Step 1 - Renal 1
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obinno59's
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2012-08-10 20:20
Gen
| Question | Answer |
|---|---|
| Course of Ureters | pass under uterine artery and under ductus deferens (retroperitoneal) - water under the bridge |
| Total body water weight percentage | 60% TBW |
| ECF vs ICF % | 1/3 ECF |
| ECF distribution | 1/4 plasma volume, 3/4 interstitial volume |
| ICF composition | ↑K+,↓NaCl [composition of what compartment] |
| How to measure plasma volume | radiolabeled albumin [measures?] |
| Extracellular volume measured by | inulin |
| Composition of Glomerular filtration barrier | 1. Fenestrated capillary endothelium (size barrier) 2. Fused basement membrane with heparan sulfate (negative charge barrier) 3. Epithelial layer consisting of podocyte foot processes |
Tubular/plasma concen. along PT
| Question | Answer |
|---|---|
| PAH | RPF |
| Creatine | approx. GFR, slightly↑ |
| Inulin&mannitol | GFR |
| Urea mech | Filtered freely, Reabsorbed MORE than PAH& Inulin |
| HCO3 | Rapidly reabsorbed |
| Glucose & AA | Rapidly reabsorb. |
| Na &K+ | reabsorb =to water |
| What subs. will be ABOVE the curve | PAH, creatine, urea, Inulin, mannitol |
| What subs. will beBELOW the curve | HCO3, Glu& AA, Na& K |
Filtration dynamics
| Question | Answer |
|---|---|
| Renal clearance | (Urine concentration x Urine flow rate) / Plasma concentration of X |
| Clearance < GFR = | net tubular reabsorption |
| Clearance > GFR = | net tubular secretion of X |
| Clearance = GFR = | no net secretion or reabsorption |
| Normal GFR | 100mL/min |
| Effective Renal plasma flow can be estimated using | PAH clearance because it is both filtered and actively secreted in the proximal tubule - All PAH entering kidney is excreted - underestimates true RPF by 10% |
| GFR estimated by | Creatinine clearance (slightly overestimates it - b/c moderately secreted) |
| Filtration Fraction | Normally 20% - GFR/RPF; Filtered load = GFR x Plasma concentration |
| Afferent Arteriole control | prostaglandins dilate afferent arteriole (↑RPF, ↑GFR so FF remains constant) - blocked by NSAIDs |
| Efferent Arteriole control | Angiotensin II constricts efferent arteriole (↓RPF, ↑GFR - FF increases) - blocked by ACE inhibitor |
| Renal blood flow | Renal artery→interlobar artery→interlobular artery→afferent→glomerulus→efferent→vasa recta→interlobular vein→interlobar vein→renal vein |
| Effects on glomerulus if Afferent arteriole constricts | ↓RPF, ↓GFR, No change in FF |
| Effects on glomerulus if Efferent Arteriole constricts [3 things] | ↓RPF, ↑GFR, ↑FF [effect on glomerulus if what happens?] |
| Effects on glomerulus with ↑ in plasma protein concentration | No change in RPF, ↓ in GFR, ↓ FF |
| Effects on glomerulus if with ↓ in plasma protein concentration | No change in RPF, ↑ GFR, ↑ FF |
| Effects on glomerulus if ureter constricts | No change RPF, ↓ GFR, ↓ FF |
| Question | Answer |
|---|---|
| Free water clearance definition | Ability to dilute urine. Given urine flow rate, urine osmolarity, and plasma osmolarIty, be able to calculate free water clearance = total urine (V) - water occupied with solute (C osm) |
| Free water clearance w/ ADH | < 0 = retention of free water |
| Free water clearance without ADH | > 0 (excretion of free water) |
| Free water clearance in isotonic urine | = 0 (seen with loop diuretic) |
| Calculation of filtered load | GFR x Plasma concentration |
| Calculation of excretion rate | Volume of urine x Cocentration in urine |
| Calculation of Reabsorption | Filtered - excreted |
| Calculation of Secretion | excreted - filtered |
| Glucosuria threshold | plasma level of 160-200 mg/dL - at 350mg/dL all transporters are fully saturated (Tm) |
| Amino acid clearance | Sodium-dependent transporters in proximal tubule reabsorb amino acids by at least 3 distinct carrier systems, with competitive inhibition within each group - Deficiency of neutral amino acid (Tryptophan) transporter is called Hartnup's disease, results in pellagra. |
renal endocrine reg
| Question | Answer |
|---|---|
| Juxtaglomerular apparatus (JGA) | modified smooth muscle of afferent arteriole and macula densa - secrete renin in response to ↓ renal blood pressure. ↓ Na+ delivery to distal tubule and ↑ sympathetic tone (beta 1) |
| Macula densa | Na+ sensor in DCT |
| Kidney endocrine functions | EPO, Vitamin D, Renin, Prostaglandins |
| Erythropoietin | released in response to hypoxia from endothelial cells of peritubular capillaries |
| 1,25-(OH)2 vitamin D | proximal tubule cells convert 25-0H vitamin D to 1,25(OH)2 vitamin D, which ↑intestinal reabsorption of both calcium and phosphate. Parathyroid hormone (PTH) acts directly on the kidney and ↑ renal calcium reabsorption and ↓ renal phosphate reabsorption.PTH also acts indirectly stimulating proximal tubule cells to make 1,25-(OH) vitamin D, which ↑ intestinal absorption of both calcium and phosphate. |
| Renin | secreted by jC cells In response to ↓ renal arterial pressure and ↑ renal sympathetic discharge (Beta 1 effect). |
| Prostaglandins | paracrine secretion vasodilates the afferent arterioles to ↑ GFR. |
tubule sites of action
| Question | Answer |
|---|---|
| Early proximal tubule | contains brush border - reabsorbs all of the glucose and amino acids and most of the bicarb, Na, Cl and water. 2. Isotonic absorption 3. Generates and secretes ammonia, which acts as a buffer for secreted H+ |
| PTH action in proximal tubule | inhibits Na+/phosphate cotransport → phosphate excretion |
| AT II action in proximal tubule | stimulates Na+/H+ exchange → ↑ Na+ and H2O reabsorption (permitting contraction alkalosis) |
| Thick ascending loop of Henle | actively reabsorps Na+, K+, Cl- and indirectly induces the paracellular reabsorption of Mg2+ and Ca2+ - impermeable to H2O - makes urine less concentrated as it ascends |
| Thin descending loop of Henle | passively reabsorbs water via medullary hypertonicity (impermeable to Na) - concentrating segment - make urine hypertonic |
| Collecting tubules | reabsorb Na+ in exchange for secreting K+ and H+ (regulated by aldosterone) |
| Aldosterone action on Collecting tubules | leads to insertion of Na+ channel on luminal side |
| ADH action on collecting tubules | acts at V2 receptors → insertion of aquaporin H2O channels on luminal side |
| Early distal convoluted tubule | actively reabsorbs Na, Cl, diluting segment - makes urine hypotonic |
| PTH actions in early distal convoluted tubule | ↑ Ca/Na exchange →↑ Ca reabsorption |
| Angiotensin II actions | 1. Vasoconstriction (receptors on vascular smooth muscle) 2. Constrict efferent arteriole of glomerulus (↑FF, preserve GFR) 3. Promote aldosterone production 4. Promote ADH production 5. ↑ proximal tubule Na/H activity increasing H2O reabsorption 6. Stimulate hypothalamus (thirst) 7. Effects baroreceptor function, limits reflex bradycardia |
| Aldosterone actions | ↑ Na channel, Na/K pump insertion in principal cells, enhances K and H excretion (upregulates principal cells K+ channels and intercalated cell H+ channels) this creates favorable Na+ gradient for Na and H2O reabsorption - primarily regulates blood volume (in low-volume state, both ADH and aldosterone act to protect blood volume) |
| ANP | released from atria in response to ↑ volume( ↑ atrial pressure) , may act as a check on RAAS, relaxes vascular smooth muscle via cGMP, causing ↑ GFR (↑ Na filtration w/ no reabsorption compensated) , ↓ renin |
| Potassium shift out of cell (causing hyperkalemia) | 1. Insulin deficiency (↓ Na+/K+ ATPase) 2. Beta -adrenergic antagonists (↓ Na+/K+ ATPase) 3 Acidosis, severe exercise (K+/H+ exchanger) 4. Hyperosmolarity 5. Digitalis (blocks Na+/K+ ATPase) 6. Cell lysis |
| K shift into cell (causing hypokalemia) | 1. Insulin (↑ Na+/K+ ATPase) 2. B-adrenergic agonists (↑ Na+/K+ ATPase) 3. Alkalosis (K/H exchanger) 4. Hypo-osmolarity |
acid base
| Question | Answer |
|---|---|
| Metabolic acidosis changes | ↓ pH, ↓PCO2, ↓↓ HCO3 - hyperventilation as compensation |
| Metabolic alkalosis changes | ↑pH, ↑pCO2, ↑↑ HCO3 - hypoventilation as compensation |
| Respiratory acidosis changes | ↓pH, ↑↑pCO2, ↑HCO3 - ↑ renal [HCO3] reabsorption |
| Respiratory alkalosis changes | ↑pH,↓↓pCO2, ↓HCO3 - ↓ renal [HCO3] reabsorption |
| Winter’s formula | Used to calculate respiratory compensation to metabolic acidosis - PCO2 = 1.5(HCO3) + 8 (+/- 2) - - - PCO2 ↑ 0.7mmHg for every ↑ 1 mEq/L HCO3 |
| Diagnosis and causes of Respiratory acidosis | arterial pH < 7.4 and pCO2>40mmHg - Hypoventilation: Airway obstruction, Acute lung disease, Chronic lung disease, Opioids, narcotics, sedatives, Weakening of respiratory muscles |
| Diagnosis of metabolic acidosis | arterial pH< 7.4 and PCO2<40mmHg and probably hyperventilation - check anion gap to determine the type |
| Anion gap calculation | Na+ - (Cl- + HCO3) - normal anion gap value (8-12 mEq/L) |
| ↑ anion gap acidosis causes | MUDPILES - Methanol (formic acid), Uremia, Diabetic ketoacidosis, Paraldehyde (or Phenformin), Iron tablets or INH, Lactic Acidosis, Ethylene glycol (oxalic acid), Salicylates |
| Normal anion gap metabolic acidosis causes | Diarrhea, Glue Sniffing, Renal tubular acidosis, Hyperchloremia |
| Respiratory Alkalosis diagnosis and causes | arterial pH>7.4, PCO2<40mmHg - Hyperventilation (early high altitude exposure), Aspirin ingestion (early) |
| Metabolic Alkalosis diagnosis and causes | arterial pH>7.4, PCO2>40mmHg - Hypoventilation compensation - Diuretic use, Vomiting, Antacid use, Hyperaldosteronism |
RTA
| Question | Answer |
|---|---|
| Type 1 Renal tubular acidosis | -Defect in collecting tubule's ability to excrete H+. -Impaired H+ secretion because of H+/K+ pump dysnfunction in the intercalated cell. So there is acidemia (metabolic acidosis) with highly alkaline urine Associated with hypokalemia and risk for calcium kidney stones |
| Type 2 Renal tubular acidosis | -Defect in proximal tubule HCO3- reabsorption . -One of the causes for proximal RTA is primary HyperPTH. PTH inhibits Na+/phosphate co-transport in prox convo tubule and causes phosphate excretion - AssocIated with hypokalemia and hypophosphatemic rickets. |
| Type 4 Renal tubular acidosis | Hypoaldosteronismor lack or collecting tubule response to aldosterone →hyperkalemia → inhibition of ammonia excretion in proximal tubule. -Hyperkalemia raises intracellular pH by exchange with protons, impairing enzymes involved in ammoniagenesis -Leads to ↓ urine pH due to ↓ buffering capacity. |
cast in urine
| Question | Answer |
|---|---|
| RBC casts are sign of | glomerulonephritis, ischemia, or malignant hypertension [casts type] |
| WBC casts are sign of | tubuiointerstltiaI inflammation, acute pyelonephritis, transplant rejection. |
| Presence of casts indicates | that hematuria/pyuria is of renal origin |
| Granular ("muddy brown" ) casts indicate | acute tubular necrosis [cast type] |
| Waxy casts indicate | advanced renal disease/CRF [cast type] |
| Hyaline casts indicate | nonspecific [casts] |
| RBCs, but no casts, in urine indicate | Bladder cancer, kidney stones [cast type] |
| WBCs (ie, pyuria), but no casts in urine indicate | Acute cystitis |
Nephritic syndromes
| Question | Answer |
|---|---|
| Nephritic syndrome | -An Inflammatory process. when it involves glomeruli, it leads to hematuria and RBC casts in urine. Associated with azotemia, oliguria, HTN,and proteinuria « 3.5 g/day). |
| Acute poststreptococcal glomerulonephritis LM | -Glomeruli enlarged and hypercellular, neutrophils, “lumpy-bumpy" appearance. |
| Acute poststreptococcal glomerulonephritis EM vs IF? | Nephritic, subepithelial immune complex (IC) humps. vs. IF= granular. |
| Acute poststreptococcal glomerulonephritis notes | Most frequently seen in children Peripheral and periorbital edema. Resolves spontaneously but pretty bad in Adults!!!! |
| Rapidly progressive (crescentic) glomerulonephritis (RPGN) LM and IF | -Nephritic , Crescent- shape. -Crescent consists of fibrin and plasma proteins with glomerular parietal cells, monocytes, and macrophages |
| These 3 diseases can result in (RPGN) diseases | Nephritic 1. Goodpasture’s (type II hypersensitivity Ab against GBM (linear IF) 2. Wegener’s granulomatosis (c-ANCA) 3. Microscopic polyarteritis (p-ANCA) |
| Goodpastures syndrome | Nephritic (RPGN) disease, type II hypersensitivity Ab against GBM (linear IF) |
| Wegener’s granulomatosis | Nephritic RPGN (c-ANCA) |
| Microscopic polyarteritis | Nephritic RPGN (p-ANCA) |
| DPGN | -Nephritic 1.Subendothelial DNA-anti-DNA ICs - wire looping of capillaries 2. Granular IF 3. MC cause of death in SLE |
| Berger’s disease (IgA glomerulonephropathy) | Nephritic 1. ↑ synthesis of IgA 2. LM and IF - ICs deposit in mesangium 3. Often presents/flares with a URI or acute gastroenteritis |
| Alport’s syndrome | Nephritic 1. Mutation in type IV collagen→split basement membrane 2. Nerve disorders, ocular disorders, deafness 3. X-linked , but can also be AR and AD |
Nephrotic syndromes
| Question | Answer |
|---|---|
| Nephrotic syndrome [presentation] | Presents with massive proteinuria (> 3. 5g/day, frothy urine), hyperlipidemia, fatty cast, edema. A/w thromboembolism and ↑ risk of infection (loss of immunoglobulins). |
| Membranous glomerulonephritis (diffuse membranous glomerulopathy) | Nephrotic, -LM =diffuse capillary and GBM thickening. -EM ="spike and dome" appearance with subepithelial deposits. -IF= granular. -SLE's nephrotic presentation |
| Membranous glomerulonephritis (diffuse membranous glomerulopathy) cause | -"SPIKE AND DOME", SUB-EPI ICs -Meds: Captopril, NSAIDs, gold, mercury, penicillamine (chelator), probenecid (gout tx) -Infections: [eg, HBV, Plasmodium, Syphilis], -Diseases: SLE, Hodgkin's |
| Minimal change disease (lipoid nephrosis) | Nephrotic - LM - normal glomeruli - EM - foot process effacement -Selective loss of ALBUMIN ONLY, not globulins, due to GBM polyanion loss 2. May be triggered by a recent infection or an immune stimulus 3. MC in children. 4. Responds to steroids. |
| Amyloidosis | Nephrotic 1. LM - congo red stain, apple-green birefringence 2. A/w MM, chronic conditions, TB, RA |
| Diabetic glomerulonephropathy and Tx? | 1.(NEG) of GBM → ↑ permeability, thickening. NEG of efferent arterioles (hyaline ateriolosclerosis of eff) ↑GFR → mesangial expansion. Type 1>Type 2 2.LM- MESANGIUM, GBM thickening, - TYPE IV COLLAGEN -Nodular glomerulosclerosis (Kimmelstiel-Wilson lesion) Tx- ACE-I |
| FSGS | Nephrotic 1.LM-segmental sclerosis and hyalinosis 2.MC glomerular disease in HIV patients - more severe in HIV patients |
| Type I MPGN | Nephrotic 1. 1.SubENDO lCs with granular IF. 2. Type I EM- “tram-track" appearance due to GBM splitting caused by mesangial ingrowth. 3. Can present as nephritic syndrome 4. Usually progresses slowly to CRF 5. Type I is associated with HBV>HCV |
| Type II MPGN | 1. Type II= EM-dense deposits. 2. Type II= a/w C3 nephritic factor((means C3 will be used up), autoab binds to C3 Convertase (C3BBB) leading to sustained activation so VERY LOW C3 |
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