module 2- renal Flashcards

1
Q

what is the job of the kidneys?

A

filter toxins out of the blood, maintains homeostasis even when several liquids are entering your body

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2
Q

what are 3 things kidneys regulate?

A

electrolytes, water balance, pH

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3
Q

7 functions of the kidney

A

1) regulate electrolytes
2) regulate water balance
3) maintain pH
4) excrete metabolic waste
5) excrete foreign compounds
6) secrete hormones
7) convert vitamin D into active form

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4
Q

why do we need to excrete wastes?

A

so it does not accumulate & become toxic

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5
Q

what 2 hormones are secreted by the kidneys

A

erythropoietin & renin

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6
Q

kidneys are located

A

retroperitoneal on back (stuck to body wall, not free)

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7
Q

ureter

A

collecting tube that takes urine to bladder

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8
Q

what is the functional unit of the kidney

A

nephron

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9
Q

3 kidney layers

A

1) renal hilus: inside
2) renal medulla: middle
3) renal cortex: outside

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10
Q

horse vs dog vs cow kidney shape

A

horse: heart
cow: lobulated cortex
dog: bean shape

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11
Q

2 parts of the nephron

A

vascular & tubular

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12
Q

vascular vs tubular

A

v: blood containing portion
t: urine/filtrate containing portion

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13
Q

what % of cardiac output goes straight to the kidneys?

A

20

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14
Q

pathway of bloodflow to the kidneys

A

renal artery -> smaller arteries -> afferent arteriole -> glomerulus

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15
Q

afferent arteriole

A

head of the nephron

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16
Q

glomerulus

A

seam where 1st level filtration occurs

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17
Q

pathway of filtration

A

efferent arteriole -> peritubular capillaries -> renal vein

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18
Q

what capillary is like meshwork

A

pertitubular

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19
Q

pathway of filtrate through the kidneys

A

bowmans capsule -> proximal tubule -> loop of henle -> distal tubule -> collecting duct

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20
Q

T or F: loop of henle always dips into the medulla

A

T

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21
Q

medulla is always on the ( ) & cortex is on ( )

A

bottom, top

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22
Q

2 types of nephrons

A

cortical & juxtamedullary

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23
Q

afferent vs efferent

A

a- blood comes in (arrives)
e- blood comes out (exits)

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24
Q

macula densea cells

A

monitors fluid

too much= stops
too low= sends signal to increase

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25
Q

difference between cortical & juxtamedullary nephrons

A

c- located in the cortex, dips slightly into medulla

j- bowmans capulse in the cortex, loop of henle extends deeply into medulla

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26
Q

3 steps to urine formation

A

1) filtration
2) tubular reabsorption
3) tubular secretion

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27
Q

where does filtration occur

A

glomerulus

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28
Q

things that get reabsorbed

A

glucose, amino acids

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29
Q

pathway of filtration

A

afferent arteriole -> filtrate into blood -> secretion from blood to fluid

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30
Q

the sieve is part of ( ) and it contains 3 layers:

A

glomerular filtration

endothelium, basement membrane, podocytes

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31
Q

basement membrane

A

negatively charged membrane that repels negatively charged things & lets in positively charged

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32
Q

what are podocytes & how do they work

A

prevent plasma proteins from being filtrated

if contracted, they flatten & slits between them become smaller to block off entrance

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33
Q

what are 3 things that are filtered out vs not filtered

A

filtered- plasma, electrolytes & small peptides

not filtered- plasma proteins, red/white blood cells & platelets

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34
Q

T or F: urine is protein free

A

T

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35
Q

what does it mean if there is very little to a lot of protein in urine

A

little- exercise pushed a bit of albumin in
lots: kidney damage

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36
Q

do large or small molecules end up in the filtrate? why?

