6. ASTHMA:
THE AIM OF THIS STUDY WAS TO INVESTIGATE:
THE CARIES RISK OF ASTHMATICS IN RELATION TO
1-DENTAL PLAQUE INDICES INCREASE
2-SALIVARY FLOW RATE DECREASE
3-PH AND BUFFER CAPACITY DECREASE
4-SALIVARY LEVELS OF STREPTOCOCCUS MUTANS INCREASE COMPARED WITH HEALTHY
SUBJECTS
AND ALSO TO EVALUATE THESE PARAMETERS WITHIN DIFFERENT GROUPS OF ASTHMATICS
ACCORDING TO THEIR MEDICATION, DURATION AND SEVERITY OF THE DISEASE.
7. . ASTHMA MEDICATION COMPRISES
BRONCHODILATORS, CORTICOSTEROIDS AND ANTICHOLINERGIC DRUGS.
MOST OF THESE DRUGS ARE INHALED USING VARIOUS FORMS OF INHALERS OR
NEBULIZERS.
THE EFFECT OF THESE DRUGS ON ORAL HEALTH IS THE SUBJECT OF DEBATE
AMONG DENTAL PRACTITIONERS. PATIENTS TAKING ASTHMA MEDICATION MAY
BE AT RISK OF DENTAL CARIES, DENTAL EROSION, PERIODONTAL DISEASES AND
ORAL CANDIDIASIS.
HENCE, PATIENTS WITH BRONCHIAL ASTHMA ON MEDICATION SHOULD RECEIVE
SPECIAL PROPHYLACTIC ATTENTION.
8. ECZEMA
SYMPTOMS INCLUDE:
ITCHY, RED, AND DRY SKIN CAUSED BY
INFLAMMATION.
IT’S MOST COMMONLY FOUND IN CHILDREN, ALTHOUGH ADULTS CAN GET IT.
IT IS ALSO CALLED ATOPIC DERMATITIS
-AND IS TREATED WITH ORAL MEDICATIONS, STEROID CREAMS AND LIGHT
THERAPY .
9. HAY FEVER (ALLERGIC RHINITIS)
IS A COMMON CONDITION THAT SHOWS
SIGNS AND SYMPTOMS SIMILAR TO A COLD
WITH SNEEZING, CONGESTION, RUNNY NOSE
AND SINUS PRESSURES.
-HAY FEVER IS CAUSED BY AN ALLERGIC
RESPONSE TO AIRBORNE SUBSTANCES,
SUCH AS POLLEN - UNLIKE A COLD WHICH IS
CAUSED BY A VIRUS. THE TIME OF YEAR IN
WHICH YOU GET HAY FEVER DEPENDS ON
WHAT AIRBORNE SUBSTANCE YOU ARE
ALLERGIC TO.
10. URTICARIA
IS A KIND OF SKIN RASH NOTABLE FOR PALE RED,
RAISED, ITCHY BUMPS.
MAY CAUSE A BURNING OR STINGING SENSATION.
THEY ARE FREQUENTLY CAUSED
BY ALLERGIC REACTIONS; HOWEVER, THERE ARE
MANY NONALLERGIC CAUSES.
MOST CASES OF HIVES LASTING LESS THAN SIX
WEEKS (ACUTE URTICARIA) ARE THE RESULT OF AN
ALLERGIC TRIGGER. CHRONIC URTICARIA (HIVES
LASTING LONGER THAN SIX WEEKS) IS RARELY DUE
TO AN ALLERGY.
THE MAJORITY OF CHRONIC HIVES CASES HAVE AN
UNKNOWN (IDIOPATHIC) CAUSE. IN PERHAPS AS
MANY AS 30–40% OF PATIENTS WITH CHRONIC
IDIOPATHIC URTICARIA, IT IS CAUSED BY
AN AUTOIMMUNE REACTION.
11. A FOOD ALLERGY
IS AN ABNORMAL IMMUNE RESPONSE TO FOOD.
THE SIGNS AND SYMPTOMS MAY RANGE FROM MILD TO SEVERE.
THEY MAY INCLUDE ITCHINESS, SWELLING OF THE TONGUE, VOMITING, DIARRHEA, HIVES,
TROUBLE BREATHING, OR LOW BLOOD PRESSURE. THIS TYPICALLY OCCURS WITHIN MINUTES
TO SEVERAL HOURS OF EXPOSURE. WHEN THE SYMPTOMS ARE SEVERE IT IS KNOWN
ASANAPHYLAXIS..
12. HISTORICALLY, PENICILLIN AND OTHER SIMILAR ANTIBIOTICS ARE THE DRUGS MOST
PEOPLE ARE ALLERGIC TO.
OTHER DRUGS COMMONLY FOUND TO CAUSE ALLERGIC REACTIONS INCLUDE SULFA
DRUGS, BARBITURATES, ANTICONVULSANTS, AND INSULIN.
THE IMMUNE SYSTEM RECOGNIZES THE DRUG AS A FOREIGN SUBSTANCE AND THE
BODY PRODUCES CERTAIN CHEMICALS, SUCH AS LARGE AMOUNTS OFHISTAMINE
WHAT ARE THE SYMPTOMS OF A DRUG ALLERGY?
SYMPTOMS OF A DRUG ALLERGY CAN RANGE FROM MILD TO LIFE-THREATENING. EVEN
IN PEOPLE WHO AREN'T ALLERGIC, MANY DRUGS CAN CAUSE INTOLERANCE AND
IRRITATION, SUCH AS AN UPSET STOMACH. BUT DURING AN ALLERGIC REACTION, THE
RELEASE OF HISTAMINE CAN CAUSE SYMPTOMS LIKE HIVES, SKIN RASH, ITCHY
SKIN OR EYES, CONGESTION, AND SWELLING IN THE MOUTH AND THROAT.
A MORE SEVERE REACTION, CALLED ANAPHYLAXIS, MAY INCLUDE DIFFICULTY
BREATHING, BLUENESS OF THE SKIN, DIZZINESS, FAINTING, ANXIETY, CONFUSION,
RAPID PULSE, NAUSEA, DIARRHEA, AND ABDOMINAL PROBLEMS.
DRUGS ALLERGIES
13. ANAPHYLAXIS
IS A SERIOUS ALLERGIC REACTION THAT IS RAPID IN ONSET
AND MAY CAUSE DEATH.
IT TYPICALLY CAUSES A NUMBER OF SYMPTOMS INCLUDING
AN ITCHY RASH, THROAT SWELLING, AND LOW BLOOD
PRESSURE. COMMON CAUSES INCLUDE INSECT BITES AND
STINGS, FOODS, AND MEDICATIONS.
ON A MECHANISTIC LEVEL, ANAPHYLAXIS IS CAUSED BY THE
RELEASE OF MEDIATORS FROM CERTAIN TYPES OF WHITE
BLOOD CELLSTRIGGERED BY EITHER IMMUNOLOGIC OR NON-
IMMUNOLOGIC MECHANISMS. CLINICIANS DIAGNOSE THE
CONDITION ON THE BASIS OF THE PRESENTING SYMPTOMS
AND SIGNS.
THE PRIMARY TREATMENT IS INJECTION OF EPINEPHRINE,
THE ADMINISTRATION OF INTRAVENOUS FLUIDS, AND
POSITIONING THE PERSON FLAT, WITH OTHER MEASURES
BEING COMPLEMENTARY.
14. SYMPTOMS TYPICALLY INCLUDE GENERALIZED HIVES,ITCHINESS, FLUSHING,
OR SWELLING (ANGIOEDEMA) OF THE AFFICTED TISSUES.
THOSE WITH ANGIOEDEMA MAY DESCRIBE A BURNING SENSATION OF THE SKIN RATHER
THAN ITCHINESS. SWELLING OF THE TONGUE OR THROAT OCCURS IN UP TO ABOUT 20%
OF CASES.
