Transport Mechanisms 2 Flashcards
(67 cards)
1
Q
effect of loops diuretics (furosemide) on ascending limb of LOH
A
- inhibits Na/K/2Cl transporter
- increases urination
2
Q
result of inhibition of Na/K/2Cl transporter in LOH
A
- decreased K+ and Ca2+ reabsorption
aka hypokalemia (and alkalosis) and hypocalcemia
3
Q
how do we have decreased Ca2+ with decreased K+
A
- electrochemical gradient that is usually formed by the back leak of K+ will lead to paracellular Ca2+ transport
- that has now been lost
4
Q
Bartter’s syndrome affects what part of the kindey
A
- ascending limb of LOH
5
Q
cause of Bartter’s syndrome
A
- defect in Na/K/2Cl transporter
6
Q
genetics of Bartter’s syndrome
A
- autosomal recessive
7
Q
symptoms of Bartter’s syndrome
A
- hypokalemia
- metabolic alkalosis
- polyuria
- polydipsia
- dehydration
- high urine calcium
8
Q
what transporter does the early distal tubule have
result
A
- Na/Cl cotransporter (NCC)
- dilutes tubular fluid
9
Q
epithelium in early distal tubule
result
A
- tight epithelial
- transcellular Na+ movement via the Na/Cl cotransporter
- impermeable to H20
10
Q
how much Na is reabsorbed in the early distal tubule
A
- 5-10%
11
Q
what transporter is located in the late distal tubule/cortical collecting duct
A
- epithelial Na Channel (ENaC)
- alpha intercalated cells
12
Q
what is the epithelial Na Channel dependent on
A
- aldosterone
13
Q
result of epithelial Na channel
A
- Na enters cell down chemical gradient through ENaC
- creates negative electrical potential
- results in K+ secretion into tubular lumen
14
Q
result of alpha intercalated cells
result of beta intercalated cell
A
- H+ secretion into tubular lumen
- HCO3/Cl- ATPase
- HCO3 extruded into the lumen
15
Q
H+ secretion into tubular lumen through what mechanisms
A
- H+ ATPase
- H/K ATPase
16
Q
what happens with the secreted H+ in late distal tubule
what happens with HCO3- in the late distal tubule
A
- binds to NH3 and other buffers
- results in HCO3 reabsorption into blood through HCO3/Cl- exchanger
17
Q
result of the thiazide diuretics such as hydrochlorothiazide and chlorthalidone
A
- inhibit the Na/Cl cotransporter in the early distal tubule
18
Q
result of amiloride/triamterene
what are they also referred to as
A
- inhibit epithelial sodium channel
- K+ sparing diuretics
19
Q
why are amiloride/triamterene referred to as K+ sparing diuretics
A
- they do not promote K+ secretion
20
Q
we generally use amiloride/triamterene in combination with
A
- thiazide or loop diuretic
21
Q
cause of Gitelman’s
result
A
- loss of function of Na/Cl cotransporter
- increased surface expression of K in collecting duct
- Na+ loss into urine
22
Q
Gitelman’s acts like what
A
- a thiazide diuretic
23
Q
symptoms of Gitelman’s
A
- hypokalemia - loss of K+ in the urine
- metabolic alkalosis
- salt craving
24
Q
cause of pseudohypoaldosteronism II
result
A
- gain of function of Na/Cl cotransporter
- increases Na and Cl reabsorption
- decreases surface expression of K channels in collecting duct.
25
symptoms of pseudohypoaldosteronism II
- hypertension - increase Na reabsorption
- hyperkalemia - potassium cannot be secreted into the urine
- Metabolic Acidosis
26
renin and aldosterone levels in pseudohypoaldosteronism II
- low
| - you're having high BP so you have increased perfusion and don't need the RAAS system
27
cause of Liddle's
result
- gain of function in epithelial Na channel
| - uncontrolled Na retention in blood
28
symptoms of Liddle's
- hypertension - increase Na+ reabsorption
- hypokalemia - you have reabsorbed all this sodium which creates an even greater gradient for K+ secretion so your K+ in blood is less.
