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Renal
FA complete Review
| Question | Answer |
|---|---|
| At which week does the pronephros degenerates? | 4th Week |
| What are the roles of the Mesonephros? | Functions as: 1. Interim kidney for the 1st trimester 2. Later contributes to male genitalia system |
| Which embryological state of the kidney is the permanent kidney? | Metanephros |
| At which week does the metanephros appear? | Week 5 |
| What is the average time of neurogenesis in the developing embryo? | 32-36 weeks |
| What structures are derived by the Ureteric bud? | Ureter, pelvises, calyces, collecting ducts |
| By which which is the Ureteric bud supposed to be fully canalized? | Week 10 |
| What is another term used for metanephric mesenchyme? | Metanephric blastema |
| What is the result from the interaction of the ureteric bud and the metanephric mesenchyme? | Differentiation and formation of glomerulus through to distal convoluted tubule (DCT) |
| Aberrant interaction of the Ureteric bud and Metanephric mesenchyme lead to: | Congenital kidney malformations, such as, Renal agenesis, multicystic dysplastic kidney |
| What embryological area or tissue is the last to be canalized? | Ureteropelvic junction |
| What area of the embryological kidney is the MC to be obstructed? | Ureteropelvic junction |
| Obstruction of the Ureteropelvic junction is diagnosed with US, and is called ___________________. | Hydronephrosis |
| What conditions are associated with the Potter sequence? | Pulmonary hypoplasia Oligohydramnios (trigger) Twisted face Twisted skin Extremity defects Renal failure in utero |
| What is the MCC of death in Potter sequence? | Pulmonary hypoplasia |
| Potter sequence is associated with Oligo- or Polyhydramnios? | Oligohydramnios |
| What are the facial abnormalities seen in Potter sequence? | Low-set ears, retrognathia, and flattened nose |
| What causes the pulmonary hypoplasia in Potter sequence? | Compression of chest and lack of amniotic fluid aspiration into fetal lungs |
| What are some common causes of Potter sequence? | ARPKD, obstructive uropathy (posterior urethral valves), bilateral renal agenesis, chronic placental insufficiency, |
| What is the common obstructive uropathy that leads to development of Potter sequence? | Posterior urethral valve obstruction |
| What is "Horseshoe kidney"? | Inferior poles of both kidneys fuse abnormally |
| What artery "traps" the normal ascend of the kidneys of the Horseshoe kidney? | Inferior Mesenteric Artery |
| What conditions are associated with Horseshoe kidney? | Hydronephrosis, renal stones, infection, chromosomal aneuploidy syndromes, and rarely renal cancer. |
| What chromosomal aneuploidy syndromes are associated with Horseshoe kidney? | Turner syndrome; trisomies 13, 18, and 21. |
| What are two common presentations of Congenital solitary functioning kidney? | Unilateral renal agenesis and Multicystic dysplastic kidney. |
| Which condition is seen with complete absence of a kidney and ureter? | Unilateral Renal agenesis |
| What is the cause of Unilateral Renal agenesis? | Ureteric bud fails to develop and induce differentiation of metanephric mesenchyme |
| What condition is seen when the ureteric bud fails to develop and induce differentiation of metanephric mesenchyme? | Unilateral renal agenesis |
| Which condition is seen when the ureteric bud only fails to differentiate the metanephric mesenchyme? | Multicystic dysplastic kidney |
| What condition is seen with an non-functional kidney consisting of cysts and connective tissue? | Multicystic dysplastic kidney |
| What is the consequence of bilateral Multicystic dysplastic kidney? | Potter sequence |
| What is Duplex Collecting system? | Bifurcation of ureteric bud before it enters the metanephric blastema creates a Y-shaped bifid ureter. |
| What are the main associated conditions with Duplex Collecting System? | Vesicoureteral reflux and/or ureteral obstruction, and increase risk for UTIs. |
| What are (embryologically) the Posterior urethral valves? | Membrane remnant in the posterior urethra in males |
| Persistence of the Posterior urethral valves leads to : | Obstruction |
| What signs can identify prenatally the presence of Posterior urethral valves obstruction? | Hydronephrosis and dilated or thick-walled bladder on US. |
| What is the MCC of bladder outlet obstruction in male infants? | Posterior urethral valves obstruction |
| Which kidney is used for donor transplantation? | Left kidney |
| Why is the Left kidney preferably used for donor transplantation? | It has a longer renal vein |
| Renal blood flow path. What structure follow the flow after the afferent arteriole? | Glomerulus |
| Renal blood flow path. Glomerulus ---> Efferent arterioles -----> ______________. | Vasa recta/peritubular capillaries --> venous outflow |
| The Juxtaglomerular cells are located between which two nephrogenic structures? | Distal convoluted tubule and the Afferent arteriole |
| Which cells line up the luminal face of the basement membrane of the glomerulus? | Podocytes |
| The podocytes form the ________ layer of the glomerular basement membrane. | Visceral |
| In a normal cross-section view of a kidney, which vessel is represented above the other, the renal vein or renal artery? | Renal artery |
| From which structure do ureters arise form? | Renal pelvis |
| Course of the ureters. Initiate at the renal pelvis then --> | Travel under the gonadal arteries --> over common iliac artery --> under uterine artery/vas deferens (retroperitoneal) |
| Ureters travel over which vascular structure? | Common iliac artery |
| Which iliac artery is associated with the course path of the ureters? | Common iliac artery |
| The ureters travel or course under two different arterial structures, which are? | First under the gonadal arteries, and lagter under the Uterine artery |
| What retroperitoneal structure is traveled under by the Ureters? | Vas deferens |
| What kind of surgical procedures may cause damage to the ureters? | Gynecologic procedures |
| What are the 3 main locations of construction of the ureters? | 1. Ureteropelvic junction 2. Pelvic inlet 3. Ureterovesical junction |
| Which female structure is described in the course of the ureters in the retroperitoneal area? | Uterine artery |
| What protein level or amount can be used to measure the plasma volume? | Albumin |
| The amount of inulin or mannitol can be measured to calculate which body volume? | Extracellular volume |
| Normal Osmolality range | 285-295 mOsm/kg H2O |
| What is the main component of ICF? | K+, Mg2+, organic phosphates |
| The ECF is mainly composed of: | Na+, Cl-, HCO3-, and albumin |
| What is the principal function or responsibility of GFR? | Filtration of plasma according to size and charge selectivity |
| What is the composition of the Glomerular filtration barrier? | 1. Fenestrated capillary endothelium 2. Basement membrane with type IV collagen chains and heparan sulfate. 3. Epithelial layer consisting of podocyte foot processes |
| How is the Glomerular filtration membrane charge? | Negatively |
| What is the symbol representing Renal clearance? | Cx |
| What is the equation used to calculate renal clearance? | (Ux V) = ---------- Px |
| What is Ux? | Urine concentration of X |
| What is Px? | Plasma concentration of X |
| What is represented by V in the equation for renal clearance? | Urine flow rate |
| If the Renal clearance is less than GFR ===> | Net tubular REABSORPTION of X |
| If the Cx is greater of GFR ===> | Net tubular SECRETION of X |
| What does it mean to be "freely filtered"? | Substance is neither reabsorbed nor secreted |
| Inulin clearance can be used to calculate===> | Glomerular filtration rate (GFR) |
| What value can be used to measure the GFR? | Inulin clearance |
| What is the normal GFR? | 100 mL/min |
| What is the equation of GFR? | (U inulin x V) = ------------------- (P inulin) |
| What measured value slightly overestimates GFR? | Creatinine clearance |
| Why is there a slight overestimation of the GFR when measured with Creatine clearance? | Moderately secreted by renal tubules |
| What is described by incremental reduction in GFR? | Define the stages of chronic kidney disease |
| PAH clearance can be used to estimate __________________. | Effective renal plasma flow (eRPF) |
| What is the equation for RBF? | (RPF) = -------------- (1 - Hct.) |
| TBV x (1-Hct) = | Plasma volume |
| What is the normal FF? | 20% |
| FF = | GFR =---------- RPF |
| What kind of drugs inhibit the afferent renal arteriole? | NSAIDS |
| The use of NSAIDS causes ____________________ of the ____________ arteriole. | Vasoconstriction ; Afferent |
| What medication types cause a dilation of the afferent arteriole? | Prostaglandins |
| Angiotensin II preferential ___________ ___________ arteriole. | Constricts efferent |
| What is the effect in the efferent arteriole of an ACE inhibitor? | Vasodilation |
| In reference to renal filtration what does the mnemonic PDA stands for? | Prostaglandins Dilate Afferent arteriole |
| In reference to renal filtration, what does the mnemonic ACE stands for? | Angiotensin II Constricts Efferent arteriole |
| In simple words, what is meant by a substance been secreted? | Going from the vasa recta/ or Peritubular arteriole into the renal glomerular tubule system |
| If a substance goes from the lumen of the PCT into the vasa recta, is its said it has been ___________________. | Reabsorbed |
| Any substance is considered FILTERED if goes from: | The Bowman space into the PCT |
| What is the main effect in glomerular dynamic in case of dehydration? | Severely decrease in RPF |
| What action can cause a decrease in both glomerular dynamics, GFR and RPF, but no changes in FF? | Afferent arteriole constriction |
| Increase in plasma protein concentration causes what kind of changes in glomerular dynamics? | Decrease in GFR and FF, but no changes in RPF |
| How is RPF affected in cases of changes of plasma protein concentration? | Unaffected |
| What causes the greatest change or decrease in RPF? | Dehydration |
| What action is the only one that keeps the FF unaffected? | Afferent arteriole constriction |
| The constriction of the efferent arteriole due to angiotensin II, causes the following glomerular dynamic changes: | Increase in GFR and FF, and a decrease in RPF |
| Where is glucose completely reabsorbed in the renal system? | Proximal convoluted tubule (PCT) |
| What mechanism in the PCT is used to reabsorb glucose? | Na+/glucose cotransporter |
| In adults, at what value of plasma glucose, starts the evidence of glucosuria? | 200 mg/dL |
| At what value or point are all transporters in charge of glucose reabsorption at PCT fully saturated? | 375 mg/min |
| What condition, causes to lower the threshold of glucosuria? | Anything that raises Filtration |
| What kind of drugs are intended or used to lower the threshold of glucose and have glycosuria at levels lower than 200 mg/dL? | Sodium-glucose cotransporter (SGLT2) inhibitors |
| What is the "Splay phenomenon"? | Tm for glucose is reached gradually rather than sharply due to the heterogeneity of nephrons |
| How is the "slay" in glucose reabsorption graph represented? | Portion f of titration curve between threshold and Tm. |
| Which part of the nephron reabsorbs most of the Na+? | Early PCT |
| Which substances are completely reabsorbed in the PCT? | Glucose and Amino Acids |
| Where do most of K+, Cl-, phosphate, bicarbonate, Na+, water and uric acid reabsorption occur in the nephron? | Early PCT |
| Which are two common hormones and/or proteins that act on the PCT? | PTH and AT II. |
| What is the role of PTH in the PCT? | Inhibition of the Na+/phosphate cotransport, which eventually leads to Phosphate excretion |
| What is the role or function of AT II in the early PCT? | Stimulation of Na+/H+ exchange, which leads to Increased reabsorption of Sodium, water, and bicarbonate. |
| What is the result of the increased reabsorption of Na+, water, and bicarbonate in the PCT due to AT II? | Contraction alkalosis |
| What compound is generated and secreted in the PCT ? | NH3 |
| What is the role or function of NH3 generation and secretion in the PCT? | Enables the kidney to secrete more H+. |
| What is the physiologic role of the Thin descending loop of Henle? | Passively reabsorbs water via medullary hypertonicity |
| Which part of the nephron makes urine hypertonic? | Thin descending loop of Henle |
| What area of the loop of Henle is known as the concentrating segment? | Thin descending loop of Henle |
| The Thin descending loop of Henle is impermeable to: | Na+ |
| Which part of the loop of Henle is impermeable to water? | Thick ascending loop |
| What is directly reabsorb by the Thick ascending loop of Henle? | Na+, K+, and Cl- |
| What is indirectly reabsorbed in the Thick ascending loop of Henle? | Mg2+ and Ca2+ |
| Urine becomes _______ concentrated as it ascends the Thick loop of Henle. | Less |
| What causes the indirect paracellular reabsorption of Mg2+ and Ca2+ in the Thick ascending loop of Henle? | K+ backleak |
| Which part of the nephron has hypotonic urine? | Early DCT |
| What ions or electrolytes are reabsorbed in the early DCT? | Na+ and Calcium |
| The DCT is impermeable to _____________. | Water |
| How does PTH work on the DCT? | Increase the Ca2+/Na+ exchange ----> Ca2+ reabsorption |
| What is the physiologic role of the Collecting tubules of the Nephron? | Reabsorbs Na+ in exchange for secreting K+ and H+ |
| What mineralocorticoid regulates the reabsorption of Na+ in the Collecting tubules of the Nephron? | Aldosterone |
| Which are the two types of cells in which Aldosterone act upon in the Collecting tubes of the Nephron? | Principal cells and a-intercalated cells |
| What is the result of Aldosterone interacting with the Principal cells in the Collecting tubes? | Increase: apical K+ conductance, Na/K pump, epithelial Na channel activity, leading to lumen negativity, which then results in K+ secretion. |
| What is happens as Aldosterone interacts with a-intercalated cells of the Collecting tubule? | The lumen negativity leads to Increase in H+ ATPase activity, leading to H+ secretion, which then results in an increase in bicarbonate/Cl- exchanger activity. |
| ADH interacts the _____ receptor of the Collecting tubules. | V2 |
| What is the result of ADH interaction at the Collecting tubule's V2 receptors? | Insertion of aquaporin H2O channels on the apical side. |
| What is the renal tubular defect seen at the PCT? | Fanconi syndrome |
| What is the renal tubular defect in the Thick ascending loop of Henle? | Bartter syndrome |
| Which part of the nephron has a renal tubular defect in Gitelman syndrome? | PCT |
| Which are the two known renal tubular defects of the Collecting tubules of the Nephron? | Liddle syndrome and Syndrome of Apparent Mineralocorticoid Excess. |
| What is the defect in nephron seen in Fanconi syndrome? | Generalized reabsorption defect in PCT, which leads to increased excretion of amino acids, glucose, bicarbonate and phosphate, among other substances reabsorbed in the PCT. |
| What are the electrolyte effects seen in Fanconi syndrome? | Metabolic acidosis (proximal RTA), hypophosphatemia, and osteopenia. |
| Which drugs are associated to the development of Fanconi syndrome? | Ifosfamide, cisplatin, and expired tetracyclines |
| Which renal tubular defect presents similar fashion as chronic use of loop diuretics? | Bartter syndrome |
| What is the main defect in Bartter syndrome? | Resorptive defect in thick ascending loop of Henle, that mainly affects the Na+/K+/2Cl- cotransporter. |
