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Renal
UWORLD Round 2 Part 1
| Question | Answer |
|---|---|
| What are common antibiotics that lead to acute interstitial nephritis? | Penicillin, cephalosporins, and sulfonamides |
| What are Urinalysis findings of acute interstitial nephritis? | WBC casts and eosinophils in the urine |
| What casts are seen in Acute Interstitial nephritis? | WBC casts |
| What type of leukocytes are found in urine in AIN sample? | Eosinophils |
| How is AIN clinically presented? | Fever, rash, and deteriorating renal function following antibiotic use |
| What are the casts found or associated with Acute Tubular Necrosis (ATN)? | Muddy brown casts |
| What conditions lead to development of ATN? | Sepsis, hypotension, or ischemic insults |
| What are the 3 main renal function tests abnormal in ATN? | 1. Cr remain elevated for weeks 2. FENa > 2% 3. Low urine osmolarity |
| What is a key difference of antibiotic-induced ATN and sepsis/ischemic-induced ATN? | ATN due to antibiotic use usually takes 5-7 days after starting the drug. |
| Muddy brown casts. Dx? | Acute Tubular Necrosis (ATN) |
| WBC casts in UA. Dx? | Acute Interstitial Nephritis (ATN) |
| What type of hypersensitivity reaction is PSGN? | Type III |
| What is the common presentation of PSGN? | Edema, proteinuria, and hematuria 2-3 weeks after bacterial infection such as strep throat |
| What common renal disease is usually seen after untreated strep throat infection? | PSGN |
| PSGN pathogenesis: | Complement activation after initial deposit of immune deposits in the glomerular to a cross reaction of antibodies raised against bacterial proteins with glomerular proteins |
| What is a "mass-like" complication of Pyelonephritis? | Perinephric abscesses |
| What common infectious condition lead to development of Perinephritis abscess? | Pyelonephritis |
| What is used to confirm diagnosis of Perinephric abscesses? | Abdominal CT scan |
| Classic clinical presentation of Pyelonephritis | Symptoms of UTI and costovertebral angle tenderness |
| Patient presents with costovertebral angle tenderness, dysuria, and feeling of incomplete voiding, and mild fever. Dx? | Pyelonephritis |
| Which type of diabetes insipidus (DI) is due to lack of ADH production? | Central DI |
| What are common causes of Central DI? | Head trauma, brain surgery, or pituitary tumors |
| _________ DI causes dilute urine that corrects with administration of ADH. | Central DI |
| Which type of DI, central or nephrogenic, corrects urine concentration by administration of ADH analogue? | Central DI |
| On which Vasopressin receptors does ADH directly bind to inhibit their activity? | V2 receptors |
| What is the result of V2-receptor inhibition by ADH? | Aquaporins will not insert into Principal cells, leading to no water reabsorption |
| Is water reabsorption by the principal cells stimulated or inhibited by ADH inhibition of V2-receptors? | Inhibited |
| Which cells have V2-receptors? | Principal cells of the Collecting duct |
| Where are V1-receptors located? | Blood vessels |
| What is the result of V1-receptor stimulated by ADH? | Blood vessels constrict leading to an increase in blood pressure |
| What acid-base disturbance is due to prolonged "vomiting"? | Contraction Metabolic Alkalosis |
| How does vomiting cause metabolic alkalosis? | Vomit leads to loss of stomach HCl and extracellular volume, resulting in decreased ECF and contraction metabolic alkalosis |
| RAAS is activated by a decrease or increase in Extracellular Fluid (ECF)? | Decrease in ECF |
| What is the direct consequence on activation of RAAS? | Increase activation of AT II |
| The increased activity of AT results in what process in the PCT? | Increased Na+ / H+ exchange in the PCT |
| The increased Na+/H+ exchange in the PCT due to increased AT II activity leads to: | Eventual increase HCO3- (bicarbonate) reabsorption |
| What measurement or value is often used to calculate GFR? | Inulin clearance |
| Inulin clearance is often used to calculate: | GFR |
| What does it mean in terms of GFR functionality when the GFR is underestimated? | There is a net reabsorption |
