CASE REPORT (19 APRIL 2012)

Patient Identity
NAME
Date of Visit NRM

Sex
Address Phone Age Occupation

: DS : 19 april 2012 : 03546902 :M : Jl KH Marzuki Blok I No 38 : 0897 8282 0521 : 58 y : retired employee

Anamnesis
Patient male 58 accompanied by her daughter complained

about sharp pain when opening mouth, drinking, and swallowing. Patients not being able to eat, so he only ate blended food. He also felt burning pain in whole mouth. No t preceded by fever, ulcers are not preceded by vesicles but patient admitted have frequent fever. Patients not admitted there are food or drugs allergic exist Patients admitted that this condition has never happened before OS has no family history with the same lesions

Anamnesis (cont)
Previously, patients came to some department in

Harapan Kita Hospital and received 12 drugs from integrated treatment. One of those is gargle but he didnt feel any better. Patients admitted that hes suffered from DM, Hypertension, Heart Disease, Pulmonary Disease, GIT Disease (Gastritis) since 3 months ago, and Kidneys problem. a week ago, dermatologist found there are pus and blood inside patients mouth so he was referred to OM with WD/ Susp SJS.

Anamnesis (cont)
RS Harapan Kita Heart and Pulmonary Disease Referred to ENT, Ophtalmology, Dermatology,

Referred to OM Department

Susp SJS

Prescribe received

Carveditol Valsartan FG Troches Is prinol Lameson Acyclovir Tobrosan C-cenclo ly Bactoderm Simarc Tantum verde Gentsimycin salt

1 x 6,25 mg 1 x 40 mg 4 x 1 mb 3 x 1 mb 1 x 16 mg 5 x 200 mg 4 x hr (2 tetes ODS) 6 x hr (1 tetes ODS) 2 x hr (setelah kompres 1 x 2 mg (kumur jangan telan) 3 x hr (untuk mata)

Extra Oral Examination

Lymph gland Right Submandibula Left Submandibula Submental Right Cervical Left Cervical Palpable, rubbery, no pain Palpable, hard, no pain Palpable, rubbery, no pain Impalpable Impalpable Desquamation and crust Simetry TAK TAK

Lips Face Circum Oral Others

Intra Oral Examination

Debris and Kalkulus (+)
OHI-S bad Buccal mucosa : erosion (right and left)

Labial mucosa : erosion

Hard palate : erosion Soft palate : erosion Dorsum of the tongue : erosion Floor of the mouth : erosion Ventral of the tongue : ulceration on right ventral 1x3 mm

Diagnosis and Treatment Plan

Diagnosis : Susp. HAEM
Treatment Plan : CIE : Cleaning teeth using sterile gauze + warm salt water / gargling warm salt water 4 times a day Replacing tantum verde with minosep 4 times a day Desquamation & Crust lips : Prednison 50mg, Avil 50 mg, Ad. Vaselin album 30 gr oles bibir 4 dd Pro periksa lab DPL, anti HSV1 anti HSV2 Pro kontrol 25 April 2012

Erythema Multiforme
Erythema multiforme (EM) is a self-limiting

hypersensitivity reaction characterized by target skin lesions and/or ulcerative oral lesions. Divided into two subtypes: a minor form, usually associated with an HSV trigger, and a major severe form, triggered by certain systemic drugs. EM may occur once or recur.

Etiology of EM
The basic cause of EM is unknown
The most common triggers : HSV and drug reactions.

Most frequently : NSAIDs, sulfonamides, anticonvulsant, trimethoprim-sulfonamide combinatios, allopurinol and penicilin. Other triggers : progesterones, mycoplasma benign and malignant tumors, radiotherapy, chrons disease, sarcoidosis, histoplasmosis and infectious mononucleosis

HAEM
20-40 % of the cases of single episodes of EM and 80% of

recurrent EM Infections frequently reported include HSV infection (due to HSV types 1 and 2) Herpes antigens have been demonstrated in the skin and immunocomplexes obtained from patients with EM. Many investigators now believe that the major cause of EM is a cellular immune response to HSV antigens deposited in keratinocyte of the skin and mucosa Tendency to develop mucous membran lesions during episodes of HAEM appears to be genetically determined and related to spesific human leukocyte antigens (HLA) types

Histopathology
The microscopic pattern of EM consists of epithelial hyperplasia and

spongiosis. Basal and parabasal apoptotic keratinocytes are also usually seen. Vesicles occur at the epithelium connective tissue interface. Epithelial necrosis is a frequent finding. Connective tissue changes usually appear as infiltrates of lymphocytes and macrophages in perivascular spaces and in connective tissue papillae. Immunopathologic studies are nonspecific for EM. The epithelium shows negative staining for immunoglobulins. Vessels have, however, been shown to have IgM, complement, and fibrin deposits in their walls. This latter finding has been used to support an immune complex vasculitis cause for EM. Autoantibodies to desmoplakins 1 and 2 have been identified in a subset, of EM major-affected patients, suggesting that both cell-mediated and humoral immune systems may contribute to the pathogenesis of EM.

Clinical Manifestation
The disease more frequently affects young men between the ages of 20 and 30 years.
The oral lesions present as

coalescing small vesicles that rupture within two or three days, leaving irregular, painful erosions covered by a necrotic pseudomembrane. Predilection : lips, buccal mucosa, tongue, soft palate, and floor of the mouth

Clinical Manifestation
The skin manifestations consist of

erythematous, flat, round macules, papules, or plaques, usually in a symmetrical pattern. The characteristic skin patterns are target- or iris-like lesions Skin bullae may occasionally be seen. Conjunctivitis, balanitis, vulvitis, and prodromal symptoms such as headache, malaise, arthralgias and fever, may also be present.

Differential Diagnosis

When target, or iris, skin lesions are present, clinical diagnosis is usually straightforward. However, in the absence of these or any skin lesions, several possibilities should be considered for the oral expression of this disease. Included would be primary HSV infections (Table 2-4), aphthous ulcers, pemphigus vulgaris, mucous membrane pemphigoid, and erosive lichen planus. The general lack of systemic symptoms; the favored oral location of the lips, buccal mucosa, tongue, and palate (rarely gingiva); the larger ulcers (usually not preceded by blisters); the presence of target skin lesions; and a history of recent drug ingestion or infection should favor a diagnosis of EM.

Treatment and Prognosis

Keeping the mouth clean with bland mouthrinses

Initiating factor should be sought

topical corticosteroids with antifungals may help control disease.

Acyclovir at 400 to 600 mg daily may be effective in patients who have an HSV-triggered disease.
Supportive measures, such as oral irrigation, adequate

fluid intake, and use of antipyretics If the patient is dehydrated as a result of an inability to eat because of oral pain , intravenous rehydration maybe necessary along with topical anesthetics agents

Gastritis
Gastritis is an inflammation of the stomach lining. Most

often the cause is infection Helicobacter pylori that causes stomach ulcers. An autoimmune disorder, a backup of bile into the stomach, or long term use of NSAIDs, such as ibuprofen, coffee and acidic beverages, too much stomach acid (such as from stress) Gastritis can occur suddenly (acute gastritis) or gradually (chronic gastritis). In most cases, gastritis does not permanently damage the stomach lining.

Sign and Symptoms

The most common symptoms of gastritis are stomach upset and pain. Other possible symptoms include: Indigestion (dyspepsia) Heartburn Abdominal pain Hiccups Loss of appetite Nausea Vomiting, possibly of blood or material that looks like coffee grounds Dark stools

Diagnosis
Several tests can be used to make a diagnosis. These

include endoscopy of the stomach and take samples from the lining if needed. The laboratory tests that may need will depend on the cause of the gastritis. A stool test may be used to check for the presence of blood, or a biopsy may be taken of the tissues of your esophagus or stomach. A breath test may detect H. pylori or samples from your esophagus or stomach may be taken to look for this bacteria

Treatment
Treatment of gastritis depends on the cause of the problem. Eliminate the causative of gastritis. Eat a fiber rich diet. Foods containing flavonoids, like apples, celery, cranberries

(including cranberry juice), onions, garlic, and tea may stop the growth of H. pylori. Avoid high fat foods. In animal studies, high fat foods increase inflammation in the stomach lining If H. pylori is present, inhibitors of gastric acid secretion and antimicrobial agents are recommended.

Diabetes mellitus (DM) is a clinically and genetically heterogenous metabolic disease characterized by:
1. 2. abnormally elevated blood glucose levels (hyperglycemia), and, dysregulation of carbohydrate, protein, and lipid metabolism

Primary feature: chronic hyperglycemia

Defect in insulin secretion

Cells resistance to insulin

Diabetes mellitus: Classification

Etiologic classification of diabetes mellitus (American

Diabetes Association, 1997):

Type 1 diabetes mellitus
(formerly juvenile diabetes, insulin-dependent diabetes, or type I) Truly dependent on insulin therapy

Type 2 diabetes mellitus

(formerly adult-onset diabetes, non-insulin-dependent diabetes, or type II) may benefit from insulin therapy but are not dependent on it for survival

Other specific types of diabetes mellitus genetic defects of beta cell function, fenetic defects in insulin action, disease of exocrine pancreas, endocrinopathies, drugs or chemical induced, infections, immune-mediated diabetes, and other genetic syndromes

Gestational diabetes mellitus

occurs during pregnancy and usually resolves after delivery

Patophysiology
Carbohydrates are broken down into glucose molecules

Glucose is absorbed into the bloodstream ( blood glucose levels )

Stimulate pancreatic beta cells Insulin

Glucose cannot enter target cells

Glucose enter target cells

Note:

Blood glucose levels

Insulin binds to specific cellular receptors and facilitates entry of glucose into the cell

CLINICAL PRESENTATION

Polydipsia (excessive thirst) Polyuria (excessive urination) Polyphagia (excessive hunger) Unexplained weight loss Changes in vision Weakness, malaise Irritability Nausea Dry mouth Ketoacidosis

Diagnostic Criteria for DM

Normal Fasting glucose 2 h postparandial plasma glucose OGTT (not recommended for routine clinical use) <110 mg/dL <140 mg/dL Impaired Fasting Glucose 110 126 mg/dL 140 200 mg/dL DM 126 mg/dL 200 mg/dL

Plasma glucose at 2 h 200 mg/dL

These criteria should be confirmed by repeating testing on a

different day Fasting: no caloric intake for at least 8 hours OGTT: oral glucose tolerance test performed using an oral load of 75 g anhydrous glucose dissolved in water

Management
The primary treatment goals : Achieving of blood glucose levels that are as close to normal as possible Prevention of complications The mainstay treatments: Diet Exercises Weight control Drugs (medication) Education

DM Medications
Primary medications:
DM type 1 insulin ; DM type 2 Oral agent + insulin

Oral Agents Sulfonylurea insulin secretion by pankreas glucose entry Meglitinides (Glinid) Stimulation of insulin secretion by pankreas (different mecanism from SU) SE : hipoglikemia Biguanides Thiazolidinedio ne A-glukosidase inhibitor derive absorption capacity of carbohidrate from bowels

Preventing Increase glikogenolisis by tissue/cell liver sensitivity for insulin and decrease hepaticglucone ogenesis Hypoglycemia less common hipoglikemia

SE : hypoglikemia

hipoglikemia

 Diagnosis : Susp. HAEM Clinical features : desquamation, crust, bleeding Prescribed : acyclovir Lesions including another mucosa : conjungtiva DD : SJS Treatment Plan : CIE : Cleaning teeth using sterile gauze + warm salt water / gargling warm salt water 4 times a day Replacing tantum verde with minosep 4 times a day Desquamation & Crust lips : Prednison 50mg, Avil 50 mg, Ad. Vaselin album 30 gr oles bibir 4 dd Lab finding : DPL, anti HSV1 anti HSV2 existence of HSV infection Pro kontrol 25 April 2012