A

small bc large are too big to be filtered

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37
Q

capillary blood pressure favours

A

filtration

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38
Q

what controls how much blood enters the kidneys

A

the diameter of the arterioles

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39
Q

(more/less) pressure is easier for molecules to be filtered

A

more

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40
Q

how to increase bloodflow to the kidneys

A

dilate afferent arteriole & increase pressure

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41
Q

2 filtration forces

A

plasma-colliod pressure & bowmans capsule hydrostatic pressure

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42
Q

plasma colloid osmotic pressure

A

opposes filtration of plasma, higher concentration (less fluid) inside = water moves in

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43
Q

bowmans capsule hydrostatic pressure

A

opposes filtration of plasma, accumulation of water = pressure increases & causes backflow

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44
Q

net filtration pressure is

A

10mmHg (low)

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45
Q

kidney stone

A

pressure in capsule increases = decrease in filtration

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46
Q

burned victims

A

loss of plasma protein = less pressure = increase in filtration

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47
Q

GFR

A

glomerular filtration rate

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48
Q

GFR equation

A

GFR= net filtration pressure by Kf

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49
Q

kf

A

filtration coefficient, how much surface is available for filtering the glomerulus

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50
Q

increase in filtration pressure = ( ) of GFR

A

increase

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51
Q

how much filtrate is produced in your kidneys every day?

A

180L

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52
Q

how much pee is produced per day?

A

1.5-2L

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53
Q

T or F: cats/dogs filtration fraction is higher than humans but lower in goats

A

T

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54
Q

2 primary autoregulation mechanisms

A

myogenic & tubuloglomerular feedback

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55
Q

myogenic stretch mechanism

A

too much pressure = vasoconstriction
too little pressure = vasodilation

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56
Q

granular cells

A

sit on side of afferent artery & cause mascula cells to send signals to dilate/constrict arterioles

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57
Q

tubuloglomerular feedback/juxtoglomerular apparatus

A

monitors flow

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58
Q

kidney failure low GFR vs high GFR

A

low- kidneys do not excrete enough = accumulation of toxins in body

high- kidneys are losing water & solutes to urine

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59
Q

extrinsic (sympathetic) nervous control of GRF

A

1) increase sodium to get better water retention after blood loss

2) podocytes

3) baroreceptor reflex

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60
Q

baroreceptor reflex

A

long term correction of BP

decrease in BP = increase in SNS activity = vasoconstrict to conserve salt = causes increase in BP b/c you are not losing the water

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61
Q

T or F: SNS signals are local

A

F, they control entire body

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62
Q

what are 2 ways the body regulates GFR?

A

autoregulation-myogenic & juxo
sympathetic innervation

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63
Q

where are fluid/solutes reabsorbed

A

tubular portion of nephron

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64
Q

T or F: reabsorption is a highly selective process

A

T

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65
Q

how does fluid get reabsorbed?

A

solutes must pass through tubule cells b/c of tight cell junctions

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66
Q

sodium reabsorption

A

uses a pump to push Na out & decrease concentration of Na inside the cell = follows concentration gradient & balances things out

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67
Q

what is the main motor or reabsorption

A

sodium

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68
Q

T or F: sodium reabsorption is active

A

T

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69
Q

Na cotransporter

A

moves Na from lumen to cell and transports glucose, AA & phosphate to be reabsorbed

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70
Q

Na cotransporter vs Na/H antitransporter

A

c- lumen -> cell
a- cell -> lumen (1 H leaves per 1 Na entering)

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71
Q

secondary active transport only relies on ( ) as energy

A

sodium gradient

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72
Q

where is 65% of filtered out sodium reabsorbed? where is the rest?

A

proximal tubule, loop of henle & collecting duct

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73
Q

what 2 hormones control some of the Na reabsorption

A

aldosterone & ANP

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74
Q

RAAS signalling

A

renin-angiotension-aldosterone system

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75
Q

RAAS signalling goal

A

increase Na and water retention, and increase BP

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76
Q

Renin

A

enzyme that helps control blood pressure & maintains levels of Na & K

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77
Q

if BP is too low/high what hormones are released in RAAS signalling system?

A

low=renin
high=ANP

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78
Q

ANP

A

atrial natriuretic peptide

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79
Q

when is renin released?

A

low Na, low BP & SNS activation

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80
Q

4 steps of RAAS

A

1) renin or ANP is released
2) angiotension -> angiotension I
3) angiotension I -> angiotension II
4) angiotension stimulates release of aldosterone by adrenal glands

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81
Q

lungs contain a lot of

A

ACE: angiotensin converting enzyme

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82
Q

effects of angiotension II on kidneys

A

vasocontriction & sodium reabsorption

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83
Q

effects of angiotension of body

A

vasoconstriction, increased BP & ADH

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84
Q

ADH

A

antidiuretic hormone

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85
Q

when cells detect aldosterone, ( ) cells increase reabsorption of NA

A

principal

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86
Q

what does aldosterone excrete more of when controlling NA reabsorption

A

K+

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87
Q

ANP net effect

A

decrease blood pressure

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88
Q

where is ANP secreted

A

cardiac smooth muscle

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89
Q

ANP causes ( ) of afferent arteriole to lower BP

A

dilation

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90
Q

all waste products but ( ) are not reabsorbed

A

urea

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91
Q

maximal tubular transport

A

not all solutes can be reabsorbed from the tubule b/c there are not enough transporters

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92
Q

renal threshold

A

max concentration of solute in the plasma that can be completely reabsorbed from filtrate into the tubule

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93
Q

filtrate solute load equation

A

= plasma [solute] x GFR

94
Q

diabetes mellitus

A

not enough transporters for glucose so glucose is lost in urine = sweet smell

95
Q

normal Tm is

A

<1.75mmol

96
Q

Tm

A

max amount of solute that can be reabsorbed

97
Q

how do we secrete things that cannot be filtered at the glomerulus?

A

secrete into tubule from peritubular capillaries

98
Q

what ion is always reabsorbed into the proximal tubule

A

K+

99
Q

if K+ is lost what is caused

A

hypokalemia

100
Q

acidosis

A

when Na is brought in & takes H out instead of K

101
Q

hyperkalemia

A

too much K+ retention

102
Q

what is secreted/what is by-product of tubular secretion

A

H- secreted
Na- by-product

103
Q

renal clearance calculation

A

[solute in urine] x urine flow / [solute in plasma]

104
Q

renal clearance measures

A

how much plasma volume is cleaned of a certain solute per unit of time

105
Q

T or F: renal clearance measures amount of solute removed

A

F

106
Q

how do dessert animals urine concentration work?

A

if no access to water = do not want to lose water = concentrate the urine

107
Q

the osmotic gradient of the kidney is

A

ECF

108
Q

medulla gets more ( ) as you get deeper into the medulla

A

hypertonic

109
Q

hypertonic areas require (more/less) energy to maintain gradient

A

more

110
Q

descending loop of henle

A

water is pulled from the tubule, and urine is more concentrated

111
Q

ascending loop of henle

A

urine becomes hypotonic by pumping out salt but not water

112
Q

3 benefits of counter current flow through loop of henle

A

hypertonic urine, hypotonic urine & osmotic gradient formation

allows control of water

113
Q

where is there dilute urine found in the loop of henle

A

top curve

114
Q

2 ways osmotic gradient is established

A

1) selective water permeability in tubule
2) selection ion transport in tubule

115
Q

maintaince of gradient

A

water gets sucked out on the way down and salt gets sucked out on the way up

116
Q

what ion follows Na when it gets pumped out

A

CI

117
Q

where does control of water occur

A

distal & proximal tubule

118
Q

T or F: distal & collecting duct are not naturally permeable to water

A

T

119
Q

how much fluid still remains after the distal nephron

A

20%. = 36L

120
Q

how do we absorb the remaining 20% of water?

A

use ADH to bind to V2 receptors on collecting duct principal cells & stimulates vesicles to unload aquaporins so the remaining water can be reabsorbed

121
Q

how do diuretics work?

A

block V2 receptors = pee more = less volume in body = BP decreases

122
Q

T or F: collecting duct is used for water reabsorption regulation

A

F

123
Q

where is collecting duct found

A

proximal tubule of loop of henle

124
Q

what occurs if no ADH is released vs it is released?

A

not released: distal & collecting tubes are impermeable to water and large volume of urine is super dilute b/c no water was reabsorbed, it all goes out in the urine

if released: distal & collecting tubes are permeable to water and small volume os urine is very concentrated b/c water was reabsorbed in the body

125
Q

ADH causes ( ) urination b/c it ( ) water in the body

A

less, keeps

126
Q

vasopressin/ADH ( ) BP

A

increases

127
Q

where is ADH/vasopressin released

A

posterior pituitary gland

128
Q

ADH release is controlled by what 3 ways

A

1) hypothalamic osmoreceptors
2) baroreceptors- sense drop in BP
3) angiotension II - sense drop in BP

129
Q

how to fix a drop in BP?

A

release ADH to put more fluid in circulatory system

130
Q

released of ADH is inhibited by what 2 things

A

1) low plasma osmolarity
2) alcohol/caffeine

131
Q

how does alcohol/caffeine inhibit ADH?

A

blocks ADH = increase water excretion b/c no pull back of water occuring

132
Q

how can ADH inhibition be overcome?

A

sleep and exercise- concentrate urine b/c do not pee during these states

133
Q

hypotonic urine in relation to ADH

A

high volume of dilute urine b/c ADH has been blocked so you pee out the water your body has not absorbed

134
Q

hypertonic urine in relation to ADH

A

max ADH response, small volume of concentrated urine produced when dehydrated b/c body is trying to conserve water

135
Q

diabetes insipitus

A

large amount of dilute urine b/c body is constantly getting rid of water via urine

136
Q

2 causes of diabetes insipitus

A

1) pituitary tumor- brain is not able to release ADH
2) kidneys cannot respond to ADH

137
Q

symptoms of diabetes insipitus

A

pee more, dilute urine, tired

138
Q

maximum urine osmolarity is based on ( ) in animals

A

aridity index- how dry the environment

139
Q

wet vs dry environment effect on kidneys in animals

A

wet- lower urine concentration b/c lots of water available to drink

dry- small concentrated urine b/c little water available to drink = trying to conserve water inside so none is being lost via urine

140
Q

what do longer loops of henle allow?

A

higher ability to concentrate urine b/c medulla is long & deep

141
Q

concentration of medulla is proportionate to what?

A

depth of medulla

142
Q

shallow cortex in animals = ( ) medulla

A

deeper medulla = longer loop of henle = concentrated urine

143
Q

T or F: all mammal plasma osmolarity is the same

A

T

144
Q

what does a higher medulla-cortex ratio mean?

A

deeper medulla compared to the cortex = more concentrated urine

145
Q

why is urine yellow?

A

b/c of urobilin

146
Q

what is urobilin

A

bilirubin metabolite

147
Q

why would urine be red or brown?

A

red- RBC from after the kidneys
brown- hemoglobin from filtration issues

148
Q

T or F: urine should be sterile (no microbes)

A

T

149
Q

why does urine smell like asparagus

A

b/c of microalbuminuria protein

150
Q

kidney stones

A

mineral crystals such as phosphate or oxalate crystals

151
Q

struvite

A

magnesium ammonium phosphate

152
Q

how to get rid of kidney stones

A

drink lots of water

153
Q

uric acid stone vs gout

A

uric- due to lots of meat/protein
gout: uric acid crystals formed in joints

154
Q

kidney stones may precipitate out of urine & cause pain if

A

mineral concentration in urine is too high

155
Q

urine pH in carnivores vs herbivores?

