Exam 6- Renal System (without pathology) Flashcards
(162 cards)
1
Q
kidney regulates
A
- long term blood pressure
- blood cell count /hemoglobin levels (produces erythropoietin)
- Ca2+ homeostasis(activates vit. D)
2
Q
kidney structure
A
v
3
Q
functional unit of the kidney=
A
nephron
4
Q
juxtaglom vs cortical neph
A
m
5
Q
renal corpuscle=
A
glomerulus + bowman’s capsule
6
Q
tubule path
A
Proximal tubule (convoluted and straight)
Loop of Henle
Distal convoluted tubule
Collecting duct (cortical and medullary)
7
Q
after collecting duct urine passes to___
A
minor calyx
major calyx
renal pelvis
ureter
8
Q
peritubular capilaries surround
A
cortical segments of tubule
9
Q
vasa recta surrounds
A
loop of henle
10
Q
blood pathways
A
- efferent arteriole -> peritubular cap-> renal vein
- efferent art. -> vasa recta -> renal vein
11
Q
three processes involved in urine production
A
glomerular filtration
tubular resorption
tubular secretion
12
Q
___+_____+______= amount excreted
A
amount filtered + amount secreted - amount reabsorbed
13
Q
filtered load
A
= “amount filtered”
14
Q
glomerular filtration barrier needs to achieve=
A
- high H20 filtration rates
- nonrestricted passage of small/mid sized molecules
- total restriction of serum albumin, proteins and cells
15
Q
layers of filtration membrane
A
endothelial cell
basement membrane
pedicels of podocytes/filtration slits with diaphragm
16
Q
diaphragm between podocytes=
A
web of nephrin
17
Q
what is freely filtered trough glom. filtration membrane
A
water
electrolytes
glucose
amino acids
urea
NOT big protiens and cells
18
Q
osmolality of plasma and filtrate
A
300mOsm/kg
19
Q
[Na+] in plasma and filtrate
A
both 140mEq/L
20
Q
[glucose] in plasma and filtrate
A
100mg/dL
21
Q
[albumin] in plasma and filtrate
A
plasma= 4mg/dL
filtrate= NONE
22
Q
forces that affect filtration
A
starling forces= hydrostatic pressure oncotic pressure
23
Q
filtration promoting forces
A
- Pgc - Glomerular capillary hydrostatic pressure
- π BS- colloid osmotic or oncotic pressure in bowman’s space (but this is practically zero…)
24
Q
filtration opposing forces
A
- Pbs- hydrostatic pressure in bowman’s space
- πGC- glomerular capillary oncotic pressure = amount of proteins in plasma
25
net filtration pressure=
"ultrafiltration pressure" NFP = (+)Pgc - Pbs- πGC
26
filtration coefficient (Kf) determined by
1. hydraulic permeability of the membrane
2. surface area of the filtration membrane - both mainly change with disease
27
glomerular filtration rate =
(equation)
= Kf x NFP = (filtration coefficient) (net filtration pressure)
28
what makes glomerulus different than other capillary beds
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
29
GFR=\_\_\_\_ ml/min or \_\_\_\_L/day
amount of filtrate/min healthy = 125ml/min or 180L/day
30
healthy people control ___ to ∆ GFR
Pgc
31
pathologies affect ____ to ∆ GFR
Pbs πGC πBS
32
\_\_\_ affect Pgc
Mean arteriole pressure
resistance at afferent and efferent arterioles
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MAP decreases = Pgc\_\_\_\_ and GFR\_\_\_
Pgc decreases GFR decreases
34
afferent arteriole dilates = Pgc\_\_\_\_ and GFR\_\_\_
Pgc increases GFR increases
35
constrict aff. arteriole = GFR \_\_\_
decreases
36
eff. arteriole dilates = Pgc\_\_\_\_ and GFR\_\_\_
Pgc decreases GFR decreases
37
constrict aff. arteriole and eff. arteriole at the same time = GFR \_\_\_\_\_
GFR stays the same
38
plasma protein concentration increases = πGC\_\_\_\_ GFR\_\_\_
πGC increases GFR decreases
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filtration membrane becomes more permeable = πBS\_\_\_\_ GFR\_\_\_
πBS increases GFR increases
40
kidney stone blocks a ureter = Pbs\_\_\_\_ GFR\_\_\_\_
Pubs increases GFR **decreases**
41
blood flow rates in
kidney cortex=
outer medulla=
inner medulla=
cortex= 4-5
outer medulla= 0.7-1
inner medulla=0.2-0.25
42
When mean arteriole blood pressure is between ____ the kidney can auto regulate it.
