Exam 3 Chapter 14 Flashcards
alcohol used to relieve everyday stress
phase 1: prealcoholic
begins with blackouts; alcohol is now required by person
phase 2: early alcoholic
person has lost control over alcohol use. physiological dependence is clearly evident
phase 3: Crucial
person is intoxicated more than they are sober
phase 4: chronic
peripheral nerve damage, pain, burning, tingling, prickly sensation of extremities
due to thiamine deficiency
-inadequate intake
-malabsorption
alcoholic peripheral neuropathy
sudden oset of muscle pain, swelling, and weakness, reddish tinge to urine, rapid rise in muscle enzymes (LDH, CPK, AST)
acute alcoholic myopathy
gradual muscle wasting and weakness of skeletal muscles
chronic alcoholic myopathy
Most serious form of thiamine deficiency
characterized by paralysis of ocular muscles, diplopia, ataxia, somnolence, and stupor
Wernicke’s encephalopathy
Syndrome of confusion, loss of recent memory, and confabulation in alcoholic pts
Korsakoff’s pyschosis
effect of alcohol on heart is an accumulation of lipids in myocardial cells, resulting in enlargement and weakened condition
Alcoholic cardiomyopathy
inflammation and pain in esophagus occurs bc of toxic effects on esophageal mucosa and also bc of frequent vomiting assoc with alcohol use
Esophagitis (esophageal varices)
inflammation of stomach lining characterized by epigastric distress, n/v, distension
gastritis
decreased exercise tolerance, tachycardia, dyspnea, edema, palpitations, nonproductive cough increased CPK, AST, ALT, LDH
Treatment is TOTAL ABSTINENCE from alcohol
alcoholic cardiomyopathy: looks like CHF or arrhythmia
usually occurs 1-2 days after binge of excessive consumption, constant, severe epigastric pain, n/v and abdominal distension
pancreatitis
leads to pancreatic insuffiency resulting in steatorrhea, malnutrition, wt loss, and DM
chronic pancreatitis
enlarged, tender liver, n/v, lethargy, anorexia, high WBC, fever, jaundice, ascites and weight loss
alcoholic hepatitis
widespread destruction of liver cells which are replaced by fibrous tissue; portal hypertension, ascites, esophageal varices, hepatic encephalopathy due to high ammonia levels
cirrhosis of liver
impaired mental fxn, apathy, euphoria/depression, sleep disturbances, increased confusion, coma or death possible
Tx: abstinence from alcohol, no protein, neomycin or lactulose
hepatic encephalopathy
Hematologic effects of alcohol
leukopenia and thrombocytopenia
abnormal facial features, small head size, shorter than ave weight, diff paying attention, poor memory, diff in school, learning diffs, speech and lang delays, poor reasoning skills, intellectual disability, sleep and sucking probs as baby, vision or hearing probs, heart, kidneys, and bone probs
FAS
BAC of 100-200mg/dL
intoxication occurs and withdrawal occurs within 4-12 hours of cessation or reduction of heavy use
barbs, non-barbs, anti anxiety agents, club drugs
sedative-hypnotic
primarily affect nervous tissue: depress activity of brain, nerves, muscles, and heart. reduce metabolism
mild sedation-death
sedative hypnotics: barbs, non barbs, antianxiety agents and club drugs
decreased dreaming while on drug but rebound insomnia and excessive dreams during withdrawal
sedative hypnotics: barbs, non barbs, antianxiety agents and club drugs
inhibits RAS for respiratory depression
sedative hypnotics: barbs, non barbs, antianxiety agents and club drugs
amphetamines, synthetic stimulants, non-amphetamine stimulants, cocaine, caffeine, nicotine
stimulants
high doses lead to hypotension (decreased CO, cerebral blood flow, and direct impairment of myocardial contractility)
sedative hypnotics: barbs, non barbs, antianxiety agents and club drugs
high doses may suppress urine formation (decrease renal fxn)
sedative hypnotics: barbs, non barbs, antianxiety agents and club drugs
stimulate liver enzyme production, produce jaundice, promote liver damage
sedative hypnotics: barbs, non barbs, antianxiety agents and club drugs
high doses will decrease body temp
sedative hypnotics: barbs, non barbs, antianxiety agents and club drugs
biphasic response (initial increase in libido, but then decreased ability to retain erection)
sedative hypnotics: barbs, non barbs, antianxiety agents and club drugs
inappropriate sexual or aggressive behavior, mood liability, impaired judgement, or impaired social or occupational functioning
sedative hypnotics: barbs, non barbs, antianxiety agents and club drugs
slurred speech, incoordination, unsteady gait, nystagmus, impairment of attention or memory, and stupor or coma
sedative hypnotics: barbs, non barbs, antianxiety agents and club drugs
withdrawal symptoms: autonomic hyperactivity (sweating or pulse rate greater than 100), increased hand tremor, insomnia, n/v, hallucinations, illusions, psychomotor agitation, anxiety, and grand mal seizures
sedative hypnotics: barbs, non barbs, antianxiety agents and club drugs
induce stimulation by augmentation of EPI, NE, or dopamine
psychomotor stimulants
exert their action on the cellular level
: general cellular stimulants: caffeine and nicotine
caffeine (cAMP)
nicotine: ganglionic neurons
most potent stimulant derived from nature
cocaine
appetite suppressants
CNS stimulants
tremor, restlessness, anorexia, insomnia, agitation, increased motor activity; increased alertness, decreased fatigue, elation and euphoria, subjective feelings of greater mental agility and muscular power
Stimulants (amphetamines, cocaine, caffeine, nicotine)
increased BP, HR, cardiac arrhythmias, relax bronchial smooth muscle, increased myocardial o2 demand, vasoconstriction, MI, vfib, pulmonary hemorrhage (inhaled cocaine)
amphetamines, synthetic stimulants, non-amphetamine stimulants, cocaine, caffeine, nicotine
result of chronic cocaine snorting
nasal rhinitis
euphoria, affective blunting, changes in sociability, hypervigilance, interpersonal sensitivity, anxiety, tensio or anger, stereotyped behaviors or impaired judgement
amphetamines or cocaine intoxication
caffeine intoxication level
+250mg
crash: fatigue, depression, nightmares, HA, profuse sweating, muscle cramps, hunger
stimulant wd
ataxia, peripheral and sensorimotor neuropathy, speech problems, and tremor
CNS effects of inhalants
coughing and wheezing to dyspnea, emphysema, and pneumonia
respiratory effects of inhalants
abdominal pain, nausea, vomiting, rash under nose or mouth, unusual breath odors, liver toxicity
GI inhalant effect
acute and chronic renal failure and hepatorenal syndrome
renal system effects of inhalants
symptoms similar to alcohol intoxication: dizziness, ataxia, euphoria, excitation, disinhibition, nystagmus, blurred vision, dbl vision, slurred speech, hypoactive reflexes, psychomotor retardation, lethargy, gen muscle weakness, stupor or coma
Inhalant intoxication
exert both a sedative and analgesic effect; medical uses include relief of pain, diarrhea, and coughing.
opioids
lethargy and indifference to the environment are common manifestations
opioid use
oral, snorting smoking SC, IM or IV
modes of using opioids
euphoria, mood changes, mental clouding, drowsiness, pain reduction, pupillary constriction, respiratory depression, suppression of cough in medulla
opioids on CNS
increased stomach and intestinal tone and peristaltic activity of intestine is diminished leading to decreased mvmt of food through the GI tract (constipation or possibly fecal impaction)
opioids on GI tract
at high doses, induce hypotension (histamine release)
opioids on heart
initial euphoria, apathy, dysphoria, psychomotor agitation, impaired judgement, pupillary constriction, drowsiness, slurred speech, and impairment in attention or memory
opioid intoxication
dysphoric mood, n/v, muscle aches, lacrimation or rhinorrhea, pupillary dilation, piloerection, sweating, diarrhea, yawning, fever, insomnia
opioid wd
anxiety, depression, ideas of reference
hallucinogen intoxication
Substance use assessment tools
MAST michigan alcohol screening test
CAGE cut back, annoyed, guilty, eyeopener
CIWA clinical institute withdrawal assessment of alcohol state
codependent must begin to let go of the denial that probs exist. Abstinence from blanket denial may be a very emotional and painful period
stage 1 the survival stage of Tx for codependency
reidentification (indiv glimpses true self through a break in denial system) accept the label of codependent and take responsibility for own dysfunctional behavior. its more painful not to enter reidentification.. accept limitations and are ready to face the issues of codependence
stage 2 the reidentification stage of tx for codependency
relationships cannot be managed by force of will. each partner must be indep. and autonomous. goal is to detach from the struggles of life that exist bc of prideful and willful efforts to control those things that are beyond the indiv’s power
stage 3 the core issues stage of tx for codependence
stage of self-acceptance and willingness to change; relinquish power over others that was not theirs in the first place. reclaim personal power; integrity is achieved out of awareness, honesty, and being in tough with one’s spiritual consciousness. Control is achieved through self discipline and self confidence
stage 4 reintegration phase of tx for codependence
naltrexone, antabuse, Campral
meds to help abstain from alcohol
gibe chlordiazepoxide (librium) and haldol
substitution for Stimulants
phenobarbital (Luminal)-barbs
benzodiazepams-non barbs
substitution for depressants
benzodiazepams clordiazepoxide (Librium) oxazepam lorazepam (ativan) diazepam (Valium)
substitution therapy for alcohol
Narcan (naloxone) naltrexone (ReVia), and nalmefene (Revex), METHADONE + clonidine, buprenorphine (less powerful than methadone but fewer side effects)
substitution for opioids
