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166 Cards in this Set

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definition of renal failure
A condition which the kidneys fail to remove the metabolic end products from blood. Also fail to regulate fluid, electrolyte and pH balance.
Chronic renal Dx
usually involve the glomerulus. In some cases they involve renal tubules or blood perfusion.
Acute renal Dx
Inablilty to maintain fluid and elctrolyte homeostasis and a failure to excrete nitrogenous waste. LOW GFR and URINE output. Reversilble.
Three types of acute renal dx
Pre-renal- affects blood flow
Renal- Acute tubular necrosis
Post-renal- obstruction
Common indicators of ARF
Azotemia- retention of nitrogenous waste

Uremia-retention of lots of toxins.
retention of nitrogenous waste either through inability to excrete them or through failure to be delivered to kidney.
INC in Waste!
Complex syndrome that occurs when azotemia becomes symptomatic. All ORGANS involved. Endocrines changes, acid base problems, etc.
7 catergories of renal dx
Acute Glomerulonephritis, Goodpasture dx,Chronic Glomerulonephritis, UTI, Renal calculi, Polycystic kidney dx, renal failure.
6 biochemical assesments to determine renal dysfunction
Proteinuria, Hematuria, Hydrogen Ion Conc, Specific Gravity,GFR, tubular function tests
if greater than 150mg/day BAD! Simple dipstick test that is suggestive of glomerular problem.
Dipstick test or microscopic exam. Blood in urine is suggestive of UTI or renal dx.
Hydrogen ion concentration
Normal is 4.5-8 thruout day. pH inc post meal but Dec with sleep and fever (metabolic acidosis). Not really helpful for diagnosing.
Specific Gravity
measure oSm. 1.01-1.025 norm but if dehyd then it can be 1.04. Kidney loses ability to concentrate urine 1st with chronic renal dx.
115-125ml/min but dec with age. Measure with creatinine. BUN also good because when BUN inc GFR will dec.
Tubular function test
Four test: PAH excretion, conc/dilut test, Sodium conc test, and urine acidification tests. Challenge kidneys to determine capacity for secretion and reabs.
6 types of morphological test for renal dyfunctoin
microscopic findings, intravenous pyelogram, retrograde pyleogram, renal angiography, renal biopsy, CT/MRI/ultrasound.
Microscopic examinations for renal dysfunction
RBC (>1 or 2)
WBC (3 or 4)
Cast exam
Cast Exam
Intravenous Pyelogram (IVP)
visualize kidney cortex with x-ray. If cortex is thin=glomerulonephritis.
If cortex look moth-eaten then it is pyelonephritis and ischemia.
Retrograde pyelogram
catheter advanced up the ureter. Contrast media inj into renal pelvis. Contrast media given then xray taken.
Renal Angiography
Will determine arterial stenosis, prescence of neoplasms, arrangements of arteries and veins.
Renal Biopsy
renal tissue taken for micro exam. Can have problems with intrarenal bleeding.
sudden impairment of renal function, oliguria. Etiology not implied. Dec renal function characterized by nitrogenous waste and azotemia.
Pre-Renal ARF
usually abnormal blood flow or myocardial dysfunction
Renal ARF
parenchymal injury
Post Renal ARF
usually tubular obstruction that interferes with elimination. oliguria.
80-95% of ARF are which types?
Pre-renal and Renal
Normal manifestation of ARF
fall in urine out put (less than 400ml/day) and dec GFR.
The 2 broad categories of causes for ARF
ischemia and nephrotoxic injury.
3 conditions that must prevail for kidney function to be normal
1. kidney must be adequately prefused with blood.
2. kidney must function normally
3.urine formed must be able to leave body
Pre-Renal Pathogenesis
See Notebook! Lots of INFO!
Normal BUN to creatinine ratio vs pre-renal ARF BUN:C
Norm ratio of BUN to Creatinine 10:1

ARF 20:1
Why avoid aspirin with pre-renal ARF
aspirin will inhibit prostaglandin synthesis. PG are vasodilators so ischemia is induced.
Best treatment for pre-renal ARF
restore adequate volume with whole blood or isotonic fluids.
four main potential causes of pre-renal ARF
Hypovolemia, dec vascular filling, heart failure/cardiogenic shock, dec renal perfusion.
Post-Renal ARF
obstruction which result in oliguria or anuria. Sometimes it's partial obstruction.
partial obstruction in post renal ARF
leads to polyuria because partial obstruction causes loss of concentrating ability and sodium wasting.
Levels where obstruction can occur
bladder (rarely causes arf), the outlet, ureter, prostate.
prostatic hyperplasia
most common underlying problem in men enlarged prostate.
How to treat obstruction and effects?
remove obstruction. diuresis and polyuria will occur and fluid replacement is needed.
Most Renal Parenchymal dx is caused by
acute tubular necrosis
5 mechanisms of renal parenchymal dx
1.immunological renal dx
2. allergic renal dx
3.obstruction which leads to necrosis
4.ischemia can lead to ATN
5.Toxic substances
ATN causes tubular damage by...
1.anoxia occurs with tub damage
2.vasoconstriction of pre-glom arterioles with damage
3.damage can led to oliguria
All will dec GFR
cisplatin causes renal damage by
accum in proximal tubules and causes mitochondrial damage
Gentamicin causes damage where in the kidney?
Proximal tubule with it's tubular toxic effects. Has some diuretic effects in addition to it's antibiotic effects so it can dec vol and inc damage.
Myoglobunuria (ATN cause)
myglobin in urine associated with rhabdomyolysis or muscle injury.
BUN:Creatinine ratio in pre-renal oliguria vs. ATN
pre-renal: >20:1
Urine concentration in pt with pre-renal oliguria vs ATN
Pre-renal urine is concentrated. Atn is not.
Pre-Renal VS ATN
Urinary Sodium
Pre: less than 20mEq/L
Pre-renal vs ATN
urinary protein
pre-renal: none
ATN: +1
Pre-renal vs ATN
Urinary sediment
a consequence of uremia
neurological manifestations
Some primary causes of ATN
trauma with blood loss, major loss of fluids, pregnancy can change bp, hypovolemia, anoxia.
Chronic Kidney Dx
decline in kidney function due to permanent loss of nephrons
Chronic kidney dx can result from
HTN, diabetes, glomerulonephritis, and other kidney dx
5 stages of kidney dx and their GFR values
stage 1- >90
stage 2- 60-89
stage 3-30-59
stage 4-15-29
stage 5 less than 15
stages 1 and 2 of CKD
no symptoms usually. the symptoms could be the underlying renal dx itself.
Stages 3 and 4 of CKD
Dec GFR. all organ systems affected but notable changes are anemia, loss of apetite, abnormalities in ionic, water, and acid base.
Stage 5 CKD
toxin accumulate and uremic syndrome occurs.
Kidney Failure definition
GFR less than 15 and accompanied by signs and symptoms or uremia or condition that need a kidney replacement (or dialysis).
End Stage renal dx
Term NOT syn with KF. end stage is used when pt is treated with dialysis and transplantation.
Functional Reserve of kidneys
as many as 90% of nephrons maybe destoryed b4 impairment is seen.
Mechanism of damage associated with CKD can be two types
initiating which is specific to the etiology (immune, toxins, or inflamm) OR progresssive involving hyperfiltration and hypertrophy of viable nephrons.
Albuminuria is helpful to measure what?
monitoring nephron injury and the response to therapy in many forms of CKD.
2 major types of CKD
Disorders of glomerular function and tubulointerstitual disorders (pyelonephritis).
infection of kidney parenchyma and renal pelvis
Chronic tubulointersitial disorders produce
intersitial fibrosis, atrophy, mononuclear infiltrates.
fluid and electrolyte imbalance in CKD can lead to
inability to concentrate urine, polyuria,nocturia,metabolic acidosis and diminished sodium tubular reabsorption.
Chronic Polynephritis
Scarring and deformation occurs. Often occurs in people with recurrent UTI or acute polynephritis. Can lead to polyuria/nocturia.
Chronic obstructive polynephritis
associated with recurrent bouts of inflammation and scarring.
Chronic polynephritis responsible for what % f ESRD?
Kidney's tolerance to drugs can vary with
age, hydration,renal function, BP and pH of urine.
Drug-related nephropathies
functional or structural damage after exposure to a drug
Drug-Related nephropathies can cause damage by..
dec renal blood flow, obstructing urine flow, damaging tublointestitial structure, prd hypersensitivity rxn.
how can NSAIDS cause drug related nephropathy?
reduce renal blood flow and cause pre-renal failure. Can cause intersitial nephritis with papillary necrosis.
Drug-related hypersensitivity rxns present how?
about 2 weeks post exposure and pt will experience fever, eosinophilia, hematuria, mild proteinuria. Can cause tubulointerstitial nephritis which will damage the tubule and interstitium.
seven types of glomerular dx
1. actue prolif glomerulonephritis
2. rapid progressive glomerulonephritis
3.nephrotic syndrome
4.membranous glomerulonephritis
5.minial change dx (lipoid nephrosis)
6.focal segmental glomerulosclerosis
7. chronic glomerulonephritis
Cellular changes associated with glomerular dx
most take place at basement membrane. Basement membrane thickening, sclerosis, fibrosis.
potential causes of glomerular dx
1. dx that cause inflammation of endothelial,mesangial, or epithelial cell of the glomeruli
2. inflammation damages capillary wall and permits rbc and proteins to get into urine.
glomerular dx can be a manifestation of which three dx?
lupus, diabetes, and HTN.
Major characteristic of glomerulonephritis
1. antibodies against glomerular basement membrane in a LINEAR pattern.
2. antibody-antigen complexes. Type 3 injury.
3. urinary changes
4. mixed nephrotic and nephritic syndromes. def diagnosis needs biopsy.
Urinary changes in glomerulonephritis
proteinuria, hematuria, pyuria, edema, dec gfr, azotemia, oliguria, htn.
Def of Nephrotic sydnrome
dx of the glomerular basement membrane and inc perm to plasma proteins
Major characteristic of nephrotic syndrome
Edema, dec in plasma osmotic presure which mean dec ECF which inc RAS. Inc in RAS mean inc in aldosterone so more fluid retention.
More characteristic of nephrotic syndrome
hypoalbumina, massive proteinuria (more than Hyperlipidia cholesterol (more than 300mg/dl).
three types of nephrotic syndromes
1.minial change glomerulonephritis (lipoid nephrosis)
2. membraneous glomerulonephritis
3.Focal segmental glomerulosclerosis
Characteristics of minimal change glomerulonephritis
glomeruli look normal under light microscope, selective protein loss to lose electroneg charge. Common in children and responds well to steroids.
Characteristics of membraneous glomerulonephritis
Most common type in adults. Caused by thickening GBM due to immune complex deposition. Non-selective protein loss. 1 in 1000 respond to steriod treatment.
Focal Segment Glomerulosclerosis
portions of the glomeruli sclerotic. More common in african americans and hispanics. Can be associated with dec oxygen, HIV, drug use. HTN present. Can treat with roids.
Nephritic Syndrome
Acute glomerular inflammation
Characteristic of Nephritic Syndrome
hematuria, oliguria and some proteinuria. Caused by inflammation that occuldes glomerular capillary lumen and damage capillary walls. DEC GFR and retention of salt and water. Edema and HTN.
HTN manifestations
inc vascular volume, elevated peripheral resistance, dec renal vasodilators, inc RAS
peripheral neuropathy
symmetrical and includes both motor and sensory nerves. Atrophy and demyelination of nerve fibers due to toxic agents and electrolyte abnormalities.
uremic encephalopathy
CNS disturbance. inability to fix attention and loss of memory.
possible cause of nausea and vomitting in pt with CKD?
decomposition of urea by intestinal flora and resulting in high conc of ammonia.
why infection more likely in pt with CKD?
defective phagocytic function, impaired humoral and cell-mediate immunity, dec granulocytes. Skin and mucosal infection may also be defective.
causes of impotence for men on dialysis
endocrine derangements, loss of libido due to anemia and dec testoterone. In women it's due to same factors.
Women on dialysis experience
cystic dx of kidney
fluid or semiseolid filled sacs of a dilated nephron.
3 types of cystic dx
2.medullary cystic dx
3.polycystic dx (autsomal recessive and autosomal dominant).
Causes of cystic dx
tubular obsruction that inc intratubular pressure. Changes in the basement membrane of renal tubules that predispose to cystic dilation.
Three main dx that lead to dialysis
glomerulonephritic, polynephritic, and polycystic dx.
Recessive polycystic dx
cysts are derived from collecting tubule. very rare and common in children.
some systemic maifestations associated with polycystic kidney dx
aneurysm, LV hypertrophy, hepatic cyst.
Medullary cystic dx complex
autsomal renal disorders with onset in childhood. Small kidneys with varying number of cyst. Initial insult is in distal tubule with progressive tubular atrophy involving both medulla/cortex. polyuria,polydipsia then salt wasting and growth retard.
simple/acquired renal cyst
common, in cortical region only, asymptomatic, tend to be in ppl over 50. If symptomatic will see HTN, pain, hematuria.
General info about Renal Obstructive disorder
1. can be insidous, partial or complete. Bi and unilateral.
2.partial occulsion of flow or complete.
3. reversible if resolved.
4. if unresolved can lead to chronic kidney dx
Causes of UT obstruction
1.developmental deficits
4.Benign prostatic hyperplasia
5.scar tissue
6. neurological disorders (spinal cord injury)
Damaging effects of Urinay obstruction
1.predisposes infection and stone formation. Calculi can contribute to infection.
2. develops back pressure that leads to kidney dilation and compresses renal vasculature. atrophy of kidney.
urine filled dilation of renal pelvis associated with atrophy of kidney due to obstruction
acute bilateral obstruction can mimic
pre-renal failure
Manifestation of partial bilateral obstruction
inability to concentrate urine. Polyuria and nocturia as well.
HTN is secondary to what disfunctions?
reduced renal blood flow and stimulation of renin release.
Most common cause of upper urinary tract obstruction is what?
urinary calculi
stone formation is dependent on what factors?
1. pH and ionic strength
2.presence of Nidus for crystal formation
3.deficiency of inhibitors for stone formation. Citrate!
What causes body to lack citrate?
Metabolic acidosis, fasting and hyperkalemia.
calcium stones
most common, inc if bone dx, renal tubulat acidosis.
Magnesium ammoniun phosphate stones
form in alkaline urine and in prescnce of bacteria ( bac splits urea into ammonia and CO2)
Uric Acid stones
develop in gout and form in urine if ph is 5-6
Cystine stones
seen in cystinuria (genetic defect) in which renal transport of cystine is dysfunctional. RARE.
Treatment for stones
diet, passing, calcium salt supp, thiazide diuretics, cellulose phosphates. Removal can also be done. Antibiotic for infections and treatment of pain with meds.
Protective mechanisms of the kidney against UTI infections
1.washout phenom
2.Mucin layer is protective.
3.IgA immune response. Local and secretory.
4.Normal flora
5.prostate secretion in men
What hormone is important in Mucin and normal flora prd?
Most common cause of UTI and most common entry path
E.Coli and Urethra
4 types of UTI
lower UTI (cystitis)
Upper UTI (pyelonephritis)
Causes of UTI assosiated with stasis of urine flow (anatomical)
stones, prostatic hyperplasis, pregnancy, malformations of ureterovesical junction. Inc P results in reflux.
Causes of UTI assosiated with stasis of urine flow (functional)
neurogenic bladder, infrequent voiding, detrusor instability, constipation.
Urethrovesical Reflux
when urine from urethra moves into bladder. interrupted voiding, coughing, squatting.
