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
Q

Causes of hypokalemia

A

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

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26
Q

Signs of hypokalemia

A
Asymptomatic until below 2-2.5mmol/L
Hyperpolarized nerve and muscle cells = less excitable
Paralysis
Muscle weakness
Cramps
Tetany
Vasoconstriction
Polyuria and thirst.
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27
Q

Causes of hyperkalemia

A

Reduced renal excretion due to AKI or CKD
K sparing diuretics
Metabolic acidosis (H moves into cell to try combat)
Artifact
Hypoaldosteronism/ ACEI

28
Q

Signs of hyperkalemia

A

Muscle weakness

Cardiac arrythmias

29
Q

What value is hyperkalmeia

A

> 6.5 mmol/L or ECG changes

30
Q

Treatment of hyperkalemia

A

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
Q

What is the role of magniesium

A

Intracellular cation
Controls mitochondrial oxidative metabolism
Regulates energy production
Vital for protein synthesis
Regulates K and Ca channels in cell membrane

32
Q

What is the normal range for magnesium

A

2.12-2.65

33
Q

How is magnesium transported across cell

A

Passive paracellular transport

34
Q

Where is magnesium reabsorbed

A

PCT 30%

LoH 60%

35
Q

What does it mean by max absorption rate

A

Absorption is equal to concentration of Mg2+ filtered. So if Mg increases and exceeds Tm then more is secreted

36
Q

What controls the absorption of Mg

A

PTH controls in LoH

37
Q

Causes of hypomagnesaemia

A
Decreased intake
Diarrhoea
Renal wasting
Diuretics
Diabetes- large urine flow
Excessive alcohol consumption- increased renal excretion
38
Q

What is hypomagnesaemia commonly associated with

A

Hypokalemia

Hypocalcemia - Mg needed to make PTH

39
Q

Signs of hypomagnesaemia

A

Uncontrolled stimulation of nerve and tetany

40
Q

Causes of hypermagnesaemia

A

Renal failure- can not excrete

Ingested Mg - incorrect IV, constipation

41
Q

Signs of hypermagnesaemia

A

Reduced muscle contraction
Inhibition of PTH release = hypocalcaemia
Can alter electrical potential across cardiac cell membrane = arrhythmias

42
Q

Treatment of hypermagnesaemia

A

Calcium gluconate- Mg and Ca compete

Furosemide- increase excretion

43
Q

Where is most glucose absorbed

A

PCT

44
Q

How is glucose reabsorbed

A

Secondary active transport driven by energy released by Na down its concentration gradient

45
Q

What transporter does glucose use on PCT

A

SGLT

46
Q

What is the Tm of glucose and what does it mean and why is it limited

A

Max tubular reabsorptive capacity for solute
Limited Na/glucose carriers
10mmol/L then start appearing in urine

47
Q

Where are amino acids reabsorbed

A

PCT by secondary transport, symporter with Na, driven by Na/K ATPase
Tm limited

48
Q

Urea in blood

A

2.6-7.5 mmol/L

49
Q

When does urea conc increase in filtrate and what does this mean

A

Result of Na, Cl and water reabsorption

This allows urea to be passively reabsorbed down conc gradient

50
Q

What areas are impermeable to urea

A

Distal tubule and outer medullary ducts

51
Q

Blood sulphate levels

A

1-1.5 mmol/L

52
Q

What is sulphate important for

A

Regulating plasma concentration

53
Q

What happens in early starvation

A

Glucose levels decline and insulin levels decline

Glucagon levels increase to release glucose

54
Q

What effects does glucagon have

A

Glucagon stimulates glycogenolysis in liver and lipolysis of TAG in fat reserves = fatty acids and glycerol

55
Q

How are fatty acids and glycerol used by body

A

As energy and converted to ketone bodies in liver

56
Q

What happens when glycogen reserves become depleted

A

Gluconeogenesis stimulated by liver using amino acids (by breaking down muscle), lactate and glycerol to make glucose for brain

57
Q

What happens when the body becomes depleted of energy

A

Reduces all energy consuming metabolic processes such as actions of cellular pumps = leaking

58
Q

Where do K, PO4, Mg leak to

A

Plasma and excreted by kidneys = deficit

59
Q

What happens to water and Na in starvation

A

Into cells and reduced ability for body to excrete excess water and Na

60
Q

What happens when you reintroduce nutrition with

A

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
Q

What happens when you reintroduce nutrition summary

A

Return to carb metabolism and increased uptake of electrolytes intracellularly = low serum levels

62
Q

Main manifestations of refeeding (6 things)

A
Hypokalemia
Hypophosphatemia
Hypomagnesaemia 
Thiamine deficiency 
Altered glucose metabolism
Body fluid disturbance
63
Q

When to consider if re-feeding is going to be an issue

A
BMI < 18.5
Low dietary intake for 5 days
3-6 months unintentional weight loss
Low electrolytes
Alcohol abuse
Malabsorption
64
Q

Serum electrolyte levels Mg, K, PO4

A

K: 2.5-3
Mg: 0.3-0.6
PO4: 0.32-0.5

65
Q

Kcal to refeed

A

10kcal/kg/day

5kcal/kg/day if BMI <14

66
Q

What to consider alongside feeding

A
Cardiac monitor
Fluid replacement
Multivitamin
Vit B with thiamine
Fluid balance