Busy. Please wait.
or

show password
Forgot Password?

Don't have an account?  Sign up 
or

Username is available taken
show password

why


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
Don't know
Know
remaining cards
Save
0:01
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
Retries:
restart all cards
share
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

Renal

QuestionAnswer
Estimated Renal Plasma Flow = [urine PAH] x Flow rate = PAH clearance (Underestimates RPF by 10%)
Renal Blood Flow = Renal Plasma Flow / (1-Hct)
Filtration Fraction = GFR / RPF
Filtered Load = GFR x plasma concentration
Angiotensin II Vasoconstriction (but not the afferent arteriole), Pressure Natriuresis (PCT Na absorption), Aldosterone & ADH release, thirst. Antagonized by ANP. Synthesized in liver.
Glucosuria Begins at 200mg/mL. Transport saturated @ 350mg/dL
Proximal Convoluted Tubule All Glucose, Protein, MOST Bicarb, Na, H20. Iso-osmotic
Thin Descending Loop of Henle Passive H20 absorption & urea excretion -> urine hypertonic
Thick ascending Loop of Henle NKCC pump (Where furosemide acts) actively reabsorbs salts, indirectly absorbs Mg & Ca. Impermeable to urea, H20 -> urine hypotonic
Distal Convoluted Tubule Na/Cl co-transporter (where Thiazides act). ENaC sodium reabsorption. PTH-mediated Ca reabsorption. Impermeable to urea (maintains at least some osmolarity to the hypotonic urine).
Collecting Tubules Aldosterone-mediated Na reabsorption for K. ADH mediated H20 & little urea reabsorption
PTH in the Kidney Increases PTC calcium absorption, decreases DCT PO4 absorption. Alpha1 hydroxylase expression to produce 1,25 (OH)2 Vitamin D.
Anion Gap Metabolic Acidosis Etiology PCO2<40. MUDPILES: Methanol, Uremia, DKA, Paraldehyde, Phenformin, Iron, INH, Lactic acidosis, Ethylene glycol, Salicylates
Non Anion Gap Metabolic Acidosis Etiology (8-12) PCO2<40. Diarrhea, Glue Sniffing, hyperchloremia, Renal tubular acidosis (Type 1: H pump defect, Type 2: renal bicarb loss, Type 4: Hyperaldo-> HyperK -> No ammonia excretion)
Respiratory Acidosis Etiology Hypoventilation (primary lung problem). PCO2 > 40
Respiratory Alkalosis Etiology PCO2<40. Early aspirin ingestion, Hyperventilation.
Metabolic Alkalosis Etiology PCO2>40. Diuretics, Vomiting, antacids, Hyperaldosteronism.
Metabolic Acidosis Formula 1.5(HCO3) + (6 to 10) = PCO2 (WINTER’S FORMULA)
Metabolic Alkalosis Formula .7(HCO3 increase above 40) = PCO2 increase
Respiratory Alkalosis Formula Acute: .2(PCO2 decrease) = HCO3 drop CHRONIC: .5(PCO2 decrease)= HCO3 drop
Respiratory Acidosis Formula Acute: .1(PCO2 elevation) = HCO3 increase Chronic: .35(PCO2 Elevation) = HCO3 increase
Nephritic Syndromes Type III Hypersensitivities (-Godpastures). Sx: Hematuria, HTN, Oliguria, Azotemia. Acute Post-Strep Glomerulonephritis, Membranoproliferative G., Rapidly Progressive/Crescentic G., Goodpasture’s, Berger’s/IgA Nephropathy, Alport’s.
Enlarged/hypercellular glomeruli, neutrophilic infiltrate. EM: Supepithelial humps. IF: Granular Acute Post-streptococcal Glomerulonephritis. Pediatric. Peripheral/periorbital edema. Self-resolves
Subendothelial Humps, Tram tracking (Mesangial cell consume Dense deposits & lay down new BM Membranoproliferative Glomerulonephritis. Slowly progressive to renal failure.
Crescent-Moon Shape LM & IF Rapidly progressive glomerulonephritis. Rapidly progresses to renal failure.
Linear IF. IgA mesangial deposits Berger’s Disease/ IgA Nephropathy. Mild, Post-infx. Recurrent hematuria.
Linear Immunofluorescence, Anti-GBM antibodies Goodpasture’s Syndrome (Type II hypersensitivity). Hemoptysis, hematuria.
Split basement membrane Alport’s Syndrome. Collagen Type IV mutation. Deafness, ocular disorders.
Nephrotic Syndromes Proteinuria. Frothy urine, hypoalbuminemia, peripheral & Periorbital edema, hyperlipidemia. Membranous Glomerulonephritis, Minimal Change Disease, Focal Segmental Glomerular Sclerosis (FSGS), Diabetic Nephropathy, SLE, Amyloidosis.
Diffuse capillary & BM thickening, granular immunofluorescence, spike & dome EM Membranous Glomerulonephritis. #1 in adults
Normal glomeruli & foot process effacement Minimal Change Disease #1 Pediatric. Tx: steroids
Segmental sclerosis & hyalinosis Focal Segmental Glomerular Sclerosis. HIV
K-W Nodules, BM thickening Diabetic Nephropathy
Diffuse capillary & BM thickening. Wire-loop leisions w/ subepithelial deposits SLE Nephropathy. 5 patterns.
Amyloid Deposits (Congo red +, Apple green) Amyloidosis: MM, TB, RA, chronic conditions.
Renal Cell Carcinoma Polycythemia, palpable mass, hematuria, flank pain. Associated w/ VHL (ch3), Smoking, obesity, 50-70yos. Paraneoplastic: EPO, ACTH, PTHrP, Prolactin
Wilm’s Tumor #1 Pediatric. Embryonic structures. WT1 deletion (Ch11). May be part of WAGR: Wilms, Anirida (no iris), GU malformation, MR
Transitional Cell Carcinoma #1 of Urinary tract. Painless hematuria. Associated w/Phenacetin, Smoking, Aniline dyes, Cyclophosphamide.
Pyelonephritis WBC casts pathognomonic. Affects cortex. Fever, CVA tenderness. Corticomedullary scaring, blunted calyx.
Diffuse Cortical Necrosis Abruptio Placentae, Septic shock -> DIC & Vasospasm -> Bilateral renal cortex infarction
Drug-Induced interstitial Nephritis Penicillins, NSAIDs, Diuretic-Hypersensitivity -> Interstitial Inflammation -> Systemic signs + Hematuria 2wks post-administration
Acute Tubular Necrosis #1 ARF. Ischemia/shock, Trauma, Toxins -> epithelial detachment, necrosis -> muddy brown casts. Death in early oliguric phase, recovery in 2-3 wks.
Renal Papillary Necrosis DM, Acute Pyelonephritis, Chronic Phenacetin use(ie-tylenol), Sickle Cell Anemia -> Hypoxic injury to medulla-> necrosis.
PRERENAL Acute Renal Failure High Osmolarity (>500), BUN/Cr Ratio (>20), low Na (10)& FeNa (1%) (Hypotension -> low RBF)
INTRINSIC Acute Renal Failure Low Osmolarity (<350), Moderate Na (20)& FeNa (2%), Low BUN/Cr (ATN, Ischemia, Toxins) Epithelial & Muddy Brown Casts.
POSTRENAL Acute Renal Failure Low Osmolarity (<350), high Na(40), FeNa (4%), Moderate BUN/Cr (>15). BPH, Stones, Neoplasia.
Chronic Renal Failure HTN, Diabetes Induced
Renal Failure Consequences Uremia & uremic encephalopathy. Anemia (no EPO), Renal Osteodystrophy (no VD), Hyperkalemia, Metabolic Acidosis (no excretion w/ typical high-acid diet), Na & H20 Excess (CHF & PE), Chronic Pyelonephritis, HTN
Fanconi’s Syndrome Proximal Tubule LOF -> No resorption of AAs, Glucose, PO4, Uric Acid, electrolytes. Consequences: Rickets, Osteomalacia, Hypokalemia, metabolic acidosis.
Dialysis Cysts Cortex & medulla. Due to Chronic Dialysis
Simple Cysts Cortex. Benign.
Medullary Cystic Disease Medullary. Small kidney. Poor prognosis
Medullary Sponge Disease Collecting ducts. Good prognosis.
Hyper & Hyponatremia Sx HypoNa: Disoriented, stuporous, coma. HyperNa: Irritable, Delirious, coma
High & Low Cl Etiologies Low Cl: Metabolic alkalosis, HypoK, Hypovolemia, High aldo. HIGH Cl: Non-Anion Gap Acidosis
Hyper & HypoKalmeia Sx HypoK: U waves, flat T waves, Arrhythmias, paralysis. HyperK; Peaked T waves, wide QRS, arrhythmias
Hyper & HypoCalcemia Sx HypoCa: Tetany, Neuromuscular irritability. HyperCa: Delirium, Renal Stones, Abdominal pain, +/-Calcuria
Hyper & HypoMagnesmia Sx HypoMg: Neuromuscular irritability, arrhythmias. HyperMg: Delirium, weak DTRs, cardiac arrest
Hyper & HypoPhosphatemia Sx HypoPO4: Bone loss, osteomalacia HyperPO4: Metastatic calcification, renal stones
Mannitol Mech: Osmotic diuresis. USE: Shock, drug OD, reduce ICP, IOccularP. SE: PE, dehydration, CI’d in anuria, CHF
Acetazolamide Mech: Carbonic anhydrase inhibitor, excreting HCO3. USE: Glaucoma, alkalinize urine, metabolic alkalosis, altitude sickness. SE: HyperCl metabolic acidosis, neuropathy, NH3 toxicity, Sulfa allergy
Furosemide & Ethacrynic Acid Mech: NKCC blocker, preventing urine concentration. USE: Edematous states, HTN, HyperCa. SE: Ototoxicity, HypoK, sulfa allergy, interstitial nephritis, gout.
HCTZ Mech: NaCl blocker in DCT. USE: HTN, CHF, HyperCa tx, Nephrogenic DI. SE: HypoK Metabolic Alkalosis, hypoNa; HyperGLUC: Glycemia, Lipidemia, Uricemia, Calcemia. Sulfa allergy
Spironolactone Spironolactone, Triamterene, Amiloride. Mech: Spiro: Aldosterone Receptor Blocker; Triam & Amil: CCT ENaC Blockers. Use: Hyperaldosteronism, HypoKalemia tx, CHF. SE: HyperK. Spironolactone: Gynecomastia, antiandrogenic.
ACE Inhibitors Capto, Elana,Lisino-pril. Use: HTN, CHF, Diabetic renal disease. SE: CAPTOPRIL: Cough, Angioedema, Proteinuria, Taste change, hypotension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Low angII + HyperK. CI’d in Renal Artery Stenosis
Losartan Angiotensin II Receptor Antagonist. Use: Same as ACE Inhibitors when patient has bradykinin-induced cough.
Henderson Hasselbach Equation pH= pKa + log [HCO3]/.03PCO2 Describes acid-base response
Cause of Hyperkalemia & Hypokalemia HyperK: Low insulin, aldosterone, sympathetic tone, acidosis, digitalis, hyperosmolarity. HypoK: High insulin, aldosterone or sympathetic tone, alkalosis, hypoosmolarity.
Anion gap Na - (Cl + HCO3)= anion gap
Created by: Kyle Tiemeier