For ALL Ye DrInkErs!!! My NaMe Is LivEr CirrHosis...

Liver Cirrhosis

The liver is the largest solid organ of the body, as commonly unknown liver is also considered the largest gland of the body. Performing complex functions, liver plays its important role
in detoxification (cleansing body toxins).

The word "Cirrhosis" came from the greek word "khirros" or tawny (yellow-orange in color) which is the typical color of the diseased liver.

Liver Cirrhosis is a condition wherein the liver tissue is replaced by scars.

For someone who does not know about scars... scars are non functional tissues and does not represent the normal body tissues... meaning it does not function as the original liver tissues... These scars were formed through biological process of wound healing and is made up of fibrous tissue.

Liver cirrhosis is the consequence of chronic liver disease... such as, Alcoholic liver disease, hepatitis caused by virus (hepatitis C and hepatitis B) and is also caused by steatohepatitis (fats build up in the liver).

Alcohol contributes 15% of individuals having liver cirrhosis and who have drink more than a 10 years already. Though there are some variability for someone to suffer cirrhosis, for men 3-4 drinks per day and 2-3 drinks for women. Alcohol blocks the livers function in properly metabolizing fats, proteins and carbohydrates, thus creating inflammation which leads to liver tissue damage and then scarring.

Typical characteristics of a person having liver cirrhosis includes, ascites(fluid leaks through the vasculature into the abdominal cavity causing bulging of the abdomen), caput medusa(spider web like appearance of the umbilical veins due to portal hypertension), esophagial varices(varicosities of the esophagial veins).

And the worst case scenario is that the process is irreversible... without prompt management it may lead to HEPATIC COMA!

ACT NOW PROTECT YOUR LIVER... AVOID EXCESSIVE ALCOHOL DRINKING!

Marasmic child: He wants to eat... Can You GIve him SOme...??

Marasmus
A form of severe muscle wasting due to malnutrition. A body weight of less than 80% of the normal body weight for that height.

Occurence may start as early as 1 year old... due to malnutrition. This malnutrition leads to extensive tissue and muscle wasting.

Picture at the left portrays a child with severe malnutrition... which is characterized by loose skin folds, dry skin, loss of adipose tissue and muscle which shows why the child is skinny and bony.

Treatment does not limit only in supplementing dietary needs but also includes treatment for impending infections and diseases.

We cannot blame them for suffering in such a horrible way... instead lets eye on those people whose greed have steal these men and children's hope.

World crisis have gone far enough... Rice cost in Asia have doubled... commodities, shelter, clothings and medicines drag those people farther than the 8 feet depth length... stop political issues and abolish tyranny... give them peace... GIVE BACK THEIR HOPES!!!

Pemphigoid... Do you Know Someone...??

Pemphigoid

Are uncommon and rare autoimmune blistering skin disease...

Pemphigoid is common and somewhat similar to pemphigus. It is more common in women than in men which mostly affects ages 60 and above than in younger ages.

Three types of pemphigoid were categorized as follows:




First is what they called Gestational pemphigoid or Pemphigoid gestationis, which was formerly called herpes gestationis. The disease usually occurs during pregnancy at the second or third trimester and/or following pregnancy.






Second they termed it as Bullous pemphigoid this type is chronic which forms blisters under the surface of the skin and produces antibodies against collagen XVII component of hemidesmosomes. It was also know to affect mucous membrane and datedly known to afflict live stocks such as pigs, dogs and cats.











Third is the Mucous membrane pemphigoid or Cicatricial pemphigoid which is very rare that occurs in one in a million population. This type is a desquamating or blistering disease in which the underlying connective tissues forms blisters then later on become scars. This type affects mucous area such as the mouth, genitalias and if it affects the eyes it may lead to blindness because of constant scarring.

Thyroid Storm

Background

Thyroid storm, also referred to as thyrotoxic crisis, is an acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones (THs) in individuals with thyrotoxicosis. Thyroid storm may be the initial presentation of thyrotoxicosis in undiagnosed children, particularly in neonates. The clinical presentation includes fever, tachycardia, hypertension, and neurological and gastrointestinal abnormalities. Hypertension may be followed by congestive heart failure that is associated with hypotension and shock. Because thyroid storm is almost invariably fatal if left untreated, rapid diagnosis and aggressive treatment are critical. Fortunately, this condition is extremely rare in children.

Diagnosis is primarily clinical, and no specific laboratory tests are available. Several factors may precipitate the progression of thyrotoxicosis to thyroid storm. In the past, thyroid storm was commonly observed during thyroid surgery, especially in older children and adults, but improved preoperative management has markedly decreased the incidence of this complication. Today, thyroid storm occurs more commonly as a medical crisis rather than a surgical crisis.

Pathophysiology

Thyroid storm is a decompensated state of thyroid hormone–induced, severe hypermetabolism involving multiple systems and is the most extreme state of thyrotoxicosis. The clinical picture relates to severely exaggerated effects of THs due to increased release (with or without increased synthesis) or, rarely, increased intake of TH.

Heat intolerance and diaphoresis are common in simple thyrotoxicosis but manifest as hyperpyrexia in thyroid storm. Extremely high metabolism also increases oxygen and energy consumption. Cardiac findings of mild-to-moderate sinus tachycardia in thyrotoxicosis intensify to accelerated tachycardia, hypertension, high-output cardiac failure, and a propensity to develop cardiac arrhythmias. Similarly, irritability and restlessness in thyrotoxicosis progress to severe agitation, delirium, seizures, and coma. GI manifestations of thyroid storm include diarrhea, vomiting, jaundice, and abdominal pain, in contrast to only mild elevations of transaminases and simple enhancement of intestinal transport in thyrotoxicosis.

Frequency

United States

The true frequency of thyrotoxicosis and thyroid storm in children is unknown. The incidence of thyrotoxicosis increases with age. Thyrotoxicosis may affect as many as 2% of older women. Children constitute less than 5% of all thyrotoxicosis cases. Graves disease is the most common cause of childhood thyrotoxicosis and, in a possibly high estimate, reportedly affects 0.2-0.4% of the pediatric and adolescent population. About 1-2% of neonates born to mothers with Graves disease manifest thyrotoxicosis.

Mortality/Morbidity

Thyroid storm is an acute, life-threatening emergency. The adult mortality rate is extremely high (90%) if early diagnosis is not made and the patient is left untreated. With better control of thyrotoxicosis and early management of thyroid storm, adult mortality rates have declined to less than 20%.

Sex

• Thyrotoxicosis is 3-5 times more common in females than in males, especially among pubertal children.
• Thyroid storm affects a small percentage of patients with thyrotoxicosis. The incidence is presumed to be higher in females; however, no specific data regarding sex-specific incidence are available.

Age

• Neonatal thyrotoxicosis occurs in 1-2% of neonates born to mothers with Graves disease. Infants younger than 1 year constitute only 1% of childhood thyrotoxicosis.
• More than two thirds of all cases of thyrotoxicosis occur in children aged 10-15 years. Overall, thyrotoxicosis occurs most commonly during the third and fourth decades of life.
• Because childhood thyrotoxicosis is more likely to occur in adolescents, thyroid storm is more common in this age group, although it can occur in patients of all ages.

History

Patients may have a known history of thyrotoxicosis. In the absence of previously diagnosed thyrotoxicosis, the history may include symptoms such as irritability, agitation, emotional lability, a voracious appetite with poor weight gain, excessive sweating and heat intolerance, and poor school performance caused by decreased attention span. Burch and Wartofsky have published precise criteria and a scoring system for the diagnosis of thyroid storm based on clinical features.

• General symptoms
• • Fever
  • Profuse sweating
  • Poor feeding and weight loss
  • Respiratory distress
  • Fatigue (more common in older adolescents)
• GI symptoms
• • Nausea and vomiting
  • Diarrhea
  • Abdominal pain
  • Jaundice
• Neurologic symptoms
• • Anxiety (more common in older adolescents)
  • Altered behavior
  • Seizures, coma

Physical

• Fever
• • Temperature consistently exceeds 38.5°C.
  • Patients may progress to hyperpyrexia.
  • Temperature frequently exceeds 41°C.
• Excessive sweating
• Cardiovascular signs
• • Hypertension with wide pulse pressure
  • Hypotension in later stages with shock
  • Tachycardia disproportionate to fever
  • Signs of high-output heart failure
  • Cardiac arrhythmia (Supraventricular arrhythmias are more common, [eg, atrial flutter and fibrillation], but ventricular tachycardia may also occur.)
• Neurologic signs
• • Agitation and confusion
  • Hyperreflexia and transient pyramidal signs
  • Tremors, seizures
  • Coma
• Signs of thyrotoxicosis
• • Orbital signs
  • Goiter

Causes

• Thyroid storm is precipitated by the following factors in individuals with thyrotoxicosis:
• • Sepsis
  • Surgery
  • Anesthesia induction
  • Radioactive iodine (RAI) therapy
  • Drugs (anticholinergic and adrenergic drugs such as pseudoephedrine; salicylates; nonsteroidal anti-inflammatory drugs [NSAIDs]; chemotherapy)
  • Excessive TH ingestion
  • Withdrawal of or noncompliance with antithyroid medications
  • Diabetic ketoacidosis
  • Direct trauma to the thyroid gland
  • Vigorous palpation of an enlarged thyroid
  • Toxemia of pregnancy and labor in older adolescents; molar pregnancy
• Thyroid storm can occur in children with thyrotoxicosis due to any cause but is most commonly associated with Graves disease. Other reported causes of thyrotoxicosis associated with thyroid storm include the following:
• • Transplacental passage of maternal thyroid-stimulating immunoglobulins in neonates
  • McCune-Albright syndrome with autonomous thyroid function
  • Hyperfunctioning thyroid nodule
  • Hyperfunctioning multinodular goiter
  • Thyroid-stimulating hormone (TSH)–secreting tumor
• Graves disease may also occur in children with Down or Turner syndromes and in association with other autoimmune conditions, including the following:
• • Juvenile rheumatoid arthritis
  • Addison disease
  • Type I diabetes
  • Myasthenia gravis
  • Chronic lymphocytic (Hashimoto) thyroiditis
  • Systemic lupus erythematosus
  • Chronic active hepatitis
  • Nephrotic syndrome
• Although the exact pathogenesis of thyroid storm is not fully understood, the following theories have been proposed:
• • Patients with thyroid storm reportedly have relatively higher levels of free THs than patients with uncomplicated thyrotoxicosis, even though total TH levels may not be increased.
  • Adrenergic receptor activation is another hypothesis. Sympathetic nerves innervate the thyroid gland, and catecholamines stimulate TH synthesis. In turn, increased THs increase the density of beta-adrenergic receptors, thereby enhancing the effect of catecholamines. The dramatic response of thyroid storm to beta-blockers and the precipitation of thyroid storm after accidental ingestion of adrenergic drugs such as pseudoephedrine support this theory. This theory also explains normal or low plasma levels and urinary excretion rates of catecholamines. However, it does not explain why beta-blockers fail to decrease TH levels in thyrotoxicosis.
  • Another theory suggests a rapid rise of hormone levels as the pathogenic source. A drop in binding protein levels, which may occur postoperatively, might cause a sudden rise in free hormone levels. In addition, hormone levels may rise rapidly when the gland is manipulated during surgery, during vigorous palpation during examination, or from damaged follicles following RAI therapy.
  • Other proposed theories include alterations in tissue tolerance to THs, the presence of a unique catecholaminelike substance in thyrotoxicosis, and a direct sympathomimetic effect of TH as a result of its structural similarity to catecholamines.

  Lab Studies

  • Thyroid storm diagnosis is based on clinical features, not on laboratory tests. If the patient's clinical picture is consistent with thyroid storm, do not delay treatment pending laboratory confirmation of thyrotoxicosis.
  • Thyroid studies
  • • Results of thyroid studies are usually consistent with hyperthyroidism and are useful only if the patient has not been previously diagnosed.
    • Test results may not come back quickly and are usually unhelpful for immediate management.
    • Usual findings include elevated triiodothyronine (T3), thyroxine (T4) and free T4 levels; increased T3 resin uptake; suppressed TSH levels; and an elevated 24-hour iodine uptake. TSH levels are not suppressed in the rare instances of excess TSH secretion.
  • CBC count reveals mild leukocytosis, with a shift to the left.
  • LFTs commonly show nonspecific abnormalities such as elevated levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatinine kinase, alkaline phosphatase, and serum bilirubin.
  • Measurement of blood gas and electrolyte levels and urinalysis testing may be performed to assess and monitor short-term management.

  Imaging Studies

  • Chest radiography
  • • Chest radiography may show cardiac enlargement due to congestive heart failure.
    • Radiography may also reveal pulmonary edema caused by heart failure and/or evidence of pulmonary infection.
  • Head CT scan may be necessary to exclude other neurologic conditions if diagnosis is uncertain after the initial stabilization of a patient who presents with altered mental status.

  Other Tests

  • ECG is useful in monitoring for cardiac arrhythmias. Atrial fibrillation is the most common cardiac arrhythmia associated with thyroid storm. Other arrhythmias such as atrial flutter and, less commonly, ventricular tachycardia may also occur.

  Medical Care

  Patients with thyroid storm should be treated in an ICU setting for close monitoring of vital signs and for access to invasive monitoring and inotropic support, if necessary. Initial stabilization and management of systemic decompensation is as follows:

  • If needed, immediately provide supplemental oxygen, ventilatory support, and intravenous fluids. Dextrose solutions are the preferred intravenous fluids to cope with continuously high metabolic demand.
  • Correct electrolyte abnormalities.
  • Treat cardiac arrhythmia, if necessary.
  • Aggressively control hyperthermia by applying ice packs and cooling blankets and by administering acetaminophen (15 mg/kg PO/PR q4h).
  • Promptly administer antiadrenergic drugs (eg, propranolol) to minimize sympathomimetic symptoms.
  • Correct the hyperthyroid state. Administer antithyroid medications to block further synthesis of THs. High-dose propyl thiouracil is preferred because of its early onset of action and capacity to inhibit peripheral conversion of T4 to T3.
  • Administer iodine compounds (Lugol iodine or potassium iodide) orally or via a nasogastric tube to block the release of THs (at least 1 h after starting antithyroid drug therapy). If available, intravenous radiocontrast dyes such as ipodate and iopanoate can be effective in this regard. These agents are particularly effective at preventing peripheral conversion of T4 to T3.
  • Administer glucocorticoids to decrease peripheral conversion of T4 to T3. This may also be useful in preventing relative adrenal insufficiency due to hyperthyroidism.
  • Treat the underlying condition, if any, that precipitated thyroid storm and exclude comorbidities such as diabetic ketoacidosis and adrenal insufficiency. Infection should be treated with antibiotics.
  • Rarely, as a life-saving measure, plasmapheresis has been used to treat thyroid storm in adults.

  Consultations

  • Endocrinologist
  • Intensivist

  Further Inpatient Care

  • A pediatric ICU is the recommended inpatient care setting.
  • Continue supportive treatment.
  • Appropriately manage the precipitating event.
  • Follow up with laboratory tests to confirm thyrotoxicosis diagnosis, if previously undiagnosed.

  In/Out Patient Meds

  • Patients may require propranolol and iodides administration for 1 week.

  Deterrence/Prevention

  • Promptly and appropriately treat thyrotoxicosis after diagnosis.
  • Perform surgery in thyrotoxic patients only after appropriate thyroid and/or beta-adrenergic blockade.
  • Thyroid storm following RAI therapy for hyperthyroidism may be related to (1) withdrawal of antithyroid medications for RAI administration (usually withdrawn 5-7 d before administration of RAI and held until 5-7 d after RAI therapy), (2) release of large amounts of thyroid hormone from damaged follicles, and (3) RAI itself. Because TH levels are often higher immediately before RAI treatment than they are afterward, many endocrinologists believe that withdrawal of antithyroid drugs is the cause of thyroid storm. One option is to stop antithyroid drugs (including methimazole) only 3 days (rather than 5-7 d) before RAI therapy and to restart antithyroid drugs 3 days after RAI administration. Early institution of antithyroid drugs after RAI therapy may decrease the efficacy of treatment, requiring a second dose.
  • Consider testing thyroid function before operative procedures in children at high risk for hyperthyroidism (eg, patients with McCune Albright syndrome).

  Prognosis

  • If untreated, thyroid storm is almost invariably fatal in adults and is likely to cause a similarly severe outcome in children, although the condition is so rare in children that these data are not available.
  • With adequate thyroid-suppressive therapy and sympathetic blockade, clinical improvement should occur within 24 hours.
  • Adequate therapy should resolve the crisis within a week.
  • Treatment for adults has reduced mortality to less than 20%.
  • In adult patients, the precipitating factor is often the cause of death.

  Patient Education

  • For excellent patient education resources, visit eMedicine's Endocrine System Center. Also, see eMedicine's patient education articles Thyroid Problems and Thyroid Storm.

  Medical/Legal Pitfalls

  • Diagnosis may be missed because of variable presentation and because thyroid storm is rare in children.
  • In younger children and neonates, thyroid storm is most likely to be confused with sepsis and septic shock in the absence of a previous thyrotoxicosis diagnosis.