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95 Cards in this Set
- Front
- Back
What are the causes of ECF volume increases? |
CHF, cirrhosis, kidney disease, hypoalbuminemia |
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How would a patient with ECF volume overload present? |
edema, weight gain, JVP elevation, pulmonary edema, pleural effusion |
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How do you manage a patient with ECF volume overload? |
treat underlying cause, Na+ restriction, diuretics |
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What are the side effects of diuretics? |
hypotension, hypokalemia, hyponatremia. |
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What are the causes of ECF volume depletion? |
diarrhea, sweating, burns, diuretics |
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How does a patient with ECF volume depletion present? |
low JVP, dry mucous membranes, weight loss, tachycardia, hypotension, depressed fontanels, oliguria |
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How do you manage a patient with ECF volume depletion? |
oral rehydration, isotonic saline IV |
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What are some of the causes of hyponatremia? |
Low Na+ due to TOO MUCH water! causes: too much ADH due to low bp, stress, pregnancy, cortisol, low tyroid, cancers, drugs |
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What are the S/S of hyponatremia? |
usually none if gradual, but if acute: headache, confusion, seizures, coma due to brain swelling. |
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How do you treat hyponatremia? |
treat underlying cause, fluid restriction, give hypertonic saline to move fluid into ICS, treat slowly to avoid brain injury |
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What are the causes of hypernatremia? |
Condition due to LOW WATER!! seen in patients who are unable to obtain fluids (elderly, infants, etc), patients in coma, glycouria (ie. DM) diabetes insipidus. |
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What are the S/S of hypernatremia? |
thirst, if acute: coma, seizures, |
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What causes hypokalemia? |
insulin therapy, diarrhea, DM, Conn's syndrome, MI, high aldosterone, diuretics, metabolic alkalosis |
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What are the S/S of hypokalemia? |
muscle weakness, ventricular arrhythmias, hyperglycemia |
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Why are patient with hypokalemia alkaline? |
When K+ is lost from cells, it gets replaced by H+ and Na+ which makes cells acidic. The kidneys then think the body is acidic and they secrete extra ammonium (acid) making the blood alkaline. |
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How do you treat hypokalemia? |
use a K+ sparing diuretic, oral KCl, IV KCl (for very low K+), high K+ foods |
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What causes hyperkalemia? |
due to K+ leaking out of cells, secondary to insulin deficiency, rhabdomyolysis, hemolysis, impaired kidney excretion, metabolic acidosis |
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what are the S/S of hyperkalemia? |
muscle weakness, stiffness, cardia arrhythmias (peaked T waves, no P waves, wide QRS) |
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How do you treat hyperkalemia? |
give calcium and insulin (stablizes ECG and shifts K+ into cells), diuretics or dialysis |
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When would you refer a diabetic patient to a nephrologist? |
1. renal insufficiency: GFR <15 2. hematuria 3. SCr elevated >30% when on ACE or ARB 4. >300mg protein in 24hr urine specimen 5. diabetic nephropathy unlikely at this time |
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What is GFR based on? (3) |
1. age 2. weight 3. creatinine clearance |
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What two areas detect changes is ECF volume? |
1. carotid baroreceptors 2. juxtaglomerular apparatus |
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What substances regulate ECF volume in the body? |
1. renin 2. aldosterone 3. angiotensin 4. catecholamine |
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What is diabetes inspidus? |
When there is not enough ADH and too much fluid is being lost. |
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What lab findings would be present in DI? |
1. high serum Na 2. high serum osmolarity (=highly concentrated) 3. low urine osmolarity (=diluted) 4. polyuria and thirst 5. ADH low (if lack of excretion from pituitary) or normal if no response from the kidneys |
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What are the S/S of DI? |
1. polyuria, 2. thirst |
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How do you treat DI? |
hormonal replacement of ADH, thiazide diuretics, oral fluid replacement. |
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What is SIADH? |
Syndrome of inappropriate ADH - too much ADH = fluid overload!! |
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What lab findings would be present in SIADH? |
1. low serum Na 2. low serum osmolarity 3. high urine osmolarity 4. high ADH levels 5. low serum Ca2+ |
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What are the S/S of SIADH? |
1. edema/fluid retention 2. olgiuria |
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What causes SIADH? |
some cancers (eg. lung), drugs |
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How do you treat SIADH? |
hypertonic solution, lithium, fluid restriction |
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What are the causes of Metabolic alkalosis? |
1. vomiting 2. loss of HCl 3. hypokalemia |
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What lab values are indicative of metabolic alkalosis? |
high pH, high bicarb, possibly low K+, low H+ |
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What are the causes of metabolic acidosis with an anion gap? (KARMEL) with out an anion gap? |
K-ketoacidosis A-aspirin R- Renal failure M- methanol E-ethalene glycol L- lactic acidosis (hypovolemic/cardiogenic shock, sepsis, cirrhosis) without - diarrhea, |
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How do you treat metabolic acidosis? |
treat underlying condition, administer NaBicarb |
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What lab values are indicative of metabolic acidosis? |
low pH, low bicarb, increased anion gap |
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What are the main characteristic of AKI? |
decreased GFR, elevation of BUN and Cr, olgiuria |
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What are major S/S of AKI? |
fatigue, altered mental status, nausea, vomiting, pruritis, seizures, anorexia, hyperkalemia, acidosis |
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What clinical findings are present in AKI? |
myoclonus, pericardial rub, edema, pulmonary rales |
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What lab investigations would you do for suspected AKI? |
BUN, SCr, lytes, CBC w/diff, urine dipstick, microscopy, urine Na, urine Cr. |
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Differentiate between nephrotic syndrome and actue nephritic syndrome |
nephrotic: >3.5g urine protein in 24 hrs, low serum albumin, high cholesterol, edema - condition of protein loss in the urine causing low oncotic pressure and subsequent edema nephritic: RBCs in urine, RBC casts, edema, HTN - condition of AKI and Na and H2O retention leading to edema. |
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Differentiate between pre, intra, and post renal AKI? |
pre-diminised blood flow to kidneys intra - damage to renal parenchyma post - UT obstruction |
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How would you investigate pre-renal AKI? |
urine dipstick, serum osmolality (>500mmol/L). BUN:Cr (>20:1), no blood or protein in the urine |
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What are the causes of pre-renal AKI? |
shock (cardiogenic, hemorrhagic), CHF |
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How do you treat pre-renal AKI? |
volume replenishment (IV NS) |
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What lab findings would be indicative of intra-renal AKI? |
normal serum osmolarity, BUN:Cr <20:1, Na excretion >3%, urine would show: RBC, RBC casts, WBC, WBC casts, proteins |
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What are the main clues in a urine analysis that AKI is glomerular in origin? |
RBCs, RBC casts, >2-3g protein in 24hr sample. |
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What is post streptococcal glomerulonephritis? What are the S/S? What is the treatment? |
immune complex build up in the glomeruli leading to AKI. usually occurs 2-3 weeks post-infection. S/S: hematuria, oliguria, HTN, proteinuria. Tx: supportive |
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What is IgA nephropathy (aka Berger's disease)? |
IgA complex build up in glomeruli usually at the time of a URTI. S/S: painless, gross hematuria Tx: steroids |
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What is Henoch Schonlein purpura? How is it different from IgA nephropathy? |
Due to deposition of IgA complex in glomeruli and may lead to CKD. Similar to IgA but has systemic presentation of: purpura, arthalgia, abd pain (triad of symptoms: abd pain, arthritis, purpura) Tx: pain killers, supportive bc spontaneously resolves |
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Name the types of focal nephritic syndromes |
1. mild postinfectious glomerulonephritis 2. mild IgA nephropathy 3. thin basement membrane disease 4. proliferative glomerulonephritis 5. early lupus |
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Name the types of diffuse nephritis syndromes |
1/ postinfectious glomerulonephritis 2. poliferative glomerulonephritis 3. advanced lupus 4. glomerulonephritis |
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If a patient had protein in the urine and hypoalbuminemia, dyslipidemia and edema but NO hematuria, what kind of kidney disease would they have? (Nephritic, nephrotic, or pre-renal?) |
nephrotic |
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How do you differentiate between glomerular vs. tubulo-interstitial AKI? |
glomerular- RBC, RBC casts, proteinuria tubulo-interstitial: WBC, WBC casts, |
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What are the two main types of tubulo-interstitial disease? How do you distinguish between the two? |
1. acute tubular necrosis 2. interstitial nephritis IN is an allergic rxn to drugs and presents with additional S/S: rash, fever, high Cr. |
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What is polycystic KD? What are the S/S? |
cyst formation on kidneys bilaterally S/S: HTN, pain, kidney stones, hematuria, UTI |
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How would you investigate polycystic KD? |
ultrasound, urine analysis |
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Who does proximal renal tube acidosis usualy occur in? What is it? What are the S/S? |
Young kids, failure of proximal tubules to reabsorb bicarb from the urine creating metabolic acidosis S/S: confusion, failure to thrive, low resp rate, dehydration, fatigue, polydispia |
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What are the S/S of renal cell carcinoma? |
hematuria, flank pain, palpable abdominal mass, weight loss, anorexia, etc. |
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What causes renal vein thrombosis? How do you investigate it? How do you treat it? |
renal veins become clogged by thrombi for various reasons, or by tumor Ix: renal vein angiography or doppler, US, CT Tx: anticoagulation w/ heparin |
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A patient presents with HTN, flank bruits, and hypokalemia. What is the main DDx? How would you investigate this? How would you manage this? |
renal artery sclerosis (bruit is main clue) Ix: angiography, doppler, CT, MRIangio, labs Tx: manage risk factors, angioplasty, meds: antiHTN |
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What is hemolytic uremia syndrome? |
When the RBC are prematurely destroyed and clog the filtering system in the kidneys leading to AKI. Usually occurs following E.coli poisoning. |
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What defines CKD? |
GFR <60ml/min for >3months proteinuria or hematuria, or anatomical abnormalities |
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What is the recommended medical therapy to improve proteinuria? |
ACE or ABR (bc acts on distal tubules) |
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List ways to prevent the progression of CKD? |
DM control, HTN control, reduce proteinuria, dyslipidemia control, smoking cessation |
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How would you investigate generalized edema? |
H&PE, urinalysis, blood tests: albumin, BUN, SCr, lytes, LFT. Further testing: abd US, CT. Want to determine if CHF, cirrhosis, kidney disease, hypoalbunemia |
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What causes the edema in nephrotic syndrome? |
high secretion of protein in the urine =low protein in the blood = low oncotic pressure = fluid is lost to the ECF |
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How do you treat nephrotic syndrome? |
corticosteroids, rare occasions: immunosuppresants. if HTN then ACEi |
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What are the S/S of acute proliferative glomerulonephritis (aka postinfectious GN)? |
hematuria, oliguria, HTN, proteinuria, edema |
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Differentiate between postinfectious GN (aka acute proliferative GN), IgA GN, and Henoch-Schnolen Purpura. |
Similar: IgA complexes clog glomeruli causing hematuria, oliguria, HTN and protienuria. Diff: PIGN: 2-3 weeks post streptococcal infection. IgA GN: at same time as URTI. HSP: has systemic symptoms of purpura, arthritis, abd pain. |
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What is Goodpasture's syndrome? What are the S/S? How is it diagnosed? How do you treat it? |
1. autoimmune disease where the basement membrane of the LUNGs and KIDNEYs are attacked by anti-glomerular basement membrane antibodies (anti-GBM) 2. fatigue, wt loss, night sweats, lung symptoms: hemoptysis, cough, SOB, crackles, resp failure, PE, chest pain. Renal symptoms: hematuria, edema, HTN, uremia. Other: hepatosplenomegaly, anemia, cyanosis 3. DDx confirmed by anti-GBM antiboides, Labs: Iron deficiency anemia, Chest x-ray, renal biopsy (cresent formation on microscopy) 4. plasma exchange, immunosuppressives, corticosteroids |
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What are the 3 main classification of AKI? Give examples of what causes each type |
1. Pre-renal: shock, vomiting, diarrhea, diuretics, CHF, Hypotension, trauma 2. intra-renal: inflammation, toxins, drugs, infection, tubular necrosis, idiopathic 3. post-renal - obstruction: enlarged prostate, kidney stones, tumors, strictures, injury |
