NUR 213
EXAM 3 3
STUDY GUIDE
Complex Health Concepts
Forsyth Technical Community College
This Document Description:
❖ This study guide for NUR 213 at Forsyth Technical
Community College focuses on Exam 3 content from the
Complex Health Concepts course.
❖ It includes essential topics.
❖ The material is clearly organized to help students understand complex
systems and prepare effectively for exam questions.
, NUR 213 – Unit 3 Study Guide
1. Exemplar: Acute and Chronic Renal Disease
Kidney function:
Excretion of wastes
Fluid and electrolyte balance
Regulation of acid-base balance
Hormone secretion
Acute kidney injury is most common in acute care settings, while chronic kidney disease is more
likely to be seen in community settings or as a coexisting condition. Both types of kidney
problems can require kidney replacement therapy (dialysis). When kidney function is
permanently or persistently impaired, as with end-stage kidney disease (ESKD), dialysis or
kidney transplant is a lifesaving approach for urinary elimination to maintain homeostasis, F&E
balance, and acid-base balance.
Gradual decline in kidney function is diagnosed as chronic kidney disease (CKD)
o Affects every body system
Sudden decline in kidney function is diagnosed as acute kidney injury (AKI)
o Affects many body systems
If AKI and CKD co-occur, the loss of kidney function and waste elimination is usually
more severe and accelerated
The problems that occur with kidney function loss are related to disturbances of F&E
balance, disturbances in acid-base balance, build-up of nitrogen-based wastes (urea), and
loss of kidney hormone function
Acute kidney injury: Rapid reduction in kidney function resulting is a failure to maintain waste
elimination, fluid and electrolyte balance, and acid-base balance. AKI can occur over a few hours
or days.
The more current definition of AKI is an increased in serum creatinine by 0.3 mg/dL o
more within 48 hours; or an increase in serum creatinine to 1.5 times or more than
baseline, which is known or presumed to have occurred in the previous 7 days; or a urine
volume of less than 0.5 mL/kg/hr for 6 hours
Although glomerular filtration (GFR) is accepted as the best overall indicator of kidney
function, it is not accurate during acute and critical illness
Duration of oliguria or anuria closely correlates with lack of recovery of kidney function;
the longer the duration of oliguria or anuria, the less likely it is that the patient will return
to full or baseline kidney function
Etiology: causes of AKI are reduced perfusion to the kidneys, damage to the kidney
tissue, and obstruction of urine flow.
o Any patient with a pre-existing reduced GFR or elevated albumin-creatinine ratio
is at increased risk for AKI during hospitalization.
o AKI is more likely to occur with advanced age or who have pre-existing
conditions such as HTN, DM, peripheral vascular disease, liver disease, or CKD.
o Sepsis, cardiac surgery, hypotension, shock, or prolonged mechanical ventilation
are also independent risk factors for the development of AKI
,o Classifications of AKI:
Pre-renal (perfusion reduction) failure: Traditionally, AKI caused by
reduced perfusion with a sustained MAP of less than 65 mmHg was
classified as pre-renal failure. It is the most common cause of AKI in acute
care. Common diseases or causes that contribute to decreased perfusion:
Blood or fluid loss (surgery, trauma, etc.), BP drugs resulting in
hypotension, heart attack or heart failure resulting in low EF and
low CO, infection, liver failure, use of ASA, ibuprofen, naproxen
or NSAIDs, anaphylaxis, severe burns, renal artery stenosis,
bleeding or clotting in the kidney blood vessels (coagulopathy),
atherosclerosis or cholesterol deposits that block blood flow in the
kidneys
Clinical manifestations:
o Hypovolemia
o Thirst
o Decreased urine output
o Dizziness
o Orthostatic Hypotension
o Elders with vague mental status changes
Intrinsic or Intra-renal failure (kidney damage): reflects injury to the
glomeruli, nephrons, or tubules. Common diseases or causes that
contribute to kidney damage:
Glomerulonephritis or inflammation of the glomeruli, bleeding in
the kidney, thrombi or emboli in the kidney blood vessels,
hemolytic uremic syndrome, systemic infection (sepsis), local
infection (pyelonephritis), lupus (causes glomerulonephritis),
certain drugs (chemo, antibiotics, contrast medium), multiple
myeloma, scleroderma, ingested toxins, vasculitis, ischemia in the
kidney (ex. hypoxemia from cardiac arrest)
Clinical Manifestations:
o Hematuria
o Edema
o Hypertension
o Acute tubular necrosis(ATN) suspected if presents after
period of hypotension secondary to cardiac arrest,
hemorrhage, sepsis, drug overdose, or surgery
Post-renal failure (urine flow obstruction): common diseases and
conditions that contribute to obstruction:
Bladder cancer, cervical cancer, colon cancer, prostate cancer,
enlarged prostate cancer, enlarged prostate, kidney stones, nerve
damage, blood clots in the urinary tract
Clinical manifestations:
o Prostatic obstruction and symptoms of urgency, frequency,
and hesitancy in older men.
