Brainscape's Knowledge GenomeTM

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


See full index

Phys pharm > Renal physiology > Flashcards

Renal physiology Flashcards

1
Q

How much of our body weight is water?

A

60%

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

What is intracellular fluid?

A

Fluid inside the cells

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

What is included in extracellular fluid? (3)

A
  • Transcellular
  • Plasma
  • Interstitial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is transcellular fluid?

A
  • Cerebrospinal fluid

- Urine stored in the bladder

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

What is interstitial fluid?

A

Fluid surrounding cells which isn’t part of the plasma

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

What is the K+ concentration in the intracellular fluid?

A

148 mM

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

What is the K+ concentration in the extracellular fluid?

A

5 mM

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

What is the Na+ concentration in the intracellular fluid?

A

10 mM

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

What is the Na+ concentration in the extracellular fluid?

A

140 mM

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

What is the Cl- concentration in the intracellular fluid?

A

4 mM

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

What is the Cl- concentration in the extracellular fluid?

A

103 mM

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

What is the protein concentration in the intracellular fluid?

A

55 mM

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

What is the protein concentration in the interstitial fluid?

A 
15 mM
(More protein in the plasma which can't cross the endothelium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What determines the total volume of the extracellular fluid?

A

Na+ concentration

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

How big is a kidney?

A

10 cm x 5.5 cm

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

Where is the kidney located?

A

Between the 12th thoracic and 3rd lumbar vertebrae

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

How much does a kidney weigh?

A

150g

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

What is renal agenesis?

A

Absence of one or both kidneys

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

How common is renal agenesis?

A

1 in 2500 foetuses

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

How serious is renal agenesis?

A

Fatal

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

What is ectopic kidneys?

A

When the kidneys develop in the wrong place

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

How common is ectopic kidneys?

A

1 in 800 live births

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

What are side effects of ectopic kidneys?

A

Increased risk of damage and stone formation

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

What is a horseshoe kidney?

A

When the kidneys are fused across midline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How common is horseshoe kidney?

A

1 in 1000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are side effects of horseshoe kidney?

A

Increased risk of stones and long term damage from stones

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

What is the capsule?

A

Fibrous layer surrounding the kidney for protection and structural integrity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the functional unit of the kidney?

A

Nephron

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

How many nephrons do you have per kidney?

A

1 - 1.5 million

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

What are the elements of the nephron? (6)

A
  • Bowman’s capsule
  • Glomerulus
  • Proximal tubule
  • Loop of Henle
  • Distal tubule
  • Collecting duct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the 2 types of nephrons?

A
  • Superficial

- Juxtamedullary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are superficial nephrons?

A

Glomerulus located near the outer part of the cortex and loop of Henle doesn’t enter the inner medulla

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

What proportion of nephrons are superficial?

A

85%

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

What are juxtamedullary nephrons?

A

Glomerulus located at the edge of the cortex and loop of Henle reaches the inner medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What proportion of nephrons are juxtamedullary?

A

15%

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

Which type of nephron plays the biggest role in urine concentration?

A

Juxtamedullary

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

What is renal failure defined as?

A

Fall in glomerular filtration rate? (GFR)

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

What does renal failure cause? (2)

A
  • Increase in serum urea

- Increase in serum creatinine

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

What is acute renal failure?

A

Reversible

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

What is chronic renal failure?

A
  • Irreversible

- Progressive

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

What is the treatment for chronic renal failure? (2)

A
  • Dialysis

- Transplant

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

How do haemoglobin levels change with acute renal failure?

A

No change

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

How do haemoglobin levels change with chronic renal failure?

A

Decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How does the size of the kidney change with acute renal failure?

A

No change

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

How does the size of the kidney change with chronic renal failure?

A

Gets smaller

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is peripheral neuropathy?

A

Peripheral nerve damage causing sensory and motor issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Which type of renal failure can cause peripheral neuropathy?

A

Chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Which type of renal failure can cause decreased haemoglobin levels?

A

Chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is uraemia? (6)

A
  • Thickening of glomerular membranes
  • Damaged glomeruli
  • Glomerulosclerosis
  • Tubular atrophy
  • Interstitial inflammation
  • Fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is glomerulosclerosis?

A

Progressive scarring of the glomeruli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is tubular atrophy?

A

Loss of nephrons

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

What symptoms arise due to failure to excrete salt and water in renal failure? (3)

A
  • Hypertension
  • Hyperkalaemia
  • Mild acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What symptoms arise due to failure to excrete urea/creatinine and leak of protein into urine in renal failure? (5)

A
  • Anorexia
  • Nausea
  • Vomiting
  • Neuropathy
  • Pericarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is pericarditis?

