Mycobacterium leprae 

- tuberculoid type has intact cellular immunity
 - forms granulomas and kill the organisms (very few present).
 - evokes a positive lepromin skin test
 - localized skin lesions that lack symmetry
 - nerve involvement (organisms invade Schwann cells) that dominates the clinical picture and leads to skin anesthesia, muscle atrophy and autoamputation.
 - lepromatous leprosy patients lack cellular immunity
 - no granulomas
 - organisms readily identified
 - negative lepromin skin test
 - Bacteremia disseminates to cooler areas like the digits.
 - symmetrical, skin lesions that produce the classic leonine facies; biopsy reveals grentz zone in superficial dermis and then organisms in macrophages.
 - neural involvement is a late feature of the disease.
 - lepromin skin test is to determine host immunity; not a diagnostic test.
 - treatment: dapsone + rifampin

Herpes simplex is subdivided into type 1 and 2, the former usually developing lesions around the lips and mouth and the latter producing vesicular lesions in the genital region 
 - contracted by physical contact; incubation 2-10 days.
 - primary HSV I usually is accompanied by systemic signs of fever and Lymphadenopathy, while recurrent herpes is not associate with systemic signs.
 - dentists often become infected by contact with patient saliva and often develop extremely painful infections on the fingers (herpetic whitlow).
 - Herpes viruses remain dormant in sensory ganglia and are reactivated by stress, sunlight, menses, etc. 

 - Herpes gingivostomatitis is MC primary HSV 1 infectionÆpainful, vesicular eruptions that may extend for the tongue to the retropharynx.
 - Herpes keratoconjunctivitis (HSV 1)
 - Kaposi's varicelliform eruption refers to an HSV 1 infection superimposed on a previous dermatitis, usually in an immunodeficient person.
 - laboratory: culture; ELISA test on vesicle fluid; intranuclear inclusions within multinucleated squamous cells in scrapings (Tzanck preps) of vesicular lesions. 

Lichen planus is an itchy, violaceous, flat-topped papule highlighted by white dots or lines called Wickham's striae.
 - lichen planus may occur in the oral mucosa, where it has a fine white net-like appearance.
 - increased epidermal proliferation; ? immunologic; initiated by epidermal injury from drugs, viruses, or topical agents.
 - characteristic histologic features include:
 - hyperkeratosis
 - absence of parakeratosis
 - prominent stratum granulosum
 - an irregular "saw toothed" accentuation of the rete pegs. 

 - dermal-epidermal junction obscured by a band-like infiltrate of lymphocytes.
 - It is generally self-limiting and resolves spontaneously 1 to 2 years after onset; however, the oral lesions may persist for years.

HAEMORRHAGIC DISORDERS

Normal homeostasis depends on

 -Capillary integrity and tissue support.

- Platelets; number and function

(a) For integrity of capillary endothelium and platelet plug by adhesion and aggregation

(b) Vasoactive substances for vasoconstriction

(c) Platelet factor for coagulation.

(d) clot retraction.

- Fibrinolytic system(mainly Plasmin) : which keeps the coagulation system in check.

Coagulation disorders

These may be factors :

Deficiency .of factors

• Genetic.
• Vitamin K deficiency.
• Liver disease.
• Secondary to disseminated intravascular coagulation.or defibrinatian

Overactive fibrinolytic system.

Inhibitors of  the factors (immune, acquired).

Anticoagulant therapy as in myocardial infarction.

Haemophilia. Genetic disease transmitted as X linked recessive trait. Common in Europe. Defect in fcatorVII   Haemophilia A .or in fact .or IX-Haemaphilia B (rarer).

Features:

• May manifest in infancy or later.
• Severity depends  on degree of deficiency.
• Persistant wound bleeding.
• Easy Bruising with Hematoma formation

Nose bleed , arthrosis, abdominal pain with fever and leukocytosis

Prognosis is good with prevention of trauma and-transfusion of Fresh blood or fTesh plasma except for danger of developing immune inhibitors.

Von Willebrand's disease. Capillary fragility and decreased factor VIII (due to deficient stimulatory factor). It is transmitted in an autosomal dominant manner both. Sexes affected equally

Vitamin K  Deficiency. Vitamin K is needed for synthesis of factor II,VII,IX and X.

Deficiency maybe due to:

Obstructive jaundice.

Steatorrhoea.

Gut sterilisation by antibiotics.

Liver disease results in :

Deficient synthesis of factor I II, V, Vll, IX and X  Incseased fibrinolysis (as liver is the site of detoxification of activators ).

Defibrination syndrome. occurs when factors are depleted due to disseminated .intravascular coagulation (DIC). It is initiated by endothelial damage or tissue factor entering the circulation.

Causes

Obstetric accidents, especially amniotic fluid embolism. Septicaemia. .

Hypersensitivity reactions.

Disseminated malignancy.

Snake bite.

Vascular defects : (Non thrombocytopenic purpura).

Acquired :

Simple purpura a seen in women. It is probably endocrinal

Senile parpura in old people due to reduced tissue support to vessels

Allergic or toxic damage to endothelium due to  Infections like Typhoid Septicemia

Col!agen diseases.

Scurvy

Uraemia damage to  endothelium (platelet defects).

Drugs like aspirin. tranquillisers, Streptomvcin pencillin etc.

Henoc schonlien purpura Widespeard vasculitis due to hypersensitivity to bacteria or foodstuff

It manifests as :

Pulrpurric rashes.

Arthralgia.

Abdominal pain.

Nephritis and haematuria.

Hereditary :

(a) Haemhoragic telangieclasia. Spider like tortous vessels which bleed easily. There are disseminated lesions in skin, mucosa and viscera.

(b) Hereditary capillary fragilily similar to the vascular component of von Willbrand’s disease

.(c) Ehler Danlos Syndrome which is a connective tissue defect with skin, vascular and joint manifestations.

Platelet defects

These may be :

(I) Qualitative thromboasthenia and thrombocytopathy.

(2) Thrombocytopenia :Reduction in number.

(a) Primary or idiopathic thrombocytopenic purpura.

(b) Secondary to :

(i) Drugs especially sedormid

(ii) Leukaemias

(iii) Aplastic-anaemia.

Idiopathic thrombocytopenic purpura (ITP). Commoner in young females.

Manifests as :

Acute self limiting type.

Chronic recurring type.

Features:

(i) Spontaneous bleeding and easy bruisability

(ii)Skin (petechiae), mucus membrane (epistaxis) lesions and sometimes visceral lesions involving any organ.

Thrombocytopenia with abnormal forms of platelets.

Marrow shows increased megakaryocytes with immature forms, vacuolation, and lack of platelet budding.

Pathogenesis:

hypersensitivity to infective agent in acute type.

Plasma thrombocytopenic factor ( Antibody in nature) in chronic type

Respiratory Pathology

A. Pulmonary infections

1. Bacterial pneumonia

a. Is an inflammatory process of infectious origin affecting the pulmonary parenchyma.

2. Bacterial infections include:

a. Streptococcus pneumoniae (most common).

b. Staphylococcus aureus.

c. Haemophilus influenzae.

d. Klebsiella pneumoniae.

e. Anaerobic bacteria from the mouth

(aspiration of oral secretions).

3. Viral infections include:

a. Influenza.

b. Parainfluenza.

c. Adenoviruses.

d. Respiratory syncytial virus.

Note: viruses can also cause pneumonia. Infection of the interstitial tissues, or interstitial pneumonia, is commonly associated with these types of infections.

Common symptoms include fever, dyspnea, and a productive cough

Two types:

(1) Lobar pneumonia

(a) Infection may spread through entire lobe(s) of lung. Intraalveolar exudates result in dense consolidations.

(b) Typical of S. pneumoniae infections.

(2) Bronchopneumonia

(a) Infection and inflammation spread through distal airways, extending from the bronchioles and alveoli. A patch distribution involving one or more lobes is observed.

(b) Typical of S. aureus, H. influenzae,and K.pneumoniae infection

Diseases that Produce a Productive Cough

Pneumonia

Lung abscess

Tuberculosis

Chronic bronchitis

Bronchiectasis

Bronchogenic carcinoma

Classification

Diseases of the respiratory system can be classified into four general areas:

• Obstructive Diseases (e.g., Emphysema, Bronchitis, Asthma)
• Restrictive Diseases (e.g., Fibrosis, Sarcoidosis, Alveolar Damage, Pleural Effusion)
• Vascular Diseases (e.g., Pulmonary Edema, Pulmonary Embolism, Pulmonary Hypertension)
• Infectious, Environmental and Other Diseases (e.g., Pneumonia, Tuberculosis, Asbestosis, Particulate Pollutants)

Eosinopenia:
Causes

-Corticoid effect (Cushing's syndrome or therapy).
-Stress.