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APEX > Unit 10 - Kidney pt 1 > Flashcards

Unit 10 - Kidney pt 1 Flashcards

1
Q

functional unit of the kidney

A

nephron

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2
Q

what is contained in the renal cortex

A
  • glomerulus
  • bowman’s capsule
  • proximal tubules
  • distal tubules
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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

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4
Q

what sections is the kidney divided into

A

renal cortex - outer section
renal medulla - inner section

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5
Q

what is contained in the renal medulla

A

loops of Henle
collecting ducts

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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

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7
Q

how is urine emptied into ureter

A

via renal pelvis
formed by multiple major calyces converging

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8
Q

controls extracellular fluid volume

A

aldosterone

water & Na+ absorbed together

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9
Q

controls plasma osmolarity

A

ADH

water absorbed, Na+ is not

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10
Q

how is long-term BP control carried out

A

thirst mechanism (intake)
sodium and water excretion (output)

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11
Q

how is intermediate-term BP control carried out

A

renin-angiotensin-aldosterone system

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12
Q

responsible for short-term BP control

A

baroreceptor reflex

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13
Q

primary regulators of acid-base balance

A

lungs
kidneys

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14
Q

how do the kidneys maintain acid-base balance

A

by titrating hydrogen in the tubular fluid, which creates acidic or basic urine

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15
Q

where is renin produced

A

juxtaglomerular apparatus

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16
Q

where is erythropoietin synthesized

A

in the kidney

secreted in response to hypoxia

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17
Q

how is the bone marrow stimulated to produce erythrocytes

A

erythropoietin stimulates stem cells in bone marrow

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18
Q

how do prostaglandins affect the renal arteries

A

PGE2 and PGI2 vasodilate the renal arteries

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19
Q

6 major functions of kidneys

A
  1. maintain ECF volume & composition
  2. long and intermediate BP regulation
  3. excretion of toxins/metabolites
  4. maintain acid-base balance
  5. hormone production
  6. blood glucose homeostasis
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20
Q

examples of times the kidneys might release EPO

A
  • anemia
  • reduced intravascular volume
  • hypoxia (high altitude, cardiac and pulmonary failure)
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21
Q

why are patients with severe kidney disease often anemic

A

severe kidney disease reduces EPO production and leads to chronic anemia

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22
Q

what is the inactive form of vitamin D3

A

calciferol - vitamin D3

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23
Q

when is calciferol synthesized

A

during exposure to ultraviolet light

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24
Q

how is calciferol converted to active vitamin D3

A

converted to 25-hydroxycholecalciferol in liver → converted to calcitriol in kidney

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25
Q

hormone that regulates serum level of calcitriol

A

PTH

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26
Q

hormone that regulates serum level of calcitriol

A

PTH

negative feedback

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27
Q

3 ways calcitriol affects serum Calcium

A

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

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28
Q

how do kidneys contribute to blood glucose homeostasis

A

Kidneys can synthesize glucose from amino acids, preventing hypoglycemia during fasting

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29
Q

3 hormones produced by the kidneys

A
  1. erythropoietin
  2. prostaglandins
  3. calcitriol
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30
Q

how much of CO do kidneys receive

A

20-25% of CO
(1,000-1,250 mL/min)

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31
Q

renal blood flow calculation

A

(MAP – Renal venous pressure) / renal vascular resistance

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32
Q

RBF received by renal cortex vs renal medulla

A

cortex receives 90%
medulla receives 10%

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33
Q

PO2 in renal cortex vs medulla

A

cortex - 50 mmHg
medulla - 10 mmHg

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34
Q

why is the renal medulla more sensitive to ischemia vs. renal cortex

A

lower PO2

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35
Q

how is RBF affected by aging

A

decreases 10% per decade of life after age 50

In the neonate, RBF doubles in the first two weeks of life and achieves an adult level by 2 yrs

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35
Q

order of renal blood flow

A

afferent arteriole → glomerular capillary bed → efferent arteriole → peritubular capillary bed

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35
Q

how much of the blood delivered to kidney is filtered at the glomerulus

A

20%

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36
Q

what happens to the blood that is filtered at the glomerulus

A

after filtration, 99% is reabsorbed into peritubular capillaries

the 1% that isn’t absorbed is excreted as urine

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37
Q

20% of blood delivered to kidney is filtered at glomerulus. where does the other 80% go

A

circulates through peritubular capillaries

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38
Q

how does blood in peritubular capillaries return to IVC

A

renal veins

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39
Q

RBF is directly proportional to:

A

difference between MAP and renal venous pressure

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40
Q

RBF is inversely proportional to

A

renal vascular resistance

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41
Q

purpose of renal autoregulation

A

ensure a constant amount of blood flow is delivered to the kidneys over a wide range of arterial blood pressures

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42
Q

what happens to GFR when MAP is outside of autoregulation range

A

becomes dependent on BP

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43
Q

how does autoregulation control RBF when renal perfusion is too high or too low

A
  • too high: decreases RBF by increasing renal vascular resistance
  • too low: increases RBF by decreasing renal vascular resistance
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44
Q

is UOP autoregulated?

A

NO - it’s linearly related to MAP > 50

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45
Q

6 key contributors to renal autoregulation

A
  1. myogenic mechanism
  2. tubuloglomerular feedback
  3. RAAS
  4. ANP
  5. prostaglandins
  6. ANS tone
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46
Q

how does the myogenic mechanism respond to renal artery pressure

A
  • pressure elevated = constricts afferent arteriole to protect glomerulus
  • pressure low = dilates afferent arteriole to increase blood flow to nephron
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47
Q

where is the juxtaglomerular apparatus located

A

in the distal tubule, specifically the region that passes between the afferent and efferent arterioles

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48
Q

how do the kidneys receive SNS innervation

A

T8-L1

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49
Q

how does the surgical stress response affect kidneys

A
  • induces a transient state of vasoconstriction and sodium retention
  • This altered physiology persists for several days, leading to oliguria and edema
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50
Q

what renal structures are innervated by SNS

A

afferent and efferent arterioles

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51
Q

Key monitor of renal perfusion and ultrafiltrate solute concentration (Na+ & Cl-)

A

Juxtaglomerular Apparatus

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52
Q

where is the Juxtaglomerular Apparatus located

A

distal tubule

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53
Q

the Juxtaglomerular Apparatus plays a vital role in:

A

regulating RBF and GFR

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54
Q

how does the Juxtaglomerular Apparatus respond to decreased renal perfusion

A

releases renin into systemic circulation

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55
Q

3 factors that increase renin output

A
  1. SNS activation (beta 1 stimulation)
  2. decreased renal perfusion (hypovolemia)
  3. decreased Na+ and Cl- delivery to distal tubule (tubuloglomerular feedback
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56
Q

how is GFR affected by RBF

A

when RBF decreases, GFR also declines

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57
Q

how can PEEP affect renin

A

reduces venous return, may reduce CO
reduces renal perfusion and stimualtes renin release

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58
Q

function of juxtaglomerular apparatus

A
  • monitors renal perfusion
  • monitors solute concentration
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59
Q

how does the juxtaglomerular apparatus maintain GFR

A

by modulating renal vascular resistance and renin release

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60
Q

senses decreased Na+ and Cl- delivery to juxtaglomerular apparatus

A

macula densa

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61
Q

how does AT2 affect GFR

A

constricts efferent arteriole, which increases GFR

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62
Q

where is angiotensinogen produced

A

liver

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63
Q

required to convert angiotensinogen to angiotensin I

A

renin

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64
Q

how is AT I converted to AT II

A

when AT I passes through lungs, ACE converts ATI to ATII

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65
Q

why can ACE inhibition manifest as cough, allergy-like symptoms, angioedema, and bronchospasm

A

ACE is involved in bradykinin metabolism

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66
Q

5 ways ATII affects BP

A
  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
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67
Q

where is aldosterone produced

A

zona glomerulosa of adrenal gland

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68
Q

functions of aldosterone in distal tubule & collecting ducts

A
  • Facilitates Na+ and water reabsorption
  • Facilitates H+ and K+ excretion
  • Increased extracellular fluid volume = ↑ CO and BP
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69
Q

how does ATII contribute to SNS activation

A

by increasing catecholamine output from adrenal medulla

70
Q

causes of decreased renal perfusion pressure that increase renin release

A
  • Hemorrhage
  • PEEP
  • CHF
  • Liver failure w/ ascites
  • Sepsis
  • Diuresis
71
Q

where is aldosterone produced

A

zona glomerulosa of adrenal gland

72
Q

functions of aldosterone

A

Facilitates Na+ and water reabsorption and K+ and H+ excretion by stimulating Na/K-ATPase in principal cells of distal tubules

