Brainscape's Knowledge GenomeTM

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


See full index

Renal System > Physio > Flashcards

Physio Flashcards

1
Q

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

A

Cortical and Juxtamedullary nephrons

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

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

What are the components of the Renal corpuscle?

A

Bowman’s capsule + glomerulus

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

What are the blood vessels that run adjacent to nephrons?

A

Vasa recta (peritubular capillaries dipping into the medulla)

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

In which part of a nephron does filtration occur?

A

Glomerulus/Bowman’s capsule

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

In which part of a nephron does reabsorption?

A

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

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

In which part of a nephron does secretion occur?

A

PCT, DCT, collecting duct

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

In which part of a nephron does excretion occur?

A

End of collecting duct

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

What % of filtered volume leaves the loop of henle?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What % of filtered volume leaves the collecting duct?

A

0.8% (1.5L/day)

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

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

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

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

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

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

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

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

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

A

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

Na+ active transport

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

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

A

No, it is proportional to plasma concentration

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is a renal threshold?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Glucoses excretion is zero until _______.

A

Plasma glucose > renal threshold

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is Fanconi syndrome?

A

Dysfunctional PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where are organic anions secreted in the nephron?

A

PCT

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the units of clearance?

A

ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the definition of clearance?

A

Amount of plasma (ml) cleared of a solute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

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

A

Clearance<GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

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

A

Clearance>GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

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

A

Urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

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

A

Penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

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

A

Inulin and Creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Why is inulin not used to estimate GFR?

A

It does not occur normally in the body

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How is creatinine clearance calculated?

A

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the T1/2 of ADH?

A

15mins

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

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

A

Positive direct relationship

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the treatment for nocturnal enuresis?

A

Desmopressin (vasopressin derivate)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is Diabetes Insipidus?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is SIADH (Schwartz-Bartter Syndrome)?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

In what form of cancer is SIADH commonly seen?

A

Small cell lung carcinoma

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

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

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions