Renal & acid base Flashcards by Ashley Long

definitions of AKI

abrupt (48 hrs) reduction of kidney function defined as
-increase in serum creatinine >/= 0.3mg/dL increase
OR
-50% increase from baseline
OR
-decrease in UO < 05mL/kg/hr for > 6 hours

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Oliguria criteria

<400 ml/d

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Nonoliguric

> 400 ml/d

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staging system used more for AKI

modified RIFLE

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↑ of sCR >/+ 0.3mg/dL or ↑ >150-200%
↑ 200-300% from baseline
↑ >300% from baseline

modified RIFLE

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most common form of AKI

prerenal

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prerenal is typically due to

decreaesd renal perfusion

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AKI type:
decreased circulation ( cardiac failure, nephrotic syndrome, cirrhosis, pancreatitis, sepsis, low BP, blood loss, trauma)
fluid loss (n/v/d, fever, increased urination, GIB

prerenal

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AKI type:
Acute tubular necrosis
glomerular disease
interstitial disease

intrarenal

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3 most common reasons for intrarenal AKI

Acute tubular Necrosis
Glomerular Disease
Interstitial Disease
(typically prerenal progresses)

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acute tubular necrosis is caused by

radiographic contrast

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lab needed for rhabdomyolosis

creatinine kinase

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2 main causes of acute tubular necrosis (leading to INTRARENAL AKI)

ischemia and nephrotoxic exposure

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Acute tubular necrosis electrolyte monitoring

↑Mg, ↑Phos, ↑Mg, ↓Ca

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rhabdomyolysis
rapid hemolysis (masssive transfusion rx, hemolytic anemia)

Intrarenal (acute tubular necrosis)

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Strep, rocky mt spotted fever, sarcoidosis and allergic rx to PCN, sulfas, etc. are all types of

intra renal interstitial nephritis (inside kidney)

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eosinophilia (↑) in blood/urine

intrarenal interstitial nephritis

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immune related and inflammatory glomerular lesions account for 5% of AKI

intrarenal glomerular nephritis

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granular casts may be seen in urine in which type of AKI

intrarenal (ATN)

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red cell casts and pyuria are typically seen in what AKI

intrarenal: glomerular

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obstruction is the usual cause of which AKI

postrenal

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stones
BPH
tumors
masses
clots
strictures

postrenal AKI

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muddy brown casts are seen in

ATN

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WBC casts are typically seen with

tubules infection/ pyelonephritis

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RBC casts are seen with

glomerular nephritis

eosinophils are seen with

acute interstitial nephritis

FeNa is only validated in what 2 patients

oliguria or AKI

FeNa can not be used in

patients with diuretics, CKD, obstruction, acute glomerular disease

test of choice for renal artery stenosis

doppler ultrasound for vascular assessment

cysts, stones, masses, and size of kidneys can be seen on

renal US

what CT is preferred for stones

non contrast

MRI is used in place of

CT with contrast

do not over hydrate in what AKI

postrenal

always consult nephrology for

intrarenal AKI

steroids may be useful in what (2)

glomerural nephritis & interstitial nephritis

sepsis, ischemia, and endogenous and exogenous nephrotoxins are causes common causes of

AKI

AKI classifcation

RIFLE criteria stands for

RISK INJURY FAILURE LOSS ESRD

diminished renal perfusion cause dfrom low blood supply to the kidneys WITHOUT nephron damage

prerenal AKA (60% of AKI cases)

ACE, NSAIDS, diuretics may cause which AKI

prerenal

patient is on max pressors and you notice a drop in UO, this could indicate

prerenal AKI due to vasoconstrictive state

intrarenal sites

abrupt decrease in GFR due to tubular cell damage that results from renal ischemia or nephrotoxic injury leads to

INTRARENAL (intrinsic) AKI

long periods of renal azotemia lead to tubular injury resulting in

ATN

*info card ENDOGENOUSIS: hemoglobinuria (hemolysis), myoglobinuria (rhabdo), hyperuricemia, multiple myeloma

ATN

*info sheet EXOGENOUS: aminoglycosides, contrast, ethylene glycol,cyclosporin, heavy metals

ATN

Contrast induced nephropathy is define das

rise in sCreat 25-50% within 48 hrs of IV contrast

Sterp, CMV, rocky mt fever are forms of bacterial pyelo that lead to

acute tubulointerstitial nephritis (intrinsic/intrarenal)

systemic lupus, Sjogrens, sacoidosis, cryoglobulinemia, can all cause

glomerulonephritis (intrinsic/intrarenal)

greatest incidence of recovery and not progressing to ESRD

post renal

conditions that cause obstruction of urinary flow and consequently a decrease in GFR

post renal

never insert a foley into

a patietn with a positive urethrogram

if there is trauma damage to a kidney who do you consult

UROLOGY (not nephro)

