Renal all Flashcards by Sumit Puri

tf kidney is located back of abd cavity

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kidney regulates blood —

composition

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kidneys To balance body water and inorganic ions maintaining stable concentrations in the —– medium

To balance body water and inorganic ions maintaining stable concentrations in the extracellular medium

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hematocrit is

rbc / blood vol

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tf wbc carry substantial vol

F minimal vol

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TF ureter comes from kidney and goes to urethra

F goes to bladder

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What are the arows and what do they do

afferent arterioles(perpendicular to interlobular artery)

constrict and dilate

regulate flow of blood

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tf aff artioles are innerve by PS innervat

Symp innerv.

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glomerular filtration happens at

glom. capillaries

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tf peritub cap come after the aff arterioles

comes after efferent arteriol

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which comes in between the 2 arteriole

thick asc. limb

bowmans capsule

thick descendning limb

thick asc limb

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number of distal tubules that drain into 1 collecting duct

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rank the right order

calyx pelvis ureter

pelvis calyx ureter

ureter calyx pelvis

calyx pelvis ureter

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TF for filtration to occur u need active transport to occur

u dont need anything to facilitate filtration

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TF in juxtaglomerular nephron the glomeruli are bigger and loop of henle are longer than cortical nephron

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granular and lot of dots

cortex with loop of henle

medulla

loop of henle

cortex with glomerular cap

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afferent arterioles

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Vasa recta

exist in cortical nephron

are peritub cap of juxtagom nephron

are convoluted

are peritub cap of juxtagom nephron

arent convoluted

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convoluted peritub cap

cotrical nephron

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tf macula densa are apart of aff. arteriole

part of distal tubule

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granular cells are derive from — — cells of the — —

smooth muscle , aff arteriole

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in between eff. arteriole aff arterioles and distal tubule

mesangial cells

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which of the following is nt a responce to stimulate renin production in the granular cells

composition of fluid going thru distal tubule

pressure in aff arteriole

sympathetic output of kidney

pressur of eff arteriole

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Na balance and Bp

Renin

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sensor of fluid inside distal tubule

Macula densa

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70 nm fenestration

endothelium covering BV

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basement membrane

3rd layer outside glom cap

+ charge

glycoproteins

allows albumin which is negative charged

glycoproteins

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correct the statement

podocytes make up parietal ep layer outside the glomerular cap. with interdigitating pedicels and form 40nm pores . they make up the 1st layer outside the BV.

podocytes make up visceral ep layer outside the glomerular cap.with interdigitating pedicels and form 4 nm pores . they make up the last layer outside the BV.

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contraction of — and — regulate filtration permeability

mesangial cells and podocytes

mesangial cells and macula densa

macula densa and podocytes

mesangial cells and podocytes

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layer preventing filtering of RBC

fenestartion

basement membrane

poocytes

fenestrations(endothelium)

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which of the follwing wil not have a big drop in pressure

renal art

aff arteriole

eff arteriol

renal art

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tf glom. cap pressure is function of pressure in aff and eff arterioles

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tf filtration is an active process

F active

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which of the following has a low reabsorption rate?

glucose

h20

urea

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reabsorption changes in — with—

parrallel ; filtration

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describe the process of urea reabs

h2o reabs

conc of urea inc in tubules

then moves down conc gradient to cap

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H20 impremeable in

thick descending limb

prox tubule

ascending limb

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which 2 structures are needed to absorb salt in prx tubule

microvilli and mitochondria

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required to absorb Na in tubules

Na/ k atpase

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thick descending limb

has lot of microvilli

dissolves salt

h20 imperm.

dissolves h20 but no NA

doesnt have much microvili or mit.

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tf na/ k atpase are on the luminal side of tubes

F on basolat. membrane

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tf Na exchange with H exists in the prox tubule (to get NA into the cell)

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early prox tubule

NA contransport with solutes

Na contransport withK and Cl

has a Na channel to get Na into the tubule cell

NA contransport with solutes

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contains cotransport of Na and Cl to get Na into tubules cell

Prox tubule

Distal tubule

TAL

Distal tubule

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which part of the renal tubule reab 67% of NA

prox tubule

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tf all glucose get reab at prox tubule

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Glucose tranport

SGLT1/2 on basolat. membrane

Na glucose cotransport on lumenal membrane

Na Glucose exchanger on luminal membane

invole GLUT 1 and 2 to get glucose into cap side

more than 1

invole GLUT 1 and 2 to get glucose into cap side

Na glucose cotransport on lumenal membrane

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filtered glucose is a function of

plasma glucose*GFR

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Tm limited

Glucose

h20

glucos

transporter get saturated and cause excretion of Glucose because glucose cant get into cap (reabs)

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2/3 get reabs in prox tubule

h20

glucoese

h2o and Na

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h20 reabs is — in the prox tubule

isosmotic(follows salt)

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high osmolarity in medulla causes H2O reabs in

descending limb

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diabetes mellitus

nill reabs of glucose

no gradient for h2o

h20 in tube and get excreted

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aqp1

exists in?

prox tubule and thick descending limb

(on luminal membrane and basolateral mem)

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ADH triggers — from vesicles to fuse on luminal membrane

AQP1

AQP2

AQP3

AQP4

AQP2

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contain proteins

Glom cap

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peritub cap

larger oncotic pressure than hydrostatic pressure of tubes

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tub. secretion important for

H and K

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H and K

secreted in tubules

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na and h2o

not secreted

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vol of ecf reg by

amt of salt in body

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most of Na available in

ECF

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pressure or vol inc from Na are detected by

baroreceptors

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responce of baroreceptors to inc(pressure or vol)

tell kidney to excrete salt

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load dependent

more Na filtered more resorbed Proxt tubule and Thick ascending limb

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maintain intak=excretion

distal tube and CD

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limited capacity for resorption of NA

distal tube and CD

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tf when u gain or lose NA the first site to be affected is distal segment

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tf when there is loss of salt then more na is resorbed in the prox tubule

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NO acts in NA constraction stimulates na resorption at prox tubulte inh na resorbtion at prox tubule

inh na resorbtion at prox tubule happens when NA inc(ecf expansion)

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tf symp and ang1 stimulate na resorption at prox tubule when there is loss of NA

F symp and ang2

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tf NA amt reabsorbed in distal tubule is low

F small percent but large amt

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which of the following doesnt inh. resorption of NA at distal tubule? no PG ANP ALdosterone

aldosterone inc NA absorption when Na is intaken(ecf expansion)

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which of the function is function of aldoesteron Na resorption by kidney inc adh sec and leads to water retention more thirst arteriolar vasoconstrictor(restore BP)

Na resorption by kidney other by Ang 2

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which of following reg how much aldosterone secreted in plasma renin ang1 ang 2 angiotensinogen

renin

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renin released

from granular cells

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ANP

inc in high ecf cases(NA intake)

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TF RAA system inc na excretion

f dec it

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h20 reabs in prox tubule is

isoosmotic follows NA

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tf most of water is reabsorbed at prox tubule anddistal tubule

F distal tubule is imperm to water

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tf passive transport maintain 200 mOsm gradient in the medulle between tubules cells and int fluid

f active transport

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equilibrates with interstitial fluid

descending limb

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oblig water loss

.5l / day

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diuresis

low adh

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in diuresis osmomolarity is more in cd osmolarity in less in cs salt cant be reabrorb in CD

osmolarity in less in cs because salt is reabsorbed in CD

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active transport out of ascending limb

concentrate the interstitium

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action of ADH to reabsorb water at CD needs

loop of henle needed to set up stage of concentrating interstitium

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wat helps maintain int. molarity

vasa recta

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adh constrict —-,; results in—- solute in medulla

vasa recta; less

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adh sec by

post pit

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tf to restore osmolarity osmorecptors alone are adequate to inc adh

f need to drink h2o

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tf baroreceptor only inh ADH receptors when you have inc vol

f they are constantly inhibiting ADH receptors

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tf osmorecptor and baroreceptor both both have adh as effectors

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vol receptor

baroreceptor

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sense plasma osmolality

osmoreceptor

ecf expansion and anp

inh thirst and adh release

tf body temp is highest from 3-6 pm

T lowest from 3-6 am

tf ovulation has .5 degree celcus dec in temp

f inc

homeotherms

maintain body temp in narrow range

major way to get heat from core to skin

convection

which of the following isnt a way to eliminate heat convection conduction radiation

radiation

convection

fluid movement

conduction

diffusion and collision of particles

bigger velocity

–> bigger gradient in temp (convection)

True false being in cold water increases the amount of heat that is lost from you

T water has higher heat capacity than air

wate vapour pressure on skin — with sweat and carries — because of the —-

inc;heat; gradient(water more pressure than air)

where do temp sensors exist

pre optic area and ant hyp, entire skin surface

tf temp sensory have merkel corpsucle

F have free nerve ending

example of acral skin

face lip finger

tf trunk and limbs have low conc of temp receptor

tf acral skin have higher onc of temp receptor

T(fine temp discrimination

tf when warm receptor stim there is depol and action potential

T ion channel open depol inc in AP

capsaicin

stim warm receptor

menthol and oil or wintergreen

stim cool sensation

tf in body core thermoreceptor there are only cold thermoceptors

F only warm

which is false about core thermceptors in brain in SC responds to 10 degree diff between mean can exist in muscles

responds to 10 degree diff between mean –> 2-4 degree

skin therm receptors tell u to turn on heat loss mech more agresive in hot env to turn on heat loss mech more agresive in cold env to turn on heat loss mech less agresive in hot env

to turn on heat loss mech more agresive in hot env

tf core body thermoceptors inc met rate same amt for diff skin thermoceptors.

