3- Refeeding, Tx AA, K, Mg, Countercurrent Flashcards
What percentages are cortical short LoH and juxtamedullary long LoH
85%
15%
Why does the LoH go into medulla
Because the medulla is hypertonic
Concentrated urine can get produced.
What is the corticopapillary gradient
Gradient from cortex to pappila
300-1200 mOsm/L
How is the corticopapillary gradient established
By urea recycling
Countercurrent multiplication
How is gradient maintained
Vasa recta
Which part of LoH are permeable to water
Thin descending
Which part of LoH are permeable to ions
Thin descending,
Thick ascending- Na/K/Cl co-transporter on apical
Countercurrent multiplication
Thick ascending limb maintains as 200 mOsm/kg difference between tubular fluid and interstitium
What is the mOsm/kg of fluid leaving LoH
100
Vasa recta
Permeable to solutes and water
Moves slowly to allow equilibrate at each point
Descends- absorbs solutes, water lost
Ascends- reabsorb water and loss of solutes
Maintains high osmolality of interstitium
Urea recycling achieves ?
Maintains medullary hypertonicity
Where is 50% of urea reabsorbed
PCT with Na
Which areas are impermeable to urea
Ascending limb and early DCT so concentration increases as water and solutes are reabsorbed
Urea concentration in tubule
Increases as urea travels down gradient from medulla
What causes increase in urea transporters and where?
ADH
Apical surface of medullary collecting tubules
What does reabsorption of urea via transporters achieve
Urea flows down conc gradient to medulla to maintain hypertonicity
How much (%) urea is excreted
40%
Why is K+ important
Tissue excitability
Determines resting membrane potential
Concentration of K+
4-5 mmol/L- extracellularly
150-160 mmol/L- intracellularly
What happens to membrane potential if extracellular K+ increases
Resting membrane potential depolarises
Where is most K+ reabsorbed
PCT - 65%
Tight junctions
Passive
Solvent drag
What is the solvent drag
Solutes in the ultrafiltrate that are transported back from the renal tubule by the flow of water rather than specifically by ion pumps or other membrane transport proteins
Secretion of K in collecting duct by what cells
By principle cells
High K diet 15-120% secretion
Reabsorption of K in collecting duct by what cells
By intercalated cells
10-12% if trying to preserve
Causes of hypokalemia
Excess insulin (increases uptake into cells)
Alkalosis- K moves into cell exchanged with H
Insufficient intake- Fasting, anorexia
Too much aldosterone- HF, cirrhosis, aldosteronism
Diuretics
D and V
Sweat
Signs of hypokalemia
Asymptomatic until below 2-2.5mmol/L Hyperpolarized nerve and muscle cells = less excitable Paralysis Muscle weakness Cramps Tetany Vasoconstriction Polyuria and thirst.
