Alcohol Use and Withdrawal  Severity of alcohol use disorder (based on >12 signs, symptoms and lab findings associated with alcohol use disorder): Definition of severity
Ref: Uptodate     Electrolyte Changes in the Alcohol Use Disorder Lab Changes Can be attributed to the following Physiological Changes 14 % : EtOH dependence 25 % of admission related to EtOH use Telltale signs of chronic alcohol ingestion are precipi-
tous decreases in plasma concentrations of phosphate, magnesium, potassium, and
calcium in the first 24 to 36 hours after admission Endocrine Impact / Neurohormonal Impact 1) Decreased Insulin / Glucagon Ratio 2) Decreased PTH level 3) Decreased GI absorption of Vitamin D 4) Increase Cortisol, GH 5) Increased ADH 6) Increased sympathetic nerve tone - due to intravascular volume depletion Changes in nutrition / metabolic pathway 1) Increase NADH /NAD ratio - - Increase in B-hydroxybutyate : metabolism of alcohol to
acetaldehyde and acetate, results in an increased ratio of reduced NADH to oxidized nicotinamide adenine dinucleotide (NAD), which
leads to preferential formation of β-hydroxybutyric
acid. The consequent increase in the level of
β-hydroxybutyrate is important to recognize,
since the use of strips or tablets that use a nitroprusside reaction, which is only sensitive to
acetoacetate, to detect the presence of ketones
may cause the clinician to mistakenly attribute
an anion-gap acidosis to some other cause. Direct
measurement of β-hydroxybutyrate levels should
be performed when alcohol abuse is suspected. - The increased ratio of NADH to NAD also favors
conversion of pyruvate to lactate, which accounts
for increased production of hepatic lactate. Peripheral tissues can oxidize lactic acid, so the degree of lactic acidosis is mild. - An increased ratio of NADH to NAD leads to
an inhibitory effect on hepatic gluconeogenesis
that predisposes patients to hypoglycemia, which
occurs in approximately one quarter of patients
with alcoholic ketoacidosis 2) Thiamine deficiency 3) Folate deficiency Associated ongoing pathological condition 1) Diarrhea 2) Vomiting 3) Increase Ethanol Level 4) Increased Ventilation 5) Decreased absorption 6) Increase Calcium carbonate use due to increase OTC med use 7) Decrease Solute Intake Impact on Kidneys 1) EtOH induced tubular dysfunction in Kidney - The described
tubular abnormalities may be related to dysfunction of apically located transporters and to decreased activity of the sodium–potassium ATPase,
both of which are related to structural changes
in the phospholipid bilayer of the cell membrane.
2) Mg loss 3) HCO3- loss 4) K loss 5) Ca loss Electrolytes and PH Changes 1) Low Na 2) Low K 3) Low Mg 3) PO43- loss - Due to : decrease intake (of PO43- rich food, antacid use, vomiting, diarrhea); increased loss (generalized tubular dysfunction, metabolic acidosis related mobilization from bone and pH direct affect in Proximal Tubule; increase PTH, Magnesium deficiency causing direct phosphateuria and functional hypoparathyroidism causing more PO4 reabsorption from bone) Drop in level after admission or Unmasking is due to : Transcellular shift (with normalization of pH, Increase glycolysis and need of PO43-, such shift exacerbated by Insulin release after glucose administration, respiratory alkalosis, increased catecholamine levels) Clinical Impact: Muscle Weakness, Rhabdomyolysis, Lactic acidosis, Tissue Ischmia (due to affect on RBC) 4) Decreased Ca++ 4) Acidosis (both AG and NAG) : Increase acid - Lactic acid, Ketoacid, small contribution of acetic acid, Bicarbonate loss Lactic acidosis : -Intracellular
deficiency of phosphate impairs generation of
adenosine triphosphate (ATP) from adenosine
diphosphate (ADP). Decreased cellular ATP stimulates phosphofructokinase activity, enhancing
glycolysis and lactate production. - The increased ratio of NADH to NAD also favors conversion of pyruvate to lactate, which accounts for increased production of hepatic lactate. Peripheral tissues can oxidize lactic acid, so the degree of lactic acidosis is mild.
5) Alkalosis (both metabolic and respiratory): Loss of HCL during vomitting; Increased Breathing     Supplement to: Palmer BF, Clegg DJ. Electrolyte disturbances in patients with chronic alcohol-use disorder. N Engl J Med 2017;377:1368-77. Benzodiazepine Withdrawal Opiates Abuse / Withdrawal
Sedative Drugs: Hypnotic Drugs: Nicotine Addition: IN GIM Section |
