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kris Endocrinology > Section 4-adrenal gland > Flashcards

Section 4-adrenal gland Flashcards

1
Q

what hormone does zona glomerulosa produce and what is its function

A

aldosterone

  • Recovery of Na+ in the kidney and enhanced K+secretion into the urine to balance charge difference
  • Therefore, adjustment of extra-cellular fluid (ECF), including blood volume
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2
Q

how physical attributes in homeostasis of blood correpsond to the control mechanisms of the system

A
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3
Q

physiological changes that influence postively and negatively sodium appetite

A

and also thirst

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4
Q

what is the primary resource to restire Na balance ( thirst of sodium appetite)

A

At first thirst increases and if it is not enough, then sodium increased

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5
Q

what is the major determinant of the blood pressure

A

The diameter of arterioles (artery, arterioles, capillaries) is a major determinant of the
blood pressure in the arteries and controls the
distribution of the blood supply to tissues

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6
Q

describe RAAS

A

v Renin from afferent arterioles in kidney
converts angiotensinogen to angiotensin I
v ACE from endothelial cells of lungs
converts angiotensin I to angiotensin II
v angiotensin II stimulates aldosterone
secretion

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7
Q

does ACTH influence aldosterone secretion

A

Modest effect

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8
Q

Angiotensin II function

A

v increases Na+ absorption and K+ excretion
v Water retention, higher blood pressure

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9
Q

is angiotensin is secrted somewhere else int he body except kidney-liver-lung

A

Renin also found in the brain. Local
production of angiotensin II ? Induction of
thirst?

not sure about the answer

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10
Q

what cells secrete renin

A

Juxtaglomerular cells

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11
Q

what juxtaglomerular apparatus sence

A

v Macula densa cells detect Na+ levels in kidney tubule
v Juxtagolomerular cells detect blood pressure

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12
Q

aldosterone is under the main influence of

A

RAAS

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13
Q

how angiotensin is disactivated

A
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14
Q

renin secretion is stimulated by

A

decreased renal arterial pressure

decreased sodium in renal tubualr fluid

increased renal sympathetic nerve activity

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15
Q

what 2 destinies angiotensin II has

A
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16
Q

angiotensin II can have 3 types of responses (speed)

A

rapid

slow

remodeling

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17
Q

describe acute effects of angiotensin II

A

Sympathetic nervous system stimulation causes vasoconstriction of most blood vessels

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18
Q

slow response of angiotensin II

A
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19
Q

what does it mena that angiotensin II have remodeling effects

A
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20
Q

how aldosterone functions

A

aldosterone through TF influence->action on structural protein of Na transport ( into the cells) and increasing regulatory proteins-kinases (SGK and K-Ras) that induces K-Na-ATPase

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21
Q

sodium transport happens in

A

vNa+ transport in
vdistal tubules of kidney
vcolon
vSalivary and Sweat glands

aldosterone will influence all of them

22
Q

function of aldosterone on the distal tubule cells

A

Aldosterone activates apical channels and more Na gets into the cell, so more Na-K ATPase

  • Na-K-ATPase , which keeps a particular voltage -60 mV),, will shuttle K from blood to the lumen of the distal tubule
  • Because Na coming in, aquaporin open and leads to reabsoprtion of water ( increased volume and Na)
23
Q

aldosterone acts mainly on what types of cells

A

v Mainly: Distal tubules and collecting ducts of the kidney.
v Also on other secretory systems (sweat glands, salivary glands,colon)

24
Q

summarize what does aldosterone do what is the net effect and what is a lag period of aldosterone

A

v Promotes plasma retention of Na+ and excretion of K+
and H+ into the lumen of the tubules
v Sensitizes arterioles to vasoconstrictor agents (to modulate activity of catecholamines ,for example)
v Net effect: Rise in plasma volume and hence blood
pressure
v Response has a lag period of 1h, reflecting that
aldosterone induced enzymes have to be synthesized
de novo

25
Q

what is conn’s syndrome

A

Hypersecretion of aldosterone usually caused
by adrenal hyperplasia (60 %) or tumor (40%)

26
Q

what is happening in conn’s syndrome

A
  • vExcess excretion of K+ and H+
  • vSerum alkalosis and neuropathy (hypocalcemia)
  • Increased water retention
  • Increased Na reabsorption
  • Increased blood pressure
27
Q

what are natriuretic peptides

A

peptides that increase the excretion of H2O and Na

produced in the heart muscle and stored in granules

28
Q

How natriuretic peptides function and where the receptors for it are

A
  • Receptors are present in the glomeruli, medullary collecting ducts of the kidney, the zona glomerulosa of the adrenal cortex and in peripheral arterioles
  • v Increases glomerular filtration
  • v Reduces blood volume and pressure
29
Q

where do sex steroids are normally synthesized and what role kidneys play in it

A
  • Sex steroids are mainly synthesized in the gonads (Females: estrogens and progestogens; Males: androgens) –regulated by gonadotrophins
  • v Adrenal cortex (mainly zonareticularis) contributes to the production of DHEAS and androstenedione – regulated by ACTH and hypothalamic CRH.
  • v Can be converted to testosterone in peripheral tissues.
30
Q

what is the role of sex steroids produced in adrenal gland

A

Role not entirely clear. Important for
body hair growth in females
.
v Responsible for growth spurt in
middle childhood (adrenarche) -Adrenarche occurs independently of an increase of estrogens, androgens, or gonadotropins associated with puberty

