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A+P 211 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

excretory system fun

A 
excretion
EPO secretion
detoxification
fluid regulation
waste reduction
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2
Q

excretion

A

blood filtration
materials filtered out and added back in
secretion and reabsorp
fluid and electro. regulation

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3
Q

EPO secretion

A

Erythropoietin
stim by low O2
inc RBC production

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4
Q

fluid regulation

A 
controlled by plasma vol and osmolarity
    affects BP and h2o vol
electrolyte balance
   rate of excretion
blood pH
  H and HCO3
nutrient conservation
    glucose and aa
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5
Q

waste elimination (N base)

A

ammonia into urea cycle
converted to uric acid or creatine
uric- non-toxic
creati- product of muscle metab

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6
Q

kidneys

A

produce urine

filter fluid

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7
Q

ureters

A

drain kidneys

urine to bladder

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8
Q

urinary bladder

A

hold urine before elimin

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9
Q

urethra

A

urine excretion

diff for e/ sex

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10
Q

renal capscule

A

outermost protective coating

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11
Q

renal cortex

A

space btw capsule and medulla

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12
Q

renal medulla

A

house renal columns and pyramids

as inc depth = in O2 conc

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13
Q

renal arteries

A

blood to kidney of abd aorta

incl afferent and efferent arteries

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14
Q

afferent artery

A

blood to glomerular

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15
Q

efferent artery

A

away from golmerular
control GFR by NaCl conce
drain into peritublar cap and renal v

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16
Q

renal v

A

collect blood from interlobar, arcuate and cortical radiate arteries
transport blood to infer. vena cava
blood filtered and has less waste
carry hormones

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17
Q

nephrons

A

renal functional unit
open 2 external world
houses tubules

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18
Q

tubules

A 
exchange waste w/ external environ
highly vasc
     inc. peritub cap
     eff and aff arterioles
function in circ and excret exchange
large SA for exchange
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19
Q

glomerulus

A

blood in by filtration
ball of cap
surr by glomerular capsule

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20
Q

flow materials through tubular system

A

glomerular (filtration)
proximal conv. tubule (bulk, unreg. absorp)
Henle loop (water absorp)
distal conv. tubule (regulation secretions and reabsorb)
collecting duct (urine transport)

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21
Q

renal corpuscle

A

area btw circ and excret
inc glomerular and glomerular capsule
fun- filtration

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22
Q

corpuscle histology

A

collection of tissues
inc. glomerular capsule
lined w/ par visceral epithe
incl podocytes and mesengial cells

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23
Q

podocyte fun

A

in glomerular caps
have filtration slits
control flow mat in and out

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24
Q

mesengial cell fun

A

in glomerular cap
alter cell v w/ contractile properties
reg. blood flow
mostly remove debris from basement mem.

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25
Q

proximal conv. tub

A

cubit. epith w/ microvilli

unreg. bulk reabsorb

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26
Q

loop of henle (nephron)

A 
ascending and descending
descending- thin mem 
easy H2O mvmnt in and out (mostly out)
ascending limb- thick mem
hard for H2O leave once get in
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27
Q

distal convoluted tubule

A

reduced absorb no microvilli
cubital epith
regul secretions and reab

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28
Q

distal conv tub and interaction w/ glomerular

A

macula densa cells react to changing NaCl levels and indicate GFR

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29
Q

juntaglomerular apparatus

A

reg. nephron act w/ macula densa and junxtaglom cells
act as physiological check
(Tubuloglomerular Feedback)

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30
Q

collecting duct

A

cubit epith
incl papill. ducts (column epith)/ aquaporins
alter amnt fluid reabsor by kidneys

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31
Q

dec urine v

A

inc. urine concentration

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32
Q

nephron types

A 
cortical N
barely discend into medulla
junxtaglomerular N
deep into medulla
point- more efficient absorp and better use volume
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33
Q

filtration

*location + process

A

location- glom and glom capsule
filt slits in glom capsule w/ podocytes
act as fenestrated cap
filtrate everything besides RBC and large proteins

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34
Q

Materials into filtrate

A

not RBC and proteins
in- glucose, elec, fatty a, urea, creatine, uric acid, H2O
only select few reabsorb

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35
Q

filtration p

A

hydrostatic and osmotic

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36
Q

hydrostatic p

A

Glomerular BHP

Capsular HP

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37
Q

glomerular BHP

A 
favors filt
circ to exre
high bp = high BHP
low bp = low BHP
materials out circ enter capsular
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38
Q

capsular HP

A

opposes filt
lrg vol and sm hole = inc P
takes long time reach proximal convolu tubule
H2O pools

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39
Q

Osmotic p

A

BCOP

capsular colloid osmotic p

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40
Q

BCOP

A

opposes filt
excret to circ
reabsorb

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41
Q

capsular COP

A

favors filt
circ to excre
usually 0
fluid moves at same rate

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42
Q

net filtration P

A 
NFP= hydrostatic- osmotic
NFP= (GBHP-CHP)- BCOP
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43
Q

glomerular filtration rate- values

A

min vol filtration
125ml/min
if below = kid not functioning
if above= kid overtaxed (break cap)

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44
Q

GFR %

A

determines amount of plasma filtered

if 20%- other 80 reverted back to efferent arteriole and peritubular capillary

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45
Q

autoregulation

A

local
inc or dec afferent arteriole diam.
myogenic mechanism (BP)
tuboglomerular feedback (Na conc)

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46
Q

myogenic mechanism

A 
regulate absorption in nephron
stim- changes local BP
high bp= high P in afferent a
   vasoconstriction, dec v blood in aff a
low bp = dilation
     blood flow inc, bp inc
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47
Q

tuboglomerular feedback

A 
regulate absorption in nephron
macula densa cells
osmasensors
na inc, dia dec
na dec, dia inc
found in distal conv tubule
inc amnt Na in DCT
   kid overtax
   fast GFR, not enough time for absorp
    dec. GFR 
          constrict affe. a
                 inc Na absorb = inc time
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48
Q

sympathetic stim

A 
regulate absorption in nephron
inc w/ stress
vasocontriction of aff a
dec GFR
good- reserve Na and Cl and H20
bad- renal failure (build up of urea)
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49
Q

systemic regulation

A

regulate absorption in nephron
hormone controlled
renin-angiotension-aldosterone system (RAAS)

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50
Q

RAAS

A

stim- low BP
recog by carotid and aortic sinus (baroreceptors)
activate sympathetic stim
produces renin
secreted by junxtaglom. or granular cells

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51
Q

renin

A

enzyme

angiotensinogen to angiotensin 1 (made by liver)

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52
Q

angiotension 1

A

act. by ACE angiotension converting enzyme to angiotension 2
in lungs

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53
Q

angiotension 2 pathways

A

cause eff. constriction
aldosterone production
inc. thirst (act. hypothal)
inc. vasoconstriction

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54
Q

angiotension and aldosteron

A 
enters adrenal glands
inc BP, inc GFR
aldosterone secreted
    kidneys uptake Na and H2o
      inc v = inc BP
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55
Q

angiotension and vasoconstic

A

dec v = inc BP

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56
Q

angiotension and thirst

A

act hypothal
intake fluid
inc v = inc bp

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57
Q

angiotension and eff. constriction

A

efferent blood away from kidney
like kinking hose
builds p = inc GFR

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58
Q

relationship btw BP and GFR

A

inc blood flow = inc bp= inc GFR
dec blood flow= dec bp= dec GFR
dec urine production
renin produced by cells in junxta apparatus

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59
Q

stim ways of renin production

A

sympathetic stim

dec GFR

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60
Q

locations of filtration, reabsorption, and secretion

A

filtration- glomerular, circ to tubules
reabsorption- tubules to circ and back if needed
secretion- circ to tubules

