ADVANCED MED SURG STUDY GUIDE
EXAM 1
Unit 1: Complex Elimination
Renal
Acute Kidney Injury (AKI)
Pathophysiology Rapid reduction in kidney function results in a failure to maintain
waste, elimination, fluid and electrolyte balance, and acid-base balance.
Can be reversible.
Pre-renal- perfusion reduction from shock, dehydration, burns, sepsis.
Intra-renal- Kidney damage from glomerulonephritis, contrast dye
and chemo, local infection. Post-renal- urine flow obstruction caused
by cancer, enlarged prostate, kidney stones.
Clinical Oliguria, pulmonary crackles, dependent and generalized edema,
Manifestations confusion, tachypnea, dyspnea.
Etiology/ Reduced perfusion to the kidneys, damage to kidney tissue, or
Risk factors obstruction of urine flow.
RF: Shock, cardiac surgery, hypotension, prolonged mechanical
ventilation, and sepsis.
Tests/ Elevated BUN (10-20), elevated creatinine (0.6-1.2), decreased GFR,
Diagnostics decreased H/H, hypocalcemia, hyperkalemia, hyperphosphatemia,
(review values)
UA, ABGs (metabolic acidosis), KUB, US, CT scan WO contrast,
nuclear med tests
Therapeutic IV fluids and fluid challenge (NS bolus) to promote kidney perfusion.
Management With loss of kidney function- hemodialysis and CKRT (ICU only) are
used.
Nursing/ Monitor electrolytes and consult RDN to establish TPN or diet with
Assessment specific amounts of protein, sodium, and fluids, strict I&Os, daily wt.
Diet: Adequate protein (may need more with dialysis), limit Na, K,
phos.
Avoid IV contrast for testing. IF contrast medium must be used, hold
metformin 24 hours before and after procedure. Push IV fluids before
and after. Avoid NSAIDS, control HTN and DM.
, Chronic Kidney Disease (CKD)
Pathophysiology Progressive, irreversible disease that occurs when the kidneys fail to
maintain waste, elimination, fluid and electrolyte balance, and acid-
base balance.
Clinical Oliguria, uremic halitosis, melena, crackles, SOB, chest pain,
Manifestations tachycardia, narrow pulse pressures, low grade fever, pericardial
friction rub, bruising, petechiae.
Etiology/ Risk AKI, pyelonephritis, glomerulonephritis, polycystic kidney disease
factors RF: HTN, DM, nephrotoxic medications,
Tests/ Hyperphosphatemia, hyperlipidemia, hypocalcemia, elevated BUN,
Diagnostics elevated creatinine, decreased GFR (90-120), decreased H/H, UA
(protein, glucose, RBCs, WBCs, decreased SG)
Kidney US, CT scan WO contrast to r/o obstruction
Therapeutic Drug therapy with diuretics (furosemide) to increase UOP to manage
Management FVO, ESAs (epoetin alpha) to prevent or correct anemia, fluid
restriction, hemodialysis, PD
Nursing/ Strict I&Os, daily weights, monitor for decreased UOP, educate pts
Assessment with DM and HTN to adhere to drug/ diet regimens, exercise, complete
annual PCP visits/ testing, limit NSAIDS, avoid IV contrast- HOLD
metformin 24 hours before and after contrast!
Diet: Adequate protein (may need more with dialysis), limit Na, K,
phos, take Ca and vit D supplements,
Dialysis considerations:
Hemodialysis: AV fistula in forearm/ upper arm, NO BPs or sticks in
limb, weight pt. before and after, palpate thrill and auscultate bruit,
cleanse access site, monitor for bleeding at vas site, BP, HA, n/v,
dizziness. Complications: hypotension, dialysis disequilibrium
syndrome, cardiac events, reactions to dialyzers.
Peritoneal dialysis: rubber cath implanted in abd cavity, warm
dialysate, monitor dwell and drainage, use aseptic technique, mask for
you and pt, use sterile technique when accessing cath site.
Complications: Peritonitis from contamination at connection site. Sxs.
cloudy dialysate outflow, fever, and abd pain. Send culture.
, Gastrointestinal
Acute Pancreatitis
Pathophysiology Inflammatory process caused by premature activation of excessive
pancreatic enzymes that destroy ductal tissue and pancreatic cells-
resulting in autodigestion and fibrosis of the pancreas.
Clinical Mid epigastric or LUQ abd pain, pain that radiates to back or left flank/
Manifestations shoulder, n/v, wt loss, Cullen sign (bruising around belly button),
turners sign (bruising in flank)
Complications: septic shock, hemorrhage, jaundice, hyperglycemia,
paralytic ileus, pleural effusion, hypovolemic shock, PNA, DIC
Etiology/ Risk Gallstones, alcoholism, blunt abd trauma, drug use, infection, CF
factors
Tests/ Elevated amylase (56-190), lipase (0-110), Bili (0.3-1), ALP (30-120),
Diagnostics ALT (, WBC, ESR, glucose
CT w/ contrast, Abd US, Abd XR, ERCP (pancreatic stones)
Therapeutic Pain control with opioids, hydration with IV fluids, NPO and or NGT,
Management famotidine, PPIs.
Nursing/ Pain control priority, assess bowel sounds, monitor for hypocalcemia
Assessment (muscle twitching, numbness, irritability)
Diet: small frequent moderate- high carbs, high protein, low fat meals.
Bland foods, no tea, coffee, cola, chocolate, alcohol.
Teach pt to monitor for acute abd pain, jaundice, steatorrhea, clay-
colored stools, or dark urine which could indicate disease progression
to chronic pancreatitis.
EXAM 1
Unit 1: Complex Elimination
Renal
Acute Kidney Injury (AKI)
Pathophysiology Rapid reduction in kidney function results in a failure to maintain
waste, elimination, fluid and electrolyte balance, and acid-base balance.
Can be reversible.
Pre-renal- perfusion reduction from shock, dehydration, burns, sepsis.
Intra-renal- Kidney damage from glomerulonephritis, contrast dye
and chemo, local infection. Post-renal- urine flow obstruction caused
by cancer, enlarged prostate, kidney stones.
Clinical Oliguria, pulmonary crackles, dependent and generalized edema,
Manifestations confusion, tachypnea, dyspnea.
Etiology/ Reduced perfusion to the kidneys, damage to kidney tissue, or
Risk factors obstruction of urine flow.
RF: Shock, cardiac surgery, hypotension, prolonged mechanical
ventilation, and sepsis.
Tests/ Elevated BUN (10-20), elevated creatinine (0.6-1.2), decreased GFR,
Diagnostics decreased H/H, hypocalcemia, hyperkalemia, hyperphosphatemia,
(review values)
UA, ABGs (metabolic acidosis), KUB, US, CT scan WO contrast,
nuclear med tests
Therapeutic IV fluids and fluid challenge (NS bolus) to promote kidney perfusion.
Management With loss of kidney function- hemodialysis and CKRT (ICU only) are
used.
Nursing/ Monitor electrolytes and consult RDN to establish TPN or diet with
Assessment specific amounts of protein, sodium, and fluids, strict I&Os, daily wt.
Diet: Adequate protein (may need more with dialysis), limit Na, K,
phos.
Avoid IV contrast for testing. IF contrast medium must be used, hold
metformin 24 hours before and after procedure. Push IV fluids before
and after. Avoid NSAIDS, control HTN and DM.
, Chronic Kidney Disease (CKD)
Pathophysiology Progressive, irreversible disease that occurs when the kidneys fail to
maintain waste, elimination, fluid and electrolyte balance, and acid-
base balance.
Clinical Oliguria, uremic halitosis, melena, crackles, SOB, chest pain,
Manifestations tachycardia, narrow pulse pressures, low grade fever, pericardial
friction rub, bruising, petechiae.
Etiology/ Risk AKI, pyelonephritis, glomerulonephritis, polycystic kidney disease
factors RF: HTN, DM, nephrotoxic medications,
Tests/ Hyperphosphatemia, hyperlipidemia, hypocalcemia, elevated BUN,
Diagnostics elevated creatinine, decreased GFR (90-120), decreased H/H, UA
(protein, glucose, RBCs, WBCs, decreased SG)
Kidney US, CT scan WO contrast to r/o obstruction
Therapeutic Drug therapy with diuretics (furosemide) to increase UOP to manage
Management FVO, ESAs (epoetin alpha) to prevent or correct anemia, fluid
restriction, hemodialysis, PD
Nursing/ Strict I&Os, daily weights, monitor for decreased UOP, educate pts
Assessment with DM and HTN to adhere to drug/ diet regimens, exercise, complete
annual PCP visits/ testing, limit NSAIDS, avoid IV contrast- HOLD
metformin 24 hours before and after contrast!
Diet: Adequate protein (may need more with dialysis), limit Na, K,
phos, take Ca and vit D supplements,
Dialysis considerations:
Hemodialysis: AV fistula in forearm/ upper arm, NO BPs or sticks in
limb, weight pt. before and after, palpate thrill and auscultate bruit,
cleanse access site, monitor for bleeding at vas site, BP, HA, n/v,
dizziness. Complications: hypotension, dialysis disequilibrium
syndrome, cardiac events, reactions to dialyzers.
Peritoneal dialysis: rubber cath implanted in abd cavity, warm
dialysate, monitor dwell and drainage, use aseptic technique, mask for
you and pt, use sterile technique when accessing cath site.
Complications: Peritonitis from contamination at connection site. Sxs.
cloudy dialysate outflow, fever, and abd pain. Send culture.
, Gastrointestinal
Acute Pancreatitis
Pathophysiology Inflammatory process caused by premature activation of excessive
pancreatic enzymes that destroy ductal tissue and pancreatic cells-
resulting in autodigestion and fibrosis of the pancreas.
Clinical Mid epigastric or LUQ abd pain, pain that radiates to back or left flank/
Manifestations shoulder, n/v, wt loss, Cullen sign (bruising around belly button),
turners sign (bruising in flank)
Complications: septic shock, hemorrhage, jaundice, hyperglycemia,
paralytic ileus, pleural effusion, hypovolemic shock, PNA, DIC
Etiology/ Risk Gallstones, alcoholism, blunt abd trauma, drug use, infection, CF
factors
Tests/ Elevated amylase (56-190), lipase (0-110), Bili (0.3-1), ALP (30-120),
Diagnostics ALT (, WBC, ESR, glucose
CT w/ contrast, Abd US, Abd XR, ERCP (pancreatic stones)
Therapeutic Pain control with opioids, hydration with IV fluids, NPO and or NGT,
Management famotidine, PPIs.
Nursing/ Pain control priority, assess bowel sounds, monitor for hypocalcemia
Assessment (muscle twitching, numbness, irritability)
Diet: small frequent moderate- high carbs, high protein, low fat meals.
Bland foods, no tea, coffee, cola, chocolate, alcohol.
Teach pt to monitor for acute abd pain, jaundice, steatorrhea, clay-
colored stools, or dark urine which could indicate disease progression
to chronic pancreatitis.
