Parvoviruses
 - smallest DNA virus
 - erythema infectiosum (fifth disease) is characterized by a confluent rash usually beginning on the cheeks ("slapped face") which extends centripetally to involve the trunk; fever, malaise and respiratory problems; and arthralgias and joint swelling (50%).
 
 other associations:
 - aplastic anemia in patients with chronic hemolytic anemias (e.g., sickle cell disease, spherocytosis).
 - repeated abortions associated with hydrops fetalis.
 - pure RBC aplasia by involving the RBC precursors (no reticulocytes peripherally).
 -chronic arthritis

Portal hypertension

 It is elevation of the portal venous pressure (normal 7 m.m Hg). 

 Causes:-
 1- Presinusoidal    
 2- Sinusoidal        
 3- Postsinusoidal
 
Presinusoidal:- 
  a. Massive splenomegaly and increased splenic blood flow.
  b. Portal vein obstruction by thrombosis or outside pressure.
  c. Portal venular obstruction at the portal tracts e.g. by fibrosis, granuloma or chronic hepatitis. 

Sinusoidal:-  
Cirrhosis due to perisinusoidal fibrosis

Postsinusoidal:-  
a.Alcoholic hepatitis leading to perivenular fibrosis.
b. Cirrhosis leading to interference with the blood flow and  to arterio -venous anastomosis resulting in increased venous blood pressure.
c. Veno -occlusive diseases of the liver caused by some drugs & plant toxins. It results in progressive fibrous occlusion of the hepatic venules and vein radicals.
d. Budd- Chiari syndrome: It is hepatic vein thrombosis. 30% of cases have no apparent cause. It produces portal hypertension and hepatomegaly. It is fatal if not treated. 
e. obstruction of major hepatic vein by tumors. 
f. Right sided heart failure and constrictive pericarditis 

Effects of portal hypertension: 

Ascitis
 
It is intraperitoneal accumulation of serous fluid which is a Transudate . It causes abdominal distension.  

Causes

a. Increased hydrostatic pressure` in the portal venous system. 
b. Decreased albumin synthesis in the liver…..decreased colloid osmotic pressure of plasma.
c. Sodium and water retension due to secondary hyperaldosteronism and ADH secretion. 
d. Leakage of hepatic lymph through the hepatic capsule due to hepatic vein obstruction.  

Splenomegaly:-   It results from chronic venous congestion.
- The spleen enlarged with capsular adhesions.
- It shows Gamma Gandi nodules.  - There may be hyperspelenism.  

Porto-Systemic venous anastomosis:-  Present in the following sites Esophageal variesis. Rupture of these vessels is the main cause of death.
Around the umbilicus  “Caput meduci”. Ano-rectal vessels. 
 

Rocky Mountain Spotted Fever (Spotted Fever; Tick Fever; Tick Typhus)

An acute febrile disease caused by Rickettsia rickettsii and transmitted by ixodid ticks, producing high fever, cough, and rash.

Symptoms and Signs

The incubation period averages 7 days but varies from 3 to 12 days; the shorter the incubation period, the more severe the infection. Onset is abrupt, with severe headache, chills, prostration, and muscular pains. Fever reaches 39.5 or 40° C (103 or 104° F) within several days and remains high (for 15 to 20 days in severe cases),

Between the 1st and 6th day of fever, most patients develop a rash on the wrists, ankles, palms, soles, and forearms that rapidly extends to the neck, face, axilla, buttocks, and trunk. Often, a warm water or alcohol compress brings out the rash. Initially macular and pink, it becomes maculopapular and darker. In about 4 days, the lesions become petechial and may coalesce to form large hemorrhagic areas that later ulcerate

Neurologic symptoms include headache, restlessness, insomnia, delirium, and coma, all indicative of encephalitis. Hypotension develops in severe cases. Hepatomegaly may be present, but jaundice is infrequent. Localized pneumonitis may occur. Untreated patients may develop pneumonia, tissue necrosis, and circulatory failure, with such sequelae as brain and heart damage. Cardiac arrest with sudden death occasionally occurs in fulminant cases.

Hematological examination

This is a method by which abnormalities of the cells of the blood and their precursors in the bone marrow are investigated to diagnose the different kinds of anemia & leukemia.

Haemolysis due to drugs and chemicals

This can be caused by :

1. Direct toxic action.
    -> Naphthalene.
    -> Nitrobenzene.
    -> Phenacetin.
    -> Lead.

Heinz bodies are seen in abundance.

2. Drug action on G-6-PD deficient RBC
3. Immunological mechanism which may be : 
    -> Drug induced  autoantibody haemolysis, Antibodies are directed against RBC.
    -> Hapten-cell mechanism where antibodies are directed against which is bound to cell surface e.g. Penicilin.
 

Immunoglobulins. (Ig)

 These are made up of polypeptide chains. Each molecule is constituted by two heavy and two light chains, linked by disulfide (S-S) bonds. The h~ chains are of 5 types, with corresponding, types or  immunoglobulin. IgG (gamma), IgM (mu µ ), IgA(alpha α), IgD(delta ), IgE(epsilon)

Each of these can have light chains of either kappa (k) or lambda type.Each chain has a constant portion (constant for the subtype) land a variable portion (antigen specific).

Enzyme digestion can split the Ig molecule into.2 Fab (antibody binding) fragments and one Fc (crystallisable, complement binding ) fragment.

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,