MOD 8 Flashcards
Kidneys functions
Filters blood
Blood pressure
Acid base balance
Make Erythropoietin
Make and release Renin
Activate Vitamin D
Kidney and acid base balance
through reabsorption or excretion of hydrogen ions and bicarbonate
w/o erythropoietin
The kidneys being damage and not making erythropoietin leads to fatigue and hypoxia (no RBC)
make and release renin
renin plays an important role in renin-angiotensin-aldosterone system, when released in works to increase blood pressure!
w/o vitamin d
patient is at risk for hypocalcemia
Blood urea nitrogen BUN
Normal range is less than 20. creation of BUN Is the most important catabolic pathway for eliminating excess nitrogen . BUN is also affected by dehydration so it only indicates kidney damage if Creatine levels are also elevated.
Creatinine
A wast product from the normal breakdown of muscle tissue. As creatinine is produced, it is filtered through the kidneys and excreted in urine as a normal production. Elevated creatinine = elevated BUN value
Glomerular filtration rate
it is a measure of how much blood gets filtered by glomeruli every minute. the GFR helps to detect kidney disease in its early stages more reliably than the creatinine test alone.
Urinalysis
abnormal substances if any of these are found it indicates a problem.
-RBCs
-WBCS
-Protein
-Glucose
-Casts
Specific gravity
1.010 - 1.030
measures how diluted r concentrated the urine is
a fixed specific gravity in which the number never changes through multiple urine tests indicates the kidney can no longer concentrate or dilute urine. Indicates severe kidney failure.
irregular RBCs urine
could be kidney stones, infection, bladder inflammation, kidney disease
irregular WBCS urine
more than a few WBCs indicates the presence of infection
irregular Protein in urine
kidney is damage allows large protein molecules to escape (proteinuria)
irregular glucose in urine
if blood sugar is too high, glucose will spill into the urine (glucosuria)
irregular casts in urine
or crystals
pieces of mineral deposits that er breaking loose and being shed into the urine
Creatine clearance
provides an estimate of kidney function and of the actual GFR. this test requires a timed urine collection (24 hrs)
* If a female patient begins menstruating during the 24 hrs of urine collection you have to notify the doctor cause yes test will not be valid
Azotemia
Increased BUN and creatine in the blood Without systemic S/S
Uremia
increased BUN and creatine with multiple system organ failures
Polyuria
increased urine output could be due to a pathologic condition such as diabetes
or just increased fluid intake in either case the kidneys are not damaged
Oliguria
decreased urine output cold be caused by dehydration or kidney failure
Anuria
No urine production (kidney failure)
Fluid/ blood pressure regulation
ADH secret by the posterior pituitary gland
released osmolarity increased blood concentration
regulates water in the body by signaling the kidney to retain water and sodium
excretion of ADH is caused by low blood volume, low sodium, high osmolarity of blood fluids
RAAS
renin-angiotensin-aldosterone system
Steps of RAAS
- initiated by decreased perfusion to the kidneys
- The kidneys release renin
- renin combines with angiotensinogen (from the liver) to form takes place in the blood stream
- angiotensin 1 is converted in the lungs to angiotensin 2 by angiotensin converting enzyme
- angiotensin 2 stimulates the adrenal cortex to release aldosterone
- aldosterone directs the kidney to reabsorb more sodium
- water follows is the sodium back into the blood stream and blood pressure is increased
Natriuretic hormones
ANP/BNP work together to lower blood pressure
atrial (ANP)
released by the heart atria, blocks aldosterone secretion and action; and inhibits renin secretion
ventricular (BNP)
produced by the heart ventricles this is important in diagnosing heart failure
ANP and BNP
are produced when the heart muscle is stretched too far
RAAS effect on B/P
Rises
ANP/BNP effect on B/P
Lowers B/P
Natriuretic
hormones cause the kidney to excrete sodium. since water follows sodium out of the body, this will decrease overall fluid volume and blood pressure will go down
Renal dysfunctions
Prerenal causes - severe decrease in blood flow to the kidneys
intrinsic causes - damage to the structures within the kidney
postrenal causes - obstruction of urine leaving the kidney
S/S of renal problems
kidney = flank pain
ureters = radiating pain from flank to groin
bladder and urethra = suprapubic and groin pain
Urinary tract obstruction
kidney stones (aka RENAL CALCULI)
risk factors: male gender, age 20-40 years, living in a desert or tropical region (dehydration), inadequate fluid intake.
Pathophys: high urine concentrations of stone forming substances precipitates into a crystal, alkaline urine increases aggregates of calcium phosphate, acid urine promotes crystallization of uric acid.
risk size of stone
> 5 mm
Clinical manifestations of kidney stones
renal colic, hematuria, nausea and vomiting, flank pain or pain that spreads to the lower abdomen/ groin. pain caused by kidney stone may change for instance shifting to a diff location or increasing in intensity
Kidney stones are considered a
POSTRENAL CONDITION
Other potential causes of urinary tract obstructions
cancer, BPH, Blood clots, malformations and inflammation response to infections. They are significant because they all CAUSE BACKFLOW of irine into the kidney. This increases pressure in the kidney LEADS TO KIDNEY DAMAGE or introduces pathogens into the kidney LEADS TO KIDNEY INFECTIONS
cystitis
infection of the bladder (lower urinary tract)
Pathophysiology of UTI
infection with bacterial organisms (E.coli is most common)
Risk factors: female, toddlers, sexually active female, diabetes mellitus, indwelling urinary catheter
Clinical manifestations of UTI’s
hematuria, WBCs and bacteria in urine
nitrates in urine
S/s of UTI in the elderly
misdiagnosed with senior dementia or Alzheimer’s disease
Confusion and other cognitive difficulties can be the result. UTI is the most common cause of LOC changes in the elderly
Pyelonephritis
Infection reaches the kidney
potential organ- and or life threatening infection that often leads to renal scarring
causes- cystitis (UTIs) urinary tract obstruction with reflux infection with E. coli, proteus, or pseudomonas
Epidemiology of pyelonephritis
females are 5 times more likely to develop acute pyelonephritis
most common cause of pyelonephritis
backward flow (reflux) of infected urine. infection began in the bladder
a blockage or abnormality of the urinary system such as those caused by stones, tumors, congenital deformities
E. Coli
Clinical manifestations of pyelonephritis
Flank pain
Fever chills
Nausea vomiting
leukocytosis
purulent urine
Glomerular disorders
Acute glomerulonephritis (GN): primary GN- untreated group A streptococcal infection
Secondary GN caused by
immune complex: antigen/ antibody complexes in glomerulus (type 3 hypersensitivity) activation of complement
-antibodies
-neutrophils and macrophages
-endothelial injury from free radicals and protease
-inflammatory mediators caused increased flomerula membrane permeability
-loss of negative charge of basement membrane
-release of growth factors
thickened glomerular membrane
Clinical manifestations of GN
Acute hematuria (Nephritic syndrome)
proteinuria (nephrotic syndrome)
Edema
Nephritic syndrome
an inflammatory process that results in hematuria and proteinuria
Nephrotic syndrome
permeability of glomerular pores allows large losses of protein molecules through the kidney just proteinuria not hematuria
Acute nephritic syndrome
acute inflammatory process
s/s hematuria, proteinuria, imparted renal function
nephrotic syndrome def
excretion of 3.5 gm or more of urinary protein per day
no hematuria
edema Periorbital edema
pathophysiology and manifestations of nephrotic syndrome
loss of plasma proteins: hypoalbuminemia leads to decreased oncotic pressure leads to full body edema and fluid overload in the lungs/heart/brain
loss of immunoglobins leads to increased susceptibility to infection
Acute tubular necrosis ATN
damage to the tubule cells of the kidneys which can lead to acute kidney failure. ATN is usually caused by a lack of oxygen to the kidney tissues (ischemia of kidneys)
ATN is one of the most common causes of acute kidney injure (failure) in hospitalized patients
Risk for acute tubular necrosis ATN
low blood pressure
septic shock
dye
medications
injury or trauma that damages the muscles
blood transfusion reaction
recent major surgery
S/s of ATN central nervous system
Change in LOC, confusion, delirium, (due to hypernatremia and cerebral edema)
S/s of ATN Oliguria or anuria
due to severe kidney disease
S/s of ATN Full body edema
due to fluid and sodium retention also due to protein loss through tubules
S/s of ATN cardiac problems
due to potassium imbalance (kidneys control excretion of potassium)
S/s of ATN fixed specific gravity
late sign of end stage kidney failure
Two different types of renal failure
acute and chronic
acute kidney injury (AKI)
formerly known as acute renal failure - has an abrupt onset and is potentially reversible
Chronic renal failure (CRF)
progresses over at least 3 months lead to permanent renal failure
Acute renal failure causes and s/s
causes: not limited to blood loss, burns, trauma, sepsis, nephrotoxic drugs, ATN, glomerulonephritis and pyelonephritis
S/s: depend on underlying cause
Chronic renal failure causes and s/s
causes: diabetes, chronic high b/p, birth abnormalities, lupus, polycystic kidney disease
s/s: high urine output (diuresis phase) or no urine output (oliguric phase)
full body edema (due to fluid retention)
change in mental alertness (na+ imbalance)
labs = high BUN and creatine
electrolyte imbalances sodium loss and potassium retention
Differences between acute and chronic kidney failure
acute: decreased blood flow (ATN), obstruction, glomerulonephritis, nephrotoxic medications
chronic: diabetes, hypertension, nephrotic syndrome, chronic obstructions
treatment for acute and chronic renal failure
hospitalization
administration of intravenous iv fluids in large volumes (to replace depleted blood volume)
diuretic therapy or medications to increase urine output
close monitoring of important electrolytes such as potassium sodium and calcium
medications to control b/p
specific diet requirements low protein because kidney cannot flush protein byproduct - urea
dialysis
treatment for chronic renal failure
depends on degree of kidney function that remains
-meds to help with growth, prevent bone density loss, and/ or treat anemia
-diuretic therapy or meds )to increase urine output
-specific diet restrictions (protein is limited due to buildup of urea)
-dialysis
-kidney transplantation
Diabetes and kidney failure
diabetes is the most common cause of kidney failure
prominent s/s that diabetes is damaging that kidney is the finding of protein in the urine
kidney failure and hypertension
hypertension is the 2nd most common cause of CRF, can be seen as not only the cause of kidney disease but also as a result of damage created by the disease
atherosclerosis causes
causes inflammation and hypertension
specific gravity
1.010 - 1.030
sodium
135 - 145
potassium
3.5 - 5.0
calcium
8.5 - 10.5
magnesium
1.5 - 3.0
nephrotic syndrome
loss of protein
acute tubular necrosis
caused by ischemia
acute renal failure
reversible
chronic renal failure
permanent
Difference between UTI and Pyelonephritis
UTI: local inflammation of bladder/ urethra/ ureters
pyelonephritis: kidney infection leads to systemic infection, with s/s of fever/ chills/ n/v, etc.
AKI 4 phases
Onset: blood loss burns trauma sepsis
Oliguric: low urine output (cause effects kidneys function)
Diuretic: kidneys start to heal
Recovery: several months to a year
