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MISCELLANEOUS lectures Flashcards

1
Q

what type of regulation is ADH involved in?

A

short term regulation of plasma osmolality

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2
Q

what type of regulation is Aldosterone involved in?

A

long term regulation of plasma volume

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3
Q

where is ADH synthesised?

A

mainly in the magnocellular cells of the paraventricular and supra-optic nuclei of the hypothalamus

some are synthesised in the parvocellular cells of the paraventricular nuclei, those are co-released with CRH, and they enhance the activity of CRH at releasing ACTH. it also means that when ACTH is secreted there is ADH action

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4
Q

how is the baroreceptor reflex involved in plasma osmolality?

A

the reflex has tonic alpha adrenergic mediated inhibition on the paraventricular neurones of the hypothalamus, preventing the release of ADH

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5
Q

how is the sub-fornical organ involved in plasma osmolality?

A

this organ stimulates drinking behaviour if the plasma osmolaility drops by 2-3%

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6
Q

how does nicotine effect plasma osmolality

A

nictonic receptors are found on the paraventricular neurones which synthesise ADH, and nicotine

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7
Q

how does nicotine effect plasma osmolality

A

nictonic receptors are found on the paraventricular neurones which synthesise ADH, and nicotine acts on them to cause the release of ADH

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8
Q

what is an orchiodemter?

A

this is used to assess the size of a boy’s testis

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9
Q

what do pubertal stages consist of?

A

assessing pubic and auxiliary hair stageing.

assessing the development of a boy’s external genitalia, and assessing the development of the female’s breast

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10
Q

what are the main effects of aldosterone concerned with increasing sodium reabsorption?

A

gene transcription of ENAC channels, which get displaced to the luminal side, those increase sodium absorption.

aldosterone also increases the transcription of a threonine/serine kinase (pKA) and this phosphorylates the Na/K+ pump on the plasma side, and the ROMK channel on the luminal side - this results in an overall loss of potassium

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11
Q

where are the osmoreceptors located in the hypothalamus?

A

they’re located around the 3rd ventricle in the organum vasculosum of the lamina terminalis

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12
Q

how does the body respond to an increase in plasma osmoality?

A

this is detected via the osmoreceptors, which signal the paraventricular nuclei to release ADH. ADH works to increase water reabsorption. the increase in blood volume increases blood pressure and this means the tonic inhibition from the baroreceptor reflex increases

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13
Q

how does the body respond to an increase in plasma volume?

A

this is detected by reduced sodium influx at the macula densa cells, increased sympathetic activation due to reduced BP and reduced transmural pressure - this activates renin and starts the RAS

angiotensin II:
- increases drinking behaviour
- sensitises the osomoreceptors
Aldosterone:
- released in response to angiotensin or increased plasma K+
- this increases sodium retention, which increases plasma osmolality
- this is detected by the osmoreceptors and leads to the release of ADH
- and the loop continues

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14
Q

what is the primary cause of mineralocorticoid excess characterised by hormonally?

A

low renin

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15
Q

what is low renin, low aldosterone indicative of? but symptoms of excessive mineralocorticoid (normal sodium, low potassium, hypertension)

A

Cushing’s disease

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16
Q

what is low renin, high aldosterone indicative of

A

Conn’s syndrome which is a primary cause of hyperaldosteronism

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17
Q

what is low renin, high aldosterone indicative of

A

Conn’s syndrome which is a primary cause of hyperaldosteronism

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18
Q

how do we treat AME

A

Spironolactone
ACE inhibitors
K+ to restore plasma K+

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19
Q

what can cause adrenal insufficeny?

A

Addison’s disease

CAH: B112 and C21 MUTATIOSN

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20
Q

What are the symptoms of diabetes insipidius?