OTHER FEATURES MAY INCLUDE A RUNNY NOSE AND SWELLING OF
THE CONJUNCTIVA.THE SKIN MAY ALSO BE BLUE TINGED BECAUSE OF LACK OF OXYGEN.
IN SEVERE CAUSES IM EPI. GIVEN IMMEDIATILLY IF AIRWAY THREATENED BY ATTACKS OF
ANGIO-OEDEMA.
ANGIO-OEDEMA
15. CONTACT DERMATITIS
IT IS REASEMBLE TO ECZEMA CLINICALLY BUT IT IS MEDIATED BY TYPE 4 REACTION.
IN DENTISTRY IT IS CAUSED BY SOME DENTAL MATERALS MAINLY LATEX ,AMALGAM
AND SOME IMPRESSION MATERIALS ETC..
-LATEX ALLERGY : PERIORAL RASH AND IN RARE CASES CAN BE SVRE AND
ANAPHYLACTOID I CHARACTER AND HAVE BE FATAL.
-MERCURY ALLERGY: LOCALLY(CONTACT DERMATITS) OR SYSTMIC DUE TO
ABSORBTION OF MERCURY COMPOUNDS SUCH AS METHYL MERCURY THAT HAVE
NEUROTOXIC EFFEECT
16. THE AUTOIMMUNE DISASES
TYPICAL FEATURES:
-COMMON IN WOMEN
-ONSET IN MID. AGES
-+ FAMILY HISORY
-AB LEVEL USUALLY RAISED
-CERCULATING AB FREQ. DETECTABLE IN UNEFFECTED FAMILY MMEBERS
-CERCULATING AB TO SEVERAL TISSUES BUT NOT ALL ATTACKED
-INCREASE RISK OF DEVELOPING OF OTHER AUTOIMMUNE DISEASES
-AB AD COMPLEMENTOFEN DETECTABLE AT SITE OF TISSUE DAMAGE
-IMMUNESUPPRESSIVE TREATMENT LIMIT THE TISSUE DAMAGE
18. CONNECTIVE TISSUE DISEASES
RHEUMATOID ARTHRITIS
-THE TMJ INVOLVED IN MOST SEVERE CASES
-DRUGS USED IN RHEUMATOID
ARTHRITIS(ASPIRIN,NSAIDS,CORTICOSTEROIDS,ANTIMALARIAL,GOLDS AND
PENCILLAMINE) AFFECT DENTAL MANAGE. OR CAUSE ORAL REACTIONS .
-MANY PT. ARE ANAEMIC DUE TO GASTRIC BLOOD LOSS INDUCED BY
ANALGESECS
19. SJOGRENS SYNDROMES
-MID. AGES
-RH. ARTHRITIS ASSOCIATED WITH SECONDARY PHASE.
-DRY MOUTH
-DRY EYE
-S.G INFILTRATED BY CD4 LYMPHOCYTES AND ACINAR DISTRUCTION
-RISK OF S.G. AND EXTRASALIVARY LYMPHOMAS
21. MANAGMENT
-GIVE REASSURANCE AND HELP DRY
MOUTH
-CONTROL CARIES
-MONITOR MUCOUSAL CANDIDOSIS
-TREAT DIFFICULTIES WITH DENTURES
SYMPTOMATICALLY
-OBSERVE REGULARY FOR POSSIBLE
DEVELOPMENT OF ASCENDING PAROTITIS
OR LYMPHOMA
23. SLE
-JOINT:PAIN AND ARTHRITIS
-SKIN: RASH(BUTTERFLY RASH ACROSS MID FACE)
-MOUTH: STOMATITIS AND SJOGREN S.
SEROUS MEM. : PERICARDITIS
-HEART : ENDOCARDITS AND MYOCARDITIS
-LUNG : PNEUNONITIS
-KIDNEYS : NEPHRITIS S.
-CNS : NEUROSIS,STROK AND CN PALSIES
-EYES . CONJUNCVTIVITIS AND RETAINAL DAMAGE
GIT: HEPATOMEGALY AND PANCREATITIS
-BLOOD : ANAEMIA AND PURPURA
24. EFFECTION ON DENTAL MANAGEMENT
-CORTICOSTEROID AND OTHER IMMUNOSUPPRESSIVE DRUGS
-PAINFUL ORAL LESIONS
-SJOGREN S.
