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Renal System > Physio > Flashcards

Physio Flashcards

1
Q

What are the 2 types of functional units in the kidney?

A

Cortical and Juxtamedullary nephrons

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2
Q

The cortex contains __________ of nephrons.

The medulla contains ________ of nephrons.

A

Cortex: Bowman’s capsule, PCT, DCT

Medulla: Loops of Henle, Collecting ducts

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3
Q

What are the components of the Renal corpuscle?

A

Bowman’s capsule + glomerulus

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4
Q

What are the blood vessels that run adjacent to nephrons?

A

Vasa recta (peritubular capillaries dipping into the medulla)

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5
Q

In which part of a nephron does filtration occur?

A

Glomerulus/Bowman’s capsule

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6
Q

In which part of a nephron does reabsorption?

A

Every part (except bowman’s capsule) but primarily in the PCT

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7
Q

In which part of a nephron does secretion occur?

A

PCT, DCT, collecting duct

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8
Q

In which part of a nephron does excretion occur?

A

End of collecting duct

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9
Q

What % of filtered volume leaves the loop of henle?

A

10%

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10
Q

What % of filtered volume leaves the collecting duct?

A

0.8% (1.5L/day)

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11
Q

Describe the changes in osmolarity as filtrate moves through the nephron.

A

Bowman’s capsule: 300mOsm (normal)
Start of Loop: 300
Mid Loop: 1200
End Loop: 100
End of collecting duct: variable depending on Aldosterone/ADH

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12
Q

↑Describe the changes in filtered volume as fluid moves through the nephron.

A

~20% of plasma passing through the glomerulus is filtered
~1% leaves (19% reabsorbed)

PCT: 70% of filtrate reabsorbed
Loop: 20% reabsorbed
By end of Collecting duct: <1% left

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13
Q

How does ultrafiltration occur?

A

High hydrostatic pressure in the glomerular capillaries
- mesangial cells can contract to ↑P
→ fluid passes through fenestrations in capillaries and through filtration slits between podocytes

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14
Q

What are the 3 layers of the glomerular filtration barrier?

A

1) Glomerular capillary endothelium
2) Basal lamina
3) Bowman’s capsule epithelium (podocytes)

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15
Q

What are the pressures influencing ultrafiltration at the renal corpuscle?

A

1) Hydrostatic/Blood pressure (55mmHg) favors filtration (higher in capillaries)

2) Colloid osmotic pressure (30mmHg) opposes filtration (more proteins in capillaries)

3) Hydrostatic pressure in bowman’s capsule (15mmHg) opposes filtration

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16
Q

What are the 2 main factors influencing GFR?

A

1) Net filtration pressure:
Hydrostatic - Colloid osmotic - fluid pressure

2) Filtration coefficient
- SA of glomerular capillaries
- permeability of 3 layers of filtration barrier

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17
Q

Describe how autoregulation of GFR occurs over a wider range of BPs.

A

Decreased GFR → constrict AA, dilate EA
Increased GFR → dilate AA, constrict EA

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18
Q

In renal artery stenosis,
GFR _____
Serum creatinine _____
K+ ______
±Edema
BP____

A

↓ Glomerular capillary pressure:
GFR ↓
Serum creatinine ↑
Hyperkalemia
Edema
BP ↑

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19
Q

What are the 3 causes of acute renal failure?

A

1) Prerenal
- ↓ BP/disrupted blood flow

2) Intrarenal
- Kidney damage

3) Postrenal
- Sudden obstruction of urine flow

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20
Q

How does the afferent arteriole constrict in response to increased GFR?

A

1) GFR ↑
2) Flow past macula densa ↑
3) Macula densa paracrine signaling to JG cells
4) JG cells contract to constrict afferent arteriole

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21
Q

What is the difference between transcellular and paracellular transport in tubule epithelial cells of the kidney?