A

polyuria, polydipsia and hypovolemic hypotension and increased renin

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21
Q

why does ADH secretion not fall to zero in neurogenic DI cause by damage to the hypothalamic tract

A

because some ADH is released from the parvocellualr neurones with CRH into the anterior pituitary

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22
Q

what is the difference between treating cranial and nephorgenic DI

A

we cannot treat nephrogenic using ADH analogues

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23
Q

what is the single most important enzyme in protecting us from AME

A

11-HSD type 2

  • this oxidise cortisol into cortisone
  • found mostly in aldosterone selective tissue
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24
Q

what is the function of 11-HSD in the placenta (Type 2)

A

This is to protect the foetus from premature exposure to cortisol which can cause premature tissue differentiation and result in intra-uterine growth restriction - which has bad effects of health of child later in their adult life

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25
Q

where is 11-HSD type 1 located mostly, and how is this significant and exploited pharmacologically?

A

located mainly in the liver–

this is important because cortisone and methyprendisone must be given orally to be first activated in the liver, from their inactive form to their active forms

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26
Q

what is a pharmacological agonist of MR

A

DOCA and fludrocortisone

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27
Q

which direutic can be used to treat DI?

A

thiazide

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28
Q

why is the MR problematic

A

has no inherent specificity for mineralocorticoids, has higher affinity than the glucocortioid receptor, and also cortisol is found at a much higher concentration than aldosterone. furthermore cortisol elves fluctuate according to the circadian rhythm

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29
Q

when can despite having functional 11-B HSD2 can AME still occur?

A

in times of excess cortisol, e.g. Cushing’s because we have exceeded the enzymatic capacity

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30
Q

what are the symptoms of AME/

A 
anti-natriuses (but not hypernatraemia) 
increased fluid reabsorption 
hypertensive hypervoleamia 
kailuresis lead to hypokalaemia 
muscle weakness and fatigue 
hypokalaemia can be life-threating 
alkalosis
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31
Q

what are the symptoms of AME/

A 
anti-natriuses (but not hypernatraemia) 
increased fluid reabsorption 
hypertensive hypervoleamia 
kailuresis lead to hypokalaemia 
muscle weakness and fatigue 
hypokalaemia can be life-threating 
alkalosis
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32
Q

what is the single most dangerous aspect of syndrome of inappropriate diruses?

A

natriuses which can lead to life-threating hyponatraemia

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33
Q

what is the co-factor that HSD type I used

A

used NADPH

34
Q

what is the co-factor that HSD type 2 uses?

A

uses NAD+

35
Q

what three factors, apart from vitamin D regulate PTH secretion?

A

magnesium, histamine and adrenaline

36
Q

how does PTH increase plasma calcium and decrease plasma phosphate?

A

increases plasma calcium directly via its action on bone and kidney and indirectly by activating Vitamin D which increases phosphate and calcium absorption from the GI tract

37
Q

How does PTH reduce phosphate plasma levels?

A

by reducing its reabsorption at the proximal tubule, thereby increasing its excretion

38
Q

what are the overall effects of PTH?

A

to increase plasma calcium levels and decrease phosphate plasma levels

39
Q

what causes primary hyperparathyrodism?

A

a benign tumour

40
Q

what causes secondary hyperparathyroidism?

and explain how renal failure can lead to it

A

this is a normal compensatory mechanism for long withstanding hypocalacaemia or low levels of calcitonin (seen in renal failure)

low calcitonin causes a decrease in vitamin D receptors in the Parathyroid gland - and this leads directly to an increase in transcription and growth of the PTH and hyperplasia of the gland

41
Q

in hypothyroidism what is the level of PTH, phosphate and calcium?

and why can it only be treated with calcitriol?

A 
PTH = LOW 
PHOSPHATE = HIGH
CALCIUM = LOW

can only be treated by calcitriol, because vitamin D activation is dependant on 1HYDROXYLASE enzyme which is dependant on PTH

42
Q

What are the levels of calcium, phosphate and PTH in pseudohypoparathyroidism? and what causes it?