A

Inflammation of the pericardium

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

What is erythropoietin?

A

Hormone produced by the kidneys

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

What symptoms arise due to failure to produce erythropoietin in renal failure? (2)

A
  • Anaemia

- Lethargy

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

What symptoms arise due to failure to excrete phosphate in renal failure? (3)

A
  • Low serum calcium
  • Metastatic calcification causes pruritus
  • Bone disease (osteomalacia, osteoporosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is metastatic calcification?

A

Deposition of calcium salts in normal tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is pruritus?

A

Skin itching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is osteomalacia?

A

Soft bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is osteoporosis?

A

Brittle bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is normal GFR?

A

125 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are examples of congenital renal abnormalities? (3)

A
  • Renal agenesis
  • Ectopic kidneys
  • Horseshoe kidney
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What can cause chronic renal failure? (4)

A
  • Glomerulonephritis
  • Diabetes mellitus
  • Hypertension
  • Polycystic kidney disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How is high phosphate levels treated?

A

Phosphate binders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How is acidosis treated?

A

Sodium bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How is sodium retention treated?

A

Diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is the GFR in end-stage chronic renal failure?

A

5-10 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the GFR in severe chronic renal failure?

A

10-25 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the GFR in moderate chronic renal failure?

A

25-50 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the GFR in mild chronic renal failure?

A

50-75 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Where does filtration occur?

A

Glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Which arteriole does blood enter the glomerulus via?

A

Afferent arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Which arteriole does blood leave the glomerulus via?

A

Efferent arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How much of the plasma that enters the glomerulus is filtered out?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How much ultrafiltrate is produced per day by both kidneys?

A

180 litres per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the total plasma volume?

A

3 litres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the diameter of the glomerulus?

A

200 micrometres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Which molecules are too big to enter the ultrafiltrate?

A
  • Blood cells

- Plasma proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Which plasma protein is filtered?

A

Albumin (small, reabsorbed later)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is paracellular transport?

A

Between cells through tight junctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is transcellular transport?

A

Across cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

How much of the filtrate is reabsorbed in the proximal tubule?

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How much of the water and Na+ in the filtrate is reabsorbed in the proximal tubule?

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How much of the glucose and amino acids in the filtrate is reabsorbed in the proximal tubule?

A

100%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

How much of the bicarbonate (HCO3-) in the filtrate is reabsorbed in the proximal tubule?

A

90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is reabsorbed at the proximal tubule? (5)

A
  • Water
  • Na+
  • HCO3-
  • Glucose
  • Amino acids
  • PO4 2-
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Which proteins are present on the basolateral membrane of proximal tubule epithelial cells? (3)

A
  • Na+/K+ ATPase
  • K+ channel
  • Phosphate/bicarbonate/amino acid/glucose transporters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the purpose of the Na+/K+ pump on the basolateral membrane of proximal tubule epithelial cells?

A

Removes Na+ from the cell into the capillaries in order to set up the driving force for Na+ uptake at the apical membrane from the filtrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the purpose of the K+ channels on the basolateral membrane of proximal tubule epithelial cells?

A

Sets a negative membrane potential to encourage Na+ to enter the cell from the filtrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

How is glucose absorbed into the blood at the proximal tubule?

A
  • Co-transport with Na+ due to the Na+ concentration gradient via SGLT1/SGLT2 on the apical membrane
  • Once inside the cell glucose diffuses into the blood across the basolateral membrane down its concentration gradient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Which proteins in the apical membrane of proximal tubule epithelial cells transport Na+ and glucose? (2)

A
  • SGLT1

- SGLT2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Where are SGLT1 and SGLT2 located in the nephron?

A

Apical membrane of proximal tubule epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

How are amino acids absorbed into the blood at the proximal tubule?

A
  • Co-transport with Na+ via a transporter on the apical membrane
  • Amino acids transported into the blood over the basolateral membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

How is Na+ reabsorbed at the proximal tubule?

A
  • Co-transport with glucose/amino acids/phosphate/exchanged with H+ into the cell
  • Enters the blood via Na+/K+ ATPase on basolateral membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Which protein in the apical membrane of proximal tubule epithelial cells transport Na+ and phosphate?

A

NaPi2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Where is NaPi2 located in the nephron?

A

Apical membrane of proximal tubule epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

How is phosphate absorbed into the blood at the proximal tubule?

A
  • Co-transport with Na+ via NaPi2

- Diffuses across the basolateral membrane into the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

How is water reabsorbed at the proximal tubule?

A

Follows Na+ reabsorption via paracellular transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What is the effect of knocking out NaPi2 in mice?

A

Low plasma phosphate levels due to more phosphate lost in the tubular fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What issues are caused when the NaPi2 transporter isn’t working properly?

A
  • Increased calcification (calcium phosphate)
  • Intraluminal stones (nephrolithiasis)
  • Nephrocalcinosis
  • Leads to damage and possible renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What does the von Kossa stain highlight?

A

Calcium phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Which protein in the apical membrane of proximal tubule epithelial cells exchanges Na+ and H+?

A

NHE3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

How does NHE3 work?

A

Transports Na+ into the cell and H+ out into the tubular fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Where is NHE3 located in the nephron?

A

Apical membrane of proximal tubule epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

How is HCO3- reabsorbed in the proximal tubule?

A
  • H+ enters tubular fluid via NHE3 and combines with HCO3- to form H2CO3
  • H2CO3 splits into CO2 and water via carbonic anhydrase which enter the cell (water via aquaporins)
  • CO2 and water reform H2CO3 which then dissociates into H+ and HCO3-
  • HCO3- reabsorbed via Na+ cotransporter, H+ recycled
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Which protein transports HCO3- from the proximal tubule cell into the blood?

A
  • Na+/HCO3- co-transporter

- 3Na+ and 1 HCO3- transported at a time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is the effect of knocking out NHE3 in mice?

A
  • Low plasma HCO3-
  • Acidosis (low plasma pH)
  • Slightly lower blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Which factor limits the maximum level of transport can occur?

A

Number of protein carriers in the membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What is the maximum reabsorption rate of glucose in the proximal tubule?

A

375 mg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Why do diabetes patients have glucose in their urine?

A
  • Plasma glucose levels are too high due to inability to respond to insulin
  • Means that 100% reabsorption of glucose in the kidneys can’t be achieved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What substances are secreted by the proximal tubule (blood to tubular fluid)?

A
  • Plasma protein bound substances

- Foreign compounds e.g. penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What occurs at the Loop of Henle?

A

Concentration of the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Where in the nephron do loop diuretics act?

A

Loop of Henle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What is reabsorbed at the Loop of Henle? (5)

A
  • Na+
  • Cl-
  • Water
  • Ca2+
  • Mg2+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What are the 3 sections of the Loop of Henle?

A
  • Thin descending limb
  • Thin ascending limb
  • Thick ascending limb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What is reabsorbed at the thin descending limb?

A

Water

118
Q

Which section of the Loop of Henle is water permeable?

A

Thin descending limb

119
Q

What is reabsorbed at the thin ascending limb? (2)

A
  • Na+

- Cl-

120
Q

What is reabsorbed at the thick ascending limb? (4)

A
  • Na+
  • Cl-
  • Ca2+
  • Mg2+
121
Q

Which proteins are present in the basolateral membrane of the thick ascending limb epithelial cells? (3)

A
  • Na+/K+ ATPase
  • K+ channel
  • CLCK (+barttin)
122
Q

Which protein in the apical membrane transports Na+ and Cl- into the thick ascending limb epithelial cells?

A

NKCC2

123
Q

What does NKCC2 transport?

A
  • Na+
  • 2Cl-
  • K+
124
Q

Where is NKCC2 found in the nephron?

A

Apical membrane of thick ascending limb cells

125
Q

Which protein in the basolateral membrane transports Cl- into the blood from inside the cell in the thick ascending limb?

A

CLCK (+barttin)

126
Q

Where in the nephron is CLCK found? (2)

A

Basolateral membrane of thick ascending limb cells and early distal tubule cells

127
Q

How is Cl- absorbed into the blood at the thick ascending limb?

A
  • 2Cl- cross the apical membrane via NKCC2

- Cl- enters the blood via CLCK on the basolateral membrane

128
Q

How is Na+ absorbed into the blood at the thick ascending limb?

A
  • Crosses the apical membrane via NKCC2

- Enters the blood via Na+/K+ ATPase on the basolateral membrane

129
Q

How is absorption of Na+ and Cl- in the thick ascending limb important for water handling?

A
  • No water reabsorption takes place in the thick ascending limb
  • Ion reabsorption sets up an osmotic driving force for water reabsorption later on in the nephron
130
Q

What is the beta/accessory subunit of CLCK?

A

Barttin

131
Q

What is barttin?

A

Beta subunit of CLCK

132
Q

How is K+ handled in the thick ascending limb cells?

A
  • Enters via NKCC2 (apical)

- Recycled by leaving via ROMK (apical) to provide enough K+ to support the function of NKCC2

133
Q

Which proteins are present in the apical membrane of thick ascending limb cells? (2)

A
  • NKCC2

- ROMK

134
Q

How are Ca2+ and Mg2+ absorbed in the thick ascending limb?

A

Follow the absorption of Na+ and Cl- via paracellular transport

135
Q

Is Bartter’s syndrome dominant or recessive?

A

Recessive

136
Q

What are the symptoms of Bartter’s syndrome? (7)

A
  • Salt wasting
  • Polyuria
  • Hypotension
  • Hypokalaemia
  • Metabolic alkalosis
  • Hypercalciuria
  • Nephrocalcinosis
137
Q

What is salt wasting?

A

Losing Na+ and Cl- in the urine that should’ve been absorbed from the tubular fluid

138
Q

How does salt wasting cause polyuria?

A
  • Reabsorption of Na+ and Cl- brings water with it via paracellular transport
  • Less reabsorption of salt and water means more water in the urine i.e. higher urine flow rate
139
Q

Why does polyuria cause hypotension?

A

Causes a decrease in extracellular fluid volume which leads to low blood pressure

140
Q

What is hypokalaemia?

A

Low plasma potassium

141
Q

What is hypercalciuria?

A

High levels of calcium in the urine

142
Q

What causes Bartter’s syndrome?

A

Mutations in NKCC2/ROMK/CLCK/Barttin (slightly different forms)

143
Q

How does a mutation in NKCC2 cause Bartter’s syndrome?

A
  • No reabsorption of Na+ and Cl- = salt wasting

- Salt wasting leads to polyuria, hypotension, hypercalciuria etc..

144
Q

How does a mutation in CLCK cause Bartter’s syndrome?

A
  • Cl- enters via NKCC2 and accumulates in the cell (can’t leave)
  • High Cl- inside the cell causes NKCC2 to stop working
  • No Na+ and Cl- reabsorption = salt wasting, polyuria, hypotension, hypercalciuria etc..
145
Q

How does a mutation in Barttin cause Bartter’s syndrome?

A
  • CLCK can’t work without Barttin
  • Accumulation of Cl- stops NKCC2 working
  • No Na+ and Cl- reabsorption = salt wasting, polyuria, hypotension, hypercalciuria etc..
146
Q

How does a mutation in ROMK cause Bartter’s syndrome?

A
  • No recycling of K+, can only leave via the K+ channel on the basolateral membrane
  • Not enough K+ in the tubular fluid to support function of NKCC2
  • No Na+ and Cl- reabsorption = salt wasting, polyuria, hypotension, hypercalciuria etc.
147
Q

Why do Bartter’s patients have hypercalciuria?

A
  • Calcium follows reabsorption of Na+ and Cl-

- No Na+ and Cl- reabsorption in Bartter’s syndrome so calcium remains in the tubular fluid

148
Q

What is the fractional excretion value?

A

Amount of a substance in the urine out of the amount of the substance that was filtered

149
Q

What does a fractional excretion value of 100% mean?

A

All of what was filtered at the glomerulus was excreted in the urine i.e. none of it was reabsorbed/secreted

150
Q

What does a fractional excretion value of less than 100% mean?

A

Some of what was filtered was reabsorbed

151
Q

What does a fractional excretion value of greater than 100% mean?

A

The substance has been filtered and then more has been secreted into the tubular fluid

152
Q

What does a difference in the fractional excretion value between a wildtype and knockout organism indicate?

A

A tubule defect

153
Q

What is the difference in symptoms between ROMK knockout mice and Bartter’s patients?

A
  • ROMK knockouts have salt wasting and polyuria like Bartter’s patients
  • ROMK knockouts have acidosis instead of alkalosis and no change in plasma K+ whereas Bartter’s patients have hypokalaemia
154
Q

What are 2 examples of loop diuretics?

A
  • Furosemide

- Bumetanide

155
Q

How do loop diuretics work?

A

Inhibit NKCC2 in the thick ascending limb

156
Q

What are loop diuretics used to treat?

A

Hypertension

157
Q

How do loop diuretics treat hypertension?

A
  • Inhibit Na+ and Cl- absorption via NKCC2
  • Therefore less water is reabsorbed
  • Decreases extracellular fluid volume
158
Q

What are the side effects of loop diuretics?

A
  • Bartter’s-like symptoms

- i.e. plasma K+ issues, pH issues, calcium issues

159
Q

What is reabsorbed at the early distal tubule?

A
  • Na+
  • Cl-
  • Mg2+
160
Q

What are the 2 types of diuretics?

A
  • Loop diuretics

- Thiazide diuretics

161
Q

Where in the nephron do thiazide diuretics act?

A

Early distal tubule

162
Q

Which proteins are present in the basolateral membrane of the early distal tubule cells? (3)

A
  • Na+/K+ ATPase
  • K+ channel
  • CLCK (+barttin)
163
Q

Which proteins are present in the apical membrane of the early distal tubule cells? (2)

A
  • NCC

- Mg2+ channels

164
Q

What does NCC transport?

A
  • Sodium/chloride cotransporter

- 1 Na+ and 1 Cl-

165
Q

How is magnesium absorbed into the blood across the basolateral membrane from the early distal tubule?

A

Unknown pathway

166
Q

Is Gitelman’s syndrome dominant or recessive?

A

Recessive

167
Q

What are the symptoms of Gitelman’s syndrome? (6)

A
  • Salt wasting
  • Polyuria
  • Hypotension
  • Hypokalaemia
  • Metabolic alkalosis
  • Hypocalciuria
168
Q

What is the difference in symptoms between Bartter’s and Gitelman’s syndrome?

A

Bartter’s patients have hypercalciuria and nephrocalcinosis but Gitelman’s patients have hypocalciuria

169
Q

Where in the nephron are the mutations for Bartter’s syndrome?

A

Thick ascending limb

170
Q

Where in the nephron are the mutations for Gitelman’s syndrome?

A

Early distal tubule

171
Q

What causes Gitelman’s syndrome?

A

Mutation in NCC

172
Q

Where in the nephron is ROMK located? (2)

A
  • Apical membrane of thick ascending limb cells

- Apical membrane of principal cells in the late distal tubule and cortical collecting duct

173
Q

Where in the nephron is NCC located?

A

Apical membrane of early distal tubule cells

174
Q

What specific mutations in NCC are seen in Gitelman’s patients? (2)

A
  • Glycine 627 valine

- Arginine 935 glutamine

175
Q

How do mutations in Gitelman’s cause loss of function of NCC?

A

Less NCC is trafficked to the membrane so there are fewer NCCs in the apical membrane of early distal tubule cells

176
Q

How do thiazide diuretics work?

A

Inhibit NCC in the early distal tubule

177
Q

What is an example of a thiazide diuretic?

A

Chlorothiazide

178
Q

What are thiazide diuretics used to treat?

A

Hypertension

179
Q

What are the side effects of thiazide diuretics?

A

Gitelman’s-like symptoms

180
Q

What does carrying one mutation for ROMK/NCCK2/NCC (Bartter’s/Gitelman’s) potentially cause?

A

Protection against hypertension

181
Q

What are the connecting tubules?

A

Connects the late distal tubule to the cortical collecting duct

182
Q

Which processes occur in the late distal, connecting tubules and the cortical collecting duct? (3)

A
  • Concentration of the urine
  • Reabsorption of Na+ and water
  • Secretion of K+ and H+ into the urine
183
Q

What are the 2 cell types in the distal tubule and the cortical collecting duct?

A
  • Principal cells

- Intercalated cells

184
Q

What is the function of the principal cells? (2)

A
  • Na+ and water reabsorption

- K+ and H+ secretion into the urine

185
Q

Where in the nephron are principal cells found? (2)

A

Late distal tubule and cortical collecting duct

186
Q

Where in the nephron are intercalated cells found? (2)

A

Late distal tubule and cortical collecting duct

187
Q

What are the 2 types of intercalated cells?

A

Alpha and beta

188
Q

What is the function of the alpha intercalated cells? (2)

A
  • H+ secretion

- HCO3- reabsorption

189
Q

What is the function of the beta intercalated cells? (2)

A
  • H+ and Cl- reabsorption

- HCO3- secretion

190
Q

Which proteins are in the apical membrane of principal cells? (3)

A
  • ENaC
  • ROMK
  • Aquaporin 2
191
Q

Which proteins are in the basolateral membrane of principal cells? (3)

A
  • Na+/K+ ATPase
  • K+ channel (Kir2.3)
  • Aquaporins (AQP3 and AQP4)
192
Q

Where in the nephron is aquaporin 2 found?

A

Apical membrane of principal cells in the late distal tubule and cortical collecting duct

193
Q

Which type of aquaporin is found on the apical membrane of principal cells?

A

Aquaporin 2

194
Q

How is Na+ reabsorbed by the principal cells?

A
  • Enters via ENaC on the apical membrane

- Leaves via Na+/K+ ATPase

195
Q

How is water reabsorbed by the principal cells?

A
  • Enters via aquaporin 2

- Leaves via aquaporins 3 and 4

196
Q

Which types of aquaporin are found on the basolateral membrane of principal cells? (2)

A
  • AQP3

- AQP4

197
Q

Where in the nephron are AQP3 and 4 found?

A

Basolateral membrane of principal cells in the late distal tubule and collecting duct

198
Q

Where in the nephron is ENaC found?

A

Apical membrane of principal cells in the late distal tubule and collecting duct

199
Q

Which protein in the principal cells transports Na+ into the cell?

A

ENaC

200
Q

Which type of K+ channel is found in the basolateral membrane of the principal cells?

A

Kir2.3

201
Q

Why do Bartter’s and Gitelman’s syndrome patients have hypokalaemia?

A
  • Tubular fluid with high Na+ content reaches the principal cells and more Na+ is reabsorbed through ENaC than usual
  • More K+ than usual is secreted and lost in the urine via ROMK so plasma K+ is lower than usual (hypokalaemia)
202
Q

Why do Bartter’s and Gitelman’s syndrome patients have metabolic alkalosis?

A
  • Tubular fluid with high Na+ content reaches the principal cells and more Na+ is reabsorbed through ENaC than usual
  • More Na+ reabsorption means more H+ secretion into the urine so pH of body fluids are too high (alkalosis)
203
Q

What is Diabetes Insipidus?

A

Patient’s struggle to reabsorb water due to issues with aquaporin 2 so have an extremely high urine flow rate

204
Q

What inherited conditions can arise from issues with the principal cells? (3)

A
  • Diabetes Insipidus
  • Liddle’s syndrome
  • Pseudohypoaldosteronism
205
Q

Which protein is not working correctly in Diabetes Insipidus?

A

Aquaporin 2 in the apical membrane of principal cells in the late distal tubule and cortical collecting duct

206
Q

What is Liddle’s syndrome?

A

Too much Na+ absorbed via ENaC and then too much water reabsorbed with it causing severe hypotension

207
Q

What causes Liddle’s syndrome?

A

Gain of function mutation in ENaC in the apical membrane of principal cells in the late distal tubule and cortical collecting duct

208
Q

What kind of drug is amiloride?

A

Diuretic

209
Q

What is amiloride used to treat?

A

Hypertension

210
Q

How does amiloride work?

A
  • Inhibits ENaC in the principal cells

- Patients lose Na+ and water in their urine

211
Q

Which proteins are in the apical membrane of alpha intercalated cells? (1)

A

Proton ATPase (i.e. H+ pump)

212
Q

Which proteins are in the basolateral membrane of alpha intercalated cells? (2)

A
  • AE1

- Cl- channel

213
Q

How do alpha intercalated cells secrete H+?

A

H+ pumped into the tubular fluid via the proton ATPase on the apical membrane

214
Q

How do alpha intercalated cells reabsorb HCO3-?

A
  • HCO3- inside the cells enters the blood via AE1 in exchange for Cl-
  • Cl- taken into the cell is recycled via the Cl- channel
215
Q

Where in the nephron is AE1? (2)

A
  • Basolateral membrane of alpha intercalated cells

- Apical membrane beta intercalated cells

216
Q

Which proteins are in the apical membrane of beta intercalated cells?

A

AE1

217
Q

Which proteins are in the basolateral membrane of beta intercalated cells? (2)

A
  • Proton ATPase

- Cl- channel

218
Q

How do beta intercalated cells reabsorb H+ and Cl-?

A
  • H+ pumped into the blood via the proton ATPase on the basolateral membrane
  • Cl- enters via AE1 on the apical membrane and enters the blood via the Cl- channel on the basolateral membrane
219
Q

How do beta intercalated cells secrete HCO3-?

A

HCO3- is pumped into the tubular fluid via AE1 in exchange for Cl- which enters the cell

220
Q

How do intercalated cells help the body adjust to changing pH?

A

Can transition between alpha and beta by moving proteins around to secrete/retain H+

221
Q

What are the features of the medullary collecting duct? (2)

A
  • Low Na+ permeability

- High water and urea permeability in the presence of vasopressin

222
Q

What is the function of aldosterone?

