RENAL Flashcards
WHAT EXITS THE HILUS?
RENAL ARTERIES, VEINS, NERVES, LYMPHATICS AND URETERS.
WHERE DOES FILTRATION TAKE PLACE?
THE GLOMERULUS
WHAT ARE THE 4 PARTS OF THE NEPHRON?
- GLOMERULUS
- GLOMERULAR (BOWMANS) CAPSULE
- RENAL TUBULE (PCT, LOOP OF HENLE, DCT)
- COLLECTING DUCT
WHERE DOES FILTRATION TAKE PLACE AND WHAT GETS FILTERED?
IN GLOMERULUS.
FILTERS…SMALL MOLECULES IE: IONS H2O GLUCOSE UREA
MACROMOLECULES (PROTEIN) IS UNTOUCHED.
WHAT HAPPENS IN THE PCT?
THE BULK OF FLUID/CONTENTS ARE REABSORBED. OSMOTIC GRADIENT STAYS THE SAME.
WHAT DOES THE LOOP OF HENLE DO?
REABSORB WATER CHLORIDE AND SODIUM.
DESCENDING LIMB: ESTABLISHES A COUNTERCURRENT BY LETTING BOTH SODIUM AND H2O OUT OF LUMEN.
ASCENDING LIMB: IMPERMEABLE TO H2O SO WATER STAYS IN LUMEN AS MORE NA IS PUMPED OUT CREATING A HYPOOSMOTIC LUMEN.
WHAT IS HAPPENING IN DCT?
NA REABSORBED CONTROLLED BY ALDOSTERONE
K SECRETED
PROTONS SECRETED
H2O PERMEABILITY CONTROLLED BY ADH
WHAT IS NET FILTRATION PRESSURE AND HOW DO YOU CALCULATE IT?
10 MM HG
BLOOD PRESSURE (HYDROSTATIC) - PROTEIN PRESSURE IN PLASMA (ONCOTIC) AND FLUID PRESSURE IN BOWMANS CAPSULE.
55-(30 + 15) = 10
WHAT MAP DOES RENAL BLOOD FLOW REMAIN CONSTANT AT?
50-150
WHAT 3 THINGS REGULATE GFR?
FILTRATION PRESSURE (BP AND RESISTANCE)
TUBULOGLOMERULAR FEEDBACK.
ANS/HORMONES (ACE/PROSTEGLANDIN)
WHAT IS GLOMERULAR TUBULAR BALANCE?
WHEN THERE IS A DECREASE IN GFR THERE IS A DECREASE IN TUBULE FLOW.
WHAT MAJOR HORMONES CONTRIBUTE TO GFR?
INCREASE GFR: ANP, NO, PROSAGLANDIN E2. ALL VASODILATE.
DECREASE GFR: ANGIOTENSIN 2, ENDOTHELIN. VASOCONSTRICT.
WHAT DOES SNS STIM. DO TO GFR?
DECREASE GFR BY VASOCONSTRICTION. THIS HAPPENS DURING EXERCISE AND HEMMORHAGE.
WHAT DOES ERYTHROPOIETIN DO?
STIM. RBC PRODUCTION. PRODUCED IN KIDNEYS….CRF PT HAS DECR. ERTYHROPOETIN AND DECREASED HGB.
WHAT DOES ALDOSTERONE DO?
PRODUCED BY ADRENALS AND NA/H2O RETENTION. RELEASE REGULATED BY RENIN-ANGIOTENSIN.
WHAT DOES ADH DO?
WITH ADH….TUBULAR PERMEABILITY INCREASED AND WATER REABSORBED. TRIGGERS FOR ADH=STRESS, PAIN, HYPOTENSION.
DO PROSTAGLANDIN AND THROMBOXANE A2 HAVE OPPOSING EFFECTS?
YES.
PROSTEGLANDIN VASODILATES AND INHIBITS PLT AGGREGATION.
HOW DOES VIT D AFFECT CALCIUM?
VIT D IS NEEDED TO ABSORB CALCIUM. RENAL PTS CANT DO THIS. LOW CA.
WHAT IS SPASTIC BLADDER DYSFUNCTION?
FAILURE TO STORE.
WHAT IS FLACCID BLADDER DYSFUNCTION?
FAILURE TO EMPTY.
WHAT ARE THE 4 PHASES OF ARF?
INITIATING=INSULT TO S/S.
OLIGURIC= U/O < 400 /24 HRS.
DIURETIC = KIDNEYS INABILITY TO CONCENTRATE URINE. LOW GFR. LABS BEGIN TO NORMALIZE.
RECOVERY = BEGINS WHEN GFR INCREASES.
WHAT IS THE #1 CAUSE OF CRF?
DIABETES
HOW MANY NEPHRONS NEED TO STOP WORKING BEFORE S/S OF KIDNEY DISEASE APPEAR?
80%
DIALYSIS IS NEEDED WHEN 90% ARE LOST.
WHAT IS THE FIRST SIGN OF DIABETIC NEPHROPATHY?
PROTEIN IN THE URINE. BASEMENT MEMBRANE THICKENS. GLOMERULUS ENLARGES.
WITH RENAL PTS WHAT DO YOU NEED TO THINK ABOUT RELATING TO BP?
THEY ARE INTRAVASCULARLY DRY SO VASODILATION FROM ANESTHESIA CAUSES BP TO BOTTOM OUT. CONSIDER ETOMIDATE FOR INDUCTION.
WHAT ARE SIDE EFFECTS OF DIALYSIS?
HYPOXEMIA, HYPOTENSION, MUSCLE CRAMPS
ARE RENAL FAILURE PREDISPOSED TO BLEEDING?
YES. DECREASED PLT FXN. CONSIDER DDAVP AND CRYO.
WHAT IS MOST EFFECTIVE TREATMENT FOR HYPERKALEMIA?
DIALYSIS. FOR K > 6.
ALSO: BICAR, HYPERVENTILATE, INSULIN/GLUCOSE, CALCIUM.
S/S OF HYPERMAGNESEMIA?
HYPOTENSION, HYPOVENT, COMA.
MUSC. RELATORS POTENTIATED.
WHAT IS NORM BUN/CR?
BUN: 10-20. LATE INDICATOR OF RENAL DX.
CR: 0.7-1.5. MOST COMMONLY USED MARKER. INVERSELY RELATED TO GFR.
WHAT IS THE MOST RELIABLE ASSESSMENT TOOL OF RENAL FX?
CREATININE CLEARANCE. NORM= 95-150
WHAT TO DO PREOP FOR A RENAL PT?
LABS: LYTES MG PHOS. CBC. TAKE HOME MEDS ENSURE NPO....DELAYED GASTRIC EMPTYING. GET CARDIAC CLEARANCE. GOOD VASCULAR ACCESS. LAST DIALYSIS.
IS REGIONAL OK FOR RENAL PTS?
YES AS LONG AS COAGS ARE NORMAL WITH ADEQUATE BP.
