for renal CA
w/renal grisk
/asbestos /comes
* · jones review
4t +Ca review
wlitis · Sh
disease
.
·
others ...
Ml
UNIT 6
ACUTE KIDNEY INJURY
● Loss of renal function d/t the kidneys
● Categories of AKI:
Vieorrhage
○ Prerenal: hypoperfusion of kidney It cardiac
⑤
output)
■ HF, hemorrhage, GI loss, sepsis, shock, renal losses -
greatest
-
○ Intrarenal: actual damage to the kidney tissue
■ Caused by nephrotoxic agents such as:
● Gentamicin, tobramycin, lead, mercury, ethylene
○ Postrenal: obstruction to urine flow
■ Blood clots, tumors, stones, BPH
● Phases of AKI:
○ Initiation period: injury happens
○ Oliguria period: ↓ urine output w/ abnormal lab values,
O -
↑ KI BUN creat Ca
-
,
■ hyPERkalemia develops
, ,
↳ indicates dehydration
-
○ Diuresis period: ↑ urine output w/ abnormal lab values *dehydration*
A○ Recovery
-
period: normal output/normal lab values *may take 3-12m*
-
● Manifestations:
○ Drowsy, HA
covery phasepotassium
○ Muscle aches
○ Seizures
● DX: Ultrasonography
○ Renal sonogram
○ CT w/ no contrast
· Normal
=
○ MRI, GFR, Metabolic acidosis
● TX:
○ Assess I&Os, & lab values
○ Monitor central venous & arterial press & hourly UO
○ Prevent infections
○ Encourage hydration for those at risk for dehydration
■ Before, during & after sx
■ Pt undergoing studies requiring fluid restriction & contrast
■ Pt w/ neoplastic or metabolism disorders
■ Pt w/ skeletal injuries & heat illnesses
○ Remove indwelling catheters ASAP
○ Monitor lab values if taking nephrotoxic meds, b/c high serum levels will cause
changes in RF
○ AVOID NSAIDS & contrast agents
○ Dialysis
○ Diuretics (furosemide)
■ HyPERKalemia is the most life-threatening imbalance seen
■ Pay att to all oral, parenteral fluids given**
ACUTE TUBULAR NECROSIS
● Damage to the kidney tubules
○ Most common intrinsic AKI
● Characteristics are:
○ Intratubular obstruction, tubular back leak, vasoconstriction
■ & changes in permeability
■ Results in a ↓ of GFR, progressive azotemia, & fluid & electrolyte
■ CKD, DM, HF, HTN
CHRONIC KIDNEY DISEASE:
● Etiology:
○ Cardiovascular disease, DM, HTN, & obesity
HTN
Urinary output
+
ESRD
=
no
, for
watch
* loss/gain tweight
weight body
75% Of
● Stages of CKD = normal GFR 125mL/min
○ Stage 1: > or less 90mL/min
■ Kidney damage w/ normal or ↑ GFR (no s/s)
○ Stage 2: 60-89mL/min
■ Mild (some fatigue/HA/vague s/s)
○ Stage 3: 30-59mL/min
■ Moderate (inc proteinuria, high creatinine, high Hct, high Ca/K/P)
■ Fatigue, HA, HTN, pain, edema, anorexia*) METABOLIC ACIDOSIS
○ Stage 4: 15-29mL/min
dialysis for ESRF
■ Severe (weight gain, bronze skin color) hum
■ Doctor will begin dialysis/ fistula or graft done -4 triglycerides (40-140m/35-1357)
*
this
"report
↳
○ Stage 5: <15mL/min 242
=
■ End-stage kidney disease or CKD
■ Scant urine, N/V *
*
● Manifestations: >-
>U Notify MD
=
○ ↑ serum CR, anemia, metabolic acidosis
○ CA & Phos abnormalities w/ mineral bone disorders
○ Fluid retention, HTN, CAD
○ Severe pain
● DX:
● TX:
○ Calculation of GFR
○ Monitor Creatinine & BUN levels
mplicationdetention
↳ report
this
○ Tx underlying cause
○ Controlling cardiovascular RF: *
e
digoxin rhythm
■ Hyperglycemia
■ Managing anemia
■ Smoking cessation
■ Weight loss & exercise programs
* Toxicity
■ Reduce salt & alcohol intake * digoxin
- halo
■ Minimize nephrotoxins yellow
-
confusion
-
● Gerontologic considerations: NIV
dysrhythmias
-
○ Kidney disease susceptible in elderly -
■ b/c # of nephrons decline
○ Diseases such as: HTN, HF, atherosclerosis DM, & cancer ↑ risk
○ Elderly taking multiple meds
GLOMERULAR DISORDERS
ACUTE GLOMERULONEPHRITIS= May lead to RF
● Patho/etiology:
○ Inflamm. of renal glomeruli & capillaries of both kidneys
○ Involves antigen-antibody reaction, causing damage to the glomerular capillaries
○ Usually accompanied by STREP infection
W
○ & impetigo (skin infection)
● Manifestations:
○ Hematuria
○ Edema, Azotemia, Proteinuria
○ Cola colored urine fluids
○ Foamy urine
○ HTN BUN creat +
fluid intake
DO NOT encourage
○ If severe: flank pain, HA, or malaise -
● DX: his
BP Q4 -
○ Throat culture (STREP)
CBC daily
○ Kidney biopsy - the golden standard -
- CMP daily
, care
avoid
A
ex
● TX:
○ C&S, UA, blood cultures 7
○ Corticosteroids (prednisone)
○ Antihypertensives
○ Control proteinuria w/ dietary rest.
