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Nephrology > Renal Physiology and Acid-base Balance/Disorders > Flashcards

Renal Physiology and Acid-base Balance/Disorders Flashcards

1
Q

What are the principle routes of H+ excretion?

A

Lungs as CO2 and H2O

Kidneys

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2
Q

What is H+ excreted as in the lungs?

A

CO2 and H2O

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3
Q

What is the initial [H+] pf glomerular filtrate?

A

40nmol/L

pH 7.4

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4
Q

In what forms is H+ found in urine?

A
  1. Free H+
  2. Attached to phosphate (Na2HPO3, NaH2PO4)
  3. Attached to ammonia (NH3, NH4+)
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5
Q

Why is urine titrated to pH 7.4?

A

pH of blood

Biologically neutral

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6
Q

Explain what a heavy meat diet would do to urine acid?

A

More H+ in urine

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7
Q

Explain what a vegetarian diet would do to urine acid?

A

Less H+

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8
Q

What is the most important vehicle for H+ excretion?

A

Ammonia NH3

NH3 + H+ –> NH4 (Excreted)

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9
Q

How is ammonia synthesised?

A

glutamine –> glutamate + ammonia (NH3)

glutaminase enzyme

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10
Q

How is ammonia regulated?

A

glutaminase enzyme can be upregulated in the liver

glutamine –> glutamte + NH3

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11
Q

In a patient with chronic kidney failure with a eGFR of 8 (normal is >60)
What does an elevated HCO3- indicate?

A

Metabolic acidosis

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12
Q

In a patient with chronic kidney failure with a eGFR of 8 (normal is >60)
What does an decreased Ca2+ indicate?

A

due to decreased vit.d hydroxylation
vit d is required for absorbing calcium

check PTH levels

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13
Q

In a patient with chronic kidney failure with a eGFR of 8 (normal is >60)
What does an elevated Phosphate indicate?

A

Bone resorption to maintain Ca2+

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14
Q

In a patient with chronic kidney failure with a eGFR of 8 (normal is >60)
What does an decreased albumin indicate?

A

filtered from blood
proteinuria

Check albuminuria levels

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15
Q

In a patient with chronic kidney failure with a eGFR of 8 (normal is >60)
What does an decreased HB indicate?

A

decreased EPO production

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16
Q

In a patient with chronic kidney failure with a eGFR of 8 (normal is >60)
What does an elevated ALP indicate?

A

High-turnover bone disease

at risk of OP

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17
Q

In a patient with chronic kidney failure with a eGFR of 8 (normal is >60)
What does an elevated K+ indicate?

A

hyperkalaemia

altered K+ distribution

Ability to excrete potassium decreases as GFR falls

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18
Q

In a patient with chronic kidney failure with a eGFR of 8 (normal is >60)
What does an elevated Cl- indicate?

A

dehydration
high salt intake
Addison’s disease (adrenal insufficiency, no aldosterone released)

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19
Q

List the body compartments and the % they represent

A

Total body water 60%
IC = 40%
EC = 20%

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20
Q

On the arterial side, which pressure is higher and which is lower?

A

High hydrostatic pressure (IC to EC)

Low oncotic pressure (EC to IC)

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21
Q

What is hydrostatic pressure?

A

IC to EC

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22
Q

What is oncotic pressure?

A

EC to IC

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23
Q

On the venous side which pressure is higher and which is lower?

A

Low hydrostatic pressure (EC to IC)

High oncotic pressure (IC to EC)

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24
Q

What is the most common ECF cation?

A

Na+

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25
Q

What is the most common ECF anion?

A

Cl-

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26
Q

What is the most common EICF anion?

A

PO43-

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27
Q

What is the most common ECF cation?

A

K+

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28
Q

What is the mmol/L of ions IC and EC?

A

152mmol/L in both compartments

Therefore iso-osmolar

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29
Q

How much CO does the kidneys receive?

A

20%

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30
Q

Where do the kidneys lie relative to vertebrae?

A

T12-L3

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31
Q

What is the kidney’s lymphatic drainage?

A

Para-aortic

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32
Q

What is normal GFR

A

approx 100mL/min

144L/day

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33
Q

What increases the SA for absorption on the PCT?

A

Epithelial cells with microvilli

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34
Q

How much NaCl is reabsorbed by the PCT?

