Term
| True or false: most of the body's potassium is in the ECF |
|
Definition
| False, mostly in the ICF, Na/K pump maintains this state |
|
|
Term
| Shift of potassium into the ECF |
|
Definition
| Hyperkalemia, excess potassium in the plasma |
|
|
Term
| Shift of potassium into the ICF |
|
Definition
| Hypokalemia, deficient potassium in the blood |
|
|
Term
| There are 7 causes of hyperkalemia, list them: |
|
Definition
| Insulin deficiency, B-adrengergic antagonism, Acidosis, Hyperosmolarity, Inhibition of Na/K pump, Exercise, Cell lysis |
|
|
Term
| There are 4 major causes of hypokalemia, list them: |
|
Definition
| Insulin activity, B-adrenergic agonism, Alkalosis and hypo-osmolarity |
|
|
Term
| True or false: Potassium is filtered, reabsorbed and secreted by the nephron |
|
Definition
|
|
Term
| 67% of the filtered potassium is reabsorbed in this part of the nephron |
|
Definition
| Proximal convoluted tubule |
|
|
Term
| 20% of the filtered potassium is reabsorbed in this part of the nephron |
|
Definition
| Thick ascending limb of the loop of Henle |
|
|
Term
| The rest of potassium handling depends on what four factors? |
|
Definition
| Dietary potassium content, Aldosterone concentration, acid-base balance, flow rate through the tubules |
|
|
Term
| This transporter, which is blocked during furosemide tx, is primarily responsible for potassium reabsorption in the ascending limb |
|
Definition
| Na-K-2Cl transporter on luminal membrane |
|
|
Term
| What is the difference between the alpha-intercalated and beta-intercalated cells in the collecting duct? |
|
Definition
| alpha-IC cells have bicarbonate-chloride antiporters on the basolateral membrane to facilitate bicarbanoate reabsorption and chloride uptake, while beta-IC cells can have them either on the basolateral membrane or the lumenal membrane depending on the presence of alkalosis |
|
|
Term
| This is the mechanism of potassium reabsorption/hydrogen ion excretion in the distal tubule |
|
Definition
| Hydrogen-potassium ATPase on the alpha-IC cells, only function in a low potassium diet when hypokalemia is present |
|
|
Term
| True or false: secretion of potassium also occurs in the alpha-IC cells? |
|
Definition
| False, potassium secretion occurs in the principal cells. The Na/K pump brings potassium into the cells from the peritubular capillaries, creating a concentration gradient to drive potassium into the lumen from the principal cells |
|
|
Term
| What are the major cations inside cells? |
|
Definition
|
|
Term
| What are the major anions of ECF? |
|
Definition
|
|
Term
| For a 100kg man, (1) is the total weight in water, (2) is the weight of the ICF and (3) is the weight of the ECF |
|
Definition
|
|
Term
| True or false: Insulin decreases serum potassium by increasing the activity of Na/K ATPase, increasing potassium uptake into cells |
|
Definition
|
|
Term
| True or false: Sympathomimetics (B2 agonists) decrease serum potassium by decreasing activity of Na-K ATPase, lowering intracellular K concentrations. |
|
Definition
| False, Na/K ATPase activity increases with B2 agonism |
|
|
Term
| True or false: Alpha and Beta adrenergics have identical effects on serum potassium |
|
Definition
| False, alpha adrenergics increase serum potassium |
|
|
Term
| True or false: Acidemia increases hydrogen ion secretion in the principal cells of the distal tubule, which increases uptake of potassium into cells causing hypokalemia. |
|
Definition
| True, in general, but acidemia need not cause hypokalemia in every case. |
|
|
Term
| Serum hyperosmolarity increases the flow of water from the (1) to the (2), resulting in (3) concentration of potassium in the ICF, resulting in an outflow of potassium to the ECF and hyperkalemia. |
|
Definition
|
|
Term
| A burn patient could develop (hyperkalemia/hypokalemia) due to cell damage and lysis |
|
Definition
| Hyperkalemia, cell lysis leads to leakage of cell contents including potassium |
|
|
Term
| This mineralocorticoid diffuses into the principal and intercalated cells of the distal tubule, binds to a receptor protein in the cytoplasm and upregulates transcription of sodium and potassium channels, and Na/K ATPase to increase sodium reabsorption and increase potassium secretion. |
