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
what is conn's syndrome
Hypersecretion of aldosterone usually caused by adrenal hyperplasia (60 %) or tumor (40%)
26
what is happening in conn's syndrome
* vExcess excretion of K+ and H+ * vSerum alkalosis and neuropathy (hypocalcemia) * Increased water retention * Increased Na reabsorption * Increased blood pressure
27
what are natriuretic peptides
peptides that increase the excretion of H2O and Na produced in the heart muscle and stored in granules
28
How natriuretic peptides function and where the receptors for it are
* 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
where do sex steroids are normally synthesized and what role kidneys play in it
* 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
what is the role of sex steroids produced in adrenal gland
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
what is congenital adrenal hyperplasia
Excessive androgen production-\> Masculinization of genitalia
32
explain what hormally happens during congention and why there is CAH
33
what defect in the organism happens that causes congenital adrenal hyperplasia
34
why congenital adrenal hyperplasia occur, is it frequent , how treated
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
total mass of medulla is
1 g
36
how adrenal medulla get its tasks
* 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
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
* 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
how epineprine and norpinephrine are disactivated
Inactivated by monoamine oxidase (MAO) and COMT (catechol-O-methyltransferase) pathways
39
what other hormones are secreted from medulla (apart from adrenalin and noradrenalin)
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
how fight-or-flight response function
41
what are acute effects of adrenalin and noradrenalin
Acute: integrated adjustment of many complex processes in organs vital to the response (e.g., brain, muscles, cardiopulmonary system, liver)
42
actiovation of organs during fight-or flight happens at the expense of
Occurs at the expense of other organs less immediately involved (e.g., skin, GI).
43
what is epinephrine and noradrenalin role in the body
* 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
what receptors bind to adrenalin and noradrenalin
vα and β1 receptors bind epinephrine and norepinephrine. β2 receptors bind primarily epinephrine (GPCR)
45
what is the drug salbutamol and what is it used for
Salbutamol activates β2 receptors and dilates bronchioles (relief of asthma); but does not affect beta1 receptors in the heart.
46
aplha, beta 1 and 2: potency for e and NE, action and target tissue/cells
47
differences between epinephrine and NE
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
adrenomedullary deficiency can happen due to
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
adrenomedullary disorders can happen due to
Hypotension, hypoglycemia (CNS and glucocorticoids are more susceptible)
50
can we live without E and NE
51
what is pheochromocytoma
tumor overproducing catecholamines
52
what is the prevalence of pheochromocytoma and its symptoms
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