the renal system Flashcards
two types of nephron
superficial cortical
juxtamedullary
superficial cortical
-glomeruli in outer cortex- shorter loop of Henle which only dips slightly into the medulla – lost entirely embedded in the outer medulla
juxtamedullary
dips deep into the medulla–> LONG loop of Henle –> near corticomeduallry border.
-larger glomeruli= higher filtration rate
glomereulus
sack of blood vessels situated in the bowman capsule
what leads into the glomeruli
afferent arterioles
what leads from he glomeruli
efferent arteries- proximal convoluted tubule, loop of henle, distal convoluted, collecting duct
corpuscle
always in the cortex–> glomerulus and bowman capsule
how does afferent and efferent arterioles control blood flow into the glomerulus
total resistance of afferent and efferent arteries, which is determined by the contraction of them, determines the renal blood flow-> contraction and dilation is important to maintain an even blood flow
what is filtered out of the blood at the bowman capsule
water,
salts,
glucose,
urea
these are filtered out due to their physical size–> water and solute have a relatively low molecular mass
of what molecular mass can be filtered at the corpuscle
68,000
what is filtrate produced at the glomerulus called
glomerulus filtrate–> forms 123cm per min in humans
what is filtration referred to at the bowman capsule
ultrafiltration–> the force of hydrostatic pressure in the glomerulus is the driving force which pushes the filtrate out of the capillary
what is ultrafiltration controlled by
1) size of the endothelium fenestrations (70-100nm)
2) filtration slits in the podocytes (25nm)
3) -ve charge of the endothelium
filtration slits and podocytes
Blood flows through the capillaries of the glomerulus (10), where it is filtered by pressure. The podocytes (3a and 3b, green) are wrapped around the capillaries. Blood is filtered through the slit diaphragm (or filtration slit), between the feet or processes of the podocytes.
how much filtrate actually leaves the body
1%–> the rest is reabsorbed
tubule reabsorption 3 types
active transport
osmosis
diffusion
reabsorption in the proximal convoluted tubule
- -> where most absorption happens–. water and glucose.
- ->most of kidneys energy goes into reabsorption of na+ ions–> through symporters therefore active transport
- -> water follows sodium (obligatory water reabsorption)
reabsorption in the loop of henle
due to counter flow arrangement, countercurrent multiplication is facilitated.–> this creates a high solute conc in the tissue fluid of the medulla
1_ descending: permeable to water, less permeable to na+ and cl- and to urea. H2O moves into the interstitum
2_Ascending (thin): not permeable to water. highly permeable to Na+ and Cl—> diffuse int the instersitium
3_Ascending (thick): more NaCl reabsorbed
why is reabsorption efficient in the loop of Henle
countercurrent system–> maintains high conc gradient
what does the distal convoluted tubule react to
the amount of anti-diuretic hormone (ADH) in the blood
the higher the ADH levels
the more water is reabsorbed - due to ADH cuisine the cells in the last section of the DCT to become more permeable to water and therefore urine will be more concentrated
the lower the ADH levels
the less water is reabsorbed due to the lasts section of the DCT being less permeable to water–> therefore urine will be more dilute
what may affect levels of ADH in the blood…
conditions like diabetes insidious or by the consumption of diuretics
diuretic
anything that increases the production of urine
what does ADH to cells
inserts aquaprotins in the membrane –> increasing permeability to water
how is water reabsorbed in the loop of Henle
- -> countercurrent multiplication
1) filtrate in proximal tubule has the same osmolarity as (300) as the instistial tissue (iso-osmotic)
2) in the ascending limb Na+ is pumped out into the instistial tissue- cl- also follows. This makes the medulla a concentrated and salty region
3) H2O moves passively into the instistial tissue and out of the nephron
4) this increases the conc of the filtrate in the LofH
what cells are there in the collecting duct
principle cells
intercalated cells
what do the principle cells in the collecting duct do
react to ADH
what do intercalated cells secrete
alpha ones secrete H+
Beta ones secrete HCO3-
what is eGFR
estimated glomeruli filtration rate
-estimate fo kidney function
IF YOUR GFR NUMBER IS LOW THEN YOU KIDNEY IS FAILING
what is used to calc GFR
serum creatine levels, cystitis c levels, age, gender, race, assays
disease of the bowman capsule
glomerulonephritis
what can glomerulonephritis do
cause blood and albumin to be found in the blood
what is glomerulonephritis
a group of diseases which injure the glomeruli–> when this structure is damaged, larger molecule like albumin and RBC will not be filters and will pass through the podacytes and be ejected from the body via the urine
what hormones are released/ synthesised from the kidneys
-erythropoietin (EPO)
Calcitriol (acts like hormone)
Erythropoietin (EPO)
a glycoprotein that control ERYTHROPOIESIS (red blood cell production)
- -> a cytokine (protein signalling molecule) which causes RBC to mature
- -> secreted from interstitial fibroblasts in the kidney
Calcitriol
activates vitamins D–> which helps with the absorption of calcium and phosphorus from food (s.intestine)
hormones in system
ADH, aldosterone, ANP
what are the capillaries surrounding nephrons called
pertitubular
cortical
80%
juxtamedullary
20%
Loop of hence gets..
