electrolytes & Acid Base
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
|
|
||||
|---|---|---|---|---|---|
| T/F exogenous alkali causes sustained metabolic acidosis. | FALSE. The healthy kidney quickly responds to excess alkali by increasing HCO3 excretion unless dietary chloride is restricted severely. in kidney failure, alkali causes met alk indep of chloride.
🗑
|
||||
| Hyperaldosteronism explained | Unregulated aldosterone secretion causesNa reabsorption w H+ and K+ secretion in collecting duct via stim Na channel & H+ATPase. K depletion then promotes NH4+ production & activation of H,K-ATPase activity w subsequent acid excretion.
🗑
|
||||
| T/F lactic acidosis causes hyperkalemia | FALSE! organic acids do not cause trans cellular potassium shifts
🗑
|
||||
| How do insulin & beta agonists lower potassium? | potassium uptake stimulated by NaK ATPase. Insulin does it directly, beta agonists increase cAMP production which then stimulates NaK ATPase. Synergistic. Since affect different cellular mechanisms.
🗑
|
||||
| Where is potassium handling regulated? | by active secretion and absorption in distal tubule and collecting duct
🗑
|
||||
| Factors affecting principal cell K secretion | located in the cortical collecting duct. Na reabsorption through apical ENaC stimulates basolateral NaK-ATPase
🗑
|
||||
| Role of intercalated cells in K secretion? | reabsorb K via apical HK-ATPase
🗑
|
||||
| __________ is the common consequence of potassium depletion. | metabolic alkalosis is seen often d/t net acid excretion.
🗑
|
||||
| Metabolic alkalosis may increase renal potassium ________ | excretion, causing K depletion
🗑
|
||||
| Pseudo-hypokalemia is seen _______ | abnormal wbc’s take up K when vials are left at room temperature. Usually seen w/ AML.
🗑
|
||||
| Explain hypokalemic periodic paralysis | CHO rich meal leads to exaggerated insulin, followed by sudden onset hypoK d/t shifting, esp at night or early AM. AD mutation of alpha subunit DHP sensitive Ca channel.
🗑
|
||||
| Explain home vomiting causes hypoK | gastric fluid contains 5-8 mmol/L of K. however, associated volume depletion causes 2cndry hyperaldo which then increases urinary K losses.
🗑
|
||||
| Hypokalemia may cause NDI when level ___. How? | K< 3.0 lowers U[] ability. Collecting tubule unresponsive to AVP: AQP2 down regulated & decreased acitivity of NaK2Cl transporter w decreased medullary [] gradient.
🗑
|
||||
| Which diuretic causes more hypoK adjusted for natriuretic effect? | Thiazides cause more K loss than loop diuretics.
🗑
|
||||
| Drugs that cause increase K excretion? | penicillin analog, info Terreson, aminoglycoside, cisplatin, toluene
🗑
|
||||
| Toluene causes? | RTA and hypokalemia
🗑
|
||||
| What effect does barium have on potassium? | blocks potassium channels diffusely, resulting in hypo K. dialysis removes barium and causes K rebound.
🗑
|
||||
| Causes hypokalemia, metabolic alkalosis and nl/low BP? | Bartter & Gitelman + diuretic use
🗑
|
||||
| Causes hypokalemia, metabolic alkalosis and HTN? | Liddle, AME, GRA
🗑
|
||||
| What is Bartter Syndrome? | variable inhritance, seen in childhood. hypoK, nl/loBP, high renin, high aldo, met alk, hypercalciuria w/ nephrocalcinosis, vol depletion, polyuria, high UCl >20 (dx young and assoc w growth retardation). Rx-indomethacin
🗑
|
||||
| What is Gitelman’s syndrome? | AR, older pts. Similar toThiazide diuretic. similar to Bartters, except add hypocalciuria, salt craving. +Salt cravings->more K loss, renal Mg wasting ->hypoMg. HYPOMAGNESEMIA defining feature. No response to indomethacin. Rx amiloride.
🗑
|
||||
| Renal K losses cause Urine K level of ______? | UK > 20 mEq/day (high).
🗑
|
||||
| What is Liddle Syndrome? | AD. ENaC mutation causes too many channels. Causes met alk + HTN + lo renin + lo aldo. Rx triamterene. no response to spironolactone.
🗑
|
||||
| What is apparent mineral corticoid excess? | AR. cortisol found at 1000x higher [] than aldo—> excess cortisol binds to mineralocorticoid receptor causing HTN & hypoK.
🗑
|
||||
| What is glucocorticoid Remediable aldosteronism? | AD w FMH hypoK and HTN.Lo renin, hi aldo. ACTH regulated promoter linked to gene for aldo synthase (rate limiting enzyme for Aldo production). So, aldo synthase expression is regulated by ACTH and hyperaldo develops.
🗑
|
||||
| hypomagnesemia + hypocalciuria + met alk + hypoK + UCl>20 | Gitelman Syn
🗑
|
||||
| met alk + lowK w nl/low BP + high renin + hypercalciuria | Bartter Syndrome. Have vol depletion.
🗑
|
||||
| met alk + lowK w nl/low BP + high renin + hypocalciuria | Gitelman’s syndrome, with similar picture toThiazide diuretic.
🗑
|
||||
| met alk + lowK + HTN + lo renin + lo aldo | Liddle Syndrome. No response to spironolactone. Rx-triamterene normalizes BP & K.
🗑
|
||||
| met alk + lowK +HTN + low renin + high aldo | Glucocorticoid Remediable Aldosteronism. Rx- steroids, triamterene, spironolactone. Distinguishing feature from AME are low renin & low aldo in AME.
🗑
|
||||
| met alk + lowK +HTN +low renin + low aldo | apparent mineral corticoid excess, cushings, congenital adrenal hyperplasia. Rx- steroids, triamterene, spironolactone. Distinguishing feature from GRA are low renin & HIGH aldo in GRA.
🗑
|
||||
| Calculate compensatory change in PCO2 in met acidosis | 1.5HCO3 + 8 +/- 2… or… HCO3 + 15 is the CO2!
🗑
|
||||
| Calculate compensatory change in PCO2 in met alkalosis | HCO3 + 15 is the CO2! (same as MA)
🗑
|
||||
| Urine anion gap formula and significance | UAG ~ (Na+K)-Cl; used to approximate ammonium excretion in cases of NAGMA
🗑
|
||||
| Positive urine AG means? | low NH4 (cannot excrete acid) thus renal cause
🗑
|
||||
| Negative urine AG means? | high NH4 (means can excrete acid) thus NON renal cause
🗑
|
||||
| For each one gram decline in albumin, the anion gap falls by ___ | 2.5 (ex alb is 2, then AG falls by 5)
🗑
|
||||
| What causes of low anion gap? | low albumin, hyperCa, hyperMg, lithium, IgG paraproteins, polymyxin B (cationic properties). Rare elevations in chloride seen from bromide and iodide, lowering AG as well.
🗑
|
||||
| What causes of high anion gap? | vol depletion (hi alb), alkalosis, anionic paraprotein IgA, severe hyperPhos (accompanied by Na)
🗑
|
||||
| Why does multiple myeloma cause low anion gap? | myeloma proteins behave like unmeasured cations but bind to HCO3 or Cl
🗑
|
||||
| Explain Distal RTA I | Cannot excrete H+;excrete K causing hypoK, urine pH > 5.5; ++stones & hypercalciuria & lo Ucitrate
🗑
|
||||
| Explain Proximal RTA II | cannot regenerate HCO3 (ie lose it; thus have too little bicarb); urine pH variable (early its < 5.5 later w rx > 5.5); cannot reabsorb K so hypoK; assoc w fanconi, rickets & osteomalacia.
🗑
|
||||
| Explain RTA IV | “distal” but not really a tubular defect! low renin & aldo; hyperK; urine pH < 5.5
🗑
|
||||
| Causes of proximal RTA | cannot reabsorb (ie lose) HCO3: MM, ifosfamide, carbonic anhydrase inh, topiramate (acts like CA), heavy metals.
🗑
|
||||
| Causes of distal RTA | autoimmune (sjogrens, thyroiditis, PB cirrhosis); hypercalciuria & nephrocalcinosis (excess vitD, HPT, Graves); drugs (amphB, ifosfamide, topiramate, lead, lithium, toluene, tetracycline); tubulointersitial d/o (MCD,analgesic nephropathy).
🗑
|
||||
| What K disorder decreases renal ammonia production? | hyperkalemia. They compete for a common site on tALH Na2ClK co-transporter.
