Term
| where is a majority of reabsorption occurring for water and Na |
|
Definition
|
|
Term
| what are two major causes of Chronic kidney disease |
|
Definition
|
|
Term
| what stage of CKD will you start to see symptoms with abnormal lab values |
|
Definition
|
|
Term
| what is the number one marker of glomerular damage |
|
Definition
| albumin levels (protienurea) |
|
|
Term
| why is the proximal tubule so important |
|
Definition
| this is where reabsorption happens, also this is where drugs are secreted |
|
|
Term
| if you had high levels of Na, K or H2o in the urine what would this indicate |
|
Definition
| damage in the proximal tubule |
|
|
Term
| why is creatinine a crude index for kidney function |
|
Definition
| since it varies by muscle mass (esp in the elderly may not see the increase associated with kidney damage) |
|
|
Term
| what are some ways to estimate kidney function |
|
Definition
| creatinine clearance, glomerular filtration |
|
|
Term
| you would normally use the cockcroft-gault equation to calculate creatinine clearance when would you not |
|
Definition
| if the patient is obese (30% above ideal body weight) |
|
|
Term
| what is the normal range for creatinine clearance |
|
Definition
|
|
Term
| what is the normal range for glomerular filtration |
|
Definition
|
|
Term
| what does the MDRD equation tell us |
|
Definition
| the glomerular filtration rate |
|
|
Term
| how do you calculate the GFR in pediatrics |
|
Definition
|
|
Term
| what is the most accurate measure of GFR |
|
Definition
|
|
Term
|
Definition
| urea production, tubular reabsorption, glomerular filtration |
|
|
Term
| how does trauma and quick flow rate affect BUN |
|
Definition
| these will both increase BUN |
|
|
Term
| list some pre-renal causes to a increased BUN |
|
Definition
| dehydration, shock, blood loss, severe heart failure |
|
|
Term
| what are post renal causes of an increased BUN |
|
Definition
| obstruction of ureter, bladder neck , or urethra |
|
|
Term
| what are the three C's of a microscopic analysis of urine |
|
Definition
|
|
Term
| what are some causes of crystal formation in urine |
|
Definition
| uric acid, alkaline urine, UTI |
|
|
Term
| proteinuria is a tell tale sign of what |
|
Definition
| problems in the glomerulus |
|
|
Term
| what is the problem with albumin not being filtered |
|
Definition
| leads to scarring, inflation, burning and ultimately nephron death |
|
|
Term
| what are two tests used to detect proteinuria |
|
Definition
| dipstick (multistix), sulfosalicylic acid test |
|
|
Term
| why is proteinuria an important biomarker |
|
Definition
| it is associated with cardiovascular disease, progressive renal disease |
|
|
Term
|
Definition
oliguria is urine output under 500 ml/day
anuria is < 100 ml/day |
|
|
Term
| what % of Na is leaves in the urine daily |
|
Definition
|
|
Term
| what is the FeNa in a patient with acute renal failure due to tubular necrosis |
|
Definition
|
|
Term
| if you have aucte oliguria with high Na levels what does this indicate |
|
Definition
|
|
Term
| if you detect microalbuminuria what are the next three steps |
|
Definition
estimate GFR and creatinine clearance
adjust meds
start on ARB or ACe |
|
|
Term
| what is the sole purpose of the parathyroid gland |
|
Definition
|
|
Term
| how does kidney failure affect the paraqthyroid and how |
|
Definition
| phosphate won't be cleared, this will cause binding to serum Ca this will then trigger the parathyroid to produce PTH hormone causing the increase of osteoclast activity |
|
|
Term
| how will kidney failure effect Ca levels in the body |
|
Definition
| it will cause phosphate to not be cleared and bind to Ca, also will not create the active form of vitamin D causing an issue in Ca absorption |
|
|
Term
| WHAT CAUSES 90% of all acute interstitial nephritis |
|
Definition
|
|
Term
| changes in cardiac output, toxic metabolites of P450, water reabsorption can all attribute to what |
|
Definition
|
|
Term
| what is the standard criteria for AKI |
|
Definition
| abrupt reduction of kidney function within 48 hrs showing an increase in serum creatinine by >.3mg/dl or 50% from base or decrease in urine output to < .5ml/kg/hr>6hr |
|
|
Term
| what are the three major types of AKI |
|
Definition
prerenal
intrinsic
post-renal |
|
|
Term
| what are the 4 types of intrinsic AKI |
|
Definition
| glomerular, interstitial nephritis, tubular injury, vascular disease |
|
|
Term
| what are the two most common AKI |
|
Definition
| tubular injury, interstitial nephritis (caused by drugs) |
|
|
Term
| what is the cause of prerenal AKI |
|
Definition
|
|
Term
| what are the most prevalent drug causes of prerenal AKI |
|
Definition
| diuretics, radio contrast media, NSAID, ACE, ARB, cyclosporine |
|
|
Term
| what are the clinical features and urinalysis results of prerenal AKI |
|
Definition
hypotension, tachycardia, dry mucous membrane
FENa<1%, urine Na<10, Osmolality>500 |
|
|
Term
| how does ACE and ARB damage the glomerulus |
|
Definition
| they cause the efferent arteriole to open allowing more blood out causing the pressure in the glomerulus to drop |
|
|
Term
| when should you hold an ACE or an ARb |
|
Definition
|
|
Term
| what is the reason behind NSAID's nephrotoxicity |
|
Definition
| they block PGE2 which causes the afferent artiole to constrict decreasing glomerulus pressure |
|
|
Term
| what is the third most common cause of ARF in hospitalized patients |
|
Definition
| contrast induced nephropathy |
|
|
Term
| what patients are at highest risk of contrast induced nephropathy |
|
Definition
|
|
Term
| what are the steps of contrast indused nephrotoxcity |
|
Definition
Contrast administration-->Renal vasodilation/osmotic diuresis->
Intense vasocontriction (in the medulla)->
Decreased medullary pO2->
Ischemic ATN |
|
|
Term
| what does a urinalysis of Acute tubular nephritis look like |
|
Definition
| muddy brown granular casts, FeNA>2%, urine Na>20, urine osmolality <300, proteinuria |
|
|
Term
| what is the most important factor for predicting aminoglycoside nephrotoxicity |
|
Definition
|
|
Term
| what dose of amphotericin B is generally nephro toxic in 80% |
|
Definition
| cumulative doses of 4 grams |
|
|
Term
| what AKI is most often caused by drugs |
|
Definition
| acute interstitial nephritis |
|
|
Term
| what is the presentation triad for acute interstitial nephritis |
|
Definition
| rash, increased eosinophils in urine and eosinophilla |
|
|
Term
| what class of drugs is most likely to cause acute interstitial nephritis |
|
Definition
| antibiotics (beta lactams) |
|
|
Term
| what are the main complications of AKI |
|
Definition
| electrolyte abnormalities (hyper- K, Mg an Phosphate, metabolic acidosis, volume overload, uremic syndrome |
|
|
Term
| who is the at risk population for AKI |
|
Definition
| elderly, diabetics, hypertension, vascular disease, heart failure, infections, poor nutrition |
|
|
Term
|
Definition
|
|
Term
| what are the goals of therapy with AKI |
|
Definition
decrease further injury
correct or treat cause
supportive care
manage complications
properly dose all meds |
|
|
Term
| what are the indices of effect for AKI |
|
Definition
| resolution of Creatinine, BUN, K, P, Mg, H,restore urine output, clear edema |
|
|
Term
| what drug class do we use for symptomatic relief of AKI |
|
Definition
|
|
Term
| how should we replace fluids in AKI |
|
Definition
| 1/2 fluid in first 24 hours then 1/2 in second 24 |
|
|
Term
| how can you prevent prerenal AKI in at risk patients |
|
Definition
hydrate
use short acting low doses of captopril (ACE or ARB)
monitor Scr, K |
|
|
Term
| how would you minimize acute intestitial nephritis damage |
|
Definition
| stop the offending agent, use prednisone 1-2mg for 4-6 weeks |
|
|
Term
| if an AKI patient has hyperkalemia what should you do |
|
Definition
get an EKG stop all K sources
use diuretics, sodium polystyrene
if moderate use insulin and glucose, NaHCO3, beta agonists (albuterol)
if severe all above as well as IV Ca and dialysis |
|
|
Term
| if patient has metabolic acidosis what should you do |
|
Definition
| give HCO3 (half the calculated dose) |
|
|
Term
| for renal replacement therapy what are the AEIOU |
|
Definition
A- acid base imbalance (metabolic acidosis)
E electolytes (hyperkalemia)
I intoxication (salicylate, lithium)
O fluid overload
Uremia |
|
|
Term
| what are all the monitoring parameters for AKI |
|
Definition
| fluids, weight, vitals, blood chem, drug concentrations, urinalysis |
|
|
Term
| what are some susceptibility factors for CKD |
|
Definition
| >65, ethnic minority, smoker, reduced kidney mass, family history of kidney disease |
|
|
Term
| what are the most common initiating factors of CKD |
|
Definition
| diabetes, hypertension, drug toxicity, autoimmune disease, polycystic kidney disease |
|
|
Term
| what is intrinsic damage in CKD |
|
Definition
| damage to any part of the nephron |
|
|
Term
| what is adaption as it pertains to the intact nephron hypothesis |
|
Definition
| the remaining nephrons componsate for the decreased number of functional units |
|
|
Term
| what is a result of nephron adaption and what is the physiological result of nephron loss |
|
Definition
nephron adaption will show an increase in creatinine and nitrogenous waste accumulation proportional to lost nephrons
the manifestation is a decrease in GFR |
|
|
Term
| what contributes to the progression of CKD |
|
Definition
| nephron injury, glomerular hypertension, hyperfiltration, angiotensin, proteinuria, scarring |
|
|
Term
| how does and ACE inhibitor work |
|
Definition
| it blocks the renin pathway not allowing angiotensin 1 changing into angiotensin 2 |
|
|
Term
|
Definition
| this will essentially block angiotensin 2 from binding to the receptor negating it's activity |
|
|
Term
| what are the beneficial effects of blocking angiotensin 2 |
|
Definition
Decreases urinary protein excretion
Decreases glomerular and systemic pressure
Decreases fibrinogenesis
Decreases the risk of serum creatinine doubling
Decreases cardiovascular events |
|
|
Term
| where is erythropoietin produced |
|
Definition
|
|
Term
| what is the main cause of anemia in CKD |
|
Definition
| decreased production of erthropoetin |
|
|
Term
| how does uremia contribute to anemia |
|
Definition
| inhibits the proliferation and differentiation of erythroid precursars |
|
|
Term
| when using an ESa to treat anemia what do you need to do first |
|
Definition
| make sure the patient has adequete levels of "building blocks" Fe, B12, folate |
|
|
Term
| when should you begin anemia screening in CKD |
|
Definition
|
|
Term
| at what hemoglobin llevels should a patient be considered anemic (and require an anemia workup) |
|
Definition
men hemoglobin<13.5 g/dl
females hemoglobin <12g/dl |
|
|
Term
| in CKD why is erthyropoietin levels not useful in diagnosing or classifying anemia |
|
Definition
| since uremia makes receptors less receptive |
|
|
Term
| when using ESA's what is the target HB level |
|
Definition
| 10-12g/dl (should not be greater then 13) |
|
|
Term
| what are the most important iron measurements for an anemic patient with CKD |
|
Definition
| ferritin and transferrin saturation |
|
|
Term
| what are the goals of treating an anemic patient with CKB |
|
Definition
maintain an adequete level of hemoglobin (not to normalize)
treat any underlying causes
prevent hypoxia complications |
|
|
Term
| when classifying someone with CKD as having metabolic bond disease what are the three manifestations used (can have 1 or combo of three) |
|
Definition
Abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism
Abnormalities in bone turnover, mineralization, volume, linear growth, or strength
Vascular or other soft-tissue calcification |
|
|
Term
|
Definition
| an alteration of born morphology |
|
|
Term
|
Definition
| enhanced osteoclast activity and bone absorption caused by excess PTH |
|
|
Term
| what is adynamic bone disorder |
|
Definition
| this is a suppression of PTH and decreases the amount of bone turnover |
|
|
Term
|
Definition
| this is defective minerlization typically due to aluminum overload or vit D deficiency |
|
|
Term
| how will you diagnose CKD-MBD |
|
Definition
| measure serum PTH and bone specefic alkaline phosphatase |
|
|
Term
| what are the diagnostic tests to diagnose renal osteodystrophy |
|
Definition
serum biomarkers
bone biopsy (gold standard) |
|
|
Term
|
Definition
turnover
mineralization
volume
used to classify renal osteodystrophy as a result of a bone biopsy |
|
|
Term
| which type of vascular classification results in the lowest survival rate |
|
Definition
| arterial intima calcification |
|
|
Term
| describe the steps in vascular calcification |
|
Definition
| during uremia you will have increased phosphorus levels, this will allow Cbfa-1 to bring osteoblasts into the smooth muscle where they will then develop matrix with collagen and non-collagen, this will allow the risk factors that will start to deposit (increased CA, P) |
|
|
Term
| how will we manage nonskeletal calcifications complications |
|
Definition
maintain Ca, phosphorus, vit D, PTH within normal ranges
manage cardiovascular risk factors
strict management and monitoring of drug therapy |
|
|
Term
| describe the progression of chronic renal failure / uremic syndrome |
|
Definition
| glomerular breakdown-> increased capillary permeability-> proteinuria, inflammation, fibrosis-> biochemical abnormalities, bone disorders |
|
|
Term
| list uremic syndrome complications |
|
Definition
| anemia, malnutrition, fluid electorlyte disorder, cardiac disease, bone metabolism disorders, hypertension, hyperlipidemia |
|
|
Term
| kidney dysfunction and uremic syndrome result in biochemical abnormalities leading to bone and vascular issues, what are they |
|
Definition
decreased vit D synthesis and activity
impaired Ca and P homeostasis
overactive parathyroid gland |
|
|
Term
| describe how you activate vitamin D |
|
Definition
sunlight transforms 7-hydrocholesterol to cholecalciferol (vit D3)
in the liver a hydroxy is added to form calcidiol
finally in the kidney 1 alpha hydroxylase adds a second hydroxy to form active 1,25 dihydroxyvitamin d3 (calcitriol) |
|
|
Term
| ergocalciferol and cholecalciferol are what |
|
Definition
|
|
Term
| what is the normal activity of vitamin D |
|
Definition
| to act on parathyroid gland causing a release of PTH |
|
|
Term
| what are the results of stage 1-3 CKD on vitamin D |
|
Definition
decreased production of calcidiol
decreased 1 alpha hydroxylase activity |
|
|
Term
| what is the affect of stages 3-5 CKD on vitamin D |
|
Definition
little to no 1-alpha hydroxylase activity
and parathyroid gland resistance to calcitriol |
|
|
Term
| describe what is happening with fibroblast growth factor 23 in uremia |
|
Definition
| phosphate is not responive to FGF23 leading to a progressive increase in FGF23 |
|
|
Term
| what contributes to hypocalcemia in CRF/uremia |
|
Definition
phosphate retention (binds Ca)
decreased vit D
parathyroid becomes resistant to Ca
increased levels of PTH |
|
|
Term
| when measuring vitamin D which analog is clinically relevant measure of vit D statud |
|
Definition
|
|
Term
| what is the normal range for Ca |
|
Definition
|
|
Term
| how do we measure parathyroid hormone |
|
Definition
using IPTH
or the more accurate alkaline phosphatases |
|
|
Term
| where is the majority of Na and HCO3 absorbed |
|
Definition
|
|
Term
| what is the main driving source for conserving electrolytes |
|
Definition
Na/K transporter using ATP to exachange Na for K+
.
++ |
|
|
Term
| aside from exchanging Na for K what does the Na/K ATPase do |
|
Definition
| sets up conditions to help reabsorb water based on solute concentrations |
|
|
Term
| in the thick ascending limb of the loop of henle what reabosrbs NaCl |
|
Definition
|
|
Term
| what establishes the counter current multiplier |
|
Definition
| Na/K atpase transporter, Na/K/2Cl co transporter |
|
|
Term
| what is a driving force for reabsorbing water |
|
Definition
| since the water becomes hypotonic once it passes through the medular regions pores will open exposing high concentration of solutes and creating reabsorption of water |
|
|
Term
| where does a loop diuretic work |
|
Definition
| Na/K/2Cl in the ascending loop of henle (also disrupts the CCM) |
|
|
Term
| how much cardiac output goes through the kidneys every minute |
|
Definition
| 1/5 of cardiac output (1 liter/min) |
|
|
Term
| electrolytes in the ultrafiltrate are excreted from where to where in the proximal tubule |
|
Definition
| from the lumen to the interstitial fluid |
|
|
Term
| in the distal tubule what measures the Na concentration and where do they communicate this info |
|
Definition
| the macula densa cells can detect Na levels and communicate it to the juxtaglomerular apparatus |
|
|
Term
| where is renin released (angiotensin precursor) |
|
Definition
| juxtaglomerular apparatus |
|
|
Term
| how does vasopressin (ADH) conserve water |
|
Definition
| it opens up the aqua pores allowing the hypotonic ultrafiltrate to force water out via concentration gradients |
|
|
Term
| what 6 things do you need for the counter current multiplier mechanism |
|
Definition
- meager blood supply
- nephrons arranged in a way to interact with one another
- active transport for Na in the ascending loop of henle
- differnetial permeability in the loop of henle (descending is freely permeable while ascending is not permeable to water)
-
Differential permeability to water in the distal tubule, collecting tubule, and collecting duct depending on the presence or absence of antidiuretic hormone (ADH, Vasopressin).
ØIn the presence of ADH the DT, CT and CD are permeable to water.
ØIn the absence of ADH the DT, CT and CD are impermeable to water.
