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Endocrinology > 5.1 CV system & adrenal medulla > Flashcards

5.1 CV system & adrenal medulla Flashcards

1
Q
  • what are the 3 physical attributes of blood? & their associated control/regulation mechanisms ish?
  • what other control mechanism is there?
  • all of them are in a ___________
A

1) volume –> H2O retention
2) blood pressure –> dilation of arterioles
3) osmolarity –> Na+ retention
- in addition to fluid intake!
- continuum!!!! 1 influences another

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2
Q

aorta –> ______ –> ______ –> ______ –> ______ –> ______ –> ______ –> vena cava
- total area of all these vessels = ?
- what is the major determinant of blood pressure in arteries? what does this thing also control? –> all of these things are under control of what?

A

aorta –> arteries –> arterioles –> capillaries –> venules –> veins –> vena cava
- total cross-sectional area
- diameter of arterioles! –> also controls distribution of blood supply to tissues
- all under control of hormones (ish)

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3
Q

what part ish of capillaries is where pressure of arteries can be regulated + allow for proper speed of blood flow at capillary levels?
- what is super important for exchange at capillaries?

A
  • precapillary sphincters!
  • slowness of blood flow at capillaries
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4
Q
  • what is sodium appetite?
    what are physiological changes that influence sodium appetite? –> which organ?
  • 3 positive
  • 4 negative
  • is sodium appetite strongly manifested in normal conditions?
    *thirst and sodium appetite graph
A
  • sodium appetite = pushes us to eat salty foods –> makes us increase salt intake
  • brain!
    POSITIVE:
  • increase aldosterone
  • increase angiotensin II
  • changes in brain [Na+] –> decrease [Na+] OR increase osmolarity –> affects Na/K channels = hinders neural propagation and membrane potential
    NEGATIVE:
  • increase [Na+] of blood plasma cerebrospinal fluid
  • post-ingestive signals from the gut (increase [Na+], distension) sensed via the vagus nerve
  • circulating & CNS peptide hormones/neuromodulators
  • arterial/venous baroreceptors (not sure if positive or negative)
  • NOT strongly manifested in normal conditions
    *thirst: fonction racine carré ish VS sodium appetite: really low and flat at first, halfway, start to increase linearly ish
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5
Q
  • aldosterone produced where?
  • main functions (2)
  • 3 functions as concepts ish
A
  • zona glomerulosa of adrenal cortex
    1. recovery/retention of Na+ in the kidney and enhanced K+ secretion into urine to balance charge difference
    2. adjustment of extracellular fluid (ECF), including blood volume (bc of osmosis) –> blood pressure!
  1. regulation of fluid volume
  2. water absorption
  3. sodium/potassium homeostasis
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6
Q

how is aldosterone synthesized? pathway!

A
  1. cholesterol enters mitochondria using StAR
  2. cholesterol –> pregnenolone, using CYP11A1
  3. pregnenolone –> progesterone, using HSD3B2
  4. progesterone –> 11-deoxycorticosterone, using CYP21A2
  5. 11-deoxycorticosterone –> corticosterone, using CYP11B1 and CYP11B2
  6. corticosterone –> 18-OH-corticosterone, using CYP11B2
  7. 18-OH-corticosterone –> aldosterone, using CYP11B2
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7
Q
  • which cells detect Na+ levels in kidney tubule?
  • vs which cells detect blood pressure?
  • which cells produce renin? in response to what?
A
  • Macula densa cells of distal convoluted tubule (near glomerulus) detect Na+ levels in kidney tubule
  • juxtaglomerular cells of afferent arterioles detect blood pressure
  • pericytes near afferent arterioles produce renin –> in response to BP or Na+ imbalance
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8
Q

RAAS
- what does renin do?
- what does ACE do?
- what does angiotensin II stimulate? (2)
- aldosterone and angiotensin II increase (3)

A
  • renin from pericytes in kidney converts angiotensinogen (produced in liver) to angiotensin I in liver –> Ang I goes into circulation until lung
  • ACE (angiotensin converting enzyme) from endothelial cells of lungs converts angiotensin I to angiotensin II –> ang II goes to kidney and drenal gland
  • angiotensin II = main regulator of aldosterone secretion (ACTH has a modest effect) + stimulates AVP, which stimulates water retention in kidney
  • increase Na+ absorption, K+ excretion and water retention in kidney
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9
Q

RAAS
- renin found in kidney but also found where?
- how is angiotensin II inactivated?

A
  • also found in brain. local production of angiotensin II? induction of thirst?
  • inactivated to angiotensin III by aminopeptidase A
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10
Q

how does aldosterone achieve its functions ish? pathway ish

A
  • aldosterone binds to mineralocorticoid receptor (MR) –> affects gene transcription in nucleus –> increase structural protein + regulatory proteins
  • increase/activates sodium potassium pumps on capillary side + increase sodium channels (epithelium sodium channels ENaC) on luminal side
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11
Q

is AVP or aldosterone faster in its action to control volume and BP?
*think about what type of receptor for each!

