Hormonal Mechanisms

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  • Created by: Becca
  • Created on: 27-12-13 16:51
What does the quantity of sodium determine?
Effective ECF volume (detected by volume sensors e.g. atrial & arterial) -> BP
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What is natriuresis?
Excretion of sodium ions in urine
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What is euvolemia?
Maintenance of normal ECF volume, by balancing NaCl ingested with that excreted
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What is hypovolemia? What causes it? What are the symptoms?
Volume depletion/ECF volume contraction. Loss of total body Na+. Serum [Na+] can be high/low/normal as it alters the amount of Na+, not conc. Causes: haemorrhage, vomiting, diarrhoea, polyuria. Symptoms: dry mucous membranes, fainting, tachycardia
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What is hypervolemia? What causes it? What are the symptoms?
Volume overload/ECF volume expansion. Increased total body Na+, can be with normal/high perfusion pressure (renal failure->nocturia, N+V, appetite/weight loss etc) or low perfusion pressure (heart failure, cirrhosis->oedema, ascites, proteinuria etc)
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What has a major influence on Na+ excretion?
GFR: determines filtered load (how much Na+ is being filtered ready to be excreted). Tubular reabsorption of Na+ (collecting duct -> fine control)
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Why is aldosterone important in normal Na+ reabsorption?
It its absence inappropriately large amount of Na+ excreted. In excess, aldosterone enhances Na+ reabsorption causing expansion of ECF volume
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What effector mechanisms stimulate renal Na+ transport?
Renin-angiotensin-aldosterone system (RAA): all increase proximal Na reabsorption, aldosterone increases late DT/CD reabsorption. Sympathetic NS: noradrenaline increases proximal Na reabsorption, activates RAA & decreases GFR (decreases Na excretion)
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What effector mechanisms inhibit renal Na+ transport?
Atrial natriuretic peptide/ANP: increase GFR (vasodilation, more Na excretion), decreases proximal/MCD Na reabsorption, inhibits aldosterone & renin release. Natriuretic factors: decrease prox Na reabsorption, inhibit renin release. ADH: inhibits RAA
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How do macula densa influence renin release?
Decrease tubular [NaCl] delivery to distal tubule -> Na+K+2Cl- co-transporter activity in macula densa cells -> increase renin release
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How do renal baroreceptors & catecholamines influence renin release?
Renal baroreceptor: decrease in renal perfusion pressure -> increase renin release. Catecholamines: decrease ECF volume/BP, increase sympathetic activity, beta-adrenoceptors -> increase renin release
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What does low blood volume & pressure stimulate?
RAA system (promotes vasoconstriction & Na reabsorption regulated by aldosterone), sympathetic NS (increase Na reab. & renin release but decrease RBF/GFR -> decrease filtered load Na), decrease ANP release, increase ADH secretion
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How does low plasma Na+/ECF volume/BP lead to aldosterone release?
Activate renin release (granular cells) -> Angiotensin (liver) -> Agiotensin I (using renin) -> Angiotensin II (using ACE) -> Aldosterone release (zona glomerulus, adrenal cortex)
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What does angiotensin II stimulate?
ADH (->CD H2O reabsorption), thirst, tubular Na reabsorption (->H2O retention), aldosterone secretion, vasoconstriction (increases BP) & sympatho-excitation (->vasoconstriction). Water & salt retention and water intake. Effective ECF volume increases
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What is the mechanism to restore low BP to normal?
Detected by baroreceptors -> activates RAA system (increase sympathetic activity) -> increase Na+ reabsorption + drinking (thirst) -> volume restored -> raises BP back to normal
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What is the mechanism to restore high BP to normal?
Detected by baroreceptors -> inhibits RAA system (decrease sympathetic activity) -> decrease Na+ reabsorption -> decrease water volume -> lowers BP back to normal
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What is the mechanism to restore low solute concentration to normal?
Detected by osmoreceptors -> decrease ADH release -> decrease water reabsorption & increase water excretion -> increase osmolality
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What is the mechanism to restore high solute concentration to normal?
Detected by osmoreceptors -> thirst & ADH release -> increase water intake & increase water reabsorption -> decreases osmolality
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What influences K+ secretion?
Renal K+ secretion is increased by aldosterone and plasma [K+] (most important), distal flow rate and Na+ reabsorption
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For osmoregulation & volume regulation: what is sensed, what are the sensors, what are the effectors & what is affected?
Osmoregulation: plasma osmolality, hypothalamic osmoreceptors, ADH/thirst, urine osmolality/water intake. Volume regulation: ECF volume, macula densa/baroreceptors/atria/carotid sinus, RAA/sympathetic NS/ANP/ADH/natriuretic factors, urinary Na/thirst
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What are the homeostatic responses to salt ingestion?
Increase osmolality -> ADH secretion/thirst -> H2O intake -> renal H2O reabsorption, osmolality normal but salt raised, increase ECF volume -> BP raised -> kidneys excrete salt+H2O (slow response) & cardiovascular reflexes lower BP (rapid) -> Normal!
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What does drinking large amounts of water cause?
Increase in volume but decrease in osmolality -> decreased ADH, decrease RAA/SNS, increase ANP/natriuretic factors -> excrete dilute urine
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What does ingestion of isotonic saline cause?
Increase in volume but no change in osmolality -> decrease RAA/SNS, increase ANP/natriuretic factors, decrease Na/H2O reabsorption -> increase urine volume -> decrease ECF volume
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What does ingestion of hypertonic saline cause?
Increase in volume & increase in osmolality -> increase ADH/thirst, decrease RAA/SNS, increase ANP/natriuretic factors -> excrete concentrated urine
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What does replacing sweat loss with plain water cause?
No change in volume but decrease in osmolality -> hyponatraemia & hypokalaemia
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What does eating salt without drinking water cause?
No change in volume but increase in osmolality -> increase ADH & thirst
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What does haemorrhage cause?
Decrease in volume but no change in osmolality -> increase RAA/SNS, decrease ANP/natriuretic factors -> increase Na/H2O reabsorption (treat with isotonic saline)
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What does dehydration e.g. sweat loss or diarrhoea cause?
Decrease in volume but increase in osmolality -> increase ADH/thirst, increase RAA/SNS, decrease ANP/natriuretic factors -> increase Na/H2O reabsorption (treat with H2O)
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What is the purpose of modulating excretion of dietary intake of K+?
Keeps plasma [K+] stable, maintains [Ki]/[Ko] & hence resting membrane potential and determines excitability of nerves & muscles
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What happens to K+ in the nephron?
Almost all filtered K+ is reabsorbed before distal sites at which secretion occurs (principal cells of cortical and outer medullary collecting duct)
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What are the major factors that affect renal K+ secretion?
Aldosterone: increase Na reabsorption -> increases Na/K-ATPase activity -> increase cell K -> increase luminal K permeability (opens K channels). Plasma [K+]: increase luminal K permeability -> increase Na/K-ATPase activity -> stimulates aldosterone
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What other factors affect renal K+ secretion?
Distal flow rate: K+ washout keeps luminal K low & allows K secretion. Na reabsorption: without Cl -> enhances luminal negativity, promotes K secretion & Na reabsorption (Na/K-ATPase). Acid-base balance: alkalosis=hypokalemia & acidosis=hyperkalaemia
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Card 2

Front

What is natriuresis?

Back

Excretion of sodium ions in urine

Card 3

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What is euvolemia?

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Card 4

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What is hypovolemia? What causes it? What are the symptoms?

Back

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Card 5

Front

What is hypervolemia? What causes it? What are the symptoms?

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