2012-01-medicine-cardinal Manifestation Of Renal Disease 6e1y3j

SY 2011-2012

Subject: Medicine Topic: Cardinal Manifestation of Renal Disease Lecturer: Dr. M. Bernardo Date of Lecture: 01/28/2012 Transcriptionist: kekie  and dj anne Pages: 14

Azotemia and urinary abnormalities Assessment of GFR (Glomerular Filtration Rate) • Primary metric for kidney function • Serum creatinine– used as surrogate to estimate GFR; most widely used for drug dosing and grading of chronic kidney disease • Low GFR leads to azotemia (retention of Creatinine, BUN, and nitrogenous wastes increase serum BUN and Creatinine) • Uremia (azotemia with signs and symptoms) will develop at significantly different levels of creatinine • Signs and symptoms: n/v, change in sensorium • Related directly to urine creatinine excretion and inversely to serum creatinine (Creatinine Clearance) Estimation of Glomerular Filtration Rate Cockcroft-Gault: Creatinine clearance (mL/min) = (140-age) x lean body weight (kg) Plasma creatinine (mg/dL) x 72 ** Multiplied 0.85 for women MDRD: (modification of diet in renal disease) -1.154 -0-203 GFR = 186 x Serum Creatinine x Age x [1.210 if Black] x [0.742 if Female] Other ways of determining GFR:  Direct GFR o Inulin clearance o Iothalamate- available in La Salle; used in renal GFR scan  EDTA  Cystatin C- member of cysteine protease inhibitors and is produced at a relatively constant rate from all nucleated cells.; more sensitive marker of early GFR decline than plasma creatinine Chronic renal failure  Define as increase creatinine for more than 3 months  Small kidneys + normal urinalysis + increase creatinine  3 major causes: o Diabetic nephropathy o Amyloidosis o HIV nephropathy Acute Renal Failure • Categories o Pre-renal  Before renal  Any condition that can cause hypoperfusion of kidney leading to azotemia  s for 40-80% of ARF and readily reversible if treated early  Causes: • Decreased circulating blood volume (GI hemorrhage, burns, diarrhea, diuretics) • volume sequestration(pancreatitis, peritonitis, rhabdomyolysis) • decreased effective arterial volume (hypotension, cardiogenic shock, sepsis) • Peripheral vasodilation ( sepsis, drugs) • Profound renal vasoconstriction (severe heart failure, hepatorenal syndrome, NSAIDs[prostaglandin production blockade], ACE-Is, and ARBs[decreased efferent arteriolar tone decreased glomerular capillary perfusion]) • Renal stenosis

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Intrinsic  Causes • Acute Tubular Necrosis o Ischemic  Common in patients that have undergone major surgery, trauma, severe hypovolemia, overwhelming sepsis, or extensive burns o Nephrotoxic  Complicates the istration of many common medications, usually by inducing a combination of intrarenal vasoconstriction, direct tubule toxicity, and/or tubule obstruction  that kidneys have a rich blood supply (25% of CO) and one of its function is to concentrate, and metabolize toxin, henceforth making it susceptible to toxins. • Interstitial nephritis  Drug-induced interstitial nephritis (antibiotics, NSAIDs, diuretics, Chinese medication chronic use)  Severe infections (bacterial and viral)  Systemic infections (SLE)  Infiltrative disorders (sarcoid, lymphoma, leukemia)  Allergic interstitial nephritis (eosinophils in urine)  Urinalysis: mild to moderate proteinuria, hematuria, and pyuria; occasionally WBC casts • Renovascular obstruction • Glomerulonephritis or vasculitis Post-renal- obstructive  Reversible, <5% of ARF  Ureteral and renal pelvic dilatation on ultrasound  Causes • Urethra or bladder outlet obstruction • Bilateral or unilateral ureteral obstruction

Table on the left compares the laboratory findings in acute renal failure, prerenal vs oliguric acute renal failure (intrinsic). In prerenal azotemia, urine sodium is less than 20 and the fractional excretion of Na is <1%, which indicates that it is still able to conserve sodium and its reabsorption is still intact, respectively. Intrinsic azotemia on the other hand, has sodium wasting leading to increased UNa [>40] and FENa [>2%].

Picture on the left showing hydronephrosis. Notice how the ureter, renal pelvic are dilated on the rt side.

In patient with azotemia, presence of hydronephrosis (dilation of renal tract.) is determined by renal ultrasound. If present, this is likely to be caused by post-renal azotemia- obstruction; and patient is managed by urologic evaluation and relieving such obstruction. If hydronephrosis is absent, urinalysis is done along with the determination of the size of renal parenchyma to differentiate chronic renal failure from acute renal failure. Small kidneys, thin cortex, bland sediment (unremarkable microscopic determination), isosthenuria and <3.5g/24 hours protein is indicative of chronic renal failure. A normal size kidney and intact parenchyma on the other hand is indicative of acute renal failure (as discussed above can be divided into pre-renal, intrinsic, and post-renal). Normal kidney with abnormal urinalysis may indicate acute tubular necrosis, glomerulonephritis, renal vessel occlusion, interstitial nephritis, and pyelonephritis depending on the abnormal sediments seen. Urine electrolytes and osmolality must be tested if kidney and urinalysis are both normal. If urine osmolality is >500 mosmol and fractional sodium excretion is <1%, its indicative of prerenal azotemia. FeNa>1% and U osmo <350mosmol with normal or abnormal urinalysis (muddy brown cast) is indicative of acute tubular necrosis. ABNORMAL URINALYSIS: Note that if >100,000 of bacteria is present in the urine, it may be indicative of pyelonephritis. WBC cast is indicative of Interstitial nephritis. Presence of RBC can indicate Artery or venous occlusion and can be confirmed by angiogram. RBC cast with proteinuria may indicate Glomerulonephritis and can be confirmed by renal biopsy.

Proteinuria • Dipstick determination • Normal <150 mg/day of total protein and <30 mg/day of albumin • Positive dipstick on urinalysis detect predominantly albumin; cannot detect urine albumin levels < 300 mg/d indication: can only detect macroalbuminuria • Microalbuminuria: o 30-300 mg/d or 30-300 mg/g o Please see the diseases to be considered on the algorithm below • Macroalbuminuria with RBC casts or RBCs on urinalysis: o 300-3500 mg/day or 300-3500 mg/g o Please see the diseases to be considered on the algorithm below • Macroalbuminuria (Heavy proteinuria): o > 3500 mg/d or 3500 mg/g Nephrotic syndrome (recall:s/s heavy proteinuria + dyslipidemia + edema) o Please see the diseases to be considered on the algorithm below • Urine protein electrophoresis can classify pattern of proteinuria (as glomerular, tubular, abnormal proteins) o Glomerular proteinuria (can be selective or nonselective) – due to abnormal glomerular permeability o Tubular proteins (TH, B2-macroglobulin) are produced by the renal tubule and shed into the urine caused by tubular injury, HPN, and CRF. o Abnormal circulating proteins (light chains and Bence Jones protein) are readily filtered because of their small size can be cause by blood cell dyscrasias such as Multiple Myeloma

Hematuria  Normal RBC excretion – 2 million RBC/day  Hematuria – 2-5 RBC/hpf  Common causes: o Stones o Neoplasms o Tuberculosis o Trauma o Prostatitis  Gross hematuria w/ blood clots - post renal source

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Single urinalysis with hematuria is common. o Menstruation  Always r/o in women o Viral illness o Allergy o Exercise o Mild trauma Persistent hematuria o >3RBC/hpf on 3 urinalysis or single urinalysis with >100 RBCs, or gross hematuria o Considerations:  Chronic anticoagulation  Urogenital neoplasms  Infection  Hypercalciuria, hyperuricosuria