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61
Q

transcellular transport

A

facilitated diff- down conc gradient , large mol
active transport- primary and secondary
primar- against conc grad. (need ATP)
second- up and down conc. gradient
powered by Na/K pump and glucose pump

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62
Q

paracellular transport

A

mat flow along conc gradient btw cells
attraction= solvent drag
Na pumped out and h2o follows (carrying o/ solv)
circ absorbs tubule fluid

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63
Q

fun proximal convoluted tubule

A

bulk, unreg. h2o reabsorption
60-70%
unreg= automatically, no ATP needed

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64
Q

proximal convoluted tubule- tubular reabsorp (NaCl) membranes

A

apical and basal mem
apical= thru tubule cells into fluid
basal= into circ system frm fluid

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65
Q

proximal convoluted tubule- tubular reabsorp (NaCl)- APICAL

A 
nephron fluid into tubules
transported w/ 
symports ex. Na cotransp and gluco
Na-H antiports
     trade Na in and H out
     reduce acidity
Cl-anion symport
       Cl in, anions out
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66
Q

proximal convoluted tubule- tubular reabsorp (NaCl)- BASAL

A 
tubular cells to circ system
Na/K pump
K/Cl symports
inc Na conc in circ system
     H2O reabsorbed
          brings o/ solutes w/
paracellular route
        Na in circ system creates conc grad. for H2O
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67
Q

proximal convoluted tubule- tubular reabsorp (Mg, Ca P)

A

paracellular

solvent drag created by NaCl

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68
Q

proximal convoluted tubule- tubular reabsorp (glucose)

A

apical- Na/ Glucose cotransport
inc. glucose symports
basal- facilitated diff (requires ATP)

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69
Q

proximal convoluted tubule- tubular reabsorp (N waste)

A 
urea, creatine and uric acid
urea- diffusion and paracell. route
          v soluble and sm
           1/2 removed from tubule (rest to circ)
contributes to kindey. h20 conc.
          osmolarity in medulla
uric acid- completely reabs (10% left)
creatine- not reabsorb
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70
Q

urea conc. change through nephron in circ system

input v output

A

in= 20 mg

out renal v =10mg

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71
Q

proximal convoluted tubule- tubular reabsorp (H2O)

A 
osmosis and solvent drag
no active transp for H20 
     need create conc. gradient (solv drag)
H2O flow thru aquaporins
       cell mem greater perm to water
60-70 reabsorb by PCT
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72
Q

obligatory H2O reabsorption

A

unregulated

automat. absorb w/ mvmnt ions (solvent drag)

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73
Q

uptake by peritubular cap

A 
inc tubular fluid
fluid flows frm high P environ tubule to low P environ of efferent arteriole
dec P more w/ angiotension 2 
      vasoconstriction of arterioles
              dec blood flow= dec P
High BCOP
   sucking force in arterioles
   opposes filtration
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74
Q

transport maximum

A

max conc. be effectively reabsorb
ex too much H2O, not enough drains
short term regul
controls reabsorption

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75
Q

solute saturation

A

when cells no longer uptake any more

ex. glucose in urine

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76
Q

renal threshold

A

max amnt effectively reabsorb
over= sub in urine
varies w/ material
bc diff transport mechanisms

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77
Q

rate of filtration value

A

125 mL/min

78
Q

ideal filtration and absorption rate

A

125mg/min
however* can’t go on forever
glucose not fully reabsorb

79
Q

how is filtration and reabsorp effected when reach transportation max and renal threshold

A 
filtration constant
 reabsorb dec (hits ceiling)
80
Q

shape of elimination curve once hits transp. max and renal threshold

A

excretion inc rapidly
absorp dec
filtr remains constant

81
Q

tubular secretion effects on pH

A 
secrete H (inc CO2) inc pH
(less in circ)

reabsorb H = dec ph
(more in circ)

82
Q

nephron (henle loop)

types of ions and their movement

A

15 % h2O reabsorp
active transport (Na, K, 2Cl transporter)
descending loop high perm to water
NaCl conc grad high (bc ascending loop)
H2O leaves descending limb (solvent drag)

83
Q

distal convoluted tubule and collecting duct

cells

A 
regulated reabsorp and secretion
principle cells
    hormone control
    H2O and NaCl
intercalated discs
    maintain acid base balance
    K and H
84
Q

distal convoluted tubule and collecting duct- hormonal influences

A 
aldosterone
  Na and H2O reabsorp
  RAAS
natriuretic peptide
  Na/H2O secretion
  made by heart
ADH
   inc H2O absorp 
        inc blood concen
PTH
   inc Ca conc and reabsorp
85
Q

H2O conservation

A 
H2O absorbed by circ
   urine V dec, conc inc
Kidney creates high osmotic grad
      cortex low, medulla high
nephron loop inc. H2O perm
      influence by ADH (aquaporins)
86
Q

osmolarity range in cortex v medulla

A

blood osmo= filtration osmo (300)

kidney medulla 300-1200

87
Q

countercurrent multiplier

A 
4x conc grad in medulla than filtrate (inside tubule)
fluids move opposite directions
   descending = down
    ascending = up
Na addedin PCT
     excreted out
         H2O leave tubule
inc chance solutes bump into transp on ascending mem
     Na, K, Cl pumped out to medulla
          inc Na conc outside more
88
Q

function of thick ascending loop and thin descending loop

A

ascending imperm H2O reabsorb w/ osmosis

inc favorability of H2O out descending limb w/ thin mem

89
Q

H2O perm. feedback loop

Hypothal branch of RAAS

A 
controlled by ADH
stim- high blood osmolarity 
         >300
              lost H2O or gained solutes
sensor- hypothal + osmoreceptors
message- release ADH thru pituitary gland
effectors- DCT cells and collecting duct
response- inc aquapor act + production
   inc. H2O perm 
      inc H2O retention in circ, urine conc inc
            max conc. 1200
if no ADH
     v diluted urine, H2O absorb by tubules, 50 mOsm
90
Q

Countercurrent exchange

A

blood and H2O
location- vasa recta
descending- lose H20, gain NaCl
ascending- lose NaCl, gain H2O

91
Q

tubule osmolarity value review

A 
glomerular (filtration 300)
PCT- 300
descending loop- 300 to 1200
ascending loop- 1200 to 300
DCT- 100
Collecting duct- 300 to 1200
vasa recta- 300 to 1200 to 300
92
Q

diss solutes in urine

A

urea, NaCl, KCl, urochrome (RBC destruction, gives yellow color)
5%

93
Q

urine specific gravity, osmolarity and pH

A 
spec. gravity- 1.001-1.008
H2O=1
ex. if dehydrated = closer to 1.001
   high v but low conc
inc diss mat = inc specific grav
osmolarity- 50-1200mOsm/L 
    50= dehydrated
pH- 4.5-8.2
usually more acidic
94
Q

urine vol

A

1-2L/day
>2L = Diuresis/ polyuria
<0.5 = Oliguria

95
Q

diabetes and polyuria

A

sympt- excessive thirst, frequent urination

96
Q

polyuria process

A

inc. Na secretion
H2O into tubules (H2O follows Na)
H2O out of circ = thirst

97
Q

diabetes mellitus

A

insulin deficiency

98
Q

gestational diabetes

A

insulin insensitivity

99
Q

insipidus diabetes

A

hypothal not produce enough ADH
ADH = H2O retention
w/out excrete 20L/day and unquenchable thirst

100
Q

Diuretics

A 
inc urine output
ex. alchohol
treats hypertension
   make nephron loop less perm to water
         excrete more fluid, dec blood vol
101
Q

renal function test

A

test urine for mat
ex. glucose, proteins, WBC’s etc.
if normal all values should be negative

