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171 Cards in this Set
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normal distributrion of sodium |
most in the ECF 140 mEq/L vs 5 mEq/L in the ICF |
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Sodium reabsorption in the proximal tubule |
~67% of Na reabsorption -apical: Na/H exchanger and Na/glucose cotransporter -basal: Na/K ATPase, Na/HCO3 cotransporter |
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Sodium reabsorption in the loop of henle |
~15-20% -apical: Na/K/2Cl cotransporter -basal Na/K ATPase |
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Sodium reabsorption in the distal tubule |
-apical: Na/Cl cotransporter (thiazide sensitive) -basal: Na/K ATPase |
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Sodium reabsorption in the collecting duct |
1-2% by principal cells -apical: epithelial sodium channel -Na/K ATPase |
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FeNa |
fractional excretion of sodium =UNa*UV*100/GFR*PNa or =UNa*PCr*100/PNa*UCr |
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aldosterone effect on Na levels |
-causes reabsorption of Na -increases # of ENaC's in collecting duct -activates Na/Cl transporter in distal tubule |
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sympathetic nervous system effect on Na |
-promotes renin secretion -enhances proximal tubule Na reabsorption |
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prostaglandin effect on Na |
-prevent local arteriolar vasoconstriction which enhances tubular reabsorption |
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ANP effect on Na |
-acts via cGMP to: inhibit ENaC, aquaporins, Renin release, and increase GFR -all producing profound diuresis |
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angiotensin II effect on Na |
-stimulates aldosterone -constricts efferent arteriole--> high GFR which promotes proximal tubular Na reabsorption |
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Na depletion |
-NOT caused by low intake -caused by renal dysfunction or extra-renal loss -distinguish these two by urine Na levels >,<10 -symptoms: decreased skin turgor, hypotension, dry mucous membranes
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Na excess |
-causes edema -caused by disruption of starling forces eg: CHF, cirrhosis, hypoalbuminemia -occurs w/ a low ECV despite high total body water/Na and therefore the kidney retains Na and increases volume further |
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serum osomolality |
(total concentration of all solutes in plasma) =2Na + glucose/18 + BUN/2.8 + EtOH/4.6 -normal = 280-310
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serum Na |
-concentration of sodium not total amount -measure of total body water not total body Na |
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urine osmolality |
=UNa+UK+Uurea -noraml = 50-1200 -surrogate measure of ADH |
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Hyponatremia assesment |
-definition: serum Na<135 (<120= danger zone) -signs: N/V, fatigue, weakness, altered mental status, seizure, coma -1st step: measure SERUM OSMOLALITY, urine osmolality, urine Na |
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isotonic hyponatremia |
'pseudohyponatremia' -extremely high levels of protein or lipids -obscures measure of sodium w/o change in osmolality of serum -treat underlying cause |
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hypertonic hyponatremia |
'pseudohyponatremia' -high levels of osmotically active substance in the blood eg. mannitol or glucose -dilutes Na concentration and increases tonicity -treat underlying cause
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hypovolemic hypotonic hyponatremia |
-decreased total body sodium more than the decrease in total body water -caused by: thiazides, mineralocorticoid deficiency, cerebral/renal salt wasting, secretory diarrhea, skin losses -UNa<20, FeNa<1% - give normal saline, stop thiazides, correct mineralocorticoid deficiency |
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euvolemic hypotonic hyponatremia causes |
-three categories: Uosmolality>300 = endocrine- hypothyroid, glucocorticoid deficiency, SIADH
Uosmolality<200= extremes: psychogenic polydipsia, tea and toast diet, beer potomania
reset osmostat- normal water excretion @ lower serum Na (diagnosis of exclusion) |
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SIADH |
syndrome of inappropriate ADH release -caused by malignancies, pulmonary issues, CNS disorders, Drugs such as antidepressants/antipsychotics/ecstasy -diagnosed by Urine Osm>serum Osm, UNa>20, hypouricemia |
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treatment of euvolemic hyponatremia |
SIADH- free water restrict, liberalize Na in diet, if Na falls below 120 and symptomatic give hypertonic saline
extremes- free water restrict, liberalize Na in diet |
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hypervolemic hyponatremia |
-increased total body water more then the increase in total body sodium -caused by CHF, cirrhosis, nephrotic, inadequate GFR -UNa<20 unless cause is low GFR -Urine Osm>350 -treatment: Na/H2O restrict, loop diuretics, ADH antagonists |
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causes of hypernatremia |
-decreased H2O intake: dementia, intubated, newborns, desert wanderers -hypertonic saline infusion -water loss: osmotic diarrhea, fever/sweating, burns, osmotic diuresis, diabetes insipidus |
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diabetes insipidus |
-ADH dysfuntion--> Urine Osm<200, polyuria -central diabetes insipidus: lack of ADH production from posterior pituitary caused by infiltrative disease, trauma, surgery etc -nephrogenic diabetes insipidus: collecting duct is non-responsive to ADH due to hypercalcemia, lithium, post obstruction, recovery from acute tubular necrosis |
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treatment of hypernatermia |
-increase water intake -IV fluids: normal saline if hypovolemic and hemodynamically unstable, or 1/2 NS or D5W |
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rate of sodium correction |
<6-10 mEq/L over 24 hrs <18 mEq/L over 48 hrs
Na change = infusedNa - serum Na/TBW+1 |
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blood pH |
=6.1 + log [HCO3-]/.03(PCO2) |
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regulation of bicarb balance |
-bicarb is freely filtered usually all reabsorbed -high PCO2, aldosterone, volume depletion, and low K+ stimulate bicarb reabsorption -1-2 mEq/Kg/Day must be regenerated by the kidney
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regulation of acid by the kidney |
-most H+ is excreted w/ buffers either phosphate (titratable acid) or ammonia (synthesized from glutamine) |
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anion gap metabolic acidosis |
defined by Na - Cl - HCO3 > 12 whether or not there is acidemia -caused by over production of non-volatile acid: M-ethanol U-ricemia D-KA P-ropylene glycol I-ron or isoniazid L-actic acidosis E-thylene glycol R-enal failure S-alicylates |
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non-anion gap metabolic acidosis |
-'hyperchloremic' -not associated w/ nonvolatile acids H-yperalimentation A-ddison's R-TA D-iarrhea A-cetazolamide S-pironolactone S-aline infusion |
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Diabetic ketoacidosis |
-most common form of acute metabolic acidosis -altered mental status, volume depletion, hyperventilation w/ acetone odor -hyperglycemic/uric, ketonemic/uric, anion gap -osmotic diuresis depletes volume/Na/K but patients are hyperkalemic from acidosis -treat w/ volume and electrolyte repletion and insulin |
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alcoholic ketoacidosis |
similar to DKA but... -lower glucose levels -low ketonuria -lipemic serum -diagnosis by betahydroxybutarate:acetoacetate ratio > 5:1 |
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metabolic acidosis w/ toxin ingestion |
-test serum osmolality -ethylene glycol may form oxylate crystals in urine -remove toxin and or block metabolism (eg. give ethanol for methanol poisoning)
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lactic acidosis |
-frequently sudden and SEVERE -reverse underlying cause: tissue hypoxia, drugs, cancer, PE, sepsis, DM, liver failure + others |
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chronic kidney disease acidosis |
-moderate CKD--> mild non-gap acidosis -advanced CKD--> anion gap acidosis -impaired ability to excrete acid -bicarb therapy when serum levels <15 |
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renal tubular acidosis |
-non gap acidosis -normal GFR -highly alkaline urine -hypokalemia -type II=proximal, high urine bicarb, defect in proximal tubule bicarb reabsorption -type I=distal, defect in hydrogen ion excretion, hypercalcuria, K depletion |
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general treatment of metabolic acidosis |
-IV bicarb only if pH < 7.1-2 -replace only half of deficit -monitor closely for hypokalemia w/ therapy |
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chloride sensitive metabolic alkalosis |
-caused by vomiting, diuretics, relief of chronic hypercapnia -in hyperemesis volume depletion--> Na reabsorption which increases bicarb reabsortion also --> aldo secretion--> H/K secretion--> paradoxically acidic urine |
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chloride resistant metabolic alkalosis |
-excess H+ excretion due to high aldo -volume expansion, hypertension -high urine chloride >20 -give KCl and treat underlying steroid disturbance |
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normal potassium distribution |
-total body K=~3000-400 mEq -98% intracellular @ 130 mEq/L -2% extracellular @ 3.5-5 mEq/L |
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functions of potassium |
-maintain transmembrane potential: hypokalemia-->hyperpolarization vice-versa -co-factor for metabolic enzymes -vasodilator in muscles -stimulates aldosterone and insulin secretion
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normal potassium balance |
-ingestion of K+ load distributes intracellular to prevent spikes in blood K -K is then excreted mostly by kidney over 4-6 hrs -some stool/skin loss |
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renal excretion of potassium |
-freely filtered and 90% reabsorbed proximally -secreted by collecting ducts in response to increases in: aldo, Na flow, pH, dietary K, poorly reabsorbable anions |
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hormonal control of serum potassium |
-insulin release is stimulated by K and causes K flux into cells -catecholamines enhance cell uptake of K -aldosterone stimulates cell uptake of K, and distal tubule/colonic secretion of K |
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non-hormonal control of serum potassium |
-inorganic acidosis causes K release from cells in exchange for H+ (organic acidosis does NOT have predictable K+ response) -exercise causes K+ release from muscle cells |
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causes of hypokalemia |
-poor intake- only in severe malnutrition states -extrarenal loss- diarrhea, villous adenoma -urinary loss- diuretics, vomiting, hyperaldo, hypoMg, osmotic diuresis -K+ shift into cells- high catecholamines, high insulin, alkalosis, familial periodic paralysis |
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consequences of hypokalemia |
-cardiac: U waves, premature beats, increased digitalis toxicity -muscle: weakness, areflexia, rhabdo -smooth muscle: gastric distention, ileus, constipation -renal/metabolic: azotemia, decreased concentrating ability, alkalosis, glucose intolerance |
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treatment of hypokalemia |
-urgent when: large, acute, ongoing loss, and underlying heart disease stepwise: high K+ foods--> oral K+-->IV K+ -risk of hyperkalemia w/ low GFR, beta-blockers, K-sparing diuretics, ACEi/ARBs |
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causes of hyperkalemia |
-artificial 'testube' psuedohyperkalemia -transcellular shift: acidemia, insulin deficiency, cell injury -increased K intake eg. salt substitutes -imparied K excretion including decreased distal Na flow, NSAIDs, ACEi |
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manifestations of hyperkalemia |
hyperacute peaked T-waves loss of P waves prolonged PR w/ wide QRS sine-waves before arrest |
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treatment of hyperkalemia |
-SEVERE: IV Ca-gluconate or CaCl for quick restoration of membrane potential, and Glucose/insulin/bicarb to drive K into cells -w/ normal renal fxn give cation exchange resin eg. kayexalate if not-->hemodialysis -MODERATE: drive K into cells, remove K form body -MILD: remove K from body LONG TERM: dietary K restriction, avoid drugs that increase K, loop diuretics, K exchange resins, correct any volume/glucose/pH abnormalities
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causes of magnesium deficiency |
-chronic alcoholism -diuretics -all hospital in patients at risk
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symptoms of magnesium deficiency |
-cardiac arrhythmias -hyponatremia -aggravated hypertension -potentiated digoxin toxicity |
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treatment of hypomagnesemia |
-confirm normal renal fxn -give IV MgSO4 in emergency otherwise elemental Mg -monitor levels, ECG |
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causes of hypermagnesemia |
-adrenal insufficiency -hypothyroidism -excessive Mg containing antacids |
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complications of hypermagnesemia |
-decreased deep tendon reflexes -low RR, muscle weakness -hypotension -bradycardia, block, arrest |
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treatment of hypermagnesemia |
IV Ca and dialysis |
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Acute kidney injury definition
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-abrupt reduction in GFR/rise in BUN/Cr
-urine volume can be normal but usually becomes oliguric (<400ml/day) or anuric (<50ml/day) -3 categories: pre-renal, intrarenal, and post-renal |
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Acute kidney injury definition
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-abrupt reduction in GFR/rise in BUN/Cr
-urine volume can be normal but usually becomes oliguric (<400ml/day) or anuric (<50ml/day) -3 categories: pre-renal, intrarenal, and post-renal |
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Pre-renal AKI
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-reduced perfusion of the kidney from intravascular volume depletion or heart failure
-BUN:Cr>20:1 -usually oliguric w/ SPGR>1.010 due to high RAAS/ADH -low urine Na/FeNa |
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Acute kidney injury definition
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-abrupt reduction in GFR/rise in BUN/Cr
-urine volume can be normal but usually becomes oliguric (<400ml/day) or anuric (<50ml/day) -3 categories: pre-renal, intrarenal, and post-renal |
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Pre-renal AKI |
-reduced perfusion of the kidney from intravascular volume depletion or heart failure
-BUN:Cr>20:1 -usually oliguric w/ SPGR>1.010 due to high RAAS/ADH -low urine Na/FeNa |
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Definition of Acute tubular necrosis
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- tubular cell apoptosis causes casts forming obstructions
- low urine SPGR and high FeNa - hallmark is muddy brown casts in urine -3 categories: ischemic, toxic, pigment induced |
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Ischemic ATN
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-prolonged pre-renal disease causes irreversible cell damage
-associated w/ prolonged cross clamping of aorta during surgery, pre-op liver failure, skin burns, necrotizing pancreatitis, hypotension |
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Toxin induced ATN
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-often occurs w/ preexisting CKD
-aminoglycosides, NSAIDs, IV contrast, heavy metals are common agents |
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Toxin induced ATN
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-often occurs w/ preexisting CKD
-aminoglycosides, NSAIDs, IV contrast, heavy metals are common agents |
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Pigment induced ATN
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Myoglobinuria: caused by rhabdomyolysis or other muscle injury
Hemoglobinuria: caused by intravascular hemolysis -urine dipstick +blood w/o RBCs -urine is pink even after centrifugation -low BUN:Cr due to Cr release from muscles |
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Post-renal AKI
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-urinary outflow obstruction--> hydronephrosis
-hesitancy, weak stream, nocturia, distended bladder -often caused by BPH |
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Phases of ATN
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-Onset: abrupt fall in GFR <10, rise in BUN/Cr, +/- oliguria
-Maintenance: 1-2 wks long, BUN/Cr plateau, oliguria assc w/ worse mortality, K rises .5/day, bicarb falls 1-2/day, may develop uremia -recovery: diuretic period, rise in GFR, slow fall in BUN/Cr, some renal dysfunction may persist |
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Treatment of ATN
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-prevent by identifying drug risk, prerenal risk, consider volume expansion
-give initial trial of loop diuretics to help volume management -control electrolytes/fluid: Na/K restriction, avoid Mg antacids -dialysis w/ AEIOU (acidosis, electrolytes, intoxication, overload, uremia) |
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MDRD equation
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GFR is inversely proportional to Cr, and age and directly proportional to sex and race
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MDRD equation
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GFR is inversely proportional to Cr, and age and directly proportional to sex and race
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Stages of CKD
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I: kidney damage w/ normal GFR
II: mild reduction in GFR III: moderate reduction in GFR~ 30-60 IV: GFR of 15-30 plan for replacement V: kidney failure start replacement if uremia is present |
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Pathophysiology of progressive CKD
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-CKD tends to be progressive
-often asymptomatic and compensated w/ up to 50% reduction in GFR -@ >75% reduction in GFR levels of phosphate, urate and potassium start to become altered -elevated trans-glomerular pressures cause glomerular hypertrophy, hyperfiltration, proteinuria and eventual focal and segmental sclerosis |
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Na and water balance in CKD
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-reductions in GFR--> Na and water retention causing hypertension
-Na/water restriction are used -loop diuretics may be required -refractory overload is and indication for dialysis -advanced CKD also prevents Na retention and may cause volume depletion |
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Potassium balance in CKD
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-hyperkalemia does not occur until late stage
-ACEi/ARBs, aldosterone antagonists may worsen hyperkalemia -hyporeninemic hypoaldosteronism renal tubular acidosis may also cause hyperkalemia -chronically treat w/ K exchange resins/loop diuretics |
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Acid base balance in CKD
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-in stages 3-4 a non-gap acidosis occurs due to decreased ammonia production
-stages 4-5 an anion gap acidosis occurs due to decreased filtration of phosphate -acidosis is usually mild due to bone buffers -chronically managed w/ sodium bicarb |
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Acid base balance in CKD
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-in stages 3-4 a non-gap acidosis occurs due to decreased ammonia production
-stages 4-5 an anion gap acidosis occurs due to decreased filtration of phosphate -acidosis is usually mild due to bone buffers -chronically managed w/ sodium bicarb |
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Hyperphosphatemia in CKD
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-occurs @~stage 4
-can cause Ca-PO4 deposition and hyperparathyroidism -use phosphate binders such as: Ca-carbonate, Ca-acetate, sevelamer-carbonate, lanthanum-carbonate |
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Acid base balance in CKD
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-in stages 3-4 a non-gap acidosis occurs due to decreased ammonia production
-stages 4-5 an anion gap acidosis occurs due to decreased filtration of phosphate -acidosis is usually mild due to bone buffers -chronically managed w/ sodium bicarb |
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Hyperphosphatemia in CKD
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-occurs @~stage 4
-can cause Ca-PO4 deposition and hyperparathyroidism -use phosphate binders such as: Ca-carbonate, Ca-acetate, sevelamer-carbonate, lanthanum-carbonate |
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Secondary hyperparathyroidism in CKD
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-results from hypocalcemia, hyperphosphatemia (via FGF-23), vit d deficiency
-causes renal osteodystrophy -raised Ca--> precipitation in tissue like the heart and joints (calciphylaxis) -May persist even after Treatment (tertiary hyperparathyroidism) |
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Vitamin D in CKD
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-loss of ability to convert 25-OH vit D to 1,25-OH vit D
-give replacement therapy -combo of hypercalcemia/hyperparathyroidism treated w/ calcimimetics (cinacalcet) |
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Hematologic abnormalities in CKD
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-anemia due to decreased Epo production
-give Epo to increase the Hgb to 10-11 -decreased platelet activity due to uremia |
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Hematologic abnormalities in CKD
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-anemia due to decreased Epo production
-give Epo to increase the Hgb to 10-11 -decreased platelet activity due to uremia |
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Metabolic/endocrine abnormalities in CKD
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-increase in cholesterol and triglycerides--> risk of CVD
-high insulin and increased resistance -high LH causes amenorrhea or low T/impotency with uremia |
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Hematologic abnormalities in CKD
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-anemia due to decreased Epo production
-give Epo to increase the Hgb to 10-11 -decreased platelet activity due to uremia |
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Metabolic/endocrine abnormalities in CKD |
-increase in cholesterol and triglycerides--> risk of CVD
-high insulin and increased resistance -high LH causes amenorrhea or low T/impotency with uremia |
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Clinical manifestations of uremia |
-pericarditis |
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infectious acute interstitial nephritis |
-can be bacterial -or viral: BK polyomavirus: occurs after renal transplant and causes elevated Cr, decoy cells in the urine, and treated by reducing immunosuppressants HIV: collapsing glomerulopathy w/ severe proteinuria, microcystic tubules, large casts |
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causes of acute allergic interstitial nephritis |
-hypersensitivity rxn to drug or infectious agent -drugs: antimicrobials (methicillin), NSAIDs, Thiazides, omeprazole -tends to recur with re-exposure |
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features of acute allergic interstitial nephritis |
Renal: -acute loss of GFR/rise in Cr -mild proteinuria, and hematuria -pyuria +/- WBC casts -urinary eosinophils -flank pain Extra renal: -fever, rash, arthralgia -peripheral eosinophilia |
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diagnosis and treatment of acute allergic interstitial nephritis |
biopsy: -T-cell/monocytes inflammation of the interstitium -variable eosinophils -tubular infiltration Treat: discontinue offending drug, consider prednisone, some fibrosis may persist |
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NSAID induced AIN |
-associated w/ nephrotic syndrome -lacks most extra-renal symptoms -may cause more severe renal impairment |
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acute phosphate nephropathy |
-precipitation of CaPO4 in/around the tubules -iatrogenic from oral phosphate before colonoscopy -volume depletion exacerbates it -Cr rises and usually never returns to baseline |
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renal manifestations of sjogren's |
-causes acute tubulointerstitial Nephritis -associated w/ distal renal tubule acidosis, moderate renal failure, nephrogenic diabetes insipidus -treat w/ prednisone and possible immunosupression |
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IgG4 related disease |
-causes acute tubulointerstitial nephritis -also associated w/ cholangitis, autoimmune pancreatitis, retroperitoneal fibrosis -predominantly affects older men -responds to steroids |
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Light chain cast nephropathy |
-seen in advanced multiple myeloma -bence-jones proteinuria (Ig light chain in urine not detected by dipstick) -kappa or lambda light chains are filtered and form crystal casts especially w/ volume depletion, infection or hypercalcemia |
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analgesic nephropathy |
-long term use of analgesics-->renal insufficiency, papillary necrosis |
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aristolochic acid nephropathy |
-seen in chinese herbal medicide and danube river -causes hypocellular fibrotic lesions |
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heavy metal nephropathy |
-rare exposures to lead or cadmium -largely affects proximal tubule -triad: saturnine gout, Hypertension, renal insufficiency -treat with chelation |
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reflux nephropathy |
-chronic vesicoureteral reflux in childhood -pressure of reflux+reccurrent infection--> interstitial scarring -can present w/ hypertension, often asymptomatic -treat w/ ACEi, may still progress if bilateral |
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sickle cell nephropathy |
-advanced renal disease occurs in 20 of sickle cell patients -sickled cells occlude microvasculature -tubular damage, nephron loss, hyperfiltration, FSGS, papillary necoris |
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Features of nephritic syndrome
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-hematuria w/ RBC casts
-hypertension -oliguria -mild proteinuria (<3g/day) -decreased GFR |
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Features of nephrotic syndrome
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-severe proteinuria (>3g/day)
- hypoalbuminemia -edema -oval fat bodies/fat casts in the urine -hyperlipidemia -hypercoagulability |
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Features of nephrotic syndrome
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-severe proteinuria (>3g/day)
- hypoalbuminemia -edema -oval fat bodies/fat casts in the urine -hyperlipidemia -hypercoagulability |
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Causes of rapidly progressive glomerular nephritis
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3 IF categories:
-Linear deposits: goodpastures/anti-GBM -granular Immune complex pattern: SLE, henoch-schonlein/IgA nephropathy, post-infectious, cryoglobulinemia -pauci immune: ANCA vasculitides |
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Features of nephrotic syndrome
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-severe proteinuria (>3g/day)
- hypoalbuminemia -edema -oval fat bodies/fat casts in the urine -hyperlipidemia -hypercoagulability |
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Causes of rapidly progressive glomerular nephritis
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3 IF categories:
-Linear deposits: goodpastures/anti-GBM -granular Immune complex pattern: SLE, henoch-schonlein/IgA nephropathy, post-infectious, cryoglobulinemia -pauci immune: ANCA vasculitides |
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Post-strep glomerulonephritis
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-mostly affects children
-occurs 1-3 wks post-pharyngitis or impetigo -reduced C3 levels -usually resolves |
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Features of nephrotic syndrome
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-severe proteinuria (>3g/day)
- hypoalbuminemia -edema -oval fat bodies/fat casts in the urine -hyperlipidemia -hypercoagulability |
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Causes of rapidly progressive glomerular nephritis
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3 IF categories:
-Linear deposits: goodpastures/anti-GBM -granular Immune complex pattern: SLE, henoch-schonlein/IgA nephropathy, post-infectious, cryoglobulinemia -pauci immune: ANCA vasculitides |
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Post-strep glomerulonephritis |
-mostly affects children
-occurs 1-3 wks post-pharyngitis or impetigo -reduced C3 levels -usually resolves |
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IgA nephropathy
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-recurrent macroscopic hematuria
-occurs during or right after a URI -focal and segmental proliferative glomerulonephritis - 60% good prognosis -henoch-schonlein purpura |
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Lupus nephritis
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Class I: minimal mesangial involvement, no clinical abnormalities
Class II: mesangial proliferation, mild hematuria/proteinuria Class III: focal proliferative nephritis, nephritic/nephrotic syndrome, reduced C3&4 Class IV: diffuse proliferative nephritis, nephritic/nephrotic low C3&4 Class V: membranous nephritis, nephrotic syndrome, normal C3&4 Class VI: advanced sclerosis, renal failure |
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Anti-GBM disease
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-can cause RPGN w/ crescents
-linear IgG on immunofluorescence -IgG against alpha-3 chain of type 4 collagen -May present w/ hemoptysis also -treat w/ plasmapheresis, steroids, immunosuppressants |
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ANCA vasculitis
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-c-ANCA=wegener's, p-ANCA= churg-Strauss or microscopic polyangitis
-causes RPGN w/ crescents -May have systemic vasculitis Sx - treat with steroids and immunosuppression |
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Alport syndrome
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-mutation in alpha-5 chain of type 4 collagen often X-linked |
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Congenital nephrotic syndrome
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-massive nephrotic syndrome early |
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Minimal change disease
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-most common cause of nephrotic syndrome in kids
-patients are otherwise healthy -effaced podocytes on EM -usually very responsive to steroids |
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Diabetic nephropathy
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-leading cause of ESRD
-early microalbuminuria, nephrotic syndrome, hypertension, renal failure -diffuse nodular glumerulosclerosis -mesangial expansion w/ thickened basement membranes -treat w/ strict glycemic control and ACEi |
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Focal and segmental glomerulosclerosis
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-most common cause of nephrotic syndrome in blacks
-podocyte effacement -non responsive to steroids -can be secondary to chronic reflux, sickle cell, obesity -HIV can cause FSGS w/ collapsing glomerulopathy |
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Focal and segmental glomerulosclerosis
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-most common cause of nephrotic syndrome in blacks |
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Membranous nephropathy
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-main cause of idiopathic nephrotic syndrome esp in whites |
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Membranoproliferative glumerulonephritis type 1 |
-Immune complex disease |
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Membranoproliferative glumerulonephritis type 1
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-Immune complex disease
-mixed nephritic/nephrotic -hematuria+proteinuria -reduced C1,2,3&4 -progressive |
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Dense deposit disease
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'Membranoproliferative glumerulonephritis type 2'
-reduced C3 due to C3 nephritic factor -assc w/ partial lypodystrophy |
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drugs for diabetic nephropathy |
ACEi's and ARBs |
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drugs for diabetes insipidus |
desmopressin for central DI thiazide and amiloride for nephrogenic DI |
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rabbit ATG |
-anti T-cell antibodies -cause a drop in T-cells and release of cytokines ---> fever chills hypotension -used for induction therapy during transplant |
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basiliximab |
-IL2-receptor blocker -used for induction therapy during transplant -not as effective as ATG |
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mycophenolate |
-prodrug that inhibits IMP dehydrogenase -purine synthesis inhibitor -more effective than azothioprine -side effects: GI, bone marrow suppression, teratogenic |
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tacrolimus |
-calcineurin inhibitor that blocks interleukin synthesis esp IL-2 -side effects: some CYP-3A drug interactions, hypertension, decreases GFR due to afferent arteriolar constriction-->vessel obliteration--> tubular atrophy and interstitial fibrosis |
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sirolimus |
-blocks mTOR preventing cell cycle progression -may not be the most effective -side effects: hyperlidipemia, increased risk of nephrotoxicity in combo w/ tacrolimus, CYP450 drug interactions |
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drugs that cause ATN |
-radiocontrast dyes -aminoglycosides -amphotericin B -cisplatin |
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nephrotoxicity of NSAIDs |
-can cause analgesic nephropathy: interstitial nephritis and papillary necrosis w/ chronic high dose therapy -may also cause acute renal insufficiency due to decreased synthesis of prostaglandins--> Na retention
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drugs that block vasopressin |
-alcohol blocks vasopressin release from the pituitary -lithium blocks vasopressin signaling of the V2 receptor which can be reversed by amiloride |
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drugs that have vasopressin effects |
these drugs cause SIADH like syndrome: -sulfonylureas -vincristine -haloperidol treated w/ furosemide, saline, conivaptan (V2 receptor antagonist) |
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autosomal dominant polycystic kidney disease |
-progressive renal failure w/ half reaching ESRD -cysts can rupture and bleed or get infected -may also have liver cysts, aneurysms, cardiac valve abnormalities -PKD1 genes mutations in the cytoplasmic domain and require a 'second hit' -PKD2 interacts w/ PKD1 possibly as a Ca channel |
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X-linked nephrogenic diabetes insipidus |
mutation in V2 receptor |
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non-X linked congenital nephrogenic diabetes insipidus |
recessive mutations in aquaporin 2 gene |
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Liddle's syndrome |
-gain of function mutation in ENaC -low-renin & aldosterone hypertension -hypokalemia -alkalosis -autosomal dominant pattern -treat w/ low Na diet and amiloride |
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Uncomplicated UTI |
-acute cystitis or urethritis -Organsims= E. coli>Staph saprophyticus> (klebsiella, proteus, GBS) -no protection from re-infection -Sx's: dysuria, frequency, urgency, suprapubic pain, hematuria -vaginitis or discharge indicates STD -urethral wash and midstream catch for samples -culture specimens rapidly >10^5 CFUs=positive -may see hematuria, pyuria, WBC casts, leukocytes esterase or nitrities |
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Complicated UTI |
-occurs w/ structural or functional abnormality in GU tract -organisms: E. coli> klebsiella, pseudomonas, serratia, proteus, enterococcus, coag-neg staph, candida -causes similar symptoms to acute cystitis or pyelonephritis
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healthcare associated UTI |
-most common hospital acquired infection -organisms: E. coli, pseudomonas, klebsiella, proteus, enterococcus, candida -must take preventative measures -often form biofilms |
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pyelonephritis |
