Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHAR255 > Kidney Disorders 1 > Flashcards

Kidney Disorders 1 Flashcards

Equations, Labs, AKI

1
Q

Why do we check renal function?

A

monitoring and early recognition of CKD
-monitoring the effect of drugs on slowing progression
-predict the time to onset of ESRD
-evaluating risk of complications
adjust doses of medications excreted by the kidneys
monitoring nephrotoxic medications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is creatinine?

A

by-product of muscle metabolism that is primarily eliminated by glomerular filtration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is serum creatinine?

A

creatinine concentration in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What happens to SCr when GFR is low?

A

SCr increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the equation we use to calculate eGFR to stage CKD?

A

CKD-EPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the equation we use to calculate CrCl for the purpose of drug dose adjustments?

A

Cockcroft-Gault

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

True or false: CKD-EPI can be used to estimate kidney function in a patient receiving dialysis

A

false
the machine is removing creatinine thus it is not a reflection of true kidney function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some sources of error in GFR estimating equations using creatinine?

A

non-steady state
-AKI
factors affecting creatinine generation
-race/ethnicity
-extremes of muscle mass and/or body size
-nutrition (high protein or supplements)
-muscle wasting diseases
-ingestion of meat
factors affecting tubular secretion of creatinine
-decrease by drug inhibition (TMP, cimetidine, fenofibrate)
factors affecting extra-renal elimination of creatinine
-dialysis
-inhibition of gut creatininase by antibiotics
-volume loss of extracellular fluids
higher GFR
interference with creatinine assay
-special or chemical interferences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which equation do we use for most patients with stable renal function?

A

CKD-EPI and Cockcroft Gault

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the main difference between the 2012 and 2021 version of CKD-EPI?

A

race has been removed from the equation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Differentiate between indexed/normalized eGFR and non-indexed/without normalization eGFR.

A

indexed/normalized
-standardized to a BSA of 1.73m2
-units: ml/min/1.73m2
-recommended for CKD staging/progression
non-indexed/without normalization
-adjusted according to patients BSA
-units: ml/min
-consider for drug dosing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When should you be cautious when using non-indexed/without normalization eGFR?

A

in the morbidly obese
-can lead to overdosing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is urea?

A

aka blood urea nitrogen (BUN)
produced as a break down product of protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the factors that can impact BUN levels?

A

dietary protein
GI bleeding
hydration status (high urea means low water)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Is BUN strictly regarded as a renal function test?

A

no
levels do rise in renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the effects of the kidney on BUN?

A

filtered by the kidney and also reabsorbed (therefore measurement underestimates GFR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is proteinuria?

A

general term for presence of increased amounts of protein in the urine
-nonspecific: albumin +/- other proteins
-persistent increase of protein in urine is a marker of kidney damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How much protein is normally lost in the urine?

A

no/minimal amounts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which type of protein is lost in the urine?

A

depends on type of kidney damage
-albumin excretion sensitive to damage from diabetes, HTN, glomerular disease
-LMW globulin excretion in tubulointerstitial kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How much albumin is normally found in the urine?

A

small amount

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is albuminuria?

A

albumin in the urine
increased levels are an early predictor of glomerular dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the screening test we use for albuminuria?

A

albumin : creatinine ratio (ACR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the categories of albuminuria?

A

A1 (normoalbuminuria): < 3mg/mmol
A2 (microalbuminuria): 3-30mg/mmol
A3: (macroalbuminuria): > 30mg/mmol
using ACR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are some potential causes of transient albuminuria?

A

recent major exercise
UTI
febrile illness
decompensated CHF
menstruation
acute severe elevation in glucose or BP
takeaway: need repeated tests to ensure its not transient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is a urinalysis?

A

provides info about the physical and chemical composition of urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What kind of information does a urinalysis provide regarding urine?

A

colour, turbidity
presence of cells, micro-organisms, casts, crystals
-granular casts, RBC casts, WBC casts
urinary eosinophils (interstitial nephritis)
pH analysis, specific gravity
glucose, ketones (diabetes/DKA)
leukocyte esterase and nitrite (UTI)

27
Q

What is the use of urinary electrolytes?

A

differentiate causes of AKI

28
Q

Describe when you are likely to see the following casts:
RBC casts
WBC casts
fatty casts
granular casts

A

RBC: proliferative glomerulonephritis
WBC: pyelonephritis or interstitial nephritis
fatty: diseases with proteinuria
granular: parenchymal diseases

29
Q

What are casts?

A

cylindrical protein structures made in the tubules
issue: not always indicative of a problem
if theres cells in the cast (WBC or RBC)=pathological

30
Q

What is an AKI?

A

a sudden decline in renal function (hours or days) as evidenced by changes in laboratory values (SCr, BUN, and urine)

31
Q

How can we classify AKI?

A

anuric
-less than 50 ml/day urine output
oliguric
-less than 500 ml/day urine output
non-oliguric
-greater than 500 ml/day urine output

32
Q

What do all staging systems use for diagnostic criteria of AKI?

A

SCr and urine output

33
Q

What are the typical timelines for the changes in SCr and urine output due to AKI?

A

SCr: may take up to 4 days before seeing an elevation
urine output: decrease is seen earlier but is non-specific

34
Q

Why do we need to know a patients baseline SCr in the context of AKI?

A

all criteria based on detecting changes in SCr

35
Q

What is the clinical presentation of AKI?