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How do you investigate AKI? |
H&PE, CBC with diff, serum Na, K, Cl, HCO, urinalysis, US of kidneys (to determine if pre, intra or post renal AKI) |
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How do you treat AKI? (generally) |
Treat is tailored to diagnosis of pre, intra or post renal AKI. 1. correct volume: if depleted-rehydrated, if overloaded: diurese. correct K+: if hyper: insulin, Calcium gluconate, saline, lasix, dialysis. metabolic acidosis: dialysis, sodium bicarb. catheter: used for obstruction |
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What are the two main causes of renal artery stenosis? Who is most likely to acquire each? |
1. atherosclerosis - older males, smokers 2. fibromuscular dysplasia - young females <30yo |
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How does angiotensin raise BP? |
1. causes generalized arteriole constriction 2. increases Na & H2O retention |
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What are the S/S of renal artery stenosis? |
severe HTN, asymmetric renal size, bruits, hypokalemia, increased SCr, pulmonary edema |
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What is the gold standard for investigating renal artery stenosis? |
renal arteriography |
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What are the causes of SIADH? (list 2 from each of the 5 categories) |
1. pulmonary disorders: acute respiratory failure, infections 2. tumors - pulmonary, mediastinal 3. CNS disorders - stroke, mass lesions 4. Drugs - SSRIs, MAOIs, carbamazapine, tricyclics 5. Misc. - HIV, idiopathic |
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List at least 5 risk factors for renal cell carcinoma |
1. obesity 2. CKD 3. PKD 4. HTN 5. smoking 6. sickle cell 7. toxicity |
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What is the classic triad of symptoms in renal cell carcinoma? |
flank pain, hematuria, abdominal mass |
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How would you investigate a suspected renal cell carcinoma? How is it treated? |
1. US, CT, MRI, labs, urinalysis, biopsy 2. surgery (partial or full nephrectomy), immunotherapy - often resistant to chemo |
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What is renal vein thrombosis? Who is most likely to acquire it? |
occlusion of the renal vein due to thrombi. Most common in children but still very rare |
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What are the symptoms of renal vein thrombosis? How does it differ from renal artery stenosis? |
S/S: flank pain, gross hematuria, nausea, anorexia, edema, scrotal swelling, proteinuria, elevated SCr, tender abdominal mass in infants, signs of dehydration Artery stenosis - more likely to affect older males with risks of athrosclerosis. causes HTN, and pre-renal AKI (possibly) |
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What is the gold standard to investigate renal vein thrombosis? |
renal venography, |
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How do you treat renal vein thrombosis? |
anticoagulation - warfarin/heparin clot buster - tPA pr PCI monitor fluids and lytes treat underlying disease (ie. nephrotic syndrome) |
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What is hemolytic uremia syndrome? |
severe life threatening complication of E.coli poisoning. E. coli toxins cause cell injury and cell death in the kidneys which induces the coagulation cascade. causes obstruction of small renal vessels but destroying RBC |
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What are the classic symptoms of hemolytic uremia syndrome? |
anemia, thrombocytosis (high platelets), renal failure other S/S: bloody diarrhea, lethargy, bruising, swelling, dehydration, oliguria, nausea, vomiting |
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How do you manage hemolytic uremia syndrome? |
supportive (fluids, lytes, analgesics, TPN, antihypertensives) blood transfusions dialysis |
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What is proximal renal tubular acidosis? |
failure of the proximal tubules to reabsorb bicarb from the urine/filtrate |
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How does a patient with proximal renal tubular acidosis present? |
metabolic acidosis - headache, confusion, LOC, lethargy, coma, hyperkalemia, warm flushed skin, nausea, vomiting, Kussmaul breathing |
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What investigations would lead you to believe a patient has proximal renal tubule acidosis? |
metabolic acidosis that is unexplained by other normal anion gap causes (ie. diarrhea, fistula, drugs) urine pH <5.3 hyperkalemia ECG suggestive of hyperkalemia |
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How do you treat proximal renal tubule acidosis? |
sodium bicarb to restore normla pH. restore lytes |
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What causes hyperkalemia? |
metabolic acidosis, DKA, renal failure, ACE inhibitors, IV intake |