31
Q

what is congenital adrenal hyperplasia

A

Excessive androgen production-> Masculinization of genitalia

32
Q

explain what hormally happens during congention and why there is CAH

A
33
Q

what defect in the organism happens that causes congenital adrenal hyperplasia

A
34
Q

why congenital adrenal hyperplasia occur, is it frequent , how treated

A

Frequency of classical CAH 1:13000 in
general population
v Both copies of 21-hydroxylase (P450c21)
mutated
v Many mutations result in partial loss of
function
v And masculinization is not as extreme
v Trt: surgical correction at birth

35
Q

total mass of medulla is

A

1 g

36
Q

how adrenal medulla get its tasks

A
  • vAdrenal medulla and chromaffin cells are part of the

sympathetic nervous system (CNS)

  • vCoordinate fight-flight response to alarm by increasing
    b. p. and cardiac output, and dilating pupils
  • vPreganglionic neurons release acetylcholine to stimulate

medulla cells to release hormones (catecholamines)

37
Q

2 types of catecholamines synthesized in medulla, the pathway, what is the rate limiting step, how epinephrine is converted to noreponephrine and what is the proportion of epinephrine to norepinephrine

A
  • Catecholamines (norepinephrine and epinephrine) synthesized from tyrosine
  • Hormones in the adrenal medulla are released in response to appropriate stimuli
  • 80 % of released catecholamines are epinephrine to 20 % norepineprine
  • tyrosine-> dopamine->norepinephrine
38
Q

how epineprine and norpinephrine are disactivated

A

Inactivated by monoamine
oxidase (MAO) and COMT
(catechol-O-methyltransferase)
pathways

39
Q

what other hormones are secreted from medulla (apart from adrenalin and noradrenalin)

A

vGranules also contain met-enkephalin and and
leu-enkephalin (related to endorphins).
vThey are co-excreted with the catecholamines
vEnkephalins may block neurotransmitters (like
morphine)
v act as an endogenous analgesics (runners
overcoming pain and being euphoric)

40
Q

how fight-or-flight response function

A
41
Q

what are acute effects of adrenalin and noradrenalin

A

Acute: integrated adjustment of many complex processes in organs vital to the response (e.g., brain, muscles, cardiopulmonary system, liver)

42
Q

actiovation of organs during fight-or flight happens at the expense of

A

Occurs at the expense of other organs less immediately involved (e.g., skin, GI).

43
Q

what is epinephrine and noradrenalin role in the body

A
  • Epinephrine: rapidly mobilizes fatty acids as the primary fuel for muscle action
  1. v increases muscle glycogenolysis
  2. v mobilizes glucose for the brain by increasing hepatic glycogenolysis and gluconeogenesis
  3. v preserves glucose for CNS by decreasing insulin release leading to reduced glucose uptake by muscle/ adipose
  4. v Increases cardiac output
  • v Norepinephrine elicits responses of the CV system - increasing blood flow and decreasing insulinsecretion.
44
Q

what receptors bind to adrenalin and noradrenalin

A

vα and β1 receptors bind
epinephrine and norepinephrine.
β2 receptors bind primarily
epinephrine (GPCR)

45
Q

what is the drug salbutamol and what is it used for

A

Salbutamol activates β2 receptors
and dilates bronchioles (relief of
asthma); but does not affect beta1
receptors in the heart.

46
Q

aplha, beta 1 and 2: potency for e and NE, action and target tissue/cells

A
47
Q

differences between epinephrine and NE

A

v Epinephrine >> norepinephrine – in terms of cardiac
stimulation leading to greater cardiac output (b
stimulation)

v Epinephrine < norepinephrine – in terms of constriction
of blood vessels – leading to increased peripheral
resistance – increased arterial pressure

v Epinephrine >> norepinephrine –in terms of increasing
metabolism

48
Q

adrenomedullary deficiency can happen due to

A

surgery, trauma.etc.

v Also if cortisol levels are suppressed for any reason
(high concentration of cortisol req’d for transcription of
PNMT) resulting in epinephrine deficiency

49
Q

adrenomedullary disorders can happen due to

A

Hypotension, hypoglycemia (CNS and glucocorticoids are more susceptible)

50
Q

can we live without E and NE

A
51
Q

what is pheochromocytoma

A

tumor overproducing catecholamines

52
Q

what is the prevalence of pheochromocytoma and its symptoms

A

Relatively rare but often not diagnosed until autopsy (about
200-1000 per million) and about 1/3 cause death prior to
diagnosis
• headache
• hypertension
• sweating
• palpitations
• chest pain
• anxiety
• glucose intolerance
• increased metabolic rate

kris Endocrinology (17 decks)

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