A

most patients are asymptomatic
-diagnosed based on lab criteria (increased SCr, BUN)
~50% are oliguric
may present with:
-signs and symptoms of dehydration (pre-renal)
-malaise, anorexia, N/V, pruritis (uremia)
-severe abdominal or flank pain (kidney stone?)
-decreased force of urine stream (obstruction)
-cola coloured urine (blood?)
-excessive foaming of urine (protein in urine)
-sudden weight gain, edema

36
Q

What are the risk factors for AKI?

A

anything that decreases blood flow to the kidneys
pre-existing renal dysfunction
drugs account for ~20% of cases

37
Q

How do we typically classify the cause of AKI?

A

based on the location of the problem
1. pre-renal (blood supply)
2. intra-renal or intrinsic (tubules, glomerulus, interstitium, vasculature)
3. post-renal (collecting tubule, ureter, bladder, urethra)

38
Q

What is the most common cause of AKI?

A

pre-renal AKI
aka prerenal azotemia

39
Q

Describe pre-renal AKI.

A

kidney not getting adequate blood supply to filter the blood
-hypoperfusion
kidneys themselves are healthy

40
Q

What are some potential causes of decreased renal perfusion which could cause pre-renal AKI?

A

intravascular volume depletion
-hemorrhage, dehydration, burns, diuretics
decreased effective circulating volume
-HF, cirrhosis
hypotension
-vasodilators, septic shock
decreased glomerular filtration pressure
-ACEI/ARBs, NSAIDs

41
Q

How does intrinsic AKI occur?

A

from direct damage to the kidneys
-due to ischemia, toxins, or disease

42
Q

What are the four main types of intrinsic AKI?

A
  1. acute tubular necrosis
    -endogenous (myoglobin) or exogenous (aminoglycosides), ischemia
  2. acute interstitial nephritis
    -idiopathic hypersensitivity immune reaction to drugs, infection
  3. acute glomerulonephritis
    -post strep antigen-antibody complexes
  4. vascular kidney injury
    -renal artery stenosis, HTN
43
Q

Which type of AKI is the least common?

A

post-renal AKI
-<5% of cases

44
Q

Describe post-renal AKI.

A

obstruction to urinary flow anywhere in the urinary tract
-urethral obstruction
-ureter obstruction
-bladder neck obstruction

45
Q

What are the causes of post-renal AKI?

A

nephrolithiasis (kidney stones)
prostate enlargement
cervical cancer tumors
drugs that crystallize (sulfonamides, acyclovir, MTX)

46
Q

What are the components in the diagnosis of AKI?

A

history
laboratory data
urinary sodium concentration (FEna)
urinalysis
others: renal ultrasound, biopsy

47
Q

What are the expected lab values for a patient with an AKI?

A

increased SCr
increased BUN
acidosis
hyperkalemia

48
Q

Why do changes in SCr lag behind the decrease in kidney function due to AKI?

A

slow accumulation, increased tubular secretion, and increased extra-renal clearance

49
Q

What is FEna?

A

fractional excretion of sodium
-% sodium filtered by the kidneys that is excreted in urine
-not specific to kidney damage (affected by other factors)

50
Q

When would you see FEna decrease? What about increase?

A

decrease: pre-renal AKI
increased: tubular damage

51
Q

What are the goals of therapy for an AKI?

A

prevent further renal injury
minimize extra-renal complications
facilitate recovery of renal function back to baseline

52
Q

What is the treatment of pre-renal AKI?

A

hydration with IV fluids if hypovolemic
-stop diuretics
BP support with vasopressors (dopamine, norepinephrine, vasopressin)
fluid removal in volume overload states with diuretics
stop/hold drugs that impair kidney function/urine flow

53
Q

What is the treatment of intrinsic renal AKI?

A

discontinue offending agent
manage underlying autoimmune disease

54
Q

What is the treatment of post-renal AKI?

A

catheter to restore urine flow
identify and remove obstruction
adequate hydration when giving drugs with potential to crystallize

55
Q

What is the normal range for potassium?

A

3.5-5mmol/L

56
Q

What is the primary route of potassium elimination?

A

kidney
-increased serum K+ seen with AKI and CKD

57
Q

What is the potassium range for mild-moderate hyperkalemia?

A

5.1-7mmol/L

58
Q

What is the potassium range for severe hyperkalemia?

A

> 7mmol/L

59
Q

What is the treatment for mild hyperkalemia due to AKI?

A

may not require therapy or can use Kayexalate (sodium polystyrene sulfonate)
-delayed onset of effect (1hr)
-15 to 60g po BID-QID until K+ normalizes
furosemide IV to increase urinary excretion

60
Q

What is the treatment for severe hyperkalemia due to AKI?

A

medical emergency
calcium gluconate to stabilize myocardium
to drive K+ into cells:
-rapid acting/regular insulin +/- glucose
-sodium bicarbonate IV infusion (if metabolic acidosis)
-salbutamol via nebulizer (if pulmonary congestion)
kayexalate
if refractory: dialysis

61
Q

What is the management of fluid overload due to AKI?

A

diuretics
-furosemide +/- metolazone

62
Q

What is the management of metabolic acidosis due to AKI?

A

sodium bicarbonate IV

63
Q

When do we dialyze in AKI?

A

AEIOU
acidosis
electrolyte abnormalities (hyperkalemia)
toxic ingestions
fluid overload
uremia

PHAR255 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions