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BR-Renal
5/24/06
| Question | Answer |
|---|---|
| Potter's syndrome | malformation of ureteric bud causes bilateral renal agenesis, oligohydraminos, limb & facial deformities, pulmonary hypoplasia; "babies with potter's can't pee in utero" |
| Horseshoe kidney results when the inferior poles..., and get stuck under... | fuse; during their ascent, they get trapped under the inferior mesenteric artery |
| Symptoms of UTI | dysuria, frequency, urgency, suprapubic pain; more common in females, babies w/ congenital defects and males w/BPH |
| Symptoms of pyelonephritis | fever, chills, flank pain, CVA tenderness |
| Community UTI infections (3) | E. coli > Staph saprophyticus > Klebsiella |
| Hospital acquired UTIs (5) | E. coli, Proteus, Klebsiella, Serratia, Pseudomonas |
| Complications of cystitis (3) | bacteremia, septic shock, ARDS |
| Is diabetes a risk factor for UTIs? | yes |
| How can you remember the UTI bugs? SSEEK PP | Serratia marcescens, Staphylococcus saprophyticus, Escherichia coli, Enterobacter cloacae, Klebsiella pneumoniae, Proteus mirabilis, Pseudomonas aeruginosa |
| Serratia | red pigment, nosocomial, drug resistant |
| Staph saprophyticus | 2nd mc in sexually active women |
| E. coli | #1mc, colonies look metallic on EMB agar |
| Enterobacter cloacae | nosocomial, drug resistant |
| Klebsiella pneumoniae | mucoid capsule, viscous colonies |
| Proteus mirabilis: activity, byproduct, stone? | motility causes "swarming" on agar; produces urease; a/w struvite stones |
| Pseudomonas aeruginosa | blue-green pigment and fruity odor; usu nosocomial and drug resistant |
| Edema d/t increased capillary pressure is: | heart failure |
| An edema d/t decreased plasma proteins is: | nephrotic syndrome or liver failure |
| Edema d/t increased capillary permeability is: | d/t toxins, infections or burns |
| Edema d/t increased interstitial fluid colloid osmotic pressure is: | lymphatic blockage |
| Embryonic derivatives of the adult kidney include: | intermediate mesoderm that forms UROGENITAL RIDGES on each side of aorta and NEPHROGENIC CORD that gives rise to: PROnephros, MESOnephros, METAnephros |
| What is the deal with the Pronephros? | it forms in the 4th wk and disappears by the 5th; it is NONFUNCTIONAL |
| What is the significance of the mesonephros? | it is the functional kidney from the 4th week until the permanent one takes over; it forms the MESONEPHRIC DUCT and URETERIC BUD |
| What arises out of the mesonephric duct? | ductus deferens, epididymis, ejaculatory duct, seminal vesicle in MALE ONLY |
| What arises from the ureteric bud? | ureter, renal pelvis, calyces, collecting tubules in BOTH SEXES |
| Where does the Adult kidney come from? | the METANEPHROS (uteric bud + metanephric mass) in the 5th wk; it is functional by the 9th week; mesoderm forms nephrons; it ascends; forms UROGENITAL SINUS and URETHRA |
| Tell me something about the urogenital sinus? | it forms the bladder, which is continuous w/ALLANTOIS |
| Which ligament does the allantois form in the adult? | MEDIAN umbilical ligament |
| The urethra is formed from? | endoderm and urogenital sinus w/ distal portion from ECTODERM |
| In the adult male/female, the ureter passes _ to the ductus deferens/uterine artery | posterior |
| The entire collecting system arises from the: | ureteric bud; the remainder is from metanephric duct |
| Fanconi's syndrome is a heretidary or acquired dysfunction of: | the proximal renal tubules; it manifests as Glycosuria, Hyperphosphaturia, Aminoaciduria and Acidosis d/t impaired glucose, AA, phosphate and bicarb reabsorption |
| Accessory renal arteries arise from? | the aorta and feed a specific part of the kidney; if cut they will infarct that part of the kidney |
| Congenital polycystic kidney disease | multiple small & large cysts that cause renal insufficiency; they are not continuous w/the collecting system; baby is death w/in days to wks |
| Where are the kidneys located? how much do they weigh? | posterior to the peritoneum at level of L1 (R is lower than L d/t liver); 150g each (if paired) |
| Left renal vein is posterior to the _ artery and anterior to the _? | superior mesenteric; abdominal aorta |
| How much blood is filtered and urine produced each day? | 1700L of blood; 1L of urine |
| The left gonadal (testicular/ovarian) vein drains into the _ vein? | left renal |
| The right gonadal vein drains directly into the _? | inferior vena cava |
| The Intracellular fluid volume equals...? | the Total body water MINUS the Extracellular fluid (measured by INULIN) |
| The Interstitial Volume is equal to the Extracellular fluid MINUS the... | Plasma volume (measured by radiolabeled ALBUMIN) |
| Total body water makes up what percentage of the body's weight? | 60% |
| Another way to consider total body water is in fractions: | 1/3 ECF+ 2/3 ICF = TBW |
| Extracellular fluid is composed of: | 14 plasma and 3/4 interstitium |
| Renal blood flow is 25% of Cardiac output and is measured as: | Renal Plasma Flow divided by (1 - hematocrit); it is autoregulated and kept fairly constant even w/arterial fluxes of 100-200mmHg |
| Renal plasma flow is measured by clearance of: | para-aminohippuric acid (PAH), which is filtered and secreted by proximal tubule |
| PAH is competitively inhibited by _ and normally mediated by _ | probenacid; a carrier system for organic acids |
| Glomerular filtration rate is normally 120ml/min; it is measured by: | inulin clearance (filtered, not absorbed or secreted) |
| Decreases in GFR cause a rise in: | BUN and creatinine levels; it decreases with age |
| Glomerular Filtration Rate = Clearance of Inulin = Urinary [inulin] x Volume of urine per minute divided by: | Plasma [inulin] |
| Factors that determine clearance are: | Filtration, Secretion, Reabsorption |
| Highly cleared substances = | those that are filtered and secreted (ex: PAH) |
| Poorly cleared substances = | those that are either not filtered (ex: protein) or are reabsorbed (ex: glucose) |
| Reabsorption is limited by | number of transporters, saturation of maximum transporters (Tm); Therefore, any concentration above the Tm is excreted as excess |
| Tm for glucose is: | 300mg/dL; concentrations above this cause osmotic diuresis seen in hyperglycemic diabetics |
| Filtration fraction is normally 20%; it is calculated by dividing the following values: | Glomerular filtration rate (~Cinulin) divided by Renal Plasma Flow (~C of PAH) |
| What do prostaglandins do to the afferent arteriole? | they dilate the vessel; this increases RPF and GFR, so FF stays constant |
| What does Antiotensin II do to the efferent arteriole? | It constricts the vessel, which decreases RPF, increases GFR and increases FF |
| The Juxtaglomerular Apparatus (afferent arteriole) produces _? Is stimulated by _ & _? | renin and erythropoietin; macula densa (baroreceptors) and b-sympathetic adrenergics |
| What exactly is the macula densa? | it is the Na+ sensor in the distal convoluted tubule |
| What does renin do? | it is secreted by JG cells to cleave angiotensinogen to AT-I which is cleaved by ACE in lungs to AT-II which increses Aldosterone levels in response to low renal BP, low Na+ delivery to distal tubule and increased sympathetic tone |
| What are the functions of Angiotensin II? (6) | 1. stimulate Aldosterone release from zona glomerulosa, 2. stimulate ADH & ACTH secretion, 3. Vasoconstrict renal arterioles w/ low plasma, 4. Vasoconstric systemically w/hi plasma levels, 5. Stimulate thirst, 6. Release E/NE from adrenal medulla |
| How is angiotensin II inactivated? | by antiotensin III, a potent stimulator of aldosterone secretion, but not a good vasoconstrictor |
| ACE-Inhibitors (captopril, enalapril) reduce hypertension by: | preventing actions of Angiotensin II on adrenal gland, thereby preventing release of aldosterone |
| Angiotensin II receptor blockers (losartan) lowers blood pressure by: | preventing angiotensin II from constricting the efferent arteriole |
