Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

structure of vasopressin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

structure of oxytocin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

neurogenic diabetes insipidus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

nephrogenic diabetes insipidus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

stimuli for oxytocin secretion

A 
parturition (giving birth)
nipple stimulation
intercourse
hypertonicity
or other intimate actions like hugging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

pituitary n optic chiasm

A

pit sits behind optic chasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

other name for pituitary gland

A

hypophysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ant pit

A

Adenohypophysis
Pars distalis

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

(oral ectoderm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

post pit

A

Neurohypophysis
Pars nervosa

neural origin
(neuroectoderm)

	neural tissue 
outgrowth from the hypothalamus. 

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

histology of post pit

A

lightly stained

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A 
TRH 
CRH 
GHRH
GHIH (SS)
GnRH
Dopamine (PIF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ant pit secrete these

A 
GH
Prolactin
FSH
LH
ACTH
TSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

acidophils secrete

A

GH PROLACTIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

basophils secrete

A

FSH
LH
ACTH
TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

neurophysin 1

A

oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

neurophysin 2

A

ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

morphine, cyclophosphamide

A

increase ADH secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

alcohol

A

decrease ADH secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

increase in osmolarity

A

detected by osmorecptors in hypothalamus

increase ADH secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

decresase in blood volume

A

detected by baroreceptors (e.g. carotid sinus)

increase ADH secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

diabetes insipidus

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

SIADH

A

Syndrome of inappropriate ADH

too much ADH released
get hypotonicity and hyponatraemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

GH job

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

excess GH in adults is

A

acromegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Excess GH in kids is

A

gigantism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

GH deficiency in kids

A

dwarfism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

acromegaly

A

=excess GH in adults
most commonly it involves a tumor called pituitary adenom

can also get arthropathy (disease of joint). cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

thyroid where

A

lobes C5-T1

isthmus-in front of 2nd to 4th tracheal rings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Addison’s disease

A

absence of glucocorticoid/mineralcoticoids

destruction of adrenal gland (autoimmune)
low cortisol, high ACTH

low aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Conn’s syndrome

A

Excess aldosterone = sodium retention and potassium excretion

adrenal adenoma
hypertension, hypernatremia, hypokalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

stimulus for aldosterone secretion

A

hyperkalaemia (raised potassium concentration)

and increased angiotensin II levels (which are associated with low sodium and volume depletion/low BP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

ANP/BNP(atrialandbrainnatriureticpeptides)

A

DECREASES sodium and water reabsorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Angiotensin II

A

Increasessodiumandwaterreabsorption.

40
Q

PTH

A

increase blood cal

decrease blood phosphate

41
Q

Cholecalciferol =

A

the one before 25 hydro….vit D3

42
Q

active Vit D3 (1,25-dihydroxycholecalciferol, also called 1,25(OH)2D3 )

A

increase blood cal

increase phosphate cal

43
Q

calcitonin

A

decrease blood cal

decrease blood phosphate

44
Q

making active vit D

A

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
Q

HYPERCALCEMIA

A

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
Q

HYPOCALCEMIA

A

Due to hypoparathyroidism
Signs:
• Chvostek’s sign-light tapping over cheek-twitching over corner of mouth
• Trousseau’s sign- the claw

47
Q

2 things from thyroid surgery:

A

bleeding n hoarseness of voice due to damage to recurrent laryngeal nerve

48
Q

structures that might be damaged during surgery of thyroid

A
  • 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
Q

calcitonin secreted from

A

Parrifocllicular cells of thyroid

50
Q

thyroid gland function

A

act on receptors in cells DNA .
increase basal metabolic rate
e.g. increase heat production, oxy production, cardiac output CNS activity etc

51
Q

cretinism

A

congenital deficiency of thyroid hormones

congentical hypothyroidsim

52
Q

T3 = triiodothyronine

A

active one

Less abundant in blood-only 15%
But 99.7% of T3s are protein bound in blood
-making it the active one