A

C- acidic b/c amino acids in meat
H- alkaline

156
Q

high pH = ( ) precipitation of minerals

A

higher

157
Q

what may cause variation in urine composition

A

urine pH changes, species, animal condition

158
Q

large kidney reserve pro & con

A

can donate kidney, but do not see clinical signs right away

159
Q

how does anti-freeze cause renal disease

A

forms oxalate crystals in the kidney = causes acute kidney damage /failure

160
Q

2 main concerns of kidney disease

A

1) decreased ability to concentrate urine
2) decreased waste removal from plasma b/c of decrease in GFR

161
Q

azotemia

A

increase of ammonia & other nitrogenous compounds in blood = ulcers, vomiting, depression

162
Q

3 other causes of kidney dysfunction

A

metabolic acidosis, hyperkalemia & anemia

163
Q

metabolic acidosis

A

H accumulates in blood = lower pH = acidic blood = metabolic problems

164
Q

hyperkalemia

A

dysfunctional hydrogen potassium exchanger causes excess H and K

165
Q

hypoproteinemia

A

proteins are filtered out= low protein in blood = more protein in urine

166
Q

anemia

A

decrease in erythropoietin = less RBC production

167
Q

dialysis

A

artificial filtering of blood

168
Q

hemodialysis

A

waste diffuses out of blood & clean blood gets pumped back into the patient

169
Q

dialysis pathway

A

blood comes out from patient -> pumps through system -> blood goes into membrane -? dialysate fluid goes through gradient & discared -> clean blood is pumped back into patient

170
Q

dialysate

A

isotonic solution with no waste products

171
Q

peritoneal dialysis

A

use peritoneal as semi-permeable membrane & empty several liters of dialysis solution

172
Q

T or F: peritoneal dialysis is less efficient than hemodialysis

A

T

173
Q

UTI

A

bad bacteria travels up urethra & settles

174
Q

UTI treatment

A

promote hydration, antibiotics & azo

175
Q

how does cranberry juice interact with UTI

A

an active ingredient in this juice reduces adherence of bacteria to bladder wall, only helps with prevention, does not help once a UTI is formed

176
Q

how does azo work for UTI

A

dye that turns urine orange & reduces pain while antibiotics have a chance to work

177
Q

urinary tract blockage

A

plugs up urethra so urine cannot be excreted = urine accumulates = bladder bursts or backs up into kidney = hyperkalemia

178
Q

autoimmune kidney disease

A

antibodies attack the glomeruls = no filtrate gets through = increase blood flow to functional nephrons = pressure increases

179
Q

ethylene glycol

A

metabolized by AD & produces metabolite called oxalic acid = binds to Ca & produces crystals = plug up renal tubules

180
Q

what de-activates AD for treatment of antifreeze?

A

4-MP and ethanol- outcompetes ethylene glycol for AD = flush it out of system

181
Q

acid vs base

A

acid- donates H
base- accepts H

182
Q

pH of venous vs arterial blood

A

A- 7.45
V- 7.35

183
Q

acidosis vs alkalosis

A

acid- blood pH falls below 7.35
alka- blood pH is greater than 7.45

184
Q

how to fix acidosis

A

increase respiration to eliminate excess H

185
Q

what can pH changes do to proteins?

A

denature proteins = ions can no longer get through specific channels = disruption of nerve/muscle conduction

186
Q

acidosis

A

drop in pH that depresses the CNS due to decrease in Ca = no AP

187
Q

T or F: acidosis can lead to a coma

A

T

188
Q

diabetic coma

A

due to ketoacidosis- brain switches to acidic ketone bodies

189
Q

diarrhea from acidosis

A

secretions from pancreas & bile = loss of bicarbonate = accumulation of H = acidosis

190
Q

alkalosis

A

increased blood pH, increased Ca, increased K

afferent- pins/needles
efferent- muscle twitches

191
Q

why does acid-base status matter?

