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Clin Med > Renal: AKI and CKD > Flashcards

Renal: AKI and CKD Flashcards

1
Q

Definitions for AKI (3)

A
  1. abrupt onset within 48 hours
  2. incr in creatinine by >0.3mg/dl OR >50% from baseline within 48 horus –>ASSOC WITH INCR MORTALITY
  3. oliguria <0.5mg/kg/hr for >6 hours
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2
Q

incidence of AKI in hosp pt

-ICU PT?

A

10-20%

ICU= 50%

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3
Q

who is at risk for AKI

A
  1. elderly >75 YO
  2. atheroscleotic dz—PVD
  3. heart and liver failure
  4. DM or other metabolic dz
  5. drug
  6. hemodynamic complications–hypotension, sepsis
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4
Q

PU is an indicator of?

-assc with?

A
  1. inflammation!!!!

A/W–>LV dysfunction, MI, stroke

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5
Q

Pre-Renal AKI

  • characterized by?
  • etiologies
  • DX—-findings in lab work, UA, urine sed
  • tx
A

charac by DECR RENAL PERFUSION WITH NEPHRONS STILL STRUCTURALLY INTACT–caused by ineffective intra-arterial volume sensed by baroreceptors

ETIOLOGIES

  • decrease intravasulcar volume
  • decr CO
  • decr effective ciruclating volume
  • impaired autoregulation
  • *hypovolemia–>GI losses (V/D), diuretic tx, blood loss, third spacing vie burns
  • *hypotension–>CHF, MI, tampdonade
  • *aff arteriole vasoconstriciton–NSAIDS, iv contrast
  • *eff arteirole constriction–ACEI, ARB
  • ascites
CM and history findings 
-vomiting 
-diarrhea 
-diuretic use 
-hemorrhage 
-burns 
-dehydration 
-cardiac dz hx 
PE 
*wt loss 
*orthostatis hypotension 
*tachycardia 
*poor skin turgor 
*dilated neck veins 
*S3 
*rales 
*periph edema 
*ascites 
*caput medussa 
*spider angiomas

DX

  • evidence of water and electrolyte conservation
    1. INCR BUN:Cr >20:1 ratio both will be incresing
    2. fractional excretion of NA–>FENA–> <1% and urine sodium <20 **
    3. oliguria
    4. Concentrated urine:
  • HIGH urine SG >1.020
  • increased urine osmolarity >500 aka increased

TX

  1. remove any offenidng meds
  2. CHF–> opitmize CO, give nitrates, ACEI, diuretics, inotropic agents
  3. Sepsis–> NaCL NSS, pressors
  4. Cirrhosis–>lasix and spironolactone, paracentesis can also be useful

**also focus on volume repletion and renal perfusion

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6
Q

general s/s of AKI

A 
hyperK 
N/V 
HTN 
Pulm edema 
Ascites 
Asterixis 
Encephaloapthy 
periph edema
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7
Q

how much dopamine causes increased renal flow

A

low doses

0.5-2 mcg/kg/min

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8
Q

ATN

-clinical features

A
  • h/o hemorrhage, severe hypotension
  • nephrotoxic drugs—NSAIDs, ABx, chemo
  • exposure to contrast dye
  • prolonged prerenal azotemia
  • hemolysis—-fever, transfusion rxn
  • ingestions—–ETHYLENE GYCOL, ODs
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9
Q

list the major types/causes of intrinsic AKI

A
  1. ATN
  2. Acute interstitial nephritis
  3. glomerulonpehritis
  4. microvascular causes: HUS and TTP
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10
Q

Acute interstitial Nephritis causes

A
  1. DRUGS
    * ABX: PCNS, cephalosporins, cipro, sulfas, antivirals
    * NSAIDS
    * GI–>COX-2 inhibs, 5-Aminosalicylates
    * allopurinol
    * chinese herbs
    * heavy metals
  2. Systemic diseases
    * Mult myeloma
    * leukemia
    * lymphoma
  3. Autoimmune dz
    * SLE
    * sarcoidosis
    * sjorgrens
  4. Tubulointersitital nephritis/uveitis
  5. infections
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11
Q

acute intersitial nephritis

  • cm
  • etiology—MC?
  • timing of s/s
  • labs
  • tx
A

MC etiology=drug hypersensitivity (70%)

