t13 urinary sys

kidneys are main organs of homeostasis because they

maintain acid base balance and water salt balance of blood

organs of the urinary sys

kidneys, ureters, urinary bladder, urethra

kidneys

filter waste products from bloodstream, convert filtrate into urine

3 regions of kidney

outer cortex, middle medulla, innermost pelvis

each kidney contains microscopic urine producing structures called

nephronsn

nephrons

microscopic urine processing structures

2 types of nephrons

cortical and juxtamedullary

cortical nephrons

majority of nephrons, short nephron loops— efferent arterioles branch into peritubular capillaries around PCT and DCT

juxtamedullary nephrons

minority of nephrons, very long nephron loops, maintain salinity gradient in the medulla/helps conserve water— efferent arterioles branch into vasa recta around long nephron loop

each nephron is associated by 2 capillary beds

glomerular capillaries and peritubular capillaries/vasa recta

3 stages of urine production

filtration, reabsorption, secretion

glomerular filtration

water/solutes smaller than proteins forced through capillary walls and pores of the glomerular capsule into the renal tubule

tubular reabsorbtion

water/glucose/amino acids/needed ions transported out of the filtrate into tubule cells and then enter the capillary blood

tubular secretion

H+/K+/creatinine/drugs removed from peritubular

as blood flows through glomerulus — — — filters through the glomerular capillaries into — —

protein-free plasma, Bowman’s capsule

almost any molecule smaller than — nm can pass frely through filtration membrane into capsular space

3

kidney infections and trauma commonly damage the filtration membrane and allow — — or — — to pass through

plasma proteins, blood cells

net filtration pressure

outward pres - inward pres / (HPgc) - (HPcs + OPgc)

filtration/reabsorbtion is always favored in renal corpuscle

filtration

hydrostatic pressure inside the glomerular capillaries favors

filtration, HPgc = 55 mmHg

colloid osmotic pressure in glomerular capillaries

favors reabsorption, OPgc = 30 mmHg

hydrostatic pressure inside capsular space favors

reabsorption, HPcs = 15 mmHg

colloid osmotic pressure of fluid in capsular space favors

filtration, OPcs= 0 mmHg (proteins are excluded from filtrate in capsular space)

glomerular filtration rate (GFR)

volume of filtrate produced by both kidneys per min

GFR (glomerular filtration rate) is — — to the NFP (net filtration pressure)

directly proportional

changes in GFR normal result from

changes in glomerular bp

when bp increases from a low 90/75 to a high 220/160 the glomerular filtration rate will not change from 125 ml/min

a

three mechanisms control the GFR

renal autoregulation (intrinsic sys), neural controls, hormonal mech (renin-angiotensin sys)

four mechanisms are in operation for autoregulation

myogenic mechanism, tubuloglomerular feedback mechanism for autoreg, glomerulotubular feedback, mesangial cells

myogenic mechanism (autoreg of gfr)

arterial pres rises/afferent arteriole stretches, vascular smooth muscles contract, arteriole resistance offsets the pressure increase— rbf remain constant

tubuloglomerular feedback mech for autoreg

feedback loop consists of flow rate sensing mechanism in macula densa of juxtaglomerular apparatus— releases paracrine factors that cause constriction of afferent cap

if bp increases — afferent arteriole and — efferent to bring GFR back to normal

constrict, dilate

mechanism of myogenic autoregulation

inc bp → inc afferent arteriolar bp → inc arterial wall stretch → sensing by myogenic stretch receptors → inc opening of voltage gated Ca+ channels → ic influx of Ca from ECF to vasuclar sm cells → inc vasoconstriction → decr minimizes changes in afferent arteriolar blood flow → decr minimizes changes in GFR

juxtaglomerular apparatus/complex

specialized region of nephron where afferent arteriole and distal convoluted tubule (DCT) come in direct contact with each other. consists of:

• juxtaglomerular cells

• macula densa cells

juxtaglomerular cells

(modded sm cells) of afferent arteriole including renin containing and sympathetically innervated granulated cells which function as mechanoreceptors to sense bp

macula densa cells

(Na+ sensors) of distal convoluted tubule (dct) which function as chemoreceptors to sense changes in solute conc and flow rate of filtrate

glomerulotubular balance

intrinsic ability of tubules to increase their reabs rate in respnse to inc tubular inflow

at rest renal bv is maximally — bc

dilated, sympathetic activity is minimal

with extreme symp stim, vasoconstriction of afferent arterioles — GFR

reduces

glomerulotubular balance

intrinsic ability of the tubules to increase reabs rate in response to increased tubular inflow

mesangial cells and how they help autoreg of gfr

surround afferent arteriole and constrict, reinforcing afferent arteriole

glucosuria

glucose in the urine, too much glucose in blood (usually is completely reabsorbed into blood)

diabetes insipidus

ADH deficiency causing increased water in urine (insipidus— tasteless) leads to hypoosmotic hypervolemia

aldosterone decreases K+ levels/increases Na+ by

increasing rate of K+ excretion, increasing rate of Na+ absorption

stimuli for aldosterone release

hyperkalemia, hyponatremia

pct reabsorbs — of glomerular filtrate and returns it to peritubular capillaries

65%

nephron loop — another 25% of filtrate

reabsorbs

dct — Na+, Cl- and water under hormonal control

reabsorbs

in addition to extracting water/solutes tubules also extract — and — them into the tubular fluid

drugs, wastes, solutes from blood; secrete

most selective reabsorption occurs in the

proximal convoluted tubule

peritubular capillaries role in absorption

provide nutrients for tubules and retrieve fluid the tubules reabsorb

descending limb of loop of henle

reabsorption of water via channels formed by aquaporin proteins— driven by high osmolarity of intersitial fluid

ascending limb of loop of henle

salt diffuses from tubule into interstitial fluid causing the filtrate to dilute

the more solutes that leave the ascending limb into the medullary interstitial fluid, the greater the — — set up around the descending limb to stimulate more water to diffuse from the descending limb

osmotic gradient

countercurrent exchanger in vasa recta function

retain solutes in the isf of medulla

dct and collecting duct are normally — to water, and require — — —

impermeable, action of hormones

two types of cells found in collecting duct

principal cells, intercalated cells

principal cells (collecting duct) contain receptors for

contain receptors for ADH and aldosterone, calso found in dct

binding of adh to principal cell increases…

increases the synthesis of aquaporing which allow more water reabsorption

in principal cells aldosterone increases synthesis of — for more — —

Na/K pumps, salt reabsorption

intercalated cells role

homeostasis of blood pH by pumping H+ ions into urine

antidiuretic hormone

secreted by pituitary gland, regulates amount of water reabsorbed by distal tubules and collecting ducts

inc ADH, inc H2O reabsorbed

renin-angiotensin → aldosterone hormonal mechanism

conserve water to help prevent further decline in BP

inc aldosterone, inc reabsorption of Na+ and Cl-

atrial natriuretic hormone hormonal mech

secreted from cardiac muscles in RA when inc in BP

inc anh: decr reabsorption: inc urine output: decr blood volume and BP

adh induces production of — — in collecting duct making it permeable to water

aquaporin complexes

excessive aldosterone will cause

excess Na+ reabsorption

urinary excretion rate eq

filtration rate - reabsorption rate + secretion rate

increases in plasma CO2 results in

respiratory acidosis

decreases in plasma CO2 results in

respiratory alkalosis

respiratory acidosis: cause and comp mech

cause: hypoventilation; inc Pco2 causing inc H+ in blood

compensatory mechanism: renal— type A intercalated cells activated to inc H+ excretion and HCO3- reabsorption

respiratory alkalosis: cause and comp mech

cause: hyperventilation, inc CO2 expired

decr blood Pco2 → decr H+ and HCO3-

compensatory mech: renal— type B intercalated cells to inc HCO3- excretion and H+ reabsorption

metabolic acidosis

incr H+/decr HCO3- in blood → decrease blood pH due to incr in metabolic acids

compensatory mech: hyperventilation to inc CO2 expired or renal— type A intercalated cells

metabolic alkalosis

inc in blood pH due to decr in metabolic acids

comp mech: hypoventilation renal— type B intercalated cells