Mesothelioma

History
In 1960s, Wagner published an article about a certain disease that is strongly linked to asbestos exposure.


Mesothelium:
The mesothelium is a membrane that forms the lining of several body cavities: the pleura (thoracal cavity), peritoneum (abdominal cavity including the mesentery) and pericardium (heart sac). Mesothelial tissue also surrounds the male internal reproductive organs (the tunica vaginalis testis) and covers the internal reproductive organs of women (the tunica serosa uteri). Mesothelium that covers the internal organs is called visceral mesothelium, while the layer that covers the body walls is called the parietal mesothelium.
(source: www.wikipedia.com)



Mesothelioma defined
A rare form of cancer in which cancer cells are found in the sac lining the chest, the lining of the abdominal cavity or the lining around the heart

is a disease in which cells of the mesothelium become abnormal and divide without control or order. They can invade and damage nearby tissues and organs. Cancer cells can also metastasize (spread) from their original site to other parts of the body. Most cases of mesothelioma begin in the pleura or peritoneum. More than 90% of mesothelioma cases are linked to asbestos exposure.

Asbestos defined
Asbestos refers to a group of minerals that occur naturally as masses of strong, flexible fibers that can be separated into thin threads and woven. Asbestos fibers, including Chrysotile asbestos, are not affected by heat or chemicals, do not conduct electricity, and therefore has been widely used in many industries. However, asbestos fiber masses tend to break easily into a dust composed of tiny particles that can float in the air and stick to clothes. The fibers may be easily inhaled or swallowed and exposure to asbestos has been shown to cause serious health problems including pleural mesothelioma.

Cholelithiasis

DEFINITION

The presence of calculi (gallstone) in the gallbladder. The medical term for gall stones is cholelithiasis. Chole is from the Greek meaning "bile". Lithos is "stone" and iasis is "condition of".

ETIOLOGY

Gallstones are crystalline structure formed by concretion (hardening) and accretion (adherence of particle, accumulation) of normal or abnormal bile constituents. According to various theories, there are four possible explanations for stone formation.

First, bile may undergo a change in composition. Studies of subject with cholesterol gallstone will indicate that their bile is supersaturated with cholesterol but deficient in bile salts. The cholesterol saturation of bile seems to increase with age. Changes in bile composition however do not completely explain hoe gallstones formed.

Second, gall bladder stasis may lead to bile stasis. Bile stasis may (1) change the composition of bile, (2)s supersaturated bile with cholesterol, and (3) precipitate some bile constituents. Gallbladder stasis may result from decreased contractility and emptying of gallbladder spasm of the sphincter of Oddi. Circumstances in which bladder stasis occur are associated with a high rate of gallstone formation. Most specifically, TPN without oral intake for longer than one month is associated with gallbladder sludge formation and cholelithiasis. Delayed emptying of gallbladder may correlate with hormonal factors. In pregnant women, the female sex hormone estrogens increases, which increases dietary uptakes of cholesterol and biliary cholesterol secretion. This may explain why gallstone seems to be associated with pregnancy. In addition, one of the precautions for administering estrogen balances to postmenopausal women is gallbladder disease.

Third, infection may predispose a person to stone formation. Inflammatory debris can form a nidus (point of origin) for stone growth. The related tissue injury may alter the composition of bile increasing the reabsorption of bile salts and lecithin. Certain organisms may also play a part in stone formation by altering the composition of bile. For example, Escherichia coli increases the amount of bilirubin available for pigment stones and Streptococcus faecalis reduces the bile salts.

Fourth, genetic and demography can affect stone formation, as shown in higher prevalence in Pima and Chippewa Native Americans, Northern Europeans, and South Americans than in Asians.

RISK FACTORS

• Overweight
• Rapid weight loss
• Estrogen intake and birth control pills(estrogen increases the concentration of cholesterol in the bile)
• Diabetes
• Over age 40 and increase in risk as one ages
• Female especially those who have had children
• Ethnicity (Pima Indians and Mexican-Americans)
• High triglycerides, high LDL cholesterol, decreased HDL cholesterol,
• Alcohol intake
• Family history of gallbladder disease (Heredity)
• Cholesterol-lowering drugs, immunosuppressive drugs and others
• Very Low Calorie Diets
• Diet high in saturated fats
• Diet high in refined foods and sugars
• Diet low in fiber (which is what the refined diets are) and not enough vegetables
• Non-fat diets
• Low-fat diets
• Constipation

Diseases such as chronic inflammatory bowel disease, chrons disease (ulcerative colitis is contraversial) Hemolytic anemias.

The Diabetes Cure

Medical Surgical Lecture Notes for Diabetes Mellitus: Definition, Diagnosis, Pathophysiology, Management, Treatment

I. DEFINITION
Diabetes Mellitus (DM) is a chronic systemic disease affecting people of all ages. It basically has three types: Type I (IDDM), Type II (NIDDM), and GDM or Gestational Diabetes which is associated with pregnancies. It is characterized by lack of or decreased ability of the body to use insulin.

Type I

• -Insulin dependent Diabetes Mellitus (Juvenile-onset Diabetes)
• -Condition marked by absolute insulin deficiency secondary to the destruction of pancreatic beta cells. (remember: beta cells of the pancreas produce insulin)

Type II

• - Non-insulin dependent Diabetes Mellitus (Adult-onset Diabetes)
• -Impaired tissue sensitivity to insulin or impaired insulin secretion

GDM- Gestational Diabetes Mellitus

• Diagnosis of Diabetes mellitus that applies to women in whom glucose intolerance develops during pregnancy (usually after 24 weeks AOG).

II. HISTORICAL BACKGROUND
In late nineteenth century, when diabetes was already a well-known abnormality in carbohydrate metabolism, scientists thru experiments that removal of the islets of langerhans in the pancreas produces DM in animals. Later on this knowledge paved way to the discovery of naturally produced insulin in 1921. Insulin was then injected to diabetic patients hence the first and proven treatment of Diabetes mellitus. Before injectible insulins were developed, diabetic patients die in a year of two after the onset of Diabetes mellitus, and even a few weeks after suffering from its symptoms.

Dr. Elliott Joslin of Boston was noted as an early pioneer in the quest for finding cure to this dramatically-brutal disease. He asserted that diabetic patients need to gain full knowledge of the disease so he could better take care of himself. A well-knowledgeable physician may not be enough, since the diabetic patient and his family play a vital role in the management of Diabetes Mellitus.

III. RISK FACTORS/PREDISPOSING FACTORS
Type 1 Diabetes mellitus
-IDDM or juvenile-onset Diabetes mellitus is inherited as a heterogenous, multigenic trait. 10% of diabetic patients suffer from type 1 DM which is usually diagnosed before the age of 30. Identical twins have a risk of 25% to 50% of inheriting this disease, whereas siblings have a 6% risk, and offspring a 5% risk. There is also an ssociation between type 1 diabetes and HLAs (Human Leukocyte Antigens).

Type 2 Diabetes mellitus
-previously called NIDDM (non-insulin dependent Diabetes mellitus), involves both genetic and environmental factors. It is not associated with HLAs and circulating ICAs are rare. It is more common in identical twins, with a risk factor of 58% to 75% than in general population. Obesity is also a major risk factor as such that 80 to 85% of diabetic patients are obese.

IV. PATHOPHYSIOLOGY (DIAGRAM)

V. CLINICAL MANIFESTATIONS (SIGNS AND SYMPTOMS)
Clinical manifestations of Diabetes mellitus is tagged as 3 P’s : Polydipsia, Polyuria, Polyphagia. Some references would use 5 P’s, with the addition of Pruritus and Paresthesia.

Polyuria is frequent urination because the water is not being reabsorbed by the body by the renal tubules. This eventually leads to dehydration, hence diabetic patients also feel excessively thirsty, a condition known as polydipsia. Increased catabolic activity of the body makes a diabetic person hungry, this is termed as polyphagia. Pruritus is a condition of the skin that is extremely uncomfortable at times and may be relieved by emollient baths.

VI. DIAGNOSIS
Laboratory tests are needed in order to establish a diagnosis of Diabetes.

a. Fasting blood Sugar/ Fasting Blood glucose

-A blood sample is taken from a patient who has taken nothing by mouth (NPO) for at least 8 hours. If the patient’s blood glucose level is 110 to 126 mg/dl, this would indicate an IFG or Impaired fasting Glucose. A diagnosis of DM is made if the patient’s blood glucose is greater than 126mg/dl.

b. Casual Blood Glucose

-A blood sample is taken from patient without a need for fasting. This is also called random blood sugar test. A blood glucose level of greater than 200 mg/dl is suggestive of diabetes. Elevation of blood glucose occur when patient is under stress, after a meal, from samples drawn from an IV site, and in diabetic patients.

c. Postload Blood glucose

-Also known as postprandial glucose test, is done two hours after a patient has taken his standard meal. Normally, blood glucose would return to fasting level within two hours. If after two hours the glucose level remains elevated at a level greater than 200 mg/dl during an OGTT, a diagnosis of Diabetes mellitus is made.

d. Glycosylated hemoglobin

-Glucose attaches to the haemoglobin molecule of an RBC (Red blood cell) and does not tend to disassociate. The higher the blood glucose level would mean higher levels of glycosylated haemoglobin (HbA1c). A1c is an average blood glucose level measured over the previous 3 months.

e. Oral Glucose Tolerance test

-usually not recommended in hospitalized clients because results are easily altered by many external and internal factors.

f. Self-Monitoring of Blood Glucose

-Provides an immediate feedback and data on blood glucose levels. SMBG is recommended for all clients with diabetes, regardless of the type of diabetes that they have. It is also a way on gaining knowledge on how a diabetic patient respond to food, insulin, exercise and stress.

When and how many times in a day an SMBG is done vary from patient to patient. It largely depends on patient needs and goals. However, it is recommended that type 1 and GDM patients taking insulin take SMBG three or more times daily. SMBG is done prior to taking a meal, before bedtime, and in the middle of the night. For type 2 DM patients, an agreement is set between the client and his health care provider. If they are taking oral medications, SMBG are usually done less frequently.

There are also some instances that a diabetic patient need SMBGs such as when feeling ill, or if experiencing hypoglycaemia ( pallor, diaphoresis or excessive sweating, cold clammy skin, faintness, weakness). It is also a standard procedure to do SMBG if patient frequently suffer from insulin reactions overnight.

VII. TREATMENT
1. Oral Antidiabetes Agents
a. Sulfonylureas (an oral hypoglycaemic agent)
b. Meglitinides (OHA)
c. Biguanides (insulin sensitizers)
d. Thiazolidinediones (insulin sensitizers)
e. Alpha-glucosidase inhibitors

2. Insulin
a. Rapid-acting
2 to 4 hours duration with peak onset of 1 hour. Examples are humalog and Novolog
b. Short-acting
4 to 6 hours duration; 2-4 hours peak time. Examples include Humulin R and Novolin R
c. Intermediate-acting
Cloudy appearance; 10-16hours duration and peaks at 4-10 hours. Examples are Humulin N (NPH), Humulin L (Lente), Humulin 70/30 (Premixed)
d. Long-acting
18-24 hours duration depending on type. Examples are Humulin U(Ultralente) and lantus (insulin glargine)

3. Exercise and Proper Diet

VIII. Injection of Insulin Dose
1. Wipe site of injection with cotton swab dipped with alcohol
2. With one hand, pinch up skin at injection site and quickly insert needle for its entire length in order to ensure injection of sufficient depth. The more rapidly the needle is inserted, the less pain will be felt.
3. Inject insulin dose. Make sure insulin temperature is at room temperature. Do not massage site of injection.
4. Rotate site of injection for best absorption of insulin.

IX. Insulin Pump Therapy
A small portable pumps for continuous administration of regular insulin are now used by diabetic patients. In this method, a small pump is worn externally and automatically injects insulin subcutaneously into the abdominal area through an indwelling needle site (changed daily).

How does it works? Insulin is infused to the patient at a low basal rate that matches a client’s basal metabolic needs. Boluses are infused before meals.

Advantage of the insulin pump includes a continuous infusion of insulin. However, it is recommended that the patient undertake SMBG (self-monitoring blood glucose) at least four times daily.