Nsg 533 pathophysiology Exam 3 Spring 2026-2027 Study guide
Urologic/Renal Content
1. Know basic renal terms like Acute vs chronic, GFR, how lab values like creatinine is important to
renal function etc.
Acute cystitis- inflammation of the urinary bladder, aka a UTI, typically bacterial Pyelonephritis-
a UTI that ascends to one or both kidneys.
Calculi- stones, in the bladder or urinary tract
Hydronephrosis- swelling of the kidney due to a buildup of urine due to a blockage GFR-
estimates kidney function by measuring how much blood passes through the glomeruli each
minute – less than 90 is kidney disease
**Minimum urine output **is about 30 ml an hour or 0.5 with the calculation
Prerenal – heart failure and hypovolemia
Intrarenal – Inflammation and infection like post strep glomerular nephritis, toxic agents
Postrenal - BPH and calculi in ureter
Decrease in GFR, decrease in urine output and increase in creatine are red flags!
2. Ureteral strictures: What can happen is there is an obstruction in one kidney? What happens to
the other kidney?
If there is an obstruction in one kidney – the other one compensates. The patient may have no
symptoms and be unaware of the compensation.
3. Renal stones: what are characteristics of the following stones?
pg. 1
, o Struvite-Staghorn (right in middle of renal pelvis and gets into urinary system) o
Calcium stones- Most common type of stone from too much oxalate or too little urine o
Uric Acid – Can result from a diet high in purine from animal proteins
4. Stress Incontinence what is it and why does it happen?
Weak pelvic floor after childbirth or menopause. Coughing, sneezing, laughing causes urine to
leak out. Women are more affected.
5. Pathophysiology of a UTI in patients with a foley catheter, what makes them difficult to treat?
Biofilm can form on the foley, urine is a good medium for bacteria growth. It can ascend up from
lower UTI to upper UTI from ureter to bladder to kidneys. Immunocompromised, females and
people with indwelling catheters are more at risk.
6. Know what nephrotic syndrome is and the Causes of edema with nephrotic syndrome.
Spilling of proteins into the urine. The oncotic pressure is decreased in the plasma which leads
to proteinuria. Now there is less protein in the blood so you can’t suck up fluid through
hydrostatic pressure into vessels which stays in the tissue – leads to major edema. Leakage of
albumin which means that there is no colloid to pull in the fluid back into the blood stream
which results in edema. Liver synthesizes proteins quickly which increases lipids to make up for
loss – hyperlipidemia results.
7. What does strep have to do with kidney disease?
Glomerular nephritis- Strep can cause the body to create an antibody-antigen immune complex
that is deposited in glomerulus. This sets off inflammation which leads to hematuria, edema
(due to decreased oncotic pressure), proteinuria, low energy, low grade fever and nephritis.
pg. 2
, 8. Pathophysiological changes in nephrons when a patient has high blood sugars.
The membrane becomes thickened and damaged which allows mesangial cells to grow and
occlude the capillaries leading to sclerosis. Filtration pressure is increased which damages the
glomeruli. Also dilates pores in glomeruli vessels which leaks protein – an indicator.
9. Pathophysiological changes of the kidney from chronic HTN?
Causes the renal arteries to become thicken to compensate for increased pressure which
narrow diameter of vessels. The means that less blood can get through which damages the
nephrons and changes the glomerulus.
10. What is a way we can detect diabetic glomerulosclerosis in patients early? What is happening?
Increased glucose entering the kidneys force them to work harder to filter out the kidneys. To
increase excretion of glucose, it needs to have increased blood flow and filtration pressure. The
increased pressure causes a change in the capillary pores. It also changes the membrane by
thickening it and damaging it. This allows mesangial cells to grow and occlude the capillaries
which leads to the glomerulus becoming sclerosed. UA that shows microalbuminuria because
albumin can now leak out through the urine.
11. RIFLE criteria- what is it and how is it used?
Risk Injury Failure Loss and ESRD. First three look at the severity and the last two look at the
outcome. It is used to assess severity of acute kidney injury.