102
Q

clearance

A

amnt blood v processed to eliminate solute in 1 min

excretion rate/ initial blood conc

103
Q

clearance range

A

depends on how much fluid recieved and reabsorption
0mL/min- 625
0= circ system retains
625= completely secreted, no mat found in blood

104
Q

clearance range 0-125

A

net solute reabsorb

0= fully reabsorb

105
Q

clearance range- 125

A

no reabsor or secretion

rate in = rate out

106
Q

clearance range- 125-625

A

leave kidney rate> filtration
no time to reabsorb
fully secreted

107
Q

Glucose clearance

A

normal conc =1
excretion rate =0
0/1 = 0 (fully reabsorb)

108
Q

inulin clearance

A

125
not reabsorbed or secreted
if below= renal failure (GFR not working)

109
Q

PAH clearance

A

625 ml/min
fully filtered and secreted
0 mg in blood

110
Q

renal dialysis

A 
filter fluid in and out
block mvmnt RBC
alter mat conc. based on condition
plasma conc> dialysis fluid conc
           materials flow out of circ system
111
Q

normal mat flow of renal dialysis

A

out circ- Ca, K
Na- constant
Glucose- variable

112
Q

micturition reflex

A 
stim- stretching
long and short reflex
long- pons and cerebellum
conscious act
pons- internal urethral sphincter
cerebellum- external urethral sphincter
short- detrusor muscle contracts 
    unconsciously w/ spinal reflex
    conscious w/ act. pons
113
Q

fluid compartments

A

intracellular
extracellular
plasma

114
Q

regulation btw plasma and extracellular

A

general homeostatic demand

hormonal and neural control

115
Q

regulation btw extracellular and intracellular

A

local ex. na/k and channels

individual homeostatic demand

116
Q

fluid intake-sources and avg.

A

2500 ml / day
metabolic h2o
ingested h2o

117
Q

fluid loss

A

urine
sensible (sweat)
insensible (respiratory + cutaneous evaporation)

118
Q

obligatory loss

A

1200-1500 ml/day

min of 400 from urine

119
Q

regulation of h2o input

A

stim- blood osmolarity inc
causes BP dec, kidney release renin= angiotensin 2
lose h2o not Na
Control- hypothal (osmorecp)
response- thirst inc
rehydrate blood, discend stomach and sm in, cools mouth
*short term input

120
Q

long term effector h2o input

A

blood osmolarity dec w/ h2o ingestion

BP inc again

121
Q

regulation h2o output

A 
control urine vol
regulated by ADH
   slows urine loss 
Na leaves too * bc of solvent drag
    blood osmolarity dec
122
Q

fluid deficiency conditions

A

hypovolemia

dehydration

123
Q

hypovolemia

A

solute + h2o mvmnt is equal
(osmol is same)
blood v dec and so blood p dec
causes- internal bleeding (hemorrhage, vomiting and diarrhea)

124
Q

dehydration

A 
more h2o is lost than Na
osmolarity inc = thirst inc
causes- sweating and diabetes
    glucose attracts h2o in tubules
    solutes never able to be excreted
125
Q

fluid shift

A 
water moves w/ osmosis
h2o dec= ECF dec= hypertonic sol
conc of ECF inc 
water moves out cell (ICF) into (ECF)
equilib restored but ICF V dec
126
Q

fluid excess problems

A

v excess

h2o intoxication

127
Q

volume excess

A 
h2o and solute retained
causes- kidney failure 
      low GFR fluids all stay in blood
             no Na excreted in urine
aldosterone hypersecretion
      inc Na reabsorb into blood
                 water follows bc solvent drag
128
Q

h2o intoxication

A

more h2o is retained in ECF than Na
fluid moves into ICF
cells swell and inc P
causes- ADH hypersecretion or overhydrating

129
Q

blood and h2o intake “danger zone”