A

Transcellular: cross apical and baso-lateral membranes of cells

Paracellular: cross through intercellular junctions

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22
Q

Which substance(s) only move(s) out of the nephron tubule lumen by transcellular transport?

A

Na+ active transport

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23
Q

Which substance(s) move(s) out of the nephron tubule lumen by both paracellular and transcellular transport?

A

1) Anions
2) Water
3) Permeable solute (K+, Ca2+, urea)

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24
Q

How do sodium transport on the apical and basolateral surface of PCT cells differ?

A

Apical: passive (ENaC)
Basolateral: active (Na+/K+ exchanger)

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25
Q

How does the Na+/K+ ATPase work?

A

1) 3 Na+ enters protein on cytosolic side
2) ATP hydrolysis → protein linked with P
3) Protein opens of extracellular side → release 3 Na+
4) 2 K+ binds to protein, P released
5) 2 K+ released into cytosol

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26
Q

How is glucose transported out of the nephron tubular lumen?

A

Apical: Secondary active transport with Na+ (SGLT symport)

Basolateral: simple/facilitated diffusion (GLUT)

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27
Q

Does glucose filtration rate in the kidney saturate with increasing plasma glucose concentration?

A

No, it is proportional to plasma concentration

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28
Q

What is the relationship between glucose reabsorption and plasma concentration?

A

Positive direct (reabsorption=Pc) UNTIL transport max (375mg/min)
(transporters are saturated)

100% of filtered glucose is reabsorbed up till ~300mg/dL

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29
Q

What is a renal threshold?

A

Plasma concentration of a solute at which transport/reabsorption is at its maximum

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30
Q

Glucoses excretion is zero until _______.

A

Plasma glucose > renal threshold

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31
Q

How is urea reabsorbed in the kidney?

A

Passive diffusion
1) Filtrate Urea conc. = ECF
2) Reabsorption of Na+ → Water osmosis → Urea gradient towards ECF
3) Urea passively diffuses across tubular epithelium (apical surface)

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32
Q

How are plasma proteins reabsorbed in the kidney?

A

Endocytosis → transcytosis
1) Proteins endocytosed and digested by lysosomes
2) Released as amino acids via transcytosis out of basolateral surface

Only small peptides and enzymes pass through filtration barrier

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33
Q

What is Fanconi syndrome?

A

Dysfunctional PCT

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34
Q

Where are organic anions secreted in the nephron?

A

PCT

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35
Q

How are organic anions secreted in the nephron?

A

1) Na+/K+ ATPase → ↓Intracellular [Na+] (Direct active)

2) NaDC (Na+/Dicarboxylate symport) → ↑ Intracellular [dicarboxylate]

3) OAT (basolateral organic ion/Dicarboxylate antiport) → ↑ Intracellular [OA-]

4) Organic ions enter via facilitated diffusion (exchange with OA-)

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36
Q

What is the units of clearance?

A

ml/min

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37
Q

What is the definition of clearance?

A

Amount of plasma (ml) cleared of a solute

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38
Q

How do you tell if there is net reabsorption of a substance?

A

Clearance<GFR

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39
Q

How do you tell if there is net secretion of a substance?

A

Clearance>GFR

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40
Q

What is an example of a substance that is net reabsorbed?

A

Urea

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41
Q

What is an example of a substance that is net secretion?

A

Penicillin

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42
Q

What are 2 substances that have no net secretion/reabsorption?

A

Inulin and Creatinine

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43
Q

Why is inulin not used to estimate GFR?

A

It does not occur normally in the body

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44
Q

Why is creatinine used to calculate GFR?

A

Production and breakdown of phosphocreatine (source of creatinine) relatively constant
→ Pc of Cr does not vary much

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45
Q

How is creatinine clearance calculated?

A

Urine Cr (mg/dL) X Urine vol. (ml/min) / Serum Cr (mg/dL)

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46
Q

The fluid within renal cortex is (more/less) concentrated than the medulla.