| Defective Na+/K+/2Cl- cotransporter. Diagnosis? | Bartter syndrome |
| What electrolyte imbalances are seen with Bartter syndrome? | Metabolic alkalosis, hypokalemia, and hypercalciuria. |
| Fanconi syndrome develops metabolic ________________, while Bartter syndrome is classically seen with metabolic ____________. | Fanconi ---- acidosis Bartter ------ alkalosis |
| Which three renal tubular syndromes are AR inheritance? | Bartter, Gitelman, and SAME |
| What renal tubular defect is due to reabsorption defect of NaCl in DCT? | Gitelman syndrome |
| Which of the renal tubular defects is the only one seen with developing metabolic acidosis? | Fanconi syndrome |
| Presents similarly to lifelong thiazide diuretic use. Dx? | Gitelman syndrome |
| What is a key electrolyte imbalance seen in Gitelman syndrome? | Hypomagnesemia, and hypocalciuria |
| Which syndrome is more severe, Bartter or Gitelman syndrome? | Bartter syndrome |
| Which renal tubular defect presents similar to hyperaldosteronism, but with aldosterone almost undetectable? | Liddle syndrome |
| What is the cause of Liddle syndrome? | Gain of function mutation --> Increase activity of Na+ channel -----> Increase Na+ reabsorption in collecting tubules |
| Metabolic alkalosis, low serum K+, hypertension, and low/undetectable aldosterone. Most likely diagnosis? | Liddle syndrome |
| What is the MC treatment of Liddle syndrome? | Amiloride |
| What enzyme deficiency is related to SAME? | 11B- hydroxysteroid dehydrogenase |
| What is the role of 11B-hydroxysteroid dehydrogenase in cells with mineralocorticoid receptors? | Conversion of cortisol into cortisone |
| In cases of SAME, the deficiency of 11B-hydroxysteroid dehydrogenase, leads to: | Excess cortisol ---> Increased mineralocorticoid receptor activity |
| What is the main treatment for SAME? | K-sparing diuretics or corticosteroids |
| What is the purpose of using K+-sparing diuretics in the treatment of SAME? | Decrease mineralocorticoid effects |
| What common substance is often indicated with the highest value of secretion and concentration along the PCT? | PAH |
| Which common substance has a very low depiction in the Relative concentrations along PCT curve? | Glucose and amino acids (glucose the lowest) |
| Why do Tubular inulin concentration increases along the length of the PCT? | As result of water reabsorption |
| If the [TF/P] > 1, it means: | Solute is secreted and water is reabsorbed less quickly than the solute. |
| What is the action of Aldosterone on a-intercalated cells? | Promote H+ secretion due to increased activity of H+ ATPase |
| Which two substances act on the Principal cells of the the collecting tubules? | Aldosterone and ADH |
| What is the result of aldosterone interaction with the Principal cells? | Sodium reabsorption and K+ secretion due to increase K+conductance, Na/K ATPase activity, and ENaC activity. |
| Which cells secrete Renin? | JG cells |
| Why do JG cells secrete Renin? | In response to: 1. decreased renal perfusion pressure, 2. Increase renal sympathetic discharge (B1 effect), and , 3. Decreased NaCl delivery to macula densa cells |
| Which kind of receptors detect a decrease in renal perfusion pressure? | Renal Baroreceptors in the Afferent arteriole |
| What is the main function or role of AT II? | Maintain blood pressure and blood volume |
| Which common endogenous enzyme limits reflex bradycardia, in cases of using a pressors in a patient? | AT II |
| Which substances serve as "check" on renin-angiotensin-aldosterone system? | ANP and BNP |
| What are the actions resulting of ANP and BNP activity? | Dilates afferent arteriole, Constricts efferent arteriole, Promotes Natriueresis |
| ANP causes ___________ in afferent arteriole. | Dilation |
| BNP and ANP cause the efferent arteriole to ________________. | Constrict |
| Which endogenous cardiac protein is secreted in order to promote natriuresis? | ANP (from atria) and BNP (from ventricles) |
| What substance primarily regulates ECF and Na+ content? | Aldosterone |
| What is the role of Renin in Angiotensin pathway? | Converts Angiotensinogen into Angiotensin I |
| Which organs can secrete ACE? | Lungs and Kidneys |
| What is the Juxtaglomerular apparatus? | Consists of mesangial cells, JG cells, and the macula densa. |
| What is the role of the JGA (Juxtaglomerular apparatus)? | Maintains GFR via renin-angiotensin-aldosterone system. |
| What is the Macula densa, and where is it located? | NaCl sensor, located at distal end of loop of Henle |
| What happens when the Macula densa senses a decrease in NaCl delivery to the DCT? | Increase renin release, which cause efferent arteriole vasoconstriction ==> Increased GFR. |
| What kind of antiarrhythmics can cause inhibition of B1-receptors of the JGA causing a decrease renin release? | B-blockers |
| What cells release Erythropoietin? | Interstitial cells in peritubular capillary bed |
| EPO is release as a response to ___________________. | Hypoxia |
| RBC proliferation in bone marrow is stimulated by? | Erythropoietin |
| How is the PCT involved in vitamin D metabolism? | Converts 25-OH vitamin D3 to 1, 25-(OH)2 vitamin D3 |
| What is the name of 1, 25-(OH)2 vitamin D3? | Calcitriol, active form |
| What is the enzyme used to convert Vitamin D3 into its active form in the PCT? | 1a-hydroxylase |
| What hormone catalyzes the action of 1a-hydroxylase? | PTH |
| What is the role of Dopamine by PCT cells? | Promotion of natriuresis |
| Dopamine in low doses causes _________________ in arterioles. | Vasodilation |
| High doses of dopamine causes __________, contrary to low doses. | Vasoconstriction |
| What conditions cause hypokalemia due to shifts of K+ into cells? | Hypo-osmolarity, alkalosis, B-adrenergic agonist, Insulin |
| Shifts K+ out of the cell causes --> | Hyperkalemia |
| What are some conditions that cause hyperkalemia by K+ shifts out of the cell? | Digitalis, Hyperosmolarity, Lysis of cells, Acidosis, B-blockers, high blood sugar, and Succinylcholine. |
| What are clinical presentation of Low Na+ concentration? | Nausea and malaise, stupor, coma, seizures |
| How is hypernatremia is clinically presented? | Irritability, stupor, coma |
| What EKG changes are seen with hypokalemia? | U waves and flattened T waves |
| Hypokalemia is seen clinically with? | Arrhythmias, muscle cramps, spasm, weakness |
| What EKG changes are seen with high serum concentration of Potassium? | Wide QRS and peaked T waves |
| How is hypocalcemia clinically presented? | Tetany, seizures, QT prolongation, twitching (Chvostek sign), spasm (Trousseau sign). |
| (+) Chvostek and Trousseau signs are presented with _____________. | Hypocalcemia |
| What are some signs of low serum Mg2+ concentration? | Tetany, torsades de pointes, hypokalemia, and hypocalcemia |
| A person with elevated serum levels of Mg2+? | Decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia |
| Low phosphate in blood is seen with: | Osteomalacia (adults) and Rickets (children) |
| What is the most significant change in Conn syndrome? | Elevated aldosterone |
| What renal disorders have most significantly low aldosterone levels? | Liddle syndrome, and SAME |
| What is the main electrolyte clue and/or change in Bartter syndrome? | Increased urine calcium |
| What is the compensatory response form Metabolic acidosis? | Hyperventilation |
| A patient with Metabolic alkalosis is immediately compensated? | Hypoventilation |
| What electrolyte change is most important in Metabolic acidosis/alkalosis? | Bicarbonate |
| Increase in [HCO3-] creates metabolic________________. | Alkalosis |
| Increased renal [HCO3-] reabsorpton is compensatory of: | Respiratory acidosis |
| A change in partial carbon dioxide (PCO2), will cause a respiratory or metabolic change? | Respiratory |
| What are the common causes of Respiratory Acidosis? | Airway obstruction, Acute lung disease, Chronic lung disease, Opioids, sedatives, weakening of respiratory muscles. |
| If a condition makes respiration difficult or weak, the patient is likely to develop: | Respiratory acidosis |
| The loss of H+ or the excess of bicarbonate lead to ---> | Metabolic alkalosis |
| What are some causes of Metabolic alkalosis? | Loop diuretics, Vomiting, Antacid use, and Hyperaldosteronism |
| What conditions are associated Respiratory alkalosis? | Anxiety/ panic attack, Hypoxemia, Salicylates, tumor, and pulmonary embolism. |
| Normal anion gap metabolic acidosis is caused by: | Hyperalimentation, Addison disease, Renal tubular acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion. |
| Increase anion gap metabolic acidosis is a caused by: | Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron tablets, INH, Lactic acidosis, Ethylene glycol, and salicylate (late) |
| What is the main defect of Renal Tubular acidosis type I? | Inability of a-intercalated cells to secrete H+ ----> no new bicarbonate is generated leading to ---> metabolic acidosis |
| What is the urine pH in RTA type I? | > 5.5 |
| What are some common causes of RTA I? | Amphotericin B toxicity, analgesic nephropathy, congenital anomalies of urinary tract, and autoimmune diseases such as SLE. |
| Distal renal tubular acidosis type I is associated with: | - Increased risk for calcium phosphate kidney stones |
| Why is there an increase risk of Ca-phosphate kidney stones in RTA I patients? | Increase urine pH and Increased bone turnover |
| What type of electrolyte disorder is caused by all types of RTA? | Normal anion gap (hypochloremic) metabolic acidosis |
| What is the pH of RTA II and RTA IV? | < 5.5 |
| What is the main defect in Proximal RTA II? | Defective PCT bicarbonate reabsorption --> Increase excretion of bicarbonate in urine ----> metabolic acidosis |
| What are some causes of Proximal RTA II? | Fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors |
| What is an associated risk of Proximal RTA II? | Hypophosphatemic rickets in Fanconi syndrome |
| Hyperkalemic Tubular acidosis main defect is: | Hypoaldosteronism or aldosterone resistance; hyperkalemia ---> decreased NH3 synthesis in PCT ------> decreased NH4+ excretion |
| What is the level (high or low) of K+ in Distal RTA and Proximal RTA II? | Low serum K+ levels |
| Which type of RTA is the only one seen with Hyperkalemia? | Type IV |
| What are the main two categories that cause RTA IV? | 1. decreased aldosterone production 2. Aldosterone resistance |
| Examples of conditions that may decrease the production of aldosterone? | Diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency |
| What are examples that demonstrate aldosterone resistance? | K+-sparing diuretics nephropathy due to obstruction, TMP-SMX use. |
| What does the presence of cast indicate? | Hematuria /pyuria is of glomerular or renal tubular origin |
| What conditions show RBC casts? | Glomerulonephritis and hypertensive emergency |
| In which conditions can we find WBC casts? | Tubulointerstitial inflammation, acute pyelonephritis, and transplant rejection |
| Fatty casts are also known as: | Oval fat bodies |
| What conditions have the presence of Fatty casts? | Nephrotic syndrome |
| What is an associated sign of Fatty casts? | "Maltese cross" sign |
| What kind of casts are found in Acute tubular necrosis (ATN)? | Granular ("muddy brown") casts |
| Waxy casts are seen with: | End-stage renal disease/ chronic renal failure |
| A patient with a long stand Hx of CKD, most likely will present with what kind of casts in the urine? | Waxy casts |
| Which kind of casts may be considered a normal finding in urine analysis? | Hyaline casts |
| It is defined as focal is the ________ of glomerulus is damaged or involved. | < 50% |
| What term or nomenclature is used to describe a condition in which more than 50% of the glomeruli is involved? | Diffuse |
| What are examples of Secondary glomerular diseases? | SLE and Diabetic nephropathy. |
| Which are the 2 Nephritic-Nephrotic syndromes? | 1. Diffuse proliferative glomerulonephritis 2. Membranoproliferative glomerulonephritis |
| What amount of protein per day must be lost in order to be consider a nephrotic syndrome? | >3.5 g/ day |
| What kind of damage is the main cause of Nephrotic syndrome pathologies? | Podocyte disruption which lead to charge barrier impaired. |
| What are the common Nephrotic syndrome diseases? | 1. Focal segmental glomerulosclerosis 2. Minimal change disease 3. Membranous nephropathy 4. Amyloidosis 5. Diabetic glomerulonephropathy |
| What are the most common Nephritic syndrome examples? | 1. Acute poststreptococcal glomerulonephritis 2. Rapidly progressive glomerulonephritis 3. Iga nephropathy (Berger disease) 4. Alport syndrome 5. Membranoproliferative glomerulonephritis |
| What kind of glomerular diseases are due to GBM disruption? | Nephritic syndromes |
| What are key characteristics of all Nephritic syndrome? | Hypertension, Increased BUN and Creatine, oliguria, hematuria, RBC casts in urine. |
| Which are the key characteristics of Nephrotic syndrome? | Massive proteinuria with hypoalbuminemia, resulting edema, hyperlipidaemia, and frothy urine with fatty casts. |
| What are state is associated with Nephrotic syndrome pathology? | Hypercoagulable state due to antithrombin (AT) III loss in urine and increase risk of infection. |
| What is the MCC of nephrotic syndrome in children? | Minimal change disease |
| What are some common triggers for MCD? | Recent infection, immunization, immune stimulus. |
| What kind of treatment has excellent response to Primary MCD? | Corticosteroids |
| What is the EM of MCD? | Effacement of podocyte foot processes |
| How is the glomeruli in MCD under LM? | Normal glomeruli |
| What is the most common cause of nephrotic syndrome African-Americans and Hispanics? | Focal segmental glomerulosclerosis |
| Focal segmental glomerulosclerosis is often secondary to: | HIV infection, sickle cell disease, heroin abuse, massive obesity, interferon treatment, or congenital malformations |
| Inconsistent response to corticosteroids in Focal segmental glomerulosclerosis leads to: | Chronic kidney disease |
| What is the LM description of FS glomerulosclerosis? | Segmental sclerosis and hyalinosis |
| IF in Focal Segmental glomerulosclerosis? | Negative but may (+) for nonspecific focal deposits of IgM, C3, and C1. |
| Membranous nephropathy is can be primary due to: | - Antibodies to phospholipase A2 receptor |
| What are secondary causes of Membranous nephropathy? | Drugs such as NSAIDs, penicillamine, gold, or Infections such as HBV, HCV, syphilis, and other SLE and solid tumors |
| What nephrotic syndrome has LM described as diffuse capillary and GBM thickening? | Membranous nephropathy |
| IF in Membranous nephropathy is? | granular due to IC deposition |
| EM described as "spike and dome" appearance of subepithelial deposits. Dx? | Membranous nephropathy |
| Another name of Membranous nephropathy? | Membranous glomerulonephritis |
| How does Membranous nephropathy respond to corticosteroids? | Poorly |
| What is the LM description of Amyloidosis? | Congo red stain shows apple-green birefringence under polarized light due to amyloid deposition in the mesangium. |
| What is the most involved organ in Amyloidosis? | Kidney |
| What is the MCC of End-stage Renal Disease (ESRD) in the United States? | Diabetic glomerulonephropathy |
| What is the result of hyperglycemia in Diabetic glomerulonephropathy? | Nonenzymatic glycation of tissue protein ---> Mesangial expansion; GBM thickening and increased permeability |
| What is seen in the LM of Diabetic glomerulonephropathy? | Mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis |
| What is the WBC seen in Diabetic glomerulonephropathy? | Eosinophils |
| What are the Kimmelstiel -Wilson lesions? | Eosinophilic nodular glomerulosclerosis seen in Diabetic glomerulonephropathy |
| Nephritic syndrome is considered an ________________________ process. | Inflammatory |
| What structure needs to be involved in nephritic syndromes in order to present with hematuria and RBC casts in urine? | Glomeruli |
| Nephritic syndromes are associated with what clinical features? | Azotemia, oliguria, hypertension, proteinuria, hypercellular/inflamed glomeruli on biopsy. |
| What type of nephritic syndrome is most common seen children? | Acute poststreptococcal glomerulonephritis |
| Common cause/Hx for Acute PSGN? | 2-4 weeks after group A streptococcal infection of pharynx or skin |
| What kind of bacteria is involved in PSGN? | Group A Streptococcus |
| PSGN is an type ______ hypersensitivity reaction. | III |
| What are the clinical features of PSGN? | Peripheral and periorbital edema, cola-colored urine, and HTN |
| What are common lab results for a patient with PSGN? | (+) strep titers/ serologies, and decreased complement levels (C3) due to consumption |
| What is the LM of PSGN? | Glomeruli enlarged and hypercellular |
| "starry sky" granular appearance ("lumpy-bumpy") due to IgG, IGgM, and C3 deposition along GBM and mesangium. Describes? | IF findings of PSGN |
| PSGN EM description is: | Subepithelial immune complex humps |
| Which nephritic syndrome is related to the shape "crescentic"? | Rapidly Progressive glomerulonephritis |
| What is the main LM description of RPGN? | Crescent moon shape |
| What is the composition of crescents seen in RPGN? | Fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes, and macrophages |
| The different disease process that lead to RPGN are differentiated by what type of pattern? | IF pattern |
| What type of IF pattern is seen in RPGN due to Goodpasture syndrome? | Linear IF due to antibodies to GBM and alveolar basement membrane. |
| What is the treatment for Goodpasture syndrome? | Plasmapheresis |
| What are some key characteristics of Goodpasture syndrome? | Hematuria/ hemoptysis; type III hypersensitivity reaction |
| RPGN due to Granulomatosis with polyangiitis has what kind of IF pattern? | Negative IF/ Pauci-immune (no Ig/C3 deposition) |
| LM- "wire looping" of capillaries | Diffuse proliferative glomerulonephritis |
| Diffuse proliferative glomerulonephritis often presents as: | Nephrotic and Nephritic syndrome concurrently |
| What is the IF pattern seen in Diffuse proliferative glomerulonephritis? | Granular |
| Which nephritic syndrome is described with EM of subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition? | Diffuse proliferative glomerulonephritis |
| Another name for IgA nephropathy? | Berger disease |
| Episodic hematuria that occurs concurrently with respiratory of GI tract infections? | IgA nephropathy |
| What renal pathology is highly associated with HSP? | IgA nephropathy |
| Which Nephritic syndrome IF, EM,and LM is related to mesangium description? | IgA nephropathy |
| IgA-based IC deposits in mesangium, describes? | IF findings in Berger disease |
| Mutation type IV collagen. Dx? | Alport syndrome |
| What is the result of mutation type IV collagen in Alport syndrome? | Thinning and splitting of glomerular basement membrane. |
| What is the most common type of inheritance of Alport syndrome? | X-linked dominant |
| What are the clinical features seen with Alport syndrome? | Eye problems (retinopathy, lens dislocation), glomerulonephritis, sensironurularl deafness |
| What is the classical description of Alport syndrome EM view? | "Basket-weave" |
| What type of hearing loss or deafness is developed in Alport syndrome? | Sensorineural deafness |
| What are common infections that develop Type 1 Membranoproliferative glomerulonephritis? | Hepatitis B or C infection |
| IF of Type 1 Membranoproliferative glomerulonephritis? | Subendothelial IC deposits with granular IF |
| What nephritic factor is associated with Type 2 Membranoproliferative glomerulonephritis? | C3 |
| What is the role of C3 nephritic factor? | IgG antibody that stabilized C3 convertase ---> persistent complement activation ---> decrease C3 levels |
| The IgG antibody stabilization of C3 convertase is due to what specific factor activity? | C3 nephritic factor |
| What is another name for the Intramembranous deposits seen in type 2 membranoproliferative glomerulonephritis? | Dense deposit disease |
| What some characteristics that both, type 1 and 2 membranoproliferative glomerulonephritis present? | GBM splitting --> "tram-track" appearance on H&E and PAS stains |
| What are stains often mentioned or used to depict the mesangial ingrowth of membranoproliferative glomerulonephritis? | H&E and PAS |
| What are serious complication of Kidney stones? | Hydronephrosis and Pyelonephritis |
| What is the typical clinical presentation of kidney stones in patient? | Unilateral flank tenderness, colicky pain radiating to groin, and hematuria |
| What is the MC kidney stone presentation? | Calcium oxalate stone in patient with hypercalciuria and normocalcemia |
| What is the MC urine Calcium level seen in a patient with a kidney stone? | Elevated Calcium urine level |
| What is the serum level MC seen in a patient with an Calcium-oxalate kidney stone? | Normal calcium level |
| What are the two types of Calcium kidney stones? | Calcium oxalate (hypocitraturia) and Calcium phosphate |
| What is the description of the Urine crystal of Calcium oxalate kidney stone? | Shaped like envelope or dumbell |
| Enveloped or dumbbell shaped kidney stone? | Calcium oxalate |
| Hypocitraturia is associated with: | Calcium oxalate nephrolithiasis due to decreased urine pH. |
| What are the most common type of Calcium kidney stones | Calcium oxalate |
| What are some common causes of development of Calcium oxalate kidney stones? | Ethylene glycol (antifreeze) ingestion, vitamin C abuse, hypocitraturia, and malabsorption (Crohn's disease). |
| What type of IBS syndrome is often associated with Calcium oxalate kidney stone formation? | Crohn disease |
| What is the MC treatment for all Calcium kidney stones? | Thiazides and low-sodium diet |
| What are the CT and X-ray findings of Calcium stones? | Radiopaque |
| Increased pH can precipitate which kind of Calcium stone? | Calcium phosphate |
| An decreased in pH value (acidosis) is commonly related precipitation of which calcium kidney stone? | Calcium oxalate |
| Which is the "basic"/"alkalotic" precipitated calcium kidney stone? | Calcium phosphate |
| Which are the two types of kidney stones that precipitate with an increase (alkalotic change) in pH? | Calcium phosphate and Ammonium-Magnesium-Phosphate stones |
| What is the shape of struvite stones? | Coffin lid |
| What is another name for ammonium magnesium phosphate kidney stones? | Struvite |
| What kind of organisms (bugs) cause Struvite formation? | Urease (+) |
| What are some organisms that are urease (+)? | Proteus mirabilis, Staphylococcus saprophyticus, and Klebsiella |
| How do urease (+) organisms cause struvite formation? | Urease (+) busgs hydrolyse urea into ammonia -->Urine alkalization |
| Staghorn calculi refers to? | Ammonia Magnesium Phosphate renal stones |
| What is the treatment for Struvite calculi? | Treat underlying infection and surgical removal of calculi |
| Rhomboid or rosettes urine crystal indicate? | Uric acid stone |
| What are the CT/and X-ray findings of Struvite? | Radiopaque |
| A ________ in pH leads to Uric acid renal stone formation. | Decrease |
| Which two, non-calcium, renal stones require acidic environments in order to precipitate? | Uric acid and Cystine stones |
| What are some strong diseases and conditions that lead to Uric acid renal stone formation? | 1. Hyperuricemia (gout) 2. Disease with increased cell turnover (Leukemia) |
| Patient with podagra, may develop more readily what kind of renal calculi? | Uric acid stone |
| What is the treatment indicated for Uric acid kidney stone? | - Alkalinization of urine, and, - Allopurinol |
| What is the description of Uric Acid stone under X-ray image? | Radiolucent |
| Which type of renal calculi is minimally visible in CT scan? | Uric acid stone |
| Cysteine kidney stone is in what shape? | Hexagonal |
| What type of renal stone is seen with a (+) Sodium Cyanide nitroprusside test? | Cystine |
| What is the treatment of Cystine stones? | Low-sodium diet, alkalinization of urine, and chelating agents if refractory |
| Defects that cause a an serum increase in cysteine levels are often associated with what kind of renal stones? | Cystine |
| What is a common AR defect that can cause cystinuria, and eventually cystine stones? | Cystine-reabsorbing PCT transporter losses function |
| What are 4 common amino acids seen with defective cysteine-reabsorption PCT reabsorption function? | COLA: Cysteine, Ornithine, Lysine, and Arginine |
| What is plasmapheresis? | Process in which liquid part of blood, the plasma, is separated from the red blood cells. |
| Why is plasmapheresis used in Goodpasture syndrome as treatment? | The plasma of the blood contains the antibodies that affect the immune system, thus, separating the plasma allow for removal of autoantibodies in GPS. |
| What is hydronephrosis? | Distension/dilation of renal pelvis and calyces |
| What are the main causes of Hydronephrosis? | 1. Urinary tract obstruction 2. Retroperitoneal fibrosis 3. Vesicoureteral reflux |
| What are some common UT obstructions that cause hydronephrosis? | Renal stones, severe BPH, congenital obstructions, cervical cancer, and injury to ureter |
| Where does dilation occur in hydronephrosis? | Proximal to site of pathology |
| What conditions of hydronephrosis may lead to an increase in serum creatine? | 1. Bilateral obstruction or, 2. Obstructed solitary kidney |
| What are some possible complications of untreated hydronephrosis? | Compression and atrophy of renal cortex and medulla |
| What is the most common primary renal malignancy? | Renal cell carcinoma |
| Polygonal clear cells filled with accumulated lipids and carbohydrate. Often golden-yellow due to increased lipid contedn. MC malgnanc? | Renal cell carcinoma |
| Where does RCC originates in the nephron? | PCT |
| What could be serious complication is RCC invades the LEFT renal vein? | Varicocele |
| What is the first and second vascular structures that RCC invades in its path to lung and bone metastasis? | First the renal vein and then the IVC. |
| What is the common clinical picture of RCC patient? | Manifest with hematuria, palpable masses, secondary polycythemia, flank pain, fever and weight loss |
| What type of renal malignancy is resistant to chemotherapy and radiation therapy? | Renal cell carcinoma |
| What is a common medication in the treatment of RCC once it cause a disseminated condition? | Aldesleukin |
| What are some risk factors or conditions for RCC development? | 1. Age -- 50-70 years old 2. Smoking 3. Obesity |
| What type of renal cancer is associated with Paraneoplastic syndromes? | Renal cell carcinoma |
| What are some associated paraneoplastic syndromes in RCC? | PTHrP, Ectopic EPO, ACTH, and Renin |
| What is a common AD condition associates with Renal cell carcinoma? | von Hippel-Lindau syndrome |
| vHL disease is associated with which chromosome gene deletion? | Chromosome 3 |
| Renal oncocytoma? | Benign epithelial cell tumor arising from collecting ducts. |
| Where in the nephron does a renal oncocytoma most likely arises from? | Collecting ducts |
| What is a common histologic description of Renal oncocytoma? | Large eosinophilic cells with abundant mitochondria without perinuclear clearing |
| What is a more common name for Nephroblastoma? | Wilms tumor |
| What is the most common child (2-4 years old) renal malignancy? | Wilms tumor |
| What malignancy is due to a "loss of function" mutations of tumor suppressor genes WT1 and WT2 on chromosome 11? | Wilms tumor |
| WT1 and WT2 are both: | Tumor suppressor genes |
| What are the 3 most common syndromes in which Wilms tumor may be a part of? | 1. WAGR complex 2. Denys-Drash syndrome 3. Beckwith-Wiedemann syndrome |
| What are the common components of WAGR complex? | Wilms tumor, Aniridia, Genitourinary malformations, mental retardation/intellectual disability |
| What is aniridia? | Absence of iris |
| What is Denys-Drash syndrome? | Condition in which Wilms tumor often seen, along with Diffuse mesangial sclerosis (early nephrotic syndrome), and dysgenesis of gonads |
| WAGR complex is usually due to a _______ of ______ gene. | Deletion of WT1 gene |
| What syndrome is often seen with a WT1 mutation? | Denys-Drash syndrome |
| What Wilms tumor-related syndrome arises from WT2 mutation? | Beckwith-Wiedemann syndrome |
| Wilms tumor, macroglossia, organomegaly, and hemihyperplasia. Dx? | Beckwith-Wiedemann syndrome |
| What is another name for Transitional cell carcinoma? | Urothelial carcinoma |
| What is the MC tumor of the urinary tract system? | Transitional cell carcinoma |
| Where in the urinary tract system can TCC can occur? | Renal calyces, renal pelvis, ureters, and bladder |
| What is common and key clinical sign of TCC? | Painless hematuria with no casts |
| What are associated problems with Transitional cell carcinoma (TCC)? | Phenacetin, Smoking, Aniline dyes, and Cyclophosphamide |
| Aniline dyes are often associated with the development of which kind of renal cancer? | Transitional cell carcinoma |
| What is the pathogenesis of the development of Squamous cell carcinoma of the bladder? | Chronic irritation of urinary bladder --> squamous metaplasia --> dysplasia and squamous cell carcinoma |
| What are some associated risk factors or Squamous cell carcinoma of the bladder? | 1. Schistosoma haematobium infection (Middle East) 2. Chronic cystitis, smoking, chronic nephrolithiasis |
| Squamous cell carcinoma of the bladder presents with _____________ hematuria. | Painless |
| What specie of Schistosoma is associated with the development of Squamous cell carcinoma of the Bladder? | Haematobium |
| What is the cause for Stress incontinence? | 1. Urethral hypermobility, or, 2. Intrinsic sphincteric deficiency |
| What is the treatment for Stress incontinence? | 1. Pelvic floor muscle strengthening (Kegel) exercises 2. Weight loss 3. Pessaries |
| Outlet incompetence describes more closely what type Urinary incontinence? | Stress |
| What type of urinary incontinence is seen with leak with increased intra-abdominal pressure? | Stress |
| What are some actions that can cause sudden increase in intra abdominal pressure and cause urine involuntary leakage? | Sneezing, cough, lifintn |
| What are some associated risk factors of Stress Urinary incontinence? | Obesity, vaginal delivery, prostate surgery |
| A positive bladder test. Dx? | Stress urinary incontinence |
| Urgency incontince is due to: | Overactive bladder --> leak with urge to void immediately |
| Detrussor instability is cause of what type of urinary incontince? | Urgency |
| UTI are often associated with ________ incontinence. | UTI |
| What kind of drugs are often used to treat urgency urinary incontinence? | Antimuscarinics (oxybutynin) |
| Patient on Oxybutynin. Suspect dx? | Urgency incontinence |
| What urinary incontinence is due to to detrusor underactivity and/or outlet obstruction? | Overflow incontinence |
| Incomplete emptying --> leak with overfilling, describes what type of urine incontinence? | Overflow |
| What are some conditions associated with overflow incontinence? | -Polyuria (diabetes), Bladder outlet obstruction (BPH), neurogenic bladder (MS) |
| What is the treatment for overflow incontinence? | Catheterization and relive obstruction |
| What type of drugs can be used to treat the overflow incontinence in a patient with severe BPH? | Beta blockers |
| Urinary tract infection is often referred as: | Acute bacterial cystitis |
| What is UTI? | Inflammation o f urinary bladder |
| How is UTI clinically presented? | Suprapubic pain, dysuria, urinary frequency, urgency. Usually no systemic symptoms. |
| What are the most common risk factors for developing UTI? | 1. Female gender (short urethra), 2. Sexual intercourse ("honeymoon cystitis") 3. Indwelling catheter 4. DM 5. Impaired bladder emptying. |
| What is the most common organism to cause an UTI? | E. coli |
| What is the second most common UTI-causing organism in a young sexually active women? | Staphylococcus saprophyticus |
| What UTI-causing organisms produces ammonia scent in urine? | Proteus mirabilis |
| What lab findings in UA indicate UTI infection due to gram negative organisms? | (+) Nitrites |
| What does Sterile pyuria and (-) urine cultures suggest as causing organism of an UTI? | N. gonorrhea or Chlamydia trachomatis |
| What is (+) result indicates UTI (E.coli)infection? | Leukocytes esterase |
| Why do women have higher risk of acquiring UTI? | Due to shorter urethra than men |
| When does Acute pyelonephritis occur? | As neutrophils infiltrate renal interstitium |
| What part of the urinary system is affected by pyelonephritis? | Affects the cortex with relative sparing of glomerular/ vessels |
| What is the typical description of flank pain in pyelonephritis? | Costovertebral angle tenderness |
| What are the two main causes of acute pyelonephritis? | Ascending UTI (E. coli MC), and Hematogenous spread to kidney |
| What are some featured finding in the UA of a acute pyelonephritis patient? | WBCs in urine and +/- WBC casts |
| What are common risk factors for Acute pyelonephritis? | Indwelling catheter, urinary tract obstruction, vesicoureteral reflux, DM, and pregnancy. |
| What are some concerning complications of acute pyelonephritis? | Chronic pyelonephritis, renal papillary necrosis, perinephric abscess, urosepsis. |
| What two conditions are most commonly present in order to develop chronic pyelonephritis? | Vesicoureteral reflux and chronically obstructed kidney stones |
| What renal pathology is often referred with the description of "Thyroidization of kidney"? | Chronic pyelonephritis |
| What is the thyroidization of kidney? | Tubules can eosinophilic casts resembling thyroid tissue |
| What is Xanthogranulomatous pyelonephritis? | Uncommon chronic destructive granulomatous process of the renal parenchyma; |
| What do the orange nodules in Xanthogranulomatous pyelonephritis may mimic? | Tumor nodules |
| What type of infection is associated with development of Xanthogranulomatous pyelonephritis? | Proteus infection |
| How is Acute Kidney injury defined? | Abrupt decline in renal function as measured by increased creatine and increased BUN or by oliguria/anuria |
| What are the main 3 types of Acute Kidney injury? | 1. Prerenal azotemia 2. Intrinsic renal failure 3. Postrenal azotemia |
| What is kind of Acute Renal injury is due to decreased RBF, such as hypotension? | Prerenal azotemia |
| Why is the BUN:Cr ratio elevated in Prerenal azotemia? | Urea is reabsorbed and not Creatine |
| What is the most common cause of Intrinsic renal failure? | Acute Tubular necrosis from ischemia or toxins |
| What less common causes of Intrinsic renal failure? | RPGN, Hemolytic uremic syndrome, or acute interstitial nephritis |
| What causes a decrease in GFR in a ATN patient with patchy necrosis? | Debris obstructing tubule and flud black low across necrotic tubule |
| What type of urine cast asr found in ATN? | Epithelial/granular casts |
| How is the BUN:Cr ratio of Intrinsic renal failure? | Decreased |
| A BUN:Cr less than 15 indicates: | Intrinsic renal failure |
| Prerenal azotemia has a BUN:Cr | Greater than 20 |
| What is the FE Na of Prerenal azotemia? | <1% |
| FE NA > 2% is seen with: | Intrinsic renal failure |
| Postrenal and Intrinsic renal failure have a Urine osmolality of: | < 350 |
| What is the common Urine osmolality value of Prerenal azotemia? | > 500 |
| What are some causes of Postrenal azotemia? | Stones, BPH, neoplasia, congenital anomalies |
| What are the 2 forms of renal failure? | 1. Acute (ATN) 2. Chronic (HTN, DM, congenital anomalies) |
| What is the definition of Renal failure? | Decline in renal filtration can lead to excess retained nitrogenous waste products and electrolyte imbalances |
| What are the consequences of Renal failure? | Metabolic Acidosis Dyslipidemia Hyperkalemia Uremia Na/water retention Growth retardation and developmental delay Erythropoietin failure Renal osteodystophy |
| What are the characteristics of Uremia due to renal failure? | Nause, anorexia, Pericarditis, Asterixis, Encephalopathy, and platelet dysfunction. |
| What is azotemia? | Abnormal condition due to abnormally high nitrogenous compounds in the blood. |
| Renal osteodystrophy is most commonly associated with which PTH condition? | Secondary hyperparathyroidism |
| What is a common result of the bones in Renal Osteodystrophy? | Thinning of the bones |
| Another term/name used for Acute Interstitial nephritis? | Tubulointerstitial nephritis |
| Acute interstitial renal inflammation is: | Acute interstitial nephritis |
| Acute interstitial nephritis is often due to: | Administration of drugs that act as haptens, inducing hypersensitive. |
| What are some common drugs associated with the development of Acute Interstitial Nephritis? | Diuretics, penicillins, proton pump inhibitors, sulfonamides, rifampin, NSAIDs |
| Pyuria with eosinophils and azotemia after administration of a new drug? | Acute interstitial nephritis |
| What is the MCC of Acute Kidney injury in hospitalized patients? | Acute Tubular Necrosis |
| What is the key finding in ATN? | Granular ("muddy brown") casts |
| What are the most common Ischemic causes of ATN? | Secondary to decreased RBF: - Hypotension, shock, sepsis, hemorrhage, HF |
| What re the most vulnerable areas of the nephron int ischemic injury in ATN? | PCT and thick ascending loop of Henle |
| ATN secondary to nephrotoxic substances is seen with: | Aminoglycosides, radiocontrast agents, lead, cisplatin, ethylene glycol, crush injury (myoglobinuria), hemoglobinuria |
| What part of nephron most susceptible to ischemic injury causing ATN? | Proximal tubules |
| Acute generalized cortical infarction of both kidneys. Dx? | Diffuse cortical necrosis |
| What is the MCC of Diffuse cortical necrosis? | Combination of vasospasm an DIC |
| What are some association of Diffuse cortical necrosis? | Obstetric catastrophes, and septic shock |
| Sloughing of necrotic renal papillae--> gross hematuria and proteinuria. Dx? | Renal papillary necrosis |
| What conditions and drugs are closely associated to Renal Papillary Necrosis? | Sickle cell disease or trait, acute pyelonephritis, NSAIDs, and Diabetes mellitus |
| What gene is the most common to cause ADPKD? | PKD1 on chromosome 16 |
| What is the most common causes of death in ADPKD? | CKD or Hypertension caused by increased renin production |
| What are some common associations of ADPKD? | Berry aneurysms, MVP, benign hepatic cysts, diverticulosis. |
| At what point should ADPKD is treated with ACE inhibitors and ARBs? | If hypertension or proteinuria develops |
| Numerous cysts in cortex and medulla causing bilateral enlarged kidneys ultimately destroy kidney parenchyma. Dx? | ADPKD |
| What gene mutation is accountable for only 15% of cases of ADPKD? | PKD2 gene mutation in on chromosome 4 |
| Cystic dilation of collecting ducts. Dx? | ARPKD |
