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88 Cards in this Set

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Kidney Functions
1.Reabsorption of water, electrolytes, all glucose, amino acids, proteins and vitamins.
2.Aids with acid base balance-excretes bicarb
3.Removal of waste from blood and formation of urine.
4. Secretion of hormones
Erythropoietin- needed for RBC formation
Renin-RAS- Renin Aldosterone System
Vitamin D
What is found in the
Cortex
Medulla
Cortex: Contains all glomeruli+85% of nephron tubules. Juxtamedullary nephrons
Medulla: Tubules, ducts, Loop of Henle
Function of
GLOMERULUS (found in cortex)

TUBULE (found in medulla)
GLOMERULUS (found in cortex)
forms a protein-free filtrate from blood

TUBULE (found in medulla)
processes the filtrate to form urine
Sympathetic innervation of kidney results in
Stimulation of SNS results in renal vasoconstriction and renin release.
1. The main driving force for filtration is
2. The most important physiologic regulator of GFR is
1. hydrostatic pressure in the glomerular capillaries.
2. blood volume. Increased fluid intake increases blood volume increasing B/P slightly increasing GFR.
How are glomerular capillaries protected from fluctuations in B/P
by autoregulation
What does the body do in response to a drop in blood pressure? (which accompanies the loss of fluid)
1. triggers the hypothalamus to rapidly release ADH from post pituitary
2. ADH increases water reabsorption by the kidney by increasing water permeability of the distal tubules and collecting ducts
3. each juxtaglomerular apparatus which responds by secreting renin
4. This triggers the formation of angiotensin II which stimulates release of aldosterone from the adrenal cortex thus slowly boosting water reabsorption by the kidneys by increasing reabsorption of Na, and thus water
glomerular filtrate contains
everything but large molecules such as proteins, contains ions, urea, glucose, minerals, vit, some drugs
99% is actively reabsorbed
nephraglia manifests as
CVA tenderness
Kidney Disease manifests as
nephraglia
Abnormal Urinalysis
Abnormal findings in: KUB, US, CT, MRI, Biopsy
Intrarenal disorder: Infection is caused by
1. Hostile environment: Intrarenal: pH, urea
Postrenal: prostatic secretions and glands in women secrete mucous
2. Unidirectional flow- back flow causes damage
3. Epithelial cells trap bacteria for inflammatory mediators to kill bacteria:
Kidney infection presents what symptoms?
Thus, pain, urgency, frequency
What populations are at risk for kidney infection
Premature newborns
Children
Sexually active and pregnant women
Women on certain Antibiotics
Older women
Diabetics Think of diabetes as chronic inflammatory disease
Indwelling catheters
Acute Pyelonephritis
Infection of renal pelvis and interstitium
Etiology Acute Pyelonephritis
Pregnancy major risk factor- due to chg hormones-look on dip stick for protein in urine
DM- diabetes
Vesicoureteral reflux esp children- urine going back into kidney, congenital malformation
E. Coli in 80% of acute cases
What is causing Acute Pyelonephritis
Ascending bacteria along the ureters may enter via bloodstream
Epithelial cells trap bacteria for inflammatory mediators to kill bacteria- sticky bomb
Inflammatory chemokines=leukocytes + inflammatory mediators=parenchymal damage.
What s/s presents with Acute Pyelonephritis
Fever, chills; Urosepsis
UTI s/s frequency, urgency and pain on urination.
CVA tenderness
How is Acute Pyelonephritis diagnosed?
Urinalysis=significant bacteria
RBC, WBC(+casts), nitrates, proteinuria
Treatment for Acute Pyelonephritis
ABX 7-10 days
urine culture if w/o improvement in 48 hrs
What do you look for in children when you can’t tell frequency or pain
Look for Fever, chills
Normal specific gravity of urine
1.003-1.030
What is the etiology of Chronic Pyelonephritis
1. Recurring or inadequately managed infections
2. Inflammation and scarring of tissue
3. Acute may lead to chronic
4. Often associated with chronic obstruction
5. At Risk Individuals such as those with obstructive disorders i.e. renal calculi (stones), neurogenic bladder, vesicoureteral reflux or Intrarenal disease
Chronic Pyelonephritis can lead to
renal failure
What is vesicoureteral reflux –
urine goes back up to kidney
Early sx of Chronic Pyelonephritis can often be minimal and may include __________.
HTN, due to renin
Dx Chronic Pyelonephritis :
IV pyelogram & ultrasound
Urinary Tract Obstruction can be caused by
Congenital
Stones
Tumors
Trauma
Edema
Pregnancy
BPH
which of the 3 is most dangerous? Calyceal stone, renal pelvic stone, upper ureter stone
upper ureter stone, can kill you because ureter is blocked off
Complications of obstruction:
Infection, sepsis, acute renal failure and ?CKD chronic kidney disease
Hydroureter-
complete obstruction of ureter, renal pelvis and tubules enlarge
Hydronephrosis-
enlarged kidney
Manifestations of renal obstructions:
Wt gain, nausea, malaise, headaches, LE edema
Renal Calculi Nephrolithiasis
kidney stones
most common Nephrolithiasis
calcium oxalate most common
contributors of renal calculi
Contributors:
High pH in urine – alkaline. Bacteria split NH3
Uric acid - gout
Prolonged immobilization
Purine diets – organ meats
Increased BMI, change from a person’s normal
If you find calcium in stone, this could indicate problems in the
parathyroid
presentations of renal calculi
Presents with acute pain:
may be flank,
CVA,
testicles or labia
n/v, hematuria, elevated VS
Diagnosis renal calculi
Diagnosis
CT, UA for pH, CBC, BUN/Creatinine; dietary history, family history, medications
treatment renal calculi
Treatment:
pain relief and prevention; maybe surgical removal of the stone. Ultrasonic or laser lithotripsy.
Glomerular Disorders
Immune or inflammatory most often implicated- is responsible for it
Proteinuria is classically the clinical manifestation
Classification r/t degree of proteinuria:
Nephrotic syndrome
Nephrosis
Nephritic syndrome
Nephrotic syndrome >3to 3.5 gm/24 hrs
Nephrosis 2 gm/24 hrs
Nephritic syndrome mild proteinuria
Glomerulonephritis
Inflammation of glomerulus and surrounding tissue
Inflammation of glomerulus and surrounding tissue r/t
drugs
Toxins
vascular disorder
systemic diseases-DM, HTN
immunologic issues
Leading cause of chronic and end stage renal failure
Glomerulonephritis
Pediatric etiology of glomerulonephritis
β-hemolytic Streptococci
Clinical manifestations of glomerulonephritis
Hematuria-smoky urine
Edema r/t decreased GFR
Proteinuria
Oliguria- absence of urine
Hypertension- renin stimulated
Reduced complement levels due to infection
What is responsible for manifestations of glomerulonephritis
Capillaries are leaking
Chronic Glomerulonephritis results from
Several years of proteinuria and hematuria but no other symptoms
Chronic Glomerulonephritis causes what changes in kidney?
Fibrotic changes with tubular dilation and atrophy may develop.
Chronic Glomerulonephritis is associated with
Associated with hypercholesterolemia, IDDM type I, and SLE
Three types of immune mechanism influencing renal disease
1. Antigen – antibody
2. Antibodies against basement membrane
3. Streptococcal release of altering enzyme β-hemolytic Streptococci
What effect does the immune response have on kidney which leads to renal failure
All alter membrane permeability and increase swelling, decreasing blood flow and filtration
What lab tests are abnormal with renal damage
Elevated serum Creatinine and BUN
Proteinuria and hematuria, casts
Renal biopsy determines extent of injury and type.
Treatment for renal damage
consists of correcting underlying cause, and controlling for:
HTN, edema, hyperkalemia, hyperlipidemia
Problems associated with Renal Disease
Calcium loss

Anemia
decreased Ca stimulates PTH, Stimulated PTH causes release of calcium from the bone and enhanced urinary excretion of phophate. Overtime with decreased GFR less phosphate is excreted, and now increases, thus hyperphosphtemia and hypocalcemia and bone disease are acclerated

inadequate production of erythropoietin, Decreased RBCS life span
Problems associated with Renal Disease
Lipids