A

approx. 70%

Active transport

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35
Q

Where is glucose and AA reabsorbed?

A

PCT
Nearly 100%
Active trasport

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36
Q

What concentration can the interstitial medulla reach?

A

1,200mOsm/kg
4x the rest of the body

in order to move water out of the renal tubule, the concentration of the surrounding interstitium must be higher than within the tubule

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37
Q

What maintains the concentration gradient in the medulla ?

A

Countercurrent exchange

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38
Q

What an the thick ascending limb transport?

A

Impermeable to water

Actively transports Na+ K+ and Cl-

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39
Q

What can the thin descending limb transport?

A

Salt and water

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40
Q

How does the vasa recta not wash away the gradient?

A

Countercurrent exchange

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41
Q

What does the hyperosmolar medulla depend on?

A

Na+ reabsorption and urea trapping

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42
Q

What concentration can the interstitial medulla reach? And what causes this?

A

Approx. 1,200mOsm/kg

  • half due to extrusion of sodium (3Na+/2K+-ATPase)
  • half due to urea accumulation (urea trapping)
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43
Q

What’s the role of ADH in urine concentration?

A

ADH activates aquaporins in the CD to allow reabsorption of water

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44
Q

What does ANP do?

A 
Secreted in response to increased plasma volume
- afferent dilation
- efferent constriction
= increased GFR
= increase Na+ excretion and water

*inhibits aldosterone

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45
Q

Where is adenosine produced? And what effect does it have?

A

Adenosine is produced by the macula densa in response to increased tubular flow, it causes afferent arteriolar constriction to maintain GFR

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46
Q

Where is renin produced?

A

Renin is produced by the macula densa in response to decreased tubular flow, it triggers the RAAS system where AngII causes systemic vasoconstriction and aldosterone secretion by adrenal cortex to reabsorb Na+ (via ENaC) and water).

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47
Q

How is GFR maintained during increase or decrease in tubular flow?

A

Increased tubular flow

  • JG apparatus secreted adenosine
  • afferent arteriolar vasoconstriction

Decreased tubular flow

  • JG apparatus secretes renin
  • RAAS
  • Ang II = systemic vasoconstriction
  • Aldosterone = Na+ (ENaC) and H2O reabsorption
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48
Q

Define oligouria

A

Decreased urine output

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49
Q

Within the intravascular space, what is the main determinant of oncotic pressure?

A

Plasma proteins

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50
Q

What drives hydrostatic pressure?

A

Heart pumping and vessels constricting

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51
Q

What is the normal healthy omsolality ?

A

approx. 300mOsm/kg

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52
Q

What are the compartments of water?

A

IC
EC
-IV
-IT

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53
Q

What happens to omsolality when water is added into ECF?

A

Nothing. water distributes evenly across 3 compartments due to osmosis

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54
Q

What happens to omsolality when NaCl is added into ECF?

A

Particles and volumes in EC space increase

Add NaCl to plasma
ITS ALWAYS WATER THAT MOVES
there will be increased omsolality in plasma
water will be driven out of cells

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55
Q

What happens to omsolality when 1L water and 300mM NaCl is added into ECF?

A

300mM is the same osmolality as normal body

therefore, increase particles and volume in the EC space
nothing moves into the IC space

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56
Q

In health, what does ECF composition depend ont?

A
  • salt intake - depends on hunger and food availability
  • water intake - depends on thirst and water availability
  • salt and water losses - sweat and GI
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57
Q

What are the structure of mesangial cells?

A

Phagocytic

Secrete amorphous BM-like material known as mesangial matrix

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58
Q

What type of collagen is the glomerular filtration barrier made of?

A

Collage type IV

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59
Q

How big is the selective barrier of glomerular filtration sieve?

A

approx. 6.5nm

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60
Q

Where does the majority of reabsorption in the kidney take place?

A

PCT

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61
Q

What is the main driver os reabsorption?

A

Na+/K+-ATPase

on basolateral surface (aka with the IT space NOT LUMEN)

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62
Q

Which part of the nephron is important in K+ and H+ excretion

A

DCT

63
Q

Where are ENaC found?

