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69 Cards in this Set
- Front
- Back
where do the ureters pass under?
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the uterine artery and the ductus deferens
water UNDER the bridge |
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60% of TBW is water...how does intra and extra cellular compare? which is high in K
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1/3 is extracellular fluid
2/3 in intracellular fluid (high in K) HIKIN': HIgh K INtracellular |
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extracelluar fluid is how much of total body water? and for it how much is plasma volume and how much is interstitial volume (how do you measure each too)
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1/4 is plasma (measure with radiolabeled albumin)
3/4 is interstitial (measured with inulin) |
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normal GFR is what?
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100ml/min
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formula for renal clearance?
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C = UV/P
U: urine concentration V: urine flow P: plasma concentration |
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what can be used to measure GFR because it is freely filtered and neither reabsorbed nor secreted?
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inulin
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the glomerular filtration barrier has three components, name em. which is lost in nephrotic syndrome
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1) fenestrated capillary endothelium (size barrier)
2) Fused basement membrane with heparan sulfate (negative charge barrier) 3) Epithelial layer with podocyte foot processes Charge barrier is lost in nephrotic syndrome Full Cup For Being My Endless Lover |
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60-40-20 rule
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60% total body water
40%ICF 20%ECF |
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creatinine clearance is only an approximate measure of GFR, why?
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it slightly overestimates the GFR because creatinine is moderately secreted by the renal tubules
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filtration fraction formula
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GFR/RPF
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what do prostaglandins do to the afferent arteriole?
what does Angiotensin II do to the efferent arteriole? |
PGs dilate the afferent arteriole
Angiotensin II preferentially constrict the efferent arteriole |
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how will NSAIDS affect blood flow in the kidney? how about ACE inhibitors?
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NSAIDS block PG formation so that will prevent the afferent arteriole from being dilated
ACE inhibitors block Angtiotensin II formation preventing efferent arteriole constriction that doesnt answer the question...oh well |
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formulas
Filtered load and excretion rate |
filtered load = GFR x P
Excretion rate = V x U P: plasma concen. V: urine flow U: urine concentration |
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where is glucose absorbed when at normal levels?
at what levels do glucosuria begin? at what levels are transporters fully saturated |
completely reabsorbed in the PROXIMAL tubule by Na/glucose transporters
glucosuria: 160-200 mg/dL saturation: 350mg/dL |
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Hartnups disease: def. seen, results in what?
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deficiency of neutral amino acid (tryptophan) transporter.
results in pellagra HarTNuP Hard to reabsorb Trytophan, a Neutral amino acid resulting in Pellagra |
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where are amino acids reabsorbed and by what?
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in the PROXIMAL tubule by sodium-dependent transporters
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in the early proximal tubule what is reabsorbed? what are the effects of PTH and AT II?
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All glucose and amino acids. Most bicarb, Na, Cl, H2O
PTH: inhibits the Na/phosphate cotransporter leading to INCREASE phosphate excretion AT II: increases Na/H exchange leading to INCREASE Na and H2O reabsorption |
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thin descending loop of henle: reabsorbs what? impermeable to what? aka what?
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passively reabsorbs water
impermeable to Na aka the concentration segment a THIN dam holds no WATER |
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thick ascending loop of Henle: reabsorbs what? impermeable to what? does what to urine?
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actively reabsorbs Na, K, Cl via NKCC pump (indirectly leading to absorption of Mg and Ca paracellularly)
Impermeable to H20 dilutes urine THICK dam holds WATER |
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early distal convoluted tubule: reabsorbs what? aka what? effect of PTH?
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actively reabsorbs Na and Cl
aka diluting segment PTH: INCREASE calcium reabsorption via increasing Ca/Na exchanger |
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Collecting tubules: reabsorb what? effects of aldosterone and ADH
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reabsorb Na in exchange for K and H
Aldosterone: inserts Na channels to increase Na reabsorption (and thus dump K) ADH: acts at V2 receptors to cause insertion of aquaporin H2O channels on luminal side |
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three triggers from the RAAS system?
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DECREASE in BP
DECREASE in delivery of Na to the macula densa cells INCREASE in sympathetic tone |
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action of AT II 6 of em
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hits AT receptors on vascular smooth muscle----INCREASE BP
constricts the efferent arteriole---INCREASE FF to preserve renal function increase aldosterone----increase Na and thus H2O reabsorption increase ADH---increase H2O reabsorption increase proximal tubule Na/H activity---increase H2O reabsorption stimulate hypothalamus---thirst |
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ADH primarily regulate what? how about aldosterone?
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ADH---osmolarity
Aldosterone---blood volume |
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JGA and its two components and their jobs?
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JG cells---secret renin in response to decrease in renal blood pressure, decrease Na delivery to distal tubule and an increase in sympathetic tone
Macula densa---Na sensor in a nutshell: maintains GFR via the RAAS system |
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kidney has endocrine functions what are they, 4 of em
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Erythropoietin--release in response to hypoxia
1,25-(OH)2 vitamin D--make active vit. D which increases intestinal reabsorption BOTH of Ca and phosphate Renin--from JG cells Prostaglandins---vasodilate afferent arteriole to increase GFR |
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how can NSAIDS kill your kidney?