A

Regulates Na+ and K+ reabsorption in the late distal tubule and collecting duct

223
Q

What is the function of vasopressin?

A

Regulates water reabsorption in the collecting duct

224
Q

How much of the Na+ that is filtered from the blood is reabsorbed?

A

99%

225
Q

How much of the water that is filtered from the blood is reabsorbed?

A

99%

226
Q

What is acute renal failure?

A

Fall in glomerular filtration rate over hours/days (very short time period)

227
Q

What is the treatment for acute renal failure?

A

Dialysis

228
Q

What are the symptoms of acute renal failure? (4)

A
  • Hypervolaemia
  • Hyperkalaemia
  • Acidosis
  • High urea and creatinine (nitrogenous waste=toxic)
229
Q

What is hypervolaemia?

A

Expansion of the extracellular fluid volume

230
Q

What is oliguria?

A

Low urine output

231
Q

Why do acute renal failure patients have hypervolaemia?

A

Low GFR so oliguria so extracellular fluid volume increases because water not being secreted in the urine

232
Q

Why do acute renal failure patients have hyperkalaemia?

A

Oliguria so lack of K+ secretion

233
Q

What results from hyperkalaemia?

A
  • Increased cardiac excitability

- Can cause sudden cardiac death

234
Q

Why do acute renal failure patients have acidosis?

A

Oliguria so lack of H+ secretion

235
Q

What results from acidosis?

A

Depression of the CNS

236
Q

What results from inability to excrete nitrogenous waste (urea/creatinine)? (2)

A
  • Impaired mental function

- Nausea/vomiting

237
Q

What could be a pre-renal cause of acute renal failure?

A

Hypotension

238
Q

How could hypotension cause acute renal failure?

A

Loss of blood causing hypotension results in poor renal perfusion which means not much glomerular filtration is occurring and urine output is low

239
Q

What is rhabdomyolysis?

A

Release of myoglobin from damaged muscle

240
Q

What could be a renal cause of acute renal failure?

A

Rhabdomyolysis

241
Q

How could rhabdomyolysis cause acute renal failure?

A

Myoglobin is released and has toxic effects on the kidney tubules

242
Q

Which ion has the highest concentration in the intracellular fluid compartment?

A

K+

243
Q

What does low plasma HCO3- indicate?

A

Acidosis

244
Q

Why does low HCO3- indicate acidosis?

A

High levels of H+ ions combine with HCO3- in the body fluids resulting in low HCO3-

245
Q

Why can IV saline be used to treat hyperkalaemia?

A

Dilutes the plasma K+ to bring it back down to normal

246
Q

Where is vasopressin released?

A
  • Made in the cell bodies of neurons in the hypothalamus whose axons project into the posterior pituitary
  • Vesicles containing vasopressin released from posterior pituitary in response to an action potential
247
Q

What does vasopressin regulate?

A

Osmolality

248
Q

What is osmolality?

A
  • Concentration of dissolved solutes in a solution

- High osmolality = lots of salt

249
Q

When is vasopressin released?

A
  • When body wants to conserve water

- In response to high plasma osmolality

250
Q

What are the units of osmolality?

A

mosmol/kg of water

251
Q

What is normal plasma osmolality?

A

270-300 mosmol/kg water

252
Q

Where are osmoreceptors located?

A

In the supraoptic and paraventricular nuclei of the hypothalamus

253
Q

What happens when plasma osmolality increases?

A
  • Osmoreceptors in hypothalamus are stimulated
  • Action potentials in neurosecretory neurons in hypothalamus causes vasopressin release from posterior pituitary
  • Less water released and feeling of thirst
254
Q

What external factors can stimulate vasopressin release? (3)

A
  • Stress
  • Nicotine
  • Ecstasy
255
Q

What external factors can inhibit vasopressin release? (2)

A
  • Excessive fluid ingestion

- Alcohol consumption

256
Q

How does increased vasopressin affect principal cells?

A
  • Binds to V2 receptors on the basolateral membrane
  • Activates PKA which causes fusion of vesicles containing AQP2 with the apical membrane
  • More water can be reabsorbed through the AQP2 channels
257
Q

What happens to principal cells when vasopressin is low?

A

AQP2 channels pulled out of the apical membrane

258
Q

What is the net effect of vasopressin release?

A
  • Increased reabsorption of water so decreased secretion in urine
  • Fall in body fluid osmolality
259
Q

How much urine can Diabetes Insipidus patients secrete per day?

