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MISCELLANEOUS lectures Flashcards

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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
where is 11-HSD type 1 located mostly, and how is this significant and exploited pharmacologically?
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
26
what is a pharmacological agonist of MR
DOCA and fludrocortisone
27
which direutic can be used to treat DI?
thiazide
28
why is the MR problematic
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
29
when can despite having functional 11-B HSD2 can AME still occur?
in times of excess cortisol, e.g. Cushing's because we have exceeded the enzymatic capacity
30
what are the symptoms of AME/
``` anti-natriuses (but not hypernatraemia) increased fluid reabsorption hypertensive hypervoleamia kailuresis lead to hypokalaemia muscle weakness and fatigue hypokalaemia can be life-threating alkalosis ```
31
what are the symptoms of AME/
``` anti-natriuses (but not hypernatraemia) increased fluid reabsorption hypertensive hypervoleamia kailuresis lead to hypokalaemia muscle weakness and fatigue hypokalaemia can be life-threating alkalosis ```
32
what is the single most dangerous aspect of syndrome of inappropriate diruses?
natriuses which can lead to life-threating hyponatraemia
33
what is the co-factor that HSD type I used
used NADPH
34
what is the co-factor that HSD type 2 uses?
uses NAD+
35
what three factors, apart from vitamin D regulate PTH secretion?
magnesium, histamine and adrenaline
36
how does PTH increase plasma calcium and decrease plasma phosphate?
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
How does PTH reduce phosphate plasma levels?
by reducing its reabsorption at the proximal tubule, thereby increasing its excretion
38
what are the overall effects of PTH?
to increase plasma calcium levels and decrease phosphate plasma levels
39
what causes primary hyperparathyrodism?
a benign tumour
40
what causes secondary hyperparathyroidism? and explain how renal failure can lead to it
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
in hypothyroidism what is the level of PTH, phosphate and calcium? and why can it only be treated with calcitriol?
``` 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
What are the levels of calcium, phosphate and PTH in pseudohypoparathyroidism? and what causes it?
``` PTH = HIGH/NORMAL CALCIUM = LOW PHOSPHATE = HIGH ``` the tissues are resistant to PTH (problems with receptors)
43
What are the levels of calcium, phosphate and PTH in pseudohypoparathyroidism? and what causes it?
``` PTH = HIGH/NORMAL CALCIUM = LOW PHOSPHATE = HIGH ``` the tissues are resistant to PTH (problems with receptors)
44
explain the structure of calcitonin, and where it is secreted from?
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
what is the action of calcitonin?
calcitonin inhibits 1 hydroxylase and reduces bone mobilisation - usually is secreted in response to hypercalcaemia to reduce plasma calcium levels
46
what is the difference between MEN I and MEN II ?
MEN -1 refers to endocrine tumours from non-neural crest origin MEN -11 refers to endocrine tumours from a neural crest origin
47
what characterises Calcitonin tumours (medullary thyroid tumours)
can occur with or without phaemchromocytoma. characterised by high calcitonin but normal calcium levels
48
what is the biochemical name from D3? where is it obtained from
cholecalciferol obtained from the slow thermal isomerisation of 7 dehydrocholestrol in the skin by UV-LIGHT
49
what happens if UV-B intensity is low or high?
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
what is the biochemical name for D2? where does it come from
ergocalciferol obtained from diet
51
what are the steps involved in activation of vitamin D
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
how is vitamin D inactivated?
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
how is vitamin D inactivated?
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
why are vitamin D analogues better at treating secondary hyperparathyrodism than calcitriol?
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
how does hypocalcaemia lead to PTH release?
this leads to inactivation of calcium sensing receptors which leads to an increase of PTH directly calcium levels rise within minutes
56
what are Chvostek's sign and Troussea's signs indicative off?
they're indicative of neuromuscular hyperexctiability cause by hypocalcaemia
57
what does secondary hyperparathyrodism lead to?
sub-periosteol bone erosion cyst formation and bone pain leading to risk of fracture and osteoporosis renal caliculi formation
58
what will hypo magnesia cause?
hypocalcaemia
59
what will renal failure cause?
hypocalcaemia
60
what are the symptoms of hypocalcaemia?
numbness and paraesthesia mood swings and depression ``` tetany and neuromuscular excitability convulsions cardiac aryhtmias (long QT interval on ECG) catarcts spasms and stridor ```
61
what are the symptoms of hypercalcaemia?
``` 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
when is phosphate levels raised?
renal failure hypoparathryodism pseudohypoparathryodism
63
when is high calcium high phosphate levels seen?
vitmain D intoxication
64
when is high calcium high phosphate levels seen?
vitamin D intoxication
65
WHAT is long QT interval associated with?
associated with hypocalcaemia
66
what is short QT interval associated with?
associated with hypercalcameia
67
briefly explain the difference between competitive assay binding and sandwich assaying? and when they're both used
• 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
what are the non-classical MHC molecules and why are they significant?
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
what contributes to immunosuppression at the foetal-maternal interface?
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
what are the function of uterine NK cells?
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
what distinguishes NK from decidual NK cells?
Peripheral NK:CD 56 dim CD57 CD16 CD62 Decidual NK: cd56 BRIGHT - CD69 c-KIT
72
what is meant by the honeymoon phase seen in T1DM?
this refers to the regenerative capacity of beta cells, after T1DM onset. this phase is only transient- because the immune system wins
73
what causes the pathology in the eye associated with Grave's disease?
• 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
what are the auto-antibodies in Hashimoto's
Thyroid perioxidase, Thyroglobuin
75
which MHC complex increases the risk of Hashimotos
HLA-DR 5
76
Which MHC complex increases the risk of Grave's
HLA-DR 3
77
which MHC complex increases the risk for diabetes and which complexes causes resistance?
MHC-DQ-8 = increases risk MHC-DQ-6 = reduction of risk
78
what are the antibodies and T-cells in Addisons' directed aganist
21 hydroxylase
79
what is the consequence of activated TH1 in the thyroid gland?
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
what is the co-stimulator molecules for Naive T-cell receptors?
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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