A

DCT

64
Q

Describe H+ excretion in the kidneys

A
  1. 3Na+/2K+-ATPase on the basolateral surface creaters concentration gradient
  2. if ENaC is present, Na+ moves into cell
  3. Tubular lumen becomes negative
  4. K+ moves out of the cells into the lumen
  5. H+ can also be driven out of the lumen in this way
65
Q

What channel is distinctively found in the thick ascending loop of Henle?

A

NKCC

Na+-K+-2CL

66
Q

Describe ion movement in the thick ascending loop of Henle

A
  1. Na+ concentration gradient created by 3Na+/2K+-ATPase
  2. Na+ moves from tubule into the endothelial cell via NKCC - K+ moves with it creating an excess of K+ within the cell
  3. K+ is actively pumped back out into the tubular lumen creating a charge within the tubular lumen
  4. This allows Mg2+ and Ca2+ to squeeze through cells and reabsorbed
67
Q

What is the functions of
PCT
DCT
LoH/CD

A
  1. PCT
    - Most NaCl and H2O reabsorption - 70%
    - 100% AA and glucose reabsorption
    - Some excretion of acid
  2. DCT
    - Fine tuning of NaCl and H2O
    - Excretion of H+ and K+ (via Na/K-ATPase–ENaC system)
  3. LoH and CD
    - Altering overall concentration of urine via AQs
68
Q

what mechanism concentrates urine?

A

Countercurrent exchange multiplier

69
Q

What is the max urine osmolality

A

1200mOsm/kg

70
Q

What two mechanisms trigger when blood volume and pressure decrease?

A
  1. RAAS via juxtaglomerular apparatus macula denasa
  2. SNS via baroreceptors
    - causes vasoconstriction of afferent arteriole to reduce amount of blood filtered
71
Q

How does the body normally respond to hyperkalaemic?

A

Release of aldosterone from the adrenal gland

  1. Na+ concentration driven by movement of Na+ by Na/K-ATPase
  2. ENaC drives Na into cell then into interstitla space
  3. Tubular lumen becomes negative
  4. K+ moves out of the cell into the tubular lumen to be excreted

(H+ can also be excreted in this manner)

72
Q

Can H+ flow freely in body compartments

A

Yes, it all body compartments

73
Q

How much H+ do we injest per day?

A

70mM

74
Q

How much H+ do we produced per day from cellular respiration?

A

15,000mM

75
Q

What is the function of HCO3-?

A

Buffering H+

76
Q

What is a volatile acid

A

Creates gas

e.g. carbonic acid

77
Q

Where is HCO3- synthesised?

A

Kidney

PCT also rapidly reabsorbs HCO3- for every 1H+ excreted as NH4+

78
Q

Where in the kidney is EPO secreted from?

And what is the function of EPO

A

Interstitial cells from the base of the loop of Henle
- kidneys are very good at detecting tissue hypoxia via countercurrent O2 exchange

EPO = erythropoietin
- regulated erythropoiesis

79
Q

What is a hypotonic solution?

Give examples

A

THINK HYPOTONIC MEANS WANTS TO GET RID OF WATER
Solution that has less solute and more water than other solution

High water concentration

  • drive water into cells
  • cells can burst

E.g.:

  • 0.25% NaCl
  • 2.5% Dextrose
80
Q

What is a isotonic solution

A

Concentration inside the cell = concentration in IV
- cell at equilibrium

E.g.:

  • 0.9% Saline NaCl (normal saline)
    • Lactated Ringer’s Solution
81
Q

What is a hypertonic solution

A

THIS: HYPERTONIC MEANS WANTS WATER

Greater concentration of solutes outside the cell that inside the cell

  • can cause cells to shrink
  • higher osmolality outside the cell
  • water leaves cell

E.g.:

  • 5% dextrose in 0.9% NaCl
  • 5% dextrose in Lactated Ringers
  • 5% dextrose in 0.45% NaCl
82
Q

What is the unit measure of kidney function?

A

Total GFR

83
Q

Define clearance

A
  • amount of fluid that has been completely cleared

Calculated by:

Clearance = [particles]urine / [particles]plasma

84
Q

What is the gold standard substance to measure GFR?

And why

A

Inulin

  • freely filtered by the glomerulus and is neither re-absorbed or secreted by the tubule
  • too expensive and cumbersome for clinical practice
  • used in animal research and in kidney donation protocols
85
Q

Why is creatinine clearance a good measure of GFR?

