterior pituitary develop from?

A

from neural cells in the third ventricle?

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3
Q

where do hormones released from the posterior pituitary synthesised?

A

in the magnocellular cells of the hypothalamus

  • those cells are the paraventricular nuclei, and the supra-optic nucleus
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4
Q

what is the pituitary stalk?

A

this is a connecting stalk containing the axons from the magnocellular cells of the hypothalamus. it contains the hypothalamo-hypophyseal tract

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5
Q

what is the posterior pituitary

A

it is a collection of nerve endings

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6
Q

how are substances released from the anterior pituitary?

A

hypothalamus releases neuropeptides into the median eminence, those are taken via the highly fenestrated capillaries of the hypophyseal portal system and transported to the anterior pituitary
NO direct projection of the hypothalamus to the anterior pituitary.

content released from the anterior pituitary to the general circulation via the seoncdary hypophyseal plexus then via the superior hypophyseal artery

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7
Q

what is the pars intermedialis?

A

this is between the anterior and posterior lobe. it is more related to the posterior lobe and is separated from the anterior lobe by the hypophyseal cleft. the main hormone here is melanoycte stimulating hormone.

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8
Q

what is the fergusson’s reflex?

A

it is the positive feedback of oxytocin release seen during childbirth

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9
Q

what are the TFG-B receptor associated with?

A

they’re associated with co-smads and R smads

1. 1.cosmad and 2 r.smads form a heterotrimer and translocates into the nucleus

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10
Q

what are the cytokine receptors associated with?

A

JAK protein kinases activating the STAT pathway or the MAPK pathway

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11
Q

what are the tyrosine kinase receptors associated with?

A

They’re associated with Grb-2 MAPK pathway

or for insulin IRS-1 MAPK pathway or PI-3K pathway (for glut 4 translocation)

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12
Q

what are the GCPR associated with (adrenoreceptors?

A

PKA with threonine/serine activity

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13
Q

give an example of a type I receptor

A

androgen, oestrogen, progesteron and glucocorticoid receptors

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14
Q

where is type I receptor located?

A

in the cystosol?

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15
Q

what is the consequence of a ligand binding to a type I receptor?

A

dissociation of heat shock proteins, homodimerisation and translocation into the nucleus

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16
Q

what type of receptors do type I receptors bind to?

A

HRE they have inverted repeats separated by a variable fragment of DNA

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17
Q

Where are type II receptors located?

A

they’re located in the nucleus?

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18
Q

what does ligand binding to type II receptors result in?

A

causes heterodimerisation (usually with RXR) the dissociation of co-repressors and recruitment of co-activators

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19
Q

what type of receptors do TYPE II receptors bind to?

A

direct repeats

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20
Q

give an example of a type II receptor

A

thryoid hormone

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21
Q

what is a type III receptor?

A

those are orphan receptors with no known endogenous ligands

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22
Q

what type of receptors do type III receptors bind to?

A

they bind to direct repeats

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23
Q

what is the consequence of ligand binding to type III receptors?

A

homodimerisation

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24
Q

what is the function of type III receptors?

A

metabolic sensors

CAR and PXR upregulate cytochrome P450 in response to xeniobiotics

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25
Q

what is an agonist response?

A

this is when ligand binding causes recruitment of co-activators are usually histone acetyl-transferases

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26
Q

what is co-repression

A

when an antagonist binds and causes a conformational shape change that favours the binding of co-repressors. those change are usually histone de-acetylases

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27
Q

what is the function of somatostatin?

A

it is a paracrine hormone ad suppresses both insulin and glucagon release from the pancreas

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28
Q

where is the major source of somatostatin?

A

from the D gastric cells, rather than delta pancreatic cells

  • those are released in response to food in stomach and reduced pH
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29
Q

what is the function of pancreatic polypeptide?

A

secreted after eating to suppress appetite

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30
Q

what is the function of IAPP or amylin?

A

suppress insulin secretion

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31
Q

what is the function of IAPP or amylin?

A

suppress insulin secretion

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32
Q

what is the function of GIP?

A

increases insulin release– this is an incretin released fro, they tend to be released from the L cells of the small intestines

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33
Q

what is the function of GIP?

A

increases glucagon release

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34
Q

how do glucocorticoids spare glucose metabolism?

A

they increase the expression of HSL

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35
Q

how do glucocorticoids spare glucose metabolism?

A

they increase the expression of HSL

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36
Q

what are the endocrine disorders that can cause diabetes?

A

cushing’s disease and acromegaly

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37
Q

what drugs can cause diabetes?

A

beta blockers, glucocorticoids and thiazides

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38
Q

what is IGT? and what implications for the patient?

A

impaired glucose tolerance - patients will usually have no symptoms.

patient more likely to develop frank diabetes and cardiovascular disease

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39
Q

what is MODY?

A

This is monogenic (autosomal dominant condition), this usually manifests pre-25yrs. also not associated with obesity

40
Q

what is fructosamine?

A

fructosamine - medium term measurement of glycated proteins especially serum proteins (albumin- with a half life of 20 days)

41
Q

what is glycosylation?

