Alcoholism (liver dz treatment)

The human body in its normal state produces about 2 shots of alcohol per day. The use of sugars and naked carbohydrates can be metabolized into alcohol. So many people that never drink alcohol die of liver disease from alcoholism from the sweets they eat. Anaerobic respiration produces alcohol, which uses one ATP molecule to produce two APT molecules, thus fatigue takes place because no energy is being produced and enzymes systems breakdown. When enough enzyme systems are broken down the cells get out of control losing their ability to differentiate, thus cancer is established. Aerobic respiration is called gluconeogenesis produces 38 molecules of ATP and provides building blocks for synthetic reactions, such as formation of fatty acids, this is what normal respiration should consist of. The burning of complex carbohydrates in the proper proportion thus produces the most efficient amount of ATP (physical & mental energy). Dietary deficiencies or genetic make-up also plays a role in the prognosis of this disease.

Reaction:

Steps in the oxidation of ethanol by the liver.

Ethanol->ADH (alcohol dehydrogenase)-> Acetaldehyde->ALDH(acetaldehyde dehydrogenase)->Acetate

NADà NADH NADà NADH

Lab Findings:

Reduced NADH = nicotinamide adenine dinucleotide

Increased NADH/NAD ratio

Hypoglycemia-Depletion of glycogen stores, it inhibits gluconeogensis.

Hyperuricemia-Increases lactate produced from pyruvate in the presence of NADH/NAD ratio, lactic acid concentrates, which inhibits Uric Acid excretion.

Hyperlipidemia-Triglycerides increase, due to inhibition effect of lipoprotein lipase by alcohol.

Thrombocytopenia-Alcohol effects the bone marrow, which decreases folic acid, vitamin B-12, causing anemia and leukopenia.

Hypomagnesemia-Decreases intracellular cations (+) Mg, Zn, Cr, causing mal-absorption with increased urine excretion, which causes irritability, tremor, and seizures.

SGOT is higher than SGPT with decreased prothrombin concentration. Elevated AKP, increased bilirubin, increased globulins, decreased albumin’s, positive SLE test, and Vit-K resistant prothrombin time.

Symptoms:

Anorexia-weight loss

Fatigue

Jaundice

Nausea

Tender hepatomegaly

Ascites

Azotemia

Impotence or irregular menstrual periods

Gastrointestinal bleeding

Hypokalemic alkalosis

Portal Hypertension

Encephalopathy

Hyperreflexia

Spider angiomas

Gynecomastia

Palmer & facial redness

Abdominal discomfort

Hematemesis

Causes of Hyperphosphatemia:

Acidosis-seen in advanced renal insufficiency-common symptom hyperventilation to increase alveolar carbon dioxide tension, which raises the pH of the blood.

Hemolysis of red blood cells-tissue destruction

Acromegly

Renal Failure

Hypoparathyroidism

Increased phosphate intake

Vit-D poisoning

Familial tumoral calcinosis

Magnesium deficiency

Chronic Aggressive Hepatitis-Affects females more than males from the 11 to 40 years of age.

Symptoms:

Fatigue

Jaundice

Abdominal pain

Puritius

Amenorrhea

Polyarthralgia

Diarrhea

Skin lesion such as acne

Hepatomegaly

Persistent infection

Spider angiomas

Gynecomastia