12. Acute tubular necrosis: Stages and symptoms
Caused by renal ischemia or nephrotoxicity. Has three stages: initiating /event, oliguric/
maintenance and diuretic /recovery.
pg. 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.
Acute cystitis- inflammation of the urinary bladder, aka a UTI, typically bacterial Pyelonephritis-
a UTI that ascends to one or both kidneys.
Calculi- stones, in the bladder or urinary tract
Hydronephrosis- swelling of the kidney due to a buildup of urine due to a blockage GFR-
estimates kidney function by measuring how much blood passes through the glomeruli each
minute – less than 90 is kidney disease
**Minimum urine output **is about 30 ml an hour or 0.5 with the calculation
Prerenal – heart failure and hypovolemia
Intrarenal – Inflammation and infection like post strep glomerular nephritis, toxic agents
Postrenal - BPH and calculi in ureter
Decrease in GFR, decrease in urine output and increase in creatine are red flags!
2. Ureteral strictures: What can happen is there is an obstruction in one kidney? What happens to
the other kidney?
If there is an obstruction in one kidney – the other one compensates. The patient may have no
symptoms and be unaware of the compensation.
3. Renal stones: what are characteristics of the following stones?
pg. 1
, o Struvite-Staghorn (right in middle of renal pelvis and gets into urinary system) o
Calcium stones- Most common type of stone from too much oxalate or too little urine o
Uric Acid – Can result from a diet high in purine from animal proteins
4. Stress Incontinence what is it and why does it happen?
Weak pelvic floor after childbirth or menopause. Coughing, sneezing, laughing causes urine to
leak out. Women are more affected.
5. Pathophysiology of a UTI in patients with a foley catheter, what makes them difficult to treat?
Biofilm can form on the foley, urine is a good medium for bacteria growth. It can ascend up from
lower UTI to upper UTI from ureter to bladder to kidneys. Immunocompromised, females and
people with indwelling catheters are more at risk.
6. Know what nephrotic syndrome is and the Causes of edema with nephrotic syndrome.
Spilling of proteins into the urine. The oncotic pressure is decreased in the plasma which leads
to proteinuria. Now there is less protein in the blood so you can’t suck up fluid through
hydrostatic pressure into vessels which stays in the tissue – leads to major edema. Leakage of
albumin which means that there is no colloid to pull in the fluid back into the blood stream
which results in edema. Liver synthesizes proteins quickly which increases lipids to make up for
loss – hyperlipidemia results.
7. What does strep have to do with kidney disease?
Glomerular nephritis- Strep can cause the body to create an antibody-antigen immune complex
that is deposited in glomerulus. This sets off inflammation which leads to hematuria, edema
(due to decreased oncotic pressure), proteinuria, low energy, low grade fever and nephritis.
pg. 2
, 8. Pathophysiological changes in nephrons when a patient has high blood sugars.
The membrane becomes thickened and damaged which allows mesangial cells to grow and
occlude the capillaries leading to sclerosis. Filtration pressure is increased which damages the
glomeruli. Also dilates pores in glomeruli vessels which leaks protein – an indicator.
9. Pathophysiological changes of the kidney from chronic HTN?
Causes the renal arteries to become thicken to compensate for increased pressure which
narrow diameter of vessels. The means that less blood can get through which damages the
nephrons and changes the glomerulus.
10. What is a way we can detect diabetic glomerulosclerosis in patients early? What is happening?
Increased glucose entering the kidneys force them to work harder to filter out the kidneys. To
increase excretion of glucose, it needs to have increased blood flow and filtration pressure. The
increased pressure causes a change in the capillary pores. It also changes the membrane by
thickening it and damaging it. This allows mesangial cells to grow and occlude the capillaries
which leads to the glomerulus becoming sclerosed. UA that shows microalbuminuria because
albumin can now leak out through the urine.
11. RIFLE criteria- what is it and how is it used?
Risk Injury Failure Loss and ESRD. First three look at the severity and the last two look at the
outcome. It is used to assess severity of acute kidney injury.
12. Acute tubular necrosis: Stages and symptoms
Caused by renal ischemia or nephrotoxicity. Has three stages: initiating /event, oliguric/
maintenance and diuretic /recovery.
pg. 3