3 categories of CKD incidence in USA

>65 y/o female > male AA, hispanic, asian, caucasion (in order)

metalic taste in the mouth, pruritus, brittle nails, SOB, ED are all s/s of

CKD

your patient with CKD comes in with an acutely elevated BUN you should be suspicious of

#1 GIB #2 dehydration

elevated sCreat, low GFR but BUN is really low could be related to

liver disease/ hepatorenal syndrome

ACUTE elevation of creatinine could likely be

toxin or drug induced.

COPD, emphysema, PNA, and asthma typically cause what acid base imbalance

resp acidosis

hyperventilation, fever, pain, anxiety, high altitude typically cause what acid base imbalance

resp alkalosis

shock, DKA, AKI, diuretics, sepsis typically cause what acid base imbalance

met acidosis

excess base, antacids, gastric suctioning, and vomiting typically cause what acid base imbalance

met alkalosis

only type of hyponatermia that requires treatment

HYPOTONIC HYPONATERMIA

hyperlipidemia is a common cause of what electrolyte imbalance

isotonic hyponatremia

hyperglycemia, mannitol and radiocontrast is a common cause of what electrolyte imbalance

hypertonic hyponatermia

what lab do you use to determine cause of hypotonic hypovolemia hyponatermia

urine sodium <10: dehydration, D/V >20: diuretics, ACE, steroid deficiency, etc

correction dose/tx for acute hypernatremia

correct no faster than 1-2mEq/L/hr (0.5 for chronic)

beer, SIADH, diuertics, CKD are all causes of what electrolyte imbalance

hypotonic euvolemic hyponatermia

what serious electrolyte abnormality must you always correct with Na if needed

hyponatermic tx with seizures

- fluid restriction <1000ml/24 - 100 ml 3% over 10m; repeat if needed; - 3% @ 0.5-2ml/kg/hr

MAX CORRECTION OF LOW NA

12 mEq/L/24 OR 20mEq/L/48 no more than 4-6mEq

fluid options for mild, oder, sev volume depletion with hypernatermia

mild: D5W mod: 1/2 NS, free water sev: 9%NS then 1/2 NS

metabolic disease, catecholamine excess, and IV insulin for DKA all cause what electrolyte disturbance

hypoKalemia

Action of Glomerulus & drug at site

Filters plasma Acetazolamide

Action at proximal convoluted tube

bicarb, sugars, & drugs re-absorbed

Action and drugs at ascending loop of henle

Site for loop diuretics

drugs at descending loop of henle

Osmotic diuretics (mannitol)

Action & drug site at Distal Convoluted tubule (Tip ** last stop to fix everything before collecting duct)

Reabsorption of water, K+ acid/base balance effected by ADH and aldosterone. Site of Action for Thiazides – HCTZ

Action & drug site for Collecting Duct

Last step in water and Na+ balance. Site of action for Potassium Sparing diuretic - Spironolactone

Acute glomerual injury, ATN, acute acute interstitial nephritis & AKI may have what in urine

EOSINOPHILS

Renal epithelial cells in urine indicate what

Tubular injury

If the glomerulus is not working what lab will be abnormal

High creatinine ( because it is the only place in the kidney where it is absorbed)

Stage 1- kidney damage

GFR > 90% (normal)

GFR 60-89

Stage 2 CKI

GFR 45-59

Stage 3 a CKI

GFR 30-44

Stage 3b CKI

GFR 15-29

Stage 4 CKI

GFR < 15

Stage 5/ kidney failure

An acute increase in BUN with CKD may indicate

Acute GIB

Acute decrease in BUN with CKD may indicate

Liver disease

Edema/weeping, high lipids, hypoalbuminemia, proteinuria, increase bleeding/clotting all could be signs of

Nephrotic syndrome

When BUN/Creat rise tighter it’s called 15:1 signifying

INTRA renal failure

Nephrotic Meds “cake man c”

Cyclosporine - ACE - keppra - erythromycin - metformin - amphotericin - NSAIDS - contrast

Urinary casts: red cell

Glomerulonephritis Vasculitis

Urinary casts: white cell

Acute interstitial nephritis

Urinary casts: fatty

Nephrotic syndrome

Urinary casts: muddy brown

ATN