EXAM #1: CONTENT REVIEW
Unit 1: Care of Patients with Complex Renal & Gastrointestinal Problems
Renal A & P
What do the kidneys do?
o Kidneys receive 20-25% of cardiac output under resting conditions – more than 1L blood/min
o Kidneys are controller of fluid & electrolyte homeostasis in the body
o Kidneys secrete erythropoietin that inc. RBC synthesis in bone marrow
o Kidneys convert Vitamin D into its active form
o Loop of Henle concentrates urine and allows water reabsorption into bloodstream
Question: The nurse is explaining to a group of nursing students that when there is a decrease in the secretion
of renin, and aldosterone it can cause
(Select all that apply.)
A. an excretion of sodium.
B. dilution of urine.
C. increased intestinal absorption of calcium.
D. increased bone density.
E. a decreased thirst.
Physical Examination
Skin color (ashen, yellow); crystals on skin (uremic frost)
Tissue turgor: to detect dehydration or edema
Periorbital edema: suggests fluid retention. Inspect the mouth for moisture and odor
Observe respiratory rate, pattern, and effort
Auscultate the lungs for crackles or rhonchi
Inspect the abdomen for scars and contours, and palpate for tenderness and bladder distention
Edema
Inspect the genitalia
Nephrotic Syndrome
Patho:
o A condition of increased glomerular permeability that allows large molecules to pass through the
membrane into the urine and then be excreted.
o This process causes severe proteinuria, high serum lipid levels, fats in the urine, edema and
hypertension.
o Identified by kidney biopsy
, Risk Factors: allergic reactions, reactions to medications, renal vein disease, sickle cell disease, HF
Clinical Manifestations
o Massive proteinuria (Increased protein) >3.5g/day in a 24-hour urine sample
o Hypoalbuminemia (Decreased albumin (serum)) <3g/dL
o Hypertension
o Edema (esp. facial and periorbital)
o Hyperlipidemia (due to low albumin)
o Fat bodies in urine
o Delayed clotting or increased bleeding with higher-than-normal values of serum activated partial
thromboplastin time (aPTT), coagulation or internation normalized ration for prothrombin (INR,
PT)
o Reduced kidney function with elevated BUN and serum creatinine and decreased GFR
Nursing Interventions: management varies, depending on which process is causing the disorder!
o Maintain fluid (NS) & electrolyte balance
o Monitor labs daily
o Monitor and record I&O daily
o Assess daily weight
o Restrict sodium & potassium intake (diet changes)
o Monitor skin due to edema
o Protein intake restriction with decreased GFR; normal GFR dietary intake of protein is needed!
o Medications:
Administer steroids if needed for inflammation
ACE inhibitors: Can decrease protein loss in the urine
Cholesterol-lowering drugs can improve blood lipid levels
NOTE! NS may progress to end stage kidney disease (ESKD) but can be prevented with
treatment!!
Kidney Injury
Acute (AKI) vs Chronic (CRF)
o Acute develops in a few hours to days with abrupt disruption in kidney function
o Chronic is progressive deterioration over years with slow loss of kidney function
o AKI affects MANY body systems. Chronic kidney disease affects EVRY body system.
AKI
What is it?
o Rapid reduction in kidney function resulting in a failure to maintain fluid & electrolyte
balance, and acid-base balance.
o Develops abruptly within hours to days
o If AKI occurs in patients with decreased kidney function already ESKD
o Increase in serum creatinine by 0.3mg/dL or more within 48 hours; OR increase in serum
creatinine to 1.5 times or more from baseline
Occurred in previous 7 days; or a urine volume less than 0.5 mL/kg/hr for 6 hours
o GFR is not accurate acute or critical illness although best overall indicator of kidney function!
