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204 Cards in this Set
- Front
- Back
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Anatomy of the kidney:
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Gross picture of renal infarct:
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Recent on left, old scarred on the right.
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CT scan of a renal infarct:
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Shows area where there is no blood flow. BUT, this will not tell you when it happened, it could be recent or old...
Typically, a renal infarct causes no pain, unless the capsule is involved - this is because there are no pain fibers in the parenchyma. |
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Two causes of a renal infarction:
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Renal vein thrombosis:
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Renal artery stenosis:
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The main complication of stenosis is renal vascular hypertension
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Pathway to hypertension from renal artery stenosis:
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Gross and histology of ischemic nephropathy:
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B: fibromuscular dysplasia with "beads on a string appearance"
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Renal artery atherosclerosis:
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Renal fibromuscular dysplasia:
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Renal atheroembolic disease:
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Can lead to renal failure in older adults.
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Systemic complications of atheroembolic disease:
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Papillary Necrosis:
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Benign Nephrosclerosis:
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Histology of benign nephrosclerosis:
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Malignant Nephrosclerosis:
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Happens rapidly
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Gross kidney with malignant nephrosclerosis:
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Histology of malignant nephrosclerosis:
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Typical presentation in childhood.
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Typical findings in all forms of thrombotic MA:
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Caused by HUS and TTP
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Pathogenesis of HUS:
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Pathogenesis of TTP:
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Comparison between HUS and TTP
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Henoch-Scholnein Purpura:
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Rash primary on the legs and the buttocks
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on a patient with Henoch-Scholnein Purpura?
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Mesangial hypercellularity
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Causes of renal agenesis:
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Unilateral renal agenesis:
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Abnormalities associated with unilateral renal agenesis:
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Prognosis of patients with unilateral renal agenesis:
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Bilateral renal agenesis:
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Potter's Syndrome:
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Prognosis of patients with bilateral renal agenesis:
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Multicystic dysplastic kidney:
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Supernumerary Kidneys:
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Ureteral Duplication:
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Ureteral Duplication part 2:
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Complications of ureteral duplication:
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Embryology of kidney ascent:
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Locations of renal ectopia (ascent problems):
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Presentation of renal ectopia:
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Horseshoe Kidney:
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Horseshoe kidney associated anomalies:
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Horseshoe kidney associated anomalies part 2:
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Complete renal fusion:
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Ureter obstruction associated with multiple renal arteries:
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Kidney stone formation risk factors:
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Types of urinary crystals:
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What type of kidney stone is the most common?
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Calcium oxalate
accounts for 70-80% of all kidney stones. |
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Risk factors for calcium oxalate stone formation:
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Uric Acid stone formation risk factors:
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Struvite stone formation:
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Cysteine stone formation:
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Kidney stone locations; three points of concern:
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Kidney stone presentation:
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Presenting symptoms of kidney stones part 2:
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Kidney stone differential diagnosis:
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Hydronephrosis = swelling of the kidney
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Kidney stone CT scan diagnosis:
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Intital treatment of kidney stones:
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Sympatholytic and CCB relax smooth muscle around ureters and help pass the stone.
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Time required for passage of a kidney stone:
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Indications for surgery to remove a kidney stone:
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Lithotripsy for kidney stone treatment:
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Evaluation of metabolic factors in a patient with kidney stones:
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What does tea contain that makes it a risk factor for kidney stones?
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Oxalate
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What type of kidney stone would you likely see in a patient with a high urine pH?
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Struvite; due to the urea splitting bacteria leading to production of alkalinizing ammonia
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In a patient with calcium oxalate stones, why would you not want them to quit taking calcium supplements?
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Oral calcium will bind to oxalate in the gut and lead to decreased absorption of oxalate.
Also, without calcium to bind to oxalate in the urine, oxalate will form a nadus on which to build kidney stones. It is better to have calcium and oxalate bind together to be able to be flushed out in the urine better. |
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What is a Randal's plaque made out of?
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Calcium phosphate
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Urinary tract obstruction:
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Microscopy findings with urinary tract obstruction:
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Gross photo of a chronically obstructed kidney:
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Histology of chronic urinary obstruction:
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Note thinning of the renal parenchyma
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Initial findings in urinary tract obstruction:
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Clinical findings in urinary tract obstruction:
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Causes of UTO:
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Diagram of locations of UTO causes:
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Uretopelvic junction obstruction:
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Happens if the ureter lacks the normal peristaltic function
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Cause of uretopelvic juction obstruction in adults:
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Patient will have pain after drinking lots of fluid, then the pain will go away as the patient becomes more dehydrated
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UPJ presentation in infants and children:
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Urinary reflux:
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Ureterovesical junction:
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The ureter does not enter the bladder at a right angle; it goes through a submucosal tunnel first
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Grading of reflux severity:
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Reflux complications:
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Reflux epidemiology:
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Developmental anomalies associated with reflux:
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Inheritance pattern of reflux:
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Primary vs Secondary reflux:
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Causes of secondary reflux:
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Ureterocele:
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Voiding cystourethrogram for diagnosis of reflux:
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Antibiotic management of reflux:
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Indications for surgical treatment of reflux:
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Renal cysts:
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Polycystic kidney disease nomeclature:
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Recessive PKD:
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Onset of cysts in recessive PKD:
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Kidney shape is preserved, but it is enlarged.
