renal disorders Flashcards

1
Q

How are the causes of renal dysfunction catergorized?

A

causes of kidney dysfunction are divided into 3 categories based on the mechanism of injury; prerenal, intrarenal, & postrenal

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2
Q

What are prerenal injuries related to?

A

decrease in blood flow & perfusion

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3
Q

What are intrarenal injuries related to?

A

secondary to actual injuries to the kidney itself

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4
Q

What are postrenal injuries related to?

A

related to obstruction of urine outflow from the kidneys

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5
Q

list possible causes of prerenal injury

A
  • hypotension
  • shock
  • diarrhea (severe)
  • vomiting (severe)
  • bleeding/hemorrhage
  • diuretics
  • diabetes insipidus
  • burns
  • HF/MI
  • cirrhosis
  • sepsis
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6
Q

list possible causes of intrarenal injury

A
  • vasculitis
  • venous occlusion
  • pre-eclampsia
  • acute tubular necrosis
  • multiple myeloma
  • hypercalcemia
  • IV contrast dyes
  • pyelonephritis
  • certain meds: NSAIDS, ACEI, heavy metals
  • transfusion reaction
  • rhabdomyolysis
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7
Q

list possible causes of post renal injury

A
  • renal calculi
  • enlarged prostate
  • cancer
  • diabetes
  • functional obstruction due to drugs
  • blood clot
  • trauma
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8
Q

What is the most common cause of acute kidney injury?

A

acute tubular necrosis (ATN)

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9
Q

What occurs when acute tubular necrosis is present?

A

damage to renal tubules causing cells to slough into the tubular lumen and lumen becomes blocked
- fluid unable to go thru lumen; decreased urine formation ; ultimately no urine if untreated
- blocked lumen exacerbates ischemic injury to cells & causes additional intrarenal injury

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10
Q

What are possible causes acute tubular necrosis?

A

post - ischemia (all causes of severe pre-renal disease)
nephrotoxins

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11
Q

is acute tubular necrosis permanant or reversible?

A

permanent injury if not reversed

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12
Q

What 3 things were mentioned to cause nephrotoxicity?

A

aminoglycosides
IV contrast dye
multiple myeloma

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13
Q

What is creatinine clearance (100-150cc/min) in prerenal azotemia vs ATN?

A

prerenal azotemia - 15-80cc/min
ATN - less than 5-10cc/min

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14
Q

What is urine sodium (10-20mEq/L) in prerenal azotemia vs. ATN?

A

prerenal azotemia - less than 10 mEq/L
ATN - greater than 20 mEq/L

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15
Q

What is specific gravity(1.005-1.025) in prerenal azotemia vs ATN?

A

prerenal azotemia - greater than 1.015
ATN - 1.010 fixed

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16
Q

What is urine osmolality (200-1200mOsm/kg) in prerenal azotemia vs ATN?

A

prerenal azotemia - concentrated >450mOsm/kg
ATN - isomotic = 300mOsm/kg

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17
Q

What is serum BUN (10-20)/ creatinine in prerenal azotemia vs ATN?

A

prerenal azotemia - greater than 15:1
ATN - 10:1 fixed

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18
Q

What is the UA like in prerenal azotemia vs. ATN?

A

prerenal azotemia - normal
ATN - red/qhite cells, casts & epithelial cells

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19
Q

What is oliguria?

A

urine output <400 ml/day

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20
Q

What is anuria?

A

urine output < 30-40 ml/day

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21
Q

What are the 4 stages of an AKI?

A

initial onset
oliguria
late diuretic
recovery

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22
Q

What happens in the initial onset phase of an AKI?

A
  • 0-2 days
  • initial insult to point when BUN/Cr rise and/or urine output drops
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23
Q

What happens in the oliguria phase of an AKI?

A
  • 1-2 days to 6-8 weeks
  • drop in GFR, rention of urea, potassium, sulfate & creatinine
  • decrease urine output & edema
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24
Q

What happens in the late diuretic phase of an AKI?

A
  • 2-8 days
  • begins with a slow, gradual increase in urine output, then high output (up to 10L in 24 hr)
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25
Q

What happens in the recovery phase of an AKI?

A
  • 2-4 months
  • labs return to pre-morbid state (full reovery; diabetics might not fully return)
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26
Q

What are the most common AKIs?

A

septic & cardiac shock

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27
Q

What should you do to help during the recovery phase of an AKI?

A
  • low sodium diet
  • fluid restriction (either IV or PO)
  • low potassium diet?
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28
Q

What clinical manifestations will an AKI have regardless of cause?

A

oligura and fluid overload

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29
Q

What are the clinical manifestations of an AKI?

A

oliguria
fluid overload
edema
build up of nitrogenous waste
- uremia
- metabolic acidosis
- thrombocytopenia
- neuromuscular irritability

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30
Q

What labs & imaging are used to dx an AKI?

A
  • UA
  • serum electrolytes
  • BUN/ Creatinine
  • ABG
  • CBC
  • CT scan
  • renal biopsy
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31
Q

What is tx of an AKI depend on?

A

depends on cause

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32
Q

What is the goal of AKI tx?

A

to restore normal chemical balance, prevent further complications until repair of renal tissue and restoration of renal function

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33
Q

How is an AKI treated?

A
  • fluid administration
  • loop diuretics (lasix)
  • monitor electrolytes → potassium
  • cardiac monitoring → tele; step down or ICU
  • hemodialysis → helps maintain a homeostatic state
  • monitor I & Os
  • might need to do daily weights
  • monitor BP
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34
Q

What is the leading cause of death in AKIs and why?

A

hyperkalemia; potassium plays a role on muscles and neves → supposed to be in ICF not ECF, do when gets ut into the ECF levels become too hight & heart will be affected

35
Q

Is dialysis longterm or shortterm in AKI?

A

should be shortterm; hope is as you recover from AKI → to get off of dialysis; non compliant pts are usually on life-long dialysis

36
Q

list indications for dialysis

A
  • volume overload
  • potassium greater than 6mEq/L → should be < 5.5 mEq/L
  • BUN greater than 120mg/dL → should be between 10-20 mg/dL
  • other signs of uremic intoxication (N/V, decreased appetite, weight loss, fatigue, impaired cognition, mucle cramps, metallic taste, seizure, coma)
37
Q

What is an irreversible and progressive disease?

A

chronic kidney disease

38
Q

chronic kidney disease is often ____________ initially until disease is far advanced

A

asymptomatic

39
Q

What classifies chronic kidney disease?

A

kidney damage or a GFR <60mL/min/1.73m^2 for 3 months or longer

40
Q

What are the causes of chronic kidney disease?

A

*hypertension
*diabetes
obesity
glomerulonephritis
SLE (lupus)
polycystic kidney disease

41
Q

What happens during chronic kidney disease?

A

loss of functioning nephrons, progressive deterioration of glomerular filtration, ability of tubules to reabsorb, endocrine functions

42
Q

as nephrons are destroyed the remaining function ____________ to take on the work of the destroyed nephrons

A

hypertrophy

43
Q

What are the tx for chronic kidney disease?

A
  • lifelong dialysis
  • kidney transplant (will get you off of dialysis)
44
Q

How many stages of renal dysfunction are there?

45
Q

What is stage 1 of renal dysfunction?

A
  • damage with normal or increased GFR (>90ml)
46
Q

What is stage 2 of renal dysfunction?

A
  • mild reduction in GFR (between 60-90ml/min)
47
Q

What is stage 3 of renal dysfunction?

A
  • moderate reduction in GFR (between 30-59ml/min)
  • decreased function because <50% of nephrons are working
  • will see lab changes
  • no longer able to compensate
48
Q

What is stage 4 of renal dysfunction?

A
  • severe reduction in GFR (15-29ml/min)
  • renal insufficiency is evident
  • nephrons no longer able to do the job
  • diet restriction of proteins
49
Q

What is stage 5 renal dysfunction?

A

kidney failure (less than 15ml/min); kidney can not longer remove waste product or maintain their normal function to sustain life; need dialysis and/or transplant

50
Q

stage 1 & 2 renal dysfunction

A
  • often asymptomatic & creatinine will be normal
  • compensation will occur for damaged nephrons
51
Q

list clinical manifestations of CKD

A
  • accumulation of nitrogenous waste
  • hyperkalemia
  • hypocalcemia
  • normochromic/normocytic anemia
  • low albumin
52
Q

What occurs due to the accumulation of nitrogenous waste in CKD?

A
  • encephalopathy
  • anemia & thrombocytopenia due to lysis
53
Q

Why does hypocalcemia occur in CKD and what can it cause?

A

hypocalcemia occurs because vitamin D is not able to be acitvated; can cause:
- hyperparathyroidism
- bone breakdown
- hyperphosphatemia

54
Q

What may the skin look like when someone has CKD?

A

grayish undertone b/c of the waste products & from the filtrated stuff used in dialysis; thin skin

55
Q

What is the tx for CKD?

A
  • treat underlying cause
  • monitor labs
  • smoking cessation → vasoconstriction
  • manage hyperglycemia → if diabetic
  • manage anemia
  • excercise program
  • decrease sodium
  • avoid alcohol
  • dialysis
  • kidney transplant
56
Q

What is glomerulonephritis?

