Advanced Med-Surg Review

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PART 1
Exam #1 Review

Renal Overview:

* Renin-angiotensin aldosterone system (RAAS) regulates renal blood flow.

* ACUTE RENAL FAILURE -rapid decline in renal function with progressive azotemia.

* AZOTEMIA An excess of metabolic waste products in the blood Urea Nitrogen and Creatinine

* OLIGURIA Urine Volume less than 400CC/24 hours for a non-trauma, non-surgical adult.

* ACUTE TUBULAR NECROSIS (ATN) Clinical syndrome of ARF secondary to ischemia or toxic injury to the renal tubules

* BUN and Creatinine DO NOT START TO RISE until GREATER than 60 % loss of renal function= Failure.

* BUN and Creatinine DO NOT GET HIGH until 90% loss of renal function = Failure.

* 24 Hour Creatinine clearance = good early indicator of renal Function (GFR).

* Elevated levels BUN/Creatinine are considered to be the “hallmarks” of acute renal failure.

* Creatinine Normal value 0.5 - 1.0 mg/dl

* In general – Creatinine is 1/10 of BUN

Acute Renal Failure
* Description: Sudden, reversible cessation of renal function associated with an identifiable toxic or ischemic trauma or obstruction - onset - hours to days.

* Risk Factors:
* Advanced Age: GFR decline by 1ml/min/year after age 40
* Renal Blood Flow 10% per decade
* Decreased muscle mass – decreased production Cr; Vit D * Diabetes Type I or II
* Severe HTN or peripheral vascular disease
* Preexisting CKD or proteinuria
* CHF
* Cirrhosis
* NSAIDS, ACEi, vasodilators
* Sepsis

Pathophysiology:

* Depressed RBF kidneys vulnerable to further insults - iatrogenic renal injury most common

* Common iatrogenic combinations:
* Preexisting renal disease, radio contrast agents, aminoglycosides, atheroembolism, or cardiovascular surgery * ACE inhibitors with diuretics
* NSAIDs
* Hypovolemia

* Recovery dependent upon restoration of RBF
Once RBF restored - remaining functional nephrons increase their filtration and eventually hypertrophy to compensate for nephrons damaged GFR recovery dependent upon the size of this remnant nephron pool.

* Causes:

* (4)phases Intrarenal ARF:
ONSET
OLIGURIC
DIURETIC
RECOVERY

* Onset Phase
* Time from the onset of injury through the cell death
* Phase can last from hours to days and is characterized by: * Renal flow at 25% of normal
* Oxygenation to the tissue at 25% of normal
* Urine output at 30 ml (or less) per hour
* Urine sodium excretion greater than 40 mEq/L.
* In this phase only 50% of the patients are noted to be oliguric. * With prompt treatment, irreversible damage can be prevented * Mild lethargy
* Mild malaise

* Oliguric/Anuric Phase
* Occurs within 48 hours of insult – lasts 1-2 wks.
* Urine output is < 400ml/day
* Nitrogenous waste accumulate
* BUN rises up to 20 – 25 mg/dl/day
* High BUN – VERY irritable to all tissues
* Creatinine 1-2mg/dl/day
* Na
* Fluid overload, acidosis & electrolyte imbalance - K+ >6 EKG ; dysrhythmias * characterized by:
* GI: n/v, gi bleed
* Neuro: drowsiness, confusion irritability, change in loc, seizures, coma * Cardio: palpitations, htn
* Skin: edema, itching, skin rash/lesions
* Respiratory: dyspnea, kussmal’s respiration, resp compensation for metabolic acidosis * Pericardial friction rub
* Pulsus paradoxus (heart sounds on inspiration that cannot be palpated radially). * Fever
* Chest pain – pericarditis - friction rub
* Crackles upon lung auscultation (due to fluid overload) * Shortness of breath (due to fluid overload)
* Jugular vein distention (due to fluid overload)

* Diuretic phase
* Good sign – source of obstruction has been removed but the residual scarring; edema of the renal tubules remains. * Gradual/abrupt return to glomerular filtration and leveling of BUN and creatinine signal diuretic...
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