Category: General Medicine

MANAGEMENT OF HYPERTENSION

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(A)

  1. Quantification of cardiovascular risk(CVR)
  2. Threshold for intervention
  3. Treatment targets
  4. Non-drug therapy
  5. Drug therapy – Antihypertensive drugs & their choice
  6. Emergency treatment of accelerated phase/Malignant hypertension
  7. Refractory HT
  8. Adjuvant drug therapy

(B)

🔅General Measures(Lifestyle Modification):
  1. Relief of stress
  2. Salt restriction – NaCl upto 5g/day help reduce BP. Diet rich in potassium & calcium should be employed
  3. Weight reduction
  4. Control of risk factors:
  • Restriction of cholesterol & saturated fat in diet reduces the atherosclerotic complications
  • Alcohol, smoking – ❌🚭
  • Control of blood sugar level in diabetics

5. Regular exercise: Jogging & swimming – ⬇️ Arterial pressure

(1) Quantification of Cardiovascular Risk:

• Objectives

🔅 To reduce the incidence of adverse cardiovascular events viz coronary heart disease, stroke & heart failure

• Benefits:

🔅Diuretics or β blockers have shown to reduce the risk of

  • CAD by 16%
  • Stroke – 13%
  • Cardiovascular death – 21%
  • Mortality – 13%

🔅Most of the excess Morbidity & Mortality associated with HT is attributable to CAD. Total CVR = CAD risk x 4/3

(2) Threshold for intervention:

  • Systolic & Diastolic BP – predictors of CVR (≥ 140/90 mm Hg)
  • The threshold for initiating AHT is lower in diabetics/cardiovascular disease as they are at a higher risk
  • The threshold for treatment of HT in elderly is same as in younger patient.

🔅 Hypertension in old age:

  1. Prevalence – half of the population over the age of 60
  2. Risks – MI, heart failure, stroke
  3. Benefit – from Anti-hypertensives is greatest in older people
  4. Target BP – similar to that for younger patient
  5. Tolerance – Well tolerated
  6. Drug of choice – low dose thiazides

Target BP during AHT

(3) Treatment Targets:

  • Optimum BP (130/83) for reduction of major cardiovascular events
  • improve screening
  • Follow up every 3 months

(4) Non-drug therapy ~ General measures

(5) Drug Therapy:

remember – ABCD👇🏻

NOTE: 🔎

A. ACE Inhibitors:

👉🏻Patients with renal artery stenosis/impaired Renal function (given with utmost care)

⬇️

Reduction of filteration pressure in the glomeruli

⬇️

Renal failure

Hence contraindicated! ❌☝🏻

👉🏻These agents also reduce the progression of Nephropathy in type II diabetes

👉🏻Level of electrolytes & creatinine should be checked before & after 1-2 weeks.

B. ARB’s

👉🏻Have lesser side effects of cough & angioedema than ACE inhibitors

C. Beta-blockers:

👉🏻These drugs are not used now as first line AHT; except in patient with Angina

👉🏻Labetalol & Carvedilol: Have better effect when combined. Labetalol is used as infusion in malignant phase HT.

D. CCB’s

👉🏻The dihydropyridines are effective, well-tolerated particularly in older people

👉🏻Rate–limiting CCB’s: HT with angina. Bradycardia may occur

  • S/E – Constipation(Verapamil)
  • Tachycardia(Nifedipine)

E. Thiazides & other Diuretics:

👉🏻The loop diuretics have few A/D over thiazides unless there’s renal impairment.