A

Less

Cortex is isosmotic to plasma.
Medulla becomes progressively concentrated

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47
Q

How does the osmolarity of filtrate change throughout a nephron?

A

1) PCT reabsorbs both solutes and water: no change in osmolarity

2) Descending limb: only water reabsorbed → ↑ Osmolarity

3) Ascending limb: only solutes/salts → ↓ Osmolarity

4) DCT reabsorbs both solutes and water: no change in osmolarity

5) Permeability of collecting tubule varies w ADH

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48
Q

What are 3 stimuli that stimulate Vasopressin secretion?

A

1) ↓BP (Carotid/aortic baroreceptors)
2) ↓Atrial stretch/↓blood vol (atrial stretch receptor)
3) Osm>280mOsm (hypothalamic osmoreceptors)

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49
Q

How is Vasopressin released?

A

1) ADH made and packaged in hypothalamic neuron cell body

2) ADH-containing vesicles transported down and stored in posterior pituitary gland

3) Released into blood

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50
Q

What is the T1/2 of ADH?

A

15mins

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51
Q

What is the moa of ADH?

A

Targets renal collecting duct
1) Binds to basolateral receptor
2) Activates cAMP messenger system
3) Triger exocytosis of AQP2-containing vesicles → ↑ aquaporin in apical membrane

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52
Q

What is the relationship between plasma vasopressin conc. and plasma osmolarity?

A

Positive direct relationship

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53
Q

What is the treatment for nocturnal enuresis?

A

Desmopressin (vasopressin derivate)

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54
Q

How is nocturnal enuresis normally prevented and compromised in enuretic children?

A

Normally, vasopressin secretion follows circadian rhythm → ↑ at night

In enuretic children, vasopressin secretion doesn’t increase at night
→ ↑ urine output
→ spontaneous emptying during sleep

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55
Q

What is Diabetes Insipidus?

A

Damage of hypothalamus → inability to produce ADH
→ ↓ permeability of collecting ducts to water
→ excessive water loss

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56
Q

What is SIADH (Schwartz-Bartter Syndrome)?

A

Syndrome of Inappropriate ADH secretion
→ Excessive release of ADH
→ Volume overload and HypoNa+

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57
Q

In what form of cancer is SIADH commonly seen?

A

Small cell lung carcinoma

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58
Q

What is the countercurrent exchange system and what is its benefit?

A

Countercurrent between the closely associated Vasa Recta and Loop of Henle

  • Filtrate in descending limb becomes progressively more concentrated as water moves into the vasa recta (opp. directions means lower down still have water potential gradient)
  • Ascending limb becomes less concentrated as more solutes are actively reabsorbed (opp. direction means vasa recta gets more concentrated for osmosis in descending limb)
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59
Q

What is the the different between osmolarity and tonicity?

A

Osmolarity: Solutes/L of solution (Osm/L)
Tonicity: How a solution affects cell vol. (no units)

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60
Q

Tonicity depends of the relative concentration of (penetrating/non-penetrating) solutes.

A

Non-penetrating

61
Q

All that apply: A hypoosmotic solution can be (hypotonic, isotonic, hypertonic).

A

Only hypotonic

(tonicity is a “subset” of osmolarity since it depends on conc. of non-penetrating solutes)

62
Q

All that apply: A isoosmotic solution can be (hypotonic, isotonic, hypertonic).

A

Isotonic and Hypotonic

(Some may not be able to equilibrate)

63
Q

All that apply: A hyperosmotic solution can be (hypotonic, isotonic, hypertonic).

A

Hypotonic, isotonic, hypertonic

(depending on relative conc. of non-penetrating solutes)

64
Q

What type of solution is given for px with intracellular dehydration (eg. Diabetes Insipidus, Dehydration)?

A

Hypotonic solution
eg. 0.45% Saline (Half normal saline)

65
Q

What type of solution is given for px with ECF depletion (eg. hypovolemia)?

