1. DISEASES OF THE RESPIRATORY SYSTEM DENTISTRY
DR HEYAM AWAD
FRCPATH

2. STRUCTURE OF THE RESPIRATORY SYSTEM

3. STRUCTURE OF THE RESPIRATORY SYSTEM

4. ALVEOLI

5. ALVEOLI: LARGE SURFACE AREA

6. ALVEOLI: RICH BLOOD SUPPLY

7. ALVEOLI: THIN MEMBRANES

8. ATELECTASIS = LUNG COLLAPSE

9. TYPES OF ATELECTASIS

10. RESORPTION ATELECTASIS
OBSTRUCTION BY:
*MUCOUS OR MUCOPURULENT PLUG (POST-OP, ASTHMA, BRONCHIECTASIS OR CHRONIC BRONCHITIS)
*TUMOUR.
*FOEIGN BODY .

11. COMPRESSION ATELECTASIS
ACCUMOLATION OF :
FLUID (PLEURAL EFFUSION)
BLOOD (HAEMOTHORAX)
AIR (PNEUMOTHORAX)
ALL WITHIN THE PLEURAL CAVITY.

12. CONTRACTION ATELECTASIS
LOCAL OR GENERALISED FIBROSIS.

13. ATELECTASIS…………….IS IT REVERSIBLE???????

14. ADULT RESPIRATORY DISTRESS SYNDROME

15. ACUTE LUNG INJURY BILATERAL PULMONARY DAMAGE.
ENDOTHELIAL AND EPITHELIAL DAMAGE.
DUE TO DIRECT OR INDIRECT LUNG INJURY.
ACUTE DYSPNEA + HYPOXEMIA + BILATERAL PULMONARY INFILTRATES WITHOUT PRIMARY LEFT SIDED HEART FAILURE.
CAN PROGRESS TO ACUTE RESPIRATORY DISTRESS SYNDROME.

16. MAIN CAUSES OF ACUTE LUNG INJURY
DIRECT LUNG DAMAGE :
PNEUMONIA.
ASPIRATION.
INDIRECT LUNG INJURY :
SEPSIS.
SEVERE TRAUMA WITH SHOCK.

17. ACUTE RESPIRATORY DISTRESS SYNDROME: CLINICAL FEATUERES.
LIFE THREATENING RESPIRATORY INSUFFICIENCY.
CYANOSIS.
HYPOXEMIA REFRACTORY TO OXYGEN THERAPY.
MAY PROGRESS TO MULTISYSTEM ORGAN FAILURE.

18. CLINICAL FEATURES 80% DEVELOP ARDS WITHIN 72 HOURS OF THE INSULT.
MORTALITY DECREASED FROM 60% TO 40% IN USA IN THE LAST DECADE.
POOR PROGNOSIS:
*OLD AGE.
*SEPSIS.
*MULTISYSTEM FAILURE.

19. OUTCOME SURVIVORS END WITH DIFFUSE INTERSTITIAL FIBROSIS.
THIS CAUSES COMPROMISE OF RESPIRATORY FUNCTION.
SURVIVALS WHO DON’T HAVE CHRONIC CONSEQUENCES RETAIN NORMAL RESPIRATORY FUNCTION WITHIN 6-12 MONTHS.

20. OBSTRUCTIVE VS RESTRICTIVE LUNG DISEASES
OBSTRUCTIVE: LIMITATION OF AIRFLOW.
RESTRICTIVE: REDUCED EXPANSION, AND DECRESED TOTAL CAPACITY.

21. OBSTRUCTIVE LUNG DISEASES
COPD: EMPHYSEMA AND CHRONIC BRONCHITIS.
ASTHMA.
BRONCHIECTASIS.

22. COPD

23. EMPHYSEMA
ABNORMAL, PERMANENT ENLARGEMENT OF AIR SPACES DISTAL TO TERMINAL BRONCHIOLES ALONG WITH DESTRUCTION TO THEIR WALLS WITHOUT SIGNIFICANT FIBROSIS.

24. TYPES OF EMPHYSEMA

25. CENTRIACINAR = CENTRILOBULAR
MORE SEVERE IN THE UPPER LOBES OF LUNGS.
SMOKING ASSOCIATED.

26. PANACINAR EMPHYSEMAM MOSTLY AFFECTS LOWER LUNG ZONES.
ASSOCIATED WITH ALPHA 1 ANTITRYPSIN DIFICIENCY.

27. MORPHOLOGY

28. HISTOPATHOLOGY

29. CLINICAL FEATURES DYSPNEA . WEIGHT LOSS. PROLONGED EXPIRATION.
BLOOD GASES RELATIVELY NORMAL.
PINK PUFFERS

30. Pink puffers

31. CHRONIC BRONCHITIS
PERSISTENT PRODUCTIVE COUGH FOR AT LEAST THREE CONSECUTIVE MONTHS FOR AT LEAST TWO CONSECUTIVE YEARS.

32. CHRONIC BRONCHITIS

33. CAUSES
SMOKING RELATED.
AIR POLLUTION.. SO2, NO.

34. PATHOGENESIS HYPERSECRETION OF MUCUS.
DUE TO HYPERTROPHY OF MUCUS SECRETING GLANDS IN TRACHEA AND MAIN BRONCHI.
INCREASE IN MUCIN SECRETING GOBLET CELLS IN THE EPITHELIUM OF SMALL BRONCHIA.

35. CLINICAL FEATURES PRODUCTIVE COUGH. HYPERCAPNIA. HYPOXEMIA. CYANOSIS.
BLUE BLOATERS

37. ASTHMA
CHRONIC INFLAMMATORY DISORDER WHICH CAUSES RECURRENT EPISODES OF WHEEZING, BREATHLESSNESS, COUGH, AND CHEST TIGHTNESS.

38. ASTHMA INTERMITTENT, REVERSIBLE : AIRWAY OBSTRUCTION.
CHRONIC BRONCHIAL INFLAMMATION WITH EOSINOPHILS.
BRONCHIAL SMOOTH MUSCLE HYPERTROPHY AND HYPERREACTIVITY.
INCREASED MUCUS SECRETION.

39. TYPES OF ASTHMA
ATOPIC: EVIDENCE OF ALLERGIC SENSITIZATION.
NONATOPIC.

40. TYPES OF ASTHMA ATOPIC : THE MOST COMMON TYPE. BEGINS IN CHILDHOOD.
TYPE 1 HYPERSENSITIVITY REACTION.
POSITIVE FAMILY HISTORY.
TRIGGERED BY ENVIRONMENTAL ANTIGENS OR INFECTIONS.

41. NON ATOPIC ASTHMA NO EVIDENCE OF ALLERGEN SENSITIZATION
SKIN TEST NEGATIVE.
POSITIVE FAMILY HISTORY IS LESS COMMON.
INFECTIONS COMMON.
VIRAL INFLAMMATION LOWERS THRESHOLD OF THE SUBEPITHELIAL VAGAL RECEPTORS TO IRRITANTS.
HUMORAL AND CELLULAR MEDIATORS SIMILAR TO ATOPIC ASTHMA.

42. DRUG INDUCED ASTHMA ASPIRIN MECHANISM UNKNOWN
ASPIRIN INHIBITS COX WITHOUT AFFECTING LIPOOXYGENASE PATHWAY SHIFTING THE BALANCE TO BRONCHOSPASM.

43. OCCUPATIONASL ASTHMA PLASTIC FUMES.
ORGANIC AND CHEMICAL DUST E.G WOOD, COTTON.
GASES: TOLUENE

44. CLINICAL FEATURES SEVERE DYDPNEA AND WHEEZING.
LABOUR TO INSPIRE AND CAN NOT EXPIRE. THIS RESULTSIN HYPERINFLATION.
ATTACKS LAST FOR 1 TO SEVERAL HOURS.

46. SARCOIDOSIS MULTISYSTEM DISEASE OF UNKNOWN ETIOLOGY.
NONCASEATING GRANULOMAS IN MULTIPLE ORGANS.

47. DIAGNOSIS: BY EXCLUSION.
NONCASEATING GRANULOMAS:
*MYCOBACTERIA.
*FUNGAL INFECTIONS.
*BERYLLIOSIS.

48. MAJOR PRESENTATION OF SARCOIDOSIS: BILATERAL HILAR LYMPHADENOPATHY AND/OR LUNG INVOLVEMENT.
EYE AND SKIN INVOLVEMENT EACH OCCUR IN 25% OF CASES.

49. EPIDEMIOLOGY
ADULTS < 40.
HIGHER PREVALENCE AMONG NONSMOKERS.

50. CLINICAL FEATURES CAN BE ASYMPTOMATIC.
PERIPHERAL LYMPHADENOPATHY, HEPATOSPLENOMEGALY, CUTANEOUS LESIONS OR EYE INVOLVEMENT.

51. OUTCOME UNPREDICTABLE COURSE.
EITHER PROGRESSIVE CHRONICITY OR RELAPSES AND REMISSIONS.
REMISSIONS ARE EITHER SPONTANEOUS OR WITH STEROIDS.

52. SARCOID GRANULOMAS

53. TUBERCULOSIS INFECTIOUS DISEASE CAUSED BY MYCOBACTERIUM TUBERCULOSIS.
CAUSES CASEATING GRANULOMAS.
MAINLY AFFECTS LUNGS, BUT OTHER ORGANS CAN BE AFFECTED.

54. EPIDEMIOLOGY A LEADING CAUSE OF DEATH IN DEPRIVED COUNTRIES.
WESTERN WORLD : DEATH DUE TO TB DECLINED IN THE 19TH CENTURAY .
RESURGENCE OF CASES SINCE 1984 DUE TO HIV INFECTION.
MORE PREVALENT IN IMMEGRANTS IN USA.

55. TRANSMISSION

56. ETIOLOGY
MYCOBACTERIA TUBERCULOSIS

57. HISTOLOGY: caseating granulomas

58. SYSTEMIC MILIARY TB BACILLI DISSIMINATE THROUGH SYSTEMIC CIRCULATION.
CAN AFFECT ANY ORGAN.
MAINLY: LIVER, BONE MARROW, SPLEEN, ADRENALS, MENINGES, KIDNEYS, F.TUBES AND EPIDIDYMIS.

59. PROGNOSIS GOOD IF LOCALISED TO LUNGS.
BAD: ELDERLY, IMMUNOSUPRESSED, MULTIDRUG RESISTENT TB.

60. TUMORS
LUNG CARCINOMA IS THE MOST COMMON CAUSE OF CANCER DEATH IN THE WEST.
TYPES: SQUAMOUS CELL CARCINOMA, ADENOCARCINOMA, SMALL CELL CARCINOMA AND LARGE CELL CARCINOMA.

61. SMALL CELL…. CHEMOTHERAPY
NONSMALL…. SURGERY, BUT ALSO CHEMO.