53
Q

T3 vs rT3

A

T3-distal ring has 1 iodine

rT3-inner ring has 1 iodine

54
Q

T4= thyroxine

A

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
Q

T3 vs T4 vs rT3

A

active
less active
not active

56
Q

transport of thyroid hormones

A

the main one carrying-TBG (high affinity, low conc)

albumin (low affinity, high conc)
TBPA (low affinity, low conc, just for T4 carrying)

57
Q

the main one doing neg feedback for thyroid hormones is

A

T3

58
Q

PRIMARY HYPERTHYROIDISM:

A

o Problem with the thyroid gland

o T3 n T4 is high, but TSH is low due to negative feedback

59
Q

SECONDARY HYPERTHYROIDISM

A
  • Problem with pituitary

* T3 T4 high, TSH also high

60
Q

graves

A

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
Q

Drugs for hyperthryoidism

A

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
Q

primary HYPOTHYROIDISM

A

Problem with thyroid

T3 T4 low, TSH high

63
Q

SECONDARY HYPOTHYROIDISM

A

Problem with pituitary or hypothalamus

T3 T4 low, TSH low as well

64
Q

Amioderone

A

Can cause both hyper or hypothyroidism

65
Q

adrennal glands: cortex from

A

mesoderm

66
Q

adrenal glands: medulla from

A

neural crest cells

67
Q

histo of adrenal gland

A
  • Glom-little balls
  • Fascilula-like fascicles- stringy
  • Reticualaris-meshy
68
Q

steroid hormones

A

synthesised from cholesterol, in the SMOOTH endoplasmic reticulum

69
Q

If 17 alpha hydroxylase gone

A

yes mineralocorticoid, no glucocorticoid or androgen

70
Q

if 21 hydroxylase gone

A

no mineralocorticoid, no glucocorticoid, only androgen

71
Q

Congenital adrenal hyperplasia

A

due to 21-hydroxylase deficiency, AMBIGUOUS genitalia

72
Q

stimulation of aldosterone

A

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
Q

cushings syndrome

A

state of excess of cortisol in body

74
Q

Cushings disease

A

high cortisol DUE to ACTH secretion often with pituitary adenoma

75
Q

BITEMPORAL HEMIANOPSIA

A

pituitary adenomas, that can compress the optic chiasm so get loss of peripheral vision

76
Q

phaeochromocytoma

A

tumour of adrenal medulla
get SNS symptoms
anxiety, hypertension, sweating etc

77
Q

aldosterone effect

A

increase na reabsorption
increase water reabsorption
increase k secretion

78
Q

mechanism of action of aldosterone

A

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
Q

fasting blood glucose

A

6.1-6.9= impaired fasting glucose/prediabetes

> 7 mmol/L= diabetes

80
Q

random blood glucose

A

7.8-11= impaired random blood glucose

> 11.1 mmol/L= diabetic

81
Q

HbA1c

A

less than 6.5% =recommendation

more than 6.5% =diabetes (T2DM)

82
Q

hypoglycaemia symptoms

A

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
Q

treatment for hypoglycaemia

A

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
Q

causes for hypoglycaemia

A

lifestyle/diet, too much insulin

85
Q

glucagon

A 
stimulate liver to to glycogenolysis (glycogen to glucose)
and gluconeogenesis (making glucose from non carbohydrate comppund)
86
Q

DKA symptoms

A 
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
Q

DKA type 1 or 2?

A

type 1 Dm

88
Q

HHS/HONK type 1 or 2?

A

type 2

89
Q

HbA1c -trend

A

the lower it is, the lower the rate of complications (e.g. retinopathy). But the greater the risk of hypoglycaemia

90
Q

HHS/HONK

A

blood glucose too hihg=extreme dehydration

often septic
uraemia
insulin is still present,so no ketosis/ketoacidosis

91
Q

A PERSON WITH DIABETES HAS AT
LEAST A __CHANCE OF DYING
FROM CARDIO-VASCULAR DISEASE

A

65%

92
Q

sympa on pancreas

A

relase glucagon

93
Q

para on pancreas

A

release insulin

94
Q

FED state

A

INCREASE INSULIN release

decrase glucagon

95
Q

FASting state

A

INCREASE GLUCAGON release

decrease insulin

MED 2031 Wks 7-12 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions