Unit 10 - Kidney pt 1 Flashcards
1
Q
functional unit of the kidney
A
nephron
2
Q
what is contained in the renal cortex
A
- glomerulus
- bowman’s capsule
- proximal tubules
- distal tubules
3
Q
where are the kidneys located
A
in the retroperitoneal space between the levels of T12 and L3
the right kidney is slightly more caudal to accommodate the liver
4
Q
what sections is the kidney divided into
A
renal cortex - outer section
renal medulla - inner section
5
Q
what is contained in the renal medulla
A
loops of Henle
collecting ducts
6
Q
what are renal papilla and what do they do
A
the apex of each pyramid
contains collecting ducts, drain urine unto minor calyces
7
Q
how is urine emptied into ureter
A
via renal pelvis
formed by multiple major calyces converging
8
Q
controls extracellular fluid volume
A
aldosterone
water & Na+ absorbed together
9
Q
controls plasma osmolarity
A
ADH
water absorbed, Na+ is not
10
Q
how is long-term BP control carried out
A
thirst mechanism (intake)
sodium and water excretion (output)
11
Q
how is intermediate-term BP control carried out
A
renin-angiotensin-aldosterone system
12
Q
responsible for short-term BP control
A
baroreceptor reflex
13
Q
primary regulators of acid-base balance
A
lungs
kidneys
14
Q
how do the kidneys maintain acid-base balance
A
by titrating hydrogen in the tubular fluid, which creates acidic or basic urine
15
Q
where is renin produced
A
juxtaglomerular apparatus
16
Q
where is erythropoietin synthesized
A
in the kidney
secreted in response to hypoxia
17
Q
how is the bone marrow stimulated to produce erythrocytes
A
erythropoietin stimulates stem cells in bone marrow
18
Q
how do prostaglandins affect the renal arteries
A
PGE2 and PGI2 vasodilate the renal arteries
19
Q
6 major functions of kidneys
A
- maintain ECF volume & composition
- long and intermediate BP regulation
- excretion of toxins/metabolites
- maintain acid-base balance
- hormone production
- blood glucose homeostasis
20
Q
examples of times the kidneys might release EPO
A
- anemia
- reduced intravascular volume
- hypoxia (high altitude, cardiac and pulmonary failure)
21
Q
why are patients with severe kidney disease often anemic
A
severe kidney disease reduces EPO production and leads to chronic anemia
22
Q
what is the inactive form of vitamin D3
A
calciferol - vitamin D3
23
Q
when is calciferol synthesized
A
during exposure to ultraviolet light
24
Q
how is calciferol converted to active vitamin D3
A
converted to 25-hydroxycholecalciferol in liver → converted to calcitriol in kidney
25
hormone that regulates serum level of calcitriol
PTH
26
hormone that regulates serum level of calcitriol
PTH
| negative feedback
27
3 ways calcitriol affects serum Calcium
**1) Stimulates intestine to absorb Ca2+ from food** (↑ serum Ca2+concentration)
**2) Instructs kidneys to reduce Ca2+ and phosphate excretion** (↑ serum Ca2+)
**3) Increases the deposition of Ca2+ into the bone** → resorption of "old" bone → increases the serum Ca2+ concentration → helps bone turnover over time
28
how do kidneys contribute to blood glucose homeostasis
Kidneys can synthesize glucose from amino acids, preventing hypoglycemia during fasting
29
3 hormones produced by the kidneys
1. erythropoietin
2. prostaglandins
3. calcitriol
30
how much of CO do kidneys receive
20-25% of CO
(1,000-1,250 mL/min)
31
renal blood flow calculation
(MAP – Renal venous pressure) / renal vascular resistance
32
RBF received by renal cortex vs renal medulla
cortex receives 90%
medulla receives 10%
33
PO2 in renal cortex vs medulla
cortex - 50 mmHg
medulla - 10 mmHg
34
why is the renal medulla more sensitive to ischemia vs. renal cortex
lower PO2
35
how is RBF affected by aging
decreases 10% per decade of life after age 50
## Footnote
In the neonate, RBF doubles in the first two weeks of life and achieves an adult level by 2 yrs
35
order of renal blood flow
afferent arteriole → glomerular capillary bed → efferent arteriole → peritubular capillary bed
35
how much of the blood delivered to kidney is filtered at the glomerulus
20%
36
what happens to the blood that is filtered at the glomerulus
after filtration, 99% is reabsorbed into peritubular capillaries
the 1% that isn't absorbed is excreted as urine
37
20% of blood delivered to kidney is filtered at glomerulus. where does the other 80% go
circulates through peritubular capillaries
38
how does blood in peritubular capillaries return to IVC
renal veins
39
RBF is directly proportional to:
difference between MAP and renal venous pressure
40
RBF is inversely proportional to
renal vascular resistance
41
purpose of renal autoregulation
ensure a constant amount of blood flow is delivered to the kidneys over a wide range of arterial blood pressures
42
what happens to GFR when MAP is outside of autoregulation range
becomes dependent on BP
43
how does autoregulation control RBF when renal perfusion is too high or too low
* too high: decreases RBF by increasing renal vascular resistance
* too low: increases RBF by decreasing renal vascular resistance
44
is UOP autoregulated?
NO - it's linearly related to MAP > 50
45
6 key contributors to renal autoregulation
1. myogenic mechanism
2. tubuloglomerular feedback
3. RAAS
4. ANP
5. prostaglandins
6. ANS tone
46
how does the myogenic mechanism respond to renal artery pressure
* pressure elevated = constricts afferent arteriole to protect glomerulus
* pressure low = dilates afferent arteriole to increase blood flow to nephron
47
where is the juxtaglomerular apparatus located
in the distal tubule, specifically the region that passes between the afferent and efferent arterioles
48
how do the kidneys receive SNS innervation
T8-L1
49
how does the surgical stress response affect kidneys
* induces a transient state of vasoconstriction and sodium retention
* This altered physiology persists for several days, leading to oliguria and edema
50
what renal structures are innervated by SNS
afferent and efferent arterioles
51
Key monitor of renal perfusion and ultrafiltrate solute concentration (Na+ & Cl-)
Juxtaglomerular Apparatus
52
where is the Juxtaglomerular Apparatus located
distal tubule
53
the Juxtaglomerular Apparatus plays a vital role in:
regulating RBF and GFR
54
how does the Juxtaglomerular Apparatus respond to decreased renal perfusion
releases renin into systemic circulation
55
3 factors that increase renin output
1. SNS activation (beta 1 stimulation)
2. decreased renal perfusion (hypovolemia)
3. decreased Na+ and Cl- delivery to distal tubule (tubuloglomerular feedback
56
how is GFR affected by RBF
when RBF decreases, GFR also declines
57
how can PEEP affect renin
reduces venous return, may reduce CO
reduces renal perfusion and stimualtes renin release
58
function of juxtaglomerular apparatus
* monitors renal perfusion
* monitors solute concentration
59
how does the juxtaglomerular apparatus maintain GFR
by modulating renal vascular resistance and renin release
60
senses decreased Na+ and Cl- delivery to juxtaglomerular apparatus
macula densa
61
how does AT2 affect GFR
constricts efferent arteriole, which increases GFR
62
where is angiotensinogen produced
liver
63
required to convert angiotensinogen to angiotensin I
renin
64
how is AT I converted to AT II
when AT I passes through lungs, ACE converts ATI to ATII
65
why can ACE inhibition manifest as cough, allergy-like symptoms, angioedema, and bronchospasm
ACE is involved in bradykinin metabolism
66
5 ways ATII affects BP
1. Among most powerful vasoconstrictors in the body (↑ arterial & venous tone)
2. Stimulates aldosterone synthesis in zone glomerulosa of adrenal cortex
3. Contributes to SNS activation by increasing catecholamine output from adrenal medulla
4. Increased ADH output from posterior pituitary gland
5. Increased thirst
67
where is aldosterone produced
zona glomerulosa of adrenal gland
68
functions of aldosterone in distal tubule & collecting ducts
* Facilitates Na+ and water reabsorption
* Facilitates H+ and K+ excretion
* Increased extracellular fluid volume = ↑ CO and BP
69
how does ATII contribute to SNS activation
by increasing catecholamine output from adrenal medulla
70
causes of decreased renal perfusion pressure that increase renin release
* Hemorrhage
* PEEP
* CHF
* Liver failure w/ ascites
* Sepsis
* Diuresis
71
where is aldosterone produced
zona glomerulosa of adrenal gland
72
functions of aldosterone
Facilitates Na+ and water reabsorption and K+ and H+ excretion by stimulating Na/K-ATPase in principal cells of distal tubules
73
how does aldosterone affect serum osmolarity
Does **not** meaningfully change serum osmolarity
74
3 ways aldosterone release can be stimulated
1. RAAS activation
2. hyperkalemia
3. hyponatremia
75
effects of ATII vs. aldosterone
* Na+ retaining effect of ATII almost immediate
* 1-2 hour delay between aldosterone release and physiologic effects
76
Conn's disease
excess aldosterone production → causes Na+ retention & K+ loss
77
Addison's disease
usually result of adrenocortical insufficiency (destruction of all of cortical zones)
78
stimulation of which adrenergic receptor increases renin release
beta 1
79
monitors of Na+ concentration in ECF
Osmoreceptors
80
principal determinant of osmolarity
Na+ concentration
| Also affected by glucose and BUN
81
principal determinant of osmolarity
Na+ concentration
| Also affected by glucose and BUN
82
where is ADH mostly produced
supraoptic nuclei of hypothalamus
83
where is ADH released
posterior pituitary gland
84
2 mechanisms that control ADH release
1. increased osmolarity of ECF
2. decreased blood volume
85
how does increased ECF osmolarity affect ADH release
* ↑ ECF Na+ concentration **shrinks osmoreceptors** in hypothalamus
* Initiates process of **transporting ADH from** hypothalamus to posterior pituitary gland
* **Thirst reflex** activated and antidiuresis prevents additional water loss
86
how does decreased blood volume control ADH release
Unloading of baroreceptors in carotid sinuses, transverse aortic arch, great veins, and RA stimulate ADH release
87
2 ways ADH restores BP
1. V1 stimulation causes vasoconstriction in vasculature
2. V2 stimulation in collecting ducts causes water retention
88
how does V1 activation cause vasoconstriction
↑ IP3, DAG & Ca2+)
89
half life of ADH
5-15 min
90
how do anesthetic agents affect ADH release
don’t directly affect ADH homeostasis but do impact arterial BP and venous blood volume, in turn increasing ADH release
91
how does V2 stimulation help restore BP
* increased cAMP
* aquaporin-2 channels facilitate water reabsorption, reduces plasma osmolarity, and increases urine osmolality
## Footnote
Net result is expansion of plasma volume
92
net result of V2 stimulation by ADH
expansion of plasma volume
93
what causes posterior pituitary to release ADH systemically? (2)
1. increased osmolarity of ECF
2. decreased blood volume
94
3 pathways that promote renal vasodilation
1) prostaglandins
2) natriuretic peptide
3) dopamine receptors
95
where are prostaglandins produced
afferent arteriole
96
how do prostaglandins play an important role in renal protection
by promoting RBF
97
what stimulates arachidonic acid liberation from cell membrane
* ischemia
* hypotension
* NE
* AT2
98
why can NSAIDs reduce RBF
they inihibit cyclooxygenase → can reduce RBF by inhibiting production of vasodilating prostaglandins
99
pathway that favors production of venal vasoconstrictors under hypoxic conditions
cyclic endoperoxide pathway
100
how does endotoxin affect renal vasculature
increases leukotriene production, which leads to renal vasoconstriction
101
how do prostaglandins & natriuretic peptides affect RAAS
* prostaglandins antagonize effects of RAAS
* natriuretic peptides inhibit RAAS
102
how do ANP & BNP affect BP
inhibit renin release
negative feedback on RAAS = vasodilation, **decreased BP**
103
where are dopamine 1 receptors present
renal vasculature, tubules, & splanchnic circulation
104
2nd messenger for DA1 receptors
increased cAMP
105
function of DA1 receptors
vasodilation, ↑ RBF, ↑ GFR, diuresis, Na+ excretion (natriuresis)
106
where are DA2 receptors present
presynaptic adrenergic nerve terminal
107
2nd messenger of DA2 receptors
decreased cAMP
108
function of DA2 receptors
decreased norepinephrine release
109
MAO of fenoldopam
selective DA1 receptor antagonist
110
low-dose fenoldopam
0.1-0.2 mcg/kg/min
111
effects of low dose fenoldopam
renal vasodilator and ↑ RBF, GFR, and facilitates Na+ excretion without affecting arterial BP
112
use of fenoldopam in CV surgery pts
* May offer protection during aortic surgery and CPB
* Reduces requirement for dialysis and in-hospital mortality in cardiac surgery patients
113
what effect do natriuretic peptides have on the kidneys?
* stimulate sodium & water excretion in collecting ducts
* inhibit renin release
114
2 components of the nephron
1. glomerulus
2. renal tubule
115
where does filtered fluid become urine
renal tubule
116
forms renal corpuscle
glomerulus & Bowman’s capsule
117
Where does the initial process of glomerular filtration begin
renal corpuscule
118
normal GFR
125 mL/min
119
normal filtration fraction
~20%
(~20% of RBF is filtered by glomerulus & ~80% is delivered to peritubular capillaries)
120
Glomerular filtrate is identical to plasma **except**
doesn’t contain plasma proteins, erythrocytes, or WBCs
121
how are proteins allowed to enter tubules with kidney disease
Kidney disease destroys basement membrane, which allows proteins to enter tubules
122
driving force that pushes fluid from blood (glomerulus) into Bowman’s capsule
Net filtration pressure (NFP)
123
NFP calculation
glomerular hydrostatic P – Bowman’s capsule hydrostatic P – glomerular oncotic P
124
most important determinant of GFR
Glomerular hydrostatic pressure
125
3 primary determinants of Glomerular hydrostatic pressure
1. arterial BP
2. afferent arteriole resistance
3. efferent arteriole resistance
126
why do pts with nephrotic syndrome or interstitial nephritis have hypoalbuminemia
they lose proteins in urine
127
glomulerar filtration depends on:
* RBF
* hydrostatic pressure at Bowman's capsule
128
how does constriction of afferent vs efferent arterioles affect GFR
* constriction of efferent increases hydrostatic pressure and GFR
* constriction of afferent decreases RBF and GFR
129
how does plasma protein concentration affect GFR
increased plasma protein concentration raises plasma oncotic pressure and reduces GFR
130
what is filtered by glomerular filtration
water, electrolytes, glucose
(proteins are not)
131
how does BP affect GFR
* increased MAP increases GFR
* decreased MAP decreases GFR
132
what is reabsorption
process where a substance is transferred from the tubule to the peritubular capillaries
133
what is secretion
process where a substance is transferred from the peritubular capillaries to the tubule
134
what is excretion
process where substance is removed from the body in the urine
135
why might diabetics have glucose in their urine
there’s a max amount that can be reabsorbed into peritubular blood. After max value is achieved, excess substance will be excreted in urine
136
urine formation is the sum of:
glomerular filtration, tubular reabsorption, and tubular secretion
137
urinary excretion rate =
filtration – reabsorption + secretion
138
how does afferent arteriole constriction affect RBF, GFR, and filtration fraction
* RBF: decreased
* GFR: decreased
* filtration fraction: no change
139
how does efferent arteriole constriction affect RBF, GFR, and filtration fraction
* RBF: decreased
* GFR: increased
* filtration fraction: increased
140
how does increased plasma protein affect RBF, GFR, and filtration fraction
* RBF: no change
* GFR: decreased
* filtration fraction: decreased
141
how does decreased plasma protein affect RBF, GFR, and filtration fraction
* RBF: no change
* GFR: increased
* filtration fraction: increased
142
where does most sodium reabsorption occur in the nephron
proximal tubule
| 65%
143
what part of the kidney is responsible for bulk reabsorption of solutes and water
proximal convoluted tubule
144
how are organic acids, bases, and hydrogen ions secreted into proximal tubule
by Na+ counter transport mechanism
145
ions that follow Na+ in direct proportion for reabsorption in the proximal tubule
K+
Cl-
bicarb
146
what % of Na+ reabsorption takes place in the loop of Helne
20%
147
primary function of descending loop of henle
participate in forming concentrated or dilute urine
| separates the handling of Na+ and water
148
primary function of descending loop of henle
participate in forming concentrated or dilute urine
| separates the handling of Na+ and water
149
part of the kidney responsible for countercurrent mechanisms + high permeability to H2O
descending loop of henle
150
Ability of kidneys to produce concentrated or dilute urine depends on?
presence of a graduated hyperosmotic peritubular interstitium
151
2 counterpart systems needed to create and maintain graduated hyperosmotic peritubular interstitium
1. loop of henle
2. vasa recta
152
role of loop of Henle in hyperosmotic peritubular interstitium
countercurrent multiplier system that creates osmotic gradient
153
role of vasa recta in maintaining countercurrent multiplier system that creates osmotic gradient
countercurrent exchanger system that maintains medullary osmotic gradient
154
where is 20% of water reabsorbed
descending loop of henle
155
what happens to the osmolarity of peritubular interstitium as the descending limb travels from cortex to medulla
progressively increases - osmolarity starts at 300 mOsm/L and increases to 1500 mOsm/L in renal pelvis
## Footnote
increasing osmolarity provides energy for passively reabsorbing water (osmosis)
156
what happens to the osmolarity of peritubular interstitium as the descending limb travels from cortex to medulla
progressively increases - osmolarity starts at 300 mOsm/L and increases to 1500 mOsm/L in renal pelvis
## Footnote
increasing osmolarity provides energy for passively reabsorbing water (osmosis)
157
what are vasa recta
peritubular capillaries that run parallel to loop of Henle
158
why are vasa recta essential
it returns the reabsorbed water to the blood, allowing osmolarity in peritubular interstitium to remain high
159
part of the loop of Henle that is **not** permeable to water
thin & thick segments of the ascending limb
160
most important pump in Ascending Loop of Henle
Na-K(2)-Cl-co transporter
161
target of loop diuretics
Na-K(2)-Cl-co transporter in ascending loop of Henle
162
function of Na-K(2)-Cl-co transporter
removes about 20% of tubular sodium
163
home to juxtaglomerular apparatus (JGA)
Distal Convoluted Tubule
164
Key process of the countercurrent multiplier system function of the loop of Henle
Water can’t follow Na+ into peritubular interstitium
tubular fluid becomes more dilute and peritubular interstitium becomes more concentrated
165
nephrons that play a more important role in countercurrent multiplier
juxtamedullary nephrons play a more signifncant role vs superficial cortical
166
how is hydrogen excreted in the ascending loop of henle
via sodium-hydrogen exchange mechanism
167
purpose of countercurrent systems in ascending loop of henle
work together to transfer water from tubular fluid into peritubular interstitium & then return water to blood
without this system, we would produce a ton of dilute urine and cause dehydration
168
function of distal convoluted tubule
fine tunes solute concentration
169
2 types of nephrons in kidney
1) superficial cortical
2) juxtamedullary
170
is the distal tubule permeable to water?
The late distal tubule is impermeable to water except in the presence of aldosterone or ADH
171
part of the nephron that adjusts urea concentration
distal convoluted tubule
172
Where do aldosterone & ADH act on the nephron?
distal convoluted tubule
collecting duct
173
part of the nephron that regulates final concentration of urine
collecting duct
174
differential when BUN:Cr is increased
dehydration
obstructive uropathy
increased protein intake
upper GI bleeding
175
why can increased BUN:Cr be due to upper GI bleeding
in the gut, heme is broken down into protein and this protein is metabolized into urea
urea is absorbed into systemic circulation - increases urea load to kidneys