A

Isotonic solution
eg. 0.9% Saline (Normal saline)

66
Q

How does drinking a large amount of water affect blood volume and osmolarity?

A

↑ volume, ↓ osmolarity

67
Q

How does drinking water throughout prolonged vigorous excercise affect blood volume and osmolarity?

A

No change in volume, ↓ osmolarity

68
Q

How does dehydration affect blood volume and osmolarity?

A

↓ volume, ↓ osmolarity

69
Q

How does 9% Saline affect blood volume and osmolarity?

A

↑ volume, no change in osmolarity

70
Q

How does bleeding/haemorrhage affect blood volume and osmolarity?

A

↓ volume, no change in osmolarity

71
Q

How does drinking sea water affect blood volume and osmolarity (immediately)?

A

↑ volume, ↑ osmolarity

72
Q

How does excessive sweating/diarrhoea affect blood volume and osmolarity?

A

↓ volume, ↑osmolarity

73
Q

What are the homeostatic responses to salt ingestion?

A

↑osmolarity → detected by osmoreceptors

1) ADH secreted from posterior pituitary → ↑ aquaporin in collecting ducts
→ ↑water reabsorption

2) Thirst → ↑ water intake

74
Q

What is the most important stimulus for thirst?

A

Osmoreceptor input

75
Q

Where is aldosterone made?

A

Adrenal cortex

76
Q

What is the T1/2 of aldosterone?

A

15mins

77
Q

What are 2 stimuli that induce aldosterone secretion?

A

1) ↓BP (via renin)
2) ↑K+

78
Q

What is 2 stimuli that inhibits aldosterone secretion?

A

1) Very high osmolarity
2) Natriuretic peptides (inhibit ATII)

79
Q

What are the target receptors and cells of aldosterone?

A

Cytosolic Mineralocorticoid Receptors on Principal cells in the distal nephron and renal collecting duct

80
Q

What is the moa of aldosterone?

A

1) Aldosterone binds to cytosolic MC receptor

2) Hormone-receptor complex initiates protein synthesis of new ion channels (ENaC, ROMK) and pumps (Na/K ATPase)

3) Aldosterone-induced proteins modulate existing pumps/channels

↑ Na+ reabsorption+ ↑K+ secretion → ↑water reabsorbed

81
Q

True or false. Na+ reabsorption is automatically coupled with water reabsorption in the PCT, DCT and collecting duct.

A

PCT: automatically coupled
DCT: requires aldosterone
Collecting duct: requires aldosterone/ADH

82
Q

True or false. Distal tubular water reabsorption occurs at all times, regardless of hormonal regulation as long as filtration is not affected.

A

False.
Distal tubular water reabsorption requires vasopressin

83
Q

What hormone is activated when there is an acute increase in blood osmolarity?

A

ADH → ↑water reabsorption → ↓osmolarity

84
Q

What hormone is activated when there is an acute loss of isotonic blood volume?

A

Aldosterone → ↑Na+ reabsorption + ↑ K+ secretion

85
Q

Which part of the nephron does acetazolamide act on?

A

PCT

86
Q

Which part of the nephron do Osmotic diuretics (eg. mannitol) act on?

A

PCT + Descending limb of LoH

87
Q

Which part of the nephron do Loop diuretics (eg. Furosemide) act on?

A

Ascending limb of LoH

88
Q

Which part of the nephron do Thiazides (eg. HCTZ) act on?

A

DCT

89
Q

Which part of the nephron do Potassium-sparing diuretics (eg. spironolactone) act on?

A

DCT

90
Q

What are 5 examples of loop diuretics?

A

ET is FABulous

1) Ethacrynic acid
2) Torsemide
3) Furosemide
4) Azosemide
5) Bumetanide

91
Q

What are 3 clinical indications for loop diuretics?

A

HE
1) HF
2) HTN
3) Edema

92
Q

What are 4 AEs of loop diuretics?