| What does it represent to GFR estimation if there is found a net secretion of Cr? | Overestimation GFR |
| BUN usually measure a net reabsorption or secretion ? | Net reabsorption |
| Cr value is usually used in GFR to represent | Net secretion |
| What are common situations that raise suspicion of a possible Hepatitis A infection? | Traveling to underdeveloped countries (eg. Mexico) and eating raw shellfish |
| Mode of transmission of Hepatitis A virus? | Fecal-oral route |
| What is the overall presentation of a person with HAV infection? | Nausea, vomiting, malaise, abdominal pain, jaundice and bilirubinemia |
| Does HBV or HAV has no carrier state and represents no risk of HCC development? | HAV |
| What part of the RAAS system is inhibited by B-blockers? | Renin release |
| Overall inactivation of the RAAS system causes an increase or decrease in blood pressure? | Decrease in blood pressure |
| What would be the concentration change or movement if a patient is treated with beta-blockers, in Renin, AT II, and aldosterone? | All would suffer a decrease due to B-blocker therapy |
| What type of antiviral (HIV medication) is Indinavir? | Protease inhibitor |
| What is the specific adverse effect of Indinavir? | Crystal-induced nephropathy |
| How is Indinavir crystal-induced nephropathy presented? | Malaise, weakness, nausea, flank pain, dark urine, and rarely, oliguria |
| Which pathogen is most common to cause peritonitis in a patient with indwelling catheter? | Staph epidermidis |
| What is the MCC of dialysis-induced peritonitis?? | Staph epidermidis |
| What is the 2nd MCC of dialysis-induced peritonitis? | Staph aureus |
| What electrolytes are increased in urine by the use of Thiazide diuretics? | Urine NaCl and urine K+ |
| Is urine Calcium increased or decreased by HCTZ? | Decreased |
| What adverse effect of thiazides lead to diabetes and gout? | Hyperglycemia and hyperuricemia, respectively. |
| On which part of the nephron does Bartter syndrome has its mutations? | Na+/K+/2Cl- transportation in the thick ascending loop of Henle |
| Mutations of the Na+/K+/2Cl- cotransporter at the loop of Henle, develop which type of renal tubular disease? | Bartter syndrome |
| Uncommon action by Furosemide: | Stimulates prostaglandin E release and reduces medullary hypertonicity to dilute urine |
| How does the loading dose changes in a patient with liver or renal failure? | Loading dose stays the same |
| How does the maintenance dose of a drug changes in a patient with liver or renal malfunctioning? | Maintenance dose is reduced |
| Which dosage is reduced in a patient with liver/renal failure, maintenance or loading? | Maintenance dose is reduced |
| What type of diuretics are the 1st line of treatment of hypertension in an osteoporotic patient? | Thiazides |
| Why are thiazides often used to treat hypertension in people with osteoporosis? | Thiazides promote the reabsorption of calcium |
| Which are known diuretics that promote the reabsorption of Calcium? | Thiazides |
| What is a common complication of CKD atha is characterized by increased urea blood levels? | Uremia |
| What type of acid-base disturbance is seen or caused by Uremia? | High anion gap metabolic acidosis |
| Normal anion gap or High anion gap metabolic acidosis. DKA? | High anion gap metabolic acidosis |
| Increased levels of BUN can be defined as: | Uremia |
| What is a common signal of kidney function deterioration, which is associated with high anion gap metabolic acidosis? | Uremia |
| Diarrhea causes high anion or normal anion gap metabolic acidosis? | Normal anion gap metabolic acidosis |
| What does the letter "D" represents in the mnemonic "MUDPILES"? | DKA |
| What is a common nephrogenic adverse or side effect of Lithium therapy? | Nephrogenic DI |
| Which condition is characterized by minimal change in urine osmolality after the Water Deprivation test? | Nephrogenic DI |
| Are ADH levels elevated or decreased in Nephrogenic DI? | Elevated |
| Which type of Diabetes insipidus, central or nephrogenic, is associated with increased levels of ADH? | Nephrogenic DI |
| What is a common complication of DM type 1? | DKA |
| WHat are symptoms of DKA? | Hyperglycemia, hyperkalemia, and high anion gap metabolic acidosis |
| What is the treatment for DKA? | IV insulin and K+ |
| What condition that causes metabolic acidosis is featured with Pseudohyperkalemia? | DKA |
| What is the main electrolyte association of SIADH? | Hyponatremia |
| What are some electrolyte and serum levels associated with SIADH? | Hyponatremia, decreased plasma osmolality, uric acid and urea |
| What is a common consequence of hypomagnesemia? | Refractory hypokalemia |
| What is often a cause of refractory hypokalemia? | Hypomagnesemia |
| Why is does refractory hypokalemia occurs due to hypomagnesemia? | Due to renal potassium wasting in the loop of Henle |
| What type of proteins are often seen with low serum Mg2+? | Alcoholics |
| What acid-base disturbance is associated with Vomiting? | Hypochloremic metabolic alkalosis |
| What common action or condition leads to Hypochloremic metabolic alkalosis? | Vomiting |
| How does prolonged vomiting cause hypochloremic metabolic alkalosis? | Excess loss of Cl- and H+ in the vomitus |
| What occurs with HCO3- levels in early stages of metabolic alkalosis due to vomiting? | Bicarbonate is loss in urine, promoting a high pH |
| What substance is freely filtered in the glomerulus, and at normal plasma levels, it is completely reabsorbed in the PCT? | Glucose |
| At what plasma levels does glucose begins to appear in the urine? | 200-375 mg/dL |
| At which plasma level does glucose transport becomes saturated in the nephron? | >375 mg/dL |
| What is the direct result of Splanchnic arterial vasodilation? | Hepatorenal syndrome |
| How is Hepatorenal syndrome (HRS) clinically presented? | Rapid-onset, acute kidney injury without evidence of ischemic or other renal insults |
| Hepatorenal syndrome is due to: | Splanchnic arterial vasodilation |
| How does Splanchnic arterial vasodilation causes HRS? | It caused by shunting of circulation away from the kidneys to the gut. |
| What condition is associated with the shunt of blood circulation away from the kidneys and into the gut? | Hepatorenal syndrome |
| Which arterial body is associated with pathogenesis of Hepatorenal syndrome? | Splanchnic arterial vasodilation |
| What acid-base disturbance is associated with Hyperventilation? | Respiratory alkalosis |
| What acid-base disturbance is associated with a high pH, low PaCO2, and rapid breathing? | Respiratory alkalosis |
| What condition is associated with excessive water intake in the setting of normally functioning kidneys? | Primary polydipsia |
| What type of patients most often develop Primary polydipsia? | Psychiatric patients |
| What occurs to urine osmolality in a patient with Primary polydipsia, as he undergoes the Water deprivation test? | Urine should immediately and robustly increase osmolality, and kidneys start retaining water |
| How is Diabetic nephropathy clinically presented? | Polyuria, an massive proteinuria, resulting in hypoalbuminemia and peripheral/periorbital edema |
| Is diabetic nephropathy associated with hyper- or hypoalbuminemia? | Hypoalbuminemia |
| How is the edema located in diabetic nephropathy? | Peripheral and periorbital edema |
| Besides peripheral and periorbital edema, what other edematous manifestation is seen with Diabetic nephropathy? | Macular edema |
| What causes Macular edema | Vascular damage due to chronic hyperglycemia |
| MOA of Thiazides: | Act on the DCT to inhibit Na+/Cl- cotransporter, thus promoting diuresis |
| What acid-base disturbance may be caused by Thiazides? | Metabolic alkalosis |
| What are some electrolyte abnormalities associated with Thiazides? | Hyperglycemia, hypercalcemia, and hyperuricemia |
| What is another way to refer to the Metanephros? | Metanephric blastema |
| What are the renal derivatives of the metanephric blastema? | Glomeruli, Bowman's space, proximal tubules, the loop of Henle, and DCT |
| What are the renal derivatives of the Ureteric Bud? | It becomes the collecting system of the kidney, including the collecting tubules and ducts, major and minor calyces, renal pelvis, and the ureters |
| The major and minor calyces derived from the Metanephric blastema or Ureteric bud? | Ureteric bud |
| Is the glomeruli and Bowman's space derived from the metanephric blastema or Ureteric bud? | Metanephric blastema |
