ACUTE v. CHRONIC RENAL FAILURE, CALCIUM/PHOSPHORUS D/O Flashcards
(40 cards)
acute renal failure
SUDDEN loss of kidney func resulting in
- lack of acid-base maintenance
- abnorm fluid and electrolyte managment
- loss of ability for excretion nitrogneous WASTE
ARF aka AKI (acute kidney injury)
ARF- Signs and symptoms
SYMPTOMS
- uremia: n/d, malaise, alt mental
- perfusion defects: edema (central or general), dizzy
- electrolyte abnorm: abd pain/ileus
SIGNS
- pericardial effusion (friction rub)
- electrolyte abnorm: arrythmias
- platelet dysfunc: bleeding
- neuro findings
ARF
- pre renal BUN:creatinine ratio
BUN:creatinine > 20:1
- due to inc urea reabsorp
ARF
- pre renal causes
MC CAUSE of ARF
due to renal hypoperfusion
- HYPOVOLEMIA, HYPOTENSION, LOW CO!
- volume depletion (dehydration, GI loss, hemorrhage)
- vasc resistance (sepsis, anaphylaxis, afterload reducing meds/ACEi, NSAIDs, renal artery stenosis)
- low CO (HF, PE, tamponade, ventilator effect pos end pressure)
ARF
- renal (intrinsic) causes
- refer when?
- admit to hospital?
- acute tubular necrosis
- interstitial nephritis
- glomerulonephritis
refer: nephro if signs present for 1-2 weeks no acute uremia, urologist if signs of urinary tract obstruction
admit to hospital: sudden loss of func + abnorm that cannot be safely managed outpt
ARF
- post renal causes
LEAST COMMON cause, easily reversed
- urethra obstruction
- bladder dysfunc/obstruction
- ureter obstruction B/L or unilat if single kidney
- BPH in men
ARF
- post renal findings
- anuria or freq but small volume voids
- suprapubic pain (distended bladder)
- palpable or percussed distended bladder or enlarged prostate
- high BUN:creatinine ratio
- US can find location of obstruction
ARF
- post renal tx
- bladder cath, allow release of urine
- correct underlying cause
- saliuresis and diuresis
loop diuretic lose Na and Ca
ARF clin criteria staging/prognosis
- RIFLE/AKIN
risk, injury, failure
RISK: 1.5x inc in serum creatinine
INJURY: 2-3x inc in serum creatinine
FAILURE: decline of urine output to <0.3 mL/kg/hr for 24hr OR anuria for 12 hrs
ARF stage based management
- high risk
- stage 1
- stage 2
- stage 3
ALL: discont nephrotoxic agents, ensure vol status and perfusion pressure, hemodynamic monitoring, serum creatinine and urine output monitoring, no radiocontrast dyes
1+2+3: diagnostic workup
2+3: durg dosing changes, ICU admission
3: renal replacement
ARF contrast induced injury
changes in kidney func after administrating intravasc contrast media
- prevent byscreening for risk
- hx of prior kidney ds, fluid status/dehydration, DM (on metformin?), CHF/vasc ds (perfusion ability), hx gout, nephrotoxic med use, recent exposure to iv contrast
ARF
- contrast induced injury RISK REDUCTION
- non pharm vs pharm
NON pharmacologic
- use lowest dose IV contrast, adequate hydration, dec exposure to nephrotoxic meds
PHARMACOLOGIC
- IV volume expansion w isotonic saline or soidum bicarb in high risk pts (renal protective)
- oral n-acetycysteine given prior (allergic rxn may occur)
- avoid diuretic use
ARF tx
- when to do renal replacement therapy v dialysis
- when to discont dialysis
- initiate renal replacement therapy if life threatening fluid, electrolyte, or acid-base abnorm
- dialysis to maintain homeostasis and prevent further injury/permit renal recovery, allow tx of underlying condition
DISCONT when patient able to maintain own ability (trials)
chronic renal failure (CRF) vs. CKD
- end stage renal ds?
CKD: gradual, progressive loss of ability to excrete wastes, concentrate urine, and conserve electrolytes
CRF: continuing irreversible reduction in nephron number (correspond to CKD stages 3-5)
end stage renal ds (ESRD): stage 5, dialysis dependent
CKD
- pre renal causes
hypoperfusion
- renal artery stenosis (fibromuscular dysplasia)
- extrinsic compression
- dec renal perfusion pressure from CHF
- dec oncotic pressure (cirrhosis, nephrotic syndromes)
CKD
- intra renal causes
intrinsic renal vasc ds
- renal artery stenosis
- glomerulosclerosis
- recurrent thromboembolic ds
glomerular ds
- nephritis/nephrotic syndromes
tubular and interstitial ds
- nephrocalcinosis due to hypercalcemia
- systemic lupus erythematosus (SLE)
- polycystic kidneys ds (mc genetic cause)
- autoimmune
CKD
- post renal causes
chronc obstruction
- BPH, neoplasm, calculi/tumors/clots, hyperplasias, strictures, inflamm
MC CAUSES CKD
- diabetic glomerular ds
- hypertensive nephropathy (primary glomerulopathy w HTN, vasc and ischemic renal ds)
- chronic glomerulonephritis
pathophys of CKD mechanisms of damage
intiating phase- nephron mass loss(first insult to kidneys)
- immune complexes (deposit in kidneys and cause inflamm)
- HTN/DM
progressive- maladaptive compensatory changes
- RAAS activation
- hyperfiltration of remaining viable nephrons
- release vasoactive hormones, cytokines, growth factors
- hypertrophy and sclerosis
- reduce renal mass more
progressive leads to fibrosis and inflamm—more scarring and nephron loss
sodium and water homeostasis
- ECFV expansion vs depletion
extracell fluid expansion
- dietary sodium intake>urinary sodium excretion = fluid overload
- tx: salt/fluid restrict, +/- diuretics, dialysis if not responsive
extracell fluid depletion
- extrarenal salt/fluid loss–> impaired salt/water reabsorp = depletion
- common cause acute on chronic RF
- excess free water consumption>urinary ree water excretion = hyponatremia
CKD issue- potassium homeostasis
- effects
- exacerbation
- management
- dec GFR–> dec ability to excrete potassium–> HYPERKALEMIA
effects- imapired neuromusc transmission (muscle weakness, arrhythmias), malaise
exacerbation: inc intake, transcellular shift, dec excretion
management: limit dietary intake, avoid meds that cause it, dialysis if ECG changes
CKD stage 4/5- metabolic acidosis
result in osteoporosis, protein catabolism, muscle wasting
tx- sodium bicarb PO daily
secondary hyperparathyroidism due to renal ds
hematologic effects of CKD
anemia
- primary cause: EPO def
- other cause: iron def, anemia of chronic ds, BM fibrosis
tx: recombinant EPO
impaired platelet function
- primary cause: uremia (dec activity platelet factor 3, abnorm aggregation, prolonged bleeding time)
impaired immune function
- primary cause: uremia (WBC suppression)
- other factors: acidosis/malnutrition
calcium and phosphorus d/o
calcium/phosphate homeostasis dysfunction
- how does it present (clinical manifestations)
CALCIUM effect
vit D is necessary for calcium absorption
- in kidney dysfunction, we are unable to inactive form into active, therefore not absorbing calcium from the gut and causing hypocalcemia
hypocalcemia–> seen in bone manifestations, myocardial dysfunc, tetany (spasm)