A

HypO

1) Hyponatremia
2) Hypokalemia
3) Hypomagnesemia
4) Ototoxicity

93
Q

What is the most dangerous complication/sequelae of hyperkalemia?

A

Cardiac arrythmias, ↑ excitability of neurons/skeletal muscles

94
Q

What is the physiological response to hyperkalemia?

A

↑ Aldosterone → ↑K+ secretion

95
Q

What is the most dangerous complication/sequelae of hypokalemia?

A

Muscle weakness → failure of respiratory and heart muscles

96
Q

What is the physiological response to hyperkalemia?

A

↓ /No Aldosterone → no secretion of K+ into collecting ducts

97
Q

Where is ACE located?

A

Capillary endothelium

98
Q

What organ produces angiotensinogen?

A

Liver

99
Q

Where does renin come from?

A

JG cells of kidneys

100
Q

What is the rate limiting factor in the RAAS pathway?

A

Plasma renin concentration

101
Q

What stimulates renin secretion?

A

↓Na+
↓BP

102
Q

What is the direct chemical stimulus for aldosterone secretion?

A

Angiotensin II

103
Q

What are the 4 systemic mechanism/responses to dehydration?

A

Dehydration: ↓BP/vol + ↑osmolarity
1) CVS
- detected by carotid/aortic baroreceptor → cardiovascular center
→ ↑sympathetic + ↓parasympathetic
→ ↑heart rate and contractility + vasoconstriction
→ ↑ CO + ↑BP

2) RAAS
- detected by macula densa → paracrine to JG cells
→ renin → AT1 → AT2 (by ACE)
→ ↑ CVS response + ↑ thirst + ↑aldosterone (but inhibited by ↑Osm)
→ ↓Na+ reabsorption (DCT + collecting duct) → ↓ osmolarity

3) Renal mechanisms
- ↓ GFR → volume conserved

4) Hypothalamus
- detected by atrial stretch, carotid/aortic baroreceptors, hypothalamic osmoreceptors
→ ↑thirst + ↑ADH release from posterior pituitary
→ ↑water intake + ↑water reabsorption

104
Q

Where do natriuretic peptides come from?

A

Myocardial cells
↑blood volume → myocardial stretch and release ANP/BNP

105
Q

What is BNP used for?

A

Indicator for HF (only ventricular stretch causes release by ventricle myocardium)

106
Q

What is the overall effect of natriuretic peptides?

A

↑ salt and water excretion
(anti-aldosterone)

107
Q

What are 4 specific tissue actions of natriuretic peptides?

A

1) Afferent arterioles
- vasodilate → ↑GFR
- inhibit renin secretion

2) Nephron
- ↓Na+ and water reabsorption

3) Adrenal cortex
- inhibit aldosterone secretion

4) Hypothalamus
- inhibit ADH secretion

5) Medulla oblongata
- ↓sympathetic output

108
Q

What are the receptors and responses to ↓BP/volume?

A

1) Direct: ↓GFR
2) Macula densa → JG cells → renin
3) Carotid/aortic baroreceptors → CVCC → ↑SNS ↓PNS
4) Carotid/aortic baroreceptors + atrial volume receptors → ↑thirst + ↑ADH secretion by posterior pituitary

109
Q

What are the receptors and responses to ↑BP?

A

1) Direct: ↑GFR
2) Myocardial cells → ANP/BNP
3) Carotid/aortic baroreceptors → CVCC → ↓SNS ↑PNS
4) Carotid/aortic baroreceptors + atrial volume receptors → ↓thirst + ↓ADH secretion by posterior pituitary

110
Q

What are the receptors and responses to ↑blood osmolarity?

A

1) Adrenal cortex → ↓aldosterone
2) Hypothalamic osmoreceptors → ↑thirst + ↑ADH secretion from posterior pituitary

111
Q

What are the receptors and responses to ↓blood osmolarity?