, o Women with history of gynecologic surgery or
abdominopelvic malignancy.
o With renal calculi or papillary necrosis:
Flank pain
Hematuria
o With pre-renal or post-renal pathology, the kidney compensates by three
responses of constricting kidney blood vessels, activating the renin-angiotensin-
aldosterone pathway, and releasing antidiuretic hormone (ADH) – this will
increase blood volume and improve kidney perfusion. However, these same
responses reduce urine elimination, resulting in oliguria (urine output <400
mL/day) and azotemia (retention and buildup of nitrogenous wastes in the blood).
Toxins can also cause blood vessel constriction in the kidney, leading to reduced
kidney blood flow, oliguria, and azotemia.
o Activated immunity and damage from kidney toxins (nephrotoxins) cause
intracellular changes of the tubular system in kidney tissue. Inflammatory proteins
and immune mediated complexes can damage cells and tissues in the kidney. With
extensive damage, tubular cells slough, and nephrons lose the ability to repair
themselves.
The presence of tubular debris and sediment in urine from kidney tissue
damage (intrarenal failure or acute tubular necrosis) is related to systemic
ischemia, reduced kidney perfusion, or nephrotoxic exposure
o Even with severe AKI, some adults will return to baseline kidney function during
recovery from illness
o Timely interventions to remove the cause of AKI may prevent progression to
ESKD and the need for lifelong renal replacement therapy or a renal transplant
Health Promotion and Maintenance:
o Remember that dehydration (severe blood volume depletion) reduces perfusion
and can lead to AKI in adults who have no known kidney problems. Teach healthy
adults to drink 2-3L of water daily
o Nurses should closely monitor lab values, perform thorough assessments, evaluate
patients I&O, and check body weight to identify changes in fluid balance. Note
characteristics of urine (sediment, hematuria, foul odor, or other worrisome
changes).
Immediately report urine output <0.5 mL/kg/hr that persists for more than
2 hours to the provider
Waiting for 6 hours of oliguria to meet AI criteria may allow progression
of kidney damage – act early!
o In the acute care setting, preventing volume depletion and providing intervention
when volume depletion occurs are nursing priorities. S&S of volume depletion:
Low urine output, decreased systolic BP, decreased pulse, orthostatic
hypotension, thirst, rising blood osmolarity
o Significant increase in creatinine, especially when the increase occurs over hours
or a few days, is a concern and must be reported urgently to the provider
o Other important labs to monitor:
BUN, serum potassium, sodium, osmolarity, urine specific gravity,
albumin-creatinine ratio, electrolytes.
EXAM 3 3
STUDY GUIDE
Complex Health Concepts
Forsyth Technical Community College
This Document Description:
❖ This study guide for NUR 213 at Forsyth Technical
Community College focuses on Exam 3 content from the
Complex Health Concepts course.
❖ It includes essential topics.
❖ The material is clearly organized to help students understand complex
systems and prepare effectively for exam questions.
, NUR 213 – Unit 3 Study Guide
1. Exemplar: Acute and Chronic Renal Disease
Kidney function:
Excretion of wastes
Fluid and electrolyte balance
Regulation of acid-base balance
Hormone secretion
Acute kidney injury is most common in acute care settings, while chronic kidney disease is more
likely to be seen in community settings or as a coexisting condition. Both types of kidney
problems can require kidney replacement therapy (dialysis). When kidney function is
permanently or persistently impaired, as with end-stage kidney disease (ESKD), dialysis or
kidney transplant is a lifesaving approach for urinary elimination to maintain homeostasis, F&E
balance, and acid-base balance.
Gradual decline in kidney function is diagnosed as chronic kidney disease (CKD)
o Affects every body system
Sudden decline in kidney function is diagnosed as acute kidney injury (AKI)
o Affects many body systems
If AKI and CKD co-occur, the loss of kidney function and waste elimination is usually
more severe and accelerated
The problems that occur with kidney function loss are related to disturbances of F&E
balance, disturbances in acid-base balance, build-up of nitrogen-based wastes (urea), and
loss of kidney hormone function
Acute kidney injury: Rapid reduction in kidney function resulting is a failure to maintain waste
elimination, fluid and electrolyte balance, and acid-base balance. AKI can occur over a few hours
or days.
The more current definition of AKI is an increased in serum creatinine by 0.3 mg/dL o
more within 48 hours; or an increase in serum creatinine to 1.5 times or more than
baseline, which is known or presumed to have occurred in the previous 7 days; or a urine
volume of less than 0.5 mL/kg/hr for 6 hours
Although glomerular filtration (GFR) is accepted as the best overall indicator of kidney
function, it is not accurate during acute and critical illness
Duration of oliguria or anuria closely correlates with lack of recovery of kidney function;
the longer the duration of oliguria or anuria, the less likely it is that the patient will return
to full or baseline kidney function
Etiology: causes of AKI are reduced perfusion to the kidneys, damage to the kidney
tissue, and obstruction of urine flow.
o Any patient with a pre-existing reduced GFR or elevated albumin-creatinine ratio
is at increased risk for AKI during hospitalization.
o AKI is more likely to occur with advanced age or who have pre-existing
conditions such as HTN, DM, peripheral vascular disease, liver disease, or CKD.
o Sepsis, cardiac surgery, hypotension, shock, or prolonged mechanical ventilation
are also independent risk factors for the development of AKI
,o Classifications of AKI:
Pre-renal (perfusion reduction) failure: Traditionally, AKI caused by
reduced perfusion with a sustained MAP of less than 65 mmHg was
classified as pre-renal failure. It is the most common cause of AKI in acute
care. Common diseases or causes that contribute to decreased perfusion:
Blood or fluid loss (surgery, trauma, etc.), BP drugs resulting in
hypotension, heart attack or heart failure resulting in low EF and
low CO, infection, liver failure, use of ASA, ibuprofen, naproxen
or NSAIDs, anaphylaxis, severe burns, renal artery stenosis,
bleeding or clotting in the kidney blood vessels (coagulopathy),
atherosclerosis or cholesterol deposits that block blood flow in the
kidneys
Clinical manifestations:
o Hypovolemia
o Thirst
o Decreased urine output
o Dizziness
o Orthostatic Hypotension
o Elders with vague mental status changes
Intrinsic or Intra-renal failure (kidney damage): reflects injury to the
glomeruli, nephrons, or tubules. Common diseases or causes that
contribute to kidney damage:
Glomerulonephritis or inflammation of the glomeruli, bleeding in
the kidney, thrombi or emboli in the kidney blood vessels,
hemolytic uremic syndrome, systemic infection (sepsis), local
infection (pyelonephritis), lupus (causes glomerulonephritis),
certain drugs (chemo, antibiotics, contrast medium), multiple
myeloma, scleroderma, ingested toxins, vasculitis, ischemia in the
kidney (ex. hypoxemia from cardiac arrest)
Clinical Manifestations:
o Hematuria
o Edema
o Hypertension
o Acute tubular necrosis(ATN) suspected if presents after
period of hypotension secondary to cardiac arrest,
hemorrhage, sepsis, drug overdose, or surgery
Post-renal failure (urine flow obstruction): common diseases and
conditions that contribute to obstruction:
Bladder cancer, cervical cancer, colon cancer, prostate cancer,
enlarged prostate cancer, enlarged prostate, kidney stones, nerve
damage, blood clots in the urinary tract
Clinical manifestations:
o Prostatic obstruction and symptoms of urgency, frequency,
and hesitancy in older men.
, o Women with history of gynecologic surgery or
abdominopelvic malignancy.
o With renal calculi or papillary necrosis:
Flank pain
Hematuria
o With pre-renal or post-renal pathology, the kidney compensates by three
responses of constricting kidney blood vessels, activating the renin-angiotensin-
aldosterone pathway, and releasing antidiuretic hormone (ADH) – this will
increase blood volume and improve kidney perfusion. However, these same
responses reduce urine elimination, resulting in oliguria (urine output <400
mL/day) and azotemia (retention and buildup of nitrogenous wastes in the blood).
Toxins can also cause blood vessel constriction in the kidney, leading to reduced
kidney blood flow, oliguria, and azotemia.
o Activated immunity and damage from kidney toxins (nephrotoxins) cause
intracellular changes of the tubular system in kidney tissue. Inflammatory proteins
and immune mediated complexes can damage cells and tissues in the kidney. With
extensive damage, tubular cells slough, and nephrons lose the ability to repair
themselves.
The presence of tubular debris and sediment in urine from kidney tissue
damage (intrarenal failure or acute tubular necrosis) is related to systemic
ischemia, reduced kidney perfusion, or nephrotoxic exposure
o Even with severe AKI, some adults will return to baseline kidney function during
recovery from illness
o Timely interventions to remove the cause of AKI may prevent progression to
ESKD and the need for lifelong renal replacement therapy or a renal transplant
Health Promotion and Maintenance:
o Remember that dehydration (severe blood volume depletion) reduces perfusion
and can lead to AKI in adults who have no known kidney problems. Teach healthy
adults to drink 2-3L of water daily
o Nurses should closely monitor lab values, perform thorough assessments, evaluate
patients I&O, and check body weight to identify changes in fluid balance. Note
characteristics of urine (sediment, hematuria, foul odor, or other worrisome
changes).
Immediately report urine output <0.5 mL/kg/hr that persists for more than
2 hours to the provider
Waiting for 6 hours of oliguria to meet AI criteria may allow progression
of kidney damage – act early!
o In the acute care setting, preventing volume depletion and providing intervention
when volume depletion occurs are nursing priorities. S&S of volume depletion:
Low urine output, decreased systolic BP, decreased pulse, orthostatic
hypotension, thirst, rising blood osmolarity
o Significant increase in creatinine, especially when the increase occurs over hours
or a few days, is a concern and must be reported urgently to the provider
o Other important labs to monitor:
BUN, serum potassium, sodium, osmolarity, urine specific gravity,
albumin-creatinine ratio, electrolytes.
