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187 Cards in this Set

  • Front
  • Back
Adrenal gland disorders
diabetes insipidus
SIADH
tasteless diabetes
diabetes insipidus
insufficiency of ADH leading to the insufficiency of ADH > lots of free water is lost
types diabetes insipidus
central type
nephrogenic type
central diabetes insipidus is
not enough ADH produced; due to
head trauma
pituitary gland tumors & infections
nephrogenic diabetes insipidus is
a renal disease that makes kidneys not respond to ADH
S/S
polyuria - excessive urine
polydipsia - excessive thrist
dehydration - dry MM, excessive Na
diabetes insipidus
treatment of central type of diabetes insipidus
ADH IV or nasally (can't be given GI)
treatment of nephrogenic type of diabetes insipidus
treat the kidney disease
Lots of Pee
diabetes insipidus
No pee
SIADH
SIADH aka
syndrome of inappropriate (excessive) ADH
Path of SIADH
excessive ADH - H2O is retained excessively

problem with pituitary
Cause of SIADH
lung cancer - ectopic production of ADH

Also caused by drugs
diuretcs
morphine
chemotherapy
general anesthesia
S/S
small amount of dark urine
retention of water marked by crackles & cellular swelling
diluted Na level
anorexia
n/v
changes in sensorium > Sz > coma/death if not treated
SIADH
treatment of SIADH
treat the cause
fluid restriction (600-800cc/day)
diuretics
changes in sensorim cause __________ becasuse
confusion
cellular swelling
increase urine specific gravity
SIADH
normal urine specific gravity
1.010 - 1.030
renal disorders
urinary tract infections
kidney stones
2nd most common infection seen by MD
urinary tract infection
cystitis
ragging bladder infection
UTI
an infection of urinary tract
Causes of urinary tract infection
1. bacteria ascends up urethra (or travels thru blood lymph)

2. foley catherters (bacteria ascends catheter)

3. Afftected by hormonal & anatomic changes
affected by hormonal & anatomic changes in women
sexual activity "honeymoon" cystitis

pregnancy > dilation of ureters > cystitis & pyelonephritis
affected by hormonal & anatomic changes in men
prostatic hypertrophy > reflux & obstruction > UTI

reflux from a sneeze or cough > forces urine into urethra & back into the bladder >

urethra has organisms (bladder is sterile)
#1 Causative organism of UTI
E.Coli
S/S of cystitis (FUB)
frequency
urgency
burning
a potential complication of urinary tract infection
acute pyelonephritis
acute pyelonephritis is
an UTI that ascends to kidney

abrupt onset of chills & fever

dysuria & frequency

back pain (also called CVA tenderness)
abrupt onset of chills & fever
back pain (also called CVA tenderness)
Dysuria
frequency
acute pyelonephritis
dx of urinary tract infections
microscopic exam urine - look WBC & bacteria
treatment of urinary tract infection
cystitis - antibotics, increased fluids, vit C

pyelonephritis - longer course of antibotics or hospitalization & IV antibotics
prevention of urinary tract infections
keep your urine acidic and drink lots of fluid
collection of crystals and protein
kidney stones (nephrolithiasis)
another name of kidney stones
nephrolithiasis
kidney stones are more common in _____ with a _________ (recurrence is common)
males

family history
Theories of Kidney stone causes
saturation theory
stone inhibitor theory
saturation theory
increase calcium & uric acid leads to stones
stone inhibitor theory
faulty inhibitor in kidney
Urine becomes concentrated/output drops (stagnant uria)
stone begins w/ a nucleus
patho of kidney stones
kidney stones are effected by
urine pH
stagnant urine
immobilization
increased calcium levels
#1 type of stone
calcium (70 - 80% of stones)
70-80% of stones are made of
calcium
other types of stone
magnesium
uric acid
cystine etc
S/S of kidney stones
no symptom if inside kidney (renal pelvis)
Pain starts when descends to ureter
"renal or urethral colic"
Hematuria
"renal or urethral colic"
abrupt, intense spasmodic pain in flank & upper quadrant of abdomen (ureter has peristalsis)
treatment for kidney stones
supportive - wait until it's passed
treat the pain w/ strong narcotics
strain the uterine to document passage
lithotropsy
ureterscopy
lithotripsy
ultrasound shock waves break up stone
Kidney stone prevention
decrease calcium alone doesn't help
Increase fiber - fiber binds w/ calcium
increase fluids
avoid calcium & tea toghther
risky food for kidney stones
rhubarb
tea
coffee
spinach
nuts
chocolate
Renal tumors
renal cell cacinoma
bladder cancer
neuroblastoma/Wilm's tumor
acute glomerulonephritis
nephrotic syndrome
most common renal neoplasm
renal cell carcinoma
renal cell carcinoma occurs most often in
men ages 50-70
exposure to petroleum products/ heavy metals/abestos
high protein diet
tobacco use
obesity
HTN
family history

are risk factors for
renal cell carcinoma
S/S of late renal cell carcinoma
hematuria
flank pain
palpable mass
only 10% of causes have S/S; mostly silent until metastasis
renal cell carcinoma
treatment for renal cell carcinoma
remove the kidneys and then start chemo
decreased cure rate if metastasis
4th most common cancer in USA
Bladder cancer
renal tumor more common in

bladder cancer
men over 60

bladder cancer
Cause of bladder cancer
unknown
#1 risk factor of bladder cancer is
smoking
other risk factors of bladder cancer include
working w/ chemicals (rubber & textiles)
family history
saccharine has not been proven to be carcinogenic in
bladder cancer
S/S of bladder cancer
hematuria - intermittent or ASYMPTOMATIC
NO PAIN
often diagnosed late in the course of disease
S/S
hematuria
no pain
bladder cancer
treatment for bladder cancer
surgery
chemo
cystectomy
renal tumor that has a high chance of recurrence
bladder cancer
rare kidney tumor found in kids under age 5
neuroblastoma/wilms tumor
tumor of embryonic orgin
neuroblastoma/wilms tumor
neuroblastoma/wilms tumor may be associated with
paternal exposure to heavy metals & hydrocarbons
neuroblastoma/wilms tumor S/S
mostly asymptomatic except for upper abd. mass
very rare and fragile tumor
neuroblastoma/wilms tumor
do not massage the abdomen
neuroblastoma/wilms tumor
treatment for neuroblastoma/wilms tumor
surgery
chemo
radiation
95% survival rate if no metastasis
neuroblastoma/wilms tumor
acute inflammation of glomerulus
acute glomerulonephritis
Acute glomerulonephritis is caused by
inflammatory cells IgG/IgM that get trapped in glomerulus

leading to damage in glomerulus
Acute clomerulonephritis is a complication from
infection
circulating immune complexes get trapped in glomerular membrane
water & Na are retained as the body slows blood flow to damaged area
blood can't be filtered
decrease in GFR (waste not excreted well)
Patho of acute glomerulonephritis
S/S of acute glomerulonephritis
abrupt onset of hematuria (cola)
oliguria
azotemia
proteinuria
H2O & Na retention (face & hands)
HTN
treatment of acute glomerulonphritis
treat original infection
usually resolves self in time
supportive treatment
azotemia
nitrogenous water in blood as GFR drops
rare tumor mostly in 2-3 year olds
neuroblastoma/wilms tumor
nephrotic syndrome
glomerular disease causing excretion of 3.5 + grams of protein in urine a day
patho of nephrotic syndrome
gleomerualr filtration membrane is injured and leaks albumin & immunoglobulins
most common cause of nephrotic syndrome
diabetes
S/S of nephrotic syndrome
#1 hypoproeinemia/hypoalbunemia
edema
proteinuria
fluid becomes trapped in tissues no proteins to pull it back in
nephrotic syndrome
losing plasma proteins
nephrotic syndrome
prevention of nephrotic syndrome
keep blood sugar even

excessive sugar gradual damage glomerulas

glomerules lets proten leak out when their damages
long term complication of renal damage

can only manage it
nephrotic syndrome
treatment of nephrotic syndrome
steroid therapy
low sodium diet
diuretics
low fat
normal protien diet
Acute renal failure (ARF)
abrupt reversible kidney failure
unable to remove wastes and regulate pH and electrolytes
ARF
Reversible kidney failure
ARF
Reversible causes of ARF
Prerenal
Intrarenal
Postrenal
Prerenal (starved to death)
any cause that impairs renal blood flow
60% of causes of reversible ARF
prerenal
Kidney is fine, but gets no blood
prerenal
what can cause prerenal
CHF
dehydration
circulatory collapse
shock
MI
Intrarenal
some type of kidney disease leading to injury to glomerulus
#1 cause of intrarenal
Injury to glomerulus
intrarenal injury to glomerulus
damage to renal tubules from extended ischemia
debris builds up
increased pressure in tubules
decreased GFR
other causes of intrarenal
trauma
antibiotics
infection
posterenal
from obstruction of urine outflow from the kidney
postrenal can be casued by
ureter obstruction
kidney stones
prostatic hypertrophy
beign prostatic hypertrophy
postrenal
decreased blood flow to kidney
prerenal
stages & S/S ARF reversible
1. Oliguria stage
2. Diuretic Phase
3. Concalescent stage
Oiguria stage
decreased GFR
occurs 1 day after ischemic event
last about 1-2 weeks
oliguria stage
Oliguria stage (list)
urine output less than 500cc day
everything builds up because it can't get out except calcium
increase BUN (azotemia) creatinine & phosphorus
increased K
fluid rention
metabolic acidosis
everything builds up because it can't et out except calcium
oliguria stage
increased K leads to
weakness
EKG change
fluid retention leads to
pulmonary edema
HTN
in oliguria stage everything is retained except
calcium
calcium blood levels in oliguria stage
are low because phosphorus is up
in this stage calcium gets pushed itno joints and tissues, bones are demineralized
Oliguria stage
#1 cause of ARF
Acute tubular necrosis
diuretic phase occurs with
start of recovery
ARF stage that last 2-14 days
diuretic phase
In the hospital for atleast two weeks
ARF
Renal blood flow is improving
increased excretion > excretes H2O & electrolytes
diuretic phase
may over excrete because tubules are still damaged
diuretic phase
Renal diet
decreased protein
carbs r better
concalescent stage may take how long
3 -12 months
ARF treatment
treat the cause
limit fluid intake during acute phase (intake = output)
adequate caloris (low proteins & high carbo)
temporary dialysis
don't let them get dehydrated
prevention of ARF for pt at risk
maintain fluid volume to keep renal perfusion normal

