Potassium balance Flashcards
(24 cards)
explain potassium input and potassium homeostasis
potassium input:
-a typical daily intake in the UK is 50-125mmol
-K+ is found in leafy vegetables and most fruit/veg.
-unlike Na+, K+ should not be restricted routinely.
Potassium homeostasis:
-intracellular levels are maintained high whilst extracellular levels are maintained low. These levels vary depdning on cell types
-internal balance maintained by inulin, adrenaline, pH changes
-external control under the kidneys
explain the importance of potasium homeostasis and potassium functions
importance of potassium homeostasis:
-regulation of K+ homeostasis implies;
* acute regulation, distrubution of K+ through ICF and ECF compartments
* chronic regulation, achieved by the kidney adjusting K+ excretion and reabsorption.
K+ functions:
1) determines ICF osmolality –> cell volume
2) Determines resting membrane potential which is very important for normal functioning of excitable cells.
3) affects vascular resistance
explain what the Na+/K+ ATPase pump does simply
Na+/K+ ATPase pump maintains HIGH [K+] and LOW [Na+]
explain internal balance/acute regulation
-ECF pool will change more dramatically with changes in body K+ distrubution which is shifted to ICF compartment
-shift mainly subject to hormonal control
-Hyperkalaemia= plasma [K+] > 5.5mM
-Hypokalaemia= plasma [K+] <3.5mM
explain how resting membrane potential is maintained and nernst equation
-membrane potential formed by creation of ionic gradients
-dynamic balance between membrane conductance to Na+ and K+ determines resting membrane potential normally.
Nernst equilibrium potential= 6.15 x log [K]0/[K]i
explain the affect of altering potassium and RMP
-Altering plasma potassium concentration can severely affect the heart by changing cardiac cell membrane potential.
-it affects the firing of action potentials producing characteristic changes in ECG.
explain hypokalaemia and hyperkalaemia
Hypokalaemia:
-hypokalaemia caused by renal or extra-renal loss of K+ or by restricted intake
-long standing use of diuretics without KCL compensation
-prolonged vomiting —-> Na+ loss —-> increased aldosterone secretion —> K+ excretion in kidneys
-profuse diarrhoea
-hypokalaemia results in decreased release of adrenaline, aldosterone & insulin
Hyperkalaemia:
-acute hyperkalaemia normal following prolongued excercise —-> normal kidneys excrete K+ easily.
disease states;
-insufficient renal excretion
-increased release from damaged body cells
-long term use of potassium sparing duiretics
-addison’s disease
explain [K+] and action potentials and ECG changes
[K+] and action potentials:
-low extracellular levels cause hyperpolarisation. This delays the firing of an action potential as it takes longer to reach resting potential.
-high extracellular levels cause depolarisation, this means the resting potential is reached too fast (shorter refractory period) so action potentials are fired too fast.
ECG changes:
-hypokalaemia; decreased amplitude of T wave, prolongued Q-U interval, prolong P-wave.
hypokalaemia; increase QRS complex, increase amplitude T wave, eventual loss of P-wave
explain external balance/chronic regulation
-in a healthy person, external balance is maintained almost entirely by the kidney
-maintenance of normal K homeostasis increasingly important limiting factor in therapy of CVD:
-drugs like B-blockers, ACE inhibitors —> risk of hypokalaemia.
-K+ excretion in the stools is not under regulatory control —> large amounts can be lost by extra-renal routes
Explain the use of plasma, insulin, glucose, and other hormones
Plasma [K+]= >7mM life threatening –> asystolic cardiac arrest
-insulin/glucose infusion used to drive K+ back into cells.
-other hormones (aldosterone, adrenaline) stimulates Na+/K+ pump to increase cellular K+ influx.
explain renal handling of Na+ and K+
-human kidneys designed to conserve Na and excrete K.
-Na+ and K+ filtered freely at glomeruli
-in 24hrs, entire glomerular filtrate contains :
* 25moles of Na+
* 0.7 moles of K+
explain K+ movement in the PCT
1) the Na+/K+ ATPase pump maintains low Na+ and high K+ levels within the kidney cells. This means Na+ can enter the cells from the tubular lumen and K+ can passively diffuse out of cells into the ECF.
2) If the Na+/K+ ATPase pump is blocked —> it disrupts the movement of ions and water.
3) There is also some passive paracellular movement of ions which causes water movement
explain Na/K+ movement in loop of Henle (LoH)
-The Na+/Cl- sympoter pulls salts out of the ascending limb lumen into the water.
-the Na+/K ATPase maintains the Na+ gradient to allow this movement
-the K+ then passively moves out of the cell through K+ channels., it contributes to the medullary osmotic effect causing the outward movement of fluid from the tubules
explain K+ movement in the DCT
> 90% of filtered K+ reabsorbed in PCT and LoH
1) ENaC channels on the luminal sides are activated by aldosterone and cause Na movement from the tubule into the epithelial cells. This is aided by the electrochemical gradient.
