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Pathophys > Exam 6- Renal System (without pathology) > Flashcards

Exam 6- Renal System (without pathology) Flashcards

1
Q

kidney regulates

A
  • long term blood pressure
  • blood cell count /hemoglobin levels (produces erythropoietin)
  • Ca2+ homeostasis(activates vit. D)
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2
Q

kidney structure

A

v

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3
Q

functional unit of the kidney=

A

nephron

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4
Q

juxtaglom vs cortical neph

A

m

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5
Q

renal corpuscle=

A

glomerulus + bowman’s capsule

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6
Q

tubule path

A

Proximal tubule (convoluted and straight)

Loop of Henle

Distal convoluted tubule

Collecting duct (cortical and medullary)

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7
Q

after collecting duct urine passes to___

A

minor calyx

major calyx

renal pelvis

ureter

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8
Q

peritubular capilaries surround

A

cortical segments of tubule

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9
Q

vasa recta surrounds

A

loop of henle

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10
Q

blood pathways

A
  1. efferent arteriole -> peritubular cap-> renal vein
  2. efferent art. -> vasa recta -> renal vein
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11
Q

three processes involved in urine production

A

glomerular filtration

tubular resorption

tubular secretion

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12
Q

___+_____+______= amount excreted

A

amount filtered + amount secreted - amount reabsorbed

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13
Q

filtered load

A

= “amount filtered”

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14
Q

glomerular filtration barrier needs to achieve=

A
  1. high H20 filtration rates
  2. nonrestricted passage of small/mid sized molecules
  3. total restriction of serum albumin, proteins and cells
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15
Q

layers of filtration membrane

A

endothelial cell

basement membrane

pedicels of podocytes/filtration slits with diaphragm

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16
Q

diaphragm between podocytes=

A

web of nephrin

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17
Q

what is freely filtered trough glom. filtration membrane

A

water

electrolytes

glucose

amino acids

urea

NOT big protiens and cells

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18
Q

osmolality of plasma and filtrate

A

300mOsm/kg

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19
Q

[Na+] in plasma and filtrate

A

both 140mEq/L

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20
Q

[glucose] in plasma and filtrate

A

100mg/dL

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21
Q

[albumin] in plasma and filtrate

A

plasma= 4mg/dL

filtrate= NONE

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22
Q

forces that affect filtration

A

starling forces= hydrostatic pressure oncotic pressure

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23
Q

filtration promoting forces

A
  1. Pgc - Glomerular capillary hydrostatic pressure
  2. π BS- colloid osmotic or oncotic pressure in bowman’s space (but this is practically zero…)
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24
Q

filtration opposing forces

A
  1. Pbs- hydrostatic pressure in bowman’s space
  2. πGC- glomerular capillary oncotic pressure = amount of proteins in plasma
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25
Q

net filtration pressure=

A

“ultrafiltration pressure” NFP = (+)Pgc - Pbs- πGC

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26
Q

filtration coefficient (Kf) determined by

A
  1. hydraulic permeability of the membrane
  2. surface area of the filtration membrane - both mainly change with disease
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27
Q

glomerular filtration rate =

(equation)

A

= Kf x NFP = (filtration coefficient) (net filtration pressure)

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28
Q

what makes glomerulus different than other capillary beds

A
  1. Kf is very high- lots of fenestrations ~20% of plasma flowing through is filtered
  2. low resistance in glomerulus, high P in glomerulus
  3. losing 20% of plasma increase πGC which would oppose filtration, but the high renal blood flow limits this
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29
Q

GFR=____ ml/min or ____L/day

A

amount of filtrate/min healthy = 125ml/min or 180L/day

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30
Q

healthy people control ___ to ∆ GFR

A

Pgc

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31
Q

pathologies affect ____ to ∆ GFR

A

Pbs πGC πBS

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32
Q

___ affect Pgc

A

Mean arteriole pressure

resistance at afferent and efferent arterioles

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33
Q

MAP decreases = Pgc____ and GFR___

A

Pgc decreases GFR decreases

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34
Q

afferent arteriole dilates = Pgc____ and GFR___

A

Pgc increases GFR increases

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35
Q

constrict aff. arteriole = GFR ___

A

decreases

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36
Q

eff. arteriole dilates = Pgc____ and GFR___

A

Pgc decreases GFR decreases

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37
Q

constrict aff. arteriole and eff. arteriole at the same time = GFR _____

A

GFR stays the same

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38
Q

plasma protein concentration increases = πGC____ GFR___

A

πGC increases GFR decreases

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39
Q

filtration membrane becomes more permeable = πBS____ GFR___

A

πBS increases GFR increases

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40
Q

kidney stone blocks a ureter = Pbs____ GFR____

A

Pubs increases GFR decreases

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41
Q

blood flow rates in

kidney cortex=

outer medulla=

inner medulla=

A

cortex= 4-5

outer medulla= 0.7-1

inner medulla=0.2-0.25

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42
Q

When mean arteriole blood pressure is between ____ the kidney can auto regulate it.

A

80 to 140mmHg

below range, then GFR is too low

above range, then glomerulus is damaged

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43
Q

two components of auto regulation

A
  1. myogenic response
  2. tubuloglomerular feedback
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44
Q

myogenic response

A

MAP increases (causes and increased RBF, Pgc, and GFR)

=stretches the afferent arteriole

=afferent arteriole then constricts which then decreases RBF, Pgc, and GFR

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45
Q

tubuloglomerular feedback

A

increased MAP

=transient increase in GFR

=increase NaCl delivery to macula densa

=release adenosine

=constricts afferent arteriole

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46
Q

small drop in MAP is dealt with by=

A

myogenic response and tubuloglomerular feedback =dilation of afferent arteriole

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47
Q

HUGE drop in MAP is dealt with by=

A

myogenic response and tubuloglomerular feedback

=dilates afferent arteriole BUT we’re out of auto regulation range… so our GFR and RBF and Pgc drop… yikes…

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48
Q

autonomic NS responds to HUGE drop in MAP by___

A

activating SNS = constricts afferent arteriole yikes!!

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49
Q

end results with HUGE decrease in MAP

A

decrease in perfusion pressure Pgc and GFR

+ autoregulation dilates aff. art.

+ SNS hugely constricts afferent arteriole (further decreasing Pgc and GFR)

=LARGE DECREASE IN PGC AND GFR

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50
Q

why does SNS constrict the aff. arteriole with huge drop in blood pressure

A

body’s trying to decrease renal blood flow so less blood goes to kidney so it can go to heart and brain

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51
Q

renal artery stenosis

A

decreased RBF, Pgc, GFR

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52
Q

auto regulatory response to renal artery stenosis

A

dilate the afferent arteriole AND constricts the efferent arteriole

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53
Q

efferent arteriole is constricted via___

A

RAAS

  • Juxtaglomerular cells =>renin
  • (+) angiotensin II which constricts eff. arteriole
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54
Q

NSAIDS effect

A

inhibits prostaglandins which normally dilate afferent arteriole

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55
Q

decreased effective circulating blood volume (heart failure) causes…

A
  1. (+) SNS = constrict afferent arteriole (alpha 1) and (+) B1 on JG to (+) RAAS
  2. (+) RAAS = constricts efferent arteriole

END RESULT= decreased RBF, but somewhat maintained GFR

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56
Q

large amounts of both NE and Ang II=

A

decreased RBF, but somewhat maintained GFR

=renal ischemia

=increased prostaglandin production

=dilate the afferent arteriole somewhat counteracts the decrease in RBF and prevents ischemia

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57
Q

why is it bad to take an NSAID if you have heart failure?

A

NSAIDS (-) prostaglandin aff. arteriole dilation which would increase GFR and RBF and therefore causes lower RBF and GFR which= ACUTE KIDNEY INJURY

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58
Q

Renal Clearance=

A

Volume of plasma cleared of a substance per unit time Volume/Time

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59
Q

Normal GFR=

A

125ml/min

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60
Q

A substance is filtered and reabsorbed but not secreted then its clearance is > GFR

A

LESS THAN

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61
Q

clearance = GFR then _____ reabsorption or secretion

A

no net

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62
Q

clearance > GFR then there has been net _____

A

secretion

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63
Q

clearance

A

reabsorption

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64
Q

p-aminohippurate (PAH)

A

-not endogenous -at low concentrations PAH is filtered, none is reabsorbed and the rest is secreted ∴ PAH is a measure of renal plasma flow

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65
Q

to measure GFR we need a substance that is ___

A

freely filtered not reabsorbed not secreted

66
Q

practically measure GFR via__-

A

creatinine clearance

67
Q

creatinine

A

=endogenous -end product of creatine metabolism -continuously exported to blood by skeletal muscle -freely filtered, not reabsorbed, only a small amount is secreted

68
Q

ways to measure creatinine

A
  1. 24hr urine collection 2. measure creatinine in serum = eGFR (“estimated” GFR)
69
Q

if your have higher serum creatinine your GFR is

A

lower than normal, bc you’re not clearing it from the blood

70
Q

how much urine is produced each day?

A

1 to 2 L

71
Q

what is reabsorbed

A

Water -up to 99%

Good solutes (ie. ions) -majority

Nutrients: glucose, AA - 100%

Urea- maybe half

72
Q

lipid soluble substances move across epithelial cells interstitial fluid by___ when___

A

diffusion only when there is a [] gradient

  • happens when H2O is reabsorbed urea follows water back into peritubular cap. when H2O is reabsorbed
73
Q

what is the osmolality of plasma, the filtrate entering the proximal tubule, and the surrounding interstitial fluid?

A

all the same 300mOsm/kg

74
Q

who de we get a concentration gradient for water

A

by resorbing Na+ via mediated transport

75
Q

mediated transport=

A

uses energy at some point

76
Q

draw how glucose is reabsorbed in the proximal tubule

A
77
Q

with the reabsorption of glucose what follows____

A

water via aquaporin-1

78
Q

movementof ions, glucose and water from interstitial space into peritubular capillary is via___

A

bulk flow

via starling forces

79
Q

how much glucose is reabsorbed in the proximal tubule?

A

all of it

80
Q

how does glucose end up in diabetic’s urine

A

the transport maximum of the glucose transporter is exceeded

81
Q

reabsorption of Na+ accomplishes…

A

1. reabsorption of solutes

glucose

amino acids

phosphate

water soluble vitamins

Cl- via leaky tight jxns.

2. reabsorption of H2O

3. reabsorption of urea

4. reabsorption of K+ and Ca2+

82
Q

glucose and amino acids are reabsorbed by primary or secondary active transport in the PCT?

A

secondary

83
Q

What is absorbed in PCt

A

65% of Na+

All the glucose

All the AA

65% of water

transport max of phosphate

lots of Cl-

most HCO3-

50% urea

65% K+

84
Q

beginig of PCT osmolality=

end of PCT osmolality=

A

both = 300mOsm/L

85
Q

what is reabsorbed in the loop of henle

A

Na+

K+

Ca2+

Mg2+

86
Q

what parts of the loop of henle are permeable to water

A

thin descending

-thick and thin ascending are impermeable

87
Q

thick/thin ascending limb have diffusion/active transport

A

thin=diffusion

thick =active

88
Q

draw reabsorption in the thick ascending limb

A
89
Q

reabsorption via the Na-K-2Cl cotransporter is considered ____ transport

A

secondary active transport

90
Q

efflux of K+ into the lumen and Cl- into the interstitum generates___

A

a positive transepithelial potential difference

=dirves the paracellurlar transport or resorption of positive ions

91
Q

___ of NaCl is reabsorbed in loop of henle

A

20%

92
Q

osmolality of the filtrate at the beginign and end of loop of henle

A

begining =300mOsm/L

end=100mOsm/L

we’re resorbing more solute water

=diluting urine

93
Q

resorption in DCT diagram

A
94
Q

what is resorbed in DCT

A

6%of NaCl

no mo H2O is resorbed and we’re taking out solute so

∴ urine becomes more dilute

95
Q

osmolality of DCT filtrate at begining and end

A

begining=100mOSm/L

end=80mOsm/L

96
Q

draw Collecting duct resorption and secretion

A

47

97
Q

aldosterone

function?

