Eosinophilia:
Causes

-Allergic disorders.
-Parasitic infection.
-Skin diseases.
-Pulmonary eosinophilia.
-Myeloproliferative lesions and Hodgkin's disease.

EMBOLISM 

An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin

99% due to dislodged thrombus

Types: 
1. Thrombo-embolism 
2. Fat embolism 
3. Air embolism 
4. Nitrogen embolism

 Emboli result in partial or complete vascular occlusion. 

 The consequences of thromboembolism include ischemic necrosis (infarction) of downstream tissue

PULMONARY THROMBOEMBOLISM
- 95% originate from deep veins of L.L

Special variants: - Saddle embolus: at bifurcation of Pulmonary artery

Paradoxical embolus: Passage of an embolus from venous to systemic circulation through IAD, IVD

CLINICAL CONSEQUENCE OF PULMONARY THROMBOEMBOLISM :

Most pulmonary emboli (60% to 80%) are clinically silent because they are small 

a. Organization: 60 – 80 % 
b. Sudden death, Right ventricle failure, CV collapse when more than 60 % of pulmonary vessels are obstructed. 
c. Pulmonary hemorrhage: obstruction of medium sized arteries. 
d. Pulmonary Hypertension and right ventricular failure due to multiple emboli over a long time.

Systemic thromboembolism

Emboli traveling within the arterial circulation 
80% due to intracardiac mural thrombi
2/3  Lt. ventricular failure

 The major targets are: 
 
 1. Lower limbs 75% 
 2. Brain 10% 
 3. Intestines 
 4. Kidneys 
 5. Spleen

Fat embolism 

Causes 
1. Skeletal injury (fractures of long bones ) 
2. Adipose tissue Injury

Mechanical obstruction is exacerbated by free fatty acid release from the fat globules, causing local toxic injury to endothelium. - In skeletal injury, fat embolism occurs in 90% of cases, but only 10% or less have clinical findings

 Fat embolism syndrome is characterized by 
 
 A. Pulmonary Insufficiency 
 B. Neurologic symptoms 
 C. Anemia 
 D. Thrombocytopenia 
 E. Death in 10% of the case 
 
 Symptoms appears 1-3 days after injury
 
 Tachypnea, Dyspnea, Tachycardia and Neurological symptoms
 
Air Embolism 

causes: 1. Obstetric procedures 
2. Chest wall injury 
3. Decompression sickness: in Scuba and deep-sea divers ((nitrogen )) 

 More then 100ml of air is required to produce clinical effect. 
 
 Clinical consequence
 1. Painful joints: due to rapid formation of gas bubbles within Sk. Muscles and supporting tissues. 
 2. Focal ischemia in brain and heart 
 3. Lung edema, Hemorrhage, atelectasis, emphysema, which all lead to Respiratory distress. (chokes) 
 4. caisson disease: gas emboli in the bones leads to multiple foci of ischemic necrosis, usually the heads of the femurs, tibias, and humeri
 
 Amniotic fluid embolism 
 - Mortality Rate = 20%-40% 
 - Very rare complication of labor 
 
 - due to infusion of amniotic fluid into maternal circulation via tears in placental membranes and rupture of uterine veins. 
 - sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures, DIC and coma 
 
 - Findings: Squamous cells, languo hair, fat, mucin …..etc within the pulmonary microcirculation

Fibrous and Fibro-Osseous Tumors

Fibrous tumors of bone are common and comprise several morphological variants.
1. Fibrous Cortical Defect and Nonossifying Fibroma 
Fibrous cortical defects occur in 30% to 50% of all children older than 2 years of age; they are probably developmental rather than true neoplasms. The vast majority are smaller than 0.5 cm and arise in the metaphysis of the distal femur or proximal tibia; almost half are bilateral or multiple. They may enlarge in size (5-6 cm) to form nonossifying fibromas. Both lesions present as sharply demarcated radiolucencies surrounded by a thin zone of sclerosis. Microscopically are cellular and composed of benign fibroblasts and macrophages, including multinucleated forms. The fibroblasts classically exhibit a storiform pattern. Fibrous cortical defects are asymptomatic and are usually only detected as incidental radiographic lesions. Most undergo spontaneous differentiation into normal cortical bone. The few that enlarge into nonossifying fibromas can present with pathologic fracture; in such cases biopsy is necessary to rule out other tumors.

2. Fibrous Dysplasia 

is a benign mass lesion in which all components of normal bone are present, but they fail to differentiate into mature structures. Fibrous dysplasia occurs as one of three clinical patterns:
A. Involvement of a single bone (monostotic)
B. nvolvement of multiple bones (polyostotic)
C. Polyostotic disease, associated with café au lait skin pigmentations and endocrine abnormalities, especially precocious puberty (Albright syndrome).

Monostotic fibrous dysplasia accounts for 70% of cases. It usually begins in early adolescence, and ceases with epiphyseal closure. It frequently involves ribs, femur, tibia & jawbones. Lesions are asymptomatic and usually discovered incidentally. However, fibrous dysplasia can cause marked enlargement and distortion of bone, so that if the face or skull is involved, disfigurement can occur.

Polyostotic fibrous dysplasia without endocrine dysfunction accounts for the majority of the remaining cases. 
It tends to involve the shoulder and pelvic girdles, resulting in severe deformities and spontaneous fractures.

Albright syndrome accounts for 3% of all cases. The bone lesions are often unilateral, and the skin pigmentation is usually limited to the same side of the body. The cutaneous macules are classically large, dark to light brown (café au lait), and irregular.

Gross features

• The lesion is well-circumscribed, intramedullary; large masses expand and distort the bone.
On section it is tan-white and gritty.

Microscopic features

• There are curved trabeculae of woven bone (mimicking Chinese characters), without osteoblastic rimming
• The above are set within fibroblastic proliferation
Individuals with monostotic disease usually have minimal symptoms. By x-ray, lesions exhibit a characteristic ground-glass appearance with well-defined margins. Polyostotic involvement is frequently associated with progressive disease, and more severe skeletal complications (e.g., fractures, long bone deformities, and craniofacial distortion). Rarely, polyostotic disease can transform into osteosarcoma, especially following radiotherapy. 

Hepatic failure 
Etiology. Chronic hepatic disease (e.g., chronic active hepatitis or alcoholic cirrhosis) is the most common cause of hepatic failure although acute liver disease may also be responsible.

- Widespread liver necrosis may be seen with carbon tetrachloride and acetaminophen toxicity. Widespread steatosis is seen in Reye's syndrome, a cause of acute liver failure most often seen in children with a recent history of aspirin ingestion for an unrelated viral illness. 
- Massive necrosis may also be seen in acute viral hepatitis, after certain anesthetic agents, and in shock from any cause. 

Clinical features. Hepatic failure causes jaundice, musty odor of breath and urine, encephalopathy, renal failure (either by simultaneous toxicity to the liver and kidneys or the hepatorerial syndrome), palmar erythema, spider angiomas, gynecomastia , testicular atrophy 

Multiple myeloma.

Blood picture:

- Marked rouleaux formation.
- Normpcytic normochromic anaemia.
- There may be leucopenia or leucoery!hrohlastic reaction.
- Atypical plasma cells may be seen in some patients
- Raised ESR
- Monoclonal hypergammaglobulinaemia 
- If light chains are produced in excess, they are excreted in urine as bence jones protein

Bone marrow

- Hyper cellular
- Plasma cells from at least 15 – 30% atypical forms and myeloma cells are seen.
 

Keloids
1. Characterized by a progressively enlarging scar.
2. Caused by an abnormal accumulation of collagen at the site of injury.
3. More common in African-Americans.