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Renal failure part 1

Renal failure part 1
42問 • 1年前
  • ユーザ名非公開
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    問題一覧

  • 1

    Progression of Renal (kidney) failure:

    Evert organ system affected with renal function loss, Acute kidney injury (AKI) most common in acute care, Chronic kidney disease (CKD) most common in community, Both types can lead to dialysis, Graudal decline=CKD, Suddne decline=AKI, Can occur simultaneously; Acute on chronic kidney disease

  • 2

    Pathophysiology of acute kidney injury (AKI):

    Rapid, sudden decline in kidney function affecting: -Elimination of metabolic wastes -Fluid & electrolyte balance -Acid-base balance, Occurs over hours to days, Often reversible, Sometimes AKI needs dialysis emergently

  • 3

    AKI Normal Renal Function Values

    BUN, Creatinine, BUN/Creatinine ratio

  • 4

    Normal BUN?

    10-20 mg/dL

  • 5

    Normal Serum creatinine m&f and fact?

    Males: 0.6-1.2 mg/dL, Females: 0.5 - 1.1 mg/dL, If someone’s serum Cr doubles in value (regardless of it being in range or not) this means there has been a 50% reduction in glomular filtration

  • 6

    What is normal BUN/ Cr ratio?

    6-25

  • 7

    What does ^BUN but normal Cr mean?

    Dehydration (give fluids)

  • 8

    Definition o AKI

    Increase in serum Cr by 0.3 mg/dL or more within 48 hours or, Increase in serum Cr to 1.5 or more from baseline (over 7 days), Urine volume < 0.5 mL/kg/he for 6 hours

  • 9

    Etiology and risk factors for AKI:

    Hypotension-even short episodes= kidney dmg., Shock- hypotension, Cardiac surgery, Sepsis- massive vasodilation, PRolongs mechinacl ventilation- stress on lungs, DM, HTN, CKD, Liver disease, Elderly

  • 10

    Etiology types of AKI:

    Prerenal, Intrinsic, Postrenal

  • 11

    Etiology and causes/examples of Prerenal AKI:

    Source outside the kidney, leading TO the kidney, Impaired renal perfusion, Cardiac failure, Sepsis, Blood loss, Dehydration, Vascular occlusion

  • 12

    Etiology and causes of Intrinsic or intrarenal AKI:

    Occurse inside kidney, Renal cortex/medulla, Glomerulonephritis Small vessel vasculitis Acute tubular necrosis:, :Toxins, :Drugs, :Prolonged hypotension, Intertsitial nephritis -, -Drugs, -Toxins, -Inflammatory disease, -Infection

  • 13

    Etiology and causes/examples of postrenal outflow obstruction:

    Unrine outflow obstruction, Urinary calculi, Retroperitoneal fibrosis, Benigin prostatic enlargement (BPH), Prostates cancer, Cervical cancer, Urethreal stricture/valves, Meatal stenosis/phimosis

  • 14

    Prerenal AKI

    Decreases renal perfusion, Causes anything that reduces blood flow into the kidneys:, :Hypovolemia: hemorrhage, burns, GI losses, :Hypotension from ↓ cardiac output: massive PE, MI, :Hypotension from vasodilation: septic shock, anaphylaxis, anesthesia administration, hepatorenal syndrome, :Renal vasoconstriction: NSAIDS

  • 15

    Here is a picture of pathophys Prerenal AKI!

    Ok great thinks. Still gonna be asystole after this 😭

  • 16

    Intrarenal AKI:

    Damage occurs inside kidney tissues • Acute tubular necrosis (damage to kidney tubules), Most common causes:, Blood clots in renal vessels, Pyelonephrtitis, Lupus (immune reaction causing glomerulonephritis, Contrast media, Nephrotoxic medications: many abx, NSAIDS, chemotherapy, Tumors

  • 17

    Here is a picture of Acute Tubular Necorisis

    Tubular epithelial cells have a high metabolic rate, Most vulnerable to ischemic injury

  • 18

    Postrenal AKI:

    Urine outflow obstruction :Causes, :Tumors, :Kidney stones, :Strictures, BPH, Urethral obstructions

  • 19

    AKI is a syndrome!! Kinda cascading!

    Ok awesomeee thanks

  • 20

    AKI incidence/Prevalence:

    In-hospital complication associated with shock, surgery, & heart conditions, 20% of hospitalized patients experience AKI, 60% of ICU patients, Higher risk: Eldrly, CKD patients, diabetics, 95% of nephrology consults are for AKI

  • 21

    Preventing AKI: **Nursing safety priority** Know the signs:

    Low urine output, Decreased systolic BP, decreased pulse pressure, orthostatic hypotension, Thirst (later sign), Rising blood osmolarity (more particles less fluid)

  • 22

    Preventing AKI: **Nursing safety priority** Interventions act early!!

    Oral fluids (if not restricted), IV fluids, Monitor lab values, I&O measurement, Daily weights, Report oliguria promptly

  • 23

    Gerontological Consideration:

    50% of hospitalized AKI patients are >60 years of age, Why?, :Dehydration decrease thirst recognition decreased mobility/access to fluids confusion, Polypharmacy, Complications of surgery

  • 24

    AKI clinical course (keep in mind don’t always have all stages)

    Onset initial phase, Oliguric phase, Diuretic phase, Recovery phase

  • 25

    AKI Onset initial phase:

    Time between the kidney injury and reduction in kidney function, Lasts hours to days, Nursing goal:minimize subsequent injury, Recoginze: -hypotension -nephrotoxic meds, Treatment: Fluid bolus, diuretics (only recommended for volume overload) med changes (BP meds may be stoppped for now too prevent hypotension)

  • 26

    AKI Oliguric phase:

    Urine output <400 ml/24hrs, Usually begins 1-7 days after injury, Typically lasts 10-14 days (can last months), Longer durations in this phase have poor outcomes

  • 27

    AKI Oliguric phase Clinical manifestations:

    ^BUN, ^Cr, ⬇️GFR, Fluid overload, Weight gain, Low urine output, HTN, Kyperkalemia, Hyponatremia, Metabolic Acidosis

  • 28

    AKI Oliguric phase interventions and management: Manage HTN

    ACE-i, ARB, Fluid restriction

  • 29

    AKI Oliguric phase interventions and management: Correct electrolyte imbalance:

    Hyponatremia: Fluid restriction, Hyperkalemia(HK): Kayexalate, HK: Lokelma, HK: Insulin & d50 protocol

  • 30

    AKI Oliguric phase interventions and management: Fluid overload:

    Fluid restriction -Yesterdays output +500ml (need to know), Diuretics (^renal blood flow and &diurese fluid/ electrolytes

  • 31

    AKI diuretic phase:

    Urine production increases, Nephrons have regained the ability to excrete urea, Result is osmotic diuresis, 1-3L per day but can be >5L, BUN, serum Cr, acid base, & electrolytes will improve

  • 32

    AKI diuretic phase Clinical manifestations & treatments:

    Hypotension, Hyponatremia, Hypokalemia, Weight loss, Neuro symptoms, Hypovolemia, TX: manage hypotension, TX: replace fluids/electrolytes

  • 33

    AKI Recover phase:

    Kidnes regain ability to maintain metabolic waste, BUN and serum Cr return to baseline, Takes several week, may continue for up to a year, Kidneys may never fully recover: may have mild, chronic elevations in BUN and Cr, Some patients will progress to CKD and need lifelong management

  • 34

    AKI Assessment History determine etiology of the AKI ASK:

    Risk factors (family hx, urinary symptoms, patterns)?, Urinary changes/issues?, Surgery/trauma, transfusions, allergic reactions?, Recent contrast media?

