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pathophysiology > test 4 > Flashcards

test 4 Flashcards

1
Q

podocyte

A

surrounds each capillary through which filtration takes place

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2
Q

mesangial cells

A

form the mesangium of the glomerulus. change size and contract when they need to filter. Barrier less leaky when contracts, K goes down

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3
Q

what charge passes through glomerulus the best

A

positive. capillary is negative. so negative is the worst to travel through

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4
Q

glomerulonephritis

A

inflammation caused by infections. makes glomerular basement membrane lose negative charge so more things will be in the urine.

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5
Q

treatment for glomerulonephritis

A

steroid therapy

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6
Q

goodpasture’s syndrome

A

anti-glomerular basement membrane disease. Antibodies develop against the basement membrane causing kidney failure and lung bleeding. symptoms never go away only controlled.

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7
Q

glomerular filtration barrier

A
  1. podocytes (epi of bowmans capsule, fenestrated, large poors, neg charge, mensangial cells)
  2. basement membrane (basal lamina - neg charged, glycoprotiens, coarse sieve)
    lies in between
  3. epithelium of Bowman’s capsule (podocytes create filtration slits)
    allows 20% plasma to enter bowman’s space
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8
Q

GFR =

A

GFR= KF [(PGC-PBS)-(πGC- πBS)], GFR is the volume tof plasma that enters bowman’s space, average 125 ml/min (above 100 good), most important regulator is blood flow

PGC: favors filtration, nearly constant
PBS: opposes filtration, constant
πGC: opposes filtration, high conc of protiens causes the rate to dec
πBS: favors filtration, no change because it can’t ever get out of capillaires

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9
Q

what happens to GFR if CO decreases

A

renal dysfunction will occur because the GFR number will be low

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10
Q

KF

A

filtration coefficient- how leaky the barrier is. mesangial contract - less leaky, KF Dec
Mesangial relax - more leaky, KF increases

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11
Q

PH - π - Pfluid = net filtration rate

A

positive to favor filtration
pH- blood pressure
π - proteins in plasma but not in bowman’s capsule
pfluid- created by bowmans’ capsule

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12
Q

efferent arteriole constrict

A

more volume in glomerulus as less is leaving, higher PH, higher GFR

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13
Q

afferent arteriole constrict

A

more volume leaving, lower PH, lower GFR

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14
Q

Renal blood flow

A

approximately 1200 ml/min

kidneys receive 20% of CO, if RBF increases then GFR increases

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15
Q

renal plasma flow (RPF)

A

= RBF X (1-Hct (%RBC))

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16
Q

what if the RPF is extremely high?

A

outstrips the filtration capacity of the capillary causing renal dysfunction - kidneys will have too much to handle

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17
Q

solvent movement in kidneys

A

moves with sodium

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18
Q

Na+ movement

A

reabsorbed by active transport,

secretion: enters on the luminal side through membrane proteins and moves down the electrochemical gradient
reabsorption: pumped out basolaterial side by the K+/Na+ ATPase

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19
Q

______ drives anion reabsorption

A

electrochemical gradient

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20
Q

______ drives water movement

A

osmosis, following solute reabsorption

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21
Q

____ filtrate reabsorbed in PCT

A

70%

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22
Q

how does reabsorption occur in the PCT

A
  1. most reabsorption occurs across the tubular epithelium- transcellular transport
  2. some reabsorption of water and certain ions occurs between cells - paracellular transport
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23
Q

Main role of PCT

A

does nothing to produce concentrated urine, just produces a smaller amount of urine - continuously establishes a Na+ gradient so the interior of PCT low Na+, favors primary active transport on the basolateral side of the membrane

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24
Q

penicillin and cimetidine

A

secreted in PCT

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25
Q

Probenecid and Penicillin

A

compete for the transporter. only can remove so many molecules. increases concentration of molecules in the body

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26
Q

loop of henle function

A

concentrating the urine, filtrate becomes larger (1200 millimoles) near the bottom of the loop reaching equilibrium with the interstitial fluid - main goal is to increase the amount of water reabsorbed back by the body without too much energy - uses

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27
Q

descending limb

A

highly permeable to water not ions. penetrates into the medulla. water moves out into the interestial fluid picked up by the vasa recta. called Thin!, no energy used! makes it hypertonic and passive diffusion because of the electrochemical gradient in the Thick ascending loop

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28
Q

how much filtrate is reabsorbed in the descending limb

A

15%

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29
Q

Thick Ascending limb

A

highly permeable to ions, not water. Na+ transported out of the filtrate, diluting it before it reaches the distal tubule. reabsorption of Na, K, Cl, THICK, uses energy to increase the solute concentration in the medulla so water can be reabsorbed in the ascending and collecting duct!

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30
Q

TAL luminal side transporter, how can this be affected by drugs?

A

1 Na+, 1 K+, 2 Cl = blocked by loop diuretics, filtrate is diluted by removal of ions and no addition of water

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31
Q

countercurrent multiplier

A

fluid in the medulla can be so high (1200 mOsm)

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32
Q

how does the bloodstream effectively reabsorb all of the water and solutes from the medulla?

A

promotes movement of water into the capillary lumen because of low hydrostatic pressure and a high protein concentration

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33
Q

vasa recta

A

capillareis that circulate around the loop of henle. associated with juxtamedullary nephrons. permeable to water and solutes. removes the water after leaving the loop of henle

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34
Q

distal convoluted tubule and collecting ductt

A

85% filtrate reabsorbed, early DCT impermeable to waste, late DCT and collecting duct may become permeable to water in the presence of ADH.

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35
Q

thiazide diruetic

A

transporter of the luminal side of the early DCT 1 Na+, 1 Cl- blocked

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36
Q

Loop diuretic

A

absorbing in the ascending on the luminal side inhibited - makes it so there is low K+ in the plasma (hypokalemia)

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37
Q

lasix

A

loop diuretic

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38
Q

urea

A

wate product
dissolved in blood
excreted in urine
regulated by ADH/Vasopressin

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39
Q

handling urea

A

nephron is impermeable to urea- want to excrete

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40
Q

what is most permeable to urea

A

papillary duct - goes back into the medulla and contriubtes to the medullary osmotic gradient

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41
Q

faster the urine flow

A

better the renal function, less urea that is reabsorbed. urea not in papillary duct to be reabsorbed

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42
Q

blood urea nitrogen

A

indicatory of renal function, if it is too high that means that the kidneys are not functioning well and are reabsorbing a waste product because it is not moving fast enough.

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43
Q

fine tuning GFR

A

controlled mostly by altering the arteriole diameters - hydrostatic pressure from volume

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44
Q

myogenic response

A

ability of the afferent arteriole to contract when high pressure - stretched - arteriole pressure stretches due to an increase in perfusion pressure

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45
Q

flow =

A

(P1 - P2) / resistance

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46
Q

tubular glomerular feedback

A

afferent arteriole senses the delivery of filtrate to the DCT (macula densa) - increases prostaglandins, dialtes - decreases resistance, decreases afferent arteriole resistance and increase in RPF and GFR

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47
Q

macula densa

A

sneses volume of filtrate

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48
Q

Renin - Angiotensin - Aldosterone System

A

RAA - important regulator of renal function and of the CV system. most important regulator of blood volume and blood pressure.

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49
Q

diseases RAA involved with

A

hypertension, CHF, diabetes mellitus, atherosclerosis, hyperlipidemia

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50
Q

how does RAA maintain GFR

A

increases PGC, blood pressure, blood volume

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51
Q

aldosterone

A

increases Na+ and water retention, and increases K+ excretion

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52
Q

what receptor is activated by RAA system

A

SNS activates systems via B1 receptor stimulation

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53
Q

activation of the RAA system

A

angiotensin (made in liver) converted by renin (RLS) to angiotensin (10AA) which is converted to angiotensin 2 (8AA) by angiotensin converting enzyme - peptidase located on pulmonary vascular endothelial cells, acts on two receptors AT1R (favored) and AT2R

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54
Q

ACE

A

luminal side of the pulmonary vascular endothelial cells to convert ang1 to ang2, benefit of it located in the lungs is that is where all of the O2 lives so it can sense the CO changes

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55
Q

ACE inhibitors

A

blocker of RAA, (“prils”) stops the conversion of ang 2

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56
Q

alskiren

A

renin inhibitor - stops the conversion to ang 2

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57
Q

AT1R blocker

A

ang 2 can’t act on

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58
Q

diabetics and RAA

A

they need to use RAA blockers/inhibitors as they have renal dysfunction

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59
Q

renin release stimuli

A

decreased flitrate delivery to the macula densa causes renin to be released from the JG cells

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60
Q

decreased filtrate is caused by

A

total volume in body low, increased urea in plasma decreases the filtrate (flow rate), decreases the pressure/volume

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61
Q

to increase renin release

A

B1 receptors on the JG cells, TGF works with others, prostaglandins

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62
Q

as arterial pressure goes down,

A

PGC goes down, GFR goes down, Macula densa delivery goes down, TGF causes the afferent arteriole resistance to go down which has a negative feedback on the PGC

as macula densa goes down also causes the renin levels to go up, ang 2 to go up, and efferent arteriole resistance to go up to have a negative feedback on the PGC

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63
Q

role of TGF

A

TGF decreases afferent arteriolar resistance by the paracrine release of vasodilatory prostaglandins, such as prostacyclin - causes vasodialation and is a drug.

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64
Q

flolan and remodulin

A

vasodialation and is a drug

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65
Q

there’s a decreased renal perfusion pressure (renal artery has occlusion so diameter is small) - what would happen if NSAID was administered

A

First decrease in perfusion pressure - relying on compensating mechanism of the afferent arteriole and releases prostaglandins to try and make the diameter bigger and improve blood flow - NSAID would inhibit this whole process

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66
Q

role of ACE inhibitor (ramipril)

A

targets the afferent arteriole, increaess GFR pressure - constricts the efferent arteriole to maintain volume. ACE inhibitor decreases ang 2 so you can’t constrict the arteriole as well

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67
Q

lisonopril affect on Renin and K+

A

renin increase in an effort to increase ang 2, K+ increases

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68
Q

aldosterone

A

produced in the renal cortex (zona glomerulosa), steroid hormone, highly lipophillic

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69
Q

3 main stimuli for aldosterone secretion

A
  1. decrease Na+ concentration in the plasma
  2. decrease total volume of plasma
  3. increase plasma concentration of K+
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70
Q

aldosterone acts on the late DCT and collecting duct to cause

A

increase in Na+ reabsorption, increase in water reabsorption, increase in K+ secretion

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71
Q

aldosterone acting on principle cells

A
  • aldosterone combines with the cytoplasmic receptor
  • hormone receptor complex initiates transcription in the nucleus
  • translation and protein synthesis make a new protein channels and pumps aldosterone-induced proteins which modulate existing channels - RESULT: increased Na+ reabsorption and K+ secretion - pumps formed by aldosterone to increae K+ and Na+ movement and increase ATPase
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72
Q

aldosterone functions

A
  1. increased basolateral Na+/K+ ATPase density and activity
  2. increased luminal ENaC - epithelial sodium channel
  3. Increased ATP production within the cell in order to maintain transport activity
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73
Q

spironolactone (aldactone)

A

aldosterone receptor antagonist for someone with congestive heart failure for effective diuretics - acts early so aldosterone can’t bind to receptor

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74
Q

eplerenone (inspra)

A

aldosterone receptor antagonist newer drugs, more specific and selective so less adverse events

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75
Q

triameterene (dyrenium)

A

inhibits ENac channels - further for formation of channels but won’t work the same

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76
Q

amiloride (midamore)

A

inhibits ENac channels- further for formation of channels but won’t work on the same

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77
Q

weak diruetics

A

help balance of loosing to much K+ like a regular diuretic - never on monotherapy of one type

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78
Q

amount excreted =

A

amount filtered - reabsorbed + secreted

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79
Q

inulin clearance

A

freely filtered at the glomerulus and not secreted or reabsorbed
renal clearance of inulin = GFR

80
Q

creatnine

A

produced by the body so better to measure than inulin. 99% filtration 1% reabosorption

81
Q

Ccr =

A

excretion rate x volume / plasma concentration

82
Q

normal GFR

A

180 L / day

83
Q

serum creatinine

A

function of muscle mass and activity - why smaller for a women than a man

84
Q

CrCl=

A

(140-age)(body wt in kg) / (SCr) (72) {cockcroft-gault formula} if a women multiply the CrCl by 85%