- metabolic alkalosis
29
cause of pseudohypoaldosteronism type I
- loss of function of epithelial Na channel
30
symptoms of pseudohypoaldosteronism type I
- hypovolemia
- metabolic acidosis
- sodium wasting
- hyperkalemia
- hyponatremia
31
aldosterone levels in pseudohypoaldosteronism type I
- elevated due to hypovolemia
32
cause of distal RTA type I
- impaired H+ secretion
33
distal RTA type I impaired H+ secretion leads to
- non-anion gap acidosis
- low bicarb
- hypokalemia
- cannot acidify urine
34
most common cause of distal RTA type I
- diminished H+ ATPase activity
35
less common causes of distal RTA type I
- increased lumenal membrane permeability leading to backleak of H+
- diminished activity of H+/K+/ATPase
36
signs of hyperkalemic RTA type 4
- hyperkalemia
| - mild non-anion gap metabolic acidosis
37
cause of hyperkalemic RTA type 4
result
- hypoaldosteronism due to a true deficiency or resistance
| - decreased Na+ reabsorption and less K+ secretion
38
syndrome of apparent mineralocorticoid excess (SAME) cause
-deficiency in enzyme that converts cortisol to cortisone
39
what binds the mineralcorticoid receptor
- cortisol
40
plasma cortisol concentration compared to aldosterone in syndrome of apparent mineralocorticoid excess (SAME) cause
- 100x higher
| - basically still acts like aldosterone
41
blood pressure in syndrome of apparent mineralocorticoid excess (SAME)
- hypertension
42
potassium levels in syndrome of apparent mineralocorticoid excess (SAME)
- hypokalemia due to K+ secretion
43
acidosis/alkalosis in syndrome of apparent mineralocorticoid excess (SAME)
- metabolic alkalosis - hydrogen ion secretion
| - ACTS LIKE ALDOSTERONE WHICH CAUSES H+ SECRETION
44
plasma renin activity in syndrome of apparent mineralocorticoid excess (SAME)
- low
45
plasma aldosterone concentration in syndrome of apparent mineralocorticoid excess (SAME)
- low
46
what hormones regulate in the early distal tubule
- none
47
what hormones regulate in the late distal tubule and cortical collecting duct - principal cells
- aldosterone
- ADH
- ANP
48
what hormones regulate in the late distal tubule and cortical collecting duct - intercalated cells
- aldosterone
49
role of aldosterone in the late distal tubule and cortical collecting duct - principal cells
- binds to intracellular receptor
| - stimulates insertion of epithelial Na channel and K channels in luminal membrane
50
role of ADH in the late distal tubule and cortical collecting duct - principal cells
- binds to V2 receptor in basolateral membrane
- V2 receptor activates adenylate cyclase to convert ATP -> cAMP to activate PKA
- phosphorylation of aquaporin 2 causes shuttling and stimulates insertion of aquaporin 2 in luminal membrane
51
role of ANP in the late distal tubule and cortical collecting duct - principal cells
- inhibits aldosterone effects
52
role of aldosterone late distal tubule and cortical collecting duct - intercalated cells
- stimulates H+ ATPase activity
53
hormonal regulation in the medullary collecting duct
- ADH dependent water reabsorption
- ADH dependent urea reabsoprtion
- aldosterone dependent Na+ reabsorption and K+ secretion
54
RAAS during hypovolemia
- decreased distal delivery of NaCl to macula densa
- increased renin release by JG cells
- increase in angiotensin II to maintain GFR
55
H2O enter lumen via which aquaporin and enters how
- 2
| - enters along osmotic gradient
56
H2O leaves via which aquaporin
- 3
57
importance of aquaporin 3
- constitutively expressed
| - not ADH regulated
58
what does high urine osmolarity reflect about ADH and urine volume
- ADH present
- water reabsorbed
- low urine volume
59
what does low urine osmolarity reflect about ADH and urine volume
- ADH not present
- water not reabsorbed
- high urine volume
60
the V2 receptor also activates which other transporter
where is this transporter expressed
- urea transporter
| - expressed in medullary collecting duct
61
urea is reabsorbed where and how
- across luminal membrane through UT1
| - along a concentration gradient
62
urea exits where and how
- exits basolateral membrane through UT3
63
what is the location of AQP2 and AQP3
- distal tubule
| - cortical and medullary collecting duct
64
which AQP is located on the apical membrane
- 2
65
which AQP is located on the basolateral membrane
- 3
66
ANP is released in response to
- atrial volume
67
result of ANP
- enhances Na+ excretion
- counters effects of RAAS
- relax vascular smooth muscle
- vasodilator
- increase diuresis