draw effects in CD

A

controls the amount of Na+ resorbed in the CD

98
Q

loop diuretic inhibits Na-K-2Cl cotransporter in the loop of henle ∴

Na+___

K+___

A
  • more Na+ int he tubule so when it hits the CD they you get more Na+ absorbed in CD
  • above causes more K+ secreted = hypokalemia
99
Q

thiazide diuretic inhibits the Na-Cl cotransporter in DCT

∴ Na+___

K+____

A

-more Na+ to CD = more Na+ is absorbed

=more K+ secreted= hypokalemia

100
Q

diuretic inhibits the Na+ channel in the CD

=Na+____

K+___

A

=decreased Na+ resorptin

=less K+ secreted

= hyper kalemia

101
Q

draw summary of where Na+ goes in nephron

A
102
Q

urine is more/less concentrated than plasm

A

less

103
Q

osmolality in different parts of the nephron

A

slide 4 of 22

104
Q

ADH function

A

puts H20 channels on CD

∴ if we want dilurte urine we want low ADH

105
Q

to prodce a concentrated urine we need:

A
  1. CD permeable to H2O

∴ high ADH

  1. interstitial fluid needs to be concentrated

= a large amout of H2O can be reabsorbed

106
Q

what makes the interstitial fluid around the CD concentrated?

A
  1. countercurrent multiplication
  2. countercurrent exchange
107
Q

counter current multiplication

diagram

A
108
Q

draw how ADH has effects in the CD

A
109
Q

without ADH we would produce ___ urine

A

dilute

about 50 mOsm/kg H2O

110
Q

with max ADH we would produce ___ urine

A

concentrated

about 1200 mOsm/kg H2O

111
Q

as filtrate goes down CD …

A

water is reabsorbed, and urine becomes more concentrated

-we can secrete urine anywhere from 50 to 1200 mOsm/kg H1O

112
Q

extra-cellurlar fluid volume

A

plasma=3.5L

itnerstitial fluid = 10.5 L

113
Q

intracellular fluid volume

A

=28L

114
Q

blood, interstitial and intracellular concentrations of

Na+

K+

protiens-

H20

A

diagram

115
Q

interstitial

A
116
Q

H20 in blood increases…

A

it shifts via osmosis form ECF to ICF to reach equillib

=cell swelling… lysis… death

117
Q

infuse person with 2L of H2O vs saline

A

H2O

Osmolality decreases (fatal)

volume of ICF increases

vol. ECF increases
vol. plasma increases

SALINE

Osmolality same

volume of ICF same

vol. ECF increases
vol. plasma increases

118
Q

a problem wiht osmolality (hyponatremia or hypernatremia) is a ___ problem

A

water

119
Q

a ∆ in ECF Na+ changes ___

A

blood volume and pressure

and NOT the Na+ concentration in the blood

120
Q

sources of water for the body

A

drinking

cellular metabolism

121
Q

how does the body lose water

A

skin (sweat)

lungs (evap.)

gi (feces)

kidney

122
Q

what organ regulates water loss

A

kidney

123
Q

what stimulates ADH

A

blood osmolality

124
Q

osmoreceptors sense increased plasma osmolarity…

A
  1. (+) thirst center
  2. (+) hypothalamic neurons

(+) ADH released from POSTERIOR pituitary

125
Q

lots of ADH = excrete ___ urine

little ADH = excrete ___ urine

A

lots of ADH = excrete small vol, concentrated urine

little ADH = excrete lots of dilute urine

126
Q

___ and ___ are main controllers of total body water and plasma osmolarity

A

ADH and thirst

127
Q

central diabetes insipidus

A

pituitary secretes too little ADH

-from head trauma/tumor/brain surgery

128
Q

nephrogenic diabetes insipidus

A

water channel on the nephron doesn’t work

  • from genetic mutation or lithium exposure
  • ADH levels will be appropriately high

bc blood osmolarity will be high

129
Q

with a large drop in BP we ___ ADH

A

increase

so to increase water resorption

(however arteriole constriction has the bigger effect)

130
Q

what takes presedence volume or osmolarity?

A

volume

-we will sacrifice osmolarity to increase blood volume

131
Q

with an high salt meal

A

total body [Na+] increases

ECF [Na+] stays the same (water shifts out of cells to compensate)

blood volume will be higher

132
Q

kidney knows total body Na+ is elevated by sensing___

A

the change in blood volume and pressure

133
Q

how does kidney regulate Na+ excretion?

