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Renal
Round 6 Review by Sections
| Question | Answer |
|---|---|
| Does hyperventilation lead to respiratory acidosis or alkalosis? | Respiratory alkalosis |
| What type of alkalosis, metabolic or respiratory, is defined with a high pH and low PCO2 level? | Respiratory alkalosis |
| What are few common causes for hyperventilation? | Pain, anxiety, aspirin overdose, and pulmonary embolus |
| What are a few actions performed by Aldosterone? | 1. Increase renal sodium reabsorption 2. Increase renal potassium excretion 3. Increased renal hydrogen ion secretion |
| Which ion renal reabsorption is increased by Aldosterone? | Sodium |
| Which electrolyte or ion renal excretion is increased by Aldosterone? | Potassium |
| Which ion renal secretion is increased by Aldosterone? | Hydrogen ion |
| What would be the direct effect on renal sodium if the actions of Aldosterone are inhibited? | Decrease renal reabsorption of sodium |
| Which hormone is inhibited if its actions include decrease renal Na+ reabsorption, K+ excretion, and H+ secretion? | Aldosterone |
| From which gland or structure is ADH secreted? | Posterior pituitary |
| What is the effect on serum osmolality and ADH release, upon pure water ingestion? | Low serum osmolality and decrease ADH secretion |
| What are the resulting effects of low ADH release from the posterior pituitary? | 1. Decrease collecting duct aquaporins 2. Decrease water reabsorption, 3. Decrease urea reabsorption from the collecting duct |
| Are aquaporins in the collecting duct increased or decreased by a decrease in ADH levels? | Decreased aquaporins |
| Which medication reverses the afferent arteriole vasodilation? | NSAIDs |
| On which renal glomerular arteriole do NSAIDs cause the most effect? | Afferent |
| What is the effect of NSAIDs regarding maintenance of GFR? | Vasoconstrict the afferent arteriole |
| Which type of acid-base disorder is seen with low pH, low bicarbonate ([HCO3-]), and low PaCO2? | Metabolic acidosis |
| What type of Metabolic acidosis is caused by diarrhea? | Normal anion gap metabolic acidosis |
| How does diarrhea cause NAGMA? | Due to loss of GI bicarbonate and potassium ions |
| What are serum and urine electrolyte changes caused by Thiazide diuretics? | Increase in serum Sodium, Chloride, and Potassium and a decrease in urine Calcium |
| An example of a diuretic that would cause a decrease in urine calcium but increase in serum K+, Na+ and Cl-? | HCTZ |
| What classification of anemia is due to PHN? | Intravascular hemolytic anemia |
| What is the result of mild respiratory acidosis in PHN? | Activation of complement and lysis RBCs because GPI is defective and cannot bind CD55 and CD59 and unable to protect RBCs from complement |
| Which condition is known to cause anemia and "cola-colored" urine in the mornings? | Paroxysmal Nocturnal Hemoglobinuria |
| Which part of the GBM is affected in MCD (or another nephrotic syndrome)? | Heparan sulfate proteoglycans |
| What is the result of a damaged heparan sulfate proteoglycans in the GBM? | Increase passage of negatively proteins through the Glomerular Basement Membrane (GBM) |
| What are some common ingestions that lead to increased anion gap metabolic acidosis? | Aspirin, ethylene glycol, propylene glycol, methanol, INH, and metformin |
| What type of acid is associated with venom against ants? | Formic acid |
| Which basic alcohol if combined with carbon monoxide leads to generation of formic acid? | Methanol |
| A person suspected of Formic acid (ant venom) toxicity develops a metabolic acidosis due to ingestion of what substance? | Methanol |
| Other than the electrolyte and serum concentrations adverse effects of Thiazides, what is another side effect of these? | Limit urinary diluting capacity |
| Which type of diuretics are known to develop a limitation on urinary diluting capacity? | Thiazide diuretics |
| What is the GFR? | Flow rate of fluid thought the glomerular basement membrane |
| What clearances can be used to determine or calculate the GFR? | Inulin or Creatine clearance |
| What is the equation for GFR? | (U inulin x V) / P inulin |
| What electrolyte imbalance is seen with alcoholism? | Hypomagnesemia |
| What is consequence of Hypomagnesemia due to chronic alcohol abuse? | Hypokalemia due to renal potassium wasting |
| Is NADH or NAD+ overproduced by excessive alcohol intake? | NADH |
| What is the difference in sodium reabsorbing by the different segments of ascending loop of Henle? | In thing ascend segment, sodium is passively reabsorbed following concentration gradient, while in the thick segment, sodium is actively reabsorbed, along with K+ and chloride, through the Na/K/2Cl cotransporter |
| What part of the nephron is ALWAYS impermeable to water? | Ascending loop of Henle |
| Why is diabetic nephropathy associated with hyponatremia? | Due to these patients have little to no glomerular filtration due to ESRD |
| What is the consequence of overuse of calcium carbonate for extended periods of time? | Milk-alkali syndrome |
| How is Milk-Alkali syndrome characterized? | Hypercalcemia, metabolic alkalosis, and renal insufficiency |
| What is a consequence or adverse effect of chronic use of OVC Calcium Carbonate? | Milk-alkali syndrome |
| Which acid base disorder is characterized by an increase in all pH, plasma bicarbonate, and PCO2? | Metabolic alkalosis |
| What are the most common type of drugs that cause AKI? | Aminoglycosides, contrast dyes, diuretics (prerenal) and NSAIDs |
| What is the effect of NSAIDs on GFR? | Decrease GFR by causing afferent arteriolar dilation constriction |
| What are the results of Furosemide therapy? | 1. Renal loss of Na, water, and H+ 2. Volume depletion 3. Hypokalemia 4 Metabolic alkalosis with a low urine clholride |
| Renal failure causes _________________- anemia. | Normocytic anemia |
| Why does a patient with renal failure eventually develops normocytic anemia? | Deficiency of EPO production |
| Description of the anemia in renal failure due to decrease EPO production | Normocytic anemia with normal platelet and WBC counts |
| What is the clinical presentation of CN poisoning? | CNS symptoms, acidosis, and increased methemoglobin |
| What is the result of CN inhibiting the ETC? | Increasing anaerobic metabolism and subsequent increasing lactic acid production |
| What kind of metabolic acidosis is eventually developed in CN poising? | Increased levels of lactic acidosis, due to increased anaerobic metabolism, lead to anion gap metabolic acidosis |
| Furosemide is a loop diuretic that cause metabolic ___________. | Metabolic alkalosis |
| Which diuretic type are associated with "contraction alkalosis"? | Loop diuretics |
| How do Loop diuretics cause metabolic alkalosis? | Rapid volume contraction due to secondary hyperaldosteronism and also by stimulation renal H+ excretion |
| What are the results of loop diuretic inhibiting the Na/K/2Cl cotransporter? | 1. Sodium chloride diuretics 2. induces sodium delivery to the Distal nephron 3. Causing volume depletion |
| What is Osmotic Demyelination syndrome? | It caused by overly rapid correctio of significant hyponatremia |
| How is Osmotic Demyelination syndrome presented? | Neurologic symptoms such as dysarthria, dysphagia, and flaccid paralysis |
| What are two common causes of Euvolemic hyponatremia? | SIADH and/or Thiazide diuretics |
| What are two commo factors that contribute to the ability of the renal medullary interstitium to concentrate urine? | Urea and NaCl |
| Proper function and concentration of which factors contribute to maximize renal free water reabsorption and urine concentration? | Urea and NaCl |
| Where in the cell is Lactic acid produced? | Cytoplasm of the cell |
| What is an example of a conditions that would lead to lactic acid production due to increased anaerobic metabolism? | Acute mesenteric ischemia |
| What type of acid-base disorder is associated with vomiting? | Metabolic alkalosis |
| What is another name or term given to the metabolic alkalosis due to vomiting? | Contraction alkalosis |
| What is the tubular response to contraction alkalosis? | Increased proximal bicarbonate reabsorption an increased aldosterone-driven collecting duct secretion of hydrogen ions |
| How is Contraction Alkalosis counteracted? | Increasing HCO3- absorption and increased H+ secretion by aldosterone activity |
| What is the most common Carbonic anhydrase inhibitor? | Acetazolamide |
| On which part of the nephron does acetazolamide act upon? | PCT |
| How does Acetazolamide work? | Causes bicarbonate diuresis and loss of buffer, reducing renal acid excreting but increasing urine excretion of Na, K, and HCO3- |
| What is the results f increase NaCl reaching the macula densa? | Afferent arteriolar vasoconstriction, which decreases the GFR back toward normal |
| Why are thiazides used for blood pressure? | Lower BP by inducing sodium diuretic an acting as mild vasodilator |
| What is Bartter syndrome? | Rare inherited cause of hypokalemia due to mutations in the Na/K+/2Cl transporters |
| Symptoms of Bartter syndrome are like those of which type of diuretic | Loop diuretics |
| What are adverse effects of Furosemide? | Hypokalemia, volume depletion, metabolic alkalosis, hypocalcemia, and hyperuricemia |
| What is the MCC of death in patients with Congenital Diaphragmatic hernia? | Pulmonary hypoplasia |
| What heart pressure is significantly increased in Pulmonary hypertension? | PCWP |
| How does Furosemide cause gout? | Reduce renal clearance of uric acid, causing hyperuricemia |
| Other than thiazides, what other diuretic is known to be cause of Gout? | Furosemide |
| What is the MCC of non-renal stone urinary obstruction in women? | Pelvic malignancies (ovarian tumor) |
| What is the initial range of albuminuria in a patient with diabetic nephropathy? | 30-300 mg albumin / 24 hours |
| What cause the benefit of treating diabetes with an AE inhibitor? | Reverse microalbuminuria |
| What are the first line of treatment for prevent progression of diabetic nephropathy? | ACE inhibitors |
| Besides using for hypertension and diabetic nephropathy, what is another benefit of ACE inhibitors? | Cardioprotective with respect to heart failure |
| What is a significant adverse effect of ACE inhibitors secondary to decreased aldosterone levels? | Hyperkalemia |
| How do ACE inhibitors exert their cardioprotective benefits? | Disrupt conversion of AT I --> AT II, which leads to decreased activation of Gq pathway and decreased activity of Phospholipase C in vascular smooth muscle |
| What are the common biopsy findings of Diabetic nephropathy? | Nodular sclerosis |
| What is the characteristic of the membrane in early diabetic nephropathy? | Thickened GBM |
| What is connected by the Cardinal ligament? | Cervix to the side wall of the pelvis and contains the uterine arteries |
| Thiazides are known to cause hypo- or hypercalcemia? | Hypercalcemia |
| What is the MOA of ARBs? | Block AT II from binding to its receptors, which lead to decreased secretion of aldosterone |
| What is a common case of Urethral obstruction? | Posterior urethral valves persistence |
| Wilms tumor tens to metastasize to the: | Lungs and liver |
| What are some pathological causes for prerenal AKI? | Volume depletion, bleeding, heart failure, liver failure, or bilateral RAS |
| What are the associated lab findings of prerenal AKI? | Urine sodium < 10 mEqL/L FeNa <1% Urine osmolaltiy of > 500 mOsm/kg Serum BUN: Cr > 20 |
| How is acute (allergic) interstitial nephritis presented? | Rash, fever, and eosinophilia |
| What RPNG is often primary or secondar to disorder like lupus? | Goodpasture syndrome |
| What is the most significant histological finding of Goodpasture syndrome sample? | Epithelial crescents |
| What is the most common cause of Hepatorenal syndrome? | Splanchnic arterial vasodilation, which cause circulation away for the kidneys to the gut, leading to renal vasoconstriction |
| What condition is characterized by shunting blood flow away from the kidneys, resulting in in rapid-onset AKI, and shunting it to the gut? | Hepatorenal syndrome |
| When is likely to suspect Rhabdomyolysis-induced ATN? | Patients with elevated creatinine, heme-positive urine, and no RBCs on UA |
| What are some causes of Rhabdomyolysis-induced ATN? | Trauma, hypo/hyperthermia, severe hypokalemia, or statins |
| What is a rare but possible complication of pyelonephritis? | Perinephric abscess |
| What is Mixed cryoglobulinemia? | Small vessel vasculitis caused by antigen-antibody deposition |
| How is Mixed cryoglobulinemia presented? | Fever, fatigue, malaise, joint pain, peripheral neuropathy, and palpable purpura with elevated serum cryoglobulins |
| IS Mixed Cryoglobulinemia associated with subepithelial or subendothelial electron deposits? | Subendothelial |
Created by:
rakomi
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