A 
PTH = HIGH/NORMAL 
CALCIUM = LOW
PHOSPHATE = HIGH

the tissues are resistant to PTH (problems with receptors)

43
Q

What are the levels of calcium, phosphate and PTH in pseudohypoparathyroidism? and what causes it?

A 
PTH = HIGH/NORMAL 
CALCIUM = LOW
PHOSPHATE = HIGH

the tissues are resistant to PTH (problems with receptors)

44
Q

explain the structure of calcitonin, and where it is secreted from?

A

it is secreted from C-cell from the thyroid gland (they’re also called amine precursor uptake decarboxylating cells.

it is a 32 aa peptide, but arises from 136aa gene

  • differential splicing of introns leads to
  • CGRP in brain
  • calcitonin in thyroid
45
Q

what is the action of calcitonin?

A

calcitonin inhibits 1 hydroxylase and reduces bone mobilisation - usually is secreted in response to hypercalcaemia to reduce plasma calcium levels

46
Q

what is the difference between MEN I and MEN II ?

A

MEN -1 refers to endocrine tumours from non-neural crest origin

MEN -11 refers to endocrine tumours from a neural crest origin

47
Q

what characterises Calcitonin tumours (medullary thyroid tumours)

A

can occur with or without phaemchromocytoma.

characterised by high calcitonin but normal calcium levels

48
Q

what is the biochemical name from D3? where is it obtained from

A

cholecalciferol

obtained from the slow thermal isomerisation of 7 dehydrocholestrol in the skin by UV-LIGHT

49
Q

what happens if UV-B intensity is low or high?

A

if low: this results in vitamin D deficiency

if high: this results in no excess vitamin D- because we make as much vitamin D as we require

50
Q

what is the biochemical name for D2? where does it come from

A

ergocalciferol obtained from diet

51
Q

what are the steps involved in activation of vitamin D

A

hydroxylation step 1 in liver:
25 hydroxylase to make 25 hydroxycholecalciferol

hydroxylation step 2 in kidney:
1 hydroxylase to make 1,25 dihydroxycholecalciferol
this is calcitriol the most active form of vitamin D

52
Q

how is vitamin D inactivated?

A

24 hydroxylase which causes further hydroxylation - and this causes inactivation.

calcitriol causes: inactivation via activation of 24 hydroxylase
calcitriol also inhibits 1 hydroxylase reducing vitmain D synthesis

53
Q

how is vitamin D inactivated?

A

24 hydroxylase which causes further hydroxylation - and this causes inactivation.

calcitriol causes: inactivation via activation of 24 hydroxylase
calcitriol also inhibits 1 hydroxylase reducing vitmain D synthesis

54
Q

why are vitamin D analogues better at treating secondary hyperparathyrodism than calcitriol?

A

because calcitriol will cause hyperphosphateamia and hypecalcaemia via its action on the GI tract

analogues tend to have higher selectivity for the parathyroid glands with lesser effect on calcium and phosphate absorption

55
Q

how does hypocalcaemia lead to PTH release?

A

this leads to inactivation of calcium sensing receptors
which leads to an increase of PTH directly
calcium levels rise within minutes

56
Q

what are Chvostek’s sign and Troussea’s signs indicative off?

A

they’re indicative of neuromuscular hyperexctiability cause by hypocalcaemia

57
Q

what does secondary hyperparathyrodism lead to?

A

sub-periosteol bone erosion
cyst formation and bone pain leading to risk of fracture and osteoporosis
renal caliculi formation

58
Q

what will hypo magnesia cause?

A

hypocalcaemia

59
Q

what will renal failure cause?

A

hypocalcaemia

60
Q

what are the symptoms of hypocalcaemia?

A

numbness and paraesthesia

mood swings and depression

tetany and neuromuscular excitability 
convulsions 
cardiac aryhtmias (long QT interval on ECG) 
catarcts 
spasms and stridor
61
Q

what are the symptoms of hypercalcaemia?