  • 35

    AKI Assessment History determine etiology of the AKI Any history of:

    Past urinary obstructions, CKD, DM,, Long-term HTN, PVD, HIV, Liver disease etc, Immune mediated AKI (acute glomerulonephritis) requires assessment for recen illness (flu, colds, gastroenteritis)

  • 36

    AKI Assessment History determine etiology of the AKI Perform a medication review:

    Abx, NSAIDS etc., Any condition that causes hypoperfusion/volume depletion

  • 37

    AKI clinical manifestations: Physical:

    Assess catheter (if present) & output q1hr after surgery, Monitor for oliguria, Daily weight (same time, same clothes, same scale), Azotemia, Fluid overload: crackles, confusion, S3, edema, ^RR, dyspnea hypoxia, Monitor VS to catch hypoperfusion and hypoxemia early:, :MAP<65 mm Hg, :Tachycardia, :Thready pulses, :Decreased cognition, : Spo2<88%

  • 38

    AKI Diagnositics:

    Blood tests: ↑BUN, ↑Cr, ↑K+, ↑Phosphorus, ↓Calcium, Imaging: US, CT (without contrast), MRI, KUB, Nuclear Med MAG3 study, Renal scan, cystoscopy or retrograde pyelogram, Other diagnostics: Kidney biopsy Manage hypo & hypertension post- procedure (BLEEDING!)

  • 39

    AKI collaborative management Drug therapy:

    If hypovolemia or hypotension, then volume repletion -Fluid chalange (bolus): 500-1000 ml NS over 1 hour, Drug dosage adjustments may be required, May need to discontinue nephrotoxic medications, ACE-I and ARBS can contribute to AKI (can be renoprotective over time)

  • 40

    AKI collaborative management Nutrition therapy:

    Register dietician, PRotien may be restricted even with non- dialysis pts (try not restric protien if we don’t have to but is hard for kidneys to filter), Protien, sodium, potassium restrictions with dialysis, Fluid restriction for dialysis: urine volume +500 ml, Monitor caloric intake, Oral supplements, enteral nutrition, TPN, etc.

  • 41

    AKI collaborative management renal replacement therapies and indications:

    Hemodialysis, CRRT (continuous renal replacement therapy), Peritoneal dialysis, Symptomatic uremia: pericarditis, neuropathy, decreased cognition, Severe metabolic acidosis: pH<7.1, Rapidly rising serum potassium >6.5 med/L, Fluid overload reduction tissue perfusion

  • 42

    A 64-year-old patient was admitted 2 days ago with hypovolemic shock secondary to traumatic injuries. Which lab value is MOST IMPORTANT to immediately report to the physician/provider?

    Serum potassium 6.8 mEq/L

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    問題一覧

  • 1

    Progression of Renal (kidney) failure:

    Evert organ system affected with renal function loss, Acute kidney injury (AKI) most common in acute care, Chronic kidney disease (CKD) most common in community, Both types can lead to dialysis, Graudal decline=CKD, Suddne decline=AKI, Can occur simultaneously; Acute on chronic kidney disease

  • 2

    Pathophysiology of acute kidney injury (AKI):

    Rapid, sudden decline in kidney function affecting: -Elimination of metabolic wastes -Fluid & electrolyte balance -Acid-base balance, Occurs over hours to days, Often reversible, Sometimes AKI needs dialysis emergently

  • 3

    AKI Normal Renal Function Values

    BUN, Creatinine, BUN/Creatinine ratio

  • 4

    Normal BUN?

    10-20 mg/dL

  • 5

    Normal Serum creatinine m&f and fact?

    Males: 0.6-1.2 mg/dL, Females: 0.5 - 1.1 mg/dL, If someone’s serum Cr doubles in value (regardless of it being in range or not) this means there has been a 50% reduction in glomular filtration

  • 6

    What is normal BUN/ Cr ratio?

    6-25

  • 7

    What does ^BUN but normal Cr mean?

    Dehydration (give fluids)

  • 8

    Definition o AKI

    Increase in serum Cr by 0.3 mg/dL or more within 48 hours or, Increase in serum Cr to 1.5 or more from baseline (over 7 days), Urine volume < 0.5 mL/kg/he for 6 hours

  • 9

    Etiology and risk factors for AKI:

    Hypotension-even short episodes= kidney dmg., Shock- hypotension, Cardiac surgery, Sepsis- massive vasodilation, PRolongs mechinacl ventilation- stress on lungs, DM, HTN, CKD, Liver disease, Elderly

  • 10

    Etiology types of AKI:

    Prerenal, Intrinsic, Postrenal

  • 11

    Etiology and causes/examples of Prerenal AKI:

    Source outside the kidney, leading TO the kidney, Impaired renal perfusion, Cardiac failure, Sepsis, Blood loss, Dehydration, Vascular occlusion

  • 12

    Etiology and causes of Intrinsic or intrarenal AKI:

    Occurse inside kidney, Renal cortex/medulla, Glomerulonephritis Small vessel vasculitis Acute tubular necrosis:, :Toxins, :Drugs, :Prolonged hypotension, Intertsitial nephritis -, -Drugs, -Toxins, -Inflammatory disease, -Infection

  • 13

    Etiology and causes/examples of postrenal outflow obstruction:

    Unrine outflow obstruction, Urinary calculi, Retroperitoneal fibrosis, Benigin prostatic enlargement (BPH), Prostates cancer, Cervical cancer, Urethreal stricture/valves, Meatal stenosis/phimosis

  • 14

    Prerenal AKI

    Decreases renal perfusion, Causes anything that reduces blood flow into the kidneys:, :Hypovolemia: hemorrhage, burns, GI losses, :Hypotension from ↓ cardiac output: massive PE, MI, :Hypotension from vasodilation: septic shock, anaphylaxis, anesthesia administration, hepatorenal syndrome, :Renal vasoconstriction: NSAIDS

  • 15

    Here is a picture of pathophys Prerenal AKI!

    Ok great thinks. Still gonna be asystole after this 😭

  • 16

    Intrarenal AKI:

    Damage occurs inside kidney tissues • Acute tubular necrosis (damage to kidney tubules), Most common causes:, Blood clots in renal vessels, Pyelonephrtitis, Lupus (immune reaction causing glomerulonephritis, Contrast media, Nephrotoxic medications: many abx, NSAIDS, chemotherapy, Tumors

  • 17

    Here is a picture of Acute Tubular Necorisis

    Tubular epithelial cells have a high metabolic rate, Most vulnerable to ischemic injury

  • 18

    Postrenal AKI:

    Urine outflow obstruction :Causes, :Tumors, :Kidney stones, :Strictures, BPH, Urethral obstructions

  • 19

    AKI is a syndrome!! Kinda cascading!

    Ok awesomeee thanks

  • 20

    AKI incidence/Prevalence:

    In-hospital complication associated with shock, surgery, & heart conditions, 20% of hospitalized patients experience AKI, 60% of ICU patients, Higher risk: Eldrly, CKD patients, diabetics, 95% of nephrology consults are for AKI

  • 21

    Preventing AKI: **Nursing safety priority** Know the signs:

    Low urine output, Decreased systolic BP, decreased pulse pressure, orthostatic hypotension, Thirst (later sign), Rising blood osmolarity (more particles less fluid)

  • 22

    Preventing AKI: **Nursing safety priority** Interventions act early!!

    Oral fluids (if not restricted), IV fluids, Monitor lab values, I&O measurement, Daily weights, Report oliguria promptly

  • 23

    Gerontological Consideration:

    50% of hospitalized AKI patients are >60 years of age, Why?, :Dehydration decrease thirst recognition decreased mobility/access to fluids confusion, Polypharmacy, Complications of surgery

  • 24

    AKI clinical course (keep in mind don’t always have all stages)

    Onset initial phase, Oliguric phase, Diuretic phase, Recovery phase

  • 25

    AKI Onset initial phase:

    Time between the kidney injury and reduction in kidney function, Lasts hours to days, Nursing goal:minimize subsequent injury, Recoginze: -hypotension -nephrotoxic meds, Treatment: Fluid bolus, diuretics (only recommended for volume overload) med changes (BP meds may be stoppped for now too prevent hypotension)

  • 26

    AKI Oliguric phase:

    Urine output <400 ml/24hrs, Usually begins 1-7 days after injury, Typically lasts 10-14 days (can last months), Longer durations in this phase have poor outcomes

  • 27

    AKI Oliguric phase Clinical manifestations:

    ^BUN, ^Cr, ⬇️GFR, Fluid overload, Weight gain, Low urine output, HTN, Kyperkalemia, Hyponatremia, Metabolic Acidosis

  • 28

    AKI Oliguric phase interventions and management: Manage HTN

    ACE-i, ARB, Fluid restriction

  • 29

    AKI Oliguric phase interventions and management: Correct electrolyte imbalance:

    Hyponatremia: Fluid restriction, Hyperkalemia(HK): Kayexalate, HK: Lokelma, HK: Insulin & d50 protocol

  • 30

    AKI Oliguric phase interventions and management: Fluid overload:

    Fluid restriction -Yesterdays output +500ml (need to know), Diuretics (^renal blood flow and &diurese fluid/ electrolytes

  • 31

    AKI diuretic phase:

    Urine production increases, Nephrons have regained the ability to excrete urea, Result is osmotic diuresis, 1-3L per day but can be >5L, BUN, serum Cr, acid base, & electrolytes will improve

  • 32

    AKI diuretic phase Clinical manifestations & treatments:

    Hypotension, Hyponatremia, Hypokalemia, Weight loss, Neuro symptoms, Hypovolemia, TX: manage hypotension, TX: replace fluids/electrolytes

  • 33

    AKI Recover phase:

    Kidnes regain ability to maintain metabolic waste, BUN and serum Cr return to baseline, Takes several week, may continue for up to a year, Kidneys may never fully recover: may have mild, chronic elevations in BUN and Cr, Some patients will progress to CKD and need lifelong management

  • 34

    AKI Assessment History determine etiology of the AKI ASK:

    Risk factors (family hx, urinary symptoms, patterns)?, Urinary changes/issues?, Surgery/trauma, transfusions, allergic reactions?, Recent contrast media?

  • 35

    AKI Assessment History determine etiology of the AKI Any history of:

    Past urinary obstructions, CKD, DM,, Long-term HTN, PVD, HIV, Liver disease etc, Immune mediated AKI (acute glomerulonephritis) requires assessment for recen illness (flu, colds, gastroenteritis)

  • 36

    AKI Assessment History determine etiology of the AKI Perform a medication review:

    Abx, NSAIDS etc., Any condition that causes hypoperfusion/volume depletion

  • 37

    AKI clinical manifestations: Physical:

    Assess catheter (if present) & output q1hr after surgery, Monitor for oliguria, Daily weight (same time, same clothes, same scale), Azotemia, Fluid overload: crackles, confusion, S3, edema, ^RR, dyspnea hypoxia, Monitor VS to catch hypoperfusion and hypoxemia early:, :MAP<65 mm Hg, :Tachycardia, :Thready pulses, :Decreased cognition, : Spo2<88%

  • 38

    AKI Diagnositics:

    Blood tests: ↑BUN, ↑Cr, ↑K+, ↑Phosphorus, ↓Calcium, Imaging: US, CT (without contrast), MRI, KUB, Nuclear Med MAG3 study, Renal scan, cystoscopy or retrograde pyelogram, Other diagnostics: Kidney biopsy Manage hypo & hypertension post- procedure (BLEEDING!)

  • 39

    AKI collaborative management Drug therapy:

    If hypovolemia or hypotension, then volume repletion -Fluid chalange (bolus): 500-1000 ml NS over 1 hour, Drug dosage adjustments may be required, May need to discontinue nephrotoxic medications, ACE-I and ARBS can contribute to AKI (can be renoprotective over time)

  • 40

    AKI collaborative management Nutrition therapy:

    Register dietician, PRotien may be restricted even with non- dialysis pts (try not restric protien if we don’t have to but is hard for kidneys to filter), Protien, sodium, potassium restrictions with dialysis, Fluid restriction for dialysis: urine volume +500 ml, Monitor caloric intake, Oral supplements, enteral nutrition, TPN, etc.

  • 41

    AKI collaborative management renal replacement therapies and indications:

    Hemodialysis, CRRT (continuous renal replacement therapy), Peritoneal dialysis, Symptomatic uremia: pericarditis, neuropathy, decreased cognition, Severe metabolic acidosis: pH<7.1, Rapidly rising serum potassium >6.5 med/L, Fluid overload reduction tissue perfusion

  • 42

    A 64-year-old patient was admitted 2 days ago with hypovolemic shock secondary to traumatic injuries. Which lab value is MOST IMPORTANT to immediately report to the physician/provider?

    Serum potassium 6.8 mEq/L