Vesicoureteral Reflux
occurs ar level of bladder to kidney. Short intravesical ureter.
hormones produced by kidneys
erythtopoietin, renin, calcitrol
juxtaglomerular apparatus
area where the late thick ascending limb of the distal tubulr passes between the afferent and efferent arterioles at the vascular pole of the renal corpuscle.
Cells with function in the JGA
Granule cells-seceret renin
Extraglomerular mesangial cells-continous with those in b.capsule
Macula Densa cells- senses sodium in lumen of nephron at end on tubule.controls gfr and renin.
tubular secretion
moving substances into lumen from capillaries
tubular reabsorption
moving substances into capil from lumen.
normal GFR
Renal blood flow
two main factors that affect RBF
Mean pressure of renal artery vs renal vein
GFR is set by 3 factors
hydraulic permeablity of capillaries, SA of capill, and net filtration pressure.
Concept of filtered load
GFR * plasma concentration. The filtered load is what is presented to the nephron to handle.
broad term for a collection of mechanisms thru which renal blood flow and GFR are kept constant across a wide range systemis arterial pressure.
why is autoregulation necessary?
excretion of salt and water is strongly regulated by GFR. and GFR is strongly regulated by arterial pressure.
Mechanisms of autoregulation
myogenic response and tubuloglomerular feedback.
Myogenic response
as MAP goes up, smooth muscle in the walls of the arteriloes are stretched and this induces constriction which induces inc vascular resistance.
Tubuloglonerular feedback
intrarenal process through which the distal tubules affect GFR. MAcula densa cells responsd to sodium levels in d.tubule.
Mechanism of tubuloglomerular feedback
high na in the d.tubule release transmitter agents from JGA. these agents loower GFR by constricting afferent arteriole. Also contract glomerular mesangial cells to dec capill SA.
Renal clearance equation
clearance= urine conc * (volume per unit time/plasma conc of s)
In order to provide an accurate measure of GFR a compound must meet the following criteria (5)
1. freely filtered
2.not reabsorbed
3.not secreted
4.not synth in tubulues
5.not metab by tubules
creatintine meets all the criteria for GFR measurement except
it's secreted by tubules in small amt
two mechanisms of reabsorption
transcellular and paracellular
Transcellular reabsorption
1.sodium pumped into interstitial space.
2. sodium enters epithelial cells from lumen of tubule
3.there is an electr and osm gradient
4. sodium,anions, and water from interstitium move into peritubular capill
major substances reabsorbed thru paracellular reabs
urea, potassium, chloride, calcium, magneium.
tubular maximum limited system
transport mechanism which can reach an upper limit because transporters are saturated. At saturation inc plasma conc does not mean inc excretion.
Gradient limited system
transport mechanism where limit is reached because of leaky junctions. substances leak back into lumen of tubule.
substances that are heavily secreted
H, K, anions and foreign chemicals.
Tubular secretion requires
active transport, usually coupled with sodium
Familial Renal Glucosuria
abnomality in the Na/glucose co transporter that mediates reabs of glucose in prox tubule.
Proximal tubule main role
reabsorb most the filtered water and non-waste solutes.
total daily intake of water and salt
water: 2850ml
both salt and water
are freely filtered and undergo considerable reabsorp but no secretion.
four mechanism by which reabsorption of sodium drives reabs of other substances
1. Osmolarity gradient
2. reabsorption of organic nutrients by co-transport
3.secretion of hydrogen ion by countertransport
4. reabs of chloride by indirect cotransport.
How is Osm not changes in the prox tubule throughout these processes?
Prox tubule highly perm to water, iso-osmotic volume reabs,
Vasopressin (ADH) stimulates insertion of....
aquaporins. When aquaporins are present water reabs is high and urine conc is increased.
Urina concetration when there is maximal reabs...
can contain less than 1% water. So urine is very hyperosmotic to plasma.
Thin ascending vs thick ascending limg in loop
thin- uses na/cl co-transporters to move salt
thick-uses diffusion
BOTH IMPERM to water!
Descending limb
no salt reabs but highly perm to water
Distal convuluted tubule
uses symport. transport salt out of lumen (like ascending limg) but is imperm to water.