| NSAIDs can cause acute renal failure in high vasoconstrictive states by: | inhibiting the renal production of prostaglandins, which keep the afferent arterioles vasodilated to maintain GFR |
| Endocrine functions of kidney: (4) | 1. Peritubular capillaries secrete erythropoietin in response to hypoxia; 2. Converts 25-OH Vit D to 1,25(OH)2 by 1a-hydroxylase d/t PTH; 3. JG cells secrete renin d/t dec renal pressure, inc symp discharge (B1); 4. Prostaglandins vasodilate to inc GFR |
| Glomerular Filtration Barrier is composed of 3 things: | 1. Fenestrated capillary (size), 2. Fused basement membrane with heparan sulfate (Negative charge barrier), 3. Epithelial layer with podocyte foot processes |
| What happens when the charge barrier is lost in the glomerulus (4)? How does it happen? | Pt exhibits albuminuria, hypoproteinemia, generalized edema, hyperlipidemia; d/t Nephrotic Syndrome |
| When the afferent arteriole is constricted, which 2 properties decrease? | RPF and GFR |
| What 2 properties increase and what decreases in response to efferent arteriole constriction? | GFR and FF (GFR/RPF); and RPF |
| If plasma protein concentration increases what will go down? | GFR and FF; nothing will happen to the RPF |
| What will happen if the plasma protein concentration goes up? | GFR and FF (GFR/RPF) will both go up |
| If the ureter is constricted, what happens to GFR and FF? | they both go down |
| AAs have 3 carrier systems with competitive inhibition w/in each group; where does this secondary transport occur? | proximal tubule; it is saturable |
| Early proximal convoluted tubule is the "workhorse of the nephron." Why? | it reabsorbs all the glucose, AAs, and most bicarb, Na and water; it secretes ammonia to buffer the secreted H+ |
| Thick ascending loop of Henle may be impermeable to water, but it reabsorbs... | Na, K and Cl (actively), Mg and Ca (indirectly) |
| Early Distal Convoluted Tubule is under hormonal control for what? and actively reabsorbs what? | Ca (via PTH) AND Na, Cl |
| Collecting Tubules is under hormonal control. 1. Aldosterone, 2. ADH (vasopresin) | 1. reabsorbs Na in exchange for secreting K or H; and 2. Reabsorbs H2O |
| How high can the osmolarity go in the medulla of the kidney? | 1200mOsm |
| What will the atria secrete to keep the RAAS in check in case of heart failure/inc atrial pressure? | ANP (atrial natriuretic peptide); it increases GFR and increases Na to lower blood volume |
| When is aldosterone secreted? | in response to low blood volume (via AT II) and increased plasma K |
| What does aldosterone do? | reabsorbes Na, secretes K and H in the distal convoluted tubule |
| When is PTH secreted? | when there is low plasma [Ca] |
| What does PTH do in the kidney? | it increases Ca reabsorption in DCT, decreases PO4 reabsorption in PCT and converts Vit D to active form |
| When is angiotensin II secreted? | when renin detects a low blood volume |
| What does angiotensin II do? | causes efferent arteriole constriction to increase GFR and inc Na and HCO3 reabsorption |
| When is Vasopressin/ADH secreted? | when plasma osmolarity increases and blood volume drops |
| What does vasopressin/ADH do? | it binds receptors on principal cells in collecting duct to increase aquaporins and increase H2O reabsorption |
| NephrItic Syndrome d/t Inflammation (6) | 1. Acute poststrep GN, 2. Rapidly progressing/Cresenteric GN, 3. Goodpasture's Syndrome, 4. Membranoproliferative GN, 5. IgA Nephropathy/Berger's, 6. Alport's Syndrome; All have: hematuria, hypertension, oliguria, azotemia |
| Acute poststreptococcal Glomerulonephritis | kids; peripheral/periorbital edema; self-limiting; "lumpy-bumpy" subepithelial humps on LM, EM |
| Rapidly progressing (cresenteric) Glomerulonephritis | cresent-moon shape on LM and IF; rapid course to renal failure |
| Goodpasture's Syndrome | type II hypersensitivity; "linear" on IF; anti-GBM antibodies; hemoptysis (affects lungs too), hematuria |
| Membranoproliferative Glomerulonephritis | "tram tracks" subendothelial humps on EM; slowly progressive to renal failure |