🗑
|
||||
| What counteracts CNI induced RTA? | CNIs activate NaCl channel, which is blocked by thiazides.
🗑
|
||||
| D-lactic acidosis | short gut allows undigested CHO to reach colon, where bacterial fermentation generate organic acids, including D lactate
🗑
|
||||
| Acid-base disorder from salicylate intoxication? | respiratory alkalosis from stimulation of medullary respiratory center andAGMA from lactate, ketoacids (salicylate anion has minor effect). Usu have hypoglycemias
🗑
|
||||
| Characteristics of milk (calcium) alkali syndrome? | nephrocalcinosis, metabolic alkalosis, renal insufficiency. DDX vitamin D excess + hypercalcemia, sippy diet(Ingestion of milk and bicarb), calcium carbonate/acetate administration
🗑
|
||||
| Metformin induced lactic acidosis by _______ | mitochondrial inhibition & decreased gluconeogenesis results in more LA
🗑
|
||||
| Findings of salicylate OD? | pure AGMA, no osmolar gap, met acidosis+ resp alk. AGMA not caused by drug itself, but by poisoned TCA cycle and uncoupled oxidative phosphorilation (LA, phosphoric, sulfuric)
🗑
|
||||
| Treatment of salicylate OD? | empty stomach, charcoal, forced saline alkaline diuresis, HD indicated if salicylate lvl >80 + severe sx, or seizures/coma, or severe acidosis
🗑
|
||||
| GTTs associated w propylene glycol toxicity | Diazepam, lorazepam, etomidate, NTG
🗑
|
||||
| Describe Propylene glycol toxicity | hi osmolal gap & hi AGMA, lactic acidosis, AKI. metabolized by alcohol dehydrogenase into D- & L-isoforms of lactic acid. It can occur with nl doses and nl GFR, but usu assoc w dosages above the recommended range. Fomepizole use unproven.
🗑
|
||||
| Which alcohols cause osmolar gap? | methanol, ethylene glycol, ETOH, propylene glycol, isopropranolol, diethylene glycol
🗑
|
||||
| Non drug causes of +osmolar gap? | DKA, alcoholic ketoacidosis, lactic acidosis, AKI, salicylate
🗑
|
||||
| T/F Ethanol ingestion may be associated with ketoacidosis. | TRUE typically after a patient stops drinking, and the osmolal gap is usually small at this point
🗑
|
||||
| Findings of isopropyl alcohol toxicity | increased osmolal gap, but NORMAL AG, high creatinine BUT normal BUN (assay interference)
🗑
|
||||
| Abnormally elevated serum creatinine with a normal BUN may be seen with ____? | isopropyl alcohol poisoning. High levels of acetone, a metabolite of isopropyl alcohol, interfere with colorimetric creatinine assays, resulting in falsely hi values
🗑
|
||||
| Abnormalities with intoxication from ETOH ketoacidosis? | met acidosis, osm gap (lactate) + AG, + ketones . Vision nl; renal fcn nl.
🗑
|
||||
| Abnormalities with intoxication from methanol? | met acidosis, osm gap + AG, neg ketones + vision changes, +/-AKI, no calcium oxalate
🗑
|
||||
| Abnormalities of putamen (putaminal hemorrhage) suggest what intoxicant(s)? | methanol. Formate causes retinal injury with optic disc hyperemia, edema—> blindness. Thought d/t disruption of mitochondrial function
🗑
|
||||
| Abnormalities with intoxication from ethylene glycol? | met acidosis, osm gap + AG, +AKI + calcium oxalate; neg ketones, Nl vision.
🗑
|
||||
| Oxalate crystals suggests what intoxicant(s) | ethylene glycol can show “envelope" Crystals
🗑
|
||||
| Indications for dialysis for methanol intoxication? | (rare since fomepizole) pH < 7.3, visual changes, AKI, methanol >50, abnl lytes unresponsive to medical rx.
🗑
|
||||
| Role of supplemental vitamins and intoxications? | Folic acid increases formate—> CO2 + H20. . Pyridoxine & thiamine may help metabolize (for EG poisoning).
🗑
|
||||
| Abnormalities with intoxication from isopropyl alcohol? | met acidosis, osm gap but NO increase in AG + ketones. No AKI, vision changes orcalcium oxalate
🗑
|
||||
| Ketones positive with intoxication from what substances? | alcoholic ketoacidosis and isopropyl alcohol
🗑
|
||||
| Treatment of aspirin/salicylate OD? | alkaline urine to keep urine pH>7.5. Alkalinization used alone if nl renal fcn. If need mech ventilation, use hi minute ventilation to keep elevated blood pH. HD when level > 80 or AMS, AKI, pulm edema, vol overload (limits alkalization).
🗑
|
||||
| When is dialysis useful for aspirin/salicylate OD? | HD when level > 80 or AMS, AKI, pulm edema, vol overload (which limits alkalization), clinical deterioration despite aggressive supportive care.
🗑
|
||||
| Effects of acetazolamide? | causes alkaline urine and severe metabolic acidosis, therefore not useful for salicylate intoxication.
🗑
|
||||
| Explain intoxication from bath salts? | Salt often inhaled/ ingested/ injected contain 3,4 methyledeedioxypyrovalerone (MDPV)—> AKI, rhabdo, seizures.
🗑
|
||||
| Ecstacy OD explained? | amphetamine derivatives causing releases serotonin, dopamine,NE, ADH, cortisol & prolactin. renal effects are AKI (rhabdo) and hypoNa. Mortality first time users 1:2000-1:50,000.
🗑
|
||||
| Ecstacy induced hyponatremia? | common, assoc w/ large H20 intake, usu females. Rx 3% NaCl if symptomatic.
🗑
|
||||
| fruity odor raises suspicion for _____ intoxication? | acetone
🗑
|
||||
| Garlic odor raises suspicion for _____ intoxication? | Arsenic, organophosphates, phosphorus, thallium, selenium
🗑
|
||||
| Wintergreen odor raises suspicion for _____ intoxication? | methyl salicylate
🗑
|
||||
| Describe toluene effects on the kidney. | extra renal acidosis w AGMA. Inhaled from paint/hydrocarbons irritate mucous membranes—>look for erythema of lips/nose, conjunctival injection. Backtitation of nonHCO3 buffers can raise CO2
🗑
|
||||
| Name complications of bicarbonate Rx. | raise CO2, lactic acid, vol overload, hyperNa, alkalosis (resp & met), decresaed O2 tissue delivery (unopposed effect of RBC2,3 DPG).
🗑
|
||||
| Describe Borr effect | acidosis shifts O2 dissociation & worsens lactic acidosis.
🗑
|
||||
| Administration of bicarbonate causes alkaline urine despite acidosis in RTA__. | RTA Type II (proximal) caused by defective HCO3 reabsorption causing mild acidosis.
🗑
|
||||
| Administration of NH4CL results in normal urine acidification with pH < 5.5 since SOME acid excretion is present in RTA ___. | Type IV RTA.
🗑
|
||||
| Ecstasy renal effects? | Most common, is hyponatremia (excess AVP release + increased H2) intake). also see AKI (nontraumatic rhabdomyolysis or setting of drug-induced liver failure and drug-induced vasculitis).
🗑
|
||||
| DDX hypercalcemia + low PTH, normal 25(OH)D, + low 1,25(OH)2D? | includes hyperthyroidism, malignancy, immobilization, Paget's disease, and milk-alkali syndrome.
🗑
|
||||
| What is Rx Rx hypercalcemia? | calcium >14 mg/dL (3.5 mmol/L) require treatment 3 ways, regardless of symptoms d/t severity: calcitonin + saline reduce Ca in 12+ hrs; bisphosphonate effective 2cnd day & maintains control
🗑
|
||||
| In the absence of AKI/CKD or HF, loop diuretic therapy to directly increase calcium excretion is/is not (choose) recommended. | Diuretics are NOT advised d/t potential complications andbetter Rx’s inhibit bone resorption, which is primarily responsible for the hypercalcemia.
🗑
|
||||
| which bisphosphonate used for hypercalcemia? | zoledronic acid (ZA; 4 mg IV) preferred over pamidronate (60-90 mg) because superior to pamidronate in reversing hypercalcemia related to malignancy. May need to repeat qmo
🗑
|
||||
| Hypercalcemia inhibits ___ reabsorption. | magnesium (and calcium) leading to hypermagnesuria and hypercalciuria. This seems to occur by activation of the calcium-sensing receptor on the basolateral membrane of TAL.
🗑
|
||||
| When is dialysis indicated for hypercalcemia? | ca levels of18-20, CNS symptoms with stable circulation, or hyperCa w renal failure. Can correct AKI. Ca 12-14 may be well-tolerated, and may not require immediate treatment.
🗑
|
||||
| Describe X-linked hypophosphatemic rickets (aka vitD-resistant rickets). | Renal phos wasting w/o hypoCa: defect in prox tubular phosphate transport d/t mutated PHEX gene. RX: po Ph + calcitriol (inc GI absorption of calcium, prevent SPTH and suppress PTH.)
🗑
|
||||
| Describe autosomal dominant hypophosphatemic rickets. | Mutant FGF-23 resistant to protease cleavage but retains its phosphaturic properties.
🗑
|
||||
| Describe Fanconi syndrome. | prox tubule dysfcn—>urinary wasting: Hypophos (can lead to osteomalacia), glucosuria (osmotic diuresis), hypouricemia, aminoaciduria, and prox RTA. [calcitriol] are low or inappropriately normal.
🗑
|
||||
| Hi alk phos and low vitD and high PTH seen in? | osteomalacia. VitD def
🗑
|
||||
| Nutritional osteomalacia usu presents with? | very low 25[OH]D (<10 ng/mL [25 nmol/L]), low to low-normal serum calcium and phosphate, and high PTH & alkphos levels. Note 1,25vitD variable (lo, nl or hi)
🗑
|
||||
| Tumor-induced osteomalacia usu presents with? | low pos + low calcitriol (expect it to be high)-[underlying tubular defect that impairs phos reabsorption also affects calcitriol synthesis].
🗑
|
||||
| High PTH + RTA, hypoPhos, hypercalciuria | prox RTAII. Causes hyperchloremic metabolic acidosis and hypoPhos. +proximal phosphate wasting and acidosis induced hypercalciuria results in SPTH
🗑
|
||||
| Drugs assoc w renal Mg wasting. | diuretics, amphora, cisplatin, pentameter, foscarnet (also hypoCa), ketogenic diet, CNI, ab against epidermal growth factor (cetuximab), ETOH, hypercalcemia.
🗑
|
||||
| How does hypercalcemia cause hypomagnesemia?(!) | Calcium binds to basolateral CaSR (ca sensing receptor)—> PGs then inhibit apical potassium channel (ROMK)>Inhibits NaCl reabsorption in TAL and reduces paracellular magnesium and calcium reabsorption.
🗑
|
||||
| HypoK can cause ____ | nephDI with polyuria
🗑
|
||||
| Describe Gitelman syndrome | most common form of familial Mg wasting & assoc w salt wasting, hypokalemic met alk, and hypocalciuria (looks like thiazide!). Caused by AR mutations in thiazide-sensitive NaCl cotransporter NCC (SLC12A3) in distal tubule.
🗑
|
||||
| Describe Familial hypocalciuric hypercalcemia (FHH) | AD disorder is characterized by very low excretion of calcium and magnesium and by a normal parathyroid hormone level.
🗑
|
||||
| AKI, low BP, edema/vol overload after stem cell txp | similar picture to HRS: Hepatic veno-occlusive disease (VOD), aka sinusoidal obstruction syn. Pathophys sinusoidal obstr, portal HTN, and microvasc intrahepatic portosystemic shunting. Risk factors: Busulfan, cyclophosphamide, total body irradiation
🗑
|
||||
| How do CNIs cause hypomagnesemia? | CNIs downregulate TRPM6 . May increase claudin-14 expression, which would inhibit paracellular magnesium transport. Mainly reduce expression of claudin 16 in the ascending limb of Henle's loop
🗑
|
||||
| Normal ca, phos, and alk phos | osteoporosis (essentially all labs normal)
🗑
|
||||
| Lytic lesions + nl alk phos+ abnl renal fcn+ hyperCa + RTAII | multiple myeloma
🗑
|
||||
| low 25OH vitD w/ variable 1,25 vit, hi alk ph, hi PTH, normal/low ca & ph | Vit D deficient. NOTE key is low vit 25OH D!!!
🗑
|
Review the information in the table. When you are ready to quiz yourself you can hide individual columns or the entire table. Then you can click on the empty cells to reveal the answer. Try to recall what will be displayed before clicking the empty cell.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Created by:
ka1usg
Popular Medical sets