| Which "tubules" are derivative of the metanephric blastema, the Proximal/Distal renal tubules or the Collecting tubules and ducts? | Proximal and Distal renal tubules (PCT and DCT) |
| Renal pelvis is derived from the _________ ______. | Ureteric bud |
| What causes the development of RPGN? | Anti-glomerular basement membrane (GBM) antibodies react with Collagen IV |
| Which type of Collagen is involved in RPGN pathogenesis? | Collagen IV |
| What is the key or featured histological finding under LM of RPGN? | Glomerular crescent formation |
| Which autoimmune condition is seen with glomerular crescent formation? | RPGN |
| What is the immunofluorescence findings of RPGN? | Linear deposits of IgG and C3 along the GBM |
| Which condition has a linear deposits of IgG and C3 along the GBM under immunofluorescence microscopy? | RPGN |
| Is C3 or C4 deposited along the GBM in RPGN? | C3 |
| What is a common cause of nephrotic syndrome in adults? | Membranous nephropathy |
| What is the EM of Membranous nephropathy? | Glomerular capillaries demonstrate irregular, subepithelial, electron-dense immune deposits on the GBM with moderate foot process effacement |
| Which two nephrotic syndrome causes are characterized with some degree of foot process effacement? | MCD and Membranous nephropathy |
| What are the IM findings of Membranous nephropathy? | Diffuse granular pattern of IgG along the capillary loops |
| Which condition is seen with a diffuse granular pattern of IgG along the capillary loops of the glomerulus under immunofluorescent imaging? | Membranous nephropathy |
| What is Fibromuscular dysplasia? | Abnormal tissue growth within arterial walls, resulting in stenotic and torturous arteries |
| What is commonly caused by Fibromuscular dysplasia? | Renal Artery Stenosis (RAS) |
| What is the pathology seen in RAS due to Fibromuscular dysplasia? | Alternating fibromuscular webs and aneurysmal dilation with absent internal elastic lamina |
| What is often the description given to the arterial walls affected by Fibromuscular dysplasia? | String of beads |
| What causes renovascular hypertension? | Due to RAS and activation of RAAS |
| What condition is due to RAS and activation of RAAS? | Renovascular hypertension |
| What is a common factor that often leads to development of atheroembolism? | Invasive vascular procedures |
| How is an atheroembolism depicted in light microscopy? | Partially or completely obstructed arterial lumen with needle-shaped cholesterol clefts within the atheromatous embolus |
| What condition is often seen the needle-shaped cholesterol clefs? | Atheroembolism |
| What is the key histological finding of atheroembolism? | Needle-shaped cholesterol clefs within the atheromatous embolism |
| What causes overactive bladder syndrome or urinary incontinence? | Uninhibited bladder contractions |
| What condition is seen with Detrusor instability? | Urinary incontinence |
| What are accompanying symptoms of Urinary incontinence? | Sense or urgency accompanied by an involuntary loss of urine |
| Which receptors are targeted by antimuscarinic drugs treating urinary incontinence? | M3 receptor |
| Why are thiazides used to prevent nephrolithiasis? | Thiazides effectively increases renal Calcium reabsorption |
| Which diuretics are know to prevent calcium nephrolithiasis? | Thiazides |
| Does a decrease in urine Ca2+ excretion, prevents or stimulate calcium stone formation by the kidneys? | Prevents |
| How is Potassium usually stored in the body? | Intracellularly due to the activity of the Na+/K+ ATPase pump |
| What is a common electrolyte abnormality seen with B-2 adrenergic activity? | Transient hypokalemia |
| How does albuterol cause hypokalemia? | B-2 receptor agonist lead to an increase transport of K+ intracellularly |
| Does beta-adrenergic agonist increases or inhibits Na+/K+ ATPase pump activity? | Increases |
| What are two common B-2 agonists? | Albuterol and Dobutamine |
| What cells produce EPO? | Peritubular fibroblast cells in the renal cortex in response to decreased renal oxygen delivery |
| How does EPO acts ? | Erythrocyte precursor cells in the bone marrow to stimulate RBC production |