A

23 litres

260
Q

What is Central Diabetes Insipidus?

A

Patient doesn’t release vasopressin

261
Q

How is Central Diabetes Insipidus treated?

A

Nasal spray containing synthetic vasopressin

262
Q

What is Nephrogenic Diabetes Insipidus?

A

Patients can’t respond to vasopressin

263
Q

What are the 2 types of Diabetes Insipidus?

A
  • Central Diabetes Insipidus

- Nephrogenic Diabetes Insipidus

264
Q

What can cause Nephrogenic Diabetes Insipidus? (2)

A
  • Defect in V2 receptor

- Defect in AQP2 channels

265
Q

Where is aldosterone released?

A

Zona glomerulosa layer in the cortex of adrenal gland

266
Q

What kind of hormone is aldosterone?

A

Mineralocorticoid

267
Q

What does aldosterone regulate?

A

Plasma Na+, K+ and body fluid volume

268
Q

When is aldosterone released? (3)

A
  • Rise in plasma K+
  • Fall in plasma Na+ (minor regulation)
  • Fall in extracellular fluid volume
269
Q

Where does aldosterone act? (2)

A
  • Late distal tubule

- Collecting duct (both principal and intercalated cells)

270
Q

What is the effect of aldosterone release? (3)

A
  • Increased reabsorption of Na+
  • Increased reabsorption of water (follows Na+)
  • Increased secretion of K+ and H+
271
Q

What is the genomic action of aldosterone in principal cells?

A
  • Diffuses across lipid membrane and binds to cytosolic receptors
  • Complex moves into the nucleus
  • Stimulates transcription and synthesis of proteins involved in Na+ reabsorption, K+ and H+ secretion
  • I.e. ENaC, ROMK, Na+/H+ exchanger, Na+/K+ ATPase, H+ ATPase
272
Q

What is the non-genomic action of aldosterone in the principal cells?

A
  • Increased activity of ENaC

- Much faster than genomic action

273
Q

What does Liddle’s syndrome cause? (3)

A
  • Hypertension
  • High Na+ reabsorption but low aldosterone
  • Too many Na+ channels in the principal cells
274
Q

How is Liddle’s syndrome treated?

A

Amiloride (blocks ENaC to reduce Na+ reabsorption, diuretic)

275
Q

What does pseudohypoaldosteronism cause? (3)

A
  • Salt loss but high aldosterone
  • Loss of response to aldosterone
  • Mineralocorticoid receptor defect
276
Q

What does the renin-angiotensin system regulate?

A

Plasma Na+, K+ and body fluid volume (same as aldosterone)

277
Q

How is the renin-angiotensin cascade initiated?

A
  • Decrease in extracellular fluid volume
  • Renin released from JGA
  • Catalyses production of angiotensin I from angiotensinogen
  • Angiotensin I converted into angiotensin II by ACE (active form)
278
Q

What is the JGA?

A

Juxtaglomerular Apparatus

279
Q

What are macula densa cells?

A

Detect changes in composition and flow rate of the tubular fluid in the early distal tubule and send signals to glomerular capillaries

280
Q

What are granular cells?

A

Renin-containing cells

280
Q

Where is angiotensinogen produced?

A

Liver

281
Q

What is ACE?

A

Angiotensin Converting Enzyme

282
Q

Where is ACE found?

A

Capillaries

283
Q

What is the active form of angiotensin?

A

Angiotensin II

284
Q

Where is the most angiotensin II produced?

A

In the lungs due to the high density of capillaries

285
Q

Where does angiotensin II act?

A

Zona glomerulosa

286
Q

What does angiotensin II do? (2)

A
  • Promotes the release of aldosterone from the zona glomerulosa
  • Causes vasoconstriction of arterioles to increase blood pressure
287
Q

Where is aldosterone released from?

A

Zona glomerulosa in the kidneys

288
Q

What is the net effect of angiotensin II? (3)

A
  • Increased Na+ reabsorption
  • Increased extracellular fluid volume
  • Increased blood pressure
289
Q

What happens when your angiotensin II levels are too high?

A
  • Hypertension
  • Excess aldosterone
  • Na+ and water retention
290
Q

How do you treat hypertension caused by increased angiotensin II levels?

A

ACE inhibitors

291
Q

Is extracellular fluid volume or plasma osmolality more important?

A
  • Extracellular fluid volume
  • Body can accommodate changes in osmolality by resetting the vasopressin system (not the aldosterone system) to favour ECFV which is more critical (blood pressure)

Phys pharm (11 decks)

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