A
  1. change the GFR to increase Na+ exretion

GFR is highly regulated so maybe not the best way

  1. Glomerulotubular balance
  2. RAAS (aldosterone increases Na+ abs. - opp of ANP)
  3. Atrial Natriuretic Peptide (ANP)
134
Q

Increaseing GFR’s effect on Na+ excretion=

=(“glomerulotubular balance”)

A

=more Na+ filtered

=more Na+ reabsorbed in PCT and loop of henle

∴ only 1-2% of extra Na+ is excreted

135
Q

draw juxtaglomerular apparatus

A
136
Q

Juxta glom. senses low Na+

A
  1. SNS senses low BP and volume

= (+) JGCs

=>RENIN

  1. macula densa senses less Na+ in DCT

(+) JGCs

=>RENIN

137
Q

renin as an enzyme pathway

A

diagram

138
Q

what will lower total body Na+ and blood pressure

A
  1. raise GFR
  2. inhibit RAS
  3. (+) ANP
139
Q

ANP

A

when blood volume increases atria stretch

= (+) ANP release

=inhibits Na+ resorption in tubules and increases GFR

140
Q

what controls K+ balance

A
  • shifting K+ either into or out of cells
  • cortical collecting duct
  • aldosterone
141
Q

normal Na+ and K+ levels

A

Na+ = 135 to 145 mEq/L

K+ =3. 5 to 5 mEq/L

142
Q

if hyperkalemic

A

insulin and epinephrine shift into skeletal muscle cell

143
Q

draw where K is moving in the nephron

A
144
Q

draw K+ excretion in CD

A
145
Q

draw aldosterone and K+ in CD

A
146
Q

Where do we get acids from?

How do we get rid of them?

A

1. CO2

2. nonvolatile acids

CO2 + H2O ⇔ H2CO3 ⇔ H+ + HCO3-

Metabolism generates CO2

Breathing eliminates CO2

147
Q

when tissues produce more CO2 blood pH is not altered because…

A

we increase RR

148
Q

nonvolatile acids

A

=any other acid other than CO2 (carbonic acid)

DONT MEMORIZE THIS LIST

=lactic acid

acetoacetic acid

ß-hydorxybutyric acid

phosphoric acid

sulfuric acid

149
Q

how do we use non volatile acids?

A

-converted to HCO3-

∴ consumes H+

150
Q

How does the body deal with this excess acid rom metabolism that generates novolatile acids?

A
  1. H+ is buffered by HCO3-, protien or PO3-
  2. Respiration
  3. Renal
151
Q

how fast does the respiratory rate to an increase in nonvolatile acids occur?

A

quickly … but this fix is limited so we need kidneys

(generally lung responds quickly and kidneys respond slowly)

152
Q

How does kidney respond to increased H+?

A
  1. reabsorption of HCO3- in PCT
  2. production of new HCO3- in nephron
    - coupled ot the excretion of H+
153
Q

producing a dilute urine is controled more by ___

producing a concentrated urine is controled more by ____

A

producing a dilute urine is controled more by loop of henle

producing a concentrated urine is controled more by CD

154
Q

draw two pathways of making new HCO3- in nephron

A

insert diagram 16 and 17/33

155
Q

renal response to an increase in non-volatile acids is fast/slow

A

slow… days

156
Q

what is respiratory vs. metabolic acidosis or alkylosis?

A

respiratory= acid base disorder from a mismatch in CO2 production and ventilation

-primary disorder is from a respiratory problem

metabolic= any base distrubance where the primary disorder is not from a respiratory problem

157
Q

patient has ketoacidosis, but a blood pH test says they’re in normal range… do they still have acidocis

A

YES

YOU HAVE TO LOOK AT THE WHOLE PICTURE!

-underlying problem is still around even though he’s in a normal range

158
Q

3 main causes of metabolic acidosis

A
  1. diabetic ketoacidosis

(ketone body acids)

  1. kidney failure

(incresased loss of bicarb, decrease excretion of ammonium and titratable acids)

  1. diarrhea

(loss of bicarb)

159
Q

hypoventialation/hyperventilation cause respiratory acidosis/alkalosis

A

hypo- acidosis

hyper- alkalosis

160
Q

how does body deal with respiratory acidosis or alkalosis?

A

kidneys!

resorb or excrete HCO3- and titratible acids

161
Q

vomiting induced acid-base disorder= metabolic/respiratory acidosis/alkalosis

A

metabolic alkalosis

-can also be caused by too many antacids…

162
Q
A

Pathophys (3 decks)

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