|
Definition
| Aldosterone, can cause hypokalemia in hyperaldosteronism and hyperkalemia in hypoaldosteronism |
|
|
Term
| In contrast to spironolactone, triamterine, and amiloride, these diuretics can cause hypokalemia by increasing potassium secretion. |
|
Definition
| Furosemide and thiazide diuretics, furosemide prevents potassium reabsorption in the thick ascending limb, diluting the luminal potassium and thus increasing diffusion pressure in the distal tubule, where thiazide diuretics block NaCl reabsorption in the DCT, increasing flow rate and increasing diffusion of potassium into the tubules |
|
|
Term
| True or false: since most serum CO2 is in the form of bicarbonate, the use of total CO2 as a marker for bicarbonate is an appropriate approximation |
|
Definition
| True, 90-95% of serum CO2 is in bicarb form, so total CO2 is an overestimate of serum bicarb |
|
|
Term
| These types of acids, in addition to CO2, make up about 50-100 mmoles of H+ that must be buffered daily to maintain a normal pH range |
|
Definition
| Fixed, or nonvolatile acids, like sulfuric acid, phosphoric acid, products of protein and lipophosphate catabolism, ketoacids, lactic acid are also fixed acids resulting from catabolism of proteins (ketoacidosis) and anaerobic metabolism (lactate) |
|
|
Term
| To be an effective buffer, the pH of the solution must be (1/2/3) units away from the pKa of the buffer |
|
Definition
| 1 unit, so phosphate has a pKa of 6.8, and can be an effective buffer to a pH of 5.8. phosphate is the primary buffer in urine. |
|
|
Term
| While HCO3 and PO4 are the major (extracellular/intracellular) buffers, organic phosphates, proteins and deoxyhemoglobin are the major (extracellular/intracellular) buffers |
|
Definition
| extracellular, intracellular |
|
|
Term
| Buffers work best in a 1.0 unit pH range of their pKa, this places the buffer in the linear portion of this curve, described by the Henderson-Hasselbach equation. |
|
Definition
| Titration curve, when the pH=pKa, the concentration of acid and buffer [HA] and [A-] are equal |
|
|
Term
| Bicarbonate, the predominant extracellular buffer, is reabsorbed mostly in this part of the kidney |
|
Definition
|
|
Term
| Describe the process of HCO3- reabsorption in the proximal tubule |
|
Definition
| Luminal carbonic anhydrase catalyzes the formation of CO2 and H2O from filtered HCO3 and H+, which are absorbed by the cells of the PCT and converted into H+ and HCO3- by intracellular carbonic anhydrase, H+ is secreted in exchange for sodium, HCO3- is reabsorbed |
|
|
Term
| True or false: bicarbonate reabsorption in the proximal tubule results in a net H+ secretion |
|
Definition
| False, virtually no H+ is freely secreted, it is either secreted as titratable acid or ammonium |
|
|
Term
| If bicarbonate is excreted in the urine, what does it imply about pH and serum bicarbonate? |
|
Definition
| Alkalosis, filtered bicarbonate is exceeded by plasma bicarbonate, causing bicarb to be excreted instead of reabsorbed |
|
|
Term
| Increased pCO2, e.g. hypoventilation, results in (increased/decreased) reabsorption of bicarbonate |
|
Definition
| Increased, the pH will decrease, increasing the number of hydrogen ions secreted in the kidney, resulting in increased bicarb formation and reabsorption |
|
|
Term
| A decrease in effective circulating volume typically results in metabolic (alkalosis/acidosis) as a result of four factors: |
|
Definition
| Alkalosis, hypovolemia induces the renin-angiotensin axis to increase formation of angiotensin II, which upregulates Na-H antiporter activity in the PCT, increasing bicarb formation and reabsorption, chloride depletion increases chloride reabsorption in the distal tuble, increasing H+ ion loss, hypokalemia for the same reason as hypochloremia, and a reduction in GFR with concomitant increase in plasma bicarb concentration |
|
|
Term
| When can volume depletion result in metabolic acidosis? |
|
Definition
| Diarrhea or intestinal fistulas, which cause bicarbonate to be lost, decreasing the serum bicarb concentration |
|
|
Term
| Proximal acidification occurs in the form this type of acid, in contrast to distal acidification, which involves ammonia |
|
Definition
| Titratable acid, phosphoric acid, which functions well until the pH lowers to 5.8, outside of its buffer range |
|
|
Term
| This enzyme, stimulated by aldosterone and contributing to the Na-H antiporter, is responsible for hydrogen ion secretion throughout the tubule |
|
Definition
|
|
Term
| Explain why, with a pKa of 9.0, NH3 can effectively buffer hydrogen ions in the collecting duct and distal tubule |
|
Definition
| The ratio of NH4 to NH3 is 1000:1 in this part of the tubule, creating a concentration gradient that constantly draws NH3 out of the intercalated cells into the lumen, plus, NH4+ cannot diffuse back into the cells surrounding the collecting duct, so a constant push for NH3 is always present |
|
|
Term
| This amino acid's catabolism is mostly responsible for producing NH3 in the intercalated cells |
|
Definition
|
|
Term
| Given its role in acid excretion, what happens to glutamine catabolism in acidosis? |
|
Definition
| Increased, to generate more NH3 and excrete more acid |
|
|
Term
| True or false: most of the day-to-day variation of potassium excretion is not due to changes in reabsorption in the proximal tubule or loop of Henle. |
|
Definition
| True, the principal cells of the DCT and CCT are the most important regulators of potassium excretion in the kidney |
|
|
Term
| True or false: during times of extreme potassium deprivation, the intercalated cells of the DCT and CCT can reabsorb potassium |
|
Definition
| True, through an energy-dependent hydrogen-potassium ATPase that exchanges potassium for hydrogen |
|
|
Term
| 90% of the epithelial cells in the DCT and CCT are this type |
|
Definition
|
|
Term
| These three factors are the most important triggers of potassium excretion in the kidney |
|
Definition
| Increased extracellular potassium concentration, increased concentration of aldosterone and increased tubular flow rate, it is decreased by an acidosis |
|
|
Term
| In what two ways does Aldosterone stimulate potassium excretion? |
|
Definition
| Increases activity of the basolateral ATPase that pumps sodium into the interstitium in exchange for potassium and increased expression of potassium channels in the luminal membrane of principal cells, allowing more potassium efflux |
|
|
Term
| Describe the difference between acute and chronic acidosis' effect on serum potassium levels |
|
Definition
| Acute acidosis reduces the activity of the basolateral Na-K ATPase, resulting in reduced potassium excretion, while chronic acidosis overcomes this reduction by increasing the secretion of sodium in the DCT by decreasing proximal sodium chloride secretion |
|
|
Term
| Describe how alkalosis/acidosis can affect serum calcium concentrations |
|
Definition
| In acidosis, the increased hydrogen concentration displaces calcium bound to albumin, increasing serum calcium (hypercalcemia), while in alkalosis a greater proportion of calcium is bound to albumin, resulting in lower serum calcium concentrations (hypocalcemia) |
|
|
Term
| True or false: most serum calcium is excreted in the feces (~90%) |
|
Definition
|
|
Term
| The largest reservoir of calcium in the body is in () |
|
Definition
| Bone, 99% of body calcium is in bone |
|
|
Term
| The process by which increased salt reabsorption in the DCT triggers a constriction in the afferent arteriole to reduce GFR is known as |
|
Definition
|
|
Term
| Describe how large increases or decreases in fluid intake cause little change in blood volume and sodium concentrations in the body |
|
Definition
| As blood volume increases pressure diuresis trigger increased ecretion of salt and water in the kidney, if blood volume decreases cardiac output increases to compensate, ensuring GFR remains stable and also increased absoprtion of salt and water |
|
|
Term
| How does increased fluid accumulation in the interstitial space initially prevent edema? |
|
Definition
| Increased hydrostatic pressure in the interstitium counteracts the pressure in the capillary bed, preventing fluid outflow, however as interstitial tissues become more compliant from constant pressure edema occurs |
|
|
Term