A
  • AVP –> GPCR –> faster, bc proteins are already there
  • aldosterone –> nuclear receptor/TF –> slower, need full transcription/translation before protein is formed
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12
Q

aldosterone acts on sodium/potassium homeostasis:
- sodium transport in which 3 areas of body?

A
  1. distal tubules of kidney
  2. colon
  3. salivary and sweat glands
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13
Q
  • which channels are needed for movement of Na+, K+ and water from where to where? after actions of aldosterone?
A
  • potassium goes out (capillary to distal tubule) –> through Na/K channel + ROMK and BK channels
  • sodium goes in (distal tubule to capillary) –> ENaC and Na/K ATPase
  • water goes in –> aquaporin 2 and aquaporin 3/4
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14
Q

ALDOSTERONE:
- mainly affects where? but also on other systems (3)
- promotes (2)
- sensitizes arterioles to (3)
- net effect: (2)
- response has a lag period of how long?, reflecting that aldosterone induced enzyme have to be what?

A
  • distal tubules and collecting ducts of kidney –> also on sweat glands, salivary glands and colon
  • promotes plasma retention of Na+ and excretion of K+
  • sensitizes arterioles to vasoconstrictor agents, AVP and angiotensin II
  • net effect = rise in plasma volume and blood pressure
  • lag period of 1 hour: reflecting that aldosterone induced enzymes have to be synthesized de novo
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15
Q
  • what is conn’s disease?
  • usually caused by (2)
  • excess excretion of (2) –> leads to (2)
  • increased (3)
A
  • hyperaldosteronism (primary alsodetronism)
  • hypersecretion of aldosterone usually caused by adrenal hyperplasia (60%) or tumor of adrenal cortex (40%)
  • excess excretion of K+ and H+ (bc high aldosterone) –> serum alkalosis and neuropathy (hypokalemia)
  • increased water retention, Na reabsorption and blood pressure
    *high blood pressure could also be from apparent mineralocorticoid from excess cortisol
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16
Q
  • what is addison’s disease?
  • caused by (2)
  • symptoms (4)
A
  • hypoaldosteronism
  • shortage/deficiency of aldosterone production OR impaired function of aldosterone
    1. low sodium (hyponatremia)
    2. too much potassium (hyperkalemia)
    3. low blood pressure
    4. metabolic acidosis
    *recall Addison’s crisis pathway!
17
Q
  • what do natriuretic peptides do?
  • produced where and stored?
  • receptors are present in (4)
  • functions: increases (3) + reduces/inhibits (4)
A
  • increase excretion of H2O and Na+ (role in BP regulation)
  • produced in heart muscle cells and stored in granules
  • present in glomeruli, medullary collecting ducts of kidney, zona glomerulosa of adrenal cortex and in peripheral arterioles
    INCREASES:
  • glomerular filtration + water loss (diuresis) + vasodilation
    REDUCES:
  • renin , blood volume and blood pressure
  • inhibits aldosterone production
18
Q
  • natriuretic peptides have opposite effects to (2) –> consequence?
A
  • opposite effects to AVP and Ang II –> renin need to make Ang II –> consequence: decrease aldosterone from direct inhibition by natriuretic peptides!
19
Q
  • where is testosterone/androgens synthesized?
  • how? pathway? (7 steps)
A
  • zone reticularis in adrenal cortex
    1. cholesterol enters mitochondria using StAR
    2. cholesterol –> pregnenolone, using CYP11A1
    3. pregnenolone –> 17OH-pregnenolone, using CYP17A1
    4. 17OH-pregnenolone –> dehydroepi-anderosterone, using CYP17A1
    6. dehydroepi-anderosterone –> androstenedione, using HSD3B2
    7. androstenedione –> testosterone, using HSD17B
20
Q
  • sex steroids are mainly synthesized where? (which sex steroids?)
  • sex steroids synthesis regulated by what?
  • what organ (mainly what region) contributes to production of (2) regulated by ACTH?
  • these 2 precursors can be converted to what? where? –> role?
A
  • in gonads! female (estrogens and progestogens) male (androgens)
  • regulated by gonadotropins
  • adrenal cortex (mainly zona reticularis, but also fasciculata) contributes to production of DHEAS and androstenedione –> regulated by ACTH (vs glomerulosa)
  • can be converted to testosterone in peripheral tissues (brain, adipose)
  • role not entirely clear –> mainly modulate effect of overall [steroid] in circulation –> important for body hair growth (adrenarche) and responsible for growth spurt in middle childhood
21
Q

CONGENITAL ADRENAL HYPERPLASIA (CAH)
- most common form involves deficiency of what? in which zonas?
- leads to reduced (2)
- exception in ZF? thus…
- low aldosterone leads to (4)
- CAH leads to excessive _________ production in which zona? –> consequence?

