It is a common, chronic and long-term disorder in which a person has uncontrollable, recurring thoughts (obsessions) and/or behaviors (compulsions) that he or she has repeated urges to repeat. There are some psychological facts about OCD that is the obsessive compulsive disorder .
According to the World Health Organization, anxiety disorders, like OCD, are more prevalent in developed countries than in developing countries.
People with family members who suffer from OCD might be predisposed to the illness. Also, as an anxiety disorder, experts believe that OCD may also be linked to levels of serotonin in the brain, stress or illness may trigger its symptoms.
Cognitive Behavioral Therapy and medication are two ways of treating OCD.
Perfectionism – a need to get everything to feel right during OCD personality traits.
An obsessive-compulsive might check their doors and windows 50 to 100 times when an obsession with security gets stuck in their head. Obsessive-compulsives are completely powerless to control their compulsions.
Obsessive-compulsives are tortured by these thoughts, which they find profoundly disgusting and distressing.
OCD sufferers are driven to carry out complex rituals known as compulsions, which are triggered by obsessions.
Some OCD sufferers are so afraid of being misunderstood by others that they become very skilful at hiding their symptoms, and can appear entirely normal. In other cases, symptoms can be so severe that sufferers receive disability compensation.
Responsibility – an exaggerated sense of responsibility for their actions during OCD personality traits.
OCD is treatable, and people who suffer from it can live a normal life.
In the U.S. 1 in 40 adults and 1 in 100 children face OCD.
OLD is a one type of OCD.Obsessive love disorder” (OLD) refers to a condition where you become obsessed with one person you think you may be in love with. You might feel the need to protect your loved ones obsessively, or even become controlling of them as if they were a possession.
People who suffer from obsessive-compulsive disorder (OCD) are plagued by intrusive thoughts that they can’t banish from their mind, no matter how hard they try.
The obsessions experienced by OCD sufferers can be grouped along with several common themes like Common obsessions, Common compulsions etc.
OCD symptoms are divided between obsessions: recurrent and persistent thoughts, urges, or impulses, and compulsions: repetitive behaviors or mental acts that the individual feels driven to perform in response to an obsession.
Many of us carry out daily rituals consisting of a series of tasks that we might otherwise forget. For example, checking that all the doors and windows are locked before we go to bed at night is a routine that guards against burglary. But in OCD, these rituals spiral out of control.
Some Common compulsions that includes,1)Cleaning – repeatedly washing hands or wiping household surfaces for hours on end.2)Checking – repeatedly questioning whether light switches are turned off, or appliances are unplugged etc.
OCD may affect men and women equally.
Neuroticism – anxious and keen to avoid dangerous situations during OCD personality traits.
Daniel Radcliffe, Cameron Diaz, Leonardo DiCaprio, Megan Fox and Justin Timberlake are all celebrities who have lived with OCD.
OCD will make your thoughts more towards to depression, Anxiety and sorrowness.It will make your personality more complex than normal human being.
Symptoms of OCD may include: an overwhelming attraction to one person’s obsessive thoughts feeling the need to “protect” the person you’re in love with,possessive thoughts & actions,extreme jealousy over other interpersonal interactions and low self-esteem. Sometimes they physically harm themselves or that person also which turns into crime and mental illness.
Most OCD compulsions are logically related to their obsession. For instance, sufferers carry out cleaning rituals in order to rid themselves of contaminants.
The difference between healthy and obsessive love is that with the latter, those feelings of infatuation become extreme, expanding to the point of becoming obsessions. Obsessive love and jealousy that is delusional is a symptom of mental-health problems and is a symptom that occurs in about 0.1% of adults.
Common obsessions include fears of contamination by germs, dirt or chemicals,flooding the house, causing a fire, or being burgled .
Indecisiveness – a tendency to take time to make decisions during OCD personality traits.
On average, people are diagnosed with OCD when they are 19-years-old.
The difference between OCD in adults and in children is that children may not be able to realize the reason for their behavior or thoughts (or that their behaviors or thoughts are unusual).
Researchers have found that people with OCD often score very highly for particular personality traits. These include: Neuroticism, Impulsivity, Responsibility, Indecisiveness and Perfectionism.
Impulsive – a tendency to engage in activities that bring instant gratification during OCD personality traits.
Intrusive thoughts, or obsessions, as psychologists call them, affect everyone. But some people can’t get rid of them as easily as the rest of us.
Perfectionism is one of the most common personality traits in OCD. Indeed, some researchers have described obsessive-compulsives as the ultimate perfectionists.
Cyst is defined as a pathological cavity may or may not be lined by epithelium and containing fluid , semi fluid or gaseous material .
Cysts are more common in the orofacial region and are the most common cause for chronic jaw swelling . They grow slowly and are usually asymptomatic . The epithelium of the cysts of oral and paraoral region is usually derived from the odontogenic apparatus and their Remnants or the epithelium entrapped at the line of fusion of various facial process during the development .
The wall of the capsule is composed of the collagenous fibrous connective tissue usually within epithelial lining and it produces various bond reserving factors for its growth and expansion .
It may occur within the bone or soft tissue . They grow by hydraulic expansion . Radiographically, they often appear radiolucency surrounded by thin radioopaque border .
TYPES OF CYSTS : TRUE CYSTS : that which is lined by epithelium e.g dentigerous cyst, radicular cyst etc. PSEUDO CYSTS: not lined by epithelium, e.g. Solitary bone cyst, Aneurismal bone cyst etc.
PARTS OF A CYST : Cyst has following parts: -> WALL (made of connective tissue) -> EPITHELIAL LINING. -> LUMEN OF CYST
Mechanism of cyst formation :
Proliferation of the epithelial lining
Food regulation within the cyst cavity
Mechanism of cyst formation Proliferation of the epithelial lining Fluid accumulation within the cyst cavity Bone resorption : Epithelial cysts A) Odontogenic cysts. 1) Developmental odontogenic cysts
Orthokeratinized odontogenic cyst
Dentigerous cyst Eruption cyst
Lateral periodontal cyst
Glandular odontogenic cyst
Calcifying odontogenic cyst
Gingival cyst of newborn
Gingival cyst of adult
2) Inflammatory odontogenic cyst
Apical periodontal cyst
Inflammatory collateral cyst
Buccal bifurcation cyst
B) non odontogenic cysts 1) developmental non odontogenic cysts
1. Cyst initiation 2. Formation 3. Cyst enlargement or expansion
Odontogenic cyst :
The odontogenic cysts are derived from epithelium associated with the development of the dental apparatus . The type of epithelium can vary with most lesions on having stratified squamous but some developmental or fissural cyst in the maxilla may have respiratory epithelium .
Dentigerous cyst / follicular cyst :
Definition: The dentigerous cyst is defined as a cyst that originates by the separation of the follicle from around the crown of an unerupted tooth.
The dentigerous cyst encloses the crown of an unerupted tooth and is attached to the tooth at the cementoenamel junction .
• The pathogenesis of this cyst is uncertain, but apparently it develops by accumulation of fluid between the reduced enamel epithelium (REE) and the tooth crown.
It is estimated to be about 20% of all jaw cysts. It is estimated that about 10% of impacted teeth have form a dentigerous cyst . The dentigerous cyst nearly always involves or is associated with the crown of a normal permanent tooth .
Clinical features :
AGE : 1st to 3rd decades.
GENDER : more frequently in males than in females.
2/3rd of follicular cyst associated with unerupted mandibular teeth, primarily III molar.
Maxillary 3rd Molar
Supernumerary tooth also can be involved
Dentigerous cysts have the potential, to attain a large size, often it is the pronounced facial asymmetry .
Pain may be a presenting symptom, if secondary infection occures.
Eggshell crackling, in large cysts
Radiographic features :
generally reveals a unilocular radiolucency associated with crowns of unerupted teeth ( multilocular effect can be seen, in large cysts due to bony trabeculations).
Cysts have a well defined sclerotic margin, unless when they are infected then the margins are poorly defined.As compared to the other jaw cysts,
The dental follicle may expand around the unerupted or impacted tooth in three variations : (a) circumferential (b) lateral (c) central or coronal
Cystic contents (aspirate): The cystic contents consist of clear yellowish fluid, in which cholesterol crystals may be present, and if the cyst infected it may show a purulent material .
A. NON INFLAMMED TYPE:
Lining derived from reduced dental epithelium, consists of 2-4 cell layers of non keratinized epithelium, without rete ridges.
Wall composed of thin fibrous connective tissue appearing immature, as it is derived from the dental papilla.
B. INFLAMMATORY TYPE :
Lining shows varying degrees of hyperplasia with rete ridges and occasionally even keratinization.
Wall is composed of mature connective tissue which shows infiltration by chronic inflammatory cells.
Focal areas of mucous cells can be seen in the lining. Small odontogenic epithelial islands can be seen in the wall.
DIFFERENTIAL DIAGNOSIS: Although it presents a unique feature, yet some lesions must be considered in its differential diagnosis : 1. Unicystic ameloblastoma 2. Adenomatoid odontogenic tumor.
1. Recurrence due to incomplete surgical removal.
2. Development of ameloblastoma either from lining epithelium or from odontogenic islands in the connective tissue wall.
3. Development of squamous cell carcinoma from same two sources.
4.Development of mucoepidermoid carcinoma from mucus secreting cells in the lining.
> Marsupialization ; It is indicated in children if the cyst is very large in size and the involved tooth/teeth are to be maintained.
> Enucleation with or without packing of defect when the possibility of the tooth erupting is low.
Behavior and prognosis : Recurrence rate is low . It is widely believed that ameloblastomas frequently arise in dentigerous cysts so lining of the cyst should be examined histopathologically . KERATOCYST
ODONTOGENIC KERATOCYST :
> The term OKC was first coined by Philisen in 1956.
> Its characteristic features first described by Pindborg & Hansen in 1963.
> Definition – According to WHO it is a benign uni or multicystic intraosseous tumor of odontogenic origin (dental lamina and its remnant) with characteristic lining of parakeratinised stratified squamous epithelium & potential for aggressive and infiltrative behavior.
> the lesion is named keratosis because the lining epithelium produces so much keratin that almost fills the cyst lumen .
> Keratin produced by cystic lining.
> Parakeratine lined cystic lesion within bone.
> Rare distinctive developmental odontogenic cyst from the dental lamina.
• The odontogenic keratocyst is a distinctive form of developmental odontogenic cyst that deserves special consideration because of its specific histopathologic features and clinical behavior.
• There is general agreement that the odontogenic keratocyst arises from cell rests of the dental lamina.
• This cyst shows a different growth mechanism and biologic behavior from the more common dentigerous cyst and radicular cyst.
• Growth may be related to unknown factors inherent in the epithelium itself or enzymatic activity in the fibrous wall.
• Several investigators suggest that odontogenic keratocysts be regarded as benign cystic neoplasms rather than cysts .
The primordial cysts are thin walled and are lined by a regular keratinized stratified squamous epithelium. The keratin formed by the epithelium is seen in two variants,
> parakeratinized – in which there is persistence of the nuclei
> orthokeratinized – in which the nuclei are absent.
Clinically, the parakeratinized variant appears to have a much higher incidence of recurrence .
COMPLICATIONS IN OKC : 1. Malignant transformation of cyst lining rare, but has been reported. 2. Recurrence high rate of recurrence.
possible reasons reported for high recurrence rate –
Presence of daughter cysts
Cystic lining is very thin and fragile, portions of which may be left behind
Epithelial lining of keratocysts have an intrinsic growth potential
new cysts can arise from basal cells of the oral mucosa
Patients with nevoid basal cell carcinoma syndrome (Gorlin- Goltz syndrome) have a particular tendency to form multiple keratocysts with other manifestations in different parts of the body (Multiple basal-cell carcinomas of the skin, rib and vertebrae anomalies, intracranial calcifications, frontal bossing, hypertelorism , and mandibular prognathism .palmar and plantar pitting ).
Other reasons are –
1. Thin, fragile lining is very difficult to remove completely.
2. New cysts develop from satellite cysts left behind.
3. Some cysts may be left behind in cases of Gorlin Gotz syndrome.
4. New cysts can also develop from basal cells of overlying oral epithelium, especially in ramus 3rd molar region .
> Swelling with or without pain > Discharge
> Displacement of teeth
> Occasionally paresthesia of lower lip.
> Expansion of the cyst is very minimal in the initial stage.
> Expansion of buccal cortical plate 30% in maxilla (third molar area followed by the cuspid region )and 50% in mandible ( occurring in the Ramus third molar area followed by the first and second molar areas and the anterior mandible ) .
Peak frequency in the 2nd and 3rd decades.
GENDER : more frequently in males than in females.
SITE : The mandible > maxilla Develop pathological fractures.
In many instances – free of symptoms until the cysts have reached a large size, involving the maxillary sinus and the entire ascending ramus, including the condylar and coronoid processes.
OKC tends to extend in the medullary cavity and clinically observable expansion of the bone occurs late.
RADIOGRAPHIC FEATURES : OKC demonstrate a well-defined radiolucent area with smooth and often corticated margins.
• Large lesions, particularly in the posterior body and ascending ramus of the mandible, may appear multilocular An unerupted tooth is involved in the lesion ; in such instances, the radiographic features suggest the diagnosis of dentigerous cyst .
• Uniform layer of stratified squamous epithelium, usually 5-8 cells in thickness.
• The basal layer exhibits a characteristic palisaded pattern with polarized and intensely stained nuclei of uniform diameter.
•The luminal epithelial cells are parakeratinized and produce an uneven or corrugated profile.
Flat epithelium and connective tissue interface absence of rete ridge.
Basal cell layer has columnar / cuboidal cells with reversely polarized nuclei, imparting a “picket fence” or “tombstone” appearance.
Small satellite cysts, cords, or islands of odontogenic epithelium may be seen within the fibrous wall.
Unilocular or multilocular radiolucency with well defined border and some times associated with sclerotic margin.
Usually extend in anteroposterior direction.
Large mandibular cysts deflect the neurovascular bundle into an abnormal position.
Neuropraxia may associated with infected cyst .
Treatment of keratocyst :
> Treatment should always be based on proper clinical assessment, accurate diagnosis and appropriate tests of the cystic aspirate.
Treatment options for keratocyst : • 1. Total enucleation and primary closer. The surgical procedure for treatment of a cyst with enucleation includes the following steps: 1. Reflection of a mucoperiosteal flap. 2. Removal of bone and exposure of part of the cyst. 3. Enucleation of the cystic sac. Care of the wound and suturing.
• 2. Enucleation with chemical fixation. recommended use of Cornoy’s solution after enucleation to destroy the daughter cysts and remnant lining. The Cornoy’s solution acts as chemo-cauterization to prevent recurrence.
•3. Marsupialization (usually not enough in keratocyst due to high recurrence rate) .
Marsupialization – the surgical opening of the (KCOT) cavity and a creation of a marsupial- like pouch, so that the cavity is in contact with outside for an extended period.
• 4. Resection.(in case of multiple recurrence)
> Surgical removal of segment of mandible or maxilla without maintaining the continuity of the bone >Recurrence rate 0%
• 5. Wide (local) surgical excision to prevent the recurrence .
It is also essential that patients with an OKC, especially if multiple, be evaluated medically to rule out the possibility of the jaw cyst-basal cell nevus-bifid rib syndrome .
A mild, tamer twist on tom yum, this iconic soup infuses sharp peppers, thinly sliced young galangal, crushed shallots, lemongrass stalks and tender strips of chicken. However, unlike its more watery cousin, its spicy blow is softened by a lashings of coconut milk. Topped with fresh lime leaves, this is a sweet-smelling concoction that’s both creamy and tempting.
Tom Kha Gai Soup is a traditional soup in Thai cooking. It is considered a ‘hot and sour’ soup (mostly from fresh lemon juice) with a base of broth and coconut milk.
Ingredients in Tom Kha Gai soup :
1 can (14 oz.) coconut milk
1 can (14 oz.) reduced-sodium chicken broth
6 quarter-size slices fresh ginger
1 stalk fresh lemongrass, cut in 1-in. pieces
1 pound boned, skinned chicken breast or thighs, cut into 1-in. chunks
1 cup sliced mushrooms
1 tablespoon fresh lime juice
1 tablespoon Thai or Vietnamese fish sauce
1 teaspoon sugar
1 teaspoon Thai chili paste
¼ cup fresh basil leaves
¼ cup fresh cilantro
Red Curry Paste: This is a paste made of red chilies, dried shrimp , lemongrass, galangal, kaffir limes, garlic, etc. It’s so flavorful and adds tons to curries, soups and marinades.
Kaffir Lime leaves: These are leaves from the kaffir lime tree and they have a spicy, and fragrant lime flavor .
Galangal: Galangal is similar to ginger, but it has a thinner skin, and a richer, spicier flavor.
Coconut Milk: Coconut milk is made by extracting the liquid from the grated meat of mature coconuts .
In a medium saucepan , First, heat up a bit of neutral oil in the pan and add sliced shallots, chopped lemongrass, and the sliced galangal over medium-low heat. Then fry the aromatics for a couple of minutes until the shallot is a little softened . Then, add the curry paste to the pan and cook it for a couple of minutes, stirring often . Then, add the kaffir lime leaves and the chicken broth and bring it to a simmer for 20 minutes.
Once the broth has reduced slightly, use a slotted spoon to scoop out the galangal, lemongrass, and lime leaves. At this point, add the chicken, fish sauce, palm sugar and coconut milk and simmer until the chicken is cooked through . Then, add the mushrooms and shrimp, season the soup with salt, add fresh lime juice and cilantro. Discard lemongrass. Garnish servings with basil and cilantro and it’s ready to go!
You can add a little chili oil to the soup to make it spicy, but it’s totally up to you !
Diabetes mellitus (DM) is a metabolic disorder characterized by hyperglycemia due to absolute or relative deficiency of insulin.
Diabetes is a metabolic dis- order whose exact cause remains still unknown. There is a disturbance of carbohydrate metabolism proper utilization with the result that there is hyper- glycaemia. The normal levels of blood sugar are dependent on the adequate amounts of insulin be- ing secreted in the body. Insulin is produced in the body by the beta cells of the islets of Langerhans of pancreas. Main stimu- lus for release of insulin is hyperglycaemia caused and there is deficiency of insulin required for its by ingestion of carbohydrates, hyperamino-acidae- mia dde to protein ingestion hormones like gluca- gon. gastrin, secretin pancreozymin and binding of insulin molecules to insulin receptors. Insulin fa- vours the entry of glucose into the liver, into mus- cles as glycogen and builds up adipose tissue by converting glucose into fat. Insulin secretion decreases with age since by the process of ageing the number of beta cells are lost by degeneration. Normally these cetls regenerate but in diabetes there is inherent defect in the regenera- tion of cells. Though mechanisms like lack of syn- thesis and release of insulin are operative in major- itý of diabetics yet other factors like defect in the transport mechanism of insulin, DNA sequence cod- ing insulin receptors and degenration of insulin on the cell surface may be operative.
Obese people are more prone to suffer from diabetes probably because obesity imposes a strain on the islets of langerhans and there is a rela- tive deficiency of insulin. Obese also show a rela- tive resistance to insulin due to reduction in the number of insulin receptors on target cells.
Exercise – Lack of physical effort and exercise promotes obesity and indirectly predisposes to dia- betes. Physical effort and leading an active life goes a long way in keeping one self trim and helps in the proper utilization of body glucose and maintains a homeostatic balance. Diet – Excessive intake of carbohydrates and re- fined sugars produces strain on the pancreas and this combined with sedentary occupation goes a long way in predisposing to diabetes.
Parity – Women with repeated pregnancies are more liable to develop diabetes since too many preg- nancies are a strain on the carbohydrate metabo- lism and often there is hormonal imbalance. Parity is an important predisposing factor in the causation of diabetes in middle aged women hav- ing more than seven children. All these factors go a long way in understanding the primary form of diabetes especially if one keeps in mind the faulty gene, over eating, obesity, lack of physical effort, racial, social and environmental factors in addition to hormonal imbalance.
Classification of diabetes mellitus 1. Type 1 diabetes mellitus A. Immune mediated B. Idiopathic 2. Type 2 diabetes mellitus 3. Other specific types: a. Genetic defects of beta cell function b. Genetic defects in insulin action c. Diseases of pancreas: pancreatitis, neoplasia, hemochromatosis, pancreatectomy d. Endocrinopathies: acromegaly, Cushing’s syndrome, hyperthyroidism pheochromocytoma, glucagonoma e. Drugs and chemicals: thiazides, corticosteroids, phenytoin, thyroid hormone f. Infections: congenital rubella, coxsackie, cytomegalo virus g. Uncommon forms of immunemediated diabetes h. Genetic syndromes: Down’s syndrome, Klinefelter’s syndrome, Turner’s syndrome 4. Gestational diabetes mellitus
TYPE 1 DM ( INSULIN DEPENDENT DIABETES MELLITUS ) : commonly in children and young adults . Pancreatic beta cells fail to respond to insulinogenic stimuli. There is also role of islet cell antibodies, insulin auto antibodies and auto immune mechanism. Most of these diabetics are under- weight, undernourished and their symptoms are se- vere. Presence of ketone bodies in the urine is quite common In such diabetics since their diabetes is brittle. These patients are more liable to develop complications. They are sensitive to insulin but do not respond to oral antidiabetic drugs. Type I A diabetes is a T-cell mediated autoimmune disease and may be associated with other autoimmune diseases like thyroid disease, Addison’s disease, vitiligo and pernicious anemia .Possible triggers are viral infections (coxsackie, rubella), bovine milk protein and nitrosuria compounds. Pancreatic islets are infiltrated with lymphocytes. Risk of developing DM is increased 10 fold in the relatives of type 1 DM patients.
TYPE 2 DM ( non insulin dependent diabetes mellitus ) : it was in adult generally above the age of 40 years (mostly obese ) . It is polygenic and multifactorial in origin involving genetic and environmental factors. Three basic pathophysiological abnormalities : a. Impaired insulin secretion b. Insulin resistance (inability of insulin to act on target tissues mainly liver and muscles) c. Increased hepatic glucose production . Patients have little tendency to ketosis and are relatively insensitive to insulin. Plasma insulin levels are either normal or raised. Genetic factors appear to play a major role in this form of diabetes and transmission is suggested to be due to an autosomal dominant trait. There are two main defects i.e. abnormal insulin secretion and insulin resistance to action in target organs. Many obese or overweight diabetics secrete large quantities of insulin but this insulin is ineffective at cellular level. There are insulin receptors on the cell wall and insulin attaches itself to these receptors before exerting its biochemical effect. Lack of adequate number of insulin receptors on the cell sur- face may be responsible for the induction of diabetes. Weight loss in such persons is known to result in increase in receptors and benefit such diabetics. In addition to the above two classical types of diabetes there is pancreatic diabetes, J type diabetes and young ketones resistant diabetes. There is hyperglycemia but endogenous insulin prevents the development of ketoacidosis. Hyperglycemia worsens insulin resistance and beta cell response to glucose (glucose toxicity) and both improve when glucose is normalized with the treatment. Many biologic products are secreted by adipocytes that modulate insulin secretion, insulin action, and body weight. Leptin and adiponectin improve insulin sensitivity while tumor necrosis factor alpha and resistin interfere with insulin action.
CLINICAL FEATURES : These are variable and may range from and due to acute complication like diabetic coma . Diabetes should be suspected if a patient has increased hunger (polyphagia ) thirst ( polydypsia ) and polyuria . Other symptoms are tiredness, fatigue, and irritability. Blurring of vision, frequent infections, and slow healing of wounds may also be present. The infections include bacterial and fungal infections of skin and genitalia. The patients with type 2 DM may present with the features of chronic neurological, cardiovascular, ophthalmic and renal complications . Chronic skin infections, generalized pruritus and fungal vaginitis are common. Females who have unexplained fetal loss or deliver large babies should be screened for DM. The patients may present with acute complications such as diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HSS) or features of chronic complications.
Complications of diabetes : Complications of diabetes may be acute in the form of diabetic coma which is a medical emergency and requires immediate management or chronic complications which are present in majority of patients. Diabetics are six to eight times more liable to heart disease than non- diabetics. Diabetes effects blood vessels both large (macrovascular disease) and small vessels particu- larly the capillaries (microvascular disease or microangiopathy). Macrovascular disease in the form of premature atherosclerosis accounts for much of morbidity in maturity onset diabetes. There is characteristic thickening of the intimal layer and li- pid material gets deposited in the intimal plaques. Aorta, carotids coronary arteries and vessels of the limbs are commonly involved. In microangiopathy there is thickening of başement membrane with hypertrophy and hyperplasia of the lining cells pro- gressing to vascular occlusion. In fact coronary heart disease is the major cause of death in diabetics after the age of 40. Ischaemic heart dis- ease in the form of myocardial infarction, angina pectoris is very common in diabetics. Again pain- less myocardial infarction explained on the basis of autonomic diabetic neuropathy or involvement of coronary vessels is common in diabetics as com- pared to non-diabetics. Diabetic cardiomyopathy, cerebrovascular accidents and hypertension are other vascular complications. gangrene of the foot occurs as a result of neuropathy microangiopathy and secondary infection. Renal lesions: Urinary tract infections, Glomerulosclerosis . GI manifestation – gastritis ( acute or chronic ) diarrhoea , nocturnal diarrhoea , paralytic ileus cholecystitis . Eye – diabetic retinopathy .
Urine Test : The urine is tested for the presence of glucose, ketones, and protein. Presence of albumin (>30 mg/dL) in the urine suggests nephropathy.
BLOOD TEST: The plasma glucose tests are performed for the diagnosis of DM (see above). The fasting plasma glucose is done after overnight fast (at least 8 hours fast). The random test is defined as without regard to time since the last meal. Oral glucose tolerance test (OGTT) is performed by giving 75 g glucose dissolved in water and measuring plasma glucose after 2 hours. The persons should be on unrestricted carbohydrate diet for 3 days before the test. The random blood sugar is performed first. If the random plasma glucose level is increased but not diagnostic (<200 mg/dL), fasting plasma glucose is measured. When the fasting plasma glucose level is <126 mg/dL, OGTT is performed. The criteria for the diagnosis of DM in pregnancy (gestational diabetes) are different and more stringent .
Serum Fructosamine Measurement : Serum fructosamine is formed by non-enzymatic glycation of serum proteins, mainly albumin. Its level reflects the glycemic control for the preceding 2 weeks. This is particularly useful for the assessment of the glycemic control in diabetic women.
Self Monitoring of Blood Glucose : Glucometers are available for the measurement of capillary blood glucose. The test can be performed by the patients themselves at home.
Continuous Blood Glucose Monitoring System : The blood glucose can be monitored continuously throughout 72 hours with the help of a subcutaneously placed sensor. This is useful in the detection of asymptomatic hypoglycemia.
Other Tests : Serum lipids are routinely measured. Patients with type 2 DM may have dyslipidemia characterized by high triglycerides, low HDL cholesterol, and presence of small dense LDL particles. These patients are more susceptible to atherosclerosis. Type 1 diabetics have raised triglycerides and LDL cholesterol but normal HDL cholesterol. Blood urea, serum creatinine, electrolytes, liver function tests are also performed.
Management of Diabetes : This includes diet modification, exercise, education and medications. Ideal goals of the glycemic control in patients with DM are as follows. However, these goals are individualized. 1. Average preprandial glucose values 90-130 mg/dL 2. Bedtime glucose value of 100-140 mg/dL 3. Peak postprandial glucose less than 180 mg/dL 4. The level of HbA1C less than 7% The management of patients with DM includes: a. Glycemic control b. Treatment of associated conditions like hyper- tension, dyslipidemia, obesity and cardiovascular disease c. Detection and management of diabetes related complications.
Complications of diabetes mellitus : Acute complications 1. Diabetic coma. 2. Non-ketotic hyperosmolar coma n 3. Skin infections (boils), urinary tract infections and pulmonary infections. Chronic complications 1. Vascular. Ischaemic heart disease, hypertension, cerebrovascular disorders, peripheral vascular disease, gangrene. 2. Renal. Chronic pyelonphritis, recurrent urinary tract infections, K.W. syndrome, papillitis necroticans, renal failure. 3. Neurological. Sensory and motor neuropathy, amyotrophy, autonomic neuropathy. 4. Gastrointestinal system. Dental sepsis, pyorrhoea, gastric distension, diarrhoea with or without steatorrhoea, cholecystitis. 5. Skin. Boils, trophic ulcer of the feet, genital infection, pruritis vulvae. 6. Eye. Retinopathy, changes in refraction requring frequent change in glasses, cataract, glaucoma, eye infections (iritis, iridocyclitis). B7. Respiratory. Pulmonary tuberculosis, bronchopneumonia, pneumonia. 8. Bones and joints. Osteoporosis, neuropathic joint. 9. Genitourinary system. Impotence in men, repeated abortions, miscarriage, stillbirths and big babies in women, hydramnios, toxaemia of pregnancy, intrauterine foetal death, prematurity, congenital anomalies and respiratory distress syndrome.
Management Steps in Diabetic Patients : Type 1 DM: The treatment of type 1 DM is lifelong insulin replacement. However, alpha glucosidase inhibitors (acarbose, miglitol) can be given to reduce carbohydrate absorption. Diet modifications, physical exercise and education are also important for the proper control of blood sugar. Type 2 DM: In obese type 2 patients, weight reduction should be achieved by diet modification and increased physical activity. Metformin is the first line therapy in obese patients. If this is inadequate, sulfonylurea, thiazolidi- nediones or alpha glucosidase inhibitors are added alone or in combination. If the combination of these drugs fails to control blood glucose levels, insulin therapy is instituted. Weight maintenance diet is prescribed to non-obese patients. Sulfonylurea is the first line therapy. If the blood glucose is not controlled by the maximum dose of sulfonylurea, other agents like biguanide or thiazoli- dinediones or both are added. If the combination of these drugs fails, insulin is indicated. Other indications of insulin in type 2 DM are (a) as a initial therapy in patients with severe weight loss, (b) patients with hepatic or renal disease where oral agents are contraindicated, (c) patients who are acutely ill (DKA, HHS) and (d) during pregnancy.
Diagnosis : The diagnosis is made by the measurement of plasma or capillary blood glucose, which is low.
Treatment : • If the patient is able to swallow, rapidly absorbable carbohydrates can be administered orally (glucose and sugar). Alternatively milk, fruit, candy bars, or biscuits may be given to patients with mild hypoglycemia. • If the patient is unable to swallow or is in severe hypoglycemia, intravenous glucose (20-50 ml of 50% dextrose) is given initially. This is followed by an infusion of 10% dextrose to maintain blood glucose above 100 mg/dL. • Glucagon injection (1 mg SC or IM) may be given in severe hypoglycemia if intravenous access can not be established promptly. • Prevention of hypoglycemia includes proper education regarding causes and symptoms of hypoglycemia and proper adjustment in medication and diet.