| What receptor is stimulated by Vasopressin and Desmopressin? | V2-receptors |
| What is the result of Vasopressin? | V2-receptor-mediated increase in water and urea permeability of the inner medullary collecting duct |
| What does a rise in Urea reabsorption causes to urine? | Enhances the medullary osmotic gradient, allowing the production of maximally concentrated urine |
| How is an increased urea reabsorption measured? | Decrease in urea clearance |
| In the retroperitoneum, what is the anatomical position of the ureters with respect to other structures? | 1. Posterior to the gonadal (ovarian) vessels 2. Cross anterior the the Common/ External Iliac arteries |
| Is the ureter anterior or posterior with respect the Ovarian vessels in the peritoneum? | Posterior |
| To which structures do the ureters are anterior in the peritoneum? | Common/ External Iliac arteries |
| What is the course or anatomical path of the ureters within the true pelvis? | 1. Anterior to the internal iliac artery 2. Posterior to the Uterine artery |
| Do ureter, within the true pelvis, lie anterior, posterior, or lateral to the internal iliac artery? | Anterior to Internal iliac artery |
| Are the ureters anterior or posterior to the Uterine artery in the true pelvis? | Posterior to the Uterine artery |
| Which arteries depict the ureters location and path in the retroperitoneum? | Posteriorly to the gonadal arteries and anterior the common/ external iliac arteries |
| Is the uterine artery posterior or anterior the ureter? | The Uterine artery is posterior with respect to the ureter |
| What cell differentiation and formation is dependent of RANK-RANK-L interaction? | Osteoclasts |
| Do osteoclasts or osteoblasts production is directly dependent on RANK--RANK-L interaction? | Osteoclasts |
| What is the function of Osteoprotegerin? | Block the binding of RANK-L to RANK and reduces formation of mature osteoclasts |
| What does a decrease in the Osteoprotegerin:RANK-L ratio produces? | Increased osteoclast activity and bone resorption |
| What is the abbreviation used for Osteoprotegerin? | OPG |
| What hormonal condition is able to produced low levels of Osteoprotegerin? | Low estrogen levels |
| What is a way or form in which menopause produce higher risk of developing Osteoporosis? | The low levels of estrogen seen with menopause, lead to decreased level of osteoprotegerin (OPG) production, which leads to increased RANK-L production and increased RANK expression in osteoclast precursors, leading to increased bone resorption |
| What is the pathological damaged caused by accidental ingestion of Ethylene glycol? | Ingestion causes ATN with vacuolar degeneration and ballooning of the proximal tubular cells |
| Which part of the nephron is most affected by ingestion of Ethylene glycol? | Proximal tubular cells (PCT) |
| What are some clinical manifestations seen with Ethylene glycol consumption? | Altered mental status, renal failure, high anion metabolic acidosis, increased osmolar gap, and calcium oxalate crystal in urine |
| What is the key histological finding of Ethylene glycol in an urine sample? | Calcium oxalate crystals |
| What type of crystals are formed and seen in urine of patient that accidentally ingested antifreeze fluid? | Calcium oxalate crystals |
| What commonly used products are known to contain Ethylene glycol? | Antifreeze, engine coolants, and brake fluid |
| How is the pathological course of disease of Contrast-induced nephropathy? | Acute rise in BUN and Cr after radiologic contrast administration, followed by a gradual return to baseline |
| What are the histological findings of Contrast-induced nephropathy? | Diffuse necrosis of PCT cells |
| Which cells are most affected by Contrast-induced nephropathy? | PCT cells |
| What is the main finding in urine analysis sample of a patient with Contrast-induced nephropathy? | Muddy Brown casts |
| Contrast-induced nephropathy is a type of: | Acute Tubular necrosis |
| Which glomerular condition or disease is associated with Crescent formation? | RPGN |
| What are crescents in RPGN made of? | Glomerular Parietal cells, lymphocytes, and macrophages along with abundant fibrin deposition |