○ Restrict protein if elevated BUN
○ Restrict NA if HTN or edema
S
○ If STREP is detected = give penicillin
○ Monitor BP, edema, daily weight & I&Os
● LAB TESTS – Renal function tests
○ Elevated BUN - > 20 & CR >1.2
○ GFR - <60mL/min (normal 90 - 120 mL/min)
○ CBC (monitor RBC count)
CHRONIC GLOMERULONEPHRITIS follow up
>
-
needs
anemia
● Manifestations: 8 ↓ RBC count
=
○ Weight loss admin "epigen"
·
* ↓RBC
○ May appear w/ a yellow pigmentation skin color
↑ Bun/creat
○ Irritability & Nocturia
○ HA, dizziness ↓ albumin
○ Digestive disturbances ↑ k+ 8 Ca
○ Pericarditis w/ pericardial friction rub
○ Pulsus paradoxus
○ Neurosensory changes
○ Diminished DTR
● DX = UA, GFR, Chest Xray
● TX:
○ BP control w/ NA & water restrict.
○ Antihypertensive meds
○ Diuretics (furosemide)
○ AVOID NSAIDS, nephrotoxins meds & IV contrast dye
○ Dialysis
○ High protein diet (eggs, meats, fish)
○ Monitor fluid & electrolyte balance
NEPHROTIC SYNDROME
● Characterized by ↑ glomerular permeability
"C
● Manifested by massive proteinuria
● Manifestations: "anasarea"
O ○ Edema (soft & & non-pitting)
-u
O
■ Usually occurs around the eyes (periorbital)
-
■ Sacrum, ankles, & hands
■ Abdomen (ascites)
○ HA, Malaise, irritability
O○ Hematuria, HTN
● DX:
O○ Proteinuria (exceeding 3.5g/day, usually the hallmark)
○ Increased WBCs in UA
○ Renal tissue needle biopsy
● Complications:
○ Infection
○ Thromboembolism
○ Pulmonary embolism
○ AKI d/t hypovolemia
○ Atherosclerosis d/t hyperlipidemia
w/renal grisk
/asbestos /comes
* · jones review
4t +Ca review
wlitis · Sh
disease
.
·
others ...
Ml
UNIT 6
ACUTE KIDNEY INJURY
● Loss of renal function d/t the kidneys
● Categories of AKI:
Vieorrhage
○ Prerenal: hypoperfusion of kidney It cardiac
⑤
output)
■ HF, hemorrhage, GI loss, sepsis, shock, renal losses -
greatest
-
○ Intrarenal: actual damage to the kidney tissue
■ Caused by nephrotoxic agents such as:
● Gentamicin, tobramycin, lead, mercury, ethylene
○ Postrenal: obstruction to urine flow
■ Blood clots, tumors, stones, BPH
● Phases of AKI:
○ Initiation period: injury happens
○ Oliguria period: ↓ urine output w/ abnormal lab values,
O -
↑ KI BUN creat Ca
-
,
■ hyPERkalemia develops
, ,
↳ indicates dehydration
-
○ Diuresis period: ↑ urine output w/ abnormal lab values *dehydration*
A○ Recovery
-
period: normal output/normal lab values *may take 3-12m*
-
● Manifestations:
○ Drowsy, HA
covery phasepotassium
○ Muscle aches
○ Seizures
● DX: Ultrasonography
○ Renal sonogram
○ CT w/ no contrast
· Normal
=
○ MRI, GFR, Metabolic acidosis
● TX:
○ Assess I&Os, & lab values
○ Monitor central venous & arterial press & hourly UO
○ Prevent infections
○ Encourage hydration for those at risk for dehydration
■ Before, during & after sx
■ Pt undergoing studies requiring fluid restriction & contrast
■ Pt w/ neoplastic or metabolism disorders
■ Pt w/ skeletal injuries & heat illnesses
○ Remove indwelling catheters ASAP
○ Monitor lab values if taking nephrotoxic meds, b/c high serum levels will cause
changes in RF
○ AVOID NSAIDS & contrast agents
○ Dialysis
○ Diuretics (furosemide)
■ HyPERKalemia is the most life-threatening imbalance seen
■ Pay att to all oral, parenteral fluids given**
ACUTE TUBULAR NECROSIS
● Damage to the kidney tubules
○ Most common intrinsic AKI
● Characteristics are:
○ Intratubular obstruction, tubular back leak, vasoconstriction
■ & changes in permeability
■ Results in a ↓ of GFR, progressive azotemia, & fluid & electrolyte
■ CKD, DM, HF, HTN
CHRONIC KIDNEY DISEASE:
● Etiology:
○ Cardiovascular disease, DM, HTN, & obesity
HTN
Urinary output
+
ESRD
=
no
, for
watch
