2012-01-medicine-cardinal manifestation of renal disease
TRANSCRIPT
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)
GFR = 186 x Serum Creatinine -1.154
x Age-0-203
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
Accounts 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
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
SY 2
011-2
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o 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 administration of many common medications, usually by inducing a combination
of intrarenal vasoconstriction, direct tubule toxicity, and/or tubule obstruction
Remember 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
o 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
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
Remember 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 administration 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
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-K-
ATPase pump.
Hence, 85-90% of all Na is extracellular.
Na loss = Na gain
Na excess edematous state
Na deficit hypovolemic state
Hypovolemia
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
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
hour for the 1st
3-4 hrs until seizures subside.
Plasma Na conc should be raised no more than 12
mmol/L during the 1st
24 hours
Osmotic Demyelination Syndrome (ODS)
Caused by correcting hyponatremia rapidly
Neurologic disorder characterized by flaccid
paralysis, dysarthria and dysphagia
No specific treatment
Assoc. w/ increase morbidity and mortality
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
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 administration
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
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
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
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
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
required over 1st
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
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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
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 administration 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.
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 supportive 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
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METABOLIC ALKALOSIS
Often accompanied by hypochloremia and
hypokalemia
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.
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
Respiratory Alkalosis
Treatment
Directed toward alleviation of underlying disorder
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!!
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