6: Alcohol Misuse Flashcards
1
Q
Describe the criteria for acute alcohol intoxication.
A
- Recent alcohol ingestion
- Clinically significant problematic behavioural or psychological changes
- > 1 of the following
○ Slurred speech
○ Incoordination
○ Unsteady gait
○ Nystagmus
○ Reduced attention/memory
○ Stupor/coma
Signs or symptoms can’t be explained by anything else
2
Q
What factors can influence the extent of acute alcohol intoxication?
A
- Intrinsic factors ○ Sex - women: § Process alcohol at slower rate § Weight less § Lower % body fluid § Reduced alcohol dehydrogenase ○ Weight § Increased weight -> increased blood volume + body fluid to dilute alcohol consumed ○ Tolerance ○ Personality and mood - Extrinsic factors ○ Size + % alcohol content of drink ○ Time spent drinking § Blood alcohol oxidised at rate of 15g/dl/hour ○ Medication § Act synergistically to compound effects of alcohol ○ Food and drink § Lines stomach § Slows absorption into blood Increased absorption rate when alcohol mixed with carbonated beverages
3
Q
What symptoms may be noted, and at what blood alcohol concentration?
A
- Excitement - BAC < 100mg%
○ Depression of higher inhibitory cortical function- Confusion - BAC 100-200mg%
○ Depression of limbic system - memory, orientation
○ Depression of cerebellum - coordination, speech - Stupor - BAC > 200mg
○ Depression of upper BS - RAS - conscious level
Depression of lower BS - breathing and vasomotive centres
- Confusion - BAC 100-200mg%
4
Q
Symptoms associated with acute alcohol intoxication
A
- Psychiatric ○ Affective disorders ○ Antisocial personality - increased risk of suicide ○ Increased risk of injury - GI ○ Nausea ○ Vomiting - causing hyponatraemia ○ Diarrhoea - increased propulsion and decreased transit time ○ Gastritis, peptic ulcer, pancreatitis ○ Oesophageal, gastric and duodenal dysmotility ○ Acute alcoholic hepatitis - Metabolic ○ Decreased glucose, albumin, K+, Mg2+, Ca2+, PO43- ○ Lactic acidosis - Cardiovascular ○ Tachycardia ○ Holiday heart syndrome ○ Peripheral vasodilation ○ Volume depletion ○ Hypotension ○ Hypothermia - Respiratory ○ Respiratory depression ○ Reduced airway sensitivity to foreign bodies ○ Decreased ciliary clearance ○ Aspiration
5
Q
Pathology of alcohol withdrawal
A
- GABA (inhibitory) and glutamate (excitory) usually balanced effect on post-synaptic neuron
In withdrawal state glutamate upregulated and over comes GABA
6
Q
Symptoms of alcohol withdrawal
A
- Autonomic symptoms ○ Increased heart rate ○ Increased resp rate ○ Increased blood pressure ○ Increased body temperature ○ Diaphoresis ○ Dilated pupils ○ Diarrhoea ○ Nauseas and vomiting - Motor symptoms ○ Increased reflexes ○ Tremors ○ Seizures ○ Ataxia ○ Slurred speech - Psychiatric symptoms ○ Illusions ○ Delusions ○ Hallucinations ○ Paranoia ○ Anxiety ○ Affective instability ○ Combativeness ○ Disinhibition - Awareness ○ Insomnia ○ Agitation ○ Irritability ○ Delirium ○ Disorientation
7
Q
What are the adverse effects of chronic alcohol misuse?
A
- Hepatobiliary ○ Liver § Steatosis § Fibrosis § Cirrhosis § Hepatocellular carcinoma ○ Leukonychia § White nails with lumulae undemarcated - hypoalbuminemia ○ Terrys nails § White proximally + distal 30% red - telangiectasis ○ Finger clubbing ○ Duputren's contracture ○ Coagulopathy ○ Hepatomegaly ○ Encephalopathy ○ Portal hypertension § Splenomegaly § Caput medudsae § Oesophageal varices § Ascites - GI effects ○ Acute and chronic pancreatitis § Pancreatic calcification ○ Gastritis § Hyperaemic gastric mucosa ○ Oesophageal varices § Linear dark blud submucosal dilated veins ○ Gastric ulcers § Shallow + sharply demarcated 1cm gastric ulcer in upper fundus § Hyperaemia and smaller ulcer - Neurological ○ Wernicke-Korsakoff syndrome § Small petechial haemorrhages in mamillary bodies ○ Cerebral atrophy § Narrowed gyri + widened sulci ○ Cerebellar degeneration § Anterior vermis atrophy of cerebellum ○ Optic neuropathy § Pale blurring of disc margins - Other ○ Alcoholic cardiomyopathy § Large, dilated left ventricle ○ Coronary artery disease § Yellow-tan lipid atherosclerotic plaque ○ Foetal alcohol syndrome § Short palpebral fissure § Flat midface § Elongated and hypoplastic philtrum § Thin upper vermillion lip border § Microcephaly § Flat nasal bridge § Epicanthal folds § Minor ear abnormalities § Micrognathia
8
Q
What are the three main forms of alcohol-induced liver injury?
A
- Hepatocellular steatosis
- Alcoholic hepatitis (steatohepatitis)
- Cirrhosis
9
Q
Factors influencing development and severity it alcohol-induced liver injury
A
- 10-15% of alcoholics develop cirrhosis
- Gender
○ M>F ) - Ethnicity/genetics
○ African-Americans worse affected than Caucasians despite similar alcohol consumption
○ 50% of Asians carry a variant aldehyde dehydrogenase gene (ALDH*2).
○ Impaired oxidation of acetaldehyde leading to flushing, nausea, headaches, increased HR - Comorbidity
○ Iron overload, NASH, viral hepatitis
- Gender
10
Q
Morphology of alcoholic liver disease
A
- Hepatocellular steatosis
○ Liver enlarged and heavy
○ Soft, yellow and greasy
○ Completely reversible with abstinence
○ Microscopic - fatty droplets in liver- Alcoholic hepatitis
○ Ballooned hepatocytes - cells injured and swollen with damaged cytoskeleton
○ Mallory hyaline - clumps of keratin formed as hepatocytes balloon
○ Inflammation
○ Hepatocyte necrosis - spotty
○ Fibrosis
○ Neutrophils more common than in NASH - Cirrhosis
○ Liver scarring - bands of scar tissue separate liver parenchyma into nodules
○ Morphology
§ Bumpy capsular surface with depressed scare and bulging regenerative nodules
§ Masson trichome stain shows blue thick bands of collagen encircle and compress nodules
- Alcoholic hepatitis
11
Q
Clinical features of alcohol related liver disease
A
- Hepatocellular steatosis ○ Completely reversible with abstinence ○ Hepatomegaly ○ Mild elevation of bilirubin ○ Raised alk phos - Alcoholic hepatitis ○ Malaise ○ Anorexia ○ Abdominal pain ○ Weight loss ○ Tender hepatomegaly ○ High bilirubin/aminotransferases/alk phos ○ AST>ALT ○ Repeated bouts cause cirrhosis - Cirrhosis ○ Commonest causes § Alcoholic liver disease § Non-alcoholic fatty liver disease § Hep B and C ○ Often asymptomatic until advanced ○ Hepatic encephalopathy ○ Haemorrhage from oesophageal varices Bacterial infection and hepatocellular carcinoma are common causes of death
12
Q
Causes of portal hypertension
A
○ Prehepatic § Obstructive thrombosis of portal vein ○ Intrahepatic § Cirrhosis § Primary biliary cholangitis § Massive fatty change § Infiltrative malignancy § Amyloidosis ○ Post-hepatic § Severe right sided heart failure § Constrictive pericarditis § Hepatic vein outflow obstruction - Increased resistance to flow ○ Contraction of SM and myofibroblasts ○ Disruption by scars and nodules - Increased flow ○ Hyperdynamic state ○ NO mediates arterial vasodilatation - Sinusoidal remodelling ○ Anastomoses in fibrous septa expose veins to arterial pressure
13
Q
Main consequences of portal hypertension
A
Hepatic encephalopathy
Ascites
Portosystemic venous shuns
Congestive splenomegaly
14
Q
What are the main sites of portosystemic shunts and the vessel involved?
A
- Small veins form/old ones open up to link portal venous system to systemic circulation
- Occur where they share a capillary bed
- Rectum - > Anorectal varices (superior/middle/inferior rectal veins)
- Oesophagogastric junction -> Oesophageal varices (submucosal veins)
- Falciform ligament of the liver (including abdominal wall veins)
○ (Periumbilical) caput medusae
15
Q
Define gastropathy and gastritis
A
- Inflammation of gastric mucosa
- Acute Gastritis: With neutrophils present
- Gastropathy: With few inflammatory cells present or absent
- Chronic Gastritis: Long-term inflammation of mucosa typically associated with H.Pylori infection
16
Q
Pathogenesis of gastropathy and gastritis
A
○ Occurs when damaging forces overwhelm protective factors § Damaging factors □ Gastric acidity □ Peptic enzymes § Protective factors □ Surface mucus secretion □ Bicarbonate secretion into mucus □ Mucosal blood flow □ Epithelial barrier function □ Epithelial regenerative capacity □ Elaboration of prostaglandins § Injury □ H.pylori infection ® Secrete urase ® Inhibit gastric bicarbonate transporters □ NSAIDs ® Inhibit cyclooxygenase (COX) dependent synthesis of prostaglandins E2 and I2 ® Contribute to mucus, phospholipid and bicarbonate secretion, mucosal blood flow and epithelial restitution □ Tobacco □ Alcohol □ Gastric hyperacidity □ Duodenal-gastric refuels □ Ischaemia □ Shock ® Decreased oxygen delivery to mucosa
17
Q
Common causes of stress related mucosal damage
A
- Stress Ulcers ○ Shock ○ Sepsis ○ Severe trauma - Curling Ulcers ○ Occur in proximal duodenum ○ Severe burns ○ Severe trauma - Cushing Ulcers ○ Intracranial disease ○ Elevated risk of perforation
18
Q
Pathogenesis of stress related mucosal damage
A
- Local ischaemia
○ Systemic hypotension or reduced blood flow due to stress-induced splanchnic vasoconstriction- Increase of endothelin-1 (vasoconstrictor)
- Intracranial injury
○ Direct stimulation of vagal nuclei
○ Hypersecretion of gastric acid - Systemic acidosis
○ Lower intracellular pH of mucosal cells
○ Reduced pH gradient promoting washout of acid that has back-diffused into lamina propria