What other substance is like this?

A
  1. produced by body at a constant rate
  2. filtered freely at the glomerulus
  3. not reabsorbed or secreted

Other substance: Cystatin C

86
Q

What is creatinine?

A
  • Normal product of muscle metabolism
  • Daily production is constant
  • [Creatinine]plasma dependent on muscle mass, kidney function and protein intake
  • Incompletely filtered but some tubular secretion (these cancel each other out)
87
Q

What is an endogenous good estimate of GFR?

A

CrCl

Creatinine clearance

88
Q

What problems are there with measuring creatinine in determining kidney function?

A

[Cr]Serum

  • inverse relationship leads to:
    1. slow recognition of loss of the first 70% of kidney function
    2. Surprise sudden rise in creatinine

__
Over estimation in women
Overestimation in elderly
Overestimation in lower mass groups (e.g. amputees)

89
Q

How were the problems involving serum creatinine measurements overcome?

A

MDRD 4-variable formula for estimated (e)GFR

  1. Serum creatinine
  2. Age
  3. Female
  4. Black ethnicity

Unit: mL/min/1.73m^2

90
Q

When is eGFR not acurate

A
  • > 60mL/min
  • <18yo
  • not accurate estimate of kidney function in steady state
91
Q

What variables are taken into consideration with the MDRD formula for eGFR calculation?

A
  1. Serum creatinine
  2. Age
  3. Female
  4. Black ethnicity
92
Q

What is “normal” eGFR?

A

approx. 100mL/min/1.73m^2

93
Q

What eGFR suggests reduced kidney function

A

<60mL/min/1.73m^2

94
Q

What does proteinuria clinically suggest?

A

Glomerular disease

*+/- blood

95
Q

How would you determine concentration of protein in urine?

A

protein:creatinine ratio

96
Q

How would you determine the level of an electrolyte being filtered?

A

Fractional excretion
e.g.

[Na]urine x Volume of urine = mmol Na excreted

[Na]urine x eGFR = mmol Na excreted

97
Q

What biochemical readers indicate the kidneys are NOT working properly?

A
  • Low eGFR <60mL/min
  • Raised [Creatinine]serum when eGFR >60mL/min

+ examine urine for proteinuria

98
Q

Describe how would you define kidney injury/disease

A
  • Reduced eGFR
  • proteinuria
  • +/- blood (haematouria)
  • once above defined, combine with Hx, examination, and investigation to identify aetiology
99
Q

What pathology does oliguria indicate?

A

oliguria = decreased urine output

  • warning for impending acute tubular necrosis
100
Q

What is acute tubular necrosis?

A

Acute tubular necrosis (ATN) is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys.

ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI.

Common causes of ATN include low blood pressure and use of nephrotoxic drugs.

101
Q

Define necrosis

A

Death of cells due to any insult

102
Q

Give an example of acute kidney injury (AKI)

A

Acute tubular necrosis due to reduced low BP or nephrotoxic drugs etc.

103
Q

Aetiology of chronic kidney disease (CKD)

A
  1. Renovscular disease
    - atherosclerosis
    - hypertension
  2. Glomerular disease
    - glomerulonephritis
  3. Tubulo-intestitial disease
    - congenital autosomal polycystic kidney disease
    - chronic nephrotoxic ingestion
    - autoimmune
  4. Obstructive uropathy
    - bladder outflow: enlarged prostate, urethral stricture
    - bladder cancer/cervical cancaer
  5. Following AKI
104
Q

What 3 categories can AKI/CKD be classified as?

A
  • Pre-renal
  • Obstructive
  • Post-renal
105
Q

What CDK classification is established renal failure?

A 
Stage 5 (final stage) 
eGFR <15 or on dialysis
106
Q

What are the main evidences of kidney damage?

A

Biochemically: proteinuria (persistant)

Or

Abnormalities such as polycystic kidney

107
Q

When is eGFR not accurate?

A

eGFR>60

108
Q

What is the most common modality used in renal imaging?

A

Ultrasound

109
Q

Upon ultrasound, what size of kidney is considered normal and abnormal?