* loss/gain tweight
weight body
75% Of
● Stages of CKD = normal GFR 125mL/min
○ Stage 1: > or less 90mL/min
■ Kidney damage w/ normal or ↑ GFR (no s/s)
○ Stage 2: 60-89mL/min
■ Mild (some fatigue/HA/vague s/s)
○ Stage 3: 30-59mL/min
■ Moderate (inc proteinuria, high creatinine, high Hct, high Ca/K/P)
■ Fatigue, HA, HTN, pain, edema, anorexia*) METABOLIC ACIDOSIS
○ Stage 4: 15-29mL/min
dialysis for ESRF
■ Severe (weight gain, bronze skin color) hum
■ Doctor will begin dialysis/ fistula or graft done -4 triglycerides (40-140m/35-1357)
*
this
"report
↳
○ Stage 5: <15mL/min 242
=
■ End-stage kidney disease or CKD
■ Scant urine, N/V *
*
● Manifestations: >-
>U Notify MD
=
○ ↑ serum CR, anemia, metabolic acidosis
○ CA & Phos abnormalities w/ mineral bone disorders
○ Fluid retention, HTN, CAD
○ Severe pain
● DX:
● TX:
○ Calculation of GFR
○ Monitor Creatinine & BUN levels
mplicationdetention
↳ report
this
○ Tx underlying cause
○ Controlling cardiovascular RF: *
e
digoxin rhythm
■ Hyperglycemia
■ Managing anemia
■ Smoking cessation
■ Weight loss & exercise programs
* Toxicity
■ Reduce salt & alcohol intake * digoxin
- halo
■ Minimize nephrotoxins yellow
-
confusion
-
● Gerontologic considerations: NIV
dysrhythmias
-
○ Kidney disease susceptible in elderly -
■ b/c # of nephrons decline
○ Diseases such as: HTN, HF, atherosclerosis DM, & cancer ↑ risk
○ Elderly taking multiple meds
GLOMERULAR DISORDERS
ACUTE GLOMERULONEPHRITIS= May lead to RF
● Patho/etiology:
○ Inflamm. of renal glomeruli & capillaries of both kidneys
○ Involves antigen-antibody reaction, causing damage to the glomerular capillaries
○ Usually accompanied by STREP infection
W
○ & impetigo (skin infection)
● Manifestations:
○ Hematuria
○ Edema, Azotemia, Proteinuria
○ Cola colored urine fluids
○ Foamy urine
○ HTN BUN creat +
fluid intake
DO NOT encourage
○ If severe: flank pain, HA, or malaise -
● DX: his
BP Q4 -
○ Throat culture (STREP)
CBC daily
○ Kidney biopsy - the golden standard -
- CMP daily
, care
avoid
A
ex
● TX:
○ C&S, UA, blood cultures 7
○ Corticosteroids (prednisone)
○ Antihypertensives
○ Control proteinuria w/ dietary rest.
○ Restrict protein if elevated BUN
○ Restrict NA if HTN or edema
S
○ If STREP is detected = give penicillin
○ Monitor BP, edema, daily weight & I&Os
● LAB TESTS – Renal function tests
○ Elevated BUN - > 20 & CR >1.2
○ GFR - <60mL/min (normal 90 - 120 mL/min)
○ CBC (monitor RBC count)
CHRONIC GLOMERULONEPHRITIS follow up
>
-
needs
anemia
● Manifestations: 8 ↓ RBC count
=
○ Weight loss admin "epigen"
·
* ↓RBC
○ May appear w/ a yellow pigmentation skin color
↑ Bun/creat
○ Irritability & Nocturia
○ HA, dizziness ↓ albumin
○ Digestive disturbances ↑ k+ 8 Ca
○ Pericarditis w/ pericardial friction rub
○ Pulsus paradoxus
○ Neurosensory changes
○ Diminished DTR
● DX = UA, GFR, Chest Xray
● TX:
○ BP control w/ NA & water restrict.
○ Antihypertensive meds
○ Diuretics (furosemide)
○ AVOID NSAIDS, nephrotoxins meds & IV contrast dye
○ Dialysis
○ High protein diet (eggs, meats, fish)
○ Monitor fluid & electrolyte balance
NEPHROTIC SYNDROME
● Characterized by ↑ glomerular permeability
"C
● Manifested by massive proteinuria
● Manifestations: "anasarea"
O ○ Edema (soft & & non-pitting)
-u
O
■ Usually occurs around the eyes (periorbital)
-
■ Sacrum, ankles, & hands
■ Abdomen (ascites)
○ HA, Malaise, irritability
O○ Hematuria, HTN
● DX:
O○ Proteinuria (exceeding 3.5g/day, usually the hallmark)
○ Increased WBCs in UA
○ Renal tissue needle biopsy
● Complications:
○ Infection
○ Thromboembolism
○ Pulmonary embolism
○ AKI d/t hypovolemia
○ Atherosclerosis d/t hyperlipidemia