A

1) HypoNa+ → Adrenal cortex → ↑aldosterone
2) Hypothalamic osmoreceptors → ↓ADH secretion from posterior pituitary

112
Q

A 0.3 change in pH corresponds to a change in [H+] by what factor?

A

2

113
Q

A decrease in pH of 1 unit corresponds to a ______ increase in [H+].

A

10x

114
Q

What is the normal range of blood pH?

A

7.38-7.42

115
Q

Acidosis causes neurons to be _____ and can lead to ______.

A

less excitable
CNS depression

116
Q

Alkalosis causes neurons to be (hyper/lessexcitable)

A

Hyperexcitable

117
Q

What are 3 components of pH homeostasis?

A

1) Buffers (eg. Hb, Bicarbonate, proteins, phosphate)
- combine with/release H+

2) Ventilation
- rapid

3) Renal
- direct via excretion/reabsorption of H+
- indirectly by changing amount of of HCO3- buffer reabsorbed/excreted

118
Q

How does acidosis lead to hyperkalaemia?

A

H+ ions displace intracellular K+ (K+ efflux)

119
Q

Alkalosis leads to (hyper/hypokalaemia)

A

Hypokalaemia (K+ influx in response to H+ efflux)

120
Q

How does hyper/hypokalemia change the excitability of neurons?

A

hyper/hypoK+ → ↑/↓ cellular K+
→ depolarise/hyperpolarise
→ ↑/↓ RMP
→ >/< excitable

121
Q

What is the Henderson-Hasselbach Equation?

A

pH= 6.1 + (log[HCO3-] / (0.03 x PCO2))

122
Q

What are 3 causes of respiratory acidosis?

A

1) COPD
2) ↑ Airway resistance (eg. asthma)
3) Respiratory depression (eg. alcohol)
4) ↓ gas exchange (fibrosis, pneumonia, muscular dystrophy)

123
Q

In respiratory acidosis:
CO2 ____
H+ _____
HCO3 ____

A

CO2 ↑ → H+↑ HCO3-↑

124
Q

Compensatory mechanism(s) for respiratory acidosis?

A

Renal: ↑HCO3- reabsorption + ↑H+ secretion (DCT)
(48-72 hrs)

125
Q

What are 2 causes of respiratory alkalosis?

A

1) Clinical/iatrogenic: Artificial ventilation
2) Physiological: Severe anxiety → hysterical hyperventilation

126
Q

Compensatory mechanism(s) for respiratory alkalosis?

A

Renal: ↑HCO3- excertion+ ↑H+ reabsorption (DCT)
(48-72 hrs)

127
Q

In respiratory alkalosis:
CO2 ____
H+ _____
HCO3 ____

A

CO2 ↓ → H+↓ HCO3-↓

128
Q

What are 3 causes of metabolic acidosis?

A

1) Dietary: Aspirin, low CHO Atkins diet
2) Metabolic: Lactic (exertion), Ketoacidosis (DM)
3) Loss of HCO3- (eg. diarrhoea)

129
Q

In metabolic acidosis:
CO2 ____
H+ _____
HCO3 ____

A

CO2 ↑
H+ ↑
HCO3 ↓

130
Q

Compensatory mechanism(s) for metabolic acidosis?

A

Respiratory: ↓CO2 by hyperventilation (immediate)

Renal: ↑HCO3- reabsorption + ↑H+ secretion (DCT)
(48-72 hrs)

131
Q

What are 2 causes of metabolic alkalosis?

A

1) Excessive vomiting of stomach contents
2) Excessive HCO3- (eg. antacids)

132
Q

In metabolic alkalosis:
CO2 ____
H+ _____
HCO3 ____

A

CO2 ↓
H+ ↓
HCO3 ↑

133
Q

Compensatory mechanism(s) for metabolic alkalosis?

