NURS 6030 - Exam 3 Review.

N6030 Study Guide Exam 3


Urologic/Renal Content

1. Know basic renal terms like Acute vs chronic, GFR, how lab values like
creatinine is important to renal function etc.
a. Acute: sudden onset, severe
b. Chronic: long standing or constantly recurring
i. End stage renal disease, renal insufficiency
c. GFR: glomerular filtration rate, is a blood test that checks how well your
kidneys are working. Kidneys have tiny filters called glomeruli. These
filters help remove waste and excess fluid from the blood. GFR estimates
how much blood passed through these filters each minute.
d. Creatinine: is a blood test that measures how much creatinine is in the
blood. Creatinine is a waste product that forms when creatine, a waste
product found in muscle, breaks down. Nephrons constantly filter blood
through a very tiny cluster of blood vessels known as glomeruli. High
levels of creatinine may indicate that your kidney is damaged.
2. Ureteral strictures: What can happen is there is an obstruction in one
kidney? What happens to the other kidney?
a. Ureteral strictures: narrowing of the ureter that causes an obstruction in
the flow of urine.
b. Urinary obstruction pathophys: urine flows out of the kidneys at
extremely low pressure. If the flow of urine is obstructed, urine backs up
behind the point of blockage, eventually reaching the small tubes of the
kidney and its collecting area (renal pelvis), swelling (distending) the
kidney and increased pressure on its internal structures. This kidney
distention is known as hydronephrosis. The elevated pressure due to the
obstruction may ultimately damage the kidney and can result in a lack of
function. Including local ischemia due to distention and increased tubular
pressures. Leading to apoptosis of renal/tubular cells causing renal failure.
c. Unilateral obstruction may have no S/S
3. Renal stones: what are characteristics of the following stones?
o Struvite-Staghorn
 Magnesium-ammonium-phosphate
 “staghorn calculus”
 Associated with urinary tract infections
 Most commonly found in women

, o Calcium stones or calcium phosphate (75%)
 most common
 Hypercalcemia: hyperparathyroidism, immobility
 They are formed from an intake of calcium, try to avoid high-oxalate
foods like potato chips, peanuts, chocolate, beets, spinach
o Uric Acid
 More common in men than in women.
 Occur in people with gout or those going through chemotherapy
 Develops when urine is too acidic.
4. Stress Incontinence what is it and why does it happen?
a. Happens when physical movement or activity—such as coughing,
laughing, sneezing, running or heavy lifting—puts pressure (stress) on
your bladder, causing you to leak urine.
5. Pathophysiology of a UTI in patients with a foley catheter, what makes
them difficult to treat?
a. Bacteria may enter the bladder through contamination of the tip during
insertion with the flora of the distal urethra or form bacteria ascending the
outside or inside of the catheter.
b. Patients with a urinary catheter have shown to develop histological and
immunological changes in the bladder that can lead to an inflammatory response,
exfoliation, edema and mucosal lesions of the bladder epithelium. Often the
catheter has bacteria growing on or inside the tubing. Once the catheter is placed
inside of the patient is can lead to inoculation of the organism into the bladder
and promote colonization. Ongoing epithelial irritation and persistent
inflammation can lead to cystitis. The ongoing inflammation of the bladder can
interfere with normal voiding and impairs the host’s defenses in the bladder
enabling more microbial colonization, multiplication and dissemination within the
urinary tract. Due to the constant mechanical damage caused by the urinary
catheter, fibrinogen accumulates in the bladder and deposits on the catheter.
Some pathogens use fibrinogen to establish colonization. The inflammation can
change the bladder environment making it more susceptible to microbial
colonization and disease causation.
c. Most of the time catheter associated UTI’s do not show any symptoms of
an infection because the patient is unable to tell when they have to
urinate, making it difficult to treat.
6. Know what nephrotic syndrome is and the Causes of edema with nephrotic
syndrome.
a. Glomerular disease where the body excretes too much protein in the urine
b. Often caused by damage to small blood vessels in the kidneys that filter
waste and excess water from the blood
i. Diabetes, lupus, amyloidosis

, c. Inflammationocclusion of glomeruli and damage of endothelial cells of
glomerulusdecreased GFR, oluguria, hematuria, edema
d. Glomerular damage causes increased permeability and a large loss of
plasma proteins (proteinuria)
i. S/S: proteinuria edema in the ankles and feet, HDL, foamy urine,
loss of immunoglobulins and complement proteins (increased risk
of infection), loss of proteins for binding drugs,
hormoneshypocalcemia (decreased vitamin D transport and
activation), hypothyroid
7. What does strep have to do with kidney disease?
a. Strep infections caused by streptococcus bacteria can develop into post-
streptococcal glomerulonephritis (PSGN). The strep bacteria travel to the
kidneys and make the filtering units of the kidney (glomeruli) inflamed,
causing the kidneys to be less able to filter urine.
b. Type III hypersensitivity: antigen-antibody complexes deposit in
glomerulus
i. Triggers inflammation, activation of complement, inflammatory
mediators
ii. Results in glomerular damage, cell proliferation, decrease GFR,
increased permeability of glomerulus
8. Pathophysiological changes in nephrons when a patient has high blood
sugars.
a. Diabetic nephropathy
i. Thickening and fibrosis of glomerulus capillary membrane
ii. Increase glucose increase blood flowinfiltration pressure
enlarged glomerular capillary pores
iii. Incorporation of glucose into glomerular capillary pores advanced
glycosylated end products
iv. Tubular endothelial cells increase reabsorption proteins damage
of nephron
9. Pathophysiological changes of the kidney from chronic HTN?
a. Hypertensive kidney disease
i. Sclerotic changes in glomerulus and arterioles
1. Thickening of vessel walls, narrowed blood vessels
ii. Changes in kidney structure
1. Change in glomerular structure and function
2. Decreased kidney size
3. Decreased perfusion of kidneyischemiatubular atrophy
iii. Can lead to end stage renal disease (ERSD)

, 10. What is a way we can detect diabetic glomerulosclerosis in patients early?
What is happening?
a. Glomerulosclerosis: increase extracellular matrix thickening of the
glomerular capillary membrane (scarring of the glomerulus)
i. can be caused by diabetes, sickle cell, obesity
ii. urinalysis will show proteins in the urine
iii. microalbuminuria
iv. urine test
11. RIFLE criteria- what is it and how is it used?
a. R: risk
b. I: injury
c. F: failure
d. L: loss of kidney function
e. E: end stage renal disease
i. It is used to define acute kidney injury
12. Acute tubular necrosis: Stages and symptoms
a. Initiation phase
i. Times from precipitating event to tubular injury
ii. 24-36 hours
iii. speed of onset determined by cause and underlying health of
kidneys
iv. can prevent injury at this phase
b. extension phase: inflammation and cell injury
c. oliguric (maintenance) phase
i. ongoing renal dysfunction; most severe symptoms
ii. weeks to months
d. Recovery (diuretic) phase:
i. Tubular epithelial repair/regeneration
ii. Diuresis
1. May be excessiveloss fluid/electrolyte
e. Tubular damage during ATN
i. Cell swelling, injury, necrosis
ii. Tubular obstruction: necrotic tissue and cells
iii. ~30% of patients may develop CKI or ESRD
1. often depends on underlying health of kidneys
f. S/S: increased creatinine and BUN, oluguria/anuria, electrolyte
abnormalities (hyperkalemia, hypocalcemia, hyperphosphatemia),
metabolic acidosis, weight gain, edema, increased BP, uremia (fatigue,
anorexia, nausea, pruriis, neuro changes)
13. Hemolytic uremic syndrome: Pathophysiology
a. Triad: hemolytic anemia, thrombocytopenia, renal impairment
b. Causes: bacterial, viral, endotoxins (E. Coli)
c. Patho: causal agent (e.g. toxins) trigger inflammation in glomerulus
i. Swollen glomerular arterioles