regulation of GFR
buffer systems:
carbonic acid
amino acid
hemoglobin
phosphate
Chronic Kidney Disease
buffer systems
Some (kinda common sense) key points:
*chemoreceptors monitor the ECF for changes in plasma volume or
composition/osmotic concentration of ECF, not the ICF
*water travels via osmosis following the ion gradient (water follows salt)
*excess water/electrolytes must be released and insufficient water/electrolytes
must be ingested to maintain homeostasis
Electrolytes:
concentration measured in Equivalents = amount of +/- ions that produces 1 mole of electric charge
1 Eq = 1000 milli eq (mEq)
most common problem = imbalance in gain/loss of Na+
imbalance of K+ less common but more dangerous
other electrolytes: Ca2+, Mg2+,PO4 3-, Cl-
Urinary Tract Infections (UTIs) are pretty common infections that happen when bacteria (likely from the skin or rectum) enter the urethra and infect the urinary tract. The most common type is a bladder infection (cystitis). Kidney infection (pyelonephritis) is another type of UTI. They’re less common, but more serious than bladder infections.
step 4: elimination
multiple nephrons dump collected wastes and water into the collecting ducts >
papillary duct > minor calyx > major calyx > renal pelvis > ureter > bladder for storage>
then micturition (urination) via urethra
transplanation
anti-diuretic hormone = ADH
Potassium
pathologies
circulation
Homeostasis requires fluid/electrolyte/pH balance
and the rest...
steps in urine formation
1. Autoregulation
low blood pressure
baroreceptors of granular cells triggered
macula densa releases adenosine
vasoconstriction of afferent arteriole occurs
GFR decreases
water loss decreases
blood volume increases
blood pressure increases
step 3: tubular secretion
substances including wastes are transferred from the peritubular capillaries to the tubular lumen. it's the opposite process of reabsorption.
Urinary Tract Infections (UTI)
primary metabolic wastes excreted are:
urea uric acid creatine
circulation
pH (acid/base) balance
Polycystic kidney disease (PKD) is a genetic disease. PKD causes cysts to grow inside the kidneys. These cysts make the kidneys much larger than they should be and damage the tissue that the kidneys are made of. PKD causes chronic kidney disease (CKD) , which can lead to kidney failure and end-stage renal disease (ESRD). PKD causes about 2 percent (2 out of every 100) of the cases of kidney failure in the United States each year.
There are two types of PKD: autosomal dominant PKD and autosomal recessive PKD. Autosomal dominant PKD causes cysts only in the kidneys. It is often called “adult PKD,” because people with this type of PKD might not notice any symptoms until they are between 30 and 50 years old. Autosomal recessive PKD causes cysts to grow in both the kidneys and the liver. Autosomal recessive PKD is often called infantile PKD because babies can show signs of the disease in their first few months of life.
Dialysis
aldosterone
Kidney stones and oxalates:
Oxalates are found in many foods. They bind to calcium during digestion in the stomach and intestines and leave the body in stool. Oxalate that is not bound to calcium travels as a waste product from the blood to the kidneys where it leaves the body in the urine. There are many different types of kidney stones, but 8 out of 10 stones are calcium oxalate stones. If there is too much oxalate and too little liquid in the urine, calcium oxalate fragments create crystals. As the crystals begin to increase in number, they stick to one another to form a larger crystal known as a kidney stone.
2. Hormonal Regulation
Triggered by:
a. low blood pressure/blood volume/decrease in GFR
c. stimulation of granular cells by sympathetic system
d. imbalance in osmotic concentrations in distal tubule next to macula densa
Response:
a. Granular cells release Renin
b. Renin triggers Angiotensin I formation
c. Angiotensin I converted to Angiotensin II by Angiotensin Converting Enzyme (ACE) in lungs
d. Angiotensin II then:
constricts efferent arterioles
increases aldosterone production by adrenal glands
which increases Na+ retention/ blood volume
stimulates brain's thirst center = increases fluid intake
increases ADH production = increases blood volume
activates sympathetic system :
constricts systemic veins
increases cardiac output
further stimulates peripheral vasoconstriction
btw...notice the countercurrent
PKD
step 1: glomerular filtration
filtrate is produced by the glomerulus when the hydrostatic pressure pushes water and solutes through the filtration membrane.
step 2: tubular reabsorption
the filtrate contains water and wastes like urea, but also glucose, amino acids, salts.
Selective reabsorption is necessary to reclaim these substances.
and when blood pressure is too high...
enter Atrial Natriuretic Peptide/ ANP
Urinary System
Water
average production via cellular respiration = 300 ml H2O/day
average loss of water via excretion/perspiration = 2500 ml H2O/day
(one degree of fever increases H2O loss by 200 ml/day...
drink plenty of water when you are sick)
Dehydration = too little
Hyperhydration = too much
Fluid shifts occur between ICF and ECF via osmosis to maintain homeostasis
Sodium
tubular secretion of K+ determined by:
K+ concentration in ECF
low pH...H+ is secreted instead of K+ in Na+ pump
amount of aldosterone released (affects NA+/K+ pump
Calcium
Welcome to Dr. Kate Brilakis' Learning Portal
juxtaglomerular apparatus
histology of urinary system