EXAM 2 REVIEW
Advanced Pathophysiology NURS-6501N Exam 2 Outline Final Exam Study
Guide
Renal: Mechanism, presentation and diagnostic tests of
- GFR = sum of GFRs in all functioning nephrons, so # of functional nephrons = GFR
- BP in glomerular capillaries > BP in Bowman’s space ( Hydrostatic pressure gradient)
- Renal auto-regulation to preserve GFR when BP/Volume drops: RAAS activated
Afferent (Approaching) arteriole dilates to increase perfusion to nephron, and Efferent
(Exiting) arteriole constricts so less blood leaves nephron
- Estimating GFR in clinical practice: Cr, BUN, eGFR, CrCl
o
Serum Cr will when GFR (Pitfall: Dependent on muscle mass; If muscle mass low,
low Cr may underestimate GFR; In trauma & muscle breakdown, high Cr may
overestimate GFR)
▪ Waste product of muscles
▪ Almost all Cr that is filtered is excreted in urine; Serum Cr reflects
kidney filtration fxn
o
When GFR , BUN (Pitfall: Depends on diet & volume status b/c it is reabsorbed to
blood w/ H20 if dehydrated, body will re-absorb more H20 & some urea too; Poor
predictor of GFR)
▪ Urea is waste product of proteins; HIGH BUN IS CALLED AZOTEMIA!!!
o
BUN to Cr Ratio: (depending on volume) 10-15:1 (b/c mostly excreted in urine)
o
eGFR: 90-120mL/min Calculated value based on age, sex, Cr, & race
o
CrCl: Measure of volume of plasma from which Cr is completely removed
▪ When GFR , CrCl
Acute Kidney Injury (Pre-renal, Intra-renal, Post-renal)
- AKI is a rise in serum Cr of at least 0.3 mg/dL within a week
o Pre-renal: blood flow to kidneys (most common cause)
Due to reduced BP or blood volume; No direct damage to kidney
▪ Caused by:
structures!
Absolute hypovolemia (hemorrhage, diarrhea, vomiting, excessive urination)
Relative hypovolemia (low effective intravascular volume e.g.
decompensated CHF, septic shock, cardiogenic shock, severe burns, anything
causing 3rd spacing/edema)
Renal artery stenosis (renal artery is prone to atherosclerosis & when plaque
building it will cause stenosis)
Medications affecting renal autoregulation (i.e. NSAIDs vasoconstrict
afferent artery by inhibiting prostaglandins & ACE/ARBs dilate the efferent
artery
▪ Mechanism of Pre-Renal AKI: BP filtration pressure gradient GFR
▪ Presentation: Asymptomatic if mild, detected by elevated Cr
Mod. to severe (significant in # of functional nephrons) presents w/ oliguria,
hyperkalemia, metabolic acidosis, uremia (symptoms caused by retention of
uremic toxins) N/V, appetite, confusion, muscle cramps, pruritis
▪ Diagnosis: Serum Cr & BUN (Azotemia), eGFR, BUN/Cr ratio (>20:1)
,EXAM 2 REVIEW
, EXAM 2 REVIEW
Urine osmolality (more concentrated urine b/c less H20 [re-absorbed] but
same amount of particles), Urine sodium (more Na+ retained, level low in
urine), UA w/ no WBC/RBC, no proteins (bland)
▪ Treatment w/ correcting hypovolemia
o Post-renal: (fluids) obstruction of urinary tract
▪ A rapid decline in GFR due to obstruction of urinary tract, but glomerulus NOT
affected & perfusion is normal
▪ Caused by: Obstruction of urinary flow from two healthy kidneys, or unilateral/
partial obstruction in pts. w/ significant underlying CKD (i.e. abdominal tumor,
stricture, BPH, anticholinergic drugs will constrict bladder sphincter & prevent urine
outflow)
▪ Mechanism: Tubular pressure Hydrostatic pressure in Bowman’s capsule
(equalized to pressure in capillaries) Pressure gradient GFR (Cr &
BUN)
▪ Presentation: Urinary output is unpredictable (i.e. can be anuria when
completely obstructed or may be normal if partial/unilateral obstruction)
Pain may or may not be present, if present due to bladder distention or
obstructions
(+/-) Abdominal/bladder distention
(+/-) Macroscopic hematuria (damage to blood vessels in wall of lower urinary
tract)
▪ Diagnosis: Serum Cr & BUN , but BUN:Cr Ratio NORMAL and Urine
Osmo NORMAL Na/ because no excessive re-absorption of H20 & Na b/c no
hypoperfusion present
Post-void residual urine volume > 200mL
Hydronephrosis on U/S
UA will show intact RBC (bleeding from ureter, bladder)
▪ Treatment: Relieve obstruction, complete recovery if relieved within 1
o Intra-renal: week damage to the structure of the kidney
▪ Decline in GFR (days-weeks) due to damage to kidney structures
▪ Renal tubules (80% of cases), Renal interstitium (supporting tissue between renal
tubules), & Glomeruli
1) Acute Tubular Necrosis (ATN) is necrosis of the tubular epithelial cells
▪ Caused by:
Ischemia (prolonged severe hypovolemia resulting in tubular cell ischemia,
septic shock, extensive burns, cardiogenic shock)
Toxins (radiocontrast materials, aminoglycosides, vancomycin,
amphotericin, myoglobin pigment of muscle byproduct in rhabdomyolysis)
▪ Mechanism: Prolonged unrelieved ischemia or direct toxic damage to epithelial
tubular cells Necrosis of tubular epithelial cells Reabsorption of H20 &
electrolytes Dead tubular cells slough off & obstruct renal tubule Pressure in
renal tubule leads to pressure gradient Equalized pressure in glomerular
capillaries & tubules GFR
Advanced Pathophysiology NURS-6501N Exam 2 Outline Final Exam Study
Guide
Renal: Mechanism, presentation and diagnostic tests of
- GFR = sum of GFRs in all functioning nephrons, so # of functional nephrons = GFR
- BP in glomerular capillaries > BP in Bowman’s space ( Hydrostatic pressure gradient)
- Renal auto-regulation to preserve GFR when BP/Volume drops: RAAS activated
Afferent (Approaching) arteriole dilates to increase perfusion to nephron, and Efferent
(Exiting) arteriole constricts so less blood leaves nephron
- Estimating GFR in clinical practice: Cr, BUN, eGFR, CrCl
o
Serum Cr will when GFR (Pitfall: Dependent on muscle mass; If muscle mass low,
low Cr may underestimate GFR; In trauma & muscle breakdown, high Cr may
overestimate GFR)
▪ Waste product of muscles
▪ Almost all Cr that is filtered is excreted in urine; Serum Cr reflects
kidney filtration fxn
o
When GFR , BUN (Pitfall: Depends on diet & volume status b/c it is reabsorbed to
blood w/ H20 if dehydrated, body will re-absorb more H20 & some urea too; Poor
predictor of GFR)
▪ Urea is waste product of proteins; HIGH BUN IS CALLED AZOTEMIA!!!