85
Q

renal handling of a drug

A

renal clearance is 200 ml/min and the calculated CrCl is 94 ml/min

86
Q

filtration rate > excretion rate

A

net reabsorption

87
Q

filtration rate < excretion rate

A

net secretion

88
Q

filtration = excretion

A

passes through the nephron without reabsorption or excretion

89
Q

CL of the drug < inulin CL

A

net reabsorption

90
Q

CL of the drug > inulin CL

A

net secretion

91
Q

CL of drug = inulin CL

A

neither reabsorbed or secreted

92
Q

renal threshold

A

conc of a substance in the blood above which the kidneys begin to remove it in the urine

93
Q

urea renal threshold

A

low renal threshold - not in the blood stream

94
Q

glucose renal threshold

A

high renal threshold

95
Q

most common reason for exceeding renal threshold:

A

diabetes mellitus - glucose in the urine to diagnose because glucose exceeds renal threshold
Low RT: wast
high RT: stays in the blood
you can tell someone has diabetes by the glucose in the urine

96
Q

threshold exceeded what happens?

A

excretion

97
Q

long term complications of diabetes

A

atherosclerosis - CV problems
nervous system, eye disease, hypertension issues, vessels occluded, protein leaky in urine, kidney disease (overworking of removing excess urine and water)

98
Q

Acute Renal Failure

A

abrupt decline due to excretion of wastes and maintaining acid/base balance
diagnosed inc serum creatnine

99
Q

classification of acute renal failures

A

increase of SCr 0.3 mg/dl or greater or 2x increase SCr from baseline, urine output <0.5 ml/kg/hr for 6 hours

100
Q

at risk groups for AKI

A

pre-existing renal impairment, hypertension, cardiac, diabetes, PVD, age

101
Q

drug induced physiology of AKI

A

loss of polarity, death of cells, migration, prolipheration, differentation and reestablismment of polarity

102
Q

prerenal azotemia

A

hemodynamics form, loss of blood volume ex: hemorrhaging

103
Q

post renal obstruction

A

drug forms crystals and causes obstruction, severe dehydration, intervene and flush out obstruction

104
Q

intrinsic AKI

A

damage to kidney from illness that damages cells of kidney (good pasutres), lots of inflammation

105
Q

glomerular nephritis

A

AKI from inflammation, once treated kidney comes out of failure

106
Q

regulation of K+

A

98% ICF, 2% ECF, normal plasma K+ is 4 mEq/L,

107
Q

role of inslulin

A

increases uptake into the cells

108
Q

role of epinephrine

A

increases

109
Q

BP decreaes

A

increases renin from kidney - ACE increases

110
Q

ang 2 increaes

A

thirst, ADH, BP, aldosterone

111
Q

aldosterone stimulation for secretion

A

stimulation for secretion- hyperkalemia (direct action on a nephron), ang 2, hypoatremia

112
Q

aldosterone inhibition for secretion

A

dehydration causes increase in ECF osmolarity (Na+) - decrease in total volume (water faster than Na+)

113
Q

end stage renal disease

A

K+ 6.9(normal 3.5-5)

114
Q

kalexalate

A

sodium polysterene sulfonate with sorbitol until K less than 5

115
Q

what is given in end stage renal disease

A

insulin 10 units IV, Dextrose IV (maintain glucose, produces insulin which causes cellular uptake of K+ because insulin release), Albuterol inhalation (B2 receptor releases epi, produces insulin)

116
Q

ADH

A

antidiuretic hormone/vasopressin/AVP

released from the posterior pituitary when dehydration occurs, kidney water reabsorption

117
Q

ADH secreted in response to

A

decrease in volume, atria stretch goes down (volume decrease, CO decrease, pumping less) - increase plasma osmolarity

118
Q

water channels in collecting duct ADH

A

vasopressin binds to the membrane receptor, receptor activates cAMP, cell inserts AQP2 water pores into the apical membrane, water is absorbed by osmosis into the blood

119
Q

diseases associated with ADH

A

diabetes insipidus ( dilute urine output, hyperatremia, polyuria, polydipsia, high plasma osmolarity, normoalkemia)
central - lack of production
nephrogenic- lack of response