more salty the further you go down–> very permeable to water in descending loop and not to salts
mechanisms that take place within the nephron
ultrafiltration
reabsorption
secretion
EXCRETION
how much blood is filtered via ultrafiltration
20%
three layers of glomerulus membrane
1) capillary endothelial fenestrations
2) gel like basement
3) slit diaphragms within filtration slits –> between foot processes of podocytes
GFR
the amount of filtrate that form sin both kidneys per min
how much cardiac output do kidneys receive
25%
normal GFR in women
105ml/min (1 litre in 9-10 mins)
daily: 150l
normal GFR of men
125 ml/min (1 litre in 8 mins)
daily:180l
GFR THAT IS TOO HIGH COULD MEAN
diabetes mellitus, diabetes insipidus
GFR THAT IS TOO LOW COULD MEAN
waste products are not excreted–> chronic renal failure
how is GFR calculated
INULIN is used
GFR= conc of insulin in urine x urine flow/conc of inulin in arteriole plasma
creatine can also be used
what sort of substance is used to measure GFR
1) freely filtered by glomerulus
2) it is not reabsorbed or secreted
3) is non toxic and not metabolised
why is creatine not great to measure GFR
some secreted and absorbed in tubule
kidney failure could lead to
- waste products accumulating in blood
- pH and electrolyte balance jeopardised
- blood volume control impaired (oedemas etc)
3 ways of GFR control
myogenic regulation
tubuloglomerular feedback
neuronal regulation
myogenic autoregulation
constriction/dilation of afferent arterioles in response to changes in blood pressure
if blood pressure drops..
GFR also drops- due to vasoconstriction of afferent arteriole , therefore decrease in pressure on glomerulus
if blood pressure increases..
GFR also increases- due to vasodilation and therefor increase in blood flow and therefor glomerular pressure increases and net filtration increases
tubuloglomerulus feedback
macla densa (specialised cells) within the distal tubule monitor filtered NA+ -if Na+ flow rate increase, GFR is decreased
countercurrent multiplier
blood flow runs in pop direction to urine –> increases the conc gradient
what is released form the pituitary which affects the renal system
ADH
if you are over hydrated you need
more ADH to cause diuresis
if you are dehydrated you need
less ADH to cause anti-diuresis
osmolarity in PCT
300
osmolarity in DCT
100
osmolarity in LoH
1200
what controls reabsorption of water in the collecting duct
ADH
Renin- angiotensin aldosterone system
BP
extra-cellular volume in the body
JGA
juxtaglomerular apparatus
2 types of cells of the JGA
1) juxtaglomerular cells- modified s.muscle cells in afferent arteriole- secretes renin
2) macula densa- distal tubule, monitors filter Na+ within DCT (also regulates GFR)
RAAS mechanism
1) blood pressure falls (low fluid vol in the nephrons)
2) renin is released and hydrolyses angiotensinogen (pre-enzyme released from the liver)
3) angiotensinogen is converted to angiotensin 1 which enter the blood
4) ACE (angiotensin converting enzyme) from the lungs reacts with angiotensin 1 to form angiotensin 2
5) angiotensin 2 has remodelling affects on the hearts, but also causes the adrenal gland to produce aldosterone (steroid hormone)
6) aldosterone causes the collecting duct to retain more water–> therefore BP increases
if calcium drops to half its amount
titanic skeletal muscle contractions
if K+ conc is reduced by 1/3-
paralysis–> nerves unable to generate action potentials
sodium in the urinary system is largely loacted
extracellulary
disorders related to Na+
HypoNatramia
HyperNatramia
Hyponatramia
Na+ conc too low in extracellular space–> causes cells to swell.