A
  • > 10cm is normal

- <9cm is abnormal and indicative of chronic disease

110
Q

Comment on ultrasound echobrightness

A
  • Normal: liver is more echobright than kidney

- Abnormal: kidney is more echobright than liver

111
Q

Define hydronephrosis

A

Swelling of kidney due to buildup of urine

- occurs when urine cannot drain out from the kidney to the bladder due to blockage or obstruction

112
Q

Give an example of an intrinsic and extrinsic blockage that can lead to hydronephrosis

A
  • intrinsic: kidney stone

- extrinsic: extrinsic compression of ureter (e.g. tumour)

113
Q

What contrast is used in CT?

A

iodine

  • its nephrotoxic therefore weigh up risks vs benefits
114
Q

What contrast is used in MRI

A

Gadolinium

115
Q

When should you avoid using contrast imaging with kidneys?

A

eGFR <30

Stage 4/5 CKD

116
Q

What type of renal stones can form?

A

Calcium
Oxalase
Urate
Cysteine

117
Q

Define kidney stones

A

A solid concretion of crystal aggregates forms within urinary space
- formed from the combination of excreted/secreted ions within glomerular filtrate

12% men and 5% women by age 70

118
Q

Classify stones by location and composition

A
  • Location
    1. Kidney: nephrolithiasis
    2. Ureter: ureterolithiasis
    3. Bladder: cystolithiasis
  • Compsition
    1. Calcium-phosphate/Calcium-oxalate
    2. Urate/cysteine etc..
119
Q

What are the risk factors for kidney stones?

A
  1. Genetic
    - Male - 50% chance
    - Family history: RR 2.5
  2. Environmental
    - BMI >27 (obese) RR 2.0
    - Immobile or sedentary (seated too much)
    - Dehydration
    - UTI
    - Rise in obesity and metabolic syndrome have caused an increase in uric acid stones
  • Protected:
  • Vegetarians RR 0.5
  • High fruit diet RR 0.6
  • High fibre diet RR 0.6
120
Q

What environmental factors protect against kidney stones?

A
  • Protected:
  • Vegetarians RR 0.5
  • High fruit diet RR 0.6
  • High fibre diet RR 0.6
121
Q

Kidney stone compositions

A
  1. Calcium containing - 80%
    - Calcium oxalate
    - Calcium phosphate
  2. Struvite stones - 5-10%
    - Magnesium
    - Ammonium
    - Phosphate
    * bound together, tends to happen with increased ammonia production e.g. persistent UTI with bacteria having urease enzyme (urea –> ammonia = stones)
  3. Uric acid - 5-10%
    - Gout (inflammatory arthritis)
  4. Cysteine - 1-2%
  5. Mixed
122
Q

What MAIN components are used to maintain acid-base balance?

A
  1. Buffering - short term process to control H+
  2. Ventilation - Control of CO2
  3. Renal regulation of HCO3- and H+ reabsorption and secretion
123
Q

What is the normal pH and [H+] of blood?

A

pH 7.4

40nmoles/L

124
Q

What blood biochemistry changes at the expense of buffering H+?

A

[HCO3-]

pCO2

125
Q

Define fixed acid

A

acid produced in body from sources other than CO2

126
Q

Define volatile acid

A

acid produced in the body from CO2

127
Q

How are CO2 and HCO3- regulated>

A

CO2 by respiration in the lungs

HCO3- by kidneys

128
Q

Are dietary acids and acids produced by anaerobic respiration fixed or volatile acids?

A

Fixed

they cannot be converted into CO2

129
Q

How do the kidneys regulate acid-base balance

A

2 mechanisms:

  1. Reabsorb the freely filtered HCO3-
  2. Secrete/titrate “fixed” acid
    - titrate non-HCO3- buffer in urine primarily phosphate
    - secretion of ammonium (NH4) into urine
130
Q

Where is HCO3- normally reabsorbed ?

A

PCT
normally ALL is reabsorbed
>4,000mmol/day

131
Q

What is the name of the disorder that results in an inability to reabsorb filtered HCO3-?

A

Renal tubular acidosis

132
Q

Mechanism for re-absorbing HCO3-

A
  1. Tubular microvilli packed with carbonic anhydrase
  2. Generates H2O and CO2 from HCO3- in filtrate
  3. H2O and CO2 diffuse into cell where they care converted back into HCO3- and H+ via carbonic anhydrase
  4. HCO3- is transported through the basolateral surface of the cell into the interstitium
  5. H+ is transported across the tubular cell membrane back into the tubule
133
Q

What buffers can be used to excrete fixed acids?

A

two bases can be used

  • Phosphate PO4: depends on delivery of filtered buffer and cannot be upregulated
  • Ammonia NH4+: can be upregulated by liver in acidosis

NEW HCO3- GENERATED

134
Q

What is the name of the condition where you cannot excrete fixed H+ in the DCT?

A

Distal tubular acidosis

135
Q

What is the difference between
Distal tubular acidosis
and
Proximal tubular acidosis

A

Proximal tubular acidosis: inability to reabsorb HCO3- in PCT

Distal tubular acidosis: inability to excrete fixed H+ in DCT

136
Q

How can ammonium buffer be upregulated?

A
  • involves the liver, people with liver failure can become acidotic
  • via glutamine metabolism
  • process regulated and can be up regulated

glutamine –> glutamate + ammonia (NH3)

NH3 binds to H+ in the urine to be excreted at NH4+ (ammonium)

and NEW HCO3- is created in the cells and reabsorbed

137
Q

What is the difference between acidosis and acidaemia

A

Acidosis: tendency to acid-base disturbance, but with normal [H+]; low HCO3- and low pCO2

Acidaemia: have high [H+]

*most patients will be acidotic

138
Q

What is the biochemical Dx of metabolic acidosis?

Explain.

A
  • increased [H+]
  • normal/decreased pCO2
  • decreased HCO3-

The body will compensate for increase [H+] by consuming a HCO3- (it’ll decrease) and then compensate by driving off CO2 (pCO2 decreases)

Consequence of driving off too much CO2 = respiratory alkalosis

*respiratory compensation

139
Q

What is the biochemical Dx of respiratory acidosis?

Explain.

A
  • increased [H+]
  • normal/increased pCO2: patient cannot ventilate CO2
  • normal/increased HCO3-: HCO3- is retained by kidneys because lungs aren’t ventilating

*renal compensation

140
Q

List main causes of metabolic acidosis

A

Vomiting
Hyperventination
Drugs

141
Q

What is the name given to hyperventilation to drive off CO2 during metablic acidosis?

A

Kassmaul’s breathing

142
Q

What is the equation for anion gap?

A

[Na+] - ([Cl- + [HCO3-]) = 6-12mmol/L

unmeasured cations - unmeasured anions
*in ECF

143
Q

What does the anion gap tell you?

A

Reflects the presence of unmeasured anions

144
Q

What is the purpose of calculating anion gap?

A

Identifying the cause of metabolic acidosis - esp. lactic acidosis, ingestion of food, poison

145
Q

What happens in lactic acidosis

A

production of lactic acid (metabolism) > renal excretion of H+

Acidosis usually results from hypo-perfusion and reduced hepatic clearance of lactate

146
Q

In what situations would you get metabolic acidosis with a raised anion gap?

A

when there is an unmeasured anion organic acid present

e.g. lactate, keto-acids, or ingestions (e.g. methanol)

147
Q

In what situations would you get metabolic acidosis with a normal anion gap?

A

In most metabolic acidosis, the acidosis is due to loss of HCO3- and therefore the anion gap does NOT increase

e.g. diarrhoea, renal tubular acidosis, chronic kidney failure

148
Q

What is the physiological anion that is not measured in the anion gap formula?

A

Albumin

149
Q

Give 2 examples of common acidosis

A
  • Lactic acidosis in shock

- Diabetic ketoacidosis (DKA)

150
Q

How would you Tx acidosis/alkalosis

A

Treat cause!

151
Q

Which values of [H+] are incompatible with life?

A

> 120nmol/L

<20nmol/L

152
Q

Name 2 sulphur containing AAs
What happens to the sulfur?
what kind of diet is this?
Whats the “risk”?

A

Cysteine and methinine
Converted into sulphuric acid H2SO4
Protein (acid) diet
Risk of acidosis

153
Q

What kind of diet give alkaline load?

What kind of salts does it contains and what is this converted to?

A

Vegetarian diet
Contains salts of carboxylic acids (sodium citrate)
- these care converted to sodium carbonate (Na2CO3) an alkali

Nephrology (6 decks)

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