Urinary system part 2 Flashcards
diverticulitis
when pressure builds up in sigmoid colon, weakened walls form out pockets called diverticula = diverticulosis
- when things get stuck and the diverticula get inflamed, it results in diverticulitis
- fistula can form = a canal b/w 2 organs
treatment of mild diverticulitis
antibiotics to treat infection
high fiber diet
fluid diet until healed
treatment of severe diverticulitis
colonoscopy: 2 parts
1. surgically remove part of inflamed colon, take healthy part and attach it to a hole in the abdominal wall called a stoma and put a bag on it
2. once colon has healed, reattach colon to rectum again
true vs false diverticula
true are made up of all layers of large intestine
false are only pockets that consist of serosa
3 processes in urine production
- glomerular filtration
- tubular reabsorption
- tubular secretion
results in fully filtered blood and production of urine
glomerular filtration
occurs in renal corpuscle,
where water and solutes move into Bowman’s capsule
renal bloodflow
20-25% of CO goes to kidneys at rest
this is about 1.2 L/min
renal plasma flow rate
55% of renal blood flow
is about 650 mL
- this is the amount of fluid that COULD be filtered
filtration fraction/ somewhat lumped with glomerular filtration rate
16-20% of the plasma flow rate
is about 125 mL/min OR 150-180 L/day
contributors to net filtration pressure (NFP)
- glomerular blood hydrostatic pressure
- capsular hydrostatic pressure
- blood colloid osmotic pressure
- the last 2 both work against GBHP
glomerular blood hydrostatic pressure (GBHP or GCP)
55mmHg
- the driving pressure in the afferent arteriole that works towards producing filtrate
- same as regular BP bc pressure in efferent arteriole is less which gives driving pressure
capsular hydrostatic pressure (CHP)
15mmHg
- pressure in capsular space due to the constant presence of some amount of glomerular filtrate
- works against producing filtrate
blood colloid osmotic pressure (BCOP)
30mmHg
- because filtration membrane doesn’t allow proteins to leave the glomerulus, the proteins on the inside are attracting the water outside to their area of higher concentration inside the glomerular capillaries
- works against producing filtrate
how is net filtration pressure calculated and what is it?
NFP = GBHP - CHP - BCOP
= 55 - 15 - 30
= 10 mmHg
glomerular filtration rate
the amount of filtrate formed in all renal corpuscles in both kidneys per minute
- average rate for women is 105 mL/min,
for men is 125 mL/min
- filtration stops if GCP (GBHP) drops to 45mmHg bc NFP becomes 0 then
what happens when GFR is too high
we may not be able to absorb things quickly enough and things that we want could be leaving the body
what happens when GFR is too low
filtrate may spend too much time in renal tubules and things we don’t want might be reabsorbed
ways GFR is regulated
2 ways:
- adjusting blood flow (by decreasing BF, we decrease the amount of filtrate produced)
- altering glomerular capillary surface area (less SA means less filtrate produced)
mechanisms of GFR control
- renal autoregulation
- neural regulation
- hormonal regulation
renal autoregulation of GFR
keeps rate relatively constant despite changes in BP, etc
incl: myogenic mechanism and tubulogomerular feedback
myogenic mechanism
a mechanism of renal autoregulation
- fast response to BP changes
- an increase in BP causes afferent arteriole walls to stretch causing smooth muscles to contract and decrease blood flow to glomerulus, thus GFR returns to normal
- prevents high BP from affecting GFR too much
- also works in response to a decrease in BP
tubuloglomerular feedback
a mechanism of renal autoregulation
- slower because have to wait for fluid to move through tubules and back to juxtaglomerular apparatus to know if adjustments need to be made or not
- GFR increases when Na+, Cl- and water are not reabsorbed, leaving more stuff in tubules
- this is detected by macula densa and inhibits release of nitric oxide (a vasodilator) from juxtaglomerular apparatus, causing afferent arterioles to constrict, decreasing blood flow to glomerulus and decreasing GFR
neural regulation of GFR
sympathetic ANS innervation
not a lot at rest
not a lot when moderate sympathetic stimulation
- larger sympathetic stimulation ex. exercise: vasoconstriction of afferent arterioles causes a decrease in blood flow and GFR, lowering urine output and allows blood flow to other tissues
hormonal regulation of GFR
2 methods:
- atrial natriuretic peptide
- angiotensin II
atrial natriuretic peptide (hormonal regulation of GFR)
increases GFR
- stretching of atria occurring bc of increase in blood volume causes ANP to be released from cells near atria
- relaxes glomerular mesangial cells which increases capillary SA, producing more filtrate, urine and decreasing blood volume to get back to norm
angiotensin II (hormonal regulation of GFR)
reduces GFR
- a vasoconstrictor that narrows afferent AND efferent arterioles therefore decreasing blood flow and GFR
tubular reabsorption
- nephron reabsorbs 99% of filtrate
- most reabsorption occurs in PCT
- water, solutes, glucose, AA, urea, ions (Na, Cl, Ca2+, bicarbonate, phosphate) and small proteins
tubular secretion
transferring materials from blood into glomerular filtrate/tubular fluid
- controls blood pH (H+ secretion)
- eliminates substances (ammonia, creatinine, K+, some drugs)
primary active transport
ATP dependant transport used to move ions against their concentration gradients
ex. Na+/K+ pump
secondary active transport
driven by ion’s electrochemical gradient via symporters and antiporters
symporter
bring substances in same direction (towards cell)
ex. Na brings glucose with in into the cell and we need active transport to create a low concentration of Na+ inside the cell, keeping the electrochemical gradient