-hypovolaemia, evvolaemia and hypervolaemia
hypernatramia
Na+ conc too high- much rarer. Associated with increase in plasma osmolarity
-stimulator of thirs
disorders related to K+
HypoKalaemia
HyperKalaemia
HypoKalemia
caused by diuretics, diarrhoea, vomiting. Majority of deficit is intracellular. Causes muscle weakness.
K+ conc too low
HyperKaleamia
renal failure, issue damage, acidosis, aldosterone impairment
-hyperventilation, ECG changes
-Depolarisation of excitable cells
K+ conc too high
majority of K+ i loacted
intracellulary
principle cells
secretes K+ (exchanges with Na+)
intercalated cells
reabsorbs K+ –> exchange with H+
types of aqua porins
1- PCT, LoH- constant presence, continous H2O absorption
2-CD, Luminal mem.-inserted in response to ADH- variable H2O absorption
3-constsnt presence
4CD, basal mem- constant presence
pH outside….. is not conducive with life
6.8-8.0
acidosis
<7.35–> depression of the CNS (coma, disorientation, death)
alkalosis
> 7.35 – over excitability of stimuli (pins and needles)
- muscle spasms and twitches
- difficulty breathing
- convulsions
acidosis is the result of..
increased secretion of H+ and zero excretion of HCO3-
-urine will be acidic
alkalosis is the result of..
created H+ secretion and increased HCO3- excretion– basic urine
how does ADH adjust body fluid
- increased body fluid levels.
ADH binds to V2 receptors on the basolateral men. in the collecting auction. The increased insertion of aquaproins 2increases the amount of water reabsorbed.
why are V2 receptor antagonist not an effective diuretic
patients with high blood pressure, who are hypervolemic (too much volume)do not produce ADH in the CD–> inhibiting the V2 receptor will not make much of a difference to H2O reabsorption in the nephron
tubuloglomerular feedback
maula dense cells within DCT lie next to the granular cells (lining of the afferent arteriole)–> which secrete vasoactive chemicals –> causing vasodilation/constriction.
If GFR increases, the amount of filtered Na+ will be deleted by macula dense cells within the DCT–> therefore granular cells will produce vasoactive chemicals causing vasoconstriction, therefore BP will decrease, as well as GFR.
the reabsorption of H2O,cl- and amino acid absorption in the PCT relies on…
reabsorption of Na+
hypervolemic
too much fluid in the blood
ADH
produced in poster pituitary (exocrine signalling). causes the secretion of K+ into the CD. Affects V2 receptors–> more aquaporins 2
aldosterone
DCT and CD–> increases reabsorption of Na+ and H2O (less excretion). Produced in the adrenal cortex/gland. Steroid hormone. Causes H2O retention and therefore causes blood pressure to increase
ANP- atria natriuretic peptide
produced in the atria of the heart in response to changes in blood pressure (increases) -prevents Na+ reabsorption from DCT and CD- increasing excretion and decreasing blood pressure.
Inhibits the release of aldosterone and renin
why does Na/K+ play a large role in Na+ and water reabsoprtion
the pump removes 3 Na for every 2K.
This keeps the conc of Na+ in the tubular cell low–> meaning there is a higher conc gradient and more Na+ will be reabsorbed from the tubules and therefore porewater will follow
how does aldosterone work
enhances the activity of Na/K+ pumps within the DCT and CD
-more Na+ reabsorbed, therefore more K+ secreted (hperkalaemia.
three types of diuretic
thiazide
loop
osmotic
there ar more types
thiazide
targets DCT and Na/cl- luminal symporters
loop
targets LofH and the Na+/K+/Cl- symporters
osmotic
targets whole nephron. Increases osmotic pressure within filtrate
aim of diuresis
increase salt load of filtrate by suppressing Na+ reabsorption within the nephron tubule
–> increases water loss in urine
diuresis helps prevent: oedemas, heart failure, hypertension, renal failure (increases GFR and restores normal renal function)
secondary role of diuretics
the removal of toxic substances e,g, drugs
-will also alte Ruhe pH of the urine