73
Q

how does aldosterone affect serum osmolarity

A

Does not meaningfully change serum osmolarity

74
Q

3 ways aldosterone release can be stimulated

A
  1. RAAS activation
  2. hyperkalemia
  3. hyponatremia
75
Q

effects of ATII vs. aldosterone

A
  • Na+ retaining effect of ATII almost immediate
  • 1-2 hour delay between aldosterone release and physiologic effects
76
Q

Conn’s disease

A

excess aldosterone production → causes Na+ retention & K+ loss

77
Q

Addison’s disease

A

usually result of adrenocortical insufficiency (destruction of all of cortical zones)

78
Q

stimulation of which adrenergic receptor increases renin release

A

beta 1

79
Q

monitors of Na+ concentration in ECF

A

Osmoreceptors

80
Q

principal determinant of osmolarity

A

Na+ concentration

Also affected by glucose and BUN

81
Q

principal determinant of osmolarity

A

Na+ concentration

Also affected by glucose and BUN

82
Q

where is ADH mostly produced

A

supraoptic nuclei of hypothalamus

83
Q

where is ADH released

A

posterior pituitary gland

84
Q

2 mechanisms that control ADH release

A
  1. increased osmolarity of ECF
  2. decreased blood volume
85
Q

how does increased ECF osmolarity affect ADH release

A
  • ↑ 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
Q

how does decreased blood volume control ADH release

A

Unloading of baroreceptors in carotid sinuses, transverse aortic arch, great veins, and RA stimulate ADH release

87
Q

2 ways ADH restores BP

A
  1. V1 stimulation causes vasoconstriction in vasculature
  2. V2 stimulation in collecting ducts causes water retention
88
Q

how does V1 activation cause vasoconstriction

A

↑ IP3, DAG & Ca2+)

89
Q

half life of ADH

A

5-15 min

90
Q

how do anesthetic agents affect ADH release

A

don’t directly affect ADH homeostasis but do impact arterial BP and venous blood volume, in turn increasing ADH release

91
Q

how does V2 stimulation help restore BP

A
  • increased cAMP
  • aquaporin-2 channels facilitate water reabsorption, reduces plasma osmolarity, and increases urine osmolality

Net result is expansion of plasma volume

92
Q

net result of V2 stimulation by ADH

A

expansion of plasma volume

93
Q

what causes posterior pituitary to release ADH systemically? (2)

A
  1. increased osmolarity of ECF
  2. decreased blood volume
94
Q

3 pathways that promote renal vasodilation

A

1) prostaglandins
2) natriuretic peptide
3) dopamine receptors

95
Q

where are prostaglandins produced

A

afferent arteriole

96
Q

how do prostaglandins play an important role in renal protection

A

by promoting RBF

97
Q

what stimulates arachidonic acid liberation from cell membrane

A
  • ischemia
  • hypotension
  • NE
  • AT2
98
Q

why can NSAIDs reduce RBF

A

they inihibit cyclooxygenase → can reduce RBF by inhibiting production of vasodilating prostaglandins

99
Q

pathway that favors production of venal vasoconstrictors under hypoxic conditions

A

cyclic endoperoxide pathway

100
Q

how does endotoxin affect renal vasculature

A

increases leukotriene production, which leads to renal vasoconstriction

101
Q

how do prostaglandins & natriuretic peptides affect RAAS

A
  • prostaglandins antagonize effects of RAAS
  • natriuretic peptides inhibit RAAS
102
Q

how do ANP & BNP affect BP

A

inhibit renin release
negative feedback on RAAS = vasodilation, decreased BP

103
Q

where are dopamine 1 receptors present

A

renal vasculature, tubules, & splanchnic circulation

104
Q

2nd messenger for DA1 receptors

A

increased cAMP

105
Q

function of DA1 receptors

A

vasodilation, ↑ RBF, ↑ GFR, diuresis, Na+ excretion (natriuresis)

106
Q

where are DA2 receptors present

A

presynaptic adrenergic nerve terminal

107
Q

2nd messenger of DA2 receptors

A

decreased cAMP

108
Q

function of DA2 receptors

A

decreased norepinephrine release

109
Q

MAO of fenoldopam

A

selective DA1 receptor antagonist

110
Q

low-dose fenoldopam

A

0.1-0.2 mcg/kg/min

111
Q

effects of low dose fenoldopam

A

renal vasodilator and ↑ RBF, GFR, and facilitates Na+ excretion without affecting arterial BP

112
Q

use of fenoldopam in CV surgery pts

A
  • May offer protection during aortic surgery and CPB
  • Reduces requirement for dialysis and in-hospital mortality in cardiac surgery patients
113
Q

what effect do natriuretic peptides have on the kidneys?

A
  • stimulate sodium & water excretion in collecting ducts
  • inhibit renin release
114
Q

2 components of the nephron

A
  1. glomerulus
  2. renal tubule
115
Q

where does filtered fluid become urine

A

renal tubule

116
Q

forms renal corpuscle

A

glomerulus & Bowman’s capsule

117
Q

Where does the initial process of glomerular filtration begin

A

renal corpuscule

118
Q

normal GFR

A

125 mL/min

119
Q

normal filtration fraction

A

~20%
(~20% of RBF is filtered by glomerulus & ~80% is delivered to peritubular capillaries)

120
Q

Glomerular filtrate is identical to plasma except

A

doesn’t contain plasma proteins, erythrocytes, or WBCs

121
Q

how are proteins allowed to enter tubules with kidney disease

A

Kidney disease destroys basement membrane, which allows proteins to enter tubules

122
Q

driving force that pushes fluid from blood (glomerulus) into Bowman’s capsule

A

Net filtration pressure (NFP)

123
Q

NFP calculation

A

glomerular hydrostatic P – Bowman’s capsule hydrostatic P – glomerular oncotic P

124
Q

most important determinant of GFR

A

Glomerular hydrostatic pressure

125
Q

3 primary determinants of Glomerular hydrostatic pressure

A
  1. arterial BP
  2. afferent arteriole resistance
  3. efferent arteriole resistance
126
Q

why do pts with nephrotic syndrome or interstitial nephritis have hypoalbuminemia

A

they lose proteins in urine

127
Q

glomulerar filtration depends on:

A
  • RBF
  • hydrostatic pressure at Bowman’s capsule
128
Q

how does constriction of afferent vs efferent arterioles affect GFR

A
  • constriction of efferent increases hydrostatic pressure and GFR
  • constriction of afferent decreases RBF and GFR
129
Q

how does plasma protein concentration affect GFR

A

increased plasma protein concentration raises plasma oncotic pressure and reduces GFR

130
Q

what is filtered by glomerular filtration

A

water, electrolytes, glucose
(proteins are not)

131
Q

how does BP affect GFR

A
  • increased MAP increases GFR
  • decreased MAP decreases GFR
132
Q

what is reabsorption

A

process where a substance is transferred from the tubule to the peritubular capillaries

133
Q

what is secretion

A

process where a substance is transferred from the peritubular capillaries to the tubule

134
Q

what is excretion

A

process where substance is removed from the body in the urine

135
Q

why might diabetics have glucose in their urine

A

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
Q

urine formation is the sum of:

A

glomerular filtration, tubular reabsorption, and tubular secretion

137
Q

urinary excretion rate =

A

filtration – reabsorption + secretion

138
Q

how does afferent arteriole constriction affect RBF, GFR, and filtration fraction

A
  • RBF: decreased
  • GFR: decreased
  • filtration fraction: no change
139
Q

how does efferent arteriole constriction affect RBF, GFR, and filtration fraction

A
  • RBF: decreased
  • GFR: increased
  • filtration fraction: increased
140
Q

how does increased plasma protein affect RBF, GFR, and filtration fraction

A
  • RBF: no change
  • GFR: decreased
  • filtration fraction: decreased
141
Q

how does decreased plasma protein affect RBF, GFR, and filtration fraction

A
  • RBF: no change
  • GFR: increased
  • filtration fraction: increased
142
Q

where does most sodium reabsorption occur in the nephron

A

proximal tubule

65%

143
Q

what part of the kidney is responsible for bulk reabsorption of solutes and water