A

Respiratory: ↑CO2 by hypoventilation (immediate, stops at PO2<60mmHg)

Renal: ↑HCO3- excretion + ↑H+ reabsorption (DCT)
(48-72 hrs)

134
Q

How does the kidney compensate for acidosis?

A

H+ secretion:
a) H+ secretion → bound to HPO42- buffer → excreted in urine
b) H+ bound to amino acids to form NH4+ → excreted in urine
c) directly dissolved in urine

HCO3- reabsorption:
a) Apical Na/H exchanger → H+ efflux
b) H+ + filtered HCO3- → CO2 (diffuses into cell)
c) CO2 + H2O → HCO3- + H+ (returns to form +ve feedback a-c)
d) Glutamine → NH4+ + HCO3-
e) Apical NH4+/Na+ exchanger → Na+ influx
f) Basolateral Na+/HCO3- transporter →
→ HCO3- added to ECF buffer

135
Q

What type of renal cells excrete H+ and reabsorb HCO3- in acidosis?

A

Type A intercalated cells in the collecting duct

136
Q

How do Type A intercalated cells compensate for acid/base disorders?

A

↑H+ excretion and ↑HCO3- reabsorption in response to acidosis

1) ↑HCO3- reabsorption via basolateral HCO3-/Cl- antiport
2) ↑H+ secretion via apical H+/K+ antiport

137
Q

What type of renal cells reabsorb H+ and secrete HCO3- in alkalosis?

A

Type B intercalated cells in the collecting duct

138
Q

How do Type B intercalated cells compensate for acid/base disorders?

A

↑HCO3- excretion and ↑H+ reabsorption in response to alkalosis

1) ↑HCO3- excretion by apical HCO3-/Cl- antiport
2) ↑H+ reabsorption via Basolateral H+ATPase

139
Q

What does an increased anion gap indicate?

A

Metabolic acidosis
↑metabolic acids eg. lactic/ketoacidosis

140
Q

What does a low anion gap indicate?

A

1) ↓ unmeasured anions (albumin)
2) ↑ unmeasured cations (hyperK+/hyperCa2+/HyperMg2+, lithium intoxication, multiple myeloma)

141
Q

How is anion gap calculated?

A

(Na+ + K+) - (Cl- + HCO3-)

142
Q

What is the normal range of an anion gap?

A

14-18mM/L

143
Q

The kidneys play a critical role in Ca2+ reabsorption through what vitamin?

A

Vitamin D in response to parathyroid hormones

144
Q

For a px with acute respiratory acidosis, how do you calculate the expected HCO3- concentration?

A

1 for 10 (above pCO2>40mmHg)

24 + (pCO2-40)/10

eg. pCO2=60mmHg → expected HCO3-=26mmol/L

145
Q

For a px with chronic respiratory acidosis, how do you calculate the expected HCO3- concentration?

A

4 for 10 (above pCO2>40mmHg)

24 + 4(pCO2-40)/10

eg. pCO2=60mmHg → expected HCO3-=32mmol/L

146
Q

For a px with acute respiratory alkalosis, how do you calculate the expected HCO3- concentration?

A

2 for 10 (above pCO2<40mmHg)

24 - 2(40-pCO2)/10

eg. pCO2=30mmHg → expected HCO3-=22mmol/L

147
Q

For a px with chronic respiratory alkalosis, how do you calculate the expected HCO3- concentration?

A

5 for 10 (above pCO2<40mmHg)

24 - 5(40-pCO2)/10

eg. pCO2=30mmHg → expected HCO3-=19mmol/L

148
Q

For a px with metabolic acidosis, how do you calculate the expected pCO2?

A

1.5 + 8

1.5 x [HCO3-] + 8

eg. [HCO3-] = 18mmol → expected pCO2= 35mmHg

149
Q

For a px with metabolic alkalosis, how do you calculate the expected pCO2?

A

7 + 20

0.7 x [HCO3-] + 20

eg. [HCO3-] = 36mmol → expected pCO2= 45mmHg

Renal System (8 decks)

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