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"unknown" etiology of disease - CORRECT ANSWER: idiopathic and cryptogenic
3 main systems regulate total body sodium - CORRECT ANSWER: 1. RAAS System -
Decreased renal perfusion is sensed by the juxtaglomerular cells in the kidney resulting
in increase renin secretion and activation of RAAS. Angiotensin causes vasoconstriction
and stimulates the release of aldosterone - promotes sodium retention.
2. Natriuretic Peptide System - Volume receptors in great veins and atria are sensitive
to small changes in venous and atrial filling. Increased atrial filling results in release of
ANF/ANP and BNF/BNP which promotes sodium excretion.
3. Pressure receptors in the aorta and carotid are stimulated by volume depletion and
activate sympathetic nervous system - renal retention of sodium.
4 common mechanisms of cell injury and death - CORRECT ANSWER: 1. ATP
Depletion
2. Oxygen and oxygen-derived free radicals
3. intracellular calcium and loss of calcium state
4. defects in membrane permeability
4 most common mechanisms of edema - CORRECT ANSWER: 1. Increased capillary
hydrostatic pressure
2. Decreased capillary oncotic pressure
3. Increased capillary membrane permeability
,4. lymphatic channel obstruction
5. sodium and water retention
4 Phases of fluid therapy - CORRECT ANSWER: Rescue - fluid admin for immediate
treatment, life threatening
Optimization - adjust fluid type, rate, and amount
Stabilize - neutral or slight neg fluid balance
De-escal - decrease admin and mobilize excess fluid balance
5 essential components of pathophysiology - CORRECT ANSWER: 1. Etiology (the why
of disease, the reason for it)
2. Epidemiology (risk factors and distributions in populations, incidence and prevalence
in disease)
3. Pathogenesis (disease mechanisms; the sequence of events that occurs between the
stimulus event and the manifestations of the disease)
4. Clinical Manifestations (signs, symptoms, diagnostic criteria)
5. Outcomes (cure, remission, chronicity, death)
Acidemia - CORRECT ANSWER: Increase in hydrogen or loss of a base
Acute Kidney Injury - CORRECT ANSWER: Increase creatinine by 0.3mg/dl or more
within 48 hours
Increase to 1.5 or more from baseline within the past 7 days
UO < 0.5ml/kg/hr >6hours
Non-oliguria >500ml/day
Oliguria <500ml/day
Anuria <100ml/day
,Acute Tubular Necrosis - CORRECT ANSWER: damage to the renal tubules due to
presence of toxins in the urine or to ischemia (aminoglycoside, NSAIDs, CT contrast)
aging is thought to be the result of: - CORRECT ANSWER: 1. faulty DNA repair
mechanisms ahd metabolic (free radical) damage
2. reduced antioxidants
AKI Clinical Course - Diuretic Stage - CORRECT ANSWER: -1 to 2 weeks
-self limiting as kidney tubular patency restored
-urine concentration, not returned
-continued healing, kidneys begin regaining lost function
-at risk for fluid volume deficit
-monitor daily weights, VS, I's and O's, assess for edema, skin turgor, mucous
membrane, hypokalemia
AKI Clinical Course - Initiating Stage - CORRECT ANSWER: -Hours to days
-S/S of impairment
-Etiology is investigated
-Tx plan for reversal
-Endocrine function not affected
AKI Clinical Course - Oliguric Stage - CORRECT ANSWER: -5 to 15 days
-Healing may begin
-Tubule cell regen. but destroyed basement membrane replaced with scar tissue
-Tubules may be clogged with inflammatory products
-Decreased GFR
-Decreased urine production
, -Decreased kidney clearance
-If persists, endocrine functions are alt.
-hyperK
-GI bleed
-infection
AKI Clinical Course - Recovery Stage - CORRECT ANSWER: -Months to years
-Scar tissue replaces basement membranes
-Nephrons become patent
-Tubular cells regenerate
-Functional loss not always clinically significant
-Urine osmo increases
-Urine volume stability
-Uremia resolves
-Pt education
Alkalosis - CORRECT ANSWER: Decrease of hydrogen ion or increase in base
Anion gap - CORRECT ANSWER: Difference between total cations in the ECF and total
anions in the ECF
Cations - sodium and a little potassium
Anions - chloride and bicarb
Normal anion gap is 10 to 14
Anion gap calculation - CORRECT ANSWER: Na - (Cl + HCO3)