NEET MDS Lessons
General Pathology
Liver cirrhosis
It is a chronic, progressive diffuse process characterized by
a. Hepatocellular necrosis
b. Replacement by fibrosis and inflammation
c. Hyperplasia of surviving liver cells forming regenerating nodules
d. Vascular derangement.
All these changes lead to loss of the normal liver architecture.
Pathology of cirrhosis
At first the liver is enlarged or of normal size. Late in the disease, it is reduced in size and weight.
Consistency- Firm.
Colour -May be yellow (fatty change), red (congestion), green (cholestaisis), or pale gray (recent nodules due to absence of pigment).
Morphologically According to the size of these nodules, cirrhosis can be classified
Micronodular (regular) cirrhosis. Small nodules 2-3 mm.in diameter.
Macronodular (irregular) cirrhosis, nodules up to one cm in diameter.
Mixed cirrhosis is the end stage of all types of cirrhosis
Microscopic picture
1 Regenerating nodulesn- Proliferated hepatocytes arranged in thick plates and separated by blood sinusoids. Central vein in abnormal sites (eccentric) - Hepatocytes may be small , large , or binucleated
2- Fibrosis- It replaces damaged hepatocytes. It develops at certain sites:-
a-perivenular b -perisinusoidal c -pericellular and d -in relation to portal tracts.
- It may be young, cellular and highly vascular or mature with diminished vasculsarity. It encloses groups of hepatocytes, lobules or regenerating nodules.
-As a result of hepatocyte injury and fibrosis, there’s loss of normal liver architecture including the lobular and acinar pattern as well as the liver cell plates
3- Bile ductular proliferation:- Occurs in the fibrous septa.Focal choestaisis with feathery degeneration of hepatocytes occur at the margins of regenerating nodules. It becomes diffuse terminally.
4- Inflammatory cells:- Lymphocytes, macrophages and plasma cells infiltrate the fibrous septa and regenerating nodules
Etiological classification of cirrhosis
Congenital Occurs at childhood
- congenital syphilis
Hereditary diseases:-
a. Primary idiopathic haemochromatosis b. Thalassemia c. Wilson’s disease d.α 1-antitrypsin deficien e. glycogen storage disease
Acquired
-Cryptogenic (10-50%).
-Alcoholic (30-70%)
-Post viral (15-20%)
- Biliary cirrhosis (16%) primary or secondary.
Characteristics of Immunoglobulin subclasses
I. Ig G:
(i) Predominant portion (80%) of Ig.
(ii) Molecular weight 150, 000
(iii) Sedimentation coefficient of 7S.
(iv) Crosses placental barrier and to extra cellular fluid.
- (v) Mostly neutralising effect. May be complement fixing.
(vi) Half life of 23 days.
2.IgM :
(i) Pentamer of Ig.
(ii) Molecular weight 900, 000
(iii) 19S.
(iv) More effective complement fixation and cells lysis
(v) Earliest to be produced in infections.
(vi) Does not cross placental barrier.
(vii) Halflife of 5 days.
3. Ig A :
- Secretory antibody. Found in intestinal, respiratory secretions tears, saliva and urine also.
- Secreted usually as a dinner with secretory piece.
- Mol. weight variable (160,000+)
- 7 S to 14 S.
- Half life of 6 days.
4.Ig D :
- Found in traces.
- 7 S.
- Does not cross placenta.
5. Ig E
- Normally not traceable
- 7-8 S (MoL weight 200,000)
- Cytophilic antibody, responsible for some hypersensitivity states,
PRIMARY LYMPHEDEMA
can occur as:
1- A congenital defect, resulting from lymphatic agenesis or hypoplasia.
2- Secondary or obstructive lymphedema
- blockage of a previously normal lymphatic; e.g. Malignant tumors
- Surgical procedures that remove lymph nodes
- Postirradiation
- Fibrosis
- Filariasis
- Postinflammatory thrombosis and scarring
Alcoholic (nutritional, Laennec’s) cirrhosis
Pathology
Liver is at first enlarged (fatty change), then return to normal size and lastly, it becomes slightly reduced in size (1.2 kg or more).
- Cirrhosis is micronodular then macronodular then mixed.
M/E
Hepatocytes:- show fatty change that decreases progressively. Few hepatocytes show increased intracytoplasmic haemochromatosis.
b. Fibrous septa:- Regular margins between it and regenerating nodules.
-Moderate lymphocytic infiltrate.
– Slight bile ductular proliferation.
Prognosis:- It Progresses slowly over few years.
Eosinophilia:
Causes
-Allergic disorders.
-Parasitic infection.
-Skin diseases.
-Pulmonary eosinophilia.
-Myeloproliferative lesions and Hodgkin's disease.
Parathyroid hormone
Parathyroid hormone (PTH) is a polypeptide (84 amino acid residues) secreted by the chief cells of the parathyroid glands (four glands: two in each of the superior and inferior lobes of the thyroid; total weight 120 mg).
The main action of PTH is to increase serum calcium and decrease serum phosphate.
Its actions are mediated by the bones and kidneys -
In bone, PTH stimulates osteoclastic bone resorption and inhibits osteoblastic bone deposition. The net effect is the release of calcium from bone.
In the kidney, PTH has the following effects:
- Increases calcium reabsorption.
- Decreases phosphate reabsorption.
- Increases 1-hydroxylation of 25-hydroxyvitamin D (i.e. activates vitamin D).
PTH also increases gastrointestinal calcium absorption.
Eczematous Dermatitis
Eczematous dermatitis includes a large category of skin lesions characterized by severe pruritus and distinctive gross and microscopic features.
- type I hypersensitivity is involved with atopic dermatitis in patients who have an allergic history.
- type IV hypersensitivity is involved in contact dermatitis (poison ivy).
- acute eczematous dermatitis is characterized by a weeping, pruritic rash, while a chronic eczematous dermatitis presents with dry, scaly, plaque-like thickening of the skin, a process called lichenification.