Renal System O1 Word Scramble
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Question | Answer |
2 most common causes of chronic kidney disease that predispose to development of acute kidney injury in setting of other exposures | Diabetes and hypertension |
"I am not making much urine" goes under which section of a note | Chief complaint |
By which mechanism does an ACE inhibitor increase risk of AKI | It blocks the conversion of Angiotensin I to Angiotensin II which inhibits vasoconstriction of the efferent arteriole which is needed to maintain GFR in decreased blood pressure or volume |
Effect of NSAID on Renal Blood flow | Vasoconstricts afferent arteriole |
Effect of ANP on Renal Blood flow | Vasodilates afferent arteriole |
Effect of Prostaglandin on Renal Blood flow | Vasodilates afferent arteriole and vasoconstricts efferent arteriole |
Effect of Angiotensin II on Renal Blood flow | Vasoconstricts efferent arteriole |
Effect of Norepinephrine on Renal Blood flow | Vasoconstricts efferent arteriole |
Effect of ACE inhibitor on Renal Blood flow | Vasodilates efferent arteriole |
Rash in a kidney patient can be indicative of | Glomerulonephritis or autoimmune (lupis) |
Frothy urine is indicative of | Proteinuria |
Tea colored urine is indicative of | Hematuria or rhabdomylosis |
Tachycardia, hypotension, reduced skin turgor with tenting and syncope are all findings supporting | Volume depletion |
Definitive way of diagnosing post-renal causes | Ultrasound |
Increased Lactic acid levels are due to | Ischemia/hypoperfusion |
Lack of blood and protein in the urine points to | Pre-renal causes |
In pre-renal disease, a decreased flow leads to increased reabsorption of | BUN |
A BUN:CR for pre-renal etiologies | >20 |
Decreased pressure and flow lead to activation of | RAAS |
Urine sodium levels for pre-renal etiologies | <20 |
Explain why urine sodium levels are low in pre-renal disease | In cases of depleted volume, Kidneys will activate RAAS and maximally reabsorb sodium and therefor increasing water retention. This will happen as long as TUBULES ARE INTACT |
RBCs or RBC casts are indicative of | Intrinsic glomerular disease |
"Muddy brown" granular casts are indicative of | Intrinsic Tubular disease |
WBCs and WBC casts with a negative urine culture are indicative of | Intrinsic Interstitial disease |
High BUN:CR and Low Na+ points to | Pre-renal disease |
Low BUN:CR and high Na+ points to | Intrinsic renal disease |
High BUN:Cr and high Na+ points to | Post-renal disease |
Pre-renal etiology is due to | True volume depletion or medications affecting renal blood flow |
Plan for patient with pre-renal causes | IV fluid hydration and holding potential offending medications |
Anuria | Absence of urine formation (<100 ml/day) |
Oliguria | Scanty urine production (<400-500 ml/day) |
Normal urine production | >500 ml/day |
Nephrotoxic | Toxic to renal cells |
Nephritic | Relating to or suffering from nephritis |
Nephritis | Inflammation of the kidneys (RBC in urine) |
Nephrotic | Relating to, caused by, or similar to nephrosis |
Nephrosis | Damage to renal tubular epithelium/glomerular basement membrane (protein in urine) |
General cause of prerenal disease | Less fluid is delivered to the kidneys for filtration |
General cause of intrinsic renal disease | The kidneys are unable to produce urine to due intrinsic disease |
General cause of Postrenal disease | The kidneys are obstructed and urine cannot be excreted |
Nephritic urine sediment suggests | Glomerulonephritis |
Sterile pyuria suggests | Interstitial nephritis |
Proteinunuria suggests | Intrinsic/Glomerular process |
Created by:
mcasto
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