120
Q

syndrome of inappropriate (too much) ADH (SIADH)

A

ADH release with normal stimuli, common in hospitalized elderly patients, caused by tumors, pulmonary disorders, TB, hyperthyroidism, drugs - dilutional hypoatremia, neurological signs

121
Q

sweat Na+ conc

A

30-50

122
Q

sweat K+ conc

A

5

123
Q

sweat H+ conc

A

-

124
Q

sweat Cl- conc

A

45-55

125
Q

sweat HCO3- conc

A

-

126
Q

gastric Na+ conc

A

40-65

127
Q

gastric K+ conc

A

10

128
Q

gastric H+ conc

A

90

129
Q

gastric cl- conc

A

100-140

130
Q

gastric HCO3- conc

A

-

131
Q

diarrhea Na+ conc

A

25-50

132
Q

diarrhea K+ conc

A

35-60

133
Q

diarrhea H+ conc

A

-

134
Q

Diarrhea Cl- conc

A

20-40

135
Q

Diarrhea HCO3- conc

A

30-45

136
Q

hypernatremia volume depletion

A

thirsting, sweating

137
Q

hypernatremia volume expansion

A

hypertonic infusion

138
Q

hypoatremia volume depletion

A

diarrhea, burns, vomiting, diuretics

139
Q

hypoatremia volume expansion

A

congestive heart failure

140
Q

natriuretic peptide

A

decrease systemic vascular resistance

141
Q

natriuretic peptide

A

induces sodium release from the kidneys
decreases systemic vascular resistance
decreases blood volume
increase CO

142
Q

atrial natriuretic peptide

A 
released from the atria from stretching when more volume is coming in
Na+/H2O excretion
decreases renin
afferent dilate efferent constrict
ENaC inhibits
PGC increases
aldosterone decreases
Antagonist RAAS
Blood volume decreases
increases lipolysis
143
Q

B-Natriuretic Peptide

A

secreted in ventricles, increases diuresis Na+ and H2O, volume decreased overall, decrease in BP,

144
Q

Nesiritide

A

BNP, treats decompensated heart failure

145
Q

BNP and clinical outcomes

A

increase in patients with worse outcomes
increase in renal failure
decrease in obesity

146
Q

why is there a resulting excretion of NaCl and H2O in natriuretic peptides

A

less vasopressin, increased GFR, decreased renin (less aldosterone), decreased blood pressure

147
Q

normal ranges of pH, Na, K

A

Na: 135-140
K: 3.5-5
pH: 7.38 - 7.42
H+: 38-42 nanomolar

148
Q

life can’t exist outside of what pH = why?

A

pH 6.8 - 7.8
K+ disturbances causes arrhythmias, contraction, acidosis, alkalosis, acidosis causes CNS suppression (respiratory issue)

149
Q

metabolism of carbs and fats generates

A

CO2

150
Q

metabolism of cys and met generates

A

sulfuric acid

151
Q

metabolism of lys, arg, his generates

A

HCl

152
Q

metabolism of Glu, Asp, citric acid generates

A

bicarbonate

153
Q

dietary intake of phosphate

A

coke, cheese, hot dogs

154
Q

3 sources of acids and bases in the body

A
  1. buffering 2. renal 3. respiratory
155
Q

phosphate site of action

A

plasma and urine

156
Q

protein site of action

A

intracellular

157
Q

organic phosophate site of action

A

intracellular

158
Q

bicarb site of action

A

extracellular

159
Q

what determiens how much acid can be buffered

A

how much before you can add before you see a change in pH

160
Q

CO2 reacts with water to produce what

A

carbonic acid

161
Q

pH =

A

6.1 + log ( [HCO3-] / 0.03 x Pco2)

162
Q

why is this such a good buffering system?