| IgA Nephropathy/Berger's Disease | Mesangial deposits of IgA on IF and EM; mild disease, often post-infectious |
| Alport's Syndrome | split basement membrane d/t Collagen IV mutation; also has nerve deafness and ocular disorders |
| NephrOtic Syndrome d/t prOteinuria (5) | 1. Membranous GN, 2. Minimal Change Disease, 3. Focal Segmental Glomerular Sclerosis, 4. Diabetic Nephropathy, 6. SLE Nephropathy; all have massive proteinuria, hypoalbuminemia, peripheral/periorbital edema, hyperlipidemia |
| Membranous glomerulonephritis | common in ADULTS; "spike and dome" on EM; diffulse capillary/BM thickening on LM |
| Minimal Change Disease (lipoid nephrosis) | mc CHILDHOOD nephrotic syndrome; responds to STEROIDS; Foot process effacement on EM; normal glomeruli on LM |
| Focal Segmental Glomerular Sclerosis | more severe in HIV pts; segmental sclerosis and hyalinosis seen on LM; nephrotic syndrome |
| Diabetic Nephropathy | Kimmelstiel-Wilson lesions and BM thickening on LM; nephrotic syndrome |
| SLE Nephropathy | 5 patterns of renal involvement; "Wire loop" appearance w/granular subendothelial BM deposits in membranous glomerulonephritis pattern |
| What complications could arise from kidney stones? | hydronephrosis and pyelonephritis |
| Calcium kidney stones | the most common type; combine w/oxalate (envelopes) or phosphate (sticks); radiopaque; w/ cancer, inc PTH, inc Vit D, milk-alkali syndrome; these RECUR |
| Ammonium magnesium phosphate (struvite) stones | 2nd mc type of stone; radiopaque "caskets"; form d/t urease positive bugs (Staph or Proteus); Can form STAGHORN calculi nidus for UTIs |
| Uric Acid Stones | highly a/w hyperuricemia (gout); commonly a result of leukemia or myeloproliferative disorders, chemotherapy and cell lysis; radiolucent w/negative birefringence |
| Cystine Stones | usu 2* to cystinuria; radiolucent or radiopaque w/sulfur (rhomboid) |
| Renal Cell Carcinoma | mc renal malignancy; men 50-70yo; smokers; a/w von Hippel-Lindau; Polygonal cells in renal tubule; Hematuria, palpable mass, 2* polycythemia, flank pain, fever; hematogenous via IVC invasion; ectopic hormones; risk w/dialysis |
| What kind of hormones are secreted from an ectopic gland d/t renal cell carcinoma | EPO, ACTH, PTHrP, prolactin |
| Wilms' tumor (nephroblastoma) | mc renal malignancy in KIDS (2-4yo); huge palpable flank mass; d/t deletion of WT1 gene on Chromosome 11; can be a/w WAGR Complex |
| What is the WAGR complex? | Wilms' tumor, Aniridia, Genitourinary malformation, mental-motor Retardation |
| Transitional Cell Carcinoma; a/w problems in your Pee SAC | mc tumor of urinary tract (calyces, renal pelvis, ureters, or bladder); RECURS after removal; Hematuria and local metastasis; caused by: Phenacetin, Smoking, Aniline dyes, Cyclophosphamide |
| COX is inhibited by aspirin and other NSAIDs, but not by: | acetaminophen |
| Acute renal failure and acute tubular necrosis often occur simultaneously, but... | acute renal failure can exist without acute tubular necrosis |
| Sheehan's syndrome (pituitary necrosis) causes: | loss of gonadotropins, TSH, ACTH d/t postpartum hemorrhage; it manifests as fatigue, wt loss and amenorrhea |
| Flea-bitten kidneys can be caused by: | SLE, HUS and TTP |
| The most common cause of acute renal failure is: | therapeutic drugs (b-lactams, sulfonamides, TMP, rifampin, COX inhibitors, diuretics, captopril) |
| Renal transplant rejection rates can be decreased by giving: | cyclosporine and muromonab-CD3 |
| Finesteride, a 5-a-reductase inhibitor is used to treat | Benign prostatic hypertrophy |
| Cold medicines and a-agonists exacerbate: | Benign prostatic hypertrophy |
| Adult polycystic kidney disease | AD; occurs in midlife; bilateral, parenchyma replaced by cysts; hematuria, HTN, palpable kidneys; progresses to renal failure; a/w BERRY aneurysms of Circle of Willis and cystic dz of other organs (especially liver) |
| Acute renal failure is d/t an abrupt decline in renal function over several days, it is indicated by: | elevated CCr and elevated BUN; 1. Prerenal azotemia, 2. Intrinsic renal failure, 3. Postrenal failure |