A

less than 1.2 L of water per day

losing at least 400 to urine and 1200-1500 for obligatory

130
Q

fluid sequestration

A

fluid in unwanted places
edema
hemorrhage

131
Q

edema

A

h2o out of circ into lymphatic or skin

ex. blister

132
Q

hemorrhage

A

internal bleeding

133
Q

relation between plasma and ECF

A

direct
if plasma change, ECF change
bulk reg

134
Q

electrolyte reg

A

indirect
hormonal control
change conc or vol
absolute quantitiy unaffected

135
Q

h2o reg

A 
osmosis
no active transp
solvent drag and cap filtration
water reabsorbed hypo to hypertonic
water secreted hypertonic to hypotonic
*in relation to flitrate
136
Q

ECF electrolytes

A

Na, Cl

137
Q

ICF electrolytes

A

K, HPO4 and proteins

138
Q 
sodium control- Aldosterone
functions
stimulus
effectors
response
A 
Fun- water reg. membrane pot (na in and depolar) + cotransport (ex. glucose)
reg- hormonal (aldosterone)
stimulit-
      hyponatremia (Na)
      hyperkalcemia (K)
      Low BP (release renin and angioten 2 = inc BP)
effectors- cells DCT + collecting duct
response
inc act Na/K pumps 
  pump more Na in= greater conc= inc osmolarity
   inc H2O too (solvent drag)
  pump K out secretion into tubules
139
Q

ADH control

A

stim- hypernatremia inc Na osmolarity in blood
sensor- osmos recp in hypothal
control- ADH produces through pit gland (no bloodb barrier)
response- inc thirst
inc H2o intake through inc Na reabsorp
dec urinary H2o loss

140
Q

Natriuretic peptide control

A 
stim- stretching atrial walls from high BP and V
sensor- cardiac musc. cells
message- ANP (counteracts ADH)
effectors- hypothal + kid. tubules
     fluid into tubules to dec BP
response- dec ADH and renin output
     dec thirst, and h20 intake
    inc h2o excretion by inc Na secretion into tubules
141
Q

low sodium

A

hyponatremia
H2O> Na
causes water intoxication

142
Q

high sodium

A

hypernatremia

results in edema and hypertension

143
Q

potassium control

A

high in ICF
regulation- by aldosterone (linked to Na)
inc Na reabsorp and K secretion

144
Q

high potassium

A

hyperkalemia
acute
higher K conc in ECF (K cannot get out)
brings excitatory cells closer to threshold
chronic
from renal failure, aldos hypersecretion or acidosis
Na not enter cell, VG channels closed
act pot prevented bc cell hyperpol by K in ICF
lowers excitability

145
Q

low potassium

A 
hypokalemia
rare
due to vomiting or diarrh
cells hyperpol w/ K in ICF
    less excitable
146
Q

chlorine regulation

A

fun- osmolarity reg in kidneys, componet of stomach acid, takes prt in chloride shift in respir (HCO3-)
regu.-
linked to Na

147
Q

low chlorine

A

hypochloremia

148
Q

high chlorine

A

hyperchloremia

149
Q

calcium control

A

fun- bone strength, blood clotting, musc. and nerve fun
reg-
PTH (low) and calcitriol (high)
hyper and hypo parathyroidism

150
Q

high Ca

A 
hypercalcemia
from alkalosis
too much PTH
osteoclast act high
     over conc. of Ca in blood
cause muscle weakness
151
Q

low Ca

A

not enough PTH
Ca stays in bone
causes muscle contraction w/ overexcit.