Protein loss
the ratio of LDL to HDL goes to LDL and an accelerated atherosclerosis occurs

Proteinuria and a negative nitrogen balance, but need to restrict dietary protein to preserve GFR
Problems associated with Renal Disease
Acid Base

Hyperkalemia
develop a acidotic state

increased plasma levels with progressive decrease of GFR
Pathophysiology Renal Disease and HTN
1. Released renin enzyme in response to the increased pressure in the renal vascular
2. Converts angiotension I to angiotension II
3. Vasoconstriction and increased arterial pressure
4. Increased aldosterone secretion
5. Systemic hypertension
6. Primary medication treatment:
ACE inhibitors
Primary medication treatment for HTN due to renal disease
ACE inhibitors
ACE inhibitors:
BLOCKS ANGIOTENSION I CONVERTING TO ANGIOTENSION II
In order for the kidney to function properly it requires:
Normal renal blood flow: RBF
Functioning Glomeruli: GFR
Functioning Tubules
Clear Urinary Outflow tract for drainage and elimination of urine formed from body’s waste
What allows for the maintenance of a near normal Intrarenal hemodynamic environment (RBF, RPF, GFR and FF ) despite changes in the systemic blood pressure
autoregulation
Interruption of renal function has significant ramifications where?
every body system
Comorbidities with kidney disease:
preexisting kidney conditions, HTN, DM, CHF, liver impairment/failure
Elderly and problems with kidneys
Autoregulation, concentrating urine, ADH/ thirst, K+, GFR.
Oliguria
<400 ml/24 hrs
Anuria
<100 ml/24 hrs
Azotemia
ALL METABOLITES ARE STAYING IN BODY
silent found by changes in BUN
Uremia
symptomatic, causes death
toxic condition of retention of waste products
clinical syndrome associated with fluid, electrolyte, and hormone imbalances and metabolic abnormalities
Prerenal acute renal failure due to
diminished perfusion of kidney due to
1.volume deficits due to fever, vomiting, diarrhea, burns, hemorrhage, overuse of diuretic
2.heart cannot generate output, CHF
3. vascular autoregulation interfered by ACE inhibitors, COX inhibitors, angiotension II receptor blocker, NSAIDS
4. nephrotic syndrome- mild protein loss due to gromular inflammation
5. hypercalcemia
6. thrombosis, embolus, dissection, stenosis
What needs to be in balance for intrarenal autoregulation?
vasodilatation and vasoconstriction
what causes vasodilation?
PG, Kinines, ANP, NO
what causes vasoconstriction?
Renin, All, ADH
influence of intrarenal constriction of afferent arterioles on GFR
loss of GFR
Area involved in intrarenal Acute Renal Failure:
vasculature, interstitial, glomerular or tubular
most common cause of ARF Acute Renal Failure
Acute tubular necrosis (ATN)
Acute tubular necrosis (ATN) is a result of
caused by prerenal ischemia
ATN may lead to
ESCRD, end stage chronic renal disease
Ischemia + inflammatory response leads to
Acute tubular necrosis
Acute Renal Failure: Post Renal
due to obstruction
intraluminal intrinsic causes of post renal ARF
stone, blood clot, papillary nec
intramural intrinsic obstruction causes
BPH, ureter stricture, carcinoma prostate, bladder tumor, radiation fibrosis
extrinsic causes of ARF, post renal
pelvic malignancies
prolapsed uterus
Stages of ATN , acute tubular necrosis
Oliguria stage
Diuretic stage
Recovery stage
describe oliguria stage
urine output drops=hypervolemia, THN, JVD
Metabolic wastes retained
Hyperkalemia, fluid electrolyte imbalance
uremic syndrome
Describe diuretic stage
polyuria due to concentrating mechanism not recovered
volume deficit
elevated BUN continues
hypokalemia
describe recover stage
full renal function recovered, serum creatine normal
why does kidney disease cause anemia?
kidneys don't manufacture erythropoietin