| Describe prerenal azotemia and how it causes acute renal failure: | a decreased RBF (ex: hypotension) lowers GFR and Na/H2) is retained by kidneys; kidney function is normal; this is usu d/t NSAIDs (not acetaminophen) or ACE-inhibitors |
| How does an intrinsic renal problem cause acute renal failure? | usu d/t acute tubular necrosis or ischemia/toxins; patchy necrosis = debris obstructing flow and decreasing GFR; urine has CASTS which are granular/epithelial mix; this is a malfunction of the kidney (DIC, GN, HUS, TTP, SLE) |
| What sort of postrenal problems will result in acute renal failure? | bilateral outflow obstruction d/t stones, BPH, neoplasia, phemosis, stricture, or neurogenic bladder |
| How can you distinguish between prerenal and renal causes of ARF when given Urine Na values? | prerenal will be <10 and renal will be >20 |
| Prerenal failure may have | hyaline casts, very high ADH, urea, Na and H2O reabsorption |
| What are some consequences of renal failure and the inability to make urine and eliminate nitrogenous wastes? (8) | 1. Anemia, 2. Renal osteodystrophy, 3. Hyperkalemia, 4. Metabolic acidosis, 5. Uremic encephalopathy, 6. Na and H20 excess, 7. Chronic pyelonephritis, 8. Hypertension |
| What are the most common causes for chronic renal failure? (2) | Hypertension and Diabetes |
| What is the most common cause of acute renal failure? | Hypoxia |
| Why is there anemia in renal failure? | the kidney endothelium does not make erythropoietin |
| Why is there osteodystrophy in renal failure? | vitamin D is no longer converted to its active form by 1-a-hydroxylase |
| Renal failure causes arrhythmias, metabolic acidosis, CHF and pulmonary edema d/t | electrolyte imbalances: hyperK, inc H, low HCO3, excess H20/Na |
| What does low [Na+] do? | causes disorientation, stupor, coma |
| What does hi [Na+] do? | causes neurologic irritability, delirium, coma |
| What does low [Cl-] do? | it occurs 2* to metabolic alkalosis |
| What does hi [Cl-] correspond with? | it is 2* to non-anion gap acidosis |
| What does low [K+] do? | causes U waves, flattens T waves, causes arrhythmias and paralysis |
| What does hi [K+] do? | it Peaks T waves and causes arrhythmias |
| What does low [Ca++] do? | causes tetany, neuromuscular irritability |
| Waht does hi [Ca++] do? | causes delirium, renal stones and abdmonial pain/constipation |
| What does low [Mg++] do? | causes neuromuscular irritability and arrhythmias |
| What does hi [Mg++] do? | causes delirium, dec DTRs, and cardiopulmonary arrest |
| What does low [PO4--] do? | causes bone loss d/t low mineral ion product |
| What does hi [PO4--] do? | causes renal stones, and metastatic calcification d/t high-mineral ion product |
| Alcoholism | physiologic dependence and tolerance w/ symtoms of withdrawal (tremor, tachycardia, HTN, malaise, nausea, delirium tremens) when intake is interrupted; affects life; Tx = Disulfiram |
| Complications of Alcoholism | hepatitis, cirrhosis, pancreatitis, dilated cardiomyopathy, peripheral neuropathy, cerebellar degeneration, Wernicke-Korsakoff, testicular atrophy, hyperestrinism, Mallory-Weiss syndrome |
| Respiratory Acidosis (w/ inc HCO3 reabsorption) | low pH, PCO2 > 40; hypoventilation (lung diseases, opioids, narcotics, sedatives, weak respiratory muscles) |
| Normal Anion Gap Metabolic Acidosis with Hyperventilation as Compensation | low pH, PCO2 <40; d/t diarrhea, glue sniffing, renal tubular acidosis, hyperchloremia; Kussmaul respirations |
| Increased Anion Gap (Na - (Cl + HCO3) Metabolic Acidosis with Compensation | MUD PILES: methanol, uremia, DKA, paraldehyde or phenformin, iron tablets or INH, lactic acidosis, ethylene glycol, salicylates; |
| Respiratory alkalosis (w/ inc HCO3 secretion) | high pH, PCO2 <40; hyperventilation, aspirin ingestion (early) |
| Metabolic Alkalosis with Hypoventilation as Compensation | low pH, PCO2 >40; Vomiting, diuretic use, antacid use, hyperaldosteronism |
Created by:
bscaryp