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MED 2031 Wks 7-12 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

overview of vasopressin n oxytocin

A

vaospressin and oxytoxin
 is
made in the magnocellular neurones in the SON(supra-optic nuclei) n PVN (paraventricular nuclei) of hypothalamus


goes down the neurons that go into posterior pit

these neutrons come up against capillaries of the inferior hypophyseal artery

hormons are stored in the posterior pit aka neurohypophysis


and are released into bloodstream wen needed

and then act on receptors (e.g. V1 n V2) at different organns n stuff

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2
Q

structure of vasopressin

A

3rd aa is Phenylalanine
8th aa is Arginine or Lysine
amides on both sides

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3
Q

structure of oxytocin

A

3rd aa is Isoleucine
8th aa is Leucine
amides on both sides

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4
Q

structure of desmopressin (synthetic replacement for vasopressin)

A

D arginine at 8 and doesnt have amide at one end.
what this means is: has 2 effects:
1. it means that it has a much much longer half life in the body


  1. it means that it interacts with one class of the AVP receptors n not the other class, and this can be for therapeutic advantage as well
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5
Q

stimuli for vasopressin secretion

A 
OSMOLARITY
BLOOD VOLUME  (can also measure bp but we tend to measure blood volume more)

vasopressin-helps u retain water

increase in osmo= will increase in vasopressin
decrease in blood volume= increase in vasopressin

alcohol can modulate vasopressin release

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6
Q

neurogenic diabetes insipidus

A

conc of vasopressin will be decreased (cos neurons can’t make them)

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7
Q

nephrogenic diabetes insipidus

A

conc of vasopressin will be increased (cause the cause is at kidneys, neurons can still make them

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8
Q

stimuli for oxytocin secretion

A 
parturition (giving birth)
nipple stimulation
intercourse
hypertonicity
or other intimate actions like hugging
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9
Q

pituitary n optic chiasm

A

pit sits behind optic chasm

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10
Q

other name for pituitary gland

A

hypophysis

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11
Q

ant pit

A

Adenohypophysis
Pars distalis

from Rathke’s
pouch (an ectodermal evagination of the
oropharynx)

(oral ectoderm)

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12
Q

post pit

A

Neurohypophysis
Pars nervosa

neural origin
(neuroectoderm)

	neural tissue 
outgrowth from the hypothalamus. 

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13
Q

histology of ant pit

A

Darkly stained
Has acidophils & basophils

basophils- base turn purple-BFLAT= basophil release=FSH,LSH, ACTH ,TSH

Acidophils-acid turn pink-
Acidophils release GH & prolactin

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14
Q

histology of post pit

A

lightly stained

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15
Q

hypo secrete these into ant pit (to regulate ant pit hormones)

A 
TRH 
CRH 
GHRH
GHIH (SS)
GnRH
Dopamine (PIF)
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16
Q

Ant pit secrete these

A 
GH
Prolactin
FSH
LH
ACTH
TSH
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17
Q

acidophils secrete

A

GH PROLACTIN

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18
Q

basophils secrete

A

FSH
LH
ACTH
TSH

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19
Q

link bw hypo and ant pit ( vasculature)

A

so basically
supeiror hypophysial artery makes a cap plexus in the median eminence.
then capillaries go down as portal vein along the anteior face of pit
veins then dive into ant pit and makes another cap plexus

hypothalamic factors that regulate ant pit hormones are released into this portal system at the median eminence, and hence get to the ant pit.

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20
Q

neurophysin 1

A

oxytocin

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21
Q

neurophysin 2

A

ADH

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22
Q

vasopressin

A

increase water reabsoption at late distal tubules and collecting ducts by inserting aquaporin-2 into tubular epithelial cells

high ADH= permeable to water
no ADH= impermeable to water

reabsorb water only. so electrolytes will still go out with urine thus decreasing the concentration of the body fluids back toward normal.

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23
Q

morphine, cyclophosphamide

A

increase ADH secretion

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24
Q

alcohol

A

decrease ADH secretion

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25
increase in osmolarity
detected by osmorecptors in hypothalamus | increase ADH secretion
26
decresase in blood volume
detected by baroreceptors (e.g. carotid sinus) | increase ADH secretion
27
diabetes insipidus
when theres too little ADH working. so not enough water reabsorbed= polyuria, thirst hypernatremia (too much na in blood) can be neurogenic (not enough ADH produced to due damage to brain) nephrogenic (hihg ADH but kidneys don't respond-kidney damage)
28
SIADH
Syndrome of inappropriate ADH too much ADH released get hypotonicity and hyponatraemia
29
GH job
No target organ, effects everywhere Direct and indirect effects: DIRECT: increased glucose synthesis (via glycogenolysis=glycogen to glucose), lipolysis (break down lipids to fatty acids n glycerol) INDIRECT: GH stimulates IGF-1/somatomedins which then stimulates cartilage formation, long bone growth
30
excess GH in adults is
acromegaly
31
Excess GH in kids is
gigantism
32
GH deficiency in kids
dwarfism
33
acromegaly
=excess GH in adults most commonly it involves a tumor called pituitary adenom can also get arthropathy (disease of joint). cardiomyopathy
34
thyroid where
lobes C5-T1 | isthmus-in front of 2nd to 4th tracheal rings
35
Addison’s disease
absence of glucocorticoid/mineralcoticoids destruction of adrenal gland (autoimmune) low cortisol, high ACTH low aldosterone
36
Conn’s syndrome
Excess aldosterone = sodium retention and potassium excretion adrenal adenoma hypertension, hypernatremia, hypokalaemia
37
stimulus for aldosterone secretion
hyperkalaemia (raised potassium concentration) | and increased angiotensin II levels (which are associated with low sodium and volume depletion/low BP)
38
ANP/BNP(atrialandbrainnatriureticpeptides)
DECREASES sodium and water reabsorption.
39
Angiotensin II
Increasessodiumandwaterreabsorption.
40
PTH
increase blood cal | decrease blood phosphate
41
Cholecalciferol =
the one before 25 hydro....vit D3
42
active Vit D3 (1,25-dihydroxycholecalciferol, also called 1,25(OH)2D3 )
increase blood cal | increase phosphate cal
43
calcitonin
decrease blood cal | decrease blood phosphate
44
making active vit D
inactive vit D (chole..) goes to liver n becomes 25-hydroxylcholecalciferol 25-bla goes to kidney where, with the help of PTH, gets converted to active Vit (1,25 dihydro...) no kidney=no active vit d
45
HYPERCALCEMIA
Due to hyperparathyroidism, malignancy, etc ``` Symptoms: Groans- constipation, nausea, vomiting Thrones-polyuria Stones- renal stones Bones-bony pain, aches, risk of fracture Moans/Psychiatric overtones-drowsiness, depression, lack of concentration ```
46
HYPOCALCEMIA
Due to hypoparathyroidism Signs: • Chvostek’s sign-light tapping over cheek-twitching over corner of mouth • Trousseau’s sign- the claw
47
2 things from thyroid surgery:
bleeding n hoarseness of voice due to damage to recurrent laryngeal nerve
48
structures that might be damaged during surgery of thyroid
* Thyroid Ima artery of Neubauer * Recurrent laryngeal nerves (right recurrent laryngeal more at risk) * Parathyroid glands (their position is variable in the body, so they might be accidentally removed)
49
calcitonin secreted from
Parrifocllicular cells of thyroid
50
thyroid gland function
act on receptors in cells DNA . increase basal metabolic rate e.g. increase heat production, oxy production, cardiac output CNS activity etc
51
cretinism
congenital deficiency of thyroid hormones congentical hypothyroidsim
52
T3 = triiodothyronine
active one Less abundant in blood-only 15% But 99.7% of T3s are protein bound in blood -making it the active one
53
T3 vs rT3
T3-distal ring has 1 iodine | rT3-inner ring has 1 iodine
54
T4= thyroxine
T4= thyroxine Less active More abundant in blood- 85% 99.9% of all T4s are protein bound in blood- hence making it the less active one In peripheral tissues, T4 is deiodinated to make more T3
55
T3 vs T4 vs rT3
active less active not active
56
transport of thyroid hormones
the main one carrying-TBG (high affinity, low conc) albumin (low affinity, high conc) TBPA (low affinity, low conc, just for T4 carrying)