| Autosomal recessive polycystic kidney disease s most associated with ____________. | Children |
| What is an important associative condition with ARPKD? | Congenital hepatic fibrosis |
| What are some concerns beyond neonatal period in cases of ARPKD? | Systemic HTN, progressive renal insufficiency, and portal hypertension form congenital hepatic fibrosis |
| What is another name for AD tubulointerstitial kidney disease? | Medullary cystic kidney disease |
| What is Autosomal dominant tubulointerstitial kidney disease? | Inherited disease causing tubulointerstitial fibrosis and prefessive renal insufficiency with inability to concentrate urine. |
| What part of the nephron does Mannitol acts on? | PCT and Thin descending loop of Henle |
| Where in the nephron des Acetazolamide works? | PCT |
| Loop diuretics work in the __________________________________. | Thick ascending loop of Henle |
| Thiazide diuretics work on the _____________ of the nephron | DCT |
| Which part of the nephron has K+sparing diuretics exert their action? | Cortical part of the Collecting duct |
| What is the mechanism of action of Mannitol? | Osmotic diuretic. Increased tubular fluid osmolarity --> increase urine flow, and decreases intranial/intraocular pressure |
| What the clinical use of Mannitol? | Drug OD, elevated intracranial or intraocular pressures |
| What are some significant side effects of Mannitol? | Pulmonary edema, dehydration, hypo-or hypernatremia. |
| What is the most significant adverse effect of Mannitol? | Pulmonary edema |
| Carbonic anhydrase inhibitor diuretic? | Acetazolamide |
| What is the mechanism of action of Acetazolamide? | Carbonic anhydrase inhibitor. Cause self limited NaHCO3 diuresis and decrease total body HCO3- stonres |
| What are the most common clinical uses of Acetazolamide? | Glaucoma, metabolic alkalosis, altitude sickness, pseudotumor cerebri. Alkalinizes urine |
| Which diuretic is commonly used to treat altitude sickness? | Acetazolamide |
| Common diuretic used to alkalinizes urine | Acetazolamide |
| Which diuretic can be used in the treatment of glaucoma? | Acetazolamide |
| What are the associated adverse effects of Acetazolamide? | Proximal RTA, paraesthesias, NH3 toxicity, sulfa allergy, and hypokalemia. |
| What type of renal stone is often precipitated in excess Acetazolamide therapy? | Calcium phosphate stone formation due to high pH |
| Which are common Sulfonamide Loop diuretics? | Furosemide, Bumetanide, and torsemide |
| What is the mechanism of action of Furosemide? | Inhibit cotransport system (Na/K/2Cl) of thick ascending limb of loop of Henle. |
| What is the result in the mechanism of action of Loop diuretics? | Abolish hypertonicity of medulla, preventing concentration of urine |
| What is release by the use of Loop diuretics? | PGE which has an vasodilatory effect on the afferent arteriole |
| Loops lose _____. | Ca2+ |
| What diuretic promotes the excretion of Calcium ion? | Loop diuretics |
| What is the non-sulfonamide loop diuretic? | Ethacrynic acid |
| What edematous states are commonly treated with Loop diuretics? | HF, cirrhosis, nephrotic syndrome, pulmonary edema |
| What are minor uses for Loop diuretics? | Hypertension and Hypercalcemia |
| What are the most significant side effects of loop diuretics? | Ototoxicity, hypokalemia, hypomagnesemia, dehydration, allergy (sulfa), metabolic Alkalosis, Nephritis (interstitial), and Gout |
| What is the difference in adverse effects between Furosemide and Ethacrynic acid? | Ethacrynic acid is more ototoxic |
| What are common Thiazide diuretics? | Hydrochlorothiazide, Chlorthalidone, and Metolazone |
| Which diuretics work by inhibiting NaCl reabsorption in early DCT leading to decreasing diluting capacity of the nephron? | Thiazide diuretics |
| Which diuretics decrease Ca2+ excretion? | Thiazide diuretics |
| What are some common uses for thiazides? | Hypertension, HF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis |
| What are some adverse effects of thiazide diuretic use? | - Hypokalemic metabolic alkalosis - Hyponatremia - Hyperglycemia - Hyperlipidemia - Hyperuricemia - Hypercalcemia -Sulfa allergy |
| What are the most common Potassium-sparing diuretics? | Spironolactone, Eplerenone, Amiloride, and Triamterene |
| Which two Potassium-sparing diuretics are competitive aldosterone receptor antagonists in the cortical tubule? | Spironolactone and Eplerenone |
| What is the mode of action of Triamterene and Amiloride? | Block Na+ channels at the cortical collecting tubule |
| What are some uses of all K+-sparing diuretics? | Hyperaldosteronism, K+ depletion, HF, and antiandrogen |
| What is an exclusive use for amiloride? | Nephrogenic DI |
| What is an exclusive Spironolactone clinical use? | Hepatic ascites |
| What side effect of potassium-sparing diuretics can lead to arrhythmias? | Hyperkalemia |
| What are the endocrine effects seen with the toxic use of Spironolactone? | Gynecomastia and antiandrogen effects |
| A man with enlarging breast and HF, is probably taking which common diuretic? | Spironolactone |
| Which diuretics cause an increase in urine NaCl? | All diuretics |
| An increase in urine NaCl by diuretics, it may lead to: | Decrease in serum NaCl |
| Which two kind of diuretics are especially significant for raising the level of urine K+? | Loop and thiazide diuretics |
| Which diuretics cause an increase in urine Ca2+? | Loop diuretics |
| Which diuretics cause a decrease in urine Ca2+? | Thiazide diuretics |
| Which diuretics cause alkalemia? | Loops and thiazides |
| Acidemia is caused by ___________________________. | Carbonic anhydrase inhibitors. |
| What are common ACE inhibitors? | Captopril, enalapril, lisinopril, and ramipril |
| What is the common suffix of ACE inhibitors | --pril |
| What action is prevented by ACE-inhibitors at the efferent arteriole? | Constriction |
| The levels of _____ are decreased with ACE-inhibitors and consequently it leads to a _______ ___________. | AT II are decreased ----> decreased GFR |
| What enzyme is produced in response to the decrease GFR caused by Captopril? | Increase in Renin |
| ACE inhibition has which secondary effect? | Inactivation of bradykinin (potent vasodilator) |
| A diabetic patient with Hx of HTN should be placed on ___________ to prevent diabetic nephropathy. | ACE inhibitors |
| What are some clinical uses for ACE inhibitors? | Hypertension, HF, proteinuria, and diabetic nephropathy |
| How does ACE inhibitors are recommended in patients with diabetic nephropathy? | Decrease intraglomerular pressure, slowing GBM thickening |
| Which adverse effects of ACE inhibitors are both due to incrased levels of Bradykinin? | Cough and Angioedema |
| What are the teratogenic effects of ACE inhibitors? | Fetal renal malformations |
| What are all adverse effects of ACE inhibitors? | Cough, Angioedema, Teratogen, increased Creatine (decrease GFR), Hyperkalemia, and hypotension |
| ACE inhibitor toxicity is seen with low or high levels of serum K+? | High |
| What is the main difference between ARB and ACE inhibitor toxicity? | ARBs do not increase levels of bradykinin |
| What type of medication selectively block binding of ATII to AT1 receptor? | ARBs |
| What is Aliskiren? | Direct renin inhibitor |
| What is a common direct renin inhibitor? | Aliskiren |
| What is prevented or blocked by Aliskiren? | Conversion of Angiotensinogen into AT I |
| What is the MC use for Aliskiren? | Hypertension |
| What are some adverse effects associated with Aliskiren? | Hyperkalemia, decreased GFR, angioedema; contraindicated in pregnant women, and those on ACE-inhibitors and/or ARBs. |
| What is the most commonly referred ARB? | Losartan |
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rakomi
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