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Urinary > 3- Refeeding, Tx AA, K, Mg, Countercurrent > Flashcards

3- Refeeding, Tx AA, K, Mg, Countercurrent Flashcards

1
Q

What percentages are cortical short LoH and juxtamedullary long LoH

A

85%

15%

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2
Q

Why does the LoH go into medulla

A

Because the medulla is hypertonic

Concentrated urine can get produced.

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3
Q

What is the corticopapillary gradient

A

Gradient from cortex to pappila

300-1200 mOsm/L

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4
Q

How is the corticopapillary gradient established

A

By urea recycling

Countercurrent multiplication

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5
Q

How is gradient maintained

A

Vasa recta

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6
Q

Which part of LoH are permeable to water

A

Thin descending

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7
Q

Which part of LoH are permeable to ions

A

Thin descending,

Thick ascending- Na/K/Cl co-transporter on apical

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8
Q

Countercurrent multiplication

A

Thick ascending limb maintains as 200 mOsm/kg difference between tubular fluid and interstitium

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9
Q

What is the mOsm/kg of fluid leaving LoH

A

100

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10
Q

Vasa recta

A

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

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11
Q

Urea recycling achieves ?

A

Maintains medullary hypertonicity

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12
Q

Where is 50% of urea reabsorbed

A

PCT with Na

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13
Q

Which areas are impermeable to urea

A

Ascending limb and early DCT so concentration increases as water and solutes are reabsorbed

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14
Q

Urea concentration in tubule

A

Increases as urea travels down gradient from medulla

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15
Q

What causes increase in urea transporters and where?

A

ADH

Apical surface of medullary collecting tubules

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16
Q

What does reabsorption of urea via transporters achieve

A

Urea flows down conc gradient to medulla to maintain hypertonicity

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17
Q

How much (%) urea is excreted

A

40%

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18
Q

Why is K+ important

A

Tissue excitability

Determines resting membrane potential

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19
Q

Concentration of K+

A

4-5 mmol/L- extracellularly

150-160 mmol/L- intracellularly

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20
Q

What happens to membrane potential if extracellular K+ increases

A

Resting membrane potential depolarises

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21
Q

Where is most K+ reabsorbed

A

PCT - 65%
Tight junctions
Passive
Solvent drag

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22
Q

What is the solvent drag

A

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

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23
Q

Secretion of K in collecting duct by what cells

A

By principle cells

High K diet 15-120% secretion

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24
Q

Reabsorption of K in collecting duct by what cells

A

By intercalated cells

10-12% if trying to preserve

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25
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
26
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. ```
27
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
28
Signs of hyperkalemia
Muscle weakness | Cardiac arrythmias
29
What value is hyperkalmeia
>6.5 mmol/L or ECG changes
30
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
31
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
32
What is the normal range for magnesium
2.12-2.65
33
How is magnesium transported across cell
Passive paracellular transport
34
Where is magnesium reabsorbed
PCT 30% | LoH 60%
35
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
36
What controls the absorption of Mg
PTH controls in LoH
37
Causes of hypomagnesaemia
``` Decreased intake Diarrhoea Renal wasting Diuretics Diabetes- large urine flow Excessive alcohol consumption- increased renal excretion ```
38
What is hypomagnesaemia commonly associated with
Hypokalemia | Hypocalcemia - Mg needed to make PTH
39
Signs of hypomagnesaemia
Uncontrolled stimulation of nerve and tetany
40
Causes of hypermagnesaemia
Renal failure- can not excrete | Ingested Mg - incorrect IV, constipation
41
Signs of hypermagnesaemia
Reduced muscle contraction Inhibition of PTH release = hypocalcaemia Can alter electrical potential across cardiac cell membrane = arrhythmias
42
Treatment of hypermagnesaemia
Calcium gluconate- Mg and Ca compete | Furosemide- increase excretion
43
Where is most glucose absorbed
PCT
44
How is glucose reabsorbed
Secondary active transport driven by energy released by Na down its concentration gradient
45
What transporter does glucose use on PCT
SGLT
46
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
47
Where are amino acids reabsorbed
PCT by secondary transport, symporter with Na, driven by Na/K ATPase Tm limited
48
Urea in blood
2.6-7.5 mmol/L
49
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
50
What areas are impermeable to urea
Distal tubule and outer medullary ducts
51
Blood sulphate levels
1-1.5 mmol/L
52
What is sulphate important for
Regulating plasma concentration
53
What happens in early starvation
Glucose levels decline and insulin levels decline | Glucagon levels increase to release glucose
54
What effects does glucagon have
Glucagon stimulates glycogenolysis in liver and lipolysis of TAG in fat reserves = fatty acids and glycerol
55
How are fatty acids and glycerol used by body
As energy and converted to ketone bodies in liver
56
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
57
What happens when the body becomes depleted of energy
Reduces all energy consuming metabolic processes such as actions of cellular pumps = leaking
58
Where do K, PO4, Mg leak to
Plasma and excreted by kidneys = deficit
59
What happens to water and Na in starvation
Into cells and reduced ability for body to excrete excess water and Na
60
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
61
What happens when you reintroduce nutrition summary
Return to carb metabolism and increased uptake of electrolytes intracellularly = low serum levels
62
Main manifestations of refeeding (6 things)
``` Hypokalemia Hypophosphatemia Hypomagnesaemia Thiamine deficiency Altered glucose metabolism Body fluid disturbance ```
63
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 ```
64
Serum electrolyte levels Mg, K, PO4
K: 2.5-3 Mg: 0.3-0.6 PO4: 0.32-0.5
65
Kcal to refeed
10kcal/kg/day | 5kcal/kg/day if BMI <14
66
What to consider alongside feeding
``` Cardiac monitor Fluid replacement Multivitamin Vit B with thiamine Fluid balance ```

Urinary (11 decks)

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