57
the main one doing neg feedback for thyroid hormones is
T3
58
PRIMARY HYPERTHYROIDISM:
o Problem with the thyroid gland | o T3 n T4 is high, but TSH is low due to negative feedback
59
SECONDARY HYPERTHYROIDISM
* Problem with pituitary | * T3 T4 high, TSH also high
60
graves
have these antibodies/immunoglobins that act on TSH receptors of thyroid like TSH, stimulate thyroid to release lots of T3, T4. primary hyperthyroidism get high T3, T4, low TSH
61
Drugs for hyperthryoidism
Carbimazole-the go to drug (inhibits iodind binding to tyrosing, decrase T3 n T4. Has less adverse effects but contradincated in 1st trimeseter preganny. So for pregnancy, give propyuracil. ) n propyuracil Betablocker for symptomatic relief
62
primary HYPOTHYROIDISM
Problem with thyroid | T3 T4 low, TSH high
63
SECONDARY HYPOTHYROIDISM
Problem with pituitary or hypothalamus | T3 T4 low, TSH low as well
64
Amioderone
Can cause both hyper or hypothyroidism
65
adrennal glands: cortex from
mesoderm
66
adrenal glands: medulla from
neural crest cells
67
histo of adrenal gland
* Glom-little balls * Fascilula-like fascicles- stringy * Reticualaris-meshy
68
steroid hormones
synthesised from cholesterol, in the SMOOTH endoplasmic reticulum
69
If 17 alpha hydroxylase gone
yes mineralocorticoid, no glucocorticoid or androgen
70
if 21 hydroxylase gone
no mineralocorticoid, no glucocorticoid, only androgen
71
Congenital adrenal hyperplasia
due to 21-hydroxylase deficiency, AMBIGUOUS genitalia
72
stimulation of aldosterone
hyperkalaemia, increased ang 2 levels/RAAS pathway (i.e. there is low bp, low salt) stimulates sodium-potassium atpase pump on basolateral sides of distal tubule n collecting ducts
73
cushings syndrome
state of excess of cortisol in body
74
Cushings disease
high cortisol DUE to ACTH secretion often with pituitary adenoma
75
BITEMPORAL HEMIANOPSIA
pituitary adenomas, that can compress the optic chiasm so get loss of peripheral vision
76
phaeochromocytoma
tumour of adrenal medulla get SNS symptoms anxiety, hypertension, sweating etc
77
aldosterone effect
increase na reabsorption increase water reabsorption increase k secretion
78
mechanism of action of aldosterone
stimulating the sodium-potassium ATPase pump on the basolateral side of principal cells increases the sodium permeability of the luminal side of the membrane (major site of action is the principal cells of the cortical collecting tubule)
79
fasting blood glucose
6.1-6.9= impaired fasting glucose/prediabetes >7 mmol/L= diabetes
80
random blood glucose
7.8-11= impaired random blood glucose >11.1 mmol/L= diabetic
81
HbA1c
less than 6.5% =recommendation more than 6.5% =diabetes (T2DM)
82
hypoglycaemia symptoms
hunger n sympa sypmtoms: sweating tremor cold palpitiations not enough sugar goes to brain: get neuro symptoms as well: visual disturbance, poor concentration, vagueness, irritablity
83
treatment for hypoglycaemia
1 single dose of simple carbohydrate (e.g. 6 jelly beans, a glass of fanta etc). wait to see if work. if no work, THEN give another single dose. follow with complex carbohydrate (cos it lasts long) if pt can't eat, give IV dextrose or glucagon
84
causes for hypoglycaemia
lifestyle/diet, too much insulin
85
glucagon
``` stimulate liver to to glycogenolysis (glycogen to glucose) and gluconeogenesis (making glucose from non carbohydrate comppund) ```
86
DKA symptoms
``` Tachycardic — Irritable — Nausea + vomiting — Confusion/mental state changes — Ketotic breath thrist, polyuria, dehydration kussmaul's breathing (to blow off some CO2) ``` ketosis n hyperglycaemia (17+)
87
DKA type 1 or 2?
type 1 Dm
88
HHS/HONK type 1 or 2?
type 2
89
HbA1c -trend
the lower it is, the lower the rate of complications (e.g. retinopathy). But the greater the risk of hypoglycaemia
90
HHS/HONK
blood glucose too hihg=extreme dehydration often septic uraemia insulin is still present,so no ketosis/ketoacidosis
91
A PERSON WITH DIABETES HAS AT LEAST A __CHANCE OF DYING FROM CARDIO-VASCULAR DISEASE
65%
92
sympa on pancreas
relase glucagon
93
para on pancreas
release insulin
94
FED state
INCREASE INSULIN release | decrase glucagon
95
FASting state
INCREASE GLUCAGON release | decrease insulin

MED 2031 Wks 7-12 (13 decks)

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