A

system is an open system: constantly changing and can add in the respiratory components. weak acid can be adjusted to meet the bodies needs. removal of CO2 by respiration or addition of CO2 by metabolism keeps the HCO3 : CO2 ratio near 20

163
Q

clinical correlation: increasing ketoacids

A

added H+, respiration will increase, renal will increase, bicarb dec, PCO2 increase

164
Q

metabolic acidosis

A

HCO3 < 24

  • respiratory compensation: PCO2 < 40 mmHg
  • Cause: addition of acid/loss of base
165
Q

respiratory acidosis

A

PCO2 > 40 mmHg

  • renal compensation, HCO3 > 24 mmHg
    cause: decreased ventilation
166
Q

metabolic alkalosis

A

HCO3 > 24

  • respiratory compensation, PCO3 > 40 mmHg
    cause: addition of base, loss of acid
167
Q

respiratory alkalosis

A

PCO3 < 40 mmHg

  • renal compensation, HCO3 < 24
    cause: increased ventilation
168
Q

renal correction in metabolic acidosis

A

increased acid titration : Increased NH3, increased HPO4-

increased acid excretion in the urine, increased bicarb regeneration. INC PH

169
Q

respiratory compensation metabolic acidosis

A

hyperventilation, dec pco2, dec H2CO3, dec H+, dec CO2 + H2O

170
Q

reabsorption of bicarbonate

A

bicarbonate enters the tubular fluid by glomerular filtration
forms H2CO3, converts to H2O and CO2 by carbonic anhydrase
CO2 can freely diffuse into proximal tubule cells, reacts with H2O inside to form HCO3- and H+, gets transported into PT capillaries across the basolateral membrane

171
Q

formation of ammonium

A

produced from glutamine in tubular cells

ammonium ion in the filtrate gets excreted removing H+

172
Q

acidosis and K+

A

collecting duct cells secrete H+ into the filtrate, this is done in exchange for K+ reabsorption, K+ increases in acidosis, secreted protons buffered by phosphate in the tubular fluid

173
Q

alkalosis and K+

A

cells in the collecting duct secrete bicarb and reabsorb H+, K+ exchanged for H+ to maintain neutrality, hypokalemia

174
Q

renal H+ excretion and HCO3- reabsorption / generation

A

normal: kidneys eliminate H+ and reabsorb new HCO3-
alkalosis: kidneys reduce secretion of H+ and secrete HCO3-
acidosis: kidneys increase secretion of H+ and increase formation/reabsorption of HCO3-

175
Q

diabetic ketoacidosis

A

increases ketoacids, K+ increase, pH < 7.4 (not complying with insulin therapy)

176
Q

profuse vomiting

A

loss of HCl, K+ decrease, pH > 7.4, metabolic

177
Q

ingestion of antacid

A

addition of base, pH > 7.4, K+ decreased

178
Q

profuse diarrhea

A

loss of HCO3-, K+ increased, pH decreased, metabolic

179
Q

hypervenhilation

A

alkylosis

180
Q

hypovenhilation

A

acidosis

181
Q

AKI stage 1 defined by

A

increase SCr 0.3 or increase from baseline 1.5-2x WITH urine output < 0.5 for 6 hrs

182
Q

pre renal injury symptoms

A

high BUN, increased SCr, edema in lower extremities

183
Q

intrinisic kidney injury symptoms

A

crush injury (inc creatinine kinase), high SCr, may have fever (inflammation)

184
Q

postrenal kidney injury symptoms

A

increased SCr, inc WBC, urine pH on low end

185
Q

prerenal cause

A

azotemia, hemodynamic form due to hypoperfusion, dec volume, hemorrhage, heart failure, narrowing of artery

186
Q

intrinsic cause

A

damage to the kidney itself from vasculitis or inflammation

187
Q

postrenal

A

due to volume contraction or drugs resulting from formation of obstruction

188
Q

treatment for kidney injury

A

hemodialysis, IV fluid, blood, blood products, dopamine dobutamine to inc CO - inc GFR

189
Q

normal range SCr

A

1 - 1.5

190
Q

normal range BUN

A

7 - 20

191
Q

normal range CrCl

A

125

192
Q

HCO3- higher in ICF or ECF

A

ECF

193
Q

pH more acidic (lower) in ICF or ECF

A

ICF

194
Q

Na / K more concentrated in ICF or ECF

A

K more in ICF

Na more in ECF

195
Q

drugs, pain, fear, anxiety, aspirin causes respiratory acidosis or alkalosis?

A

alkalosis

196
Q

some dugs, emphysemia, pulmonary edema cause acidosis or alkalosis?

A

acidosis

pathophysiology (11 decks)

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