1. Alcohol increases the risk for the following cancers: oral, larynx, pharynx, esophagus, liver, and lung. It may increase the risk for gastric, colon, pancreatic, and breast cancer.
I. Alcohol is the most common cause of cirrhosis and esophageal varices.
3. Alcohol is involved in roughly 50% of fatal car accidents, 67% of drownings and homicides, 70—80% of deaths in fires, and 35% of suicides.
4. Always give thiamine before glucose in an alcoholic; if you give them in the reverse order, you may precipitate Wernicke's encephalopathy.
Wernicke's vs. Korsakoff's syndromes. Wernicke's syndrome - ophthalmoplegia, nystagmus, ataxia, and confusion; acute and often reversible; may be fatal. Korsakoff's syndrome = anterograde amnesia and confabulation, chronic and irreversible. Both are due to thiamine deficiency. The most likely cause is damage to the mamillary bodies and thalamic nuclei.
Alcohol withdrawal can be fatal. Treat on an inpatient basis. Use benzodiazepines (chlor-diazepoxide and other long-acting benzodiazepines) or, rarely, liar bit urates. Gradually taper the dose over days.
Withdrawal stages/symptoms. First comes acute withdrawal syndrome, 12-48 hours after last drink. Symptoms include tremors, sweating, hyperreflexia, and seizures (rum fits). Next is alcoholic hallucinosis, which consists of hallucinations (auditory/visual) and illusions without autonomic symptoms. Finally comes delirium tremens, which usually occurs 2-4 days after the last drink and involves hallucinations and illusions plus confusion, poor sleep, and autonomic lability (sweating, increased pulse and temperature), which occasionally is fatal.Treat on an inpatient basis.
Stigmata of chronic liver disease in alcoholics: varices, hemorrhoids, caput medusae, jaundice, ascites, palmar erythema, spider angiomas, gynecomastia, testicular atrophy, encephalopathy, asterixis, prolonged prothrombin time, hyperbilirubinemia, spontaneous bacterial peritonitis, hypoalbuminemia, and anemia.
Conditions commonly caused by alcohol include gastritis, Mallory-Weiss tears, pancreatitis (acute and chronic), peripheral neuropathy (via thiamine deficiency), brain damage, and cardiomyopathy (dilated). It also causes testicular atrophy, fatty change in the liver, hepatitis, cirrhosis, hepatocellular liver cancer, Wernicke/Korsakoff syndrome (via thiamine deficiency), cerebellar degeneration, and rhabdornyolysis (acute and chronic).
Alcohol is a definite teratogen. You should be able to recognize fetal alcohol syndrome: mental retardation, microcephaly, microphthalmia, short palpebral fissures, midfacial hypoplasia, and cardiac defects. No alcohol is good alcohol during pregnancy. An estimated 1 in 3000 births is affected by fetal alcohol syndrome, which is the most common cause of preventable mental retardation.
Incidence. Alcohol abuse is more common in men. Roughly 10-15% of people abuse alcohol. Alcoholism has a heritable component and is especially passed from fathers to sons.
1. Skid-row alcoholics commonly develop aspiration pneumonia with weird bugs such/as Klebsiella species (currant-jelly sputum) and enteric organisms (e.g., anaerobes, Escherichia coli, streptococci, staphylococci).
2. Alcohol may precipitate hypoglycemia (but give thiamine first).
3. Alcoholics develop just about every type (if vitamin and mineral deficiency; especially common are deficiencies of folate, magnesium, and thiamine.
4. Bleeding varices are treated with stabilization (lluids, blood), then upper endoscopy and sclerotherapy with cauterization, banding, or vasopressin.The mortality rate is high, and rebleeding is common, especially early.Try transjugular intrahepatic portosystemic shunt (TIPS) before portacaval shunting procedures (splenorenal is the most physiologic sliunt type).
You must know how to interpret simple blood gases, when given pH, O , , CO? , and bicarbonate. Here are good basic hints:
1. pH tells you whether you are dealing with acidosis or alkalosis.
2. Look at CO}. If it is high, the patient has either respiratory acidosis (pH < 7.4) or is compensating for metabolic alkalosis (pH > 7.4-). If CO, is low, the patient has either respiratory alkalosis (pH > 7.4) or is compensating for metabolic acidosis (pH < 7.4).
3. Look at bicarbonate. If it Is high, the patient: has either metabolic alkalosis (pH > 7.4) or is compensating for respiratory acidosis (pH < 7.4). If bicarbonate is low, the patient either has metabolic acidosis (pH < 7.4) or is compensating for respiratory alkalosis (piI > 7.4).
Clinical correlation: common causes of different primary disturbances
1. Respiratory acidosis: chronic obstructive pulmonary disease, asthma, drugs (opioids, benzodiazepines, barbiturates, alcohol, and other respiratory depressants), chest wail problems (paralysis, pain), sleep apnea
3. Metabolic acidosis: ethanol, diabetic ketoacidosis, uremia, lactic acidosis (sepsis/shock), methanol/ethylene glycol, aspirin/salicylate overdose, diarrhea, carbonic anhydrase inhibitors
4. Metabolic alkalosis: diuretics (except carbonic anhydrase inhibitors), vomiting, volume contraction, antacid abuse/milk-alkali syndrome, hyperaldosteronism
5. Salicylate/aspirin overdose causes two primary disturbances (respiratory alkalosis and metabolic acidosis). Look for coexisting tinnitus and/or hypoglycemia, vomiting, and history of "swallowing several pills." Alkalinizatjon of the urine (with bicarbonate) speeds excretion.
i. In certain patients with chronic lung disease, pH may be alkaline during the day (especially in patients with sleep apnea) because they breathe belter when they are awake or have just recovered from an episode of bronchitis. The metabolic alkalosis that usually compensates for respiratory acidosis is no longer compensatory and becomes the primary disturbance (elevated pH and bicarbonate).
7, Sleep apnea, if severe, may cause right-sided heart failure (cor pulmonale).
Treatment. Do not use bicarbonate to treat low pH unless the pH is < 7.0 and other measures have failed (always try saline first).
Note: Beware the asthmatic whose blood gas goes from alkalotic to normal. The patient is probably about to crash and needs intubation.
Signs and symptoms of hyponatremia are confusion, lethargy, mental status changes, anorexia, seizures, disorientation, cramps, and coma. The first step in determining the cause of true hyponatremia is to look at the volume status:
HYPOVOLEMIC' KUVOI.EMJÇ ' HY'mvptEMIC- '
. Dehydration;' diuretics, diabetic ■■; .. Syndrome of inappropriate secretion' of ■ ■ '.'Cohgt-sf iye héárt failure, nephrotic syndrome,
''tóoácidoaís/éiabéí^ mdjitus,- .•-..-.• antidiuretic hormone psychogenic" 'y".\> ' 'drrJïosis,.lóxsmta, renal failure '.
Addison's -fiypâàWostarQmsm■ 'polydipsia,'.oxytocin use-..1;-.'.
1. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) commonly results from head trauma or surgery, meningitis, small cell cancer of lung, postoperative, or other painful states, pulmonary infections (pneumonia or tuberculosis), opioids, or chlorpropamide. Treatment is water restriction. Occasionally, when refractive to conservative management, SIADH is treated with demeclocycline (a tetracycline that causes renal diabetes insipidus).
2. With Addison's disease and. hypoaldosteronisrn, potassium is elevated.
3. Hypovolemic hyponatremia should be treated with saline, Euvolemic and hypervolemic hyponatremia should be treated with free water restriction and possibly diuretics for hypervolemia.
4. Never correct hyponatremia rapidly, because you may cause brainstem damage (central pontine myelinolysis). Hypertonic saline is used only when the patient has seizures due to hyponatremia and, even then, only briefly and cautiously. Normal saline is « better choice 99 times out of J 00 for board purposes.
5. Correct the sodium when the patient has hyperglycemia (once glucose exceeds 200 mg/dl, sodium decreases by 1.6 mEq/L for each increase of 100 mg/dl in glucose). Hyperlipidemia and severe hyperproteinemia may cause a false (spurious) hyponatremia by their osmotic effect.
5, In a surgical patient, the most common cause of hyponatremia is inappropriate or excessive fluid administration.
1. Oxytocin administration may cause hyponatremia in pregnant women (oxytocin has an ADH like effect).
The signs and symptoms of Hypernatremia and hyponatremia are similar: confusion, mental status changes, hyperreflexia, seizures, and coma. Common causes include, dehydration, inability to drink (paralysis, dementia), diuretics, diabetes insipidus (pituitary or nephrogenic), diarrhea, renal disease, and iatrogenic administration of excessive salt. Sickle cell disease also may cause hypernatremia due to kidney damage that impairs renal concentrating ability. Hypokalemia and. hypercalcemia also cause a similar impairment in renal concentrating ability that may mimic diabetes insipidus (DI). Treatment involves water replacement. Often the patient is so dehydrated that normal saline may be used at first until the patient is hemodynamic cally stable; then switch to one-half normal saline (0.4.5% NaCl). Five-percent dextrose in water should not be used
Pituitary vs. nephrogenic diabetes insipidus. Pituitary DI responds to vasopressin; nephrogenic DI does not. Nephrogenic 1)1 may be caused by medications (lithium, demecJocycline, methoxyflurane, and amphotericin B) and. is treated with a thiazide diuretic (paradoxical effect). Central DI .may be caused by Sbeehan's syndrome (postpartum hemorrhage causes shock and pituitary infarction [apoplexy]); look for inability to breast feed and other endocrine deficiencies.
Hypokalemia causes muscular weakness, including weakness of smooth muscles. The patient may have an ileus and/or hypotension. Muscular weakness may lead to paralysis and ventilatory failure. The most famous (and most tested) effect of hypokalemia, however, is on the heart. EKG findings include loss of T wave, U waves, premature ventricular and. atrial contractions and ventricular and atrial tachyarrhythmias.
Changes in pH may cause changes in. serum potassium (alkalosis causes hypokalemia, acidosis causes hyperkalemia). For this reason, bicarbonate is given to severely hyperkalemic patients. Normalization of deranged pH most likely will correct the potassium derangement automatically (no need to give or restrict potassium).
1. The heart i.s particularly sensitive to hypokalemia when the patient is taking digitalis. Potassium should be watched carefully in all patients taking digitalis, especially if they also take diuretics (a very common occurrence).
2. Do not replace potassium too quickly! The best method of replacement is oral, but if potassium must be given IV, do not exceed 20 rnEq/hr. Monitor the EKG if potassium must be given quickly.
3. If hypomagnesemia is present, it is difficult to correct the hypokalemia unless you also correct the hypomagnesemia.
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