Causes of hyperkalemia
Reduced renal excretion due to AKI or CKD
K sparing diuretics
Metabolic acidosis (H moves into cell to try combat)
Artifact
Hypoaldosteronism/ ACEI
Signs of hyperkalemia
Muscle weakness
Cardiac arrythmias
What value is hyperkalmeia
> 6.5 mmol/L or ECG changes
Treatment of hyperkalemia
Calcium gluconate- stabilize myocardium
Insulin- drives K into cells (give with glucose)
Calcium resonium increased bowel excretion
Salbutamol neb- drives K into cells
Sodium bicarbonate- corrects acidosis so drives K into cells
RRT- dialysis
What is the role of magniesium
Intracellular cation
Controls mitochondrial oxidative metabolism
Regulates energy production
Vital for protein synthesis
Regulates K and Ca channels in cell membrane
What is the normal range for magnesium
2.12-2.65
How is magnesium transported across cell
Passive paracellular transport
Where is magnesium reabsorbed
PCT 30%
LoH 60%
What does it mean by max absorption rate
Absorption is equal to concentration of Mg2+ filtered. So if Mg increases and exceeds Tm then more is secreted
What controls the absorption of Mg
PTH controls in LoH
Causes of hypomagnesaemia
Decreased intake Diarrhoea Renal wasting Diuretics Diabetes- large urine flow Excessive alcohol consumption- increased renal excretion
What is hypomagnesaemia commonly associated with
Hypokalemia
Hypocalcemia - Mg needed to make PTH
Signs of hypomagnesaemia
Uncontrolled stimulation of nerve and tetany
Causes of hypermagnesaemia
Renal failure- can not excrete
Ingested Mg - incorrect IV, constipation
Signs of hypermagnesaemia
Reduced muscle contraction
Inhibition of PTH release = hypocalcaemia
Can alter electrical potential across cardiac cell membrane = arrhythmias
Treatment of hypermagnesaemia
Calcium gluconate- Mg and Ca compete
Furosemide- increase excretion
Where is most glucose absorbed
PCT
How is glucose reabsorbed
Secondary active transport driven by energy released by Na down its concentration gradient
What transporter does glucose use on PCT
SGLT
What is the Tm of glucose and what does it mean and why is it limited
Max tubular reabsorptive capacity for solute
Limited Na/glucose carriers
10mmol/L then start appearing in urine
Where are amino acids reabsorbed
PCT by secondary transport, symporter with Na, driven by Na/K ATPase
Tm limited
Urea in blood
2.6-7.5 mmol/L
When does urea conc increase in filtrate and what does this mean
Result of Na, Cl and water reabsorption
This allows urea to be passively reabsorbed down conc gradient
What areas are impermeable to urea
Distal tubule and outer medullary ducts
Blood sulphate levels
1-1.5 mmol/L
What is sulphate important for
Regulating plasma concentration
What happens in early starvation
Glucose levels decline and insulin levels decline
Glucagon levels increase to release glucose
What effects does glucagon have
Glucagon stimulates glycogenolysis in liver and lipolysis of TAG in fat reserves = fatty acids and glycerol
How are fatty acids and glycerol used by body
As energy and converted to ketone bodies in liver
What happens when glycogen reserves become depleted
Gluconeogenesis stimulated by liver using amino acids (by breaking down muscle), lactate and glycerol to make glucose for brain
What happens when the body becomes depleted of energy
Reduces all energy consuming metabolic processes such as actions of cellular pumps = leaking
Where do K, PO4, Mg leak to
Plasma and excreted by kidneys = deficit
What happens to water and Na in starvation
Into cells and reduced ability for body to excrete excess water and Na
What happens when you reintroduce nutrition with
Increased insulin production = increased cell uptake of glucose, PO4 and K = deficit
Reactivation of Na/K ATPase = more K taken up and Na and water out of cells
Na/K ATPase uses Mg as cofactor so = decrease Mg
Decreased renal function = decrease ability to excrete Na and fluid = overload
PO4 used for energy storage as ATP
Increase demand for thiamine for carb met
Protein synthesis = increase anabolic tissue growth = increased demand for PO4, K, glucose and water
What happens when you reintroduce nutrition summary
Return to carb metabolism and increased uptake of electrolytes intracellularly = low serum levels
Main manifestations of refeeding (6 things)
Hypokalemia Hypophosphatemia Hypomagnesaemia Thiamine deficiency Altered glucose metabolism Body fluid disturbance
When to consider if re-feeding is going to be an issue
BMI < 18.5 Low dietary intake for 5 days 3-6 months unintentional weight loss Low electrolytes Alcohol abuse Malabsorption
Serum electrolyte levels Mg, K, PO4
K: 2.5-3
Mg: 0.3-0.6
PO4: 0.32-0.5
Kcal to refeed
10kcal/kg/day
5kcal/kg/day if BMI <14
What to consider alongside feeding
Cardiac monitor Fluid replacement Multivitamin Vit B with thiamine Fluid balance