-BLEEDING TENDENCIES
-ANAEMIA
-CARDIAC DISEASE AND RISK OF ENDOCARDITIS
25. DLE
SIMILAR TO SLE BUT WITHOUT LATTERS
SEROLOGICAL CHANGES AND SYSTEMIC
DISORDERS.
26. SYSTEMIC SCLEROSIS(SCLERODERMA)
-SJOGREN SS.
-LIMITED ORAL OPENING
-WIDENING IN PDL SHADOW
-GROSS RESORPTION OF JAW
-FIRM WHITISH-YELLOW FIBROTIC MUCOUSAL
PLAQUE
-STIFNESS OF SKIN ,GIT,HEART,LUNGS AND KIDNEY
-FACIAL FEATURES BECOME SMOOTH (MASK LIKE)
-RAYNAUDS PHNOMENON.
27. PERNICIOUS ANEMIA
UNTREATED PERNICIOUS ANEMIA CAN LEAD TO:
- NEUROLOGICAL COMPLICATIONS, AND IN SERIOUS CASES, DEATH. HOWEVER, IN 20% OF
CASES OF COBALAMIN DEFICIENCY, ANEMIA IS NOT OBSERVED. WHILE IT MAY CONSIST OF
THE TRIAD OF PARESTHESIAS, SORE TONGUE, AND WEAKNESS, THIS IS NOT THE CHIEF
SYMPTOM COMPLEX. COMMON SYMPTOMS INCLUDE ANEMIA, FATIGUE, DEPRESSION, LOW-
GRADE FEVERS, DIARRHEA,DYSPEPSIA, WEIGHT LOSS, NEUROPATHIC
PAIN, JAUNDICE, GLOSSITIS (SWOLLEN, RED AND SMOOTH APPEARANCE OF THE
TONGUE), ANGULAR CHEILITIS (SORES AT THE CORNER OF THE MOUTH),
DEHYDRATED/CRACKED AND PALE LIPS AND DARK CIRCLES AROUND THE EYES (LOOK OF
EXHAUSTION), BRITTLE NAILS, AND THINNING AND EARLY GREYING OF THE HAIR. BECAUSE
PA MAY AFFECT THE NERVOUS SYSTEM, SYMPTOMS MAY ALSO INCLUDE DIFFICULTY
INPROPRIOCEPTION, MEMORY CHANGES, MILD COGNITIVE IMPAIRMENT (INCLUDING
DIFFICULTY CONCENTRATING AND SLUGGISH RESPONSES, PSYCHOSIS, IMPAIRED
URINATION, LOSS OF SENSATION IN THE FEET, UNSTEADY GAIT, DIFFICULTY IN
WALKING, MUSCLE WEAKNESS AND CLUMSINESS ANEMIA MAY CAUSE TACHYCARDIA (RAPID
HEARTBEAT) AND CARDIAC MURMURS, ALONG WITH A YELLOW WAXY PALLOR, LOW BLOOD
PRESSURE, HIGH BLOOD PRESSURE, AND SHORTNESS OF BREATH.
28. IDIOPATHIC THROMBOCYTOPENIC PURPURA (ITP)
ALSO KNOWN AS PRIMARY IMMUNE THROMBOCYTOPENIA, PRIMARY IMMUNE THROMBOCYTOPENIC
PURPURA OR AUTOIMMUNE THROMBOCYTOPENIC PURPURA
IS DEFINED AS ISOLATED LOW PLATELET COUNT (THROMBOCYTOPENIA) WITH NORMAL BONE
MARROW AND THE ABSENCE OF OTHER CAUSES OF THROMBOCYTOPENIA. IT CAUSES A
CHARACTERISTIC PURPURIC RASH AND AN INCREASED TENDENCY TO BLEED.
