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Renal
First Aid: Renal
| Question | Answer |
|---|---|
| This structure passes under the uterine artery and under the ductus deferens (retroperitoneally) | Ureters |
| What percentage of total body weight is total body water, ICF, and ECF? | 60/40/20 rule; 60% TBW, 40% ICF, 20% ECF (which is 1/4th plasma volume, 3/4ths interstitial volume) |
| What is the equation for renal clearance? | C=UV/P |
| What does it mean if renal clearance is greater then GFR? What does it mean if it is less then GFR? | If renal clearance is greater than GFR then there is net secretion; if less than GFR then there is net reabsorption |
| What substance is used to calculate GFR? | inulin (creatinine clearance is an approximate measure, but 10-15% is secreted so not as accurate as inulin) |
| What substance is used to calculate effective renal plasma flow (ERPF)? | PAH is used as it is both filtered and actively secreted |
| This substance dilates afferent arteriole leading to increased GFR and RPF. | prostaglandins; inhibited by NSAIDs |
| This substance constricts efferent arteriole leading to increased GFR and decreased RPF resulting in an increased filtered fraction. | Angiotensin II; inhibited by ACEi's |
| What is the equation for free water clearance? | CH2O=V-Cosm; Cosm=Uosm*V/Posm |
| What is the Tm of glucose transport? | 350 mg/dL, but glucosuria begins at 200 mg/dL |
| Where is glucose reabsorbed in the nephron? | It is absorbed in the proximal tubule via cotransport with sodium; a basolateral Na/K ATPase restores the intracellular sodium balance |
| How is bicarb reabsorbed in the proximal tubule? | Sodium/hydrogen exchanger pumps hydrogen into the lumen so that it can combine with bicarb via CA in the lumen and be reabsorbed as water and CO2; in the cell CA splits it back to hydrogen (exchanged for sodium) and bicarb is pumped into interstitium |
| How is potassium reabsorbed in the thick ascending limb? | Na/K/2Cl cotransporter; this is the site of action for loop diuretics (furosemide) and the reason they cause increase potassium loss; sodium is then pumped into interstitium via Na/K ATPase |
| How is chloride reabsorbed in the distal convoluted tubule? | Na/Cl cotransport; sodium is then pumped into interstitium via Na/K ATPase |
| Where does PTH act to increase calcium reabsorption? | Distal convoluted tubule |
| On what cells does aldosterone act to increase Na reabsorption? | In the collecting tubules; principal cells (where Na is reabsorbed in exchange for K) and intercalated cells (where Na is reabsorbed in exchange for H) |
| What causes renin release from JGA? | Decreased Na return (can be caused by decreased BP, decreased renal blood flow, etc), also secreted in response to increased sympathetic tone |
| What are the actions of angiotensin II? | Potent vasoconstriction (especially efferent arteriole), increase in proximal tubule Na reabsorption, release of aldosterone, release of ADH, stimulation of hypothalamus (thirst) |
| What is the action of ANP? | released by atria in response to increased atrial pressure, decreases renin and increases GFR |
| In metabolic acidosis bicarb would be increased or decreased? | Decreased, as its buffering action would cause it to combine with hydrogen to form CO2 and water |
| In metabolic alkalosis bicarb would be increased or decreased? | Increased, as water and CO2 would be split to generate H+ to offset alkalosis |
| What are common causes of anion gap metabolic acidosis? | MUDPILES; methanol, uremia, diabetic ketoacidosis, paraldehyde, intoxication (iron or isoniazid), lactic acidosis, ethylene glycol, salicylates |
| What are common causes of normal anion gap metabolic acidosis? | diarrhea, renal tubular acidosis, hyperchloremia (decreased bicarb reabsorption to maintain neutrality, not total picture but helps me remember) |
| What are common causes of metabolic alkalosis? | vomiting, diuretic use, antacid use, and hyperaldosteronism (Na/H exchange in intercalated cells) |
| What is Potter's syndrome? | bilateral renal agenesis resulting in oligohydramnios--> pulmonary hypoplasia and limb and facial abnormalities |
| Horseshoe kidneys get trapped under what artery when ascending from the pelvis? | Inferior mesenteric artery |
| What are common causes of RBC casts? | Glomerular inflammation (nephritic syndrome), ischemia, or malignant hypertension |
| What are common causes of WBC casts? | acute pyelonephritis, tubulointerstitial disease, glomerular disorders |
| What are causes of waxy casts? | advanced renal disease, chronic renal failure |
| What condition is associated with granular casts? | acute tubular necrosis |
| Lumpy bumpy appearance on LM, subepithelial humps on EM, what is expected on IF? | granular pattern; acute poststrep glomerulonephritis |
| Crescent moon shape on LM and IF is associated with this syndrome. | Rapidly progressive (crescentic) glomerulonephritis; rapid progression to renal failure (prognosis in number of crescents) |
| In Goodpasture's syndrome, what pattern is seen on IF? | Linear staining pattern of basement membrane; anti-GBM antibodies |
| Subendothelial humps on EM with "tram track" appearance of basement membrane is seen in what disorder? | Membranoproliferative glomerulonephritis; slow progression to renal failure |
| IgA deposits in mesangium are seen on IF and EM in this disorder. | Berger's disease (IgA nephropathy, often postinfectious) |
| A split glomerular basement membrane is seen in this disorder, often associated with nerve deafness and ocular disorders. | Alport's syndrome; collagen IV mutation |
| Non-diabetic patient with diffuse capillary and basement membrane thickening, what can be expected on EM? | "spike and dome" appearance; membranous glomerulonephritis |
| EM shows foot process effacement in this disease. | Minimal change disease |
| Segmental sclerosis and hyalinosis is seen on LM in this disease. | Focal segmental glomerular sclerosis |
| IF congo red stain, apple green birefringence | Amyloidosis |
| This type of kidney stone is secondary to urease positive buts (proteus, staph, klebsiella). | ammonium magnesium phosphate (struvite) |
| This renal malignancy is associateed with von Hippel-Lindau disease and gene deletion in chromosome 3. | Renal cell carcinoma; originates in renal tubule cells, may produce secondary polycythemia |
| What is von Hippel-Lindau disease? | Autosomal dominant condition where hemangioblastomas are found in cerebellum, retina, and spinal chord; associated with renal cell carcinoma and pheochromocytoma |
| Deletion of the WT1 gene on what chromosome leads to Wilm's tumor? | chromosome 11; can be part of WAGR (Wilms tumor, Aniridia (colorless eye), Gonadoblastoma, mental Retardation) |
| Thyroidization of the kidney is seen in this disease. | Chronic pyelonephritis |
| Acute pyelonephritis affects what part of the kidney? | The cortex |
| This common cause of renal failure is associated with renal ischemia (shock), crush injury (myoglobinuria), and some intoxications. | Acute tubular necrosis; granular casts often seen |
| Renal papillary necrosis is seen in what diseases? | DM, acute pyelonephritis, and sickle cell anemia |
| What is the cause of prerenal ARF? | decreased renal blood flow (hypotension) leading to decreased GFR and Na/H20 retention; BUN/Cr ratio is often greater than 20 |
| What is the cause o intrinsic renal ARF? | generally due to ATN or ischemia/toxins with debris obstructing tubule and fluid backflow; BUN/Cr ratio is often less than 15 |
| What is Fanconi syndrome? | defect in proximal tubule transport of amino acids, phosphate, uric acid, protein, and electrolytes. |
| Osmotic diuretic which acts by keeping water in the lumen. | Mannitol |
| What is the mechanism of action of acetazolamide? | carbonic anhydrase inhibitor --> bicarb reabsorption drives the Na/H exchanger in the proximal tubule --> NaHCO3 excreted; causes acidosis |
| Na/K/2Cl cotransport inhibitor. | Furosemide; acts in ascending limb |
| This diuretic inhibits NaCl reabsorption in early distal tubule. | Hydrochlorthiazide |
| This diuretic is a competitive aldosterone receptor antagonist. | Spironolactone, triamteren, amiloride |
| What is the contraindication of ACE inhibitors? | Bilateral renal artery stenosis |
Created by:
rahjohnson
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