| Which is kidney and bone condition is often developed in patients with CKD? | Renal Osteodystrophy |
| How is Renal Osteodystrophy developed in CKD patients? | Due to secondary hyperparathyroidism induced by hyperphosphatemia and hypocalcemia |
| What is the result of CKD-induced hypocalcemia and hyperphosphatemia? | Secondary hyperparathyroidism |
| Is serum phosphate increased or decreased in CKD patients? | Increased |
| CKD leads to secondary hyperparathyroidism, and then if the patient has increased bone resorption, it develops into: | Osteitis fibrosa cystica |
| Ectopic production of ADH from malignancy (MC lung cancer). Dx? | SIADH |
| What is SIADH? | Condition of impaired urinary water excretion due to ectopic and excessive production of ADH |
| List of symptoms associated with SIADH: | 1. Low serum osmolality 2. Hyponatremia 3. High urine osmolality 4. High urine sodium 5. Euvolemia |
| Urine sodium in SIADH. Low or high? | High urine sodium |
| Urine osmolarity in SIADH. Low or high? | High urine osmolality |
| What are the two main serum levels of concern in SIADH? | Low serum osmolality and hyponatremia |
| Is SIADH associated with hyponatremia or hypernatremia? | Hyponatremia |
| What does a low serum osmolality indicates? | Diluted blood |
| What does a high urine osmolality indicate? | Concentrated urine |
| What does Euvolemic hyponatremia implies? | Normal sodium stores and a total body excess of free water. |
| Which condition is associated commonly with Euvolemic hyponatremia? | SIADH |
| What common antiepileptic is associated to cause SIADH? | Carbamazepine |
| What important renal-associated condition is often an adverse effect of Carbamazepine therapy? | SIADH |
| How does Carbamazepine cause SIADH? | Increasing ADH secretion and renal sensitivity to ADH |
| Common drug used to treat Hyperkalemia | Patiromer |
| What is Patiromer? | Nonabsorbable cation exchange resin |
| What is treated with Patiromer? | Hyperkalemia |
| MOA of Patiromer: | Binds to colonic K+ in exchange for Ca2+, trapping K+ within the resien where is then excreted in the feces |
| What are the associated adverse effects of Patiromer? | Diarrhea, hypokalemia, hypercalcemia, and hypomagnesemia |
| What are clinical manifestations highly indicative of RAS? | Severe hypertension (acute onset), and abdominal bruits |
| Why does RAS activate the RAAS system? | RAS causes a decreased renal artery perfusion |
| What is the consequential effect of increased levels of Renin released to activate the RAAS? | Increase peripheral resistance and elevated systemic blood pressure |
| How is K+ serum levels affected by the activation of RAAS? | Relative hypokalemia |
| Is increased activity of RAAS associated with metabolic acidosis or metabolic alkalosis? | Metabolic alkalosis |
| How does increased RAAS activity lead to relative hypokalemia? | Increased aldosterone secretion causes increased renal Na+ reabsorption and K+ and H+ excretion |
| Which hormone is responsible for the increased excretion of potassium and H+ in increased RAAS activity? | Aldosterone |
| What are the effects of ACE inhibitors? | Block AT II-mediated vasoconstriction, which can reduce systemic blood pressure and lower renal perfusion |
| Which arteriole is affected by ACE inhibitors, efferent or afferent? | Efferent arteriole |
| What is the result of ACE inhibitors on the Renal efferent arteriole? | Dilation, leading to a reduction in GFR and renal filtration fraction (FF) |
| What are the effect on GFR and renal FF when patient using ACE inhibitors? | Reduction in GFR and FF |
| Which part of the nephron has the lowest osmolality? | DCT |
| What is the approximate osmolarity value at the DCT? | 100 |
| What is the luminal osmolality at the bottom of the loop of Henle? | 1, 200 |
| Which part of the nephron has an approximate osmolality of 100? | DCT |
| Which part of the nephron has an approximate 300 value in osmolality? | PCT and early cortical collecting tubes |
| What is the approximate osmolality value of the Thick ascending loop of Henle? | 200 |
| What are the electrolyte abnormalities most commonly associated with CKD? | Hyperphosphatemia and hypocalcemia |
| What causes chronic inflammation in patients with CKD? | Usually due to secondary atherosclerosis and/or uremia |
| What causes the vascular calcification observed in CKD patients? | Electrolyte abnormalities and chronic inflammation |
| What is Refeeding syndrome? | Occurs after the reintroduction of carbohydrates in patients with chronic malnourishment, which stimulates insulin secretion an drives phosphorus intracellular in an effort to maintain energy |
| What is the result of the phosphate redistribution seen with Refeeding syndrome? | Severe hypophosphatemia |
| What is a common cause of severe hypophosphatemia in children living in third world countries? | Refeeding syndrome |
| How is serum phosphate distributed in Refeeding syndrome? | It is shunted intracellularly in order to maintain cellular energy metabolism |
| What occurs in Renal ammoniagenesis? | Renal tubular epithelial cells metabolize Glutamine into Glutamate, generating ammonium |
| What nephrogenic process is known to produce ammonium? | Renal ammoniagenesis |
| What is the amino acid conversion taken place in renal ammoniagenesis that leads to increased NH4+? | Glutamine into Glutamate |
| What are the final products of renal ammoniagenesis? | 1. Ammonium excreted in the urine 2. Bicarbonate absorbed into the blood |
| What process is responsible for majority of renal acid excretion in chronic acidotic states? | Renal ammoniagenesis |
| What type hypersensitivity is PSGN? | Type III hypersensitivity reaction |
| Which type of hypersensitivity reactions are Type III? | Immune-complex mediated |
| What is the cause of PSGN? | Nephrogenic strains of group B-hemolytic streptococcus infection |
| Another name for IgA nephropathy? | Berger disease |
| How is IgA nephropathy clinically presented? | Recurrent, self-limited, painless hematuria, and URI symptoms that are concurrent with infection |
| What is the main histological finding of Berger disease? | Mesangial IgA deposits on IM |
| Which glomerular condition is seen in IM mesangial IgA deposits? | Berger disease |
| What are features of PSGN that make it different from IgA nephropathy? | 1. PSGN occurs 1-3 weeks after strep infection vs concurrent URI 2. PSGN is does not present with recurrent painless hematuria |
| What is the main description of hematuria in IgA nephropathy? | Recurrent, self-limited, painless hematuria |
| What is the main histological finding of PSGN? | EM ---> Subepithelial humps |
| What glomeruli disease is associated with EM showing subepithelial humps? | PSGN |
| What is the IF of Anti-GBM disease? | Linear stating of IgG |
| Which immunoglobulin stains linearly on IF of Anti-GBM disease? | IgG |
| Which is the LM characteristic of RPGN? | Glomerular crescents |
| Which condition of the glomerulus is seen on LM with glomerular crescents? | RPGN |
| EM of Alport syndrome? | Lamellated appearance on GMB |
| Which nephrogenic disease is characterized with an EM showing lamellated appearance of the GMB? | Alport syndrome |
| What leads to the development of Hypertensive nephropathy? | Homogeneous deposition of eosinophilic hyaline material in the intima and media of small arteries and arterioles |
| What is Hyaline arteriosclerosis? | Deposition of hyaline material in the intima and media of small arteries and arterioles |
| What condition is often due to ongoing or chronic hyaline arteriosclerosis of renal vasculature? | Hypertensive nephropathy |
| What toxins are often associated with Hypertensive nephropathy? | Uremic toxins |
| What is the result or consequence of uremic toxins accumulation in Hypertensive nephropathy? | Fatigue, weakness, and itching |
| How is acute Urinary tract obstruction characterized? | Anuria and bladder distension and can result in hydronephrosis and acute kidney injury (AKI) |
| What is a possible cause of anuria and bladder distension leading to hydroneprhosis? | Urinary tract obstruction |
| How is a urinary tract obstruction diagnosed or indicated in a physical examination? | Palpable, distended bladder, along with abdominal and flank pain |
| What is the MCC of urinary rentention? | Bladder outlet obstruction due to BPH |
