Pathways
Acronym RAAS
The renin-angiotensin-aldosterone system
Organs the kidneys are connected to
Cardiovascular system, Ureter (ultimately bladder), adrenal gland.
Function of the kidney (at least one)
Filtration of blood
Homeostasis of blood pH long term
etc
What is an acute kidney injury (definition)
an abrupt loss of kidney function in a few days
unlike
Chronic Kidney Disease (CKD): in which there is progressive loss of function of more and more nephrons that gradually decreases overall kidney function.
Stimulus for vasopressin secretion
Increased plasma osmolarity sensed by the hypothalamus
Most permeable capillary
sinusoidal/ discontinuous
different types of pressure
hydrostatic (fluid pressure)
osmotic (solute concentrations)
oncotic (proteins and particles)
What can uncontrolled prostatitis lead to?
Pain, difficulty urinating, muscular growth in the bladder
perhaps prostate cancer if mutations occur
An example of something that would activate the RAAS system
Hypotension, Low Serum Na, ect
List the order of blood flow in the kidneys
Renal artery
Afferent Arteriole
Glomerulus
Efferent arteriole
Peritubular capillary
Renal Vein
Regions of the kidney where water and solutes are reabsorbed
proximal tubule, loop of henle, distal tubule, collecting duct
Three promoters of crystal formation
Dead cells (act as nucleation points),
secondary crystallization (crystals form on crystals),
aggregation of crystals
Function of Parathyroid hormone and what acts as the negative stimulus of PTH
Parathyroid hormone (PTH) blocks reabsorption of phosphate in the proximal tubule while promoting calcium reabsorption in the ascending loop of Henle, distal tubule, and collecting tubule.
[increased calcium]
What structure(s) concentrates the urine
loop of henle, collecting ducts
What are the components of the natural buffer system (serum formula and enzyme)
Carbon dioxide + water->(carbonic anhydrase) <- Carbonic acid (H2CO3) -> <- Bicarbinate and H+
Mechanisms for correcting metabolic alkalosis
(looking for short and long term fixes)
Secretion of HCO3- into the urine (long term)
changes in breathing (short term)
Assume one side effect of a given drug is that it is an antagonist for Na/K ATP channels in the peritubular capillaries.
What are the potential adverse effects of this (3)
What are the mechanisms available to correct this (specific hormones)
Sodium would be unable to leave the cells that make up the proximal nephron. These are the cells that drive water reabsorption, so there would be an increased amount of urine in the lumen. This would dilute the urine, could potentially stress the kidneys and cause damage, it could lead to dehydration and changes in solute transport. This could lead to changes in pH. Sodium and potassium toxicity.
The RAAS system is available for correction of this disorder. (aldosterone and vasopressin)
How can low cardiac output increase the toxicity of drugs?
Low cardiac output causes decreased GFR, acute kidney injury, and other decreased clearance of drugs by the kidney.
This can then lead to toxic buildup of drugs, and drug metabolites.
In some cases, the blood brain barrier can fail. What could be some possible causes for failure, and what would be the effects.
How can this be used to treat infections of the brain?
Causes; meningitis, infection, hemorrhagic stroke, etc
Effects; increased permeability of drugs, pathogens, and other fluids
Increased permeability of drugs allows for increased treatment of meningitis and other brain infections as the BBB breaks down.
Say a drug has the effect of chelating calcium out of solution. What could be effects of this if the drug is renally excreted (be specific), what if it is hepatically metabolized.
Effects if renally processed; kidney stones (calcium oxalate, calcium phosphate), kidney damage
Effects if hepatically processed; increased calcium in the blood (insoluble), calcium buildup in the liver, cirrhosis