L21 Flashcards
in a Low K diet what segments of the nephron will be reabsorbing K
all the segments of the nephron will be reabsorbing K
in a normal to high K diet what is the nephron doing
A normal to high the upper parts of the nephron will still do reabsorption and the lower parts will do secretion
What is the concentration of K+ in the ICF and the ECF?
- ICF - generally 150 mM
* ECF ~ 4 mM
what is hyperkalemia
–ECF > 5 mM = hyperkalemia (High K+ blood)
what is hypokalemia
–ECF < 3.5 mM = hypokalemia (Low K+ blood)
Why is high K+ in the
ICF important?
there’s 5
- maintain cell volume
- regulation of pH
- controlling cell enzyme function
• controlling DNA and
protein synthesis
• controlling cell growth, cell cycling and cell proliferation
Why is low K+ in the
ECF important?
theres 2
• maintain the steep K+
gradient across the
membrane to maintain the potential of cells
• Low K+ prevents problems with excitation and contraction – action potential – muscle contraction – cardiac rhythmicity
what is a low extracellular K effect on the membrane potential
it makes the MP more -ive theefore the cell is less excitable
this would be the opposite if the ECF conc of K was high
what is ataxia and what causes it
Ataxia leads to tremors and loss of fine motor control which is what happens when you have high K in extracellular fluid
what is the intracellular effect of K on the volume of the cell
net loss of intracellular K = cell shrinks
gain of K = cell swells
what is the intracellular effect of K on the pH of the cell
loss of K = cell acidosis
gain of K = alkalosis
what is the P wave?
Atrial depolarisation
what is the QRS wave?
Ventricular
depolarisation
what is the T wave?
Ventricular
repolarisation
repolarisation of a cardiac myocyte is dependent on how many K channels
6
what is the effect of an ECF conc of K of 2.5mM (hypokalemia) on an ECG
low T wave
high U wave
low ST wave
the ecg looks very different therefore you have altered cardiac function
what is the effect of an ECF conc of K of 10mM (hyperkalemia) on an ECG
initially
prolonged PR interval, depressed ST segment and high T wave
auricular standstill/intraventricular black
ventricular fibrillation = death
Which of the following statements is TRUE?
A. A typical diet does not contain the proper amount of daily K+.
B. Low ICF K+ is very important for proper enzyme function.
C. K+ is the most abundant cation in the body.
D. K + is not invoved in the nerve action potential.
C is correct
how do we get K into our bodies
then what happens
through our diet where it is absorbed through the intestine and absorbed into the blood
from her it goes into the ECF where it is either stored in the tissues via insulin, adrenaline or aldosterone (extra renal)
or excreted into the urine via ADH or aldosterone (and plasma conc)
How does your body respond to changes in K+ to maintain K+ homeostasis?
external factors
• Extrarenal - to increase K+ uptake into cells (skeletal muscle, bone, liver, red blood cells)
– epinephrine
– insulin
– aldosterone
Occurs rapidly to prevent hyperkalemia (stops it by “hiding” the K away)
How does your body respond to changes in K+ to maintain K+ homeostasis?
internal factors
• Intrarenal - regulation of reabsorption and
secretion of K+ along the nephron
Occurs over several hours
what are the extrarenal effects of Epinephrine,Insulin, and
Aldosterone on uptake of K+
acute rise in plasma conc causes Epinephrine,Insulin, and Aldosterone to increase Na/K ATPase activity in some way
The mussle cells have an insulin and adrenaline receptor in the membrane and a aldosterone receptor intracellularly
adrenaline is produced in the chromaffin cells of the adrenal medulla.
When it binds to the receptor it increases intracellular cAMP which activates Na/K ATPase to get more K into the cell
insulin is produced by the b cells in the pancreas and when it binds to its receptors in acts on Na/K ATPase as well
Aldosterone also increases Na/K ATPase activity produced from zonular glomerulosa cells of the adrenal cortex
how can we calculate the intrarenal effects of an increase in K
If we know the Glomerular Filtration Rate (GFR), we can calculate the daily filtered load of K+
GFR x [K+]plasma = Daily filtered load
eg
[K+]plasma = 4 mmol/L
180 L/day x 4 mmol/L = 720 mmoles/day
(filtered)
how can you figure out the filtered load of an ion (eg K)
GFR x [K+]plasma = Daily filtered load
the proximal tubule reabsorbs what % of the K+ filtered load
67%
this is where majority is absorbed
in the PT is mainly reabsorbed through what mechanism
the paracellular pathway (because of the leaky absorptive epithelium and local environmental voltage)
what causes K in the PT to be mostly reabsorbed through the paracellular pathway
local environmental voltage
the thick ascending limb reabsorbs what % of the filtered load of K
20%
how is K reabsorbed in the thick ascending limb
through NKCC2 (transcellular)
and paracellular pathways
the cortical collecting duct contains 2 kinds of cells
these are the intercalated cells and the principal cells
what is their roles in terms of K
• Intercalated cells (~30% of the cells)
– K+ reabsorption (9% of K filtered load via K/H ATPase)
• Principal cells (~70% of the cells)
– Na+ reabsorption
– K+ secretion
what transporters are located in an intercalated cell of the collecting duct
reabsorbs K in a low NA diet
These are tight absorbitive epithelial cells
Contain H ATPase
and K/H exchanger (also ATPase) in apical membrane
Basolateral = Cl bicarbonate exchanger and K/Cl channel and Na/K ATPase
Carbonic anhydrase and K/H exchanger is for pH regulation
how do the principal cells and the late distal tubule secrete K
in a high K diet you get K+ secretion (luminal K+ channel ROMK) under the influence of aldosterone and the K+-Cl- cotransporter (electroneutral)
aldosterone increases the activity of these channels via increasing more ENaC into the apical membrane, this brings more Na into the cell increasing the activity of the Na/K ATPase which makes the inside of the cell more positive (more K inside the cell) which increases the driving force of K across the apical membrane
If you have a low K+ diet, which statement is TRUE?
A. Your body would increase K+ secretion by the collecting duct cells.
B. Your body would reduce insulin release to reduce uptake of K+ into cells.
C. Your body would increase the release of epinephrine to increase uptake of K+ into cells.
D. Your body would decrease the amount of aldosterone
A. you wouldn’t increase secretion in a low K diet
C. decrease the release
D. aldosterone is not secreted actively in response to K it is so Na is reabsorbed and loss of K is just a byproduct maybe???
what regulates K excretion/secretion
- high plasma K+ concentrations
- aldosterone
- flow rate of the filtrate
how does an increase in K concentration in the plasma (hyperkalemia) increase K excretion
increase in plasma K is detected by the adrenal gland which causes aldosterone to be secreted which acts on the kidney to increase K secretion
what is the effect of Aldosterone on K+ secretion by the
LDT and CD
there is an increase in activation and amount of the epithelial sodium channel (ENaC) which brings more Na into the cell increasing the Na driving force for the Na/K ATPase
an increase in the amount and activity of the Na+-K+-ATPase;
entry of K+ across basolateral membrane
entry of Na+ makes the cell potential more
positive enhancing the driving force for K+ exit
across the apical membrane (K+ secretion)
what is the effect of flow of tubular fluid on K secretion
Low K+ diet = low flow rate = K+ secretion is low
• Normal or High K+ diet then K+ secretion is high when compared at a single flow rate
flow is about 5nL/min