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What in utero disorder can recessive PKD lead to?
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Potter's syndrome
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Liver involvement in recessive PKD:
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What two diseases will patients with recessive PKD develop at some point in their life?
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Renal failure, congestive heart failure or both
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Dominant PKD:
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Inheritance patterns of dominant PKD:
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Pathology of dominant PKD:
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Dominant PKD can affect any portion of the nephron unit, whereas recessive PKD only affects the tubules.
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Dominant PKD related mortality:
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Other GI manifestations of dominant PKD:
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Cardiovascular manifestations of dominant PKD:
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Renal/urinary manifestations of dominant PKD:
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What is important to control in dominant PKD patients?
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Tuberous sclerosis; another syndrome that can be caused by mutations responsible for ADPKD:
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Tuberous Sclerosis:
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An angiomyolyoma can be a risk factor for developing renal cell carcinoma
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Incidence of simple cysts according to age:
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A non-genetic disease
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Multicystic dysplastic kidney:
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Caused by the failure of the ureter to enter the bladder. Kidney makes urine but it has nowhere to go - causing cysts.
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Acquired renal cystic disease:
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Findings in acquired renal cystic disease:
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Complications associated with acquired renal cystic disease:
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Urinary incontinence definitions:
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Is incontinence more common in men or women?
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Physiology of urination:
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Physiology of urination part 2:
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What are risk factors for stress incontinence?
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Obesity, multiparity, smoking, pelvic surgery, menopause and constipation
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What are some risk factors for urge incontinence?
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Important history to get when evaluating incontinence:
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Examinations to perform when evaluating incontinence:
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Labs and studies to get when evaluating incontinence:
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Treatment options for stress incontinence:
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Treatment options for urge incontinence:
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Benign adult renal tumors:
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Papillary, collecting duct, clear cell and chromophobe (in order)
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Things to remember about renal clear cell carcinoma:
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Rests are peices of embryological tissue sitting among normal tissue
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Transitional cell bladder cancer pearls:
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In an asymptomatic patient, what bacterial count is needed to diagnose a UTI?
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At least 10 to the 5th power.
With a symptomatic patient, a lower count is acceptable. |
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Cystitis vs. Urethritis:
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Pyelonephritis:
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Uncomplicated vs. complicated UTI:
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Pathobiology of UTI's:
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Pathobiology of UTI's part 2:
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Common causative agents of UTI's:
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Common causative agents of complicated UTI's:
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Catheters and nosocomial UTI's:
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Indications for catheter use:
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Pyelonephritis gross picture:
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Microabscesses
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Is there a connection between chronic UTI's and chronic kidney disease?
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Chronic pyelonephritis caused by VU reflux leads to damaged compound papilla.
Chronic pyelonephritis caused by obstruction leads to both compound and simple papilla damage. |
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Gross kidney as a result of chronic pyelonephritis with obstruction:
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Histology of kidney with chronic infection damage vs. normal:
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Diagram of potassium homeostasis:
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The colon is where K+ gets excreted through the fecal route.
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Reabsorption of potassium through the tubules:
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The distal tubule is the only site where potassium reabsorption or excretion is regulated.
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Major factors in potassium regulation:
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Causes of spurious hyperkalemia:
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Spurious = lab result is high, but in reality the patients potassium level is normal
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If the lab reports a patient's K+ as 7.0 with hemolysis, what should you do?
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Get an EKG first to check...then have the blood re-drawn.
* The K+ value may actually be high even without the hemolysis. |
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Causes of external balance hyperkalemia:
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Causes of internal balance hyperkalemia:
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Hyper/Hypokalemia and membrane potential:
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Hyperkalemia and it's effect on the heart:
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Causes of external hypokalemia:
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Causes of internal hypokalemia:
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Effects of hypokalemia on the EKG:
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Systemic effects of chronic hypokalemia:
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Urine potassium algorithm for determining renal vs. non-renal causes of imbalance:
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Serum sodium measurements relate directly to water in the ECF:
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Osmoregulation vs. Volume regulation mechanisms:
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Total body water calculation:
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Fluid compartment rules:
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What is the difference between tonicity and osmolarity?
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Tonicity is osmoles that can make the cell shrink or swell - not every osmole can do that.
*The most important thing that determines tonicity in the body is sodium* |
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The difference between tonicity and osmolality:
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The effect of tonicity on red blood cells:
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Hyponatremia:
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Algorithm for determing causes of hyponatremia:
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The effect of hyponatremia and it's correction on the brain:
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Hypernatremia:
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Serum osmolarity thresholds for ADH release and thirst:
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Diabetes Insipidus:
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Causes of diabetes insipidus:
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Symptoms of hypertonicity:
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Consequences of hypertonicity:
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Treatment of hypernatremia:
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In a patient with severe life threatening hyperkalemia, what are the first steps you should take to correct the high K+?
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Insulin + glucose
Calcium to stabilize the myocardium Loop diuretics |
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Treatment of hyperkalemia:
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Low magnesium can cause wasting of what electrolyte from the kidney?
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Potassium!
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Times required for buffering acid/base changes:
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Renal excretion of acids:
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Renal Acid Transporters:
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Interpretation of the urine anion gap:
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