Chart showing Mode of Action & Side effects of AHT’s☝🏻

The influence of comorbidity on the choice of antihypertensive drug therapy

Management of hypertension: British hypertension society guidelines

🔅Choice of AHT drug:

Criteria:

  • Age & ethnic background
  • Cost, convenience
  • Response to initial therapy
  • S/E

A = ACE inhibitor (consider AT-II receptor antagonist if ACE-intolerant); C = Calcium channel blocker; D = thiazide-type diuretic)

(6) Emergency treatment of accelerated phase/Malignant hypertension

🔅 In accelerated phase HT, lowering BP too quickly may compromise tissue perfusion & can cause –

  • Cerebral damage
  • Occipital blindness
  • Coronary/Renal insufficiency

🔅150/90 mm Hg within 48 hours is ideal along with cardiac failure/hypertensive encephalopathy

🔅Avoid parenteral therapy

  • iv/im: Labetalol (2mg/min)
  • iv: Glyceryl trinitrate(0.6-1.2mg/hour)
  • im: Hydralazine(5-10 mg aliquots repeated at 1/2 hourly interval)
  • iv: Na Nitroprusside(0.3 – 1 μg/kg body wt/min)

(7) Refractory HT:

🔅Causes of treatment failure include:

  1. Non-adherence to drug therapy
  2. Inadequate therapy
  3. Renal artery stenosis

(8) Adjuvant Drug Therapy:

📌Aspirin – Antiplatelet

  • ⬇️ Cardiovascular risk
  • S/E: Bleeding

📌Statins – Reduced risk by treating hyperlipidaemia

Dr. Mehnaz Memon🖊

References: Davidson’s Principles and Practice of Medicine Textbook

10 Steps to Accurate Manual Blood Pressure Measurement

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Image Via: medical.docs

Step 1 – Choose the right equipment: 
What you will need: 
1. A quality stethoscope 
2. An appropriately sized blood pressure cuff 
3. A blood pressure measurement instrument such as an aneroid or mercury column sphygmomanometer or an automated device with a manual inflate mode.

Step 2 – Prepare the patient:Make sure the patient is relaxed by allowing 5 minutes to relax before the first reading. The patient should sit upright with their upper arm positioned so it is level with their heart and feet flat on the floor. Remove excess clothing that might interfere with the BP cuff or constrict blood flow in the arm. Be sure you and the patient refrain from talking during the reading.

Step 3 – Choose the proper BP cuff size: Most measurement errors occur by not taking the time to choose the proper cuff size. Wrap the cuff around the patient’s arm and use the INDEX line to determine if the patient’s arm circumference falls within the RANGE area. Otherwise, choose the appropriate smaller or larger cuff.

Step 4 – Place the BP cuff on the patient’s arm: Palpate/locate the brachial artery and position the BP cuff so that the ARTERY marker points to the brachial artery.  Wrap the BP cuff snugly around the arm.

Step 5 – Position the stethoscope: On the same arm that you placed the BP cuff, palpate the arm at the antecubical fossa (crease of the arm) to locate the strongest pulse sounds and place the bell of the stethoscope over the brachial artery at this location.

Step 6 – Inflate the BP cuff:Begin pumping the cuff bulb as you listen to the pulse sounds. When the BP cuff has inflated enough to stop blood flow you should hear no sounds through the stethoscope. The gauge should read 30 to 40 mmHg above the person’s normal BP reading. If this value is unknown you can inflate the cuff to 160 – 180 mmHg. (If pulse sounds are heard right away, inflate to a higher pressure.)

Step 7 – Slowly Deflate the BP cuff: Begin deflation. The AHA recommends that the pressure should fall at 2 – 3 mmHg per second, anything faster may likely result in an inaccurate measurement.

Step 8 – Listen for the Systolic Reading: The first occurence of rhythmic sounds heard as blood begins to flow through the artery is the patient’s systolic pressure. This may resemble a tapping noise at first.

Step 9 – Listen for the Diastolic Reading: Continue to listen as the BP cuff pressure drops and the sounds fade. Note the gauge reading when the rhythmic sounds stop. This will be the diastolic reading.

Step 10 – Double Check for Accuracy: The AHA recommends taking a reading with both arms and averaging the readings. To check the pressure again for accuracy wait about five minutes between readings. Typically, blood pressure is higher in the mornings and lower in the evenings. If the blood pressure reading is a concern or masked or white coat hypertension is suspected, a 24 hour blood pressure study may be required to assess the patient’s overall blood pressure profile.

Further Reading/References:

https://www.suntechmed.com/support/product-training-tutorials/1692-how-to-measure-blood-pressure

BURKITT LYMPHOMA

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It is also called as ‘African jaw lymphoma’. It is a lymphoreticular cell malignancy. In the African form jaw involvement is 75% and in cases of the American form, abdomen involvement is more common. It is a B-cell neoplasm.

Etiology

• Epstein-Barrvirus(EBV)which also causes nasopharyn- geal carcinoma and infectious mononucleosis is considered to be the etiological factor. There are higher EBV antibody levels in patients of Burkitt’s lymphoma.

Clinical Features

  • Age and sex—peak incidence is in children between 6to 9 years. Males are affected more commonly than the females, with a ratio of 2:1.
  • Site distribution—more are found in maxilla than in mandible, where it may spread rapidly to the floor of the orbit. Almost always occurs in molar area. In the African form, more than one quadrant is involved while in the American form, only one quadrant is involved.
  • Onsetandprogress—the most important hall mark of this tumor is the fast growth with a tumor doubling time of less than 24 hours.
  • Symptoms—the most common presenting features are swelling of the jaws, abdomen and paraplegia. It is painless.
  • Sign—peripheral lymphadenopathy is common.
  • Prognosis—it is rapidly fatal in the absence of treatment,with death occurring within 6 months.

Oral Manifestations

  • • Onset and extent—it begins generally as a rapidly growing tumor mass of the jaws, destroying the bone with extension to involve maxillary, ethmoid and sphenoid sinus as well as orbit.
  • Symptoms—loosening or mobility of permanent teeth.There is gross distortion of the face due to swelling. Paresthesia and anesthesia of inferior alveolar canal or other sensory facial nerves are common.
  • Signs—gingiva and mucosa adjacent to the affected teeth become swollen, ulcerated and necrotic. As the tumor mass increases, the teeth are pushed out of their sockets. Swelling of the jaw occurs and it may cause facial asymmetry. They are capable of blocking nasal passages, displacing orbital contents and eroding through skin. There is derangement of arch and occlusion. There may be large quantity of mass protruding into the mouth, on the surface of which may be seen rootless, developing permanent teeth.
  • Spread—once the tumor perforate the bone, it is initially confined by the periosteum, but subsequently it spreads to the soft tissues of the oral cavity and face where rapid tumor growth soon obliterates the entire face and skin becomes tense and shiny.

Histology

Shows characteristic starry sky appearance.

  1. Radiographic Features
    • Motheaten appearance—small radiolucent foci scattered throughout the affected area. These small foci coalesce and form a multilocular moth eaten appearance.
    • Sunray appearance—if periosteum is elevated, it will produce sunray appearance.
    • Margins—margins are ill defined and non-corticated.
    • Shape—they expand rapidly and are ballooned shaped.
    • Teeth—Lesions are osteolytic with loss of lamina dura about the erupted teeth and crypts of developing teeth are enlarged.
    • Effect ons urrounding structures—they expand very rapidly and breach its outer cortical limits.
  1. Diagnosis
  2. • Clinical diagnosis—swelling of the jaw and abdomen with peripheral lymphadenopathy can give clue to the diagnosis.

• Radiological diagnosis—moth eaten appearance is seen with loss of lamina dura around the teeth.

• Laboratorydiagnosis—monotonous sea of un differentiated monomorphic lymphoreticular cells, usually showing abundant mitotic activity. There is also hyperchro- matosis and loss of cohesiveness. Characteristic ‘starry sky’ appearance is seen.

Management

• Cytotoxicdrugs—cytotoxicdrugs like cyclophosphamide 40 mg/kg in single IV administration and repeated about 2 weeks later. Vincristine and methotrexate have been successful in some cases.

• Multiagent chemotherapy—combination of drugs such as cyclophosphamide, vincristine and methotrexate give better results than any single drug. Majority of patients show dramatic response to the therapy. The swelling regresses and the displaced teeth return to their normal position within 1 to 2 weeks.