| What are the four most common causes of edema? |
|
Definition
| Increased capillary hydrostatic pressure, increased capillary permeability, decreased plasma oncotic pressure and lymphatic obstruction |
|
|
Term
| Describe the effect of ACE inhibitors and ARBs on pressure natriuresis |
|
Definition
| Blockade of Angiotensin II decreases the MAP at which the kidneys begin excreting salt and water |
|
|
Term
| These diuretics work in the proximal tubules by increasing tubular fluid osmolarity, thus inhibiting water resorption |
|
Definition
| Osmotic diuretics like mannitol |
|
|
Term
| These diuretics work in the thick ascending limb of the LoH by blocking the Na-2K-Cl transporter, disrupting the countercurrent mechanism and increasing the osmolarity of the filtrate |
|
Definition
| Loop diuretics, furosemide |
|
|
Term
| These diuretics work in the early DCT by inhibiting NaCl transport |
|
Definition
| Hydrochlorothiazide and other thiazide diuretics |
|
|
Term
| These diuretics work in the proximal tubules by inhibiting HCO3 resorption, and can cause what negative side effect? |
|
Definition
| Acetazolamide, a carbonic anhydrase inhibitor, can cause metabolic acidosis from excessive excretion of bicarb |
|
|
Term
| These diuretics work in the collecting duct by inhibiting aldosterone |
|
Definition
| Spironolactone, competitively inhibits aldosterone at its receptor, thus decreasing Na resoprtion and K excretion |
|
|
Term
| These diuretics work in the collecting duct by blocking sodium channels on the luminal membrane |
|
Definition
| Sodium channel blockers like triamterene and amiloride |
|
|
Term
| Because they inhibit sodium resorption in the collecting duct, what two types of diuretics are known as potassium-sparing diuretics? |
|
Definition
| Spironolactone and triamterene |
|
|
Term
| In what three ways can acute kidney injury be classified? Give an example of each. |
|
Definition
| Pre-renal by septic or hemorrhagic shock, renal by acute tubular necrosis and glomerulonephritis, post-renal by kidney stone obstruction |
|
|
Term
| What three materials most commonly cause kidney stones? |
|
Definition
| Calcium, urate and cystine |
|
|
Term
| True or false: 20-25% of cardiac output is directed to the kidneys to maintain GFR and perfusion |
|
Definition
|
|
Term
| True or false: Diminished renal blood flow results in diminished GFR and decreased urine output |
|
Definition
|
|
Term
| True or false: Decreased renal perfusion won't necessarily damage nephrons as long as it stays about 20-25% of normal |
|
Definition
| True, decreased GFR->decreased sodium chloride transport which uses the most ATP of any process in the kidney, thus reducing energy need |
|
|
Term
| These bacteria are the most common cause of acute glomerulonephritis |
|
Definition
| GAS, indirectly, the antibody-antigen complex formed following infection deposits on the basement membrane of the glomerulus resulting in inflammation and blockage, or increased vascular permeability resulting in proteinuria and hematuria |
|
|
Term
| What is the most serious consequence of acute kidney injury? |
|
Definition
| Hyperkalemia, can be exacerbated by metabolic acidosis, another common sequale of AKI |
|
|
Term
| This criteria for AKI is a serum creatinine increase over the course of <2 weeks of at least .5mg/dl given baseline<2.5 or 20% if baseline over 2.5 |
|
Definition
|
|
Term
| This criteria for AKI is a urine output of 100-400 ml over 24 hours or <100ml over 12 |
|
Definition
| Urine output, oliguria or anuria |
|
|
Term
| True or false: though reversible if treated in a timely fashion, AKI still has a mortality rate of 20-70% |
|
Definition
|
|
Term
| In addition to true volume depletion from hemorrhage or shock, what other blood volume defects can cause prerenal AKI |
|
Definition
| Decrease in ECV such as in CHF or cirrhosis, Renal artery stenosis, and disruption of renal vasoregulation such as ACEI or NSAIDs, ACEI inhbitis Angiotensin II in constrcting the efferent arteriole and NSAIDS constrict the afferent arteriole via inhibition of prostaglandin synthesis |
|
|
Term
| What two conditions account for 75% of AKI |
|
Definition
| Prerenal AKI due to volume depletion and ischemic ATN |