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inhibiting the formation of prostaglandins which causes the afferent arteriole to dilate and maintain GFR in times of dire need
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PTH has a couple of effect on the kidney which almost counteract each other...detail them
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it works on the proximal tubule to increase the excretion of phosphate
it also indirectly increases phosphate reabsortion in the gut by stimulating the formation of vit. D in the kidney |
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ANP: source, cause for release, effect and result
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from the atria
released in response to increase in atrial pressure causes an increase in GFR and Na filtration with NO compensatory Na reabsorption in distal nephron results in Na and volume loss |
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PTH: cause for release, effect and result
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released in response to decrease in Ca, increase in phosphate, decrease in active vit. D
Causes increase in Ca reabsorption, decrease in phosphate reabsorption, increase in vit. D production results in increase in Ca and phosphate absorption in the gut |
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AT II: cause for release, effect and result
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release in response to decrease in BP
results in increase if efferent arteriole constriction---increases GFR and FF WITH a compensatory Na reabsorption in proximal and distal nephron results in preservation of renal function in low-volume state |
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causes of a K shift INTO cell...4 of em
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high insulin
Beta adrenergic agonist alkalosis hypo-osmolarity |
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causes of a K shift OUT of cell..6 of em
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insulin deficiency
Beta adrenergic antagonists acidosis hyperosmolarity digitalis cell lysis (duh) |
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the respiratory compensation in response to metabolic acidosis can be calculated using what?
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Winters formula
PCO2 = 1.5 (HCO3) + 8 +/- 2 |
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Anion gap formula?
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AG=Na - (Cl + HCO3)
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pt has wide AG acidosis...causes?
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MUDPILES
Methanol Uremia DKA Paraldehyde or Phenformin Iron tablets or INH Lactic acidosis Ethylene glycol Salicylates |
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Type 1 RTA: defect, associated risks
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defect in collecting tubule ability to excrete H
assoc. with hypokalemia and risk of calcium containing kidney stones "distal" |
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Type 2 RTA: defect, associated risks
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defect in proximal tubule HCO3 reabsorption
associated with hypokalemia and hypophosphatemic rickets "proximal" |
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Type 4 RTA: defect, associated risks
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defect (lack thereof) in collecting tubule response to aldosterone
risk of hyperkalemia and inhibition of ammonium excretion in proximal tubule, leads to decrease in urine pH d/t buffering capacity "hyperkalemic" |
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RBC cast sign of? 3 things
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glomerulonephritis, ischemia, malignant HTN
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WBC cast sign of ? 3 things
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tubulointerstitial inflammation, actue pyelonephritis, transplant rejection
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granular (muddy brown) casts sign of?
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acute tubular necrosis
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waxy cast sign of what?
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advanced renal disease
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hyaline casts sign of?
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nonspecific
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what mediates the damage in nephritic syndrome?
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immune-complex deposition activates complement; C5a attracts NUETROPHILS which mediate the damage
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what is the most common cause of death in SLE?
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diffuse proliferative glomerulonephritis
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what kind of stones CAN NOT be seen on xray?
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uric acid stones
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what leads to formation of staghorn calculi?
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infection with urease-positive bugs (proteus mirabilis, staph, klebsiella)
or cysteine-based stones |
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what is the most common renal malignancy? where does it originate? what increases its incidence? classic triad
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renal cell carcinoma, originates in the renal tubular cells, smoking
triad: hematuria, flank pain, palpable mass |
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what kind of stones are commonly seen in kids? what can they form?
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cysteine, form staghorn calculi
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what is part of the pathogenesis of renal cell carcinoma (gene deletion)
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loss of VHL (3p) tumor suppressor gene, leads to increased IGF-1 (promotes growth)
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a disease associated with VHL inactivation and thus renal cell carcinoma
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von Hippel-Lindau syndrome
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in nephrotic syndrome what component of the filtration barrier gets lost?
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the charge barrier
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traumatic crush injuries can lead to an elevation of what electrolyte?
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potassium due to it being release from muscles when they are crushed and their cellular contents are spewed out.
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what is the imaging study of choice for kidney stones?
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abdomen/pelvis CT
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what bug is the most common cause of pyelonephritis?
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e coli
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what is the primary use of mannitol?
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decrease intracranial pressure
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how would heart failure affect your acid/base balance?
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cause metabolic alkalosis due to a lower level of blood being delivered the kidney activating the RAAS system. this will lead to increase in aldosterone, this will lead to K dumping. low K levels will cause a shift of K out of cells and H into cells leading to an increase in the pH
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bicarb (and inorganic phosphorus, amino acids and glucose) are absorbed faster than water in the proximal tubule so its concentration is higher in the plasma than the tubule
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just remember that
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SIADH will lead to what kind of levels of Na in the urine and plasma?
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high urine sodium levels
low (diluted) sodium levels in blood |
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what is the DOC for patients with SIADH
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demeclocycline (an ADH antagonist)
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a patient with renal cell carcinoma also has von hippel-lindau syndrome what is a pertinent finding on physical examination elsewhere in the body?
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retinal angiomas
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bugs that cause struvite kidney stones?
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urease-producing organisms, including Proteus, Pseudomonas, Providencia
The P's make it so you can Pee less commonly: klebsiella, staph and mycoplasma |
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increased redness of skin and mucosal membranes occurs due to polycythemia when a patient has renal cell carcinoma
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make that connection!
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ADPKD will do what to the BUN and creatinine levels? anemia Y or N?
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INCREASE THEM
YES for anemia |
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losartan blocks what two things on its way to decrease blood pressure?
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vasoconstriction and aldosterone release
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which will help decrease chances of getting a kidney stone: increase or decrease sodium intake?
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DECREASE Na intake
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henoch-schonlein purpura present with rash on butt and extensor surface of legs...it is due to IgA deposits where and follow what kind of illness?
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in the mesangium and it follows a viral URT infection
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what parasite is associated with transitional cell carcinoma, how do you Rx it?
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shistosoma
Rx with praziquantel |