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196 Cards in this Set
- Front
- Back
Alcoholic fatty liver
Give signs and symptoms |
-History of several days of heavy drinking and/or long term drinking
-Anorexia -Nausea -Right upper quadrant discomfort -Hepatomegaly -May have tender liver |
|
Signs and symptoms of alcoholic hepatitis
|
Signs and symptoms of hepatitis in association with heavy alcohol use
-Severe alcoholic hepatitis has very high mortality rate severe alcoholic hepatitis also has anorexia, nausea, abdominal pain, impaired liver function with jaundice, bruising, encephalopathy -+/- Ascites -With or without neutrophilic leukocytosis |
|
Alcoholic cirrhosis.
List signs and symptoms |
Nausea
weight loss usually complications such as Portal hypertension Variceal bleeding and/or ascites Liver failure May lead to hepatocellular carcinoma |
|
Treatment of ascites
|
Salt restriction to reduce fluid retention
manage portal hypertension with beta blockers spironolactone, furosemide transjugular intrahepatic porta-systemic shunting |
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Treatment of hepatic encephalopathy
|
-Treat precipitating factors
decrease colonic production absorption of ammonia with lactulose treat H. pylori |
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Discuss hepatitis A
|
-RNA virus
Past fecal oral contamination -Almost universal in underdeveloped countries -More severe with advancing age -Does not persist as chronic infection -More associated with poverty and crowding then injection indications vaccination High-risk occupations Travelers Homosexual man Patients with chronic liver disease |
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Discuss Hepatitis B
|
Most prevalent chronic infectious viral disease in humans
really transmitted among intravenous drug users |
|
Hepatitis B
Risk groups for |
-Risk group = multiple sexual partners
-risk group = homosexual man Risk group = Asians, Southern Europeans, med geraniums risk group = indigenous people risk group = health care workers risk group = children infected parents Risk group = IV drug use |
|
Hepatitis B
prodrome symptoms |
Transient serum sickness prodrome (polyarthralgia, fever, malaise, proteinuria)
|
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Hepatitis B
symptoms of acute infection |
Anorexia
Nausea sometimes vomiting jaundice pale stools dark urine often subclinical |
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Hepatitis B
chronic disease |
Converts to chronic hepatitis B in 5% of adults
|
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Hepatitis B
Diagnoses of chronic hepatitis B |
HBsAg process for more than 6 months
|
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Hepatitis B
complications of chronic active hepatitis B |
Chronic hepatitis
cirrhosis hepatocellular carcinoma |
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Hepatitis B
treatment of active chronic hepatitis B |
Only if active liver inflammation
pegylated interferon is 30% effective Use 2 or more agents |
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Discuss hepatitis C
|
Strongly associated with injection of drugs
incidence of approximately 20% per year of IV drug use Most IV drug users are infected low sexual transmission |
|
Hepatitis C
Risk factors |
Contaminated drug injection equipment
blood transfusions prior to 1990 incarceration (drug use) body piercing and tattoos 10% transferred from mother to baby low risk sharing toothbrushes, razors etc. healthcare workers, needlesticks birth or medical procedures sexual activity Use a snorting straws No evidence of transmission to casual household contacts no evidence of transmission through breast milk |
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Hepatitis C
Primary infection |
Usually subclinical.
Peak viremia usually in week 2 or 3. |
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Hepatitis C
Chronic infection |
Chronic infection develops and three fourths of patient's with acute infection.
Liver damage results from immune damage to infected cells. 8% well-developed cirrhosis after 20 years 20% well-developed cirrhosis after 40 years |
|
Hepatitis C
symptoms of chronic hepatitis C |
Severity does not correlate with disease activity well.
Usually nonspecific, mild, intermittent. Most common symptoms are fatigue, nausea, muscle aches, right upper quadrant pain, weight loss |
|
hepatitis C
percentage of acute infections that develop persistent chronic infection |
60-70%
|
|
hepatitis C
mechanism of liver injury |
Hepatitis C cause liver damage predominantly by immune damage to affected liver cells
|
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hepatitis C
percentage of people developing cirrhosis |
8% of hepatitis C. patient will develop cirrhosis in 20 years
-20% will develop cirrhosis in 40 years |
|
Hepatitis C
how to make the diagnosis |
Enzyme immunoassay or hepatitis C, it is good but many false positives.
does not differentiate between current and resolved infections.. Positive hepatitis C RNA tests indicates active infection. |
|
Hepatitis C.
How to determine if infection has resolved? |
Hepatitis C RNA test negative.
And Positive antibody tests suggests cleared infection |
|
Hepatitis C.
Assessing severity of disease |
Symptoms do not correlate with severity of liver disease.
Spider nevi common but nonspecific. Plasma ALT is best indicator of active viral hepatitis but does not indicate severity. |
|
Hepatitis C.
Effect of alcohol and disease |
Alcohol consumption in the presence of chronic hepatitis C has added effect of liver inflammation and accelerates hepatic fibrosis.
Heavy alcohol use: increases viral load increase risk of progression to hepatocellular carcinoma |
|
Hepatitis C.
Dietary guidelines |
No dietary guidelines for hepatitis C.
However dietary treatment of diabetes and obesity can slow progression of hepatitis |
|
Hepatitis C.
Indications for antiviral treatment |
Name indication for treatment of active hepatitis isn't elevated ALT and (if performed) biopsy evidence of fibrosis
|
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+16
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24
|
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Hepatitis C.
Goal of antiviral therapy |
The goal of antiviral therapy and hepatitis C is a sustained virologic response evidenced by normal ALT and negative hepatitis C PCR at least 6 months after treatment
|
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Hepatitis C.
Risk of cirrhosis during sustained urologic response |
There is a very low risk of cirrhosis after 6 months of sustained virologic response with normal PCR normal ALT
|
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Hepatitis C.
Duration of treatment. Drugs used |
Pegylated interferon and ribavirin are drugs of choice.
Genotype 2 or 3 is treated for 6 months. Genotype is one, 4, 5, 6 or cirrhosis are treated for 12 months |
|
Hepatitis C.
Treatment of patient's with positive hepatitis CRNA and normal transaminases. |
This disease is mild. Can treat if patient really desires. Generally, mildly discouraged treatment until ALT is abnormal or signs of progressive liver disease
|
|
Hepatitis C.
Treatment of patients with ongoing substance abuse |
NIH recommends against treating patients with ongoing substance abuse (except methadone or buprenorphine).
|
|
Hepatitis C.
Side effects of interferon |
Interferon therapy.
Flulike symptoms in 4-6 hours of injection. Also may have more persistent symptoms of fatigue mood alterations moderate suppression of white cell count moderate suppression of platelet count skin rash anorexia and weight loss Dryness of mucous membranes Hair loss major side effects severe depression retinopathy Interstitial fibrosis lung thyroid disease |
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Hepatitis C.
At what rate does hepatitis C cirrhosis progressed to hepatocellular carcinoma? |
Annual rate of 3-5%
|
|
List of treatment for small primary hepatocellular carcinomas?
|
Excision
|
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Whatever the indications for liver transplantation in the presence of hepatitis C?
|
Major complications of their cirrhosis.
Life expectancy of one-2 years without transplantation. |
|
What is a 3 year post transplantation survival rate after hepatitis C?
|
84% = 3 year survival rate.
Equal to survival of other patients with transplantation of liver |
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What is hepatitis D?
|
Delta agent isn't effective viral RNA particle they cannot replicate without co-infection with hepatitis B.
|
|
What is cocaine hepatitis?
|
Cocaine hepatitis is uncommon condition causing about 1% of hepatic failures.
Probably occurs as a result of heat shocklike features of cocaine toxicity. Is both dose and time-dependent. |
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What is the mechanism of cocaine hepatitis injury?
|
Cocaine hepatitis injury most likely cause by ischemia from the vaso constrictive effects of cocaine and possibly toxic metabolites.
|
|
What is the effect of alcohol and cocaine taken together?
|
Ethel cocaine (coca ethylene) is produced.
Has similar effects as cocaine Has a little longer half-life, therefore accumulates at a higher dose. Has lower LD 50 |
|
Can ecstasy produce hepatic injury?
|
Ecstasy and MDMA rarely cause hepatic injury.
When it occurs it is probably due to hypothermia and volume depletion at rave parties |
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What is the most common toxic material designed for oral use but injected?
|
Talc
accumulation causes damage at several sites, especially lung and liver |
|
What is the pathogenesis of injected talc?
|
Talc is strongly fibrogenic in the long and leads to pulmonary granulomatous disease with progressive or fatal outcome.
Talc in liver is inconsequential |
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What is effects of opioids on the liver?
|
No hepatotoxicity from pure preparations of opiate agonists.
Opioid antagonist such as naltrexone can cause minor elevation of liver enzymes, but rarely serious. |
|
What are the possible effects of anabolic steroids?
|
Cholestasis.
Toxic hepatitis. Hepatic adenomas. Hepatic carcinomas hepatotoxicity from contaminants |
|
Why is GFR important in drug treatment?
|
GFR can be reduced because of nephrotoxicity.
GFR is used to adjust medication dosages. |
|
List renal problems associated with opiate use.
|
HIV nephropathy.
Hepatitis C associated glomerulonephropathy is. Hepatitis B associated polyarteritis nodosa. Bacterial endocarditis and acute glomerulonephritis. Subcutaneous injection amyloidosis. Nontraumatic rhabdomyolysis and acute renal failure. heroin nephropathy |
|
List renal problems associated with cocaine usage.
|
Cocaine usage can cause:
Rhabdomyolysis and acute renal failure. Accelerated hypertension and renal failure. HIV nephropathy. Hypertensive nephrosclerosis. Renal infarction. Thrombotic microangiopathy and renal failure. |
|
List renal problems associated with alcohol consumption
|
Alcohol consumption is associated with:
Hepatorenal syndrome. Rhabdomyolysis and acute renal failure. Increased incidence and severity of postinfectious glomerulonephritis. Electrolyte disorders |
|
Define
nephrotic syndrome |
Nephrotic syndrome characterized by
heavy proteinuria (>3.5 g per day). Hypoalbuminemia. Hyperlipidemia. Lipid area. Edema. Not all characteristics must be present to diagnose |
|
State differences between nephritic and nephrotic syndromes
|
Both have:
Proteinuria greater than 3.5 g per 1.73 m² body surface. Hypoalbuminemia. Hyperlipidemia. Edema. Hypertension. Renal insufficiency. Nephritic syndrome also has hematuria due to larger pore size. |
|
What is the most common presentation of renal disease with hepatitis C?
|
Renal disease in the presence of the hepatitis C. most often presents with:
-Nephritic and nephrotic syndrome. Urine contained large amounts of protein, red blood cells, red blood cell casts |
|
Heroin nephropathy.
Discuss. |
Heroin nephropathy is a secondary cause of focal and segmental glomerulonephritis,
often associated with hypertension Often associated with slow progression to ESRD rarely encountered |
|
The frequency of coexistence of hepatitis C and HIV drug users is__?
|
78% of HIV drug users have hepatitis C.
|
|
What is the treatment of acute hypertension in connection with cocaine use?
|
Steroids
|
|
Drugs of abuse associated with rhabdomyolysis
|
Phencyclidine.
Methamphetamines. MDMA. Cocaine. Heroin. Alcohol. |
|
Discuss
hepatorenal syndrome. |
Hepatorenal syndrome is a result of chronic alcohol ingestion producing liver damage.
Is a state of profound renal vasoconstriction and splanchnic basal dilatation associated with severe liver function impairment. Often with hypertension and ascites. |
|
Diagnosis and prognosis of
hepatorenal syndrome |
Diagnosis of hepatorenal syndrome is a diagnosis of exclusion.
Must have trial of volume replacement with salt poor albumin (NOT saline). Removal of any potentially nephrotoxic agents. No improvement of oliguric acute renal failure makes diagnosis of hepatorenal syndrome probable. Prognosis is almost always fatal unless successful liver transplant |
|
What is
Ecstasy? |
Ecstasy =
MDMA = methylenedioxymethamphetamine. |
|
Effects of MDMA at rave party
|
MDMA can lead to
agitation high fever hyperventilation impaired sensorium increase insensible fluid losses leading to dehydration, hypernatremia and fluid depletion this results in hypotension, shock, brain damage, rhabdomyolysis and renal failure |
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Major targets of alcohol and other drug toxicity
|
Liver is major target for toxicity
|
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Hepatic cirrhosis is___leading cause of death in. US
___Most common cause of death in middle-age American man |
12th
fifth |
|
Number of dead Puryear from hepatic cirrhosis
|
28,000
|
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Most common causes for liver transplantation
|
Hepatitis C
alcoholic cirrhosis |
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Amount of alcohol needed to produce fatty liver.
|
Fatty liver can occur after a single heavy drinking episode
usually needs 10 years of alcohol consumption at 100 g per day to develop alcoholic liver disease |
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How much alcohol is in a standard drink
|
Standard drink contains 14 g of alcohol
|
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How much alcohol as needed to develop hepatic cirrhosis?
|
Hepatic cirrhosis usually requires long-term alcohol consumption a 40 g per day for men or 20 g per day for women.
Very heavy drinkers have only 50% chance of developing cirrhosis. |
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Risk factors for alcoholic liver disease
|
Women require only half the amount of alcohol as men to develop alcoholic liver disease.
Genetics can produce threefold susceptibility to liver disease. Nonalcoholic fatty disease progresses more common with obesity. Obesity increases risk of alcoholic liver disease |
|
Chronic alcohol consumption increases hepatotoxicity of what classes of drugs?
|
Chronic alcohol consumptions increases hepatotoxicity of:
Acetaminophen. Industrial solvents. Anesthetic gases. Illicit drugs |
|
What is the cause of alcoholic liver damage?
|
Alcoholic liver damage was previously thought to be due to poor nutrition. Today, thought to be direct result of alcohol ingestion even with adequate nutrition
|
|
How does chronic alcohol consumptions increases hepatotoxicity?
|
Alcohol induces CP Y2 E1 which also metabolizes many other things
|
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Alcoholic fatty liver
history, signs and symptoms |
alcoholic fatty liver occurs.
After heavy or long term drinking, even for several days anorexia Nausea Right upper quadrant discomfort enlarged liver plus/minus liver tenderness |
|
Alcoholic hepatitis
signs and symptoms |
Alcoholic hepatitis produces
signs and symptoms of hepatitis in association with heavy drinking. Anorexia Nausea Abdominal pain impaired liver function Jaundice Bruising. Encephalopathy Fever and/or leukocytosis +/- Ascites Rare a high mortality |
|
Alcoholic cirrhosis
Signs and symptoms |
Alcoholic cirrhosis
Nausea Weight loss Portal hypertension Variceal bleeding and/or ascites Liver failure May lead to hepatocellular carcinoma |
|
Alcoholic liver disease
make diagnosis |
Diagnosis of alcoholic liver disease
liver function tests Gamma GT almost always raised Transaminases usually elevated if transaminases greater than 500, suggest additional disorders such as acetaminophen ingestion viral hepatitis or liver ischemia |
|
Significance of AST/ALT ratio
|
If ALT >AST,
suspect chronic hepatitis C, acetaminophen ingestion Other liver injury It AST >ALT (usually 2:1) suspect alcoholic liver disease |
|
Alcoholic hepatitis
described pathogenesis |
Pathogenesis of alcoholic hepatitis
neither predictable nor preventable Multifactorial factors include host, toxin, metabolic ethanol metabolizes to cetyl aldehyde via ADH and a.l. pH enzymes. Acetyl aldehyde affects many aspects of normal so function Second pathway and chronic alcoholism involves cytochrome P4 52 E1. |
|
Alcoholic liver disease
Treatment |
Treat alcoholic liver disease mainly by avoiding further alcohol.
If 6 weeks abstinence resolves elevated liver function tests, may return to drinking had low-level if able to control |
|
Alcoholic liver disease
what is apparent half-life of gamma GT? |
Gamma GT has an apparent half-life of 26 days. Of failure to drop suggest coexisting disease
|
|
Pharmacotherapies for alcohol dependence
baclofen Disulfiram Acamprosate Naltrexone Cortisone |
Pharmacotherapies for alcohol dependence:
baclofen has shown promise Disulfiram contraindicated in advanced liver disease Acamprosate contraindicated in severe decompensated liver disease Naltrexone associated with dose-dependent hepatotoxiciities. Cortisone prednisone 40 mg per day x28 days sometimes works |
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Effect of alcohol on myocardial contractility
|
alcohol depresses cardiac contractility
|
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What are metabolites of alcohol
What are their pharmacologic effects? |
The metabolites of alcohol are
acetyl aldehyde acetate. Acetyl aldehyde and acetate at adrenergic and vasodilatory effects. |
|
Why does cardiac output increased with alcohol and healthy patient's?
|
Alcohol increases heart rate and reduces peripheral resistance.
However, left ventricular ejection fraction is reduced alcohol increases skin and splanchnic blood flow but reduce his pancreatic flow |
|
What is effect of alcohol on ischemic myocardium?
|
In ischemic myocardium, alcohol cannot increase fail a so dilation because it is already maximally dilated.
Dilatation of is adjacent tissue vessels produces a "coronary steal" which increases myocardial damage Alcohol may mask angina. Alcohol may precipitate coronary spasms |
|
Alcoholic heart disease.
List effects of alcohol |
Excessive alcohol can produce
hypocontractile heart. Reduced cardiac output. Increased systemic vascular resistance in alcohol cardiomyopathy. Hyperdynamic heart. Four-chamber dilatation cardiomegaly. Interstitial and perivascular fibrosis. |
|
Alcoholic cardiomyopathy
Described cause and effects |
Alcoholic cardiomyopathy is a clinically distinct disorder in alcoholics without nutritional deficiency.
Dilated hypocontractile heart. Probably due to toxic effect of acetyl aldehyde. Requires prolonged excessive use of alcohol for greater than 10 years. 90% of patients are black. |
|
What is holiday heart?
|
Excessive alcohol, especially binge drinking produces cardiac arrhythmias.
Atrial fibrillation most common. Therefore always look for alcohol in the presence of cardiac arrhythmias. |
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What is thought to be the cause of sudden cardiac death in alcoholics?
|
Sudden cardiac death in alcoholics is thought to be due to arrhythmias most likely produced by alcohol withdrawal symptoms.
|
|
Nicotine
effect on heart rate and blood pressure on skin |
Nicotine increases heart rate and blood pressure for at least 30 minutes
reduces blood flow to skin |
|
Nicotine
effect on coronary arteries On hemoglobin. On platelet aggregation and blood viscosity. On HCL in conjunction with women taking oral contraceptives |
Effects of nicotine.
Coronary artery spasm. Increasing carboxyhemoglobin decrease his oxygen delivery. Induces platelet aggregation and blood viscosity. Lowers HDL |
|
Coronary risk reduction by stopping smoking
|
Nicotine replacement does not cause heart disease.
2 years of nicotine abstinence reduces coronary risk by 50%. 20 years nicotine abstinence reduces coronary risk to that of nonsmokers |
|
Cannabis
effects on circulatory system and heart |
Cannabis, regardless of method abuse.
Increases heart rate up to 50%. May increase, decrease I have no effect on blood pressure. Causes basal dilatation. Cardiac output increases because of increased heart rate and basal dilatation. Increases carboxyhemoglobin. 5 times more likely to have AMI within one hour of smoking cannabis. |
|
Opioids
effects on cardiovascular system |
Opioids.
Lower blood pressure. Reduce heart rate. Have favorable effect on myocardial ischemia. |
|
what are the four neurotransmitter systems within the brainstem reticular formation?
|
serotonin, acetylcholine, dopamine, noradrenaline
|
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Cocaine
treatment of cocaine-induced vasoconstriction A. What not to use |
Cocaine induced vasoconstriction of coronary arteries is enhanced by a beta adrenergic blocker propanolol!
|
|
Cocaine
treatment of cocaine-induced vasoconstriction B. What to use |
Coronary vaso constrictive action of cocaine is attenuated by alpha adrenergic blocker phentolamine
|
|
Cocaine
acute coronary syndrome |
Acute coronary syndrome with cocaine.
Occurs in adolescence in young people. Occurs in both occasional and habitual cocaine users. First hour after cocaine use as greatest risk. Coronary thrombosis is usual cause |
|
Cocaine
Acute coronary syndrome Treatment |
Treatment of acute coronary syndrome produced by cocaine.
Nitroglycerin both sublingual IV. Prevent seizures with benzodiazepines. May need angiography and thrombolysis. Morphine can attenuate cocaine-induced vasospasm therefore useful for continuing chest pains Do not give beta blockers until coronary patency established |
|
Cocaine.
Effects of chronic cocaine usage on heart |
Chronic cocaine usage.
Increases atherosclerosis increases myocardial injury Increases vascular complications related to hypertension. Part of damage to his from repeated elevations of blood pressure. Can also cause sudden cardiac death by producing arrhythmias |
|
Amphetamines
list significant amphetamines of abuse |
Amphetamines and related compounds are.
T., L., amphetamine. Methylphenidate. Methamphetamine. MDMA |
|
Amphetamines. Effects on cardiovascular system
|
Amphetamines effect on cardiovascular system.
Dose-dependent elevation of blood pressure and heart rate |
|
Phencyclidine and lysergic acid diethylamide.
Effects on cardiovascular system |
Phencyclidine (PCP) and lysergic acid diethylamide.
Increased heart rate |
|
Anabolic steroids
side effects |
Anabolic steroids (mainly testosterone at its congeners) use in 100-1000 times therapeutic doses can produce.
Marked cardiac hypertrophy. Acute myocardial infarction even with patent coronary arteries stroke |
|
Physical signs of addiction
skin HEENT cardiovascular |
Physical signs of addiction
skin Wrinkles from tobacco Scars from injection Palmar erythema of alcoholism HEENT Mouth cancer Tooth staining from tobacco Extreme tooth decay from methamphetamine (causes xerostomia and bruxism) cardiovascular murmurs from valvular disease |
|
Physical signs of addiction
Abdomen breasts Male genitourinary Female genitourinary Lymph nodes |
Physical signs of addiction
Abdomen Especially liver breasts Gynecomastia Male genitourinary Prostatism Colon and breast cancer increased with alcoholism Female genitourinary STDs Lymph nodes supraclavicular suggest lung cancer axillary and inguinal nodes |
|
Best lab test for nutritional status
|
The best test for nutritional status is
serum pre-albumin |
|
Treatment of heroin addict in the hospital
|
Give 10-20 mg of methadone and repeat in 2 hours.
Repeat methadone daily. If history of prior withdrawal give diazepam 10-20 mg orally or 5-10 parenterally |
|
Treatment of pain in opiate addict
|
Opioid addicts must have higher doses to control pain.
Control the pain then put on schedule. Do not use p.r.n. dosing |
|
Alcohol withdrawal.
How long after last drink before DTs start? |
DTs we'll begin in 6-48 hours after last drink
|
|
what are the sympathetic splanchnic nerves to the GIT?
|
thoracic, lumbar
|
|
Alcohol withdrawal. What are symptoms of delirium tremens?
|
The symptoms of delirium tremens are:
Tremor. Moist warm skin. Hypertension (treat with clonidine) Agitation (treat with haloperidol). Tachycardia (treat with benzodiazepines and maybe beta blockers). Seizures (treat with benzodiazepine, NOT DILANTIN! |
|
which structures are suspended by mesentery?
|
jejunum, ileum
|
|
Cause and treatment of Wernicke-Korsakoff syndrome
|
Wernicke-Korsakoff syndrome Caused by thiamine deficiency.
Give 100 mg thiamine IM before giving glucose |
|
Korsakoff syndrome
Symptoms |
Main symptom of Korsakoff syndrome is confabulation
|
|
Alcoholic cerebellar dysfunction.
Symptoms |
Alcoholic cerebral dysfunction
Ataxia and incoordination Often irreversible |
|
Alcoholic peripheral neuropathy symptoms
|
Symptoms of alcoholic peripheral neuropathy.
Burning pain numbness in stocking glove distribution |
|
Symptoms of alcoholic hepatitis
|
Alcoholic hepatitis symptoms.
Fever. Leukocytosis. Right upper quadrant pain and tenderness. Elevation of AST greater than ALT. |
|
Complications of hepatic cirrhosis
|
Complications of hepatic cirrhosis are.
Hypoalbuminemia. Coagulopathy. Hyperbilirubinemia. Hepatic encephalopathy. Esophageal or gastric variceal bleeding. Ascites. Spontaneous bacterial peritonitis. Volume overload and edema. Hepatorenal syndrome |
|
Was a five-year prognosis for cirrhosis if continues drinking
|
50%
|
|
Alcoholism
hematologic consequences |
Iron deficiency from gastrointestinal hemorrhage, Mallory-Weiss tears
pancytopenia. Folate deficiency producing megaloblastic anemia |
|
Alcoholism, cardiovascular consequences
|
Cardiovascular consequences of alcoholism.
Hypertension, especially during withdrawal. Alcoholic cardiomyopathy and congestive heart failure. |
|
Effects of alcoholism on EKG
|
EKG shows diffuse hypokinesis and four-chamber dilatation
|
|
Effects of alcoholism on esophagus
|
Alcoholism effects of esophagus.
Gastroesophageal reflux. |
|
Characteristic lesions of alcoholic gastritis
|
Characteristic lesions of alcoholic gastritis her subepithelial hemorrhages and epithelial erosions.
|
|
Predisposing factors to pancreatitis are...
|
Heavy alcohol consumption.
Gallstones these account for 75% of pancreatitis |
|
What percentage of heavy drinkers develop pancreatitis?
|
5% heavy drinkers develop pancreatitis
|
|
Factors leading to tissue injury in pancreatitis are...
|
Oxidative stress.
Autodigestion |
|
Mechanism of alcohol causing pancreatitis.
|
Alcohol contracts the sphincter of Oddi and inhibits pancreatic secretion.
Results in the cascade of autodigestion |
|
Diagnoses of pancreatitis
|
Attack of severe abdominal pain and tenderness.
Elevation of serum amylase more than 3 times normal. Imaging studies suggestive of inflammation |
|
Treatment of pancreatitis
|
Bedrest.
Analgesics. Intravenous fluids. Fasting |
|
Chronic pancreatitis.
Cause. Clinical features |
Principal cause of chronic pancreatitis is excessive consumption of alcohol (75% of cases).
Clinical features pain his chief problem. Upper abdominal pain that may radiate to the back. Pain increases with meals. Anorexia and weight loss. Can lead to diabetes and steatorrhea. |
|
The most common cause of pancreatitis and children is...
|
Most common cause of pancreatitis and children is
cystic fibrosis |
|
Mechanism of diarrhea in acute and chronic alcoholism
|
Diarrhea in alcoholics occurs from
altered motility. Altered permeability. Nutritional disorder. Small intestinal mucosal injury |
|
Treatment of opiate-induced constipation
|
Increase fluid intake
fiber supplementation lactulose |
|
Body packing
|
Ingestion of condoms or other bags filled with cocaine or other drugs.
Absorption can occur without rupture of the bag. Takes 3-6 days to clear GI tract. Give dilute contrast media to assist visualization |
|
Effective cocaine and amphetamines on gut
|
Cocaine mainly causes ischemic injury of the gut producing
intestinal perforation Infarction Ischemic colitis |
|
Drugs associated with pulmonary complications.
Central nervous system stimulants |
Drugs associated with pulmonary complications.
Central nervous system nicotine. Cocaine and crack. Amphetamines. MDMA. Methylphenidate. Caffeine |
|
Drugs associated with pulmonary complications.
Central nervous system depressants |
Drugs associated with pulmonary complications.
Central nervous system depressants. Alcohol. Barbiturates. Benzodiazepines. GHB (gamma hydroxyl butyrate). Opiates |
|
Drugs associated with pulmonary complications.
Central nervous system |
Drugs associated with pulmonary complications.
Central nervous system Volatile substances Aromatic hydrocarbons Nitrous oxide. Nitrites. Refrigerants |
|
Where is automaticity of respiration controlled in the brain?
|
Automaticity of respiration is controlled by the medulla oblongata.
But modulated by reticular activating system, cerebral cortex, and peripheral sensors |
|
Where is hypoxic drive regulated?
|
Hypoxic drive comes from the carotid body. When stimulated it causes hypotension and bradycardia
|
|
Described respiratory depression symptoms
|
Patients with respiratory depression are:.
Somnolent or postictal. Rapid and shallow respirations. Limited ability to cough. |
|
What are the medical complications of respiratory depression?
|
Medical complications of respiratory depression are.
Atelectasis. Hypoxemia. Hypoventilation. Inability to clear secretions. Broncho-aspiration. |
|
What is the management of respiratory depression?
|
Management of respiratory depression.
Look for history of drug abuse. Look for positive toxicology screen. electrocardiogram. Blood gas. Chest x-ray treat with. Thiamine. Glucose. Naloxone |
|
Discuss
atelectasis. Causes, pathophysiology, treatment |
Atelectasis
In respiratory depression, shallow respirations may not exceed critical closing volume and result in airway collapse. Ineffective cough and aspirated secretions, loss of surfactants lead to atelectasis. Unventilated areas are still perfused causing shunting and therefore hypoxemia. Treat with. incentive spirometry, respiratory suctioning. Chest physiotherapy. Supplementary oxygen. Possible bronchoscopy |
|
Discuss.
Aspiration pneumonitis |
Aspiration Pneumonitis.
Usually caused by aspiration of oral secretions or gastric contents. Usually only chemical pneumonitis but can lead to noncardiogenic pulmonary edema and respiratory failure with or without bacterial superinfection. Infiltrates develop within hours to days. Do not treat prophylactically with antibiotics |
|
What are the causes of respiratory infections with chronic use of drugs?
|
Chronic addictive drug users her susceptible to a variety of infections.
Many drugs affect leukocyte function. Malnutrition. Immune d deficiency occurs. Septic injections. May need cortisone for COPD plus producing immunosuppression. |
|
What are contaminants of illegal injected drugs ?
|
Common contaminants of illegal injected drugs are.
Mannitol. Cellulose. Talc. . Sugars. Phenobarbital. Methyl quinolone. Caffeine. Procaine |
|
Discuss.
Talc Granulomatosis |
Talc granulomatosis.
= Magnesium silicate. Widely use is a filler in oral medications. Can be added as a contaminate of injected drugs. Produces a syndrome similar to sarcoidosis. Insidious onset of granulomatous interstitial fibrosis. Symptoms are. Dyspnea. Dyspnea with exertion. Cough. Talc retinopathy in half of the patient's. Chest x-ray shows micral nodular interstitial capacity in some patients. CT me revealed diffuse groundglass opacity and confluent perihilar masses. PFT shows low diffusion capacity as first abnormality. Lung biopsy often needed to establish diagnosis. Sometimes improve with steroids |
|
Discuss
Pulmonary Hypertension |
Pulmonary Hypertension
multiple mechanisms. Chronic hypoxemia related to interstitial lung disease and vasoconstriction. Pulmonary arterial thrombosis at sites of foreign body granulomatosis. Primary pulmonary hypertension can occur as a result of HIV infection. Common presentations involve dyspnea on exertion. Physical exam an EKG often normal or right ventricular enlargement. |
|
What is the most common pulmonary complication of intravenous heroin users?
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Septic thromboemboli is the most common pulmonary complication of intravenous heroin use.
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What are the advantages of inhaling drugs?
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Inhalation route of drug administration has the following advantages.
Ease of administration. Rapid onset of action. Dose minimalization. Avoidance of intravenous injection. Avoidance of hepatic first pass effect. |
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Discuss
Barotrauma with Inhalation of Drugs |
Barotrauma can occur with inhalation of cocaine, heroine, 3, 4 methylenedioxymethamphetamine. Marijuana. Tobacco and volatile substances.
Produced by extreme breath-holding against closed glottis e.g. prolonged Valsalva maneuver, to increase drugs effect Alveolar bleb rupture. Dissection of air along peribronchial pass into mediastinum, pleural cavities, skin and retropharyngeal space some users exhale smoke forcibly into another users mouth, sometimes producing barotrauma |
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Components of tobacco causing lung cancer
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Cigarette tardus associated with high rates of
lung cancer, emphysema, bronchitis, airway reactivity |
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What are the adverse effects of environmental tobacco smoke?
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Adverse effects of environmental tobacco smoke in children are.
Lower respiratory illness. Chronic respiratory symptoms. And middle ear disease. Reduced lung function. Asthma. And wheezing in early childhood. Adults. Increase risk of lung cancer. Cardiovascular disease. Acute respiratory symptoms of illness |
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Criteria for diagnosis of
Chronic Bronchitis |
Criteria for diagnosis of chronic bronchitis.
Sputum production for at least 3 months and 2 consecutive years in the absence of other causes of chronic cough. Nonspecific airway changes, but usually. Mucous gland hypertrophy of intermediate size airways. Overproduction of the mucus may overwhelm mucociliary escalator |
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Described
Pulmonary Emphysema |
Pulmonary emphysema develops with irreversible a large dose of airspaces distal to the terminal bronchial, with destruction of the alveolar wall
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Components of tobacco causing lung cancer
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Cigarette tardus associated with high rates of
lung cancer, emphysema, bronchitis, airway reactivity |
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What are the adverse effects of environmental tobacco smoke?
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Adverse effects of environmental tobacco smoke in children are.
Lower respiratory illness. Chronic respiratory symptoms. And middle ear disease. Reduced lung function. Asthma. And wheezing in early childhood. Adults. Increase risk of lung cancer. Cardiovascular disease. Acute respiratory symptoms of illness |
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Criteria for diagnosis of
Chronic Bronchitis |
Criteria for diagnosis of chronic bronchitis.
Sputum production for at least 3 months and 2 consecutive years in the absence of other causes of chronic cough. Nonspecific airway changes, but usually. Mucous gland hypertrophy of intermediate size airways. Overproduction of the mucus may overwhelm mucociliary escalator |
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Described
Pulmonary Emphysema |
Pulmonary emphysema develops with irreversible a large dose of airspaces distal to the terminal bronchial, with destruction of the alveolar wall
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Discuss
Blue Bloater |
•Chronic bronchitis (blue bloaters)
◦Patients may be obese. ◦Frequent cough and expectoration are typical. ◦Use of accessory muscles of respiration is common. ◦Coarse rhonchi and wheezing may be heard on auscultation. ◦Patients may have signs of right heart failure (ie, cor pulmonale), such as edema and cyanosis. ◦Because they share many of the same physical signs, COPD may be difficult to distinguish from congestive heart failure (CHF). One crude bedside test for distinguishing COPD from CHF is peak expiratory flow. If patients blow 150-200 mL or less, they are probably having a COPD exacerbation; higher flows indicate a probable CHF exacerbation. |
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Discuss
Pink Puffer |
•Emphysema (pink puffers)
◦Patients may be very thin with a barrel chest. ◦They typically have little or no cough or expectoration. ◦Breathing may be assisted by pursed lips and use of accessory respiratory muscles; they may adopt the tripod sitting position. ◦The chest may be hyperresonant, and wheezing may be heard; heart sounds are very distant. ◦Overall appearance is more like classic COPD exacerbation. |
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Cause of pulmonary hypertension and cor pulmonale
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Pulmonary hypertension and cor pulmonale.
Caused by chronic hypoxic vasoconstriction the pulmonary vasculature leading to pulmonary arterial hypertension and right heart strain |
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Symptoms of pulmonary hypertension and cor pulmonale
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Symptoms of pulmonary hypertension and cor pulmonale.
Tachycardia. Prominent neck veins are. Tricuspid insufficiency murmur. Right ventricular third heart sound. Hepatojugular reflex. Peripheral edema |
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What are the products of marijuana combustion?
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Marijuana combustion produces the same chemicals as cigarette smoke except that it does not contain nicotine. It also contains THC and other cannabinoids.
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Compare marijuana and tobacco smoke.
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Marijuana smoke has 3 times as much tar cigarettes. Produces 5 times the carboxyhemoglobin level is cigarettes.
Marijuana does not contain nicotine. Marijuana is just as dangerous as cigarettes except that it produces less emphysema or accelerated decline of FEV1 |
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What effects does cocaine have on neurotransmitters?
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Cocaine blocks
norepinephrine reuptake. Serotonin reuptake Cocaine causes release of Norepinephrine Serotonin! Dopamine |
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How much cocaine actually reaches the lung when cocaine is inhaled
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About one third of inhaled cocaine reaches along
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Discuss speedballing
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Speedballing = combining cocaine with heroin or morphine to attenuate the sudden decrease of euphoria
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Discuss freebasing
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Freebasing = process of using volatile solvents to convert cocaine from assault the base and remove adulterants.
Freebase product is highly potent with rapid onset of action and more likely to produce side effects |
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What are the physiologic effects of cocaine?
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Cocaine produces
marked vasoconstriction reduced diffusion capacity damage to the alveolar capillary membrane alveolar hemorrhage noncardiogenic pulmonary edema Reduction and immunologic capacity inhibits function of natural killer cells. |
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What are upper airway complications of cocaine use?
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Cocaine may produce the following and upper airways.
Nasal septal perforation because of the vasoconstrictive effect. Sinusitis, epiglottitis. Vasculitis |
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Discuss pulmonary edema with cocaine
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Cocaine reproduce cardiogenic pulmonary edema or noncardiogenic pulmonary edema.
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Discuss "Crack Lung"
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Crack lung occurs 1-48 hours after heavy cocaine smoking.
Consists of chest pain, cough, hemoptysis, dyspnea, bronchospasm, pruritus, fever, diffuse alveolar infiltrates without effusions, pulmonary and systemic eosinophilia. |
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What are the general effects of amphetamines? On the respiratory system
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Amphetamines. Increased sympathetic stimulation.
By causing release of biogenic amines. By inhibiting reuptake of biogenic amines. Effects of amphetamine are primarily cardiovascular and neurologic. Also cause some bronchodilatation |
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What is caffeine?
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Caffeiine is a phosphodiesterase that raises intracellular cyclic adenosine monophosphate
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Where the effects of caffeine on the respiratory system?
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Caffeine produces smooth muscle relaxation therefore mild bronchodilator are properties
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What are the effects of opioids on the respiratory system?
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Opioids affect the respiratory system mostly at the alveolar walls, but also tracheal and bronchial smooth muscle.
Most dramatic effect of opioids and respiratory system is indirect by acting on the CNS to reduced responsiveness to carbon dioxide and depress respiratory automaticity and cough. |
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How long does respiratory depression last with opioids?
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Maximal respiratory depression occurs within 10 minutes after IV dose of opioid oral up to 90 minutes after subcutaneous or IM dose.
Respiratory depression lasts 4-5 hours |
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Where the principal respiratory complications of opioid overdose?
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The complications of opioid overdose are pulmonary edema and respiratory failure
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Discuss pulmonary edema and heroin
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Opioid overdose, especially heroin is a common cause of pulmonary edema in younger patients. 50% of overdose patient's present with pulmonary edema.
20% of this group will die |
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Further respiratory effects of alcohol?
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Alcohol intoxication can produce respiratory depression as well as.
Atelectasis. Hypoxemia. Respiratory acidosis. Aspiration. Adult respiratory syndrome. Respiratory failure |
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What is the mechanism metabolic acidosis and respiratory alkalosis with alcohol ingestion?
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Alcohol ingestion can produce alcoholic ketoacidosis.
Which produces metabolic acidosis. Which stimulates compensatory respiratory alkalosis. |
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Described hepatopulmonary syndrome
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Hepatopulmonary syndrome occurs in 8 days 15% of patients with cirrhosis.
Triad of. Liver dysfunction. Intrapulmonary or other vascular dilatation. Arterial hypoxemia |
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Discuss effects of sedative hypnotics on respiratory system
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Sedative hypnotic drugs. Her significant respiratory depressants when abuse or mix with alcohol or opiates
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What is the most common cause of barbiturate overdose?
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Most common cause of barbiturate overdose is accidental or intentional oral ingestion by a seizure patient or family member.
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What is the usual cause of death and sedative hypnotic overdose?
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Most sedative hypnotic overdose tests occur as a result of adult respiratory distress syndrome secondary to either a chemical aspiration pneumonitis or bacterial pneumonia
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What are the symptoms of sedative hypnotic withdrawal?
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Sedative hypnotic withdrawal symptoms are.
Tachypnea (most common).. Anxiety. Tremor. Headache. Diaphoresis. Difficulty concentrating. Insomnia. Hallucinations. Fatigue withdrawal occurs to-5 days after last dose |
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What the symptoms are barbiturate withdrawal?
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Barbiturate withdrawal.
Occurs 2-7 days after last dose. Agitation. Hyperreflexia. Anxiety. Tremor. Less often and symptoms are. Confusion and hallucinations. Seizures (often refractory to phenytoin). |
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What are the effects of benzodiazepines on sleep disorders?
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The effects of benzodiazepines on sleep disorders.
Decreased tone of upper airway muscles. Reduction in ventilatory response to carbon dioxide. Worsening nocturnal hypoxia. Pulmonary hypertension |
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What are the effects of inhalation of multiple substances?
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Volatile substance inhalation. Produces intoxicating and dysphoric effects within section.
Affect CNS with lethargy, stupor, agitation, hallucinations, dizziness, seizures. Pulmonary complications include severe respiratory depression, barotrauma, persistent cough, suffocation |
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what are the most common volatile inhalants?
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The most common volatile substance of abuse are.
Paramedic and short-chain hydrocarbons such as Toluene. Gasoline. Butane. Butyl and animal nitrites. Freon |