TWO DISTINCT CLINICAL SYNDROMES MANIFEST AS AN ACUTE CONDITION IN CHILDREN AND A
CHRONIC CONDITION IN ADULTS. THE ACUTE FORM OFTEN FOLLOWS AN INFECTION AND HAS A
SPONTANEOUS RESOLUTION WITHIN 2 MONTHS. CHRONIC IDIOPATHIC THROMBOCYTOPENIC
PURPURA PERSISTS LONGER THAN 6 MONTHS WITH A SPECIFIC CAUSE BEING UNKNOWN.
ITP IS AN AUTOIMMUNE DISEASE WITH ANTIBODIES DETECTABLE AGAINST SEVERAL PLATELET
SURFACE ANTIGENS.
ITP IS DIAGNOSED BY A LOW PLATELET COUNT IN A COMPLETE BLOOD COUNT (A COMMON BLOOD
TEST). HOWEVER, SINCE THE DIAGNOSIS DEPENDS ON THE EXCLUSION OF OTHER CAUSES OF A
LOW PLATELET COUNT, ADDITIONAL INVESTIGATIONS (SUCH AS A BONE MARROW BIOPSY) MAY BE
NECESSARY IN SOME CASES.
IN MILD CASES, ONLY CAREFUL OBSERVATION MAY BE REQUIRED BUT VERY LOW COUNTS OR
SIGNIFICANT BLEEDING MAY PROMPT TREATMENT WITH CORTICOSTEROIDS, INTRAVENOUS
IMMUNOGLOBULIN, ANTI-D IMMUNOGLOBULIN, OR IMMUNOSUPPRESSIVE DRUGS.REFRACTORY
ITP (NOT RESPONSIVE TO CONVENTIONAL TREATMENT) MAY REQUIRE SPLEENECTOMY, THE
SURGICAL REMOVAL OF THE SPLEEN.PLATELET TRANSFUSIONS MAY BE USED IN SEVERE BLEEDING
TOGETHER WITH A VERY LOW COUNT. SOMETIMES THE BODY MAY COMPENSATE BY MAKING
ABNORMALLY LARGE PLATELETS.
29. SIGNS INCLUDE
-THE SPONTANEOUS FORMATION OF BRUISES (PURPURA) AND PETECHIAE (TINY
BRUISES), ESPECIALLY ON THE EXTREMITIES,BLEEDING FROM THE
NOSTRILS AND/OR GUMS
- MENORRHAGIA (EXCESSIVE MENSTRUAL BLEEDING), ANY OF WHICH MAY OCCUR IF THE
PLATELET COUNT IS BELOW 20,000 PER ΜL
-A VERY LOW COUNT (<10,000 PER ΜL) MAY RESULT IN THE SPONTANEOUS FORMATION
OFHEMATOMAS (BLOOD MASSES) IN THE MOUTH OR ON OTHER MUCOUS MEMBRANES.
BLEEDING TIME FROM MINOR LACERATIONS ORABRASIONS IS USUALLY PROLONGED.
-SERIOUS AND POSSIBLY FATAL COMPLICATIONS DUE TO EXTREMELY LOW COUNTS
(<5,000 PER ΜL) INCLUDE SUBARACHNOID OR INTRACEREBRAL HEMORRHAGE (BLEEDING
INSIDE THE SKULL OR BRAIN), LOWER GASTROINTESTINAL BLEEDING OR OTHER
INTERNAL BLEEDING.
30. SOME MEDICATIONS CAN HAVE AN IMPACT ON THE NUMBER AND FUNCTION OF WHITE
BLOOD CELLS.
1- CLOZAPINE, AN ANTIPSYCHOTIC MEDICATION WITH A RARE ADVERSE EFFECT LEADING TO
THE TOTAL ABSENCE OF ALL GRANULOCYTES (NEUTROPHILS, BASOPHILS, EOSINOPHILS).
2-THE ANTIDEPRESSANT AND SMOKING ADDICTION TREATMENT DRUG BUPROPION HCL
(WELLBUTRIN) CAN ALSO CAUSE LEUKOPENIA WITH LONG-TERM USE.