2) This Na+ is moved out into the blood by the Na+/K+ ATPase which also transports K+ in.
3) The K+ then moves out passively through K+ channels or actively through the Cl-/K+ symporter (into the lumen)
4) The ENaC channels are inhibited by K- sparring diuretics which disrupts the concentration gradient for the Na+/K+ ATPase, this ultimately limits K+ movement into the lumen
Explain K+ excretion into urine in DCT
-increased K+ intake
-changes in blood pH:
* Aklalosis —> increased excretion of K+—-> decreased serum [K+]
* acute acidosis —> decreased excretion of K+ —> increased serum [K+]
explain how this is achieved
1) actvity of Na+/K ATPase pump
2) electrochemical gradient
3) permeability of luminal membrane channel
explain aldosterone and K+ secretion
-Aldosterone is a major regulator of K+ balance in the body. it acts to:
-increased activity of Na+/K+ pump to increased K+ influx into cells, increases cell lumen K+ concentration gradient so more secreted into lumen.
-increased ENaC channels to increased Na+ reabsorption= decreased cell negativity and increased lumen negative creates a voltage gradient.
-redistrubutes ENaC from intracellular localisation to membrane
-increased permeability of luminal membrane to K+
explain how increased plasma [K] increases [K] secretion in 3 ways
1) slows exit from basolateral membrane, cell lumen concentration gradient
2) increased activity of Na+/K+ ATPase, increased [K] within cell
3) increased plasma [K] stimulates aldosterone secretion
explain alkalosis and acidosis
Alkalosis; increases intracellular K+ so favours the concentration gradient for K+ secretion
Acidosis; decreases intracellular K+ by inhibiting the Na/K ATPase, this reduces the passive diffusion of K+ into the lumen reduces secretion of K+
explain tubular flow rate and K+ secretion and reabsoprtion of K+
Tubular flow rate and K+ secretion:
-increased tubule fluid flow rate; weeps away the secreted K+, making the [K] low so that the concentration gradient for K+ is favourable to more K entering. This increases K+ secretion
-ADH increases K+ secretion by increasing the K+ conductance of luminal membrane
Reabsorption of K+:
-a-intercalated cells of late DCT/CD; active in severe hypokalaemia
explain Na+ and K+ balance
Na+ and K+ balance:
-depedence of potassium secretion on Na+ and flow poses problems. This is because K+ levels may be normal but K+ may be lost as a result of modifying Na+
-a decrease in ECFV increases aldosterone secretion and Na reabsorption.
-Na+ reabsorption reduces flow rate which reduces K+ secretion whilst aldosterone—> increases K+ secretion. This means the two effects counteract each other and K+ levels remain constant
explain renin-angiotension-aldosterone
-a decrease in fluid volume will reduce BP (sensed by JGA) and Na+ (sensed by macula densa)
-this signals the release of renin which ultimately causes vasoconstricton (reducing BP) and aldosterone release.
-aldosterone has differeing effects on different cells
-in principle cells, it increases the number of ENaC channels and Na/K ATPase pumps. This leads to more K+ being secreted.
-in intercalated cells, it increases the activity of the Na+ symporter and causes the movement of K+ into the blood so less is secreted.
explain characteristics of Addison’s disease
Addison’s disease aka primary adrenal insufficiency is very rare compared to secondary:
-cortex produces glucocorticoid hormones, mineralcorticoid hormones and sex hormones
-damage to cortex causes a reduction in hormone production —> numerous symptoms
-deficiency in aldosterone means the body secrets too much Na+ and retains too much K+ (hyperkalaemia)
-treatment usually involves corticosteroid (steroid) replacement therapy for life
explain secondary adrenal insufficiency and conn’s syndrome aka primary aldosteronism
Secondary adrenal insufficiency:
-failure to produce ACTH which stimulates the adrenal glands to produce cortisol
Conn’s syndrome aka primary aldosteronism:
causes;
-due to aldosterone producing adenoma (tumour) of zona glomerulosa of adrenal gland
-usually <3cm, unilateral and renin unresponsive
-hyperaldosteronism due to variety chronic disease
-most common due to Conn’s syndrome, remaining 40-50% is due to bilateral adrenal hyperplasia
-Aldosterone releases in absence of stimulation by angiotension II
-increased plasma aldosterone causes kidneys to stimulate Na+ reabsorption & K+ excretion leading to hypertension.
-this increased fluid volume causes hypokalaemia, hypersa natremia and alkalosis
-increase in BP and Na+ delivery to macula densa reduces renin release —> renin independent cause of hypertension
treatment:
-surgical removal of tumour containing adrenal gland
-hypertension and hypokalaemia controlled with K+ sparing agents