o
BUN to Cr Ratio: (depending on volume) 10-15:1 (b/c mostly excreted in urine)
o
eGFR: 90-120mL/min Calculated value based on age, sex, Cr, & race
o
CrCl: Measure of volume of plasma from which Cr is completely removed
▪ When GFR , CrCl
Acute Kidney Injury (Pre-renal, Intra-renal, Post-renal)
- AKI is a rise in serum Cr of at least 0.3 mg/dL within a week
o Pre-renal: blood flow to kidneys (most common cause)
Due to reduced BP or blood volume; No direct damage to kidney
▪ Caused by:
structures!
Absolute hypovolemia (hemorrhage, diarrhea, vomiting, excessive urination)
Relative hypovolemia (low effective intravascular volume e.g.
decompensated CHF, septic shock, cardiogenic shock, severe burns, anything
causing 3rd spacing/edema)
Renal artery stenosis (renal artery is prone to atherosclerosis & when plaque
building it will cause stenosis)
Medications affecting renal autoregulation (i.e. NSAIDs vasoconstrict
afferent artery by inhibiting prostaglandins & ACE/ARBs dilate the efferent
artery
▪ Mechanism of Pre-Renal AKI: BP filtration pressure gradient GFR
▪ Presentation: Asymptomatic if mild, detected by elevated Cr
Mod. to severe (significant in # of functional nephrons) presents w/ oliguria,
hyperkalemia, metabolic acidosis, uremia (symptoms caused by retention of
uremic toxins) N/V, appetite, confusion, muscle cramps, pruritis
▪ Diagnosis: Serum Cr & BUN (Azotemia), eGFR, BUN/Cr ratio (>20:1)
,EXAM 2 REVIEW
, EXAM 2 REVIEW
Urine osmolality (more concentrated urine b/c less H20 [re-absorbed] but
same amount of particles), Urine sodium (more Na+ retained, level low in
urine), UA w/ no WBC/RBC, no proteins (bland)
▪ Treatment w/ correcting hypovolemia
o Post-renal: (fluids) obstruction of urinary tract
▪ A rapid decline in GFR due to obstruction of urinary tract, but glomerulus NOT
affected & perfusion is normal
▪ Caused by: Obstruction of urinary flow from two healthy kidneys, or unilateral/
partial obstruction in pts. w/ significant underlying CKD (i.e. abdominal tumor,
stricture, BPH, anticholinergic drugs will constrict bladder sphincter & prevent urine
outflow)
▪ Mechanism: Tubular pressure Hydrostatic pressure in Bowman’s capsule
(equalized to pressure in capillaries) Pressure gradient GFR (Cr &
BUN)
▪ Presentation: Urinary output is unpredictable (i.e. can be anuria when
completely obstructed or may be normal if partial/unilateral obstruction)
Pain may or may not be present, if present due to bladder distention or
obstructions
(+/-) Abdominal/bladder distention
(+/-) Macroscopic hematuria (damage to blood vessels in wall of lower urinary
tract)
▪ Diagnosis: Serum Cr & BUN , but BUN:Cr Ratio NORMAL and Urine
Osmo NORMAL Na/ because no excessive re-absorption of H20 & Na b/c no
hypoperfusion present
Post-void residual urine volume > 200mL
Hydronephrosis on U/S
UA will show intact RBC (bleeding from ureter, bladder)
▪ Treatment: Relieve obstruction, complete recovery if relieved within 1
o Intra-renal: week damage to the structure of the kidney
▪ Decline in GFR (days-weeks) due to damage to kidney structures
▪ Renal tubules (80% of cases), Renal interstitium (supporting tissue between renal
tubules), & Glomeruli
1) Acute Tubular Necrosis (ATN) is necrosis of the tubular epithelial cells
▪ Caused by:
Ischemia (prolonged severe hypovolemia resulting in tubular cell ischemia,
septic shock, extensive burns, cardiogenic shock)
Toxins (radiocontrast materials, aminoglycosides, vancomycin,
amphotericin, myoglobin pigment of muscle byproduct in rhabdomyolysis)
▪ Mechanism: Prolonged unrelieved ischemia or direct toxic damage to epithelial
tubular cells Necrosis of tubular epithelial cells Reabsorption of H20 &
electrolytes Dead tubular cells slough off & obstruct renal tubule Pressure in
renal tubule leads to pressure gradient Equalized pressure in glomerular
capillaries & tubules GFR