A

proximal convoluted tubule

144
Q

how are organic acids, bases, and hydrogen ions secreted into proximal tubule

A

by Na+ counter transport mechanism

145
Q

ions that follow Na+ in direct proportion for reabsorption in the proximal tubule

A

K+
Cl-
bicarb

146
Q

what % of Na+ reabsorption takes place in the loop of Helne

A

20%

147
Q

primary function of descending loop of henle

A

participate in forming concentrated or dilute urine

separates the handling of Na+ and water

148
Q

primary function of descending loop of henle

A

participate in forming concentrated or dilute urine

separates the handling of Na+ and water

149
Q

part of the kidney responsible for countercurrent mechanisms + high permeability to H2O

A

descending loop of henle

150
Q

Ability of kidneys to produce concentrated or dilute urine depends on?

A

presence of a graduated hyperosmotic peritubular interstitium

151
Q

2 counterpart systems needed to create and maintain graduated hyperosmotic peritubular interstitium

A
  1. loop of henle
  2. vasa recta
152
Q

role of loop of Henle in hyperosmotic peritubular interstitium

A

countercurrent multiplier system that creates osmotic gradient

153
Q

role of vasa recta in maintaining countercurrent multiplier system that creates osmotic gradient

A

countercurrent exchanger system that maintains medullary osmotic gradient

154
Q

where is 20% of water reabsorbed

A

descending loop of henle

155
Q

what happens to the osmolarity of peritubular interstitium as the descending limb travels from cortex to medulla

A

progressively increases - osmolarity starts at 300 mOsm/L and increases to 1500 mOsm/L in renal pelvis

increasing osmolarity provides energy for passively reabsorbing water (osmosis)

156
Q

what happens to the osmolarity of peritubular interstitium as the descending limb travels from cortex to medulla

A

progressively increases - osmolarity starts at 300 mOsm/L and increases to 1500 mOsm/L in renal pelvis

increasing osmolarity provides energy for passively reabsorbing water (osmosis)

157
Q

what are vasa recta

A

peritubular capillaries that run parallel to loop of Henle

158
Q

why are vasa recta essential

A

it returns the reabsorbed water to the blood, allowing osmolarity in peritubular interstitium to remain high

159
Q

part of the loop of Henle that is not permeable to water

A

thin & thick segments of the ascending limb

160
Q

most important pump in Ascending Loop of Henle

A

Na-K(2)-Cl-co transporter

161
Q

target of loop diuretics

A

Na-K(2)-Cl-co transporter in ascending loop of Henle

162
Q

function of Na-K(2)-Cl-co transporter

A

removes about 20% of tubular sodium

163
Q

home to juxtaglomerular apparatus (JGA)

A

Distal Convoluted Tubule

164
Q

Key process of the countercurrent multiplier system function of the loop of Henle

A

Water can’t follow Na+ into peritubular interstitium

tubular fluid becomes more dilute and peritubular interstitium becomes more concentrated

165
Q

nephrons that play a more important role in countercurrent multiplier

A

juxtamedullary nephrons play a more signifncant role vs superficial cortical

166
Q

how is hydrogen excreted in the ascending loop of henle

A

via sodium-hydrogen exchange mechanism

167
Q

purpose of countercurrent systems in ascending loop of henle

A

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
Q

function of distal convoluted tubule

A

fine tunes solute concentration

169
Q

2 types of nephrons in kidney

A

1) superficial cortical
2) juxtamedullary

170
Q

is the distal tubule permeable to water?

A

The late distal tubule is impermeable to water except in the presence of aldosterone or ADH

171
Q

part of the nephron that adjusts urea concentration

A

distal convoluted tubule

172
Q

Where do aldosterone & ADH act on the nephron?

A

distal convoluted tubule
collecting duct

173
Q

part of the nephron that regulates final concentration of urine

A

collecting duct

174
Q

differential when BUN:Cr is increased

A

dehydration
obstructive uropathy
increased protein intake
upper GI bleeding

175
Q

why can increased BUN:Cr be due to upper GI bleeding

A

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

APEX (54 decks)

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