80 to 140mmHg
below range, then GFR is too low
above range, then glomerulus is damaged
43
two components of auto regulation
1. myogenic response
2. tubuloglomerular feedback
44
myogenic response
MAP increases (causes and increased RBF, Pgc, and GFR)
=stretches the afferent arteriole
=afferent arteriole then constricts which then decreases RBF, Pgc, and GFR
45
tubuloglomerular feedback
increased MAP
=transient increase in GFR
=increase NaCl delivery to macula densa
=release adenosine
=constricts afferent arteriole
46
small drop in MAP is dealt with by=
myogenic response and tubuloglomerular feedback =dilation of afferent arteriole
47
HUGE drop in MAP is dealt with by=
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...
48
autonomic NS responds to HUGE drop in MAP by\_\_\_
activating SNS = constricts afferent arteriole yikes!!
49
end results with HUGE decrease in MAP
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
50
why does SNS constrict the aff. arteriole with huge drop in blood pressure
body's trying to decrease renal blood flow so less blood goes to kidney so it can go to heart and brain
51
renal artery stenosis
decreased RBF, Pgc, GFR
52
auto regulatory response to renal artery stenosis
dilate the afferent arteriole AND constricts the efferent arteriole
53
efferent arteriole is constricted via\_\_\_
RAAS
- Juxtaglomerular cells =\>renin
- (+) angiotensin II which constricts eff. arteriole
54
NSAIDS effect
inhibits prostaglandins which normally dilate afferent arteriole
55
decreased effective circulating blood volume (heart failure) causes...
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
56
large amounts of both NE and Ang II=
decreased RBF, but somewhat maintained GFR
=renal ischemia
=increased prostaglandin production
=dilate the afferent arteriole somewhat counteracts the decrease in RBF and prevents ischemia
57
why is it bad to take an NSAID if you have heart failure?
NSAIDS (-) prostaglandin aff. arteriole dilation which would increase GFR and RBF and therefore causes lower RBF and GFR which= ACUTE KIDNEY INJURY
58
Renal Clearance=
Volume of plasma cleared of a substance per unit time Volume/Time
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Normal GFR=
125ml/min
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A substance is filtered and reabsorbed but not secreted then its clearance is \> GFR
LESS THAN
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clearance = GFR then _____ reabsorption or secretion
no net
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clearance \> GFR then there has been net \_\_\_\_\_
secretion
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clearance
reabsorption
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p-aminohippurate (PAH)
-not endogenous -at low concentrations PAH is filtered, none is reabsorbed and the rest is secreted ∴ PAH is a measure of renal plasma flow
65
to measure GFR we need a substance that is \_\_\_
freely filtered not reabsorbed not secreted
66
practically measure GFR via\_\_-
creatinine clearance
67
creatinine
=endogenous -end product of creatine metabolism -continuously exported to blood by skeletal muscle -freely filtered, not reabsorbed, only a small amount is secreted
68
ways to measure creatinine
1. 24hr urine collection 2. measure creatinine in serum = eGFR ("estimated" GFR)
69
if your have higher serum creatinine your GFR is
lower than normal, bc you're not clearing it from the blood
70
how much urine is produced each day?
1 to 2 L
71
what is reabsorbed
Water -up to 99%
Good solutes (ie. ions) -majority
Nutrients: glucose, AA - 100%
Urea- maybe half
72
lipid soluble substances move across epithelial cells interstitial fluid by\_\_\_ when\_\_\_
diffusion only when there is a [] gradient
- happens when H2O is reabsorbed urea follows water back into peritubular cap. when H2O is reabsorbed
73
what is the osmolality of plasma, the filtrate entering the proximal tubule, and the surrounding interstitial fluid?
all the same 300mOsm/kg
74
who de we get a concentration gradient for water
by resorbing Na+ via mediated transport
75
mediated transport=
uses energy at some point
76
draw how glucose is reabsorbed in the proximal tubule
77
with the reabsorption of glucose what follows\_\_\_\_
water via aquaporin-1
78
movementof ions, glucose and water from interstitial space into peritubular capillary is via\_\_\_
bulk flow
via starling forces
79
how much glucose is reabsorbed in the proximal tubule?
all of it
80
how does glucose end up in diabetic's urine
the transport maximum of the glucose transporter is exceeded
81
reabsorption of Na+ accomplishes...
**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
glucose and amino acids are reabsorbed by primary or secondary active transport in the PCT?
secondary
83
What is absorbed in PCt
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
beginig of PCT osmolality=
end of PCT osmolality=
both = 300mOsm/L
85
what is reabsorbed in the loop of henle
Na+
K+
Ca2+
Mg2+
86
what parts of the loop of henle are permeable to water
thin descending
-thick and thin ascending are impermeable
87
thick/thin ascending limb have diffusion/active transport
thin=diffusion
thick =active
88
draw reabsorption in the thick ascending limb
89
reabsorption via the Na-K-2Cl cotransporter is considered ____ transport
secondary active transport
90
efflux of K+ into the lumen and Cl- into the interstitum generates\_\_\_
a positive transepithelial potential difference
=dirves the paracellurlar transport or resorption of positive ions
91
\_\_\_ of NaCl is reabsorbed in loop of henle
20%
92
osmolality of the filtrate at the beginign and end of loop of henle
begining =300mOsm/L
end=100mOsm/L
we're resorbing more solute water
=diluting urine
93
resorption in DCT diagram
94
what is resorbed in DCT
6%of NaCl
no mo H2O is resorbed and we're taking out solute so
∴ urine becomes more dilute
95
osmolality of DCT filtrate at begining and end
begining=100mOSm/L
end=80mOsm/L
96
draw Collecting duct resorption and secretion
47
97
aldosterone
function?
draw effects in CD
controls the amount of Na+ resorbed in the CD
98
loop diuretic inhibits Na-K-2Cl cotransporter in the loop of henle ∴
Na+\_\_\_
K+\_\_\_
- 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
thiazide diuretic inhibits the Na-Cl cotransporter in DCT
∴ Na+\_\_\_
K+\_\_\_\_
-more Na+ to CD = more Na+ is absorbed
=more K+ secreted= hypokalemia
100
diuretic inhibits the Na+ channel in the CD
=Na+\_\_\_\_
K+\_\_\_
=decreased Na+ resorptin
=less K+ secreted
= hyper kalemia
101
draw summary of where Na+ goes in nephron
102
urine is more/less concentrated than plasm
less
103
osmolality in different parts of the nephron
slide 4 of 22
104
ADH function
puts H20 channels on CD
∴ if we want dilurte urine we want low ADH
105
to prodce a concentrated urine we need:
1. CD permeable to H2O
∴ high ADH
2. interstitial fluid needs to be concentrated
= a large amout of H2O can be reabsorbed
106
what makes the interstitial fluid around the CD concentrated?
1. countercurrent multiplication
1. countercurrent exchange
107
counter current multiplication
diagram
108
draw how ADH has effects in the CD
109
without ADH we would produce ___ urine
dilute
about 50 mOsm/kg H2O
110
with max ADH we would produce ___ urine
concentrated
about 1200 mOsm/kg H2O
111
as filtrate goes down CD ...
water is reabsorbed, and urine becomes more concentrated
-we can secrete urine anywhere from 50 to 1200 mOsm/kg H1O
112
extra-cellurlar fluid volume
plasma=3.5L
itnerstitial fluid = 10.5 L
113
intracellular fluid volume
=28L
114
blood, interstitial and intracellular concentrations of
Na+
K+
protiens-
H20
diagram
115
interstitial
116
H20 in blood increases...
it shifts via osmosis form ECF to ICF to reach equillib
=cell swelling... lysis... death
117
infuse person with 2L of H2O vs saline
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
a problem wiht osmolality (hyponatremia or hypernatremia) is a ___ problem
water
119
a ∆ in ECF Na+ changes \_\_\_
blood volume and pressure
and NOT the Na+ concentration in the blood
120
sources of water for the body
drinking
cellular metabolism
121
how does the body lose water
skin (sweat)
lungs (evap.)
gi (feces)
kidney
122
what organ regulates water loss
kidney
123
what stimulates ADH
blood osmolality
124
osmoreceptors sense increased plasma osmolarity...
1. (+) thirst center
2. (+) hypothalamic neurons
(+) ADH released from POSTERIOR pituitary
125
lots of ADH = excrete ___ urine
little ADH = excrete ___ urine
lots of ADH = excrete small vol, concentrated urine
little ADH = excrete lots of dilute urine
126
\_\_\_ and ___ are main controllers of total body water and plasma osmolarity
ADH and thirst
127
central diabetes insipidus
pituitary secretes too little ADH
-from head trauma/tumor/brain surgery
128
nephrogenic diabetes insipidus
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
with a large drop in BP we ___ ADH
increase
so to increase water resorption
(however arteriole constriction has the bigger effect)
130
what takes presedence volume or osmolarity?
volume
-we will sacrifice osmolarity to increase blood volume
131
with an high salt meal
total body [Na+] increases
ECF [Na+] stays the same (water shifts out of cells to compensate)
blood volume will be higher
132
kidney knows total body Na+ is elevated by sensing\_\_\_
the change in blood volume and pressure
133
how does kidney regulate Na+ excretion?
1. change the GFR to increase Na+ exretion
GFR is highly regulated so maybe not the best way
2. Glomerulotubular balance
3. RAAS (aldosterone increases Na+ abs. - opp of ANP)
4. Atrial Natriuretic Peptide (ANP)
134
Increaseing GFR's effect on Na+ excretion=
=("glomerulotubular balance")
=more Na+ filtered
=more Na+ reabsorbed in PCT and loop of henle
∴ only 1-2% of extra Na+ is excreted
135
draw juxtaglomerular apparatus
136
Juxta glom. senses low Na+
1. SNS senses low BP and volume
= (+) JGCs
=\>RENIN
2. macula densa senses less Na+ in DCT
(+) JGCs
=\>RENIN
137
renin as an enzyme pathway
diagram
138
what will lower total body Na+ and blood pressure
1. raise GFR
2. inhibit RAS
3. (+) ANP
139
ANP
when blood volume increases atria stretch
= (+) ANP release
=inhibits Na+ resorption in tubules and increases GFR
140
what controls K+ balance
- shifting K+ either into or out of cells
- cortical collecting duct
- aldosterone
141
normal Na+ and K+ levels
Na+ = 135 to 145 mEq/L
K+ =3. 5 to 5 mEq/L
142
if hyperkalemic
insulin and epinephrine shift into skeletal muscle cell
143
draw where K is moving in the nephron
144
draw K+ excretion in CD
145
draw aldosterone and K+ in CD
146
Where do we get acids from?
How do we get rid of them?
**1. CO2**
**2. nonvolatile acids**
CO2 + H2O ⇔ H2CO3 ⇔ H+ + HCO3-
**Metabolism generates CO2**
**Breathing eliminates CO2**
147
when tissues produce more CO2 blood pH is not altered because...
we increase RR
148
nonvolatile acids
=any other acid other than CO2 (carbonic acid)
DONT MEMORIZE THIS LIST
=lactic acid
acetoacetic acid
ß-hydorxybutyric acid
phosphoric acid
sulfuric acid
149
how do we use non volatile acids?
-converted to HCO3-
∴ consumes H+
150
How does the body deal with this excess acid rom metabolism that generates novolatile acids?
1. H+ is buffered by HCO3-, protien or PO3-
2. Respiration
3. Renal
151
how fast does the respiratory rate to an increase in nonvolatile acids occur?
quickly ... but this fix is limited so we need kidneys
(generally lung responds quickly and kidneys respond slowly)
152
How does kidney respond to increased H+?
1. reabsorption of HCO3- in PCT
2. production of new HCO3- in nephron
- coupled ot the excretion of H+
153
producing a dilute urine is controled more by \_\_\_
producing a concentrated urine is controled more by \_\_\_\_
producing a dilute urine is controled more by loop of henle
producing a concentrated urine is controled more by CD
154
draw two pathways of making new HCO3- in nephron
insert diagram 16 and 17/33
155
renal response to an increase in non-volatile acids is fast/slow
slow... days
156
what is respiratory vs. metabolic acidosis or alkylosis?
**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
patient has ketoacidosis, but a blood pH test says they're in normal range... do they still have acidocis
YES
YOU HAVE TO LOOK AT THE WHOLE PICTURE!
-underlying problem is still around even though he's in a normal range
158
3 main causes of metabolic acidosis
1. diabetic ketoacidosis
(ketone body acids)
2. kidney failure
(incresased loss of bicarb, decrease excretion of ammonium and titratable acids)
3. diarrhea
(loss of bicarb)
159
hypoventialation/hyperventilation cause respiratory acidosis/alkalosis
hypo- acidosis
hyper- alkalosis
160
how does body deal with respiratory acidosis or alkalosis?
kidneys!
resorb or excrete HCO3- and titratible acids
161
vomiting induced acid-base disorder= metabolic/respiratory acidosis/alkalosis
metabolic alkalosis
-can also be caused by too many antacids...
162
