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DT3-Exam 3 > Acute & Chronic Renal Failure + Cases-- Melissa > Flashcards

Acute & Chronic Renal Failure + Cases-- Melissa Flashcards

1
Q

Define acute renal failure.

What are the three general causes?

A

Sudden decrease in renal function that may or may not be primary to the kidney…

Can be pre renal (decreased perfusion), intrinsic, or post renal (obstructive)

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2
Q

What do we use to measure GFR and therefore renal function? What are two problems with this measurement?

A

Cr clearance

  • Cr is secreted slightly in the PT
  • Cr does not increase until ~24 hrs after ARF starts
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3
Q

Is imaging of the renal system required to make ARF Dx?

A

Not unless you have suspicion of obstruction–it is not emergent
*Note that US may miss stones and CT has radiation risk

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4
Q

Describe what you should look for on microscopic exam to dx ARF?

A

Look for any casts or cells in the urine; note cell types

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5
Q

How does FENa change with volume depletion?

A

FENa will DECREASE with volume depletion (^RAAS)

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6
Q

What are some systemic symptoms that may manifest with ARF? (2)

A
  • Decreased mental status
  • Urea flecks on skin
  • These are uremia symptoms
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7
Q

What are some indications that volume depletion may be the etiology behind a patient’s ARF? (2)

A
  • Elderly patient on diuretics
  • Patient has N/V
  • *NORMALIZE VOLUME STATUS STAT**
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8
Q

What are two renal vascular diseases that might present with HTN?
How do irregularities in BP cause renal dysfunction

A
  • post strep glomerulonephritis
  • PAN

HypoTN: Under-perfusion and ischemic injury
HTN: vascular injury

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9
Q

What is one thing you should never forget to check in males with ARF?

A

Prostate enlargement!

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10
Q

What is one commonly associated disease state with ARF?

A

CHF: cardiorenal syndrome–patients are more likely to have renal problems

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11
Q

What might WBCs in the urine indicate?

RBCs?

A
  • UTI; if casts think pyelonephritis or interstitial nephritis
  • There are many states that will cause hematuria!
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12
Q

Specifically EOS in the urine is indicative of…

A

Drug induced nephrotoxicity

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13
Q

Ethylene glycol poisoning will predispose one to…

A

Ca oxalic acid crystals (Remember in general that Ca crystals are the most common)

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14
Q

What is one renal disease state that will cause low urine pH? High urine pH?

A
  • RTA (2, 4)–> LOW pH

- Proteus infection–> HIGH pH

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15
Q

What should you think when you see red/ brown pigmented urine WITHOUT RBCs?

A

Rhabdomyolysis!

Be on the lookout in elderly w bc of falls

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16
Q

Very common cause of proteinuria?

A

DM!

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17
Q

Dimorphic RBCs that are shaped like mickey mouse ears come from…

A

The glomerulus

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18
Q

What is a normal BUN: Cr ratio?
What does it mean if the ratio is high?
What does it mean if the ratio is low?

A

Normal- 20: 1
HIGHER than 20:1 - Prerenal azotemia (renal underperfusn.)
LOWER than 20:1: Intrinsic renal failure

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19
Q

What are two extra renal factors that might cause ^ BUN?

A
  • corticosteroid

- GI bleed

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20
Q

3 Factors that might cause falsely LOW Cr or BUN?

A
  • cirrhosis
  • cachexia
  • severe protein malnutrition
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21
Q

What are two factors that might complicate determining FENa?

A
  • patient taking diuretic (by definition wastes Na)

- patient with chronic renal disease

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22
Q

How does the FENa change with…
Pre renal azotemia?
Chronic kidney disease at baseline?
Acute Glomerulonephritis?

A

Pre renal azotemia: FENa less than 1%
Glomerulonephritis: NENa less than 1%;
CKD: RARELY less than 1% at baseline

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23
Q

How does prerenal (hypo perfusion) ARF present (4)?

Is it reversible?

A
  • ^BUN, ^Cr (give fluids to ^ filtration of blood )
  • Possible association with HypoTN
  • Can be induced by diuretics or BP meds
  • Hypercalcemia–> renal vasoconstriction
  • Typically reversible
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24
Q

How does postrenal (obstructive) ARF present? (2)

A
  • Flank pain (radiates to inner thigh if stone in ureter)
  • Hyperkalemia (indicates malfxn in DT)
  • Reversible if caught quickly
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25
Q

List 4 causes of obstructive ARF:

A
  • stones
  • enlarged prostate
  • ureteral compression
  • clots
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26
Q

What are 4 causes of intrinsic ARF?

A
  • (#1) AKI
  • glomerulonephritis
  • interstitial nephritis
  • atheroembolic renal disease
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27
Q

Describe how AKI can lead to intrinsic ARF:

A

AKI–> sepsis/ HypoTN–> ARF unresponsive to fluids

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28
Q

What are two markers of intrinsic ARF?

A

Cr and urine flow are LATE markers

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29
Q

What is the end result of untreated pre renal azotemia?

A

Acute kidney injury (AKI)! this is how pre renal ARF can cause intrinsic kidney disease

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30
Q

What is one clinical phenomenon that commonly occurs with AKI?

A

Sepsis/ SIRS: diffuse inflammation–> poor renal perfusion

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31
Q

3 potential causes of AKI?

A
  • Decreased perfusion
  • Rhabdomyolysis
  • Contrast dye
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32
Q

Glomerulonephritis is usually…

A

nephritic

33
Q

RBC casts are almost pathonumonic for…

A

glomerulonephritis

34
Q

4 common clinical signs of glomerulonephritis:

A
  • Urine: casts, proteinuria, dysmorphic RBCs
  • HTN
  • ~systemic disease
  • FENa less than 1%
35
Q

What are three examples of glomerulonephritis?

A
  • PSGN
  • Lupus nephritis
  • Wegners
36
Q

Most common cause of interstitial nephritis?

A

DRUGS! ABX, NSAIDS, Proton pump inhibitors

*This is a rare phenomenon

37
Q

Describe three clinical findings of interstitial nephritis.
Will patients present with oliguria?
What is the BUN:Cr?

A
  • Rise in Cr weeks after exposure
  • Eosinophilia/ Eosinophiluria
  • +/- rash or fever
  • Patients will NOT have oliguria
  • BUN:Cr LESS than 20:1
38
Q

Describe how an atheroembolus to the kidney will present:

When does this occur?

A

Vascular procedure–> athroemboli–> purple toes, unremarkable urine sediment, LOW complement

39
Q

How does rhabdomyolysis happen?
What is are three marker of disease?
How do we treat it?

A

Severe muscle injury–> myoglobinuria + ARF–> oliguria

  • ^ CPK
  • Cr»BUN
  • Treat with aggressive hydration +/- mannitol; requires dialysis if oliguria/anuria
40
Q

4 potential causes of rhabdomyolysis?

A

1 Elderly falls (Initially described in crush injury)

  • Hypothyroid
  • Statins
  • Neuroleptic malignant syndrome
41
Q

2 populations at risk for contrast induced AKI:

A

patients with DM or myeloma (basically baseline kidney disease…)

42
Q

Two ways to protect against contrast induced AKI:

A

Premedication and hydration

43
Q

3 types of meds that can INDIRECTLY cause AKI:

A
  • NSAIDS–> stop dilation at afferent arteriole
  • DIURETICS
  • ACEi’s –> stop constriction of efferent arteriole
44
Q

3 drugs that are directly nephrotoxic:

A
  • cisplatin
  • amphotericin
  • aminoglycocides
45
Q

Describe how ethylene glycol and methanol can cause renal toxicity:

A

ethylene glycol–> oxalic acid–> Ca/oxalic acid crystals

methanol–> formic acid

46
Q

How do we treat drug induced AKI?

A

Discontinue offending agent and hydrate but do not over hydrate because that is bad

47
Q

Describe the AKI associated with lactic acidosis/ketoacidosis:

A

Keto/Lactate–> Oliguric AKI–>

HYPERKALEMIA + ACIDEMIA–> Need DIALYSIS!!

48
Q

Remember that AKI often occurs as a part of…

A

SIRS!!!

49
Q

How do we define chronic kidney disease?

How is it typically discovered?

A

GFR LESS than 60 for LONGER than 3 mos

*Typically discovered as incidental finding on screening

50
Q

How do we measure kidney function?

A

Estimate the GFR using serum Cr, weight, and age.

51
Q

What is a NORMAL Cr?

When might this be deceptive?

A

0.6-1.3 ; Typically LOWER in males and females with less lean muscle mass

Note that this may UNDERESTIMATE renal disease in elderly females

52
Q

What are the stages of Chronic Renal disease (1-5)

A 
1= normal GFR, disease present 
2= GFR 60-90, disease present 
3= GFR 30-60
4= GFR 15-30
5= GFR
53
Q

6 common associations with chronic kidney disease?

A
  • DM (mostly glomerular at first)
  • HTN (slower progression)
  • Atherosclerotic vascular disease
  • Glomerulonephritis (less nephrons at baseline)
  • Meds
  • Obstruction
54
Q

What are the symptoms of chronic kidney disease?

What do we look for on PE?

A

Usually NONE!
May have fatigue, nocturne, swelling (stage 5) or confusion (uremic encephalopathy)…

Look for loss go muscle mass, HTN, edema, and mental status on PE

55
Q

BUN and Cr in patient with Chronic Kidney Disease (CKD):

A

HIGH!

56
Q

Potassium in patient with CKD:

A

HIGH!

57
Q

PO4 in patient with CKD:

A

HIGH

58
Q

Why do patients with CKD get anemia?

A

NO EPO!!!

59
Q

Patients with which type of CKD are more likely to have severe proteinuria?

A

Glomerular more than tubular disease

60
Q

In which vitamin will CKD patients be deficient?

A

vitamin D (1,25)

61
Q

How do CKD patients get renal osteodystrophy?

A

No active vit D–> Hypocalcemia–> ^ PTH–> Demineralize bone

62
Q

Patients with CKD will have what kind of pH disturbance?

A

METABOLIC ACIDOSIS

63
Q

When do we typically implement renal replacement therapy?

A

GFR LESS than 15

*It is important to plan ahead when patients are deteriorating; putting in emergency dialysis has high infection risk

64
Q

What are the dietary restrictions of patients with CKD?

A

Limit: protein, Na, K, PO4 (patients generally have poor quality of life)

65
Q

What is peritoneal dialysis?

A

Dialysate –> peritoneum via indwelling cath–>

  • Works overnight
  • ^ risk infection, nausea and pain
66
Q

How does hemodialysis work?

A

Uses naive shunt/ artificial graft

  • Can have vascath as emergent portal (^ infection risk)
  • Risks: infection, N/V, dizziness
67
Q

What are some complications associated with CKD?

What is the #1 cause of death in these patients?

A

1 cause of death = CAD

  • CVA/ PAD/ CKD
  • DM/ HTN
  • Immunosuppression w/ dialysis–> infection
  • Patients commonly debilitated w poor quality of life
68
Q

How do we prevent progression of CKD?

What are 4 drug classes used to treat these patients?

A
  • Manage causative factors (DM, HTN, etc.)
  • Exercise and decrease salt intake
  • ACEi’s to decrease protein excretion
  • ARBs, Ca++ channel blockers, Statins
69
Q

What does specific gravity tell you about urine?

A

the osmolality!

70
Q

1 presentation of rhabdo?

A

Elderly patient with falls

Can also occur with neuroleptic malignant syndrome (look for ^CPK), statin use

71
Q

Dark urine without cells is…

A

Rhabdomyolysis

72
Q

Spironolactone moa?

ACEi moa?

A

Remember that both ultimately diminish effects of ALDO

73
Q

How can a stomach bug cause kidney injury?

What does the patients’ urine sodium/ K+ look like in this case?

A

Prolonged hypo perfusion to kidney–> Acute tubular necrosis

  • Urine Na is LOW because patient is reabsorbing it to ^ plasma volume (^RAAS)
  • Urine K+ is probably ^.
74
Q

Note on elderly folks and hypernatremia:

A

Elderly patients with volume depletion may not demonstrate hypernatremia. I am not sure why, but I think he said this.

75
Q

1 cause of muscarinic poisoning?

A

organophosphates from pesticide exposure

76
Q

How do we prevent contrast nephropathy?

A

Administer prophylactic fluids and “athetylcystine”

…He says the word. I had no opportunity to read it.

77
Q

What do we give/ not give patients with contrast nephropathy? When do we suspect this? What does the urinalysis look like?

A

Obviously suspect this if there is hx of imaging with contrast; be on the lookout in patients with advanced kidney disease (contrast = ^ osmotic load)

  • Administer fluids and drug
  • Do not give K+ binding resin (not useful)
  • This is pre renal azotemia–> may see waxy casts on urinalysis, otherwise there is little sign on urine sediment
78
Q

How do we filter blood for stage 5 kidney disease?

How do patients present?

A
  • Plasmapheresis + dialysis; patient should be on transplant list
  • Patients will have alveolar edema in the lungs and cardiomegaly
79
Q

Atheroembolism to kidney: three findings?

A

Renal insufficiency, purple toes, low blood complement levels

DT3-Exam 3 (9 decks)

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