152
Q

hyperparathyroidism

A

stim osteoclast act
from vitm d defic, dirrh, and pregnancy
ca from bone to circ

153
Q

hypoparathyroidism

A

inhibit osteoclast act

ca stays in bone NOT to circ

154
Q

magnesium control

A

fun- intracell. metab act (cofactor)
reg- source = diet via paracellular route
reabsorb in PCT of nephron
inc w/ PTH and vitamin D

155
Q

hypomagnesemia

A

loss through vomiting
over excit of tissues
nerve cells depol
musc. contract

156
Q

hypermagnesemia

A

from renal failure

excit tissues depressed

157
Q

phosphates control

A

fun- nucleic acid/ATP structure and fun + acid base balance
regu-
inc PTH = inc phos secretion
inc or dec pH= change in phos concen

158
Q

pH

A

conc. of H+ ions
inc. in H+ = DEC pH
dec in H+= inc pH

159
Q

normal pH range

A

7.35-7.45
<7.35 = acidosis
>7.45 = alkalosis
range favors enzyme function, hemoglobin affinity and nervous system fun (excitability)

160
Q

pH and Hb affinity

A

inc pH= dec H = inc affinity
dec pH= inc H= dec O2 affin.
Hb can bind to O2 if not high conc. of H+ ions

161
Q

acid sources

A

dietary- fat and proteins-H+ in kidneys
fixed acids (only altered w/ excretion) taking H out of sol.
metabolic- CO2, lactic/keto acids
CO2= volatile acid (fixed easily w. respi)

162
Q

general acidosis

A 
H+ diffuse into cells
K+ out of cells to ECF
charge less -
H+ bind cations in ICF
      cell becomes hyperpol.
           less excitable
cause- CNS depression (coma and confusion)
163
Q

general alkalosis

A 
cause- spasms and convulsions
H+ conc. in ICF dec bc goes out to ECF
      hyperpol cell
K+ enters and depolarized 
   inc excitability (lwrs distance to threshold)
164
Q

acid-base disturbance categories

A

respiratory- CO2
metabolic- not alter CO2
functions by reabsorp, secretion and excretion

165
Q

respir. acidosis

A 
inc in conc CO2 (hypercapnia)
    move to right inc in co2= inc H
causes
   hypoventilation
       high co2, low o2
respir. distress
        ex. COPD 
        O2 can get in but cannot escape
166
Q

respir. alkalosis

A 
dec in conc CO2 (hypocapnia)
dec co2= dec H
causes
   hyperven (co2 expelled too quickly)
 emotional shock, fever (inc metabolism), high altitude (low o2 inc breathing and co2 out)
167
Q

metabolic acidosis

A 
inc in organic acid (H)
amnt bicarb dec (no buffer capacity)
         inc PCO2 (fix= inc respir rate)
causes
high protein diet
    brkdwn protein for energy
high fat diet
      free f acids and ketone bodies released
starvation
        brkdown own muscle, keto acids inc
heavy exercise
         lactic acid produced inc
diarrhea
         bicarb not reabsorb in tubules
                H+ not counteracted
renal failure
         kidney cannot expell H and therefore HCO3 not produced
168
Q

metabolic alkalosis

A 
excessive loss H
due to vomiting
fix
   dec resp rate= inc co2
   kidney generate H and secrete HCO3 (allow H to inc)
   buffer systems donate H+ ions
169
Q

chemical buffering composition

A

weak acid and base
if buffering capacity is met a change in pH will rapidly occur
(not enough HCO3 to consume H+ ions)

170
Q

bicarbonate buffer

A

inc co2= inc HCO3
can alter pH from organic (fixed acids) NOT volatile or CO2
normal HCO3 conc= 24mmol/L
need respir and renal function to work! (CO2 and HCO3)

171
Q

HCO3 reserve

A 
hind HCO3 w/ Na = NaHCO3
storaged w/ Na
if regen HCO3 have to remove Na
used when all available HCO3 is bound to organic acids
*inc buffering capacity
172
Q

protein buffer

A

inc pH= carboxyl group lose H (C-O-OH) to (C-O-O-)
dec pH to normal
dec pH= amnio group accept H (NH2) to NH3)
inc pH to normal

173
Q

hemoglobin buffer

A 
apart of protein buffer
buffers blood
inc H+ = inc in bond w/ Hb
CO2 inc = HCO3 out of circ
          H attracted to Hb
CO2 dec= H cleaved from Hb to inc pH
174
Q