A

this is a non-enzymic process, where glucose reacts with lysine residues of a protein

42
Q

what are the different analogues of insulin?

A

those that inhibit hexamerisation: rapidly acting
bind albumin: medium actin
insoluble depots under the skin: very long acting

43
Q

what are the histological differences between T1DM and T2DM

A

T1DM:
- lymphocyte infiltration and autoantibody infiltration of the pancreas

T2DM;

  • amyloid deposits
  • in early stages of the disease hypertrophy of the islets occur, to compensate for insulin resistance (hyperinsulinamie)
  • then beta cells reach exhaustion and the islets shrink and form amyloids (those are islet amyloid peptides)
44
Q

what are the histological differences between T1DM and T2DM

A

T1DM:
- lymphocyte infiltration and autoantibody infiltration of the pancreas

T2DM;

  • amyloid deposits
  • in early stages of the disease hypertrophy of the islets occur, to compensate for insulin resistance (hyperinsulinamie)
  • then beta cells reach exhaustion and the islets shrink and form amyloids (those are islet amyloid peptides)
45
Q

what does unopposed glucagon lead to?

A

increased protein breakdown
increased lipolysis and ketogeneiss
increased hepatic glucose output
increase in gluconeogeneiss

46
Q

what does reduced insulin sensitivity lead to?

A

inability to inhibit hepatic glucose ouptut
inability to have IMGD
and inabiity to inhibit lipolysis in adipocytes

47
Q

what are dysfunctional adipose tissue?

A

this explains why some obese patients have diabetes and others do not

dysfunctional tissue has:

  • low adiponectin
  • high leptin, IL-6 and TNF and MCP-1

this is usually associated with ectopic deposits around the abdomen

48
Q

how are AGE-p formed?

A

glucose + proteins form schiff base (rapid and reversible reaction)

schiff base undergoes and amadori re-araangemt to form a ketoamine (this is slow and irreversible)

this then forms AGE-P

49
Q

how does AGE-P affect protein turnover?

A

intra-crosslinking within the protein, and cross linking with other proteins

50
Q

what is the biggest problem with T1DM?

A

keto-acidosis

51
Q

what is the biggest problem with T2DM?

A

AGE-products

52
Q

what does the presence of auto-antibodies indicate

A

the number of different types of auto bodies predict the rate of onset and whether or not the individual will develop diabetes

53
Q

why do some individuals with autoantibodies in their circulation not develop frank T1DM?

A

because they have anti-idiotypic antibodies. those bind to the antigen binding site of the auto-antibodies. so that those anti-iodotypic antibodies and autontibodies exist in equilibrium

54
Q

what are the two effects of autoantibodies?

A

those cause the neutralisation of the auto antibodies and they also prevent the secretion of auto-antibodies

55
Q

at least in the early phases of T2DM what distinguishes it from T1DM?

A

the presence of high levels or normal levels of insulin within the circulation

56
Q

what is T2DM caused by?

A

insulin resistance and beta cell dysfunction (and the inability of insulin to suppress hepatic gluconeogenesis)

57
Q

what does insulin resistance manifest as?

A

the inability of the reduced ability to clear a glucose load

58
Q

where does insulin resistance first manifest?

A

first seen in adipose tissue and skeletal muscle and then goes on to effect the over

59
Q

what are some of the factors inducing insulin resistance?

A

elevate fatty acids
inflammatory mediators
high concentration of hormones antagonising insulin (GC and adrenaline and glucagon)

60
Q

what is the effect of insulin resistance on skeletal muscle?

A

less IMGD via GLUT 4 receptors

61
Q

what is the effect of insulin resistance on the liver?

A

the inability of insulin to suppress hepatic gluconeogenesis increases hepatic glucose output

(insulin does not affect glucose intake into the liver but antagonises the effect of glucagon within the liver)

62
Q

what are the effects of insulin resistance on adipocytes?

A

cannot suppress lipolysis, this increases the concentration of fatty acids within the circulation

63
Q

what are the effects of insulin resistance on adipocytes?

A

cannot suppress lipolysis, this increases the concentration of fatty acids within the circulation. those are transported to the liver and converted into TAG which recirculate as VLDL and cause dyslipidaemia

64
Q

what is the effect of insulin resistance on the sympathetic nervous system?

A

it stimulates the sympathetic nervous system causing hypertension

65
Q

what is the effect on insulin on the ovaries?

A

it increases androgen production and this could contribute to the metabolic disturbances seen in PCOS

66
Q

what causes serine phosphorylation and what’s the problem with it?

A

serine phosphorylation is caused by;

  1. inflammatory mediators released from adipocytes
  2. NEFAs and DAG

they cause serine phosphorylation of IRS-1 and IRS-2 and this inhibits their ability to stimulate growth and metabolism

67
Q

what is IRS-1 associated with?

A

associated with insulin resistance

68
Q

what is iRS-2 associated with?

A

important in the pancreatic secretion of insulin - impaired action leads to pancreatic insufficiency

69
Q

what is MODY?

A

this is an autosomal dominant condition not associated with diabetes or autoantibodies it is monogenic

70
Q

what is mitochondrial diabetes?