A 
stones 
bone pain 
abdominal pain, nausea and vomitting 
polyuria 
neuromuscular symptoms caused are due to calcium blocking the sodium channels and inhibiting depolarisation of nerve and muscle fibres

decreases heart rate, but increases contractility - leading to short QT interval on ECG

icnreases gastrin production which increases gastric acidity and leads to peptic ulcers

62
Q

when is phosphate levels raised?

A

renal failure
hypoparathryodism
pseudohypoparathryodism

63
Q

when is high calcium high phosphate levels seen?

A

vitmain D intoxication

64
Q

when is high calcium high phosphate levels seen?

A

vitamin D intoxication

65
Q

WHAT is long QT interval associated with?

A

associated with hypocalcaemia

66
Q

what is short QT interval associated with?

A

associated with hypercalcameia

67
Q

briefly explain the difference between competitive assay binding and sandwich assaying? and when they’re both used

A

• SANDWICH ASSAY (ELISA and immunometric)
o Amount of label increases with concentration of hormone
o Can only be used for hormones greater than 1000 molecular weight (cannot be used for T3/T4 or steroids)
• Competitive binding assay
o Used when hormone has a molecular weight of less than 1000
o Amount of label decreases as the concentration of hormone increase

68
Q

what are the non-classical MHC molecules and why are they significant?

A

those are HLA -G, E and F

they’re not found anywhere else in the body except from the placenta. those non-classical MHC prevent the NK from killing the foetus which does not express MHC

69
Q

what contributes to immunosuppression at the foetal-maternal interface?

A

o No expression of MHC I or II molecules
o IL-10, TGF-B and IDO expression
o Fas-L expression
o Non-classical MHC molecules (HLA-G, E and F)
• Prevent natural killer cell from killing cells that do not express MHC molecules

70
Q

what are the function of uterine NK cells?

A

those are found in the endometrium, and up-regulated during pregnancy. their cytotoxic action is down regulated by HLA-G but they cause secretion of VEGF and vasoactive mediators

71
Q

what distinguishes NK from decidual NK cells?

A

Peripheral NK:CD 56 dim
CD57
CD16
CD62

Decidual NK: cd56 BRIGHT
- CD69
c-KIT

72
Q

what is meant by the honeymoon phase seen in T1DM?

A

this refers to the regenerative capacity of beta cells, after T1DM onset. this phase is only transient- because the immune system wins

73
Q

what causes the pathology in the eye associated with Grave’s disease?

A

• Pathology associated in the eye with grave’s is not associated with antibodies, but rather T-cell secreting cyotkines including IL-1 and TNF and IFN-Y which cause activation of fibroblasts

recall that TSH-R are not exclusive to the thyroid gland, but some are also found in the orbital fibroblasts

74
Q

what are the auto-antibodies in Hashimoto’s

A

Thyroid perioxidase, Thyroglobuin

75
Q

which MHC complex increases the risk of Hashimotos

A

HLA-DR 5

76
Q

Which MHC complex increases the risk of Grave’s

A

HLA-DR 3

77
Q

which MHC complex increases the risk for diabetes and which complexes causes resistance?

A

MHC-DQ-8 = increases risk

MHC-DQ-6 = reduction of risk

78
Q

what are the antibodies and T-cells in Addisons’ directed aganist

A

21 hydroxylase

79
Q

what is the consequence of activated TH1 in the thyroid gland?

A

this causes secretion of IL-1 AND IFN-Y (which leads to aberrant expression of MHC-11 by thyroid epithelial cells)

  • this does not initiate the autoimmune disease, but can exacerbate the autoimmune disease
80
Q

what is the co-stimulator molecules for Naive T-cell receptors?

A

CD40 to CD4O-L (on T-cell)
CD28 (on T-cell) to CD80/CD86
CTLA-4 (on T-cell) to CD80/CD86

Endocrinology (6 decks)

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