Excretory System Flashcards
function of kidneys
responsible for water-solute balance
deamination in excretion
amino group + other molecules -> ammonia -> urea
deamination occurs at liver, produces ammonia, ammonia changes to urea and travels to kidneys via blood
nucleotide breakdown in excretion
nucleotides (dna/rna) breakdown into uric acid
creatine phosphate
creatine phosphate (molecule found in liver, used to store energy by turning ADP to ATP as a last resort) becomes creatinine and is excreted in urine
Pressure Filtration
due to glomerular blood pressure of 60 mmHg, blood is filtered at the glomerulus - bowman’s capsule interface
tubular excretion
- unwanted substances enter dct from peritubular capillaries (histamines, penicillin, ammonium ion, H+ (regulate pH), creatinine)
- uses active transport
threshold levels
the amount of any substance that is reabsorbed by peritubular capillaries is limited to a threshold level (tubular max/T-max)
T-max
maximum amount of any substance in the blood after which no more of it will be reabsorbed because carriers are saturated
threshold level of urea vs glucose
low t-max for urea, high t-max for glucose (little urea is reabsorbed, lots of glucose reabsorbed)
diabetes
- lack of insulin
- increased glucose concentration in blood
- glucose concentration exceeds threshold
- not all glucose will be reabsorbed
- sugary urine
ADH function
hormone that increases the permeability of the collecting duct (opens channels) to increase H2O reabsorption to increase blood pressure & decrease solute concentration
Aldosterone
hormone that increases Na+ retention and therefore H2O reabsorption to increase blood pressure
structure that senses low BP and produces renin
juxtaglomerular apparatus (next to glomerulus, near afferent arteriole)
renin
an enzyme that turns angiotensinogen (plasma protein) into angiotensin I during aldosterone production (for BP regulation)
angiotensin converting enzyme
an enzyme in the lungs that converts angiotensin I into angiotensin II
angiotensin II functions
- vasoconstriction (increase BP)
- causes release of aldosterone by the adrenal cortex
Atrial Natriuretic Peptide/Hormone (ADP/ADH)
peptide/hormone produced by cardiac cells in atria (when blood volume increases stretch), inhibits the production of renin and therefore aldosterone, increasing how much Na+ and therefore H2O are excreted, causing decrease in blood volume
permeability of loop of henle to water
ascending limb is impermeable to H2O (can not be reabsorb into blood), descending limb is permeable
countercurrent exchange
- ascending loop of henle (impermeable to H2O) contains Na+ pumps for active transport
- Na+ is extruded into interstitial space of renal medulla
- increase in salt and urea concentration in medulla - hypertonic
- H2O diffuses out of descending loop of henle due to the concentration gradient generated
non-filterable
formed elements (blood cells etc), plasma proteins
when is active transport used
- active reabsorption phase during selective reabsorption from pct cells to capillaries (nutrients and salts)
- tubular excretion from capillaries to dct (unwanted substances like histamines, penicillin, ammonium ion, H+, creatinine)
- countercurrent exchange uses active transport (pumps)
what situation exceeds threshold levels
threshold level for glucose exceeded with diabetes
production & secretion of ADH
produced in hypothalamus, released by posterior pituitary
which hormone is released due to sweating
aldosterone
how does ADH work
- increased permeability of collecting duct to H2O (opens channels in duct)
- increased H2O reabsorption into blood (dilutes solute and increased blood pressure)
- decreases amount of urine
why does alcohol increase excretion
inhibits adh, adh decreases urine by increasing reabsorption of water
where is aldosterone released
adrenal cortex
aldosterone function
pumps Na+ out of DCT (and loop of henle) into blood, H2O follows due to osmotic pressure
aldosterone production
low blood volume & Na+ sensed by juxtaglomerulus apparatus releases renin -> renin breaks down angiotensinogen to angiotensin 1-> ACE in lung breaks down angiotensin 1 into angiotensin 2 -> angiotensin 2 causes release of aldosterone
ANP production
stretch of cells in atria sense high blood volume, release anp/anh
ANP function
inhibit renin production, decrease in aldosterone, - decrease Na+ retention from dct and loop of henle
- increased Na+ excretion, therefore H2O excretion (H2O follows by osmosis)
- decrease of H2O concentration in blood, less volume