F for higher skin thermoceptor the temp is less skin thermoceptors alter sensitivity to body core thermceptor

Brown adipose tissue

inc rate of metab

cutaenous ciruclation

inc blood to skin

vasocontrict to skin

less heat loss

TF ANS control cut circulation

shivering

invol clonic rhythmic contractions and relaxation

which of the following has noradrenagenic stim for cut circ of skin vasoconstrition vasodil of acral skin vasodil of non acral skin

vasoconstriction

tf vasodil of acral skin involves bypassing cap

tf vasodil of acral skin use symp ns

F doesnt

kallikrein is released in vasoconstrition vasodil of acral skin vasodil of non acral skin

vasodil of non acral skin

kallikrein; bradykin 1st second second 1st vasodil; comes from activated sweat gland involved in vasodil of acral skin

1st second

tf brown adipose tissue only found in infants

Infants

thin shell of fat and skin and more susceptible to heat loss

which 2 inc UCP T3 and FA FA and T2 protein kinase and T3 5 deiodinase and alpha 1 receptor

T3 and FA

in brown adipose tissue B3 stim by NE ultimately make Lipase (convert TG to FA) B3 stim by NE make 5’ deiodinase T3 converts to T2 via 5’ deiodinase

B3 stim by NE ultimately make Lipase (convert TG to FA)

TF in brown adipose tissue UCP reverse gradient of H + into inner mit membrane. ATP synthase does the opposite

Non shiver thermogenesis happens in

brown addpose cells

hyperthermia

core temp above limits

hyperthermia

hot humid env with phys activity

tf in hyperthermia inc in core temp by less radiative heat loss less conductive heat loss more evap heat loss 1 and 2

1 and 2

inc radiation and metabolism

cause hyperthemia

tf in hypothermia shivering and cutaneous constriction is sufficient

F not sufficienct have to get out of water

fever in hot env

heat loss mech off

fever in cold env

heat loss mech on

fever in—

fever in cold env

inc of temp in fever

improve t lymph proliferation

tf t lymphocyte proliferate greater in vitro when at 39 then 37 degrees Celsius

heat loss neurons on

fever i cold

shift balance point of temp of 37 dgress celcius

Fever or excersize

at the thick ascending limb

K is transferred to caps at basolateral membrane by

cotransport wih Cl

pump

channel

1 and 3

at prox tubule k is reabs intracellularly and secondary to water and diffusion

reabs paracellularly

how does K get into tubular cell at luminal membrane

cotransport wih 2 cl and na

TF collecting duct and distal convoluted tubule

can reabsorb and sec K

hypokalemia (low plasma K) which cells in CD reab K

intercalated cells

tf principla cell secrete K into urine

Lot of K in diet

Principle cells work to take secrete K in CD andDCT

At basolateral membrane of Principle cells

K/Na atpase bring K into cell from cap

K/Na atpase bring K into cap from tubular cell

K channels bring K into tubular cell to be secreted

K/Na atpase bring K into cell from cap

What is on the lumanal membrane of principle cells to secrete K

K channel

K channels are on intercalated cells to

transfer K from lumen to Tubular cell

reabsorb K from tub. cell to cap

take ATP to reabs K

reabsorb K from tub. cell to cap

In urine

1-20% excreted of K

determine amt of K goes to urine

principle cells of CD

tf hyperkalemia stimulates NaK pump and inc. luminal permeability independent of Aldosterons sec.