A
  • involves deficiency of CYP21A2 (zone glomerulosa and zona fasciculata)
  • reduced aldosterone and cortisol
  • ZF: produces 21-deoxycortisol –> similar to cortisol but lower glucocorticoid activity (can act though! therefore low aldosterone is the main problem)
  • low aldosterone leads to salt wasting, salt and water craving, vomiting and dehydration, low blood pressure (death)
  • excessive production of androgen in ZR (hyperactivation of ZR bc not affected by CYP21A2)–> masculinization of genitalia
22
Q
  • total mass of adrenal medulla? about ___% of total adrenal glands weight
  • adrenal medulla and _______ cells are part of the what?
A
  • 1g –> 15% of total weight
  • chromaffin cells –> part of sympathetic nervous system
23
Q
  • what are chromaffin cells&
  • what stimulates chromaffin cells to release what?
  • what do these released compounds do?
A
  • modified post-ganglionic cells
  • preganglionic neurons release acetylcholine to stimulate chromaffin cells to release catecholamines
  • coordinate fight/flight response to alarm by increasing blood pressure and cardiac output + dilating pupils
24
Q
  • catecholamines (which 2) –> synthesized from what?
  • pathway? (4 steps)
  • rate limiting step?
  • which enzyme does cortisol stimulate? (in catecholamine synthesis pathway)
A
  • norepinephrine and epinephrine –> synthesized from tyrosine
    1. tyrosine to dopa by tyrosine hydroxylase (rate limiting step! + commits Tyr to cetacholamine synthesis)
    2. dopa to dopamine by dopa decarboxylase
    3. dopamine to norepinephrine by dopamine b-hydroxylase
    4. norepinephrine to epinephrine by PNMT (phenylethanolamine N-methyltransferase)
    *cortisol stimulates PNMT!
25
Q
  • hormones in adrenal medulla are released in response to what?
  • which % of catecholamines are epinephrine vs norepinephrine?
A
  • in response to appropriate stimuli?
  • 80% epinephrine (or adrenaline)
  • 20% norepinephrine (or noradrenaline)
26
Q

explain the fight or flight response –> schéma!
- hypothalamus perceives _______, then activates 2 pathways

A
  • perceives stress!
    1. activates SNS:
    a) activates adrenal medulla –> releases NE and E into bloodstream
    b) impulses activate glands and smooth muscles
  • both a) and b) lead to neural activity combines with hormones in bloodstream to constitute fight or flight response
    2. ALSO activates adrenal-cortical system by releasing CRF –> pituitary gland secretes hormone ACTH –> ACTH arrives at adrenal cortex and release approximately 30 hormones (cortisol, aldosterone, androgens…) –> bloodstream –> leads to neural activity combines with hormones in bloodstream to constitute fight or flight response
27
Q

FIGHT OR FLIGHT RESPONSE:
- (2) initiate fight or flight response
- __________ adjustments of many complex processes in ________ vital to response (ie: 4)
- occurs at expense of what?

A
  • norepinephrine and epinephrine
  • integrated adjustments of many complex processes in organs vital to response (ie brain, muscles, cardiopulmonary system, liver)
  • occurs at expense of other organg less immediately involved (ie skin, GIT)
28
Q

functions of
- epinephrine (5)
- norepinephrine (2)

A

EPINEPHRINE:
- rapidly mobilizes FA as primary fuel for muscle action
- increases muscle glycogenolysis
- mobilizes glucose for the brain by increase in hepatic glycogenolysis and gluconeogenesis
- preserves glucose for CNS by decreasing insulin release leading to reduced glucose uptake by muscle/adipose (opposes insulin)
- increases cardiac output
NOREPINEPHRINE:
- increase blood flow
- decrease insulin secretion

29
Q

adrenergic receptors:
- why are there different responses depending on different target tissues?
- drugs specific for ________ of receptors have different effects –> ie salbutamol does what?

A
  • bc different target tissues have different receptor distributions and hence have different responses
  • drugs (subtypes) specific for subtypes of receptors have different effects:
    Salbutamol activates/ is agonist to b2 receptors and dilates bronchioles (relief of asthma) –> does not affect b1 receptors in the heart
30
Q

explain pathway of what leads to adrenergic receptors:
- a vs b1 vs b2

A
  1. sympathetic preganglionic fiber –> releases acethylcholine –> to sympathetic postganglionic fiber –> releases NE which binds to a and b1 receptors
  2. sympathetic preganglionic fiber –> releases acethylcholine to adrenal medulla –> secretes E and NE into bloodstream –> E and NE act on a and b1 receptors + E acts on b2 receptors
31
Q

which receptors (a1/2 vs b1 vs b2) bind which catecholamine?
- potency?
- action?
- target?

A
  • a1/2 and b1 receptors bind NE and E VS b2 receptors bind primarily E
  • a1: NE > E –> Gq –> smooth muscle (skin, GI, uterus)
  • a2: E > NE –> Gi –> nerve terminals (synaptic transmission)
  • b1: NE > E –> Gs –> heart, cerebral cortex
  • b2: E > NE –> Gs –> lung, smooth muscle, cerebellum
32
Q

differences btw NE and E:
- Epinephrine&raquo_space; norepinephrine for 2 things
- norepinephrine > epinephrine for 1 thing –> leads to what?

A

E&raquo_space; NE:
- cardiac stimulation leading to greater cardiac output (b stimulation)
- in terms of increasing metabolism
E < NE:
- in terms of constriction of blood vessels –> leading to increased peripheral resistance –> increased arterial pressure

Endocrinology (14 decks)

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