Mannitol
mannitol
dilates renal arteries & increased GFR
chronic renal failure
progressive and IRREVERSIBLE destruction of the kidney
occurs 1 day after ischemic event
last about 1-2 weeks
oliguria stage
Oliguria stage (list)
urine output less than 500cc day
everything builds up because it can't get out except calcium
increase BUN (azotemia) creatinine & phosphorus
increased K
fluid rention
metabolic acidosis
everything builds up because it can't et out except calcium
oliguria stage
increased K leads to
weakness
EKG change
fluid retention leads to
pulmonary edema
HTN
in oliguria stage everything is retained except
calcium
calcium blood levels in oliguria stage
are low because phosphorus is up
in this stage calcium gets pushed itno joints and tissues, bones are demineralized
Oliguria stage
#1 cause of ARF
Acute tubular necrosis
diuretic phase occurs with
start of recovery
ARF phase that last 2-14 days
diuretic phase occurs with start of recovery
renal blood flow is improving
increased excretion leads to excretion H2O & electrolytes
diuretic phase
may over excrete because tubules are still damaged
diuretic phase
increased excretion leads to
excretes H2O & elctrolytes
Hospital stay for ARF pt
at least 2 weeks
renal diet
decreased protein
carbs good
concalescent stage of ARF may take
3-12 months
treatment of ARF
treat the cause
limit fluid intake during scute phase (intake=output)
adequate calories (low proteins & high carbs)
temporary dialysis
don't let them get dehydrated
prevention of ARF for pts. at risk
maintain fluid volume to keep renal perfusion normal

Mannitol
mannitol
dilates renal arteries and increases GFR
Chronic renal failure
progressive & IRREVERSIBLE destruction of the kidney
causes of chronic renal failure
anything that leads to permanent loss of nephrons

complications of many diseases
chronic renal failure #1 cause
diabetes
stages of chronic renal failure
decrease renal reserves
renal insufficiency
end stage renal disease
50% of renal function is gone (chronic renal failure)
1st stage - decreased renal reserves
S/S of renal reserves
None because kidney can adapt
75-90% of renal function is gone (chronic renal failure)
2nd stage renal insufficiency
renal insufficiency s/s
slighly eleveted BUN & creatinine
polyuria (because kidney's can't concentrate urine)
may be controlled w/ diet and medicaiton
end stage renal disease s/s
profund S/S
need dialysis or transplant
more than 90% of function is gone in kidney
end stage renal disease
S/S of chronic renal failure
Azotemia
fluid & Na buildup
elevaed potassium
metabolic acidosis
elevated phosphorus levels
increased loss of calcium
RBC decreased
pale dry pruitis skin uremic frost
uremic frost
filtering; dandruff flakes off skin
with chronic renal failure elevated potassium leads to
arrythmias (irregular beat)
with chronic renal failure calcium loss leads to
stimulation of PTH and bones dissolve
Chronic renal failure cause elevated resp because
trying to get rid of acid
edema
#1 sign of chronic renal failure
azotemia
azotemia
increased nitrogen in blood
with chronic renal failure fluid & Na build up leads to
bounding pulses
JVD
crackles
edema
HTN
complication of chronic renal disease
congestive heart rate CHF
acid is part of regular
metabolism
treatment for chronic renal failure
decrease protein (decrease nitrogenous wastes)
adequate calories (meet engery needs)
Low K
decrease fluids
dialysis/kidney transplant
decrease fluids prevents
circulatory overload (but don't decrease to much)
Urinalysis checks urine for
color
specific gravity
pH
There should be no _______(6) in urinalysis
glucose
RBC
WBC
protein
cast
crystals
creatinine is a product of
muscle mass
estimates glomerular filtration rate very well and is a very reliable measure

doesn't vary much
creatinine
creatinine normal levels
.7 - 1.5
Blood Urea Nitrogen
nitrogen in the blood
substance normally in blood
by product of protein metabolism - substance normally in blood
blood urea nitrogen
BUN is easily effected by
intact protien
GI bleeding
hydration
BUN is a less reliable estimate of GFR than
creatinine
Normal BUN level
10 - 20 mg/dl
urine specific gravity
a measure of the concentration of solutes (chunks) in the urine
normal range of urine specific gravity
1.010 - 1.030
very dilute would have specific gravity of
1.0
very dark concentrated urine would have a spefic gravity of
1.03
this test _________ compares the urine to ______, which has the specific gravity of _____
urine specific gravity
10
30