6. recirculation and concentration of urea
|
|
|
Term
| how does vasopressin creat aquaporin |
|
Definition
coupling to V2 receptors activating GS-adenylyl cyclase-cAMP-PKA pathway
|
|
|
Term
|
Definition
|
|
Term
| why would you use an osmotic diuretic |
|
Definition
| for acute situations like poisoning |
|
|
Term
| explain how loop diuretics work (furosemide) |
|
Definition
they cause 15-20% od filtered Na to be excreted, as well as lots of water, K, Ca
they block the NA/K/2cl co transporter in the thick ascending limb to be inhibited |
|
|
Term
| what blocks the aldosterone dependent channels |
|
Definition
|
|
Term
| how long will carbonic anhydrase inhibitors be active for |
|
Definition
| a few days since it will deplete bicarb |
|
|
Term
| how will carbonic anhydrase get sodium bicarb from the lumen to the urine |
|
Definition
| NaHCO3 loses Na picks up a hydrogen then carbonic anhydrase will break it up to H2O and CO2 which can easily pass the membrane onse through carbonic anhydrase will reform H2CO3 then eventually NAHCO3 |
|
|
Term
| diuretics can cause hypokalemia how |
|
Definition
| it decreases Na in the loop of henle causing further down the line a frantic attempt to restore Na by pushing out K |
|
|
Term
| when would you use a loop diuretic |
|
Definition
| acute pulmonary edema, hypercalcemia, congestive heart failure, hypertension, renal failure, chemical intoxication |
|
|
Term
| what would you use a thiazide for |
|
Definition
| heart failurre, renal failure, hypercalciuria, diabetes, hypertension |
|
|
Term
| what are the unwanted side affects of a loop diuretic |
|
Definition
| hypokalaemia, metabolic alkalosis, hypovolameia,0 temporary deafness, retention of lithium, displacement of plasma bound drugs, cross sensitivity with sulfa drugs |
|
|
Term
|
Definition
| they inhibit the Na/Cl cotransporter in distal convoluted tubule |
|
|
Term
| what is the side effects of a thiazide |
|
Definition
| hypokalaemia (can lead to hyperglycemia), metabolic alkalosis, retention of lithium, elevated uric acid and lipids, cross sensitivity to sulfa drugs |
|
|
Term
| what are examples of K sparing diuretic |
|
Definition
| triamterene, amiloride, spironolactone |
|
|
Term
| how can a thiazide cause a gouty attack |
|
Definition
| they are are organic acids and compete with uric acid in renal handling causing plasma concentration of uric acid to increase |
|
|
Term
| what is the mechanism of action for the loop diuretics |
|
Definition
| block the Na/K/2Cl transporter this will also create an isotonic solution in the interstitium which will force out more water |
|
|
Term
| what are the two mechanism of action for K sparing diuretics |
|
Definition
1.) sodium channel blocker
2.) aldosterone receptor blockers |
|
|
Term
| what are some side effects of K sparing diuretics |
|
Definition
| impotence, decreased libido, gynecomastia, menstrual irregularities, hyperkalemia |
|
|
Term
| what is a good diuretic combo and why would you do this |
|
Definition
loop diuretic with a thiazide
this is done to overcome tolerance |
|
|
Term
| how does hypokalemia effect loop diuretic action |
|
Definition
| you will develop tolerance since you really need K to bind to expose the second Cl site where the action of the drug is |
|
|
Term
| what is the concept of using an osmotic diuretic |
|
Definition
| put a high concentration of anontoxic, not metabolized, freely filtered by glomerulus and not reabsorbed from renal tubule |
|
|
Term
| how does an osmotic diuretic work |
|
Definition
| the high osmotic gradient developed in the vascular system will draw in water and brings the water through the kidneys with it |
|
|
Term
| what are some issues with using osmotic diuretics |
|
Definition
| cardiovascular overload, hypersensitivity, inablity to clear the agent |
|
|
Term
| what is the target of the vasopressin receptor antagonist |
|
Definition
| V2 receptor in the collecting duct |
|
|
Term
| what are the effects of the carbonic anhdrase inhibitors on acid base balance and K |
|
Definition
depletes base and retains hydrogen cause metabolic acidosis
acidosis causes a shift in intracellular H/K and increased Na/K exchange causing hypokalemia |
|
|
Term
| wht would you use a carbonic anhydase inhibitor |
|
Definition
| glaucoma, epilepsy, alkalinize urine |
|
|
Term
| the Na/K co-transporter is driven by ATP under the influence of |
|
Definition
|
|
Term
| the Na/K/2CL transporter is principle mech for conservation of water in concert with |
|
Definition
|
|
Term
| when dealing with net filtration what will you use |
|
Definition
| glomerular hydrostatic force-( COP+ bowmans capsular preassure) |
|
|
Term
| the clearance of inulin will show you what |
|
Definition
|
|
Term
| what is the measure of renal plasma flow |
|
Definition
|
|
Term
| how can you calculate renal blood flow |
|
Definition
|
|