A

potassium homeostasis & H concentration

192
Q

3 primary mechanisms of acid production

A

1) carbonic acid formation
2) nutrient breakdown- inorganic acids
3) metabolism- organic acids

193
Q

henderson hasselblach equation

A

pH = pK + log [base]/[acid]

194
Q

breakdown of acids vs bases

A

acids- meats = increase H
bases- fruits/vegetables = decrease H

195
Q

fat metabolism

A

triglycerides converted to long chain FA

196
Q

3 types of metabolism of organic acids

A

fat metabolism, fermentation, anaerobic

197
Q

fermentation

A

short chain FA produced by rumen & absorbed in bloodstream

198
Q

anaerobic metabolism causes

A

lactic acid production

199
Q

3 controls of acid-base status

A

1) chemical buffers
2) respiratory compensation
3) metabolic (renal) compensation

200
Q

what is the ratio for bicarbonate to H

A

20:1

201
Q

T or F: bicarbonate cannot be used to drive the equation backwards

A

T

202
Q

pK of bicarbonate

A

6.1

203
Q

build up CO2 causes bicarb to H ratio to change to

A

21:2

204
Q

protein buffer system

A

amino acids in proteins can accept or donate H

205
Q

protein vs carbonate buffer locations

A

proteins = ICF buffer
carbonate = ECF buffer

206
Q

hemoglobin buffer system

A

de-oxygenated hemoglobin has a greater affinity for H than oxygenated hemoglobin

allows H to be bound not free floating = maintains & buffers pH

207
Q

phosphate buffer system

A

ICF & urinary buffer system

phosphate can bind H = more H umped out in urine = good

208
Q

peripheral chemoreceptors detect H concentration in ( ) and central chemoreceptors detect H concentration in ( )

A

arterial blood, brain

209
Q

what occurs when central chemoreceptors detect H in the brain?

A

signals respiratory centre to breathe more to bring in more CO2 & exhale H

210
Q

when H decreases, receptors will cause a ( ) in ventilation so CO2 can ( )

A

decrease, build up

211
Q

when does respiratory compensation kick in?

A

when chemical buffers are not sufficient

212
Q

2 limitations of respiratory compensation

A

1) cannot fully correct it, just minimize
2) cannot compensate for respiratory induced acid-based problems

213
Q

what is the 3rd line of defence for acid-base disturbances? what does it do?

A

kidneys- takes excess things in the blood & put into urine and reabsorb what we need from the urine & put it back in the blood

214
Q

hydrogen potassium exchangers

A

move 1 H out & 1 K in

215
Q

T or F: kidneys can regulate bicarb excretion

A

T

216
Q

kidney reabsorption of bicarbonate

A

bicarb must form CO2 to diffuse bc it is negatively charged molecule & cannot diffuse across the cell

217
Q

during alkalosis, bicarb is ( ) in the urine

A

stuck

218
Q

what occurs if blood pH drops below 4.5

A

transporters cannot function

219
Q

how to increase H secretion during acidosis

A

phosphate buffers = soak up excess H so more can be secreted

220
Q

what is the 1st buffer in urine?

A

phosphate, and then ammonia

221
Q

metabolic acidosis is fixed via

A

respiratory alkalosis

222
Q

what is hypoventilation & how is it fixed?

A

PCO2 increases = H increase = acidosis

compensate with metabolic alkalosis

223
Q

respiratory alkalosis is caused by

A

hyperventilation

224
Q

what is hyperventilation

A

blowing off too much CO2 = PCO2 drops = H drops

225
Q

normal [HCO3] in blood is (). what happens if it is over or under that?

A

24 mEq/L, metabolic acidosis if over and metabolic alkalosis if under

226
Q

metabolic acidosis from gain of acid causes

A

1) diabetes- ketone bodies
2) animals in negative energy balance = uses ketone bodies
3) anaerobic metabolism = lactic acid production
4) grain overload = VFA increase = drops pH
5) uremia

227
Q

uremia

A

cannot secrete H & reabsorb bicarb

228
Q

metabolic acidosis causes from a loss of bicarb

A

diarrhea = fast = cannot absorb bicarb

229
Q

metabolic alkalosis cause from a loss of H in body

A

severe vomiting = loss of H

230
Q

metabolic alkalosis cause from a trap of H in GI tract

A

twisted abomasum=cuts off blood supply = H is not reabsorbed

231
Q

metabolic alkalosis cause from a gain of bicarb

A

too many antacids