A

inflammation of the glomerular capillaries

57
Q

What causes about 25-30% of all ESRD cases?

A

glomerulonephritis

58
Q

is glomerulonephritis acute or chronic?

A

can be acute or chronic

59
Q

What is the most common cause of glomerulonephritis?

A

post-streptococcal glomerulonephritis

60
Q

What are the sx of glomerulonephritis?

A
  • pink or cola-colored urine
  • proteinuria
  • hematuria
  • hypertension
  • fluid retention/edema
  • decreased urine
  • N/V
  • muscle cramps
  • fatigue
61
Q

What are complications of glomerulonephritis?

A
  • accumulation of waste or toxins in the bloodstream
  • poor regulation of essential minerals & nutrients
  • loss of RBCs
  • loss of blood proteins
62
Q

What causes glomerulonephritis to begin with?

A

begins with an antigen-antibody reaction

63
Q

What does the antigen antibody complex do in glomerulonephritis?

A

damages structures of the glomeruli which causes nephron dysfunction

64
Q

What does nephron dysfunction in glomerulonephritis cause?

A
  • decreased filtration of blood
  • decreased urine production
  • hypervolemia
  • hypertension
65
Q

What are the clinical manifestations of glomerulonephritis?

A
  • oliguria often 1st sx
  • followed by hematuria, proteinuria → cola colored urine
  • edema often in face & hands
  • HTN
  • elevated anti-strep antibodies (ASO)
  • increased creatinine
  • decreased serum albumin
  • cast in urine
66
Q

What are casts in urine?

A

tiny tube-shaped partickes that can be found when urine is examined under the microscope; may be made up of WBC, RBC, kidney cells, or substances such as protein or fat

67
Q

What is the goal of tx for glomerulonephritis?

A
  • increase urine output
  • decrease urinary protein
68
Q

What types of medications are used to tx glomerulonephritis?

A
  • corticosteroids
  • antibiotics, if needed
  • antihypertensives, if needed
  • antipyretics
69
Q

What diet modifications should be made for a patient who has glmomerulonephritis?

A
  • low sodium
  • low protein
70
Q

What complications should you monitor for during glomerulonephritis tx?

A
  • HTN
  • encephalopathy
  • HF
  • pulmonary edema
71
Q

What is nephrotic syndrome?

A

damage to the glomerulus; the filter is damaged and things which should stay in are able to leak out through the pores which become bigger due to the damage

72
Q

What does damage to the glomerulus lead to?

A

increased permeability of proteins & other substances in the blood

73
Q

What is the most common type of nephrotic syndrome?

A

diabetic nephropathy

74
Q

What are the top 3 causes of nephrotic syndrome?

A
  • diabetic nephropathy
  • lupus
  • amyloidosis
75
Q

What percentage of cases do the top 3 causes of nephrotic syndrome account for?

76
Q

list other possible causes of nephrotic syndrome

A
  • vasculitis
  • allergies
  • preeclampsia
  • HTN
  • other infections
77
Q

What are the clinical manifestations of nephrotic syndrome?

A
  • albuminuria (AKA proteinuria) → often also have WBC in urine
  • edema
78
Q

What is used to dx nephrotic syndrome?

A
  • UA → proteinuria, hematuria
  • elevated BUN/Cr
  • low serum albumin
  • test for lupus & HepB & C may be performed
  • 24 hr urine
  • renal ultrasound
  • renal biopsy
79
Q

What is the tx for nephrotic syndrome?

A
  • diet → low protein & sodium
  • adequate fluid intake but avoid overload
  • pneumococcal & flu vaccines
  • ACEI or ARBs
80
Q

What are complications related to tx of nephrotic syndrome?

A
  • hyperlidemia
  • thromboembolism
81
Q

nephrotic syndrome (slide)

A
  • increase in glomerular permeability
  • massive loss of plasma proteins in the urine
  • generalized edema
  • elevated triglycerides & LDL
  • Na & water retention
  • ascites +/-
82
Q

nephritic syndrome (slides)

A
  • inflammatory response r/t immune complexes & antibody-antigen complexes lodged in capillary
  • immune response develops against the antigens
  • occlusion of glomerular capillary lumen & damage of capillary wall
  • damage allows RBC to escape into urine
  • decreased GFR, fluid retnenion & nitrogen waste accumulation
  • protein uria & oliguria
83
Q

post-strep glomerular nephritis (chart)

A
  • seen ages 4-7
  • 10-14 days after strep inf.
  • anti-streptolysin titer→ pos
  • urine → cola-colored
  • hematuria → massive
  • proteinuria → minimal
  • HTN
  • edema → moderate
  • hyperkalemia
  • elevated BUN