3- MINOCYCLINE, A COMMONLY PRESCRIBED ANTIBIOTIC, IS ANOTHER DRUG KNOWN TO
CAUSE LEUKOPENIA.
4-THERE ARE ALSO REPORTS OF LEUKOPENIA CAUSED BY DIVALPROEX SODIUM
OR VALPROIC ACID (DEPAKOTE), A DRUG USED FOR EPILEPSY (SEIZURES) AND MIGRAINE.
5-THE ANTICONVULSANT DRUG, LAMOTRIGINE, HAS BEEN ASSOCIATED WITH A DECREASE IN
WHITE BLOOD CELL COUNT.
6-OTHER MEDICATIONS INCLUDE IMMUNOSUPPRESSIVE DRUGS, SUCH
AS SIROLIMUS, MYCOPHENOLATE MOFETIL, TACROLIMUS, CYCLOSPORINE, LEFLUNOMIDE
(ARAVA) AND TNF INHIBITORS.
7- INTERFERONS USED TO TREAT MULTIPLE SCLEROSIS, SUCH AS REBIF, AVONEX,
AND BETASERON,
DRUGS ASSOCIATED LEUCOPENIA
31. ADDISON’S DISEASE CHRONIC ADRENAL INSUFFICIENCY, HYPOCORTISOLISM,
ANDHYPOADRENALISM
IS A RARE, CHRONIC ENDOCRINE SYSTEM DISORDER IN WHICH THE ADRENAL GLANDS DO NOT
PRODUCE SUFFICIENTSTEROID HORMONES (GLUCOCORTICOIDS AND MINERALOCORTICOIDS). IT IS
CHARACTERISED BY A NUMBER OF RELATIVELY NONSPECIFIC SYMPTOMS, SUCH AS ABDOMINAL PAIN
AND WEAKNESS, BUT UNDER CERTAIN CIRCUMSTANCES, THESE MAY PROGRESS TO ADDISONIAN CRISIS,
A SEVERE ILLNESS WHICH MAY INCLUDE VERY LOW BLOOD PRESSURE AND COMA. AN ADRENAL CRISIS
OFTEN OCCURS IF THE BODY IS SUBJECTED TO STRESS, SUCH AS AN ACCIDENT, INJURY, SURGERY,
SEVERE INFECTION OR ILLNESS; DEATH MAY QUICKLY FOLLOW.
THE CONDITION ARISES FROM PROBLEMS WITH THE ADRENAL GLAND, PRIMARY ADRENAL
INSUFFICIENCY, AND CAN BE CAUSED BYDAMAGE BY THE BODY'S OWN IMMUNE SYSTEM,
ADDISON'S DISEASE AND OTHER FORMS OF HYPOADRENALISM ARE GENERALLY DIAGNOSED VIA BLOOD
TESTS AND MEDICAL IMAGING.
TREATMENT INVOLVES REPLACING THE ABSENT HORMONES
(ORAL HYDROCORTISONE AND FLUDROCORTISONE).[2] LIFELONG, CONTINUOUS STEROID REPLACEMENT
THERAPY IS REQUIRED, WITH REGULAR FOLLOW-UP TREATMENT AND MONITORING FOR OTHER HEALTH
PROBLEMS.
32.
33. HYPOTHYROIDISM
IS A COMMONDISORDER OF THE ENDOCRINE SYSTEM IN
WHICH THE THYROID GLAND DOES NOT PRODUCE
ENOUGH THYROID HORMONE.
-WORLDWIDE, TOO LITTLE IODINE IN THE DIET IS THE MOST
COMMON CAUSE OF HYPOTHYROIDISM.[1][2] IN COUNTRIES
WITH ENOUGH IODINE IN THE DIET, THE MOST COMMON
CAUSE OF HYPOTHYROIDISM IS THE AUTOIMMUNE
CONDITION HASHIMOTO'S THYROIDITIS. LESS COMMON
CAUSES INCLUDE THE FOLLOWING: PREVIOUS TREATMENT
WITH RADIOACTIVE IODINE, INJURY TO
THE HYPOTHALAMUS OR THEANTERIOR PITUITARY GLAND,
CERTAIN MEDICATIONS, A LACK OF A FUNCTIONING THYROID
AT BIRTH, OR PREVIOUS THYROID SURGERY.
- THE DIAGNOSIS OF HYPOTHYROIDISM, WHEN SUSPECTED,
CAN BE CONFIRMED WITH BLOOD
TESTS MEASURING THYROID-STIMULATING HORMONE (TSH)
AND THYROXINE LEVELS.
HYPOTHYROIDISM CAN BE TREATED WITH MANUFACTURED
LEVOTHYROXINE MEDICATIONS SUCH AS BETA
BLOCKERS MAY CONTROL THE SYMPTOMS AND ANTI-
THYROID MEDICATIONS SUCH AS METHIMAZOLE
34. HYPERTHYROIDISM
IS THE CONDITION THAT OCCURS DUE TO
EXCESSIVE PRODUCTION OF THYROID HORMONE BY
THE THYROID GLAND
-CAUSES INCLUDE MULTINODULAR GOITER, TOXIC
ADENOMA, INFLAMMATION OF THE THYROID, EATING
TOO MUCH IODINE, AND TOO MUCH SYNTHETIC
THYROID HORMONE. A LESS COMMON CAUSE IS
A PITUITARY ADENOMA.
-TREATMENT DEPENDS PARTLY ON THE CAUSE AND
SEVERITY OF DISEASE. THERE ARE THREE MAIN
TREATMENT OPTIONS: RADIOIODINE THERAPY,
MEDICATIONS, AND THYROID SURGERY. MAY
TEMPORARILY HELP PEOPLE WHILE OTHER
TREATMENTS ARE HAVING EFFECT. SURGERY TO
REMOVE THE THYROID IS ANOTHER OPTION.
35. HYPOPARATHYROIDISM
IS DECREASED FUNCTION OF THE PARATHYROID
GLANDS WITH UNDERPRODUCTION OF PARATHYROID
HORMONE. THIS CAN LEAD TO LOW LEVELS OF
CALCIUM IN THE BLOOD, OFTEN CAUSING CRAMPING
AND TWITCHING OF MUSCLES
OR TETANY(INVOLUNTARY MUSCLE CONTRACTION),
AND SEVERAL OTHER SYMPTOMS. THE CONDITION
CAN BE INHERITED, BUT IT IS ALSO ENCOUNTERED
AFTER THYROID OR PARATHYROID GLAND SURGERY,
AND IT CAN BE CAUSED BY IMMUNE SYSTEM-
RELATED DAMAGE AS WELL AS A NUMBER OF RARER
CAUSES.
-THE DIAGNOSIS IS MADE WITH BLOOD TESTS
-THE TREATMENT OF HYPOPARATHYROIDISM IS
LIMITED BY THE FACT THAT THERE IS NO ARTIFICIAL
FORM OF THE HORMONE THAT CAN BE
ADMINISTERED AS REPLACEMENT; CALCIUM
REPLACEMENT OR VITAMIN D CAN AMELIORATE THE
SYMPTOMS BUT CAN INCREASE THE RISK OF KIDNEY
STONES AND CHRONIC KIDNEY DISEASE.
36. PEMPHIGUS VULGARIS
IS A CHRONIC BLISTERING SKIN DISEASE WITH SKIN
LESIONS THAT ARE RARELY PRURITIC, BUT WHICH ARE
OFTEN PAINFUL IT IS CLASSIFIED AS A TYPE II
HYPERSENSITIVITY REACTION, WITH THE FORMATION OF
ANTI-DESMOSOME ANTIBODIES.
-THE PATHOGENESIS OF THE DISEASE INVOLVES
AUTOANTIBODIES AGAINST DESMOSOME PROTEINS,
SEPARATING KERATINOCYTES FROM THE BASAL LAYER OF
THE EPIDERMIS. ON HISTOLOGY, THE BASAL KERATINOCYTES
ARE USUALLY STILL ATTACHED TO THE BASEMENT
MEMBRANE
TRANSUDATIVE FLUID ACCUMULATES IN BETWEEN THE
KERATINOCYTES AND BASEMENT MEMBRANE (SUPRABASAL
SPLIT), FORMING A BLISTER AND RESULTING IN WHAT IS
KNOWN AS A POSITIVE NIKOLSKY'S SIGN
37. MUCOUS MEMBRANE
PEMPHIGOID
IS A RARE CHRONIC AUTOIMMUNE
SUBEPITHELIAL BLISTERING DISEASE
CHARACTERIZED BY EROSIVE SKIN LESIONS OF
THE MUCOUS MEMBRANES AND SKIN THAT
RESULTS IN SCARRING OF AT LEAST SOME SITES
OF INVOLVEMENT.
-CICATRICIAL PEMPHIGOID HAS BEEN REFERRED
TO BY A VARIETY OF DESIGNATIONS BASED
LARGELY ON ITS SITE OF INVOLVEMENTS, WITH
EXAMPLES OF SUCH TERMINOLOGY INCLUDING
"DESQUAMATIVE GINGIVITIS," "OCULAR
PEMPHIGUS" AND "BENIGN MUCOUS MEMBRANE
PEMPHIGOID
38. ERYTHEMA MULTIFORME
IS A SKIN CONDITION OF UNKNOWN CAUSE,
POSSIBLY MEDIATED BY DEPOSITION
OF IMMUNE COMPLEX(MOSTLY IGM) IN THE
SUPERFICIAL MICROVASCULATURE OF THE
SKIN AND ORAL MUCOUS MEMBRANE THAT
USUALLY FOLLOWS AN INFECTION OR DRUG
EXPOSURE. IT IS AN UNCOMMON DISORDER,
WITH PEAK INCIDENCE IN THE SECOND AND
THIRD DECADES OF LIFE.
39. -THE CONDITION VARIES FROM A MILD, SELF-LIMITED RASH (E. MULTIFORME MINOR) TO A
SEVERE, LIFE-THREATENING FORM KNOWN AS ERYTHEMA MULTIFORME MAJOR THAT ALSO
INVOLVES MUCOUS MEMBRANES.
THE MILD FORM USUALLY PRESENTS WITH MILDLY ITCHY (BUT ITCHING CAN BE VERY
SEVERE), PINK-RED BLOTCHES, SYMMETRICALLY ARRANGED AND STARTING ON THE
EXTREMITIES. IT OFTEN TAKES ON THE CLASSICAL "TARGET LESION"
APPEARANCE, WITH A PINK-RED RING AROUND A PALE CENTER. RESOLUTION WITHIN 7–10
DAYS IS THE NORM.
40. CAUSE OF EM:
-INFECTIONS:
BACTERIAL: HAEMOLYTIC STREPTOCOCCI, LEGIONELLOSIS, LEPROSY, NEISSERIA
MENINGITIDIS,MYCOBACTERIUM, PNEUMOCOCCUS, SALMONELLA SPECIES, STAPHYLOCOCCUS S
PECIES, MYCOPLASMA PNEUMONIAE), CHLAMYDIAL.
FUNGAL (COCCIDIOIDES IMMITIS)
PARASITIC (TRICHOMONAS SPECIES, TOXOPLASMA GONDII),
VIRAL (ESPECIALLY HERPES SIMPLEX)
-DRUGS REACTION: MOST COMMONLY TO: ANTIBIOTICS
(INCLUDING, SULPHONAMIDES, PENICILLIN), ANTICONVULSANTS
(PHENYTOIN, BARBITURATES), ASPIRIN, ANTITUBERCULOIDS, AND ALLOPURINOL AND MANY
OTHERS.
-PHYSICAL FACTORS: RADIOTHERAPY, COLD, SUNLIGHT
OTHERS: COLLAGEN DISEASES, VASCULITIDES, NON-HODGKIN LYMPHOMA, LEUKAEMIA, MULTIPLE
MYELOMA, MYELOID METAPLASIA, POLYCYTHEMIA