o HYPOPERFUSION (reduction in blood flow)
Kidney compensates by constricting blood vessels and by activating renin-angiotension-
aldosterone which RELEASES ADH
ADH- increase blood volume increasing perfusion BUT will decrease UOP causing:
OLIGURIA = <400ml/24hour period
o Less than 0.5mL/kg/hr for 2 or more hours
o Min. UOP Q24 hours=720mL or 30mL/hr
, Symptoms of reduced blood volume MAP <65, tachycardia, thread peripheral pulses,
decreasing cognition
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
S/S: same as fluid overload Hypertension, dec. O2, high HR
AKI Causes
o Reduced perfusion to the kidneys, damage to kidney tissue and obstruction of urine outflow
o Pre-renal: decreased perfusion to glomeruli
Reduced perfusion with a sustained mean arterial pressure (MAP) of less than 65mm Hg
Conditions that contribute: Blood or fluid loss, BP drugs, heart attack/HF, infection, liver
failure, use of aspirin/ibuprofen/NSAIDS, dehydration, burns, atherosclerosis
o Intra-renal: nephrotoxic agents, kidney infections, occlusion of intrarenal arteries, hypertension,
diabetes mellitus, or direct trauma to the kidney
Reflects injury to the glomeruli, nephrons or tubules
Conditions that contribute: glomerulonephritis, bleeding in the kidney, sepsis, lupus,
TTP, drugs, multiple myeloma, scleroderma, vasculitis
o Post-renal: caused by backward pressure on the kidney from an obstruction somewhere lower in
the urinary system (Effects normal urine flow)
Conditions that contribute: Kidney stones, cancers (bladder, cervical, colon, prostate),
enlarged prostate, nerve damage, blood clots in the urinary tract
Table 68-4 Conditions Contribute to AKI
Prerenal (Perfusion Reduction)
o Blood or fluid loss (surgery, trauma, sepsis, shock, hypovolemic shock)
o BP drugs resulting in hypotension
o MI or heart failure
o Infection
o Liver failure
o Use of aspirin, ibuprofen, Naproxen, NSAIDS
o Severe allergic reaction
o Severe burns
o Severe dehydration
o Renal artery stenosis
o Bleeding or clotting in kidney blood vessels
o Atherosclerosis or cholesterol deposits that block blood flow
Intrarenal (Kidney Damage)
o Glomerulonephritis or inflammation
o Bleeding in kidney
o Thrombi or emboli
o Hemolytic uremic syndrome (premature destruction of RBC’s)
, o Sepsis & local infection
o Lupus
o Chemo agents, abx, iodinated or hyperosmolar contrast, zoledronic acid
o Multiple myeloma
o Scleroderma
o Thrombotic thrombocytopenic purpura
o Ingested toxins (etoh, heavy metals, cocaine)
o Vasculitis
o Ischemia in kidney tissue
Postrenal (Urine Flow Obstruction)
o Bladder, cervical, colon, prostate cancer
o Enlarged prostate
o Kidney stones
o Nerve damage involving nerves that control bladder
o Blood clots in urinary tract
Phases of AKI
o Onset stage: from time of initial event to renal manifestations, symptoms can occur immediately
up to a week after event
increased BUN & serum creatinine with normal to decreased urine output.
o Oliguric stage: can last 1 to 8 weeks (the longer this phase last the worse the prognosis.
urine output decreases to 400 mls or less per day
o Diuretic stage: gradual or abrupt return of glomerular filtration.
Urine output may be 1-2L per day. Serum BUN & creatinine levels decrease.
Need a place of care that focuses on fluid and electrolyte REPLACEMENT and
monitoring.
Onset of polyuria can signal the start of recovery from AKI.
o Recovery stage: as renal tissue recovers, serum electrolytes, BUN & creatinine return to normal.
Can last 3-12 months
Nursing Care of Patients with AKI
o Avoid hypotension and maintain normal fluid balance to prevent and manage AKI
o Thorough assessment and close monitoring of laboratory values is essential for signs of
impending kidney dysfunction. (Na, K, USG, albumin creatine ratio, osmolarity, BUN and
electrolytes)
Evaluate fluid status
Accurately measure I&O
Measure body weight
Note characteristics of urine (report of new sediment, hematuria (smoky or red color)),
foul odor
Report urine output < 0.5 mL/kg/hr for more than 2 hours ACT EARLY!
Monitor kidney lab values
Increase in creatinine, esp. over hours or a few days (report to PCP)
BUN
Potassium, sodium, urine specific gravity, albumin-creatinine ratio and
electrolytes
Reduced GFR makes pt more vulnerable for AKI
Keep MAP at 80 mm/hg
NO nephrotic agents
Check kidney function before contrast dye
Unit 1: Care of Patients with Complex Renal & Gastrointestinal Problems
Renal A & P
What do the kidneys do?
o Kidneys receive 20-25% of cardiac output under resting conditions – more than 1L blood/min
o Kidneys are controller of fluid & electrolyte homeostasis in the body
o Kidneys secrete erythropoietin that inc. RBC synthesis in bone marrow
o Kidneys convert Vitamin D into its active form
o Loop of Henle concentrates urine and allows water reabsorption into bloodstream
Question: The nurse is explaining to a group of nursing students that when there is a decrease in the secretion
of renin, and aldosterone it can cause
(Select all that apply.)
A. an excretion of sodium.
B. dilution of urine.
C. increased intestinal absorption of calcium.
D. increased bone density.
E. a decreased thirst.
Physical Examination
Skin color (ashen, yellow); crystals on skin (uremic frost)
Tissue turgor: to detect dehydration or edema
Periorbital edema: suggests fluid retention. Inspect the mouth for moisture and odor
Observe respiratory rate, pattern, and effort
Auscultate the lungs for crackles or rhonchi
Inspect the abdomen for scars and contours, and palpate for tenderness and bladder distention
Edema
Inspect the genitalia
Nephrotic Syndrome
Patho:
o A condition of increased glomerular permeability that allows large molecules to pass through the
membrane into the urine and then be excreted.
o This process causes severe proteinuria, high serum lipid levels, fats in the urine, edema and
hypertension.
o Identified by kidney biopsy
, Risk Factors: allergic reactions, reactions to medications, renal vein disease, sickle cell disease, HF
Clinical Manifestations
o Massive proteinuria (Increased protein) >3.5g/day in a 24-hour urine sample
o Hypoalbuminemia (Decreased albumin (serum)) <3g/dL
o Hypertension
o Edema (esp. facial and periorbital)
o Hyperlipidemia (due to low albumin)
o Fat bodies in urine
o Delayed clotting or increased bleeding with higher-than-normal values of serum activated partial
thromboplastin time (aPTT), coagulation or internation normalized ration for prothrombin (INR,
PT)
o Reduced kidney function with elevated BUN and serum creatinine and decreased GFR
Nursing Interventions: management varies, depending on which process is causing the disorder!
o Maintain fluid (NS) & electrolyte balance
o Monitor labs daily
o Monitor and record I&O daily
o Assess daily weight
o Restrict sodium & potassium intake (diet changes)
o Monitor skin due to edema
o Protein intake restriction with decreased GFR; normal GFR dietary intake of protein is needed!
o Medications:
Administer steroids if needed for inflammation
ACE inhibitors: Can decrease protein loss in the urine
Cholesterol-lowering drugs can improve blood lipid levels
NOTE! NS may progress to end stage kidney disease (ESKD) but can be prevented with
treatment!!
Kidney Injury
Acute (AKI) vs Chronic (CRF)
o Acute develops in a few hours to days with abrupt disruption in kidney function
o Chronic is progressive deterioration over years with slow loss of kidney function
o AKI affects MANY body systems. Chronic kidney disease affects EVRY body system.
AKI
What is it?
o Rapid reduction in kidney function resulting in a failure to maintain fluid & electrolyte
balance, and acid-base balance.
o Develops abruptly within hours to days
o If AKI occurs in patients with decreased kidney function already ESKD
o Increase in serum creatinine by 0.3mg/dL or more within 48 hours; OR increase in serum
creatinine to 1.5 times or more from baseline
Occurred in previous 7 days; or a urine volume less than 0.5 mL/kg/hr for 6 hours
o GFR is not accurate acute or critical illness although best overall indicator of kidney function!
o HYPOPERFUSION (reduction in blood flow)
Kidney compensates by constricting blood vessels and by activating renin-angiotension-
aldosterone which RELEASES ADH
ADH- increase blood volume increasing perfusion BUT will decrease UOP causing:
OLIGURIA = <400ml/24hour period
o Less than 0.5mL/kg/hr for 2 or more hours
o Min. UOP Q24 hours=720mL or 30mL/hr
, Symptoms of reduced blood volume MAP <65, tachycardia, thread peripheral pulses,
decreasing cognition
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
S/S: same as fluid overload Hypertension, dec. O2, high HR
AKI Causes
o Reduced perfusion to the kidneys, damage to kidney tissue and obstruction of urine outflow
o Pre-renal: decreased perfusion to glomeruli
Reduced perfusion with a sustained mean arterial pressure (MAP) of less than 65mm Hg
Conditions that contribute: Blood or fluid loss, BP drugs, heart attack/HF, infection, liver
failure, use of aspirin/ibuprofen/NSAIDS, dehydration, burns, atherosclerosis
o Intra-renal: nephrotoxic agents, kidney infections, occlusion of intrarenal arteries, hypertension,
diabetes mellitus, or direct trauma to the kidney
Reflects injury to the glomeruli, nephrons or tubules
Conditions that contribute: glomerulonephritis, bleeding in the kidney, sepsis, lupus,
TTP, drugs, multiple myeloma, scleroderma, vasculitis
o Post-renal: caused by backward pressure on the kidney from an obstruction somewhere lower in
the urinary system (Effects normal urine flow)
Conditions that contribute: Kidney stones, cancers (bladder, cervical, colon, prostate),
enlarged prostate, nerve damage, blood clots in the urinary tract
Table 68-4 Conditions Contribute to AKI
Prerenal (Perfusion Reduction)
o Blood or fluid loss (surgery, trauma, sepsis, shock, hypovolemic shock)
o BP drugs resulting in hypotension
o MI or heart failure
o Infection
o Liver failure
o Use of aspirin, ibuprofen, Naproxen, NSAIDS
o Severe allergic reaction
o Severe burns
o Severe dehydration
o Renal artery stenosis
o Bleeding or clotting in kidney blood vessels
o Atherosclerosis or cholesterol deposits that block blood flow
Intrarenal (Kidney Damage)
o Glomerulonephritis or inflammation
o Bleeding in kidney
o Thrombi or emboli
o Hemolytic uremic syndrome (premature destruction of RBC’s)
, o Sepsis & local infection
o Lupus
o Chemo agents, abx, iodinated or hyperosmolar contrast, zoledronic acid
o Multiple myeloma
o Scleroderma
o Thrombotic thrombocytopenic purpura
o Ingested toxins (etoh, heavy metals, cocaine)
o Vasculitis
o Ischemia in kidney tissue
Postrenal (Urine Flow Obstruction)
o Bladder, cervical, colon, prostate cancer
o Enlarged prostate
o Kidney stones
o Nerve damage involving nerves that control bladder
o Blood clots in urinary tract
Phases of AKI
o Onset stage: from time of initial event to renal manifestations, symptoms can occur immediately
up to a week after event
increased BUN & serum creatinine with normal to decreased urine output.
o Oliguric stage: can last 1 to 8 weeks (the longer this phase last the worse the prognosis.
urine output decreases to 400 mls or less per day
o Diuretic stage: gradual or abrupt return of glomerular filtration.
Urine output may be 1-2L per day. Serum BUN & creatinine levels decrease.
Need a place of care that focuses on fluid and electrolyte REPLACEMENT and
monitoring.
Onset of polyuria can signal the start of recovery from AKI.
o Recovery stage: as renal tissue recovers, serum electrolytes, BUN & creatinine return to normal.
Can last 3-12 months
Nursing Care of Patients with AKI
o Avoid hypotension and maintain normal fluid balance to prevent and manage AKI
o Thorough assessment and close monitoring of laboratory values is essential for signs of
impending kidney dysfunction. (Na, K, USG, albumin creatine ratio, osmolarity, BUN and
electrolytes)
Evaluate fluid status
Accurately measure I&O
Measure body weight
Note characteristics of urine (report of new sediment, hematuria (smoky or red color)),
foul odor
Report urine output < 0.5 mL/kg/hr for more than 2 hours ACT EARLY!
Monitor kidney lab values
Increase in creatinine, esp. over hours or a few days (report to PCP)
BUN
Potassium, sodium, urine specific gravity, albumin-creatinine ratio and
electrolytes
Reduced GFR makes pt more vulnerable for AKI
Keep MAP at 80 mm/hg
NO nephrotic agents
Check kidney function before contrast dye