A

inherited maternally

  • it is associated with muscle weakness and deafness and lactic acidosis
  • the mutations in the mitochondria reduce its oxidative ability
  • this manifests in pancreatic insufficiency because insulin release is dependant on glycolysis
71
Q

what is gestational diabetes?

A

severe insulin resistance caused by hormonal changes and metabolic stress of pregnancy,

in women with low insulin secreting capacity this can result in diabetes

72
Q

what is gestational diabetes?

A

severe insulin resistance caused by hormonal changes and metabolic stress of pregnancy,

in women with low insulin secreting capacity this can result in diabetes

73
Q

what is the effect of hyperthyroidism on sugar levels?

A

causes increased insulin resistance and diabetes for unknown cause

74
Q

how does acromegaly affect plasma glucose levels?

A

GH is counter regulatory to ACTIONS of SST and insulin. GH has no effect on insulin secretion.

GH causes insulin resistance

75
Q

what are the effects of glucocorticoids on plasma glucose levels?

A

glucocorticoids increase insulin resistance and cause frank T2DM (mainly by causing resistance in target tissues) - because patients have normal beta function, they can secrete insulin to compensate, so only patients with compromised secretory capacity are affected

attributed to lower phosphorylation of IRS

76
Q

what is the effect of adrenaline on plasma glucose levels

A

it inhibits insulin secretion (a2) AND causes insulin resistance

reduces phosphorylation of IRS-1

77
Q

how can we measure the level of insulin released over a period of time?

A

by measuring amount of C-peptide in circulation

78
Q

how do we diagnose T1DM?

A

presence of autoantibodies and absence of C-peptides

79
Q

what is the main cause of insulin insensitivity

A

because of an increase in lipolysis

80
Q

what is the aim of insulin injections

A

increase glucose metabolism and inhibit gluconeogenesis

81
Q

explain how PCOS causes diabetes?

A

insulin increases androgen secretion by the ovaries, and excess androgens cause insulin resistance

82
Q

what is the mechanism (molecular) by which insulin resistance manifests?

A

through problems in downstream signalling involving the IRS proteins

83
Q

where does the adrenal cortex arise from?

A

mesothelium of the mesonephros of the embryonic adrenal cortex

84
Q

where does the adrenal medulla arise from?

A

neural crest origin, phaeochromaffinoblasts invade the cortex and establish cords around the vascular spaces to form the medulla

85
Q

what structure provides the corticosteroids to the medulla?

A

the cortical capillaries (cortical venues)

86
Q

give the steps in catecholamine biosynthesis

A

Tyrosine –> DOPA (tyrosine hydroxylase - this is the rate limiting step)
Dopa –> Dopamine (dopa decarboxylase)
dopamine–> noradrenaline (dopamine hydroxylase)
noradrenaline —> adrenaline (PMNT)

87
Q

what is the activity of PMNT (phenoethaloamine N-meythyl-transferase) dependant on?

A
  • sympathetic acitivty

- corticosteroids delivered from the adrenal cortex

88
Q

why do neural cells not synthesise adrenaline?

A

because they do not have PMNT

89
Q

what are alpha receptors coupled to

A

PLC/calcium

90
Q

what are beta receptors coupled to

A

cAMP-PKA

91
Q

What are the metabolic affects mediated by catecholamines? and what are they mediated through?

A

mainly mediated though adrenaline (because they’re in circulation)

  • hyperglycaemia
    A2 receptors inhibits insulin release (this reduces IMGD)
  • increase in lactate and free fatty acid plasma concentration
    mediated through beta receptors

noradrenaline has very little effect on plasma glucose, although may slightly increase plasma insulin

92
Q

what are the two enzymes involved in catecholamine metabolism?

A

MAO AND COMT - THEY PRODUCE INERT METABOLITES FOR EXCRETION E.G. VMA

the order at which the enzymes work in is unimportant, because they end up producing the same end production

93
Q

what type of tumours occur in MEN-11

A

medullary carcinoma of the thyroid
phaechromocytoma
primary hyperparathyroidism

94
Q

what does adrenomedullalry hypofuntion result in?

A

hypoglycaemia and hypotension

95
Q

what does adrenomedullalry hyperfunction result in?

A

hyperglycaemia and hypertension

96
Q

how do we treat phaemochromocytoma?

A

• We must first stabilise the tumour, this is done via alpha and beta blockade
o Alpha blockade is done first, and this is to prevent a hypertensive crisis occurring due to unopposed alpha adrenoreceptors stimulation
o This manipulation before surgery is essential otherwise the tumour can cause catastrophic release of stored catecholamines
• After stabilisation the tumour is removed

97
Q

how do we diagnose phaemochromocytoma?

A

• Release is episodic so excess catecholamines can be determined by assay of urine collected over 24 hours
o Usually VMA is measured, but other end-products can be measured depending on the cells the tumour has hijacked
• Imaging with uptake scans with meta-iodobenzylguanidine (mIBG)
o Also MRI or PET scanning
• Individual chromaffin cells usually secrete either adrenaline or noradrenaline
• BUT phaeochromocytomas usually over-secrete both hormones

Endocrinology (6 decks)

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