inc plasma K levels will:

inc Na/K pump at prox tubule

inc. luminal permeability of CD
dec. aldosterone secretion

inc. luminal permeability of CD
inc. ald and inc. Na k pumps on basolater side of CD cells

aldosterone

insert transport proteins

and make transporter

acidosis

inc. k excretion
dec. K excretion

inc. K excretion

effect of inc. tubular flow

inc. k excretion

metabolism produces

h ions

gain H; lose H

kidney ;urine

buffer for H

bicarb

resp acidosis

accum of CO2 which makes H

any problem with ventilation

inc CO2

diabetics and hypoxia

produce acid

normal diet

make diet

net exogenous acid production

acid made from protein digestion and diabetes and hypoxia

tf amt of acid in body is less than ingest per day

true

tf most of bicarb reabsorption occurs in prox tubule an none goes into urine

tf bicarb is reabsorbed at all parts of renal tubule

at the prox tubule — bicarb is reabs and — h+ is secreter

1;1

prox tubule luminal mebrane how do you get H+ out into lumen

thru exchanger(with NA) and pumP

how does HCO3 get to cap at basolat membrane of Prox tubule

cotransport with NA

exchange with Cl

at luminal side of the collecting duct

H get secreted by

pump with H+

and exchange with K(need ATP)

how does hco3 get to cap side in CD

exchange with CL

tf in prox tubule and collecting duct

h secreted and HCO3 reabsorbed

and both 1;1

intercalated alpha type cell occurs

at CD to resorb bicarb

in intercalated beta cells of the cd

hco3 secreted in eaxchanged for

principal cells have wat features

aqp2 and Na channel

located in CD

exhange of h with urinary buffer

h+ with atp pump

bicarb exchange for CL

interacalated cells

H pump

beta intercalated types cells are used to

transfer hco3 to tube in alkalosis(excess hco3 in blood)

purpose of interacalated alpha; vs beta cells

reabsorb bicarc; secrete bicarb

reabs H+ and secretion of Bicarb occurs in

interacalate alpha

intercalated beta

prox tubule

intercalated beta

tf ammonium production and bicarb reabsorption are 1;1 in the proximla tubule

(h excretion from urine)

NH4 reabsorbs —–

and get resecreted as —–

at thick ascending limb

nh3 in the collecting duct

contributes to 2/3 of acid excretion from urine

ammonium production

tf ammonium production to excrete acids in urine is ridge and take up 2/3 of total acid excretion in urine

flexible

2/3 correct

during ammonium formation to excrete acid in urine

glut braks down to bicarb and nh4(1;1)

nh4 dissolves away to tubular fluid alone

nh3 is exchanged for na on the tub. membrane

glut braks down to bicarb and nh4(1;1)

renal failure

patient cant get rid of acid

diabetic acidosis

inc nh4 and ta in cap

acidosis

inc in acid in tubular cells

what does acidosis trigger

transporter and enzyme secretion to transport acids(nh4 and TA) to urine

excersizing

met. acidosis

diahrreha

met. acidosis

vomit

met. alkalosis

trigger hypervent

met acid.

trigger hypovent

met. alk.

tf metabolic acidosis results in low ph and high pCO2

low both

tf most of k is in interceullular fluid

t/f 2/3 of fluid in body is ecf

f it is icf(28l to 14 l)

plasma k when lower than 3.5 meq/l

hypokalemia

normal plasma conc

3.5-5 meq/l

what is the effect on the right

low k outside

hyperpolarized and hard to get to threshold

symptoms of the curve on right

increased K on outside

very excitable

det resting potential

k out

after a meal plsma k increases stim k uptake thru

na/ k atpase

insuline and epeniephrine

inc k uptake by inc. na k atpase turnover rate

hyperkalemia

caused by insulin deficiency and beta antagonist

epinephrine bind to – to inc na/k atpase turnover rate and k is brought into the cell

beta receptor

treatment for hyperkalema

b agonist and insulin

2 factors inc na/k atpase pump

so that k can be absorbed in tissue cells

plasma k

insulin and epinephrine

tf after plasma K inc after a meal it immediately get translocated in a tissue cell and then immediately the plasma k level goes down to normal

F the plasma k level stays elvated to signal kidney to get rid of K by having more pumps activated

tf after k accumulates in tisses cells after intestinal absorption there is fast renal excretion

renal excretion is very slow (little by little goes ijnto urine)

plasma k

and aldosterone

signal excretion k in urine

tf after K is absorbed in the intestines it immediately stays in the ECF

ECF doesnt want to saturate and it get transferred to Tissues

inc volume

signal for kidney to excrete more salt

less o2 and insulin

cause Acid from fat and carb

carotid bodie and chemoreceptor

trigger hypervent when there is in H from food

tf int.alpha cells reabsorb most HCO3

proximal kidney cells do

tf K is more prevalent in ECF

alpha int and principle cells

K transport in CD

Alkalosis

stimulates potassium secretion

heat loss to water

ex of convection

inc. flow thru arteriovenus anastomoses

cut. circulation

symp. vasodil

non acral skin

kallikrein released in cut circ of

non acral skin

sweat gland act by

symp.

impaired ability to shiver and sweat

infants

tf warm core thermoreceptors are always on

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Renal all Flashcards

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