Phosphate buffer

A

predom in ICF
H + HPO4 = H2PO4
reserve= Na2PO4

175
Q

respir. control of pH- acidosis response

A

resp rate inc= CO2 dec= pH inc
H+ expelled
renal comp inc H and HCO3 reabsorb

176
Q

respir. control of pH- alkalosis response

A

respr rate dec= inc CO2= pH dec
dec affinity
renal comp= inc H and HCO3 secretion (stop resisting inc in H+)

177
Q

renal control pH (general)

A

secretion or reabsorp of H and HCO3
pH dec= inc H+ secretion and inc HCO3 reabsorp
pH inc= inc H+ reabsorb and inc HCO3 secretion

178
Q

buffering capacity

A

pH=4.5

below this H will not be removed from circ system

179
Q

renal control- acidosis response

A

CO2 absorb into kidney cells
secretion of H+ and Cl into tubules (filtrate)

free H in cells binding
reabsorb HCO3 into circ (bind to free H+)
create H+HCO3= H2CO3 into CO2 and H2O
H+ ions leave via H2O in urine
H bind to Na2HPO4
H bind w/ NH4Cl

180
Q

renal control- alkalosis response

A

inc H+ reabsorb to circ
Cl follows
inc HCO3 secretion to filtrate
Cl exchanged (HCO3 out, Cl in)

181
Q

relationship btw pH level of urine and kidney function

A

low pH <7.35= acidosis

high pH> 7.45= alkalosis

182
Q

diagnosing acidosis

A

check PCo2 conc (indicates lung function)
not inc = metabolic acidosis
>50 mmHg= respir acidosis

183
Q

diagnosing acidosis- metabolic acidosis

A

lung fun is ok
if normal PCO2 (40)= acute metabolic acidosis
caused by loss of HCO3 (ex. diarrhea)
if PCO2< 35 = chronic (compensated) metabolic acidosis
caused by the retention of organic acids
due to high fat/protein diet, kidney failure, starvation or heavy exercise

184
Q

diagnosing acidosis- respiratory acidosis

A

know that lung fun is >50mmHg
if normal conc of HCO3= acute resp. acid.
ex.CNS damage
if HCO3 conc >28
kidneys are doing work of lungs= Chronic respir. acid.
ex. long term disease like asthma
fix= inc respir rate to dispel CO2

185
Q

diagnosing alkalosis

A

check PCO2 lvl
inc >45 mmHg= Metabolic alkalosis
dec <35 mmHg= Respiratory alkalosis

186
Q

diagnosing alkalosis-Metabolic alkalosis

A

due to inc in HCO3
and dec in H+ ions
ex. vomiting

187
Q

diagnosing alkalosis- respir. alkalosis

A 
hyperventilation
check HCO3 lvls
if low/normal= acute respir. alka
     ex. fever or panic attack
     fix=dec respir rate to inc O2
if <24 mmHg HCO3= chronic (compensated) respir. alkal
  ex. CNS damage
188
Q

kidney compensation-acidosis

A

chronic respir acidosis
CO2 not expelled
HCO3 production inc by kidneys

189
Q

relation btw PCO2 and pH

A

PCO2 inc = pH dec = more acidic (more H ions)

PCO2 dec= pH inc = more basic (less H ions)

190
Q

value of constant PCO2

A

40mmHg

191
Q

davenport diagram- left v right

A 
left straight- acute respir acidosis
right straight- acute respir alkalosis
left down- metabolic acidosis
right down- metabolic alkalosis
left = acidosis (dec. pH)
right= alkalosis (in. pH)
192
Q

davenport diagram- curve representation

A

curve = lung function
measured by PCO2
low PCO2= hyperventilation
high PCO2= lung failure
HCO3 value= kidneys ability to regulate H present in blood
inc H= inc HCO3 production or inc in reabsorp
dec H = dec in HCO3 production or inc in secretion

A+P 211 (5 decks)

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