REFERENCE- SHAFER’S TEXTBOOK OF ORAL PATHOLOGY AND ANIL GHOM TEXTBOOK OF ORAL MEDICINE

HODGKIN’S AND NON-HODGKIN’S LYMPHOMA

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  • Primary tumors of the lymphoid system
  • Cancers involving lymphocytes during maturation or storage in the bone marrow
  1. Hodgkin’s lymphoma
  2. Non-Hodgkin’s lymphoma
  3. Burkitt’s lymphoma

Hodgkin’s Lymphoma

Hodgkin’s disease (HD) is a lymphoid malignancy characterized by the presence of Reed-Sternberg cells of B cell origin. The disease arises usually in single nodal area and successively spreads to contiguous lymph node areas. Extranodal involvement is rare.

Types (Histological)

• Lymphocyte predominant—abundant lymphocytes, few plasma cells, occasional Reed-Sternberg cell, localized involvement of one side of diaphragm and most favorable prognosis.

• Mixed cellularity—lymphocytes, plasma cells, eosino- phils, easily identified Reed-Sternberg cell.

• Nodular sclerosis—sparse lymphocytes, stromal cells, fibrosis and numerous but bizarre Reed-Sternberg cells. It has poor prognosis.

• Lymphocyte depletion—lymphocytes, plasma cells, eosinophils with localized involvement.

ETIOLOGY

  • Unkonown
  • However both genetic and environmental factors including EBV ( Ebstein Barr Virus) play role in pathogenesis.

CLINICAL FEATURES

  • • Age and sex—it is characterized by a bimodal age incidence, peak one in young adults and the second in the 5th decade of life with equal distribution between sexes.
  • First sign – asymptomatic enlargement of a supradiaphragmatic lymph node often in the neck
  • .Symptoms—theinvolvednodesarepainless.Generalized weakness, loss of weight, cough, dyspnea and anorexia are seen. Pain in back and abdomen owing to splenic enlargement, due to pressure of enlarged nodes or involvement of vertebrae.
  • Pel Ebstein fever—characteristic features of this disease are Pel-Ebstein fever, a cyclic spiking of high fever and generalized severe pruritis of unknown etiology.
  • Mediastinal lymph node involvement is common
  • Night sweats, fever, weight loss
  • Rarely produces oral manifestations

Hodgkin’s lymphoma. This high-power photomicrograph shows the characteristic Reed-Sternberg cell (arrow) of Hodgkin ‘s lymphoma, identifiedby its “owl-eye” nucleus.

  1. Radiographic Features
    • Site—it is rarely seen in jaws. The common regions are the posterior maxilla and mandible.
    • Appearance—malignant lymphoma arising in the oral cavity spreads to bone and cause irregular bone loss to the area of the lesion. There are radiolucent areas sepa- rated from each other by normal appearing bone which later become confluent, unless treatment is carried out.
    • Margins—typically,theradiolucentlesionshavediffuse ill defined margins which suggest infiltration of bone.
    • Osteoblastic type—osteoblastic type is uncommon in jaws, but it is seen in the vertebrae and pelvis. In it, there is frank sclerosis with filling of the marrow spaces by bone. It presents as grayness or whiteness which is abnormal. The margins may be well defined and sharp or irregular and trailing off gradually into the normal bone.

Diagnosis

  • Clinicaldiagnosis—discreteenlargementoflymphnode which is rubbery in consistency with some systemic signs.
  • Radiologicalfeatures—thereisfociofradiolucencyseen in the jaw.
  • Laboratorydiagnosis—itischaracterizedbyreplacement of normal lymph node architecture by an admixture of malignant lymphoid cells and non-neoplastic inflammatory cells. Characteristic Reed Sternberg cells are present. Multinucleated giant cells are also present. There is also presence of anemia which is normocytic and normochromic. ESR is raised. There is also raised level of LDH.

MANAGEMENT

Localized disease: The patients with localized disease (IA, IIA) are treated with 3 cycles of chemotherapy (ABVD-doxorubicin, bleomycin, vinblastine and dacarbazine) followed by radiotherapy of involved nodal areas. 

Extensive disease: Patients with B symptoms or extensive disease receive complete course (6-8 cycles) of ABVD chemotherapy.

Long-term cure can be achieved in >90% patients with localized disease and in 50-75% patients with extensive disease.

Non-Hodgkin’s Lymphoma

It is also called as ‘lymphosarcoma’. In this group, there is neoplastic proliferation of lymphoid cells, usually affecting the B-lymphocytes. Unlike Hodgkin’s lymphoma, the disease is frequently widespread at the time of diagnosis, often involving not only the lymph nodes but also bone marrow, spleen and other tissue. Early involvement of bone marrow is typical of this lymphoma.

Types (Histological)

  • Nodular—neoplastic cells tend to aggregate in such a way that large clusters of cells are seen.
  • Diffuse—thereismonotonousdistributionofcellswith no evidence of nodularity or germinal center pattern.
  • Etiology
  • Viral—the etiology is unclear but herpes virus and Epstein barr etiology has been suggested.
  • Immunological—there may be induced immunologic effect permitting a malignant clone to proliferate.
  1. Clinical Features
    • Age and sex—it affects persons of all ages from infants to the elderly. But is commonest in middle age group. Males are affected more commonly than the females.
    • Onset—the onset of symptoms may be insidious. Painless lymph node enlargement of abdominal and mediastinal region are the most common finding. Very often the first group of lymph nodes affected may be cervical, axillary or inguinal.
    • Symptoms—the patient complains of tiredness, loss of weight, fever and sweating. Pain is the main symptom of bone involvement which may present as a patho- logical fracture. Patient may complain of abdominal pain, nausea, vomiting, diarrhea or intestinal obstruc- tion which may occur due to involvement of gastro- intestinal tract. Pressure effect of lymphoma may cause dysphagia, breathlessness, vomiting, intestinal obstruction or ascites and paraplegia.
    • Signs—if liver and spleen are involved, hepato- splenomegaly is present. The growth is fleshy and is prone to ulceration.

The matted, nontender lymph node enlargement in the lateral cervical region represents a common presentation of lymphoma.

Oral manifestations

  • Gingival or mucosal tissue swelling or masses
  • Rapid growth of tumour from non-healing tooth extraction site.
  • Paresthesia or anaesthesia due to nerve invasion

Radiographic Features

• Appearance—asthediseaseprogressessmallradiolucent foci scattered throughout the area may be seen. Subsequent radiographs of the expanding lesion will show that these small foci have coalesced to form large multilocular moth eaten radiolucency with poorly defined margins.

• Margins—lesion blends imperceptibly with adjacent normal bone, in most of the cases.

• Effect on surrounding structures—lesions may cause marked expansion of bone. Erosion and perforation of cortex may occur.

• Maxillary sinus involvement—if the lesion involves maxillary sinus, possible opacification with breached cortical walls and associated paracentral or intracentral mass.

• Teeth—cortices of unerupted tooth buds and lamina dura of adjacent teeth are lost. Teeth may be resorbed.

Diagnosis

  • Clinical diagnosis—bluish color mass of the palate with multiple lymph node involvement may suspect the diagnosis of non-Hodgkin’s lymphoma.
  • Radiological features—expansion of bone with radio- lucency is present.
  • Laboratory diagnosis—blood count usually shows hypersplenism or hemolytic anemia. The reduced WBC and RBC counts are seen along with reduced hemo- globin levels and reticulocytosis. In some cases, there may be slight increase in lymphocytes and thrombo- cytopenia. Moderate degree of anemia will also present when there is considerable bone marrow involvement. Some very aggressive high grade non-Hodgkin’s lymphomas are associated with very high urate levels which can precipitate renal failure.

Treatment

The disease stage is determined after clinical evaluation and investigations.
Treatment of low grade lymphoma: It depends on the stage of the disease and clinical status.

  • Asymptomatic patients generally do not require therapy.
  • Symptomatic localized (stage I) disease can be treatedwith radiotherapy.
  • Symptomatic patients with extensive disease (stage III,IV) are treated with chlorambucil or combination chemotherapy (CVP; cyclophosphamide, vincristine, and prednisolone or CHOP; cyclophosphamide, doxorubicin, vincristine and prednisolone).
  • Other newer effective agents are fludarabine, monoclonal antibody (anti-CD20) with or without radionuclides, and lymphoma vaccine.
  • The relapse following therapy is common. Hence, low grade NHL is generally not curable. However, the cure is now possible in some cases with the use of radio- immunotherapy.
  • Treatment of high grade lymphoma:
  • Localized high grade NHL (stage I and non-bulky stage II) is treated with three cycles of chemotherapy (CHOP with monoclonal antibody, anti-CD20) followed by radiotherapy.
  • Extensive disease (bulky stage II, stage III, and stage IV) is treated with six to eight cycles of chemotherapy.
  • Autologous bone marrow transplantation is indicatedin relapsed cases.
  • The cure rate is 60-90% in stage I and II and 30-40% instage III and IV.

REFERENCE- SHAFER’S TEXTBOOK OF ORAL PATHOLOGY, ANIL GHOM TEXTBOOK OF ORAL MEDICINE AND GOGLE SLIDE SHARE

REITER’S SYNDROME

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Reiter’s syndrome is associated with urethritis, balanitis, conjunctivitis, and mucocutaneous lesions.

 It is a disease of unknown aetiology, although there is evidence of an infec- tious origin.

It is one of the most common complications of non-specific urethritis and it clinically mimicks gonorrhoea, although the urethral discharge is negative for Neisseria.

CLINICAL FEATURES

>Reiter’s syndrome is more prevalent in young adult men, usually between 20 and 30 years of age. 

>The male-to-female ratio is 9:1. 

>There is a typical tetrad of manifestations: non- gonococcal urethritis, arthritis, conjunctivitis, and mucocutaneous lesions. 

>Urethritis may be the first sign. The urethral discharge is usually associated with itching and burning sensation. 

>The arthritis is often bilaterally symmetrical and usually polyarticular.

 >Conjunctivitis is often so mild as to be overlooked. 

>The skin lesions are similar to those seen in keratoderma blennorrhagica and consist of red or yellow keratotic macules or papules which eventually desquamate.

Oral Manifestations

Sites—it is seen on the buccal mucosa, lips and gingiva.

Oral lesions appear as painless, red, slightly elevated areas, some- times granular or even vesicular, with a white circinate border on the buccal mucosa, lips, and gingiva. 

The palatal lesions appear as small, bright red purpuric spots, which darken and coalesce, while the lesions on the tongue closely resemble ‘geographic’ tongue.

Laboratory Findings

The patients usually have a mild leukocytosis, an elevated erythrocyte sedimentation rate, and pyuria.

  • Differential Diagnosis
  • • Geographic tongue and stomatitis—no skin changes, no visceral lesions are seen.
  • • Pustularpsoriasis—Auspitz’ssignpresent.
    • Behcet’ssyndrome—nourethritis,aphthaewithredhalo.
  • • Stevens-Johnson syndrome—acute appearance, moresevere clinical course, no arthritis or urethritis.
    • Benign mucosal pemphigoid—blister formation, nourethritis, found in older patients.
Histologic Features
The microscopic findings are not diagnostic. They consist of parakeratosis, acanthosis, and polymorphonuclear leukocyte infiltration of epithelium, sometimes with mi- croabscess formation similar to psoriasis. The connective tissue shows a lymphocyte and plasma cell infiltrate.
  • Management
  • • Spontaneous remission—many patients undergo spontaneous remission.• Antibiotics—incasesymptomaticpatient,doxycycline or minocycline may be given.
  • • Analgesics—nonsteroidalanti-inflammatorydrugsare given to manage arthritis.
  • • Immunosuppressiveagents—immunosuppressiveagents like azathioprine and methotrexate are given in cases of most resistant cases.

REFERENCE- SHAFER’S TEXTBOOK OF ORAL PATHOLOGY [8TH ED} AND ANIL GHOM TEXTBOOK OF ORAL MEDICINE

WEGNER’S GRANULOMATOSIS

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Wegener’s granulomatosis is a disease of unknown aetiology, which basically involves the vascular, renal and respiratory systems. It involves the nose, paranasal air sinuses, lower respiratory tract, gut, joints, nervous system, and kidneys. Involvement of the kidney is the common cause of death.

This disease is caused by an abnormal immune reaction secondary to a nonspecific infection or a hypersensitivity reaction to an unknown antigen.

Clinical Features

>Wegener’s granulomatosis may occur at any age, although the majority of cases are in the fourth and fifth decadesof life.

 >There is a slight predilection for occurrence in males.

 >It is best described as a multisystem disease, which is usually first characterized clinically by the development of rhinitis, sinusitis, and otitis or ocular symptoms.

 >The patient soon develops a cough and hemoptysis as well as fever and joint pain. 

>Hemorrhagic or vesicular skin lesions are also commonly present. 

>Granulomatous lesions of the lungs are found on the chest radiograph, while the glomerulonephritis, which develops ultimately, leads to uraemia and terminal renal failure.

 >In nervous system, sensory neuropathy may be an occasional finding.

>Prognosis—the disease is usually fatal, with mean survival time of 5 months. Death occurs due to involvement of kidney.

Oral Manifestations

Involvement of the gingiva has been the most common and characteristic manifestation, and is termed as strawberry gingivitis.Gingival lesions may manifest as ulcerations, friable granular lesions, or simply enlargements of the gingiva. 

The inflammatory process starts in the interdental papilla and spreads rapidly to the periodontal structure and leads to bone loss and tooth mobility. 

Palate—orallesionstypicallyincludeulcerationofthe palate by extension of nose lesions and destruction of nasal septum. This will lead to perforation of palate.

• Teeth—theremaybelooseningofteethwithinsomecases spontaneous exfoliation. After extraction of teeth patient is usually noticed poor healing.

Laboratory Findings

Laboratory findings include anaemia, leukocytosis, elevated erythrocyte sedimentation rate, and hyperglobulinaemia. Because of kidney involvement, haematuria is common, as well as the finding of albumin, casts, and leukocytes in the urine. Circulating immune complexes have been demonstrated in some patients, but this is not a consistent finding.

Histologic Findings

Wegener’s granulomatosis presents a pattern of mixed inflammation centred around the blood vessels. 

The lesions in the upper respiratory tract and lungs consist of giant cell necrotizing granulomatous lesions showing vasculitis. 

Oral biopsy specimens show pseudoepitheliomatous hyperplasia and subepithelial abscesses. The gingival and other lesions show a nonspecific granulomatous process with scattered giant cells.

Diagnosis

  • Clinical diagnosis—typical strawberry gingivitis with necrotic ulceration in the oral cavity.
  • Laboratorydiagnosis—cytoplasmiclocalizationispresent with Wegener’s granulomatosis. Histopathologically chronic inflammatory cells and multinucleated giant cells are found.
  • Differential Diagnosis
  • Agranulocytosis, leukemia, lymphoma—diagnosis by blood picture, possibly histology.
  1. Management
    • Cotrimoxazole—it is combination of trimethoprim and sulfamethoxazole. It has proved to be effective as an adju- vant or sole therapy in both localized and generalized forms.
    • Corticosteroids—regimenofcyclophosphamide12mg/ kg body weight/day with prednisolone 1 mg/kg body weight have been utilized to obtain complete remission.
    • Others—other treatment modalities includes cyclo- sporine, intravenous pooled immunoglobulin, and local irradiation.

REFERENCE- SHAFER’S TEXTBOOK OF ORAL PATHOLOGY {8TH ED} AND ANIL GHOM TEXTBOOK OF ORAL MEDICINE