-local inflammation in the kidneys -pyuria/leukocytosis -fever, flank pain/CVA tenderness, can cause sepsis and renal failure -antibiotic susceptibility testing important |
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bacterial prostatitis |
-severe fever w/ pelvic pain, urinary retention, swollen/tender prostate -organsims: E. coli, staph aureus -prostate stones may harbor persistent organisms |
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staph saprophyticus |
-gram positive -teichoic acid and glycocalyx -non hemolytic -coag negative -resistant to novobiocin treat w/ TMP-SMX |
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step agalactiae |
-gram + -teichoic acid, capsule -antibodies provide immunity -beta hemolytic -bacitracin sensitive -hydrolyzes hippurate -positive CAMP test -treat w/ penicillin G
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Enterococcus |
-gram + cocci -can be any hemolytic type -grows in 6.5 % NaCl, hyrdolyzes esculin in bile -high antibiotic resistance |
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enterobacteriaceae |
-gram - rods -facultative anaerobes -flagella and pili -oxidase neg -grow on blood and MacConkey agar -LPS, capsules, antigenic variation, Type III secretion, growth factor sequestration -includes: escheria, klebsiella, proteus, shigella, salmonella, yersinia |
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E. coli |
-enterobacteriaceae -adhesins and exotoxins -can cause septicemia and UTI -H fimbriae associated w/ acute cystitis -P fimbriae associated w/ pyelonephritis -MacConkey agar lactose fermenter |
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klebsiella |
-enterbacteriaceae -MacConkey agar lactose fermenter -urease positive -test susceptibilities
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Proteus |
-enterobacteriaceae -swarms on agar plates -non-lactose fermenter -urease positive
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psuedomonas |
-gram- rods in pairs -motile, aerobes, oxidase+ -non-lactose fermenter -capsule, LPS, pili, flagella -resistant to disinfectants and lives in water -important hospital acquired opportunistic infection -exotoxin A, pyocyanin |
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candida |
-yeasts w/ pseudohyphae and hyphae -normal flora that can overgrow -OTC preparations available for treatment |
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types of kidney stones |
Ca-oxalate Ca-phosphate Uric acid struvite cystine |
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citrate |
-most important inhibitor of crystal formation -chelates Ca -can be low in metabolic acidosis due to malabsorption/diarrhea predisposing to stone formation |
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Urine pH effect on crystals |
-alkaline urine favors CaPO4 stone formation -acidic urine favors uric acid crystal formation -calcium oxalate not affected by pH |
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randall's plaque |
-calcium oxalate deposits under the urothelium precursor to Ca-oxalate stones |
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calcium stones risk factors |
low urine volume, hypocitraturia, hyperoxaluria (due to intake of vit C, choco, spinach, rhubarb), hyperPTH, high vit D, low dietary Ca, malabsorption syndromes |
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uric acid stones |
-risk increased w/ urine pH<5.5 -radiolucent on X-ray -protein rich diet increases risk -~20% have concurrent gout -rhomboid on microscopy |
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struvite stones |
-forms in the presence of a UTI caused by a urease positive organism such as proteus or klebsiella -composed of Mg-NH4-PO4 -form large staghorn calculi that need to be surgically removed but often recurr -coffin lid shaped on microscopy |
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cystine stones |
-only occur with cystinuria (autosomal recessive disease) -stones begin in 1-4 decades of life -often large and bilateral -crystals are hexagonal (stop sign) |
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drugs that form crystals in the urine |
indinavir and acyclovir |
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presentation of kidney stones |
-hematuria -acute renal colic -nausea vomiting -if in the: upper ureter-->flank pain lower ureter-->may radiate to the testicle/labium UV junction-->mainly urinary symptoms -unable to find comfortable position -CVA tenderness -leukocytosis -helical CT |
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management of stones |
-IV NSAIDs like ketorolac -volume expand -stones>5-6mm not likely to pass spontaneously -indications for surgery: obstructed UTI, decreased renal function, intractable pain/nausea/vomiting -extracorporeal shock wave lithotripsy except w/ obesity or cystine stones -flexible ureteroscopic removal is best -percutaneous nephrostolithotomy for larger stones |
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prevention of stones |
-increase fluid intake so that Urine output>2.5L/day -correct low citrate levels For Ca stones: -do not restrict dietary Ca but do restrict Na -thiazide diuretics For Uric acid stones: -alkalinize the urine w/ potassium citrate -lower dietary protein For cystine stones: -alkalinize the urine -thiol containing drugs like penicillamine, tiopronin, captopril For struvite stones: -surgical removal -antibiotics |