|
|
Term
| Other than ATN, what are some less common causes of intrinsic ATI? |
|
Definition
| Acute interstitial nephritis, acute glomerulonephritis and vascular diseases such as vasculitis or malignant hypertension |
|
|
Term
| What is the most common cause of acute interstitial nephritis? |
|
Definition
| Drug toxicity, penicillin, cephalosporins, sulfa and NSAIDs |
|
|
Term
| What populations are most at risk of obstructive kidney disease |
|
Definition
| Older men with enlarged prostates and patients with only one kidney or pelvic cancer |
|
|
Term
| What are the three phases of ATN? |
|
Definition
| Initiation, maintenance and recovery |
|
|
Term
|
Definition
| Pathology of ATN, patchy loss of tubular epithelial cells, detachment from basement membrane, proximal tubule dilation, casts and cellular regeneration |
|
|
Term
| What two events distinguish maintenance and recovery from initiation of ATN? |
|
Definition
| Oliguria of the maintenance phase, when diuresis begins the the patient is in recovery, sodium handling lags behind tubular repair so diuresis occurs before normal urine output is restored |
|
|
Term
| Fractional excretion of sodium is useful in distinguishing what two causes of acute kidney injury? |
|
Definition
| Pre-renal from intrinsic, ie ATN |
|
|
Term
| T or F: Hyperkalemia is a rare occurrence in normal subjects, because the body is extremely effective in preventing excess K accumulation in the ECF |
|
Definition
|
|
Term
| What two steps makeup the body's response to a potassium load? |
|
Definition
| Cells take up excess K mediated by insulin and the Na-K pump, then urinary excretion through aldosterone |
|
|
Term
|
Definition
| The ability to handle waht might be a lethal K load if given acutely |
|
|
Term
| What mechanism facilitates kaliuresis? |
|
Definition
| Enhanced excretion in the late distal nephron |
|
|
Term
| What two events are required to increase K excretion in the prinicpal cells of the CCT and MCT? |
|
Definition
| Increased secretion of aldosterone and a small elevation in the plasma K concentration are required |
|
|
Term
| What is the model of K adaptation? |
|
Definition
| Chronic renal failure due to loss of nephrons requiring greater excretion per nephron |
|
|
Term
| What facilitates increased K excretion in the late distal nephron? |
|
Definition
| Upregulation of Na/K ATPase activity via aldosterone |
|
|
Term
| T or F: Chronic hyperkalemia is rarely associated with an impairment in urinary K excretion due to hypoaldesteronism or decreased distal flow |
|
Definition
| False, it is always associated with impairment in K excretion |
|
|
Term
| What term describes a condition in which the elevation in the measured K concentration is due to K mvmt out of the cells during or after the blood draw |
|
Definition
|
|
Term
| How does metabolic acidosis cause hyperkalemia? |
|
Definition
| K moves out of cells in exchange with protons to maintain pH balance |
|
|
Term
| By what mechanism does Beta-blockade induce hyperkalemia? |
|
Definition
| Down-regulation of the Na/K pump leading to K outflow into serum |
|
|
Term
| T or F: Severe exercise can cause hyperkalemia |
|
Definition
|
|
Term
| True or false: Three major causes of decreased K excretion in the urine are renal failure, decreased effective circulating volume and hyperaldosteronism |
|
Definition
|
|
Term
| True or false: hyperkalemia as a result of renal failure is due to damage to exchange mechanisms in the distal nephron |
|
Definition
| False, loss of total number of nephrons, not any defect to excretion mechanisms |
|
|
Term
| What two mechanisms, as a result of ECV depletion, result in decreased flow? |
|
Definition
| Low GFR and enhanced Na resoprtion in the proximal tubule |
|
|
Term
| What are the three most common causes of hypoaldosteronism? |
|
Definition
| hyporeninemic or K sparing diuretic use, CAH in children |
|
|
Term
| T or F: Use of ACE inhibitors can decrease GFR and result in hyperkalemia |
|
Definition
|
|
Term
| TB/AIDS, metastatic tumors, autoimmunity and genetic defects can all cause this condition in the adrenal glands, resulting in hyperkalemia |
|
Definition
| Primary hypoaldosteronism |
|
|
Term
| True or false: Secondary adrenal insufficiency also causes hyperkalemia |
|
Definition
| False, aldosterone secretion in secondary adrenal insufficiency is unchanged |
|
|
Term
| T or F: Heparin can cause hyperkalemia |
|
Definition
| True, by reduction of aldosterone secretion |
|
|
Term
| How does hyperkalemia cause muscle weakness? |
|
Definition
| Persistent depolarization inactivates sodium channels in the cell membrane, producing a net decrease in membrane excitability |
|
|
Term
| T or F: Hyperkalemia typically spares muscle weakness in the cranial nerve innervated muscles and the diaphragm |
|
Definition
|
|
Term
| T or F: Cardiac arrhythmia is the most dangerous consequence of hyperkalemia |
|
Definition
| True, elevated EC K concentration increases the permeability of K channels in the cardiomyocyte membrane which increases the rate of depolarization and gives rise to ectopic foci |
|
|
Term
| T or F: The alteration in T wave configuration seen in hyperkalemia is prominent when K concentration exceeds 5 meq/L |
|
Definition
|
|
Term
| T or F: Hyperkalemia eventually leads to merged QRS and T waves and ventricular fibrillation or cardiac arrest |
|
Definition
|
|
Term
| T or F: The endocardium is more prominently affected than the epicardium by hyperkalemia |
|
Definition
| False, epicardium more affected than endocardium |
|
|
Term
| T or F: Hyperkalemia's cardiac toxicity is augmented by hypocalcemia, hyponatremia and is blunted by acidemia |
|
Definition
| False, all augment cardiac toxicity in hyperkalemia |
|
|
Term
| What three processes should be considered when diagnosing the source of hyperkalemia? |
|
Definition
| Increased intake, decreased uptake into cells or decreased excretion |
|
|
Term
| What four treatments can be used in acute hyperkalemia to increase movement of potassium into cells? |
|
Definition
| Insulin+Glucose, sodium bicarb (not CaBicarb), Beta agonists and hypertonic saline if hyponatremic as well |
|
|
Term
| What three treatments for hyperkalemia work by increasing excretion? |
|
Definition
| Diuretics, kayexalate and hemodialysis/peritoneal dialysis |
|
|
Term
| T or F: Each mg of sodium polystyrene sulfate can bind up to 1 meq of potassium |
|
Definition
| False, each gram can bind K in the the GI tract and be excreted in the feces, major side efx include nausea, constipation, overuse and sodium retention |
|
|
Term
| T or F: chronic glomerulonephritis is best considered a pool of end-stage glomerular disease fed by a number of streams of specific types of glomerulonephritis |
|
Definition
| True, poststreptococcal glomerulonephritis is a rare antecedent in children |
|
|
Term
| Pathologic findings including thinned renal cortex, increased peripelvic fat and hyaline obliteration of the glomeruli indicate what condition? |
|
Definition
| Chronic glomerulonephritis |
|
|
Term
| List some complications of uremia due to chronic glomerulonephritis |
|
Definition
| uremic pericarditis, uremic gastroenteritis, secondary hyperparathyroidism, LVH from hypertension and uremic pneumonitis |
|
|
Term
| What three clinical syndromes are most associated with diabetic nephropathy? |
|
Definition
| Non-nephrotic proteinuria, nephrotic syndrome and chronic renal failure, as well as hyalinizing arteriolar sclerosis |
|
|
Term
| T or F: over proteinuria is preceded by a 5-10 year period of microalbuminuria |
|
Definition
| True, during this time the capillary basement membrane thickens and there is diffuse mesangial sclerosis and nodular glomerulosclerosis |
|
|
Term
| Nodular glomeruosclerosis, also known as (), results from mesangiolysis and disruption of capillary anchoring to mesangial stalks |
|
Definition
| Kimmelstiel-Wilson disease or intercapillary glomerulosclerosis |
|
|
Term
| What is the clinical definition of microalbuminuria? |
|
Definition
| 30-300 mg of albumin in the urine per day. |
|
|
Term
| T or F: GFR < 60 ml/min for 3+ months is the definition of chronic kidney disease |
|
Definition
|
|
Term
| T or F: Kidney size is of poor diagnostic utility in differentiating chronic from acute kidney disease |
|
Definition
| False, it is the most sensitive marker for a kidney <9cm in span |
|
|