| How does BPH cause urinary retention? | The urethral compression by BPH causes a bladder outlet obsruction |
| Why is the MCC of neprhotic syndrome in children? | MCD |
| What are some classic clinical manifestations of Minimal Change disease (MCD)? | Proteinuria, hypoalbulinemia, and edema tha are usually reversible with corticosteorids |
| Is MCD responsive or non-responsive to corticosteroids? | Responsive |
| What is the main lesion of MCD? | Diffuse foot process effacemen on electron microscopy (EM) |
| How are the LM and IF of MCD? | Normal glomeruli |
| Histological findings: IF - normal glomeruli, LM - normal ; EM - diffuse foot process effacement of glomeruli. DX? | MCD |
| Recurrent hematuria that occurs spontaneously or within 5-7 of an upper or pharyngeal infection. Dx? | IgA nephropathy |
| How are the serum complements levels in IgA nephropathy? | Normal complement levels in the blood |
| What is Rhabdomyolysis? | Renal/muscular condition due to the release of intracellular muscle contents, such as myoglobin and electrolytes, due to myocyte injury |
| Which condition is often a result of myocyte injury - release of muscle contents into blood? | Rhabdomyolysis |
| What are common causes of Rhabdomyolysis? | Crush injuries, seizures, and drug use (statins) |
| How is Heme pigment released? | It is release from myoglobin after degradation in the kidney |
| What is common condition due to release of heme by degraded myoglobin? | ATN |
| What cells are affected by Heme pigment? | Tubular cells |
| What lab results indicate Myoglobinuria? | (+) blood in urine dipstick in the absence of RBC on microscopic UA |
| What is Analgesic Nephropathy? | Form of CKD caused by prolonged, heavy intake of NSAIDs and/or acetaminophen |
| What are the pathologic characteristics caused by Analgesic nephropathy? | Chronic interstitial nephritis and papillary necrosis of the kidney tissue |
| What are some compensatory mechanisms activated by hypovolemia in order to maintain tissue perfusion? | 1. Activation of RAAS pathway, 2. Increased Vasopressin release, 3. Increase sympathetic tone |
| What is the result of increased activation of RAAS due to hypovolemia? | Increase in aldosterone and endothelin release |
| What acid-base disturbance is FIRST seen with Salicylate toxicity? | Primary respiratory alkalosis |
| What type of metabolic acidosis, normal anion or anion-gap, is seen with late aspirin toxicity? | Anion gap metabolic acidosis |
| Respiratory alkalosis ---> anion gap metabolic acidosis. Dx? | Salicylate poisoning |
| What is the primary cause of Metabolic acidosis due to Salicylate poisoning? | Increased production of Lactate (lactic acid) |
| What are some associated symptoms of Aspirin (Salicylate) poisoning? | Tinnitus, tachypnea, hyperthermia, vomiting, and altered mental status |
| How do Thiazides cause Hypokalemia? | Decrease intravascular fluid volume, which stimulates aldosterone secretion and leads to increased excretion of K+ and H+ ions in the urine |
| Which type of diuretics are known to cause hypokalemia due to increase aldosterone secretion and increased K+ excretion of urine? | Thiazides |
| How is significant hypokalemia clinically presented? | Muscle weakness, cramps, and possible rhabdomyolysis |
| What is a common electrolyte imbalance seen with Thiazides and loop diuretics? | Hypokalemia and metabolic alkalosis |
| Loop diuretics and Thiazides are known to cause which acid-base disturbance as a side effect? | Metabolic alkalosis |
| What type of anemia is seen in CKD? | Normocytic anemia due to EPO deficiency |
| How does a recombinant-EPO treat symptoms of EPO-deficiency normocytic anemia? | Improve tissue oxygen delivery and reduce mortality |
| What are the significant and dangerous adverse effects of prolonged recombinant-EPO therapy? | Hypertension and thromboembolism |
| What is a possible adverse effect of initiating ACE inhibitors or ARBs in a patient with RAS? | Precipitate acute renal failure |
| How is the UA of a patient with RAS and wrongfully given ARBs or ACE inhibitors? | Unremarkable, meaning no hematuria, proteinemia, or casts |
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rakomi
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