Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why does the LoH go into medulla

A

Because the medulla is hypertonic

Concentrated urine can get produced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the corticopapillary gradient

A

Gradient from cortex to pappila

300-1200 mOsm/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is the corticopapillary gradient established

A

By urea recycling

Countercurrent multiplication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is gradient maintained

A

Vasa recta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which part of LoH are permeable to water

A

Thin descending

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which part of LoH are permeable to ions

A

Thin descending,

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Countercurrent multiplication

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the mOsm/kg of fluid leaving LoH

A

100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Urea recycling achieves ?

A

Maintains medullary hypertonicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where is 50% of urea reabsorbed

A

PCT with Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which areas are impermeable to urea

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Urea concentration in tubule

A

Increases as urea travels down gradient from medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes increase in urea transporters and where?

A

ADH

Apical surface of medullary collecting tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does reabsorption of urea via transporters achieve

A

Urea flows down conc gradient to medulla to maintain hypertonicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How much (%) urea is excreted

A

40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why is K+ important

A

Tissue excitability

Determines resting membrane potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Concentration of K+

A

4-5 mmol/L- extracellularly

150-160 mmol/L- intracellularly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What happens to membrane potential if extracellular K+ increases

A

Resting membrane potential depolarises

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where is most K+ reabsorbed

A

PCT - 65%
Tight junctions
Passive
Solvent drag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Secretion of K in collecting duct by what cells

A

By principle cells

High K diet 15-120% secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Reabsorption of K in collecting duct by what cells

A

By intercalated cells

10-12% if trying to preserve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

Urinary (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions