Showing posts with label Psychiatry. Show all posts
Showing posts with label Psychiatry. Show all posts

Tuesday, September 22, 2015

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Alcoholic liver disease

Chronic and excessive use of alcohol is one of the major causes of liver disease.

90% of daily heavy drinkers (>60 g alcohol/day) as well as binge drinkers have fatty liver but a smaller percentage (10-35%) of drinkers progress to alcoholic hepatitis which is a precursor for cirrhosis.

The long-term risk is 9 times higher in patients with alcoholic hepatitis compared to those with fatty liver alone.

Some population-based surveys have documented that men must drink 40 to 80 g of alcohol daily and women must drink 20 to 40 g daily for 10 to 12 years to achieve a significant risk of liver disease.

Liver pathology consists of 3 major lesions that are progressive and rarely exist in a pure form:
1) fatty liver (usually reverses quickly with abstinence),
2) alcoholic hepatitis and
3) cirrhosis.

histologic staging alcoholic liver disease

Prognosis of severe alcoholic liver disease (ALD) is bad. Mortality of patients with alcoholic hepatitis concurrent with cirrhosis id nearly 60% at 4 years.

Although alcohol is a direct hepatotoxin, it is unclear why only 10-20% of alcoholics will develop alcoholic hepatitis. It appears to involve a complex interaction of facilitating factors like drinking patterns, diet, obesity and gender.

Harmful use of alcohol results in 2.5 million deaths each yr. Most of the mortality is due to cirrhosis. The mortality is declining now because of decreased consumption of alcohol in the Western countries except in the U.K, Romania, Russia and Hungary.

a) Quantity and duration of alcohol intake - are the most important risk factors. Time taken to develop liver disease is directly related to the amount of alcohol consumed.
b) There is no clear role of the type of beverage and the pattern of drinking.
c) Genetic - some people are genetically predisposed  for alcoholism and subsequently to the ill effects of alcohol on the liver.
d) Gender - It is a strong determinant for ALD. Women are more susceptible to alcoholic liver injury. They develop advanced liver disease with substantially less alcohol intake. Gender-dependent differences may be due to the effects of estrogen, proportion of body fat and gastric metabolism of alcohol.
e) Chronic infection with Hepatitis C virus - It is an important comorbidity in the progression of ALD to cirrhosis in chronic and excessive drinkers. Even moderate alcohol intake of 20-50 g/day increases the risk of cirrhosis and hepatocellular cancer. Intake of more than 50 g/day decreases the efficacy of interferon-based antiviral therapy.

It is unclear but what is known is that alcohol can act as a direct hepatotxin and malnutrition does not play a major role.
- Alcohol is metabolised to acetyldehyde which in turn initiates an inflammatory cascade that results in a variety of metabolic responses.
- Steatosis from lipogenesis, fatty acid synthesis and depression of fatty acid oxidation occur secondary to effects on sterol regulatory transcription factor (SRTF) and peroxisome proliferator-activated receptor alpha (PPAR-alpha).
- Intestinal derived endotoxin initiates a pathogenic process through toll-like receptor-4 and TNF-alpha. This facilitates hepatocyte apoptosis and necrosis.
- Cell-injury endotoxin also activates innate and adaptive immunity pathways. There is release of pro-inflammatory cytokines (TNF-alpha) and proliferation of T/B cells.
- Production of toxic protein-aldehyde adducts, generation of reducing equivalents and oxidative stress also contribute to liver injury.

Finally hepatocyte injury and impaired regeneration are associated with stellate cell activation and collagen production which are key events in fibrogenesis. The resulting fibrosis causes architectural derangement of the liver and the associated pathophysiology.

Fatty liver is the initial and most common histologic response to hepatotoxic stimuli, including excess alcohol ingestion. Accumulation of fat within the perivenular hepatocytes coincides with the location of alcohol dehydrogenase. Continuing alcohol ingestion results in deposition of fat throughout the entire hepatic lobule.

Alcoholic fatty liver - traditionally regarded as benign but appearance of steatohepatitis and certain features like giant mitochondria, perivenular fibrosis and microvesicular fat are associated with progressive liver injury.

Hallmarks of alcoholic hepatitis include: (hepatocyte injury)
a) ballooning degeneration,
b) spotty necrosis,
c) polymorphonuclear infiltrate and
d) fibrosis in the perivenular and perisinusoidal space of Disse.

Mallory-Denk bodies are often present in florid cases but these are neither specific nor necessary to establish the diagnosis.

Usually the patients are asymptomatic.
Hepatomegaly is often the only clinical finding.
It is very important to assess the drinking history and estimate how much alcohol is consumed per day and for how long.
1 beer, 4-5 ounces of wine, 1.5 oz of 40% liquor and 1 ounce (approximately 30 mL) of 80% spirits all have around 12 g of alcohol.

Alcohol content of various beverages

- Patients with fatty liver may have:
1) right upper quadrant discomfort,
2) nausea and
3) rarely jaundice.

- Patients with alcoholic hepatitis may have:
1) fever
2) spider nevi
3) jaundice
4) abdominal pain.
We can also see portal hypertension, ascites and variceal bleeding even in the absence of cirrhosis.

These are most identified through routine screening tests.

Fatty liver - laboratory abnormalities are non-specific
Modest elevation of AST, ALT, GGTP are seen. Triglycerides and bilirubin may also be increased.

Alcoholic hepatitis
a) increased AST and ALT - by 2-7 fold but rarely greater than 400 IU.
b) AST/ALT ratio greater than 1.
c) hyperbilirubinemia
d) modest increase in alkaline phosphatase

If synthetic function is deranged then the condition is more serious. Hypoalbuminemia and coagulopathy are more common in advanced liver disease.

Ultrasonography is also a useful investigation as it can determine the size of the liver and detect any fatty infiltration. If it demonstrates portal vein flow reversal, ascites and intraabdominal venous collaterals then the condition has less potential for complete reversal.

Below is an ultrasonographic picture of hepatic steatosis. Fatty infiltration produces an increased reflectivity of hepatic parenchyma, known as ‘bright liver pattern’. This feature can be assessed by comparing liver parenchyma with the right kidney’s cortex, which normally presents an echogenicity equal to or slightly lower than that of the liver. Severe steatosis produces a strong attenuation in the deepest liver sections, resulting in poor explorability.

bright liver with posterior attenuation

Critically ill patients with alcoholic hepatatis have short term (30-day) mortality rates exceeding 50%.
A Discriminant Function (DF) above 32 and a Model for End-stage Liver Disease (MELD) greater than 21 is associated with poor prognosis.
Worse prognosis if there is associated:
a) ascites,
b) variceal hemorrhage,
c) deep encephalopathy and
d) hepatorenal syndrome.

mortality alcoholic liver disease

a) Complete abstinence from alcohol is the mainstay for treatment.
b) Patients with severe alcoholic hepatitis i.e. DF>32 and MELD>21 should be given Prednisone 40mg/day or Prednisolone 32mg/day for 4 weeks followed by tapering over 4 weeks.
c) Alternatively Pentoxifylline, a non-specific TNF inhibitor, can be used in a dosage of 400mg 3 times per day for 4 weeks.
d) Liver transplantation is an accepted indication for treatment in selected and motivated patients with end-stage cirrhosis.

Below is an algorithm showing how to manage alcoholic hepatitis:
algorithm alcoholic hepatitis

N.B Monoclonal antibodies that neutralize serum TNF-alpha should not be used as studies have reported an increase in the number of deaths secondary to infections and renal failure.

First published on: 23 September 2015

Thursday, June 21, 2012


Delirium - definition, common causes, physical examination

Delirium is defined by the acute onset of fluctuating cognitive impairment and a disturbance of consciousness. Cognition includes memory, language, orientation, judgement, conducting interpersonal relationships, performing actions (praxis), and problem solving. Delirium is thus marked by short-term confusion and changes in cognition. There is also rapid improvement in most cases when the causative factor is identified and eliminated.

Abnormalities of mood, perception, and behavior are common psychiatric symptoms. Tremor, asterixis, nystagmus, incoordination, and urinary incontinence are common neurological symptoms.

Common causes of delirium:
1) Central nervous system disorder
Seizure (postictal, nonconvulsive status, status)
Head trauma, brain tumor, subarachnoid hemorrhage, subdural, epidural hematoma, abscess, intracerebral hemorrhage, cerebellar hemorrhage, nonhemorrhagic stroke, transient ischemia
2) Metabolic disorder
Electrolyte abnormalities
Diabetes, hypoglycemia, hyperglycemia, or insulin resistance
3) Systemic illness
Infection (e.g., sepsis, malaria, erysipelas, viral, plague, Lyme disease, syphilis, or abscess)
Change in fluid status (dehydration or volume overload)
Nutritional deficiency
Uncontrolled pain
Heat stroke
High altitude (usually >5,000 m)
4) Medications
Pain medications (e.g., postoperative meperidine or morphine)
Antibiotics, antivirals, and antifungals
Cardiac medications
Antineoplastic agents
Anticholinergic agents
Neuroleptic malignant syndrome
Serotonin syndrome
5) Over-the-counter preparations
Herbals, teas, and nutritional supplements
6) Botanicals
Jimsonweed, oleander, foxglove, hemlock, dieffenbachia, and Amanita phalloides
7) Cardiac
Cardiac failure, arrhythmia, myocardial infarction, cardiac assist device, cardiac surgery
8) Pulmonary
Chronic obstructive pulmonary disease, hypoxia, SIADH, acid base disturbance
9) Endocrine
Adrenal crisis or adrenal failure, thyroid abnormality, parathyroid abnormality
10) Hematological
Anemia, leukemia, blood dyscrasia, stem cell transplant
11) Renal
Renal failure, uremia, SIADH
12) Hepatic
Hepatitis, cirrhosis, hepatic failure
13) Neoplasm
Neoplasm (primary brain, metastases, paraneoplastic syndrome)
14) Drugs of abuse
Intoxication and withdrawal
15) Toxins
Intoxication and withdrawal
Heavy metals and aluminum

Physical examination of a delirious patient:

Clinical Implication

1. Pulse
Stokes-Adams syndrome
Increased intracranial pressure

Heart failure

2. Temperature
Thyroid storm

3. Blood pressure
Addison's disease

Intracranial mass

4. Respiration
Cardiac failure
Acidosis (metabolic)

Alcohol or other substance intoxication

5. Carotid vessels
Bruits or decreased pulse
Transient cerebral ischemia

6. Scalp and face
Evidence of trauma

7. Neck
Evidence of nuchal rigidity
Subarachnoid hemorrhage

8. Eyes
Hypertensive encephalopathy

Pupillary dilatation
Autonomic overactivity (e.g., delirium tremens)

9. Mouth
Tongue or cheek lacerations
Evidence of generalized tonic-clonic seizures

10. Thyroid

11. Heart
Inadequate cardiac output, possibility of emboli

Heart failure
Hypertensive disease

12. Lungs
Primary pulmonary failure
Pulmonary edema

13. Breath


14. Liver
Liver failure

15. Nervous system
a. Reflexes
Asymmetry with Babinski's signs
Mass lesion
Cerebrovascular disease
Preexisting dementia
Frontal mass
Bilateral posterior cerebral artery occlusion
b. Abducent nerve
(sixth cranial nerve)
Weakness in lateral gaze
Increased intracranial pressure
c. Limb strength
Mass lesion
Cerebrovascular disease
d. Autonomic

Friday, January 27, 2012

Difference between factitious disorder and malingering

Persons with factitious disorder fake illness. They simulate, induce, or aggravate illness. They also often inflict painful and even life-threatening injury on themselves or those under their care.

Unlike malingerers who have material goals, such as monetary gain or avoidance of duties, patients with factitious disorder bear the sufferings primarily to gain the emotional care and attention that comes with playing the role of the patient. The disorders have a compulsive quality, but the behaviors are considered voluntary in that they are deliberate and purposeful, even if they cannot be controlled.

Thursday, October 27, 2011


Depression - cause, signs and symptoms

Depression is a mood disorder whereby mood is sad. About 30% of psychiatric cases deal with depression. Both males and females are affected but females are slightly more prone to be depressed.

The biological cause is that there is a decrease in the serotonin neurotransmitter.

Signs and symptoms:
A simple mnemonic to remember is SIPS CAGE.

1) Sleep - There is late onset of sleep, intermittent awakening and early morning awakening i.e. around 2 hours before the normal waking up time. Rarely, the patient may over sleep.
2) Interest - Patient will have a decrease interest in the daily activities. This can result in social withdrawal, decreased ability to function in occupational and interpersonal areas. At times there is the inability to experience pleasure aka anhedonia.
3) Psychomotor activity - In younger patients, there is slowness in the thinking process and activities also are carried out at a slow pace. In elderly on the other hand, there is restlessness and increased activity.
4) Suicidal ideas - There is recurrent thoughts of death or suicide.
5) Concentration - There is decreased ability to concentrate on a particular task.
6) Appetite - It is usually decreased but can also be increased in many cases. This leads to weight changes.
7) Guilty feelings
8) Energy - There is decreased energy level.

A major depressive episode must last at least 2 weeks and have at least 4 of the above named symptoms.

In addition to the above symptoms, patient will have a feeling of hopelessness, helplessness and worthlessness.

Somatic complaints like heaviness in head, vague body aches, vertigo and generalised weakness are also commonly encountered.
In 20% of cases there may be psychotic features like delusions and hallucinations.