Congestive heart failure (CHF)
A. Left-sided CHF

1. May result from nearly any heart disease affecting the left ventricle (e.g., ischemic heart disease, hypertension, valvular disease).
2. Common signs and symptoms include:
a. Dyspnea (shortness of breath) exacerbated by exertion.
b. Paroxysmal nocturnal dyspnea.
c. Orthopnea.
d. Tachypnea.
e. Pleural effusion.
f. Consequences include pulmonary edema.

B. Right-sided CHF

1. The most common cause of right heart failure is left heart failure. It uncommonly occurs in isolation. Other causes include left-sided lesions (mitral stenosis), pulmonary hypertension, cardiomyopathy, and tricuspid or pulmonary valvular disease.
2. Frequently presents with peripheral edema, especially in the ankles and feet (i.e., dependent edema), enlarged liver or spleen, and distention of the neck veins.

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. 
 

Primary vs. secondary disorders - Most nutritional disorders in developed countries are not due to simple dietary deficiencies but are rather a secondary manifestation of an underlying primary condition or disorder.

• Chronic alcoholism
• Pregnancy and lactation
• Renal dialysis
• Eating disorders
• Prolonged use of diuretics
• Malabsorption syndromes
• Neoplasms
• Food fads
• Vegans
• AIDS 

The Specific Immune Response

Definition

The immune response comprises all the phenomenon resulting from specific interaction of cells of the immune-system with antigen. As a consequence of this interaction cells  appear that mediate cellular immune response as well cells that synthesis and secrete immunoglobulins

Hence the immune response has 2 components.

1. Cell mediated immunity (CMI).

2:. Humoral immunity (antibodies)

(I) Macrophages. Constituent of the M. P. S. These engulf the antigenic material.

(i) Most of the engulfed antigen is destroyed to' prevent a high dose paralysis of the Immune competent cells.

(ii) Some of it persists in the macrophage, retaining immunogenecity for continued stimulus to the immune system.

(iii)The antigenic information is passed on to  effectors cells. There are two proposed mechanisms for this:

(a) As messenger RNA with code for the specific antibody.

(b) As antigen-RNA complexes.

(2) Lymphocytes. There are 2 main classes recognized by surface characteristics.

(A) T-Lymyhocytes (thymus dependant) :- These are responsible for cellular immunity . On exposure to antigen 

• They transform to immunoblasts  which divide to form the effectors cells.
• They secrete lymphokines These are
  • Monocyte migration inhibition factor
  • Macrophage activation factor
  • Chemotactic factor
  • Mitogenic factor
  • Transfer factor
  • Lymphotoxin which kills target cell
  • Interferon.
  • Inflammatory factor which increases permeability. .
• Some remain as 1onglived memory cell for a  quicker recognition on re-exposure
• They also modify immune response by other lymphocytes in the form of “T – helper cells “ and “T-suppressor” cells
• They are responsible for graft rejection

(B) B-Lymphocytes (Bursa dependent). In birds the Bursa of Fabricious controls

these cells. In man, its role is taken up by," gut associated lymphoid tissue)

(i) They are responsible for antibody synthesis. On stimulation they undergo blastic transformation and then differentiation to plasma cells, the site of immunoglobulin synthesis.

(ii) They also form memory cells. But these are probably short lived.

(C) In addition to T & B lymphocytes, there are some lymphocytes without the surface markers of either of them. These are 'null' cells-the-natural Killer (N,K.) cells and cells responsible for antibody dependent cellular-cytotoxicity.

(3) Plasma cells. These are the effectors cells of humoral immunity. They produce the immunoglobins, which are the effector molecules.

FUNGAL INFECTION

Mucormycosis (Zygomycosis; Phycomycosis)

Infection with tissue invasion by broad, nonseptate, irregularly shaped hyphae of diverse fungal species, including Rhizopus, Rhizomucor, Absidia, and Basidiobolus.

Infection is most common in immunosuppressed persons, in patients with poorly controlled diabetes, and in patients receiving the iron-chelating drug desferrioxamine.

Symptoms and Signs

Rhinocerebral mucormycosis is the most common form, but primary cutaneous, pulmonary, or GI lesions sometimes develop, and hematogenous dissemination to other sites can occur. Rhinocerebral infections are usually fulminant and frequently fatal. Necrotic lesions usually appear on the nasal mucosa or sometimes the palate.

Metastatic Tumors 

These are the most common malignant tumor of bone. Certain tumors exhibit a distinct skeletal prediliction. In adults more than 75% of skeletal metastases originate from cancers of the prostate, breast, kidney, and lung. In children, neuroblastoma, Wilms' tumor, osteosarcoma, Ewing sarcoma, and rhabdomyosarcoma are the common sources of bony metastases. Most metastases involve the axial skeleton (vertebral column, pelvis, ribs, skull, sternum), proximal femur, and humerus. The radiologic appearance of metastases can be purely osteolytic, purely osteoblastic, or mixed osteolytic-osteoblastic (majority of cases). In lytic lesions (e.g., kidney& lung), the metastatic cells secrete substances such as prostaglandins, interleukins, etc. that stimulate osteoclastic bone resorption; the tumor cells themselves do not directly resorb bone. Similarly, metastases that elicit a blastic response (e.g., prostate adenocarcinoma) do so by stimulating osteoblastic bone formation.