  • inections
  • idiopathic
  • autoimmune

CM =variable +/- arthralgias
s/s usually 7-10 days after drug ingestion

TRIAD

  • Fever
  • Serum Eosinohphilia
  • maculopapular rash
  • **rarely seen together tho

LABS

  • non-nephrotic PU
  • WBC casts are pathognomonic
  • urine eosinophils on Wright’s or Hansel’s stain

TX

  • remove offending agent
  • most recover kidney function within 1 year
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12
Q

TTP

  • cause
  • labs
  • tx
A

reduced activitty of Von Willebrand factor—cleased protease on ADAMTS13

  • *thrombocytopenias
  • small vessel thrombi—-lots of platelts
  • microangiopathic hemolytic anemia

LABS

  • very elevated LDH
  • incr bili
  • negative coombs
  • DIC in severe

TX=plasma, steroids, Ritixumab

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13
Q 
Contrast Induced Nephropathy
-define 
rf 
-prevention 
-what happens if pt has a gfr <30
A

*****0.5mg/dl rise or 25% increase of Creatinine 48hrs AFTER contrast given

RF

  • renal insuff GFR >50
  • DM
  • CHF
  • urgent
  • intra-aortic balloon pump
  • large volumes of dye
  • age >80
  • dehydration

prevention

  • SALINE
  • low-osmolality media
  • N-acetylcysteine
  • mesure CR 48 hrs after dye given
  • consider mri wtihout gadolinum

**in patients with renal dz (GFR <30)—association with NEPHROGENIC FIBROSIS—which is irreversible

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14
Q

Nephrogenic Systemic Fibrosis

  • what causes it
  • patho
  • areas it causes
A

GADOLINIUM CONTRAST DYE

  • non-reversible
  • pt with gfr <30

PATHO: fibrosis of fascia forming coalescnece of erythematous plaques that form a “peau d’orange” pattern

affected areas=lungs, pleural cavity, diaph, heart, dura mater, muscle

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15
Q

Renal Atheroembolic Dz

-what can cause this

A

Cardiac cath—-atheromatous debris and emboliation of cholesterol–can trael to retinal, cerebral, skin, renal (ARF), or the gut

**Cr wont improve with IV hydration

***dx of exclusion– must do renal biopsy

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16
Q

Post renal azotemia

  • etiology
  • CM
  • dx
A

etiology

  • urinary flow obstruction–>leads to renal insuff
  • *anatomic
  • *ureteric obstruction–BILATERAL STONES, tumor, stricutre
  • *bladder outlet syndrome
  • *tubular—myeloma casts, crystals, drugs

CM
*Hx of BPH
*usually asympto—– change in urine OP…HTN.. rarely pain
PE: distended bladder, pelvic mass, large prostate

LABS:

  • incr CR usually assoc with bilateral kidney obstruction —
  • US: inital imaging choice
  • BLAND sedement
17
Q

Hepato-renal syndrome
-what is it
-define it in terms of GFR
UA results

A

profound renal vasoconstriction despite normal kidneys
-only improves with liver transplant

GFR: creatiine >1.5 mg or GFR <40

UA
*oliguira <500 
*NA <10 Meq/L 
*FENA <1 
*urine osm >>> serum osm 
RBCs>50

serum NA < 130
BLAND URINE *****

18
Q

indications to HD

A 
A-->acidemia metabolic 
E-->electrolytes--HYPERK 
I-->ingestion of drugs/ischemia 
O-->overload fluid 
U -->uremia
19
Q

one of the most important prognostic factors for CKD

A

degree of PU—tells us response to tx

20
Q

stages of CKD

A

stage 1: kidney damage with normal GFR (>90) ****
stage 2: mild decr GFR 60-89
stage 3: moderate decr in GFR 30-59
stage 4: severe decr in GFR 15-29
stage 5: kidney failure with GFR <15—–not on dialysis YET ****
stage 6: ESKD– gfr <15 ON dialysis

21
Q

CKD on US

A

hyperechoic, small kidney

22
Q

Uremic Syndrome

-when does this ocur

A

when GFR <10 in CKD

  • acidosis unresponsive to medical tx
  • hyerpK unresponsive to medical tx
  • volume overload refracrtory to diuresis
  • uremic pericarditis can occur

CM of uremia

  • n/v
  • fatigue
  • malaise
  • metalic taste
  • hiccups
  • ams
  • irritabilit y
  • muscle cramps
  • easy bruising
  • fluid overload
  • encephalopathy
  • pericarditis

Clin Med (52 decks)

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