Hematuria without proteinuria and dysmorphic RBCs or RBC casts but with pyuria and WBC casts is indicative of UTI and confirmed by urine culture. Hematuria with proteinuria and dysmorphic RBCs and RBC casts indicates glomerulonephritis and can be further evaluated with serologi, hematologic examinations and renal biopsy. Hematuria + (-) proteinuria + (-) pyuria:  (+) IVP +/- renal ultrasound  stones, renal cysts  (+) cystoscopy  bladder neoplasm needing biopsy and evaluation  (+) renal CT scan  renal neoplasm, renal cell CA All negative, follow-up periodic urinalysis PYURIA AND CASTS  Isolated pyuria is unusual since inflammatory reactions in the kidney are also associated with hematuria.  Waxy Casts - degenerated cellular cast  Broad Casts - dilated tubule of enlarged nephrons

ABNORMALITIES OF URINE VOLUME Oliguria and Anuria  Oliguria - urine output of <500 ml/24hr  Anuria –urine output of < 50 ml/24 hr o Causes  Total urinary tract obstruction (note that obstruction to just one kidney will not cause anuria since one kidney is enough to maintain kidney function)  Total renal artery or vein occlusion  Shock  Cortical necrosis, ATN and RPGN  Nonoliguria: >500 ml/day in patients with acute or chronic azotemia

Polyuria  polyuria is INCREASED in VOLUME and not increased in frequency  Should be differentiated from urinary frequency – small volumes  24 hour urine collection, urine output is >3L/day  Mechanisms: o Excretion of nonabsorbable solutes o Excretion of water (defect in ADH production or renal responsiveness)  Urine osmolality o solute diuresis (excretion of nonabsorbable solutes), high urine osmolality o water diuresis (excretion of water), low urine osmolality

Check urine osmolality  If patient is excreting a urine high in osmolality, it means that the polyuria is caused by solute diuresis. There are solutes in the renal tubules that causes the water to stay in the renal tubules and move out of the body as urine.  If the patient is excreting a dilute urine, then the polyuria is from water diuresis.  Water deprivation test will distinguish between primary polydipsia versus diabetes insipidus.  If you decrease the water intake of a patient and the results is correction of polyuria, then the cause of polyuria is a primary polydipsia. Drugs and hypothalamic disease all cause increase in water intake by changes in the brain. Primary polydipsia may also be caused by psychogenic processes.  Diabetes insipidus is divided into 2 types: central and nephrogenic.  To differentiate between the 2 causes of DI, ADH level is needed.  Low ADH level means px is experiencing Central DI, and the polyuria will correct with istration of exogenous vasopressin.  Normal to high ADH points to a nephrogenic DI. Even with exogenous vasopressin, polyuria from vasopressin will not resolve since nephrogenic DI is caused by insensitivity of the renal tubules to vasopressin.

FLUID AND ELECTROLYTE DISTURBANCE Sodium and Water Composition of Body Fluids  Water - most abundant constituent of the body.  50% of body weight in women, 60% in men  Osmolality - solute or particle concentration of a fluid +  Major ECF particles are Na and its accompanying anions Cl and HCO3 +  Major ICF osmoles: K and organic phophate esters (ATP, creatine phosphate, and phospholipids)  Ineffective osmoles - do not contribute to water shift  eg. Urea, glucose

Hypovolemia

Water Balance  Normal plasma osmolality is 275-290 mosmol/kg  Water intake = water excretion  Disorders in water homeostasis: o Hyponatremia o Hypernatremia Water Intake  THIRST – primary stimulus for water ingestion  Ineffective osmoles do not play a role in stimulating thirst.  Average osmotic threshold for thirst is approx. 295 mosmol/kg Water Excretion  Arginine vasopressin (AVP) – principal determinant of renal water excretion  HYPERTONICITY - major stimulus for AVP secretion  Major ECF solutes are Na salts, effective osmolality is primarily determined by plasma Na concentration.  Inc Na  inc AVP secretion  Nonosmotic factors that affect AVP secretion: ◦ Effective circulating (arterial) volume ◦ Nausea ◦ Pain ◦ Stress ◦ Hypoglycemia ◦ PregnancyDrugs (e.g. morphine) Sodium Balance  Sodium is actively pumped out of cells by Na-KATPase pump.  Hence, 85-90% of all Na is extracellular.  Na loss = Na gain  Na excess  edematous state  Na deficit  hypovolemic state

Clinical Features  Nonspecific and secondary to electrolyte imbalances and tissue hypoperfusion o Fatigue, weakness, muscle cramps, thirst, postural dizziness  More severe degrees of hypovolemia  End-organ ischemia o manifest as oliguria, cyanosis, abdominal and chest pain, confusion or obtundation Treatment  Mild – oral route  More severe – requires IV therapy with isotonic or normal saline  Hypernatremia – greater deficit of water than Na o Tx: hypotonic solution such as half-normal saline or D5W  Pxs w/ sig. hemorrhage, anemia or intravascular volume depletion: BT or colloid-containing solutions (albumin, dextran) HYPONATREMIA • Plasma Na conc of < 135 mmol/L • Not a disease but a manifestation Clinical Features  Related to osmotic water shift leading to increased ICF volume  Sxs primarily neurologic o Brain cell swelling or cerebral edema  Severity is dependent on rapidity of onset and absolute decrease in plasma Na conc.  Asx, or complain of nausea and malaise  As plasma Na conc falls, sxs progress o Headache, lethargy, confusion, and obtundation  Plasma Na conc falls acutely below 120 mmol/L or decreases rapidly o Stupor, seizures, and coma

HYPERNATREMIA  Plasma Na conc of > 145 mmol/L  Majority due to loss of water Clinical Features  Hypertonicity  water shifts out of cells leading to contracted ICF volume  Decreased brain cell volume is assoc with increased risk of subarachnoid or intracerebral hemorrhage.

Treatment of Hyponatremia  Mild asymptomatic hyponatremia requires no treatment.  Asx hyponat + volume contraction  isotonic saline  Hyponat due to edematous states  restriction of Na and water intake  Rate of correction of hyponat depends on absence or presence of neurologic dysfunction. No neurologic dysfunction  Plasma Na conc should be raised by no more than 0.5-1.0 mmol/L per hr and by < 10-12 mmol/L over the first 24h Severe symptomatic hyponat  Treated with hypertonic saline  Plasma Na conc should be raised by 1-2 mmol/L per st hour for the 1 3-4 hrs until seizures subside.  Plasma Na conc should be raised no more than 12 st mmol/L during the 1 24 hours Osmotic Demyelination Syndrome (ODS)  Caused by correcting hyponatremia rapidly  Neurologic disorder characterized by paralysis, dysarthria and dysphagia  No specific treatment  Assoc. w/ increase morbidity and mortality

flaccid

Treatment  Goal: 1. Stop ongoing water loss (treat underlying cause) 2. Correct water deficit Water deficit = Plasma Na conc – 140 x TBW 140 Treatment  GIT – safest route of water istration  IV – using D5W or hypotonic saline  CDI – desmopressin  Sxic polyuria due to NDI – low-Na diet and thiazide diuretics

POTASSIUM HYPOKALEMIA  Plasma K conc of < 3.5 mmol/L Etiology  Redistribution into cells – metabolic alkalosis and insulin  Nonrenal loss of K o Excessive sweating, diarrhea o Renal loss of K o Primary hyperaldosteronism, Liddle’s syndrome, Bartter’s syndrome, RTA Clinical Features  Fatigue, myalgia and muscular weakness of the lower extremities are common complaints. o Due to a lower (more negative) resting membrane potential  More severe hypokalemia: progressive weakness, hypoventilation (due to respiratory muscle involvement), and eventually complete paralysis.  Sxs seldom occur unless plasma K conc is < 3 mmol/L Diagnosis  Pseudohypokalemia o Marked leukocytosis (e.g. AML)  low measured plasma K due to WBC uptake of K at room temp o Avoided by storing blood sample on ice or rapidly separating plasma (or serum) from the cells.

TTKG – ratio of the K conc in the lumen of the CCD to that in peritubular capillaries or plasma K Hypokalemia with TTKG greater than 4 suggests renal K loss due to increased distal K secretion.

Treatment  A decrement of 1 mmol/L in plasma conc (4.0 to 3.0 mmol/L)  deficit of 200-400 mmol  Plasma K < 3.0 mmol/L – deficit of < 600 mmol  KCl - – preparation of choice o Promote more rapid correction of hypokalemia and metabolic acidosis  KHCO3 and citrate (metabolized to HCO3) tend to alkalinize px o More appropriate for hypokalemia assoc with chronic diarrhea or RTA  Max conc o Peripheral vein not more than 40 mmol/L o Central vein not more than 60 mmol/L  Rate of infusion should not exceed 20 mmol/L HYPERKALEMIA  Plasma K conc > 5.0 mmol/L Etiology  Increased K intake is rarely the sole cause of hyperK  K adaptation ensures rapid K excretion in response to increases in dietary consumption.  Pseudohyperkalemia o K movement out of cells immediately prior to or following venipuncture o Contributing factors: prolonged use of torniquet w/ or w/o repeated fist clenching, hemolysis, marked leukocytosis or thrombocytosis o Leukocytosis and thrombocytosis  increases K conc due to release of intracellular K following clot formation Clinical Features  Resting membrane potential is related to ratio of ICF to ECF K conc. o hyperK – partially depolarized cell membrane  Prolonged depolarization impairs membrane excitability, manifest as weakness o May progress to flaccid paralysis and hypoventilation  Caridac toxicity – most serious effect o Does not correlate well with plasma K conc

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Dialysis

HYPERCALCEMIA AND HYPOCALCEMIA

Decrease in ECF calcium triggers increase in PTH secretion PTH results in increased tubular reabsorption of calcium by the kidney, resorption of calcium from bone; stimulates renal 1,25 hydroxyvitamin D3 production  increase intestinal calcium absorption

Treatment  Approach depends on the ff: ◦ Degree of hyperkalemia (as determined by plasma K conc) ◦ Assoc muscular weakness ◦ Changes on the ECG  Potential fatal hyperK rarely occurs unless plasma K exceeds 7.5 mmol/L  Severe hyperK – emergent tx directed at ◦ Minimizing membrane depolarization ◦ Shifting K into cells ◦ Promoting K loss  Calcium gluconate – decreases membrane excitability; has no effect in decreasing K concentration  K shift: o Insulin – causes K to shift into cells o Alkali tx w/ IV Na HCO3 – shift K into cells o B2-adrenergic agonists – cellular uptake of K 

Removal  Diuretics (loops and thiazides) – renal K excretion  Cation-exchange resin (Na poysterene sulfonate) – promotes exchange of Na for K in the GIT

HYPERCALCEMIA

Clinical Manifestations  Mild hyperCa (up to 11-11.5 mg/dL) – asx  Neuropsch sxs – trouble concentrating, personality changes, or depression  Other presenting sxs – PUD, nephrolith, increased fracture risk Diagnostic Approach  First step in diagnostic evaluation of hyper- or hypocalcemia is ensure that the alteration in serum Ca levels is not due to abnormal albumin conc  About 50% of total calcium is ionized and the rest is bound principally to albumin.  Every 1 g/dL below 4.1 g/dL albumin, add 0.2 mM (0.8 mg/dL) to total Ca. vice versa for hyperalb  Primary hyperparathyroidism – most common cause of chronic hyperCa

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Malignancy is second most common cause of chronic hyperCa. Second step – PTH E.g., elevated Ca and low phosphorus (as in primary hyperparathyroidism) what is expected PTH?  low, but if you have inc PTH or inapprop N PTH then think of primary hyperparathyroidism Dec PTH in the face of hypercalcemia – consistent with non-parathyroid mediated hypercalcemia, most often due to underlying malignancy

Treatment • Mild asx hyperCa – no immediate tx, mgt should be dictated by underlying diagnosis • Symptomatic hypercalcemia o Volume expansion – since hyperCa invariably leads to dehydration; 4-6 L of IV saline may be st required over 1 24 hours o Drugs that inhibit bone resorption – if there is increased calcium mobilization from bone (malignancy, severe hyperparathyroidism) o zolendronic acid, pamidronate, etidronate o Glucocorticoids – preferred therapy for patients with 1,25(OH)2D-mediated hypercalcemia o Decrease 1,25(OH)2D production o IV hydrocortisone, oral prednisone HYPOCALCEMIA  Suppressed (or “inappropriately low”) PTH level in the setting of hypocalcemia establishes absent or reduced PTH secretion (hypoparathyroidism) as the cause of hypocalcemia.  Elevated PTH level (secondary hyperparathyroidism) should direct attention to the vitamin D axis as the cause of hypocalcemia  Causes of hypocalcemia can be divided into 2, either a hypoparathyroidism or secondary hyperparathyroidism.  Hypoparathyroidism – even if low Ca, body cannot increase PTH  2 hyperpara – persistently inc PTH causing Ca to remain low

Clinical Manifestations  Asx if decreases in serum Ca are relatively mild and chronic  Mod to severe hypoCa assoc with paresthesias (fingers, toes and circumoral regions); caused by increased neuromuscular irritability  Chvostek’s sign – twitching of the circumoral muscles in response to gentle tapping of the facial nerve just anterior to the ear  Trousseau’s sign – induced by inflation of BP cuff to 20mmHg above the px’s systolic BP for 3 minutes causing carpal spasm  Severe hypocalcemia can induce seizures, carpopedal spasm, bronchospasm, laryngospasm, and prolongation of QT interval Treatment  Acute sxic hypocalcemia – IV calcium gluconate  Continuing hypocalcemia often require constant IV infusion of calcium gluconate  Chronic hypocalcemia due to hypopara is treated with oral calcium supplements and either vitamin D2 or D3 or calcitriol [1,25(OH)2D].  Vitamin D deficiency is best treated with vitamin D supplementation. ACIDOSIS AND ALKALOSIS Normal Acid-Base Homeostasis  Normal arterial pH 7.35-7.45  Henderson-Hasselbach equation

pH = 6.1 + log _ HCO3_ ___ PaCO2 x 0.301 Metabolic acidosis – decrease HCO3, pH will decrease Respiratory acidosis – increase PaCO2, pH will decrease Metabolic alkalosis – increase HCO3, pH will increase Respiratory alkalosis – decrease PaCO2, pH will increase Normal Acid-Base Homeostasis  Metabolic acidosis/alkalosis – compensation is regulation of PaCO2 (respiratory)  Respiratory acidosis/alkalosis – compensation is regulation of HCO3 (metabolic)

METABOLIC ACIDOSIS  High anion gap acidosis  Hyperchloremic non-gap acidosis  ANION GAP (Plasma) o Unmeasured anions in the plasma o N 10-12 mmol/L AG = Na – (Cl + HCO3) High-anion-gap acidoses Lactic Acidosis  2 types: o Type A – secondary to poor tissue perfusion o Type B – aerobic disorders  Tx: Correct underlying condition that disrupts lactate metabolism o Type A – circulatory insufficiency (shock, cardiac failure), severe anemia, mitochondrial enzyme defects, and inhibitors (carbon monoxide, cyanide) o Type B – malignancies, nucleoside analogue reverse transcriptase inhibitors in HIV, DM, renal or hepatic failure, thiamine deficiency, severe infections (cholera, malaria), seizures, or drug toxins (biguanides, ethanol, methanol, propylene glycol, isoniazid, and fructose)

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Diabetic Ketoacidosis  Cause: increased fatty acid metabolism and accumulation of ketoacids  Occurs in insulin-dependent DM in association with cessation of insulin or intercurrent illness  Intercurrent illness – infection, gastroenteritis, pancreatitis, or MI, increases insulin requirements temporarily and acutely  Volume expansion with isotonic saline if patient is dehydrated.  Mainstay of tx is IV regular insulin. Alcoholic Ketoacidosis  Chronic alcoholics  abrupt cessation of alcohol consumption with poor nutrition  Assoc. with binge drinking, vomiting, abdominal pain, starvation, and volume depletion  Mixed acid-base disorders are common: hypoperfusion may enhance lactic acid production  Chronic respiratory alkalosis accompany liver disease  Metabolic alkalosis can result from vomiting.  Treatment: correction of extracellular fluid deficits with IV saline and glucose  Correction of hypophosphatemia, hypokalemia and hypomagnesemia

Isopropyl Alcohol Toxicity  Ingested isopropanol is absorbed rapidly and may be FATAL when as little as 150 mL is consumed.  Rubbing alcohol, solvent, or de-icer  Treatment: watchful waiting and ive therapy  Vasopressors if patient is hypotensive, mechanical ventilation Renal Failure  Reduced rate of NH4 production and excretion, primarily die to decreased renal mass.  Renal failure require oral alkali replacement to maintain HCO3 between 20 and 24 mmol/L. Hyperchloremic (nongap) metabolic acidosis

Drug- and Toxin-induced Acidosis  Salicylates  Ethylene glycol  Methanol  Isopropyl alcohol Salicylate-induced Acidosis  Respiratory alkalosis  Mixture of high-AG metabolic acidosis and respiratory alkalosis  Treatment: vigorous gastric lavage with isotonic saline immediately followed by istration of activated charcoal per NG tube  In acidotic patient, IV NaHCO3 is given to alkalinize urine (urine pH > 7.5)  In presence of renal failure, hemodialysis can be performed. Ethylene glycol-induced Acidosis  Commonly used in antifreeze  Ingestion leads to metabolic acidosis and severe damage to the CNS, lungs, heart, and kidneys  Diagnosis is facilitated by recognizing oxalate crystals in the urine, the presence of an osmolar gap in serum, and a high-AG acidosis.  Treatment includes institution of saline or osmotic diuresis, thiamine and pyridoxine supplements, fomepizole or ethanol, and hemodialysis. Methanol-induced Acidosis  Wood alcohol  Treatment is similar to ethylene glycol intoxication.

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METABOLIC ALKALOSIS  Often accompanied hypokalemia

Respiratory Alkalosis by

hypochloremia

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Treatment  Directed toward alleviation of underlying disorder

Treatment   

Primarily directed at correcting the underlying stimulus for HCO3 generation. Remove the factors that sustain the inappropriate in HCO3 reabsorption NaCl therapy -is usually sufficient to reverse the alkalosis if ECFV contraction is present, as indicated by low urine Cl.

End of Transcription Sorry di ko na carry hanggang abnormalities of urine volume lang ung napakinggan ko kasi kailangan ko ng mag-aral at ang toxic ni doc..nagjump sya ng bongga. Anyways, most naman e nasa ppt nya..but if u need to clarify anything, nasa Harrison’s Chapter 44 to 46. God bless!!

Respiratory acidosis

Treatment  Depends on its severity and rate of onset  Acutundere resp acidosis can be life-threatening  Measures to reverse the underlying cause should be undertaken  Simultaneously with restoration of adequate alveolar ventilation

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