Acne vulgaris is a chronic inflammatory disorder usually present in the late teenage years characterized by comedones, papules, nodules, and cysts.
 - subdivided into obstructive type with closed comedones (whiteheads) and open comedones (blackheads) and the inflammatory type consisting of papules, pustules, nodules, cysts and scars.
 - pathogenesis of inflammatory acne relates to blockage of the hair follicle with keratin and sebaceous secretions, which are acted upon by Propionibacterium acnes (anaerobe) that causes the release of irritating fatty acids resulting in an inflammatory response.
 - pathogenesis of the obstructive type (comedones) is related to plugging of the outlet of a hair follicle by keratin debris.
 - chocolate, shellfish, nuts iodized salt do not aggravate acne.
 - obstructive type is best treated with benzoyl peroxide and triretnoin (vitamin A acid)
 - treatment of inflammatory type is the above plus antibiotics (topical and/or systemic; erythromycin, tetracycline, clindamycin).

Valvular disease
A. Generally, there are three types:
1. Stenosis—fibrotic, stiff, and thickened valves, resulting in reduced blood flow through the valve.

2. Regurgitation or valvular insufficiency— valves are unable to close completely, allowing blood to regurgitate.

3. Prolapse—“floppy” valves; may occur with or without regurgitation. The most common valvular defect.

Immunodeficiency

This may be :-

• Congenital (Primary)
• Acquired (Secondary)

Features : Complete or near complete lack of T & B lymphoid tissue. Fatal early in life Even with marrow grafting, chances of graft versus host reaction is high.

B. T Cell Defects :

• Thymic dysplasia
• Digeorge’s syndrome
• Nazelof’s syndrome
• Ataxia teltngiectaisa
• Wiscott Aldrich’s syndrome

These  lessons show predominantly defective cell mediated immunity. But they may also show partial immunoglobulin defects cell mediated immunity. But they may also show partial immunoglobulin defects due to absence og T-B co-operation.

C. Humoral immunity defects.

Bruron type- aggammaglobulinaemia.

• Dysgammaglobulinaemias-variable immunodeficiency’s of one or more classes.

Acquired deficiency

A. Immuno suppression by :

• Irradiation.
• Corticoids.
• Anti metabolites.
• Anti lymphocyte serum.

B. Neaplasia  of lymphoid system :

• Hodgkin's and Non Hodgkin's lymphomas.
• Chronic lymphocytic leukaemia..
• Multime myeloma and other paraproteinaemias (normal immunoglobulins reduced in spite of hyperglobulinaemia).

c. excessive protein loss.

• Nephrotic Syndrome.
• Protein losing enteropathy.

Lymphocytosis:
Causes
-Infections in children and the neutropenic infections in adults.
-Lymphocytic leukaemia.
-Infectious mononucleosis.
-Toxdplasmosis.
-Myast'henia gravis.

Aneurysm

An aneurysm is a localized abnormal dilation of a blood vessel or the heart

Types:
1. True aneurysm - it involves all three layers of the arterial wall (intima, media, and adventitia) or the attenuated wall of the heart.
 e.g. Atherosclerotic, syphilitic, and congenital aneurysms, and ventricular aneurysms that follow transmural myocardial infarctions. 

2 False aneurysm 
(also called pseudo-aneurysm) is a breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space ("pulsating hematoma"). 
E.g. ventricular ruptures after MI that are contained by a pericardial adhesion
E.g. a leak at the junction of a vascular graft with a natural artery.

Aneurysms are classified by macroscopic shape and size 
Saccular aneurysms 

spherical outpouchings (involving only a portion of the vessel wall, and often contain thrombi. 

Fusiform aneurysms

diffuse, circumferential dilation of a long vascular segment; 

they vary in diameter and length and can involve extensive portions of the aortic arch, abdominal aorta, or even the iliacs.

Aortic Aneurysm 

The two most important causes are: 

1- atherosclerosis : the most common cause 
It causes thinning and weakening of the media. The intimal plaques compress the underlying media and also compromise nutrient and waste diffusion from the vascular lumen into the arterial wall. The media consequently undergoes degeneration and necrosis, thus allowing the dilation of the vessel 

2- cystic medial degeneration of the arterial media. E.g. Marfan syndrome.

3- Other causes include: trauma, congenital defects (e.g., berry aneurysms), infections (mycotic aneurysms), systemic diseases, such as vasculitis.

Mycotic  Aneurysm :  
Infection of a major artery that weakens its wall is called a mycotic aneurysm

possible complications: thrombosis and rupture. 

It can originate from: 
(1) embolization of a septic thrombus, usually as a complication of infective endocarditis 
(2) extension of an adjacent suppurative process; 
(3) circulating organisms directly infecting the arterial wall 

Mycotic AAAs are atherosclerotic lesions infected by lodging of circulating microorganisms in the wall 

- e.g.  bacteremia from a primary Salmonella gastroenteritis. 

Abdominal Aortic  Aneurysm

Atherosclerotic aneurysms occur most frequently in the abdominal aorta ,the common iliac arteries, the arch, and descending parts of the thoracic aorta can also be involved 

Pathogenesis 

AAA occurs more frequently in men and rarely develops before age 50. 

Atherosclerosis is a major cause of AAA 

 hereditary defects in structural components of the aorta (e.g., defective fibrillin production in Marfan disease affects elastic tissue synthesis) 
 
 Morphology :
  Usually positioned below the renal arteries and above the bifurcation of the aorta 
  
  AAA can be saccular or fusiform 
  
  as large as 15 cm in diameter, and as long as 25 cm. 
  
  Microscopically: atherosclerosis with destruction and thinning of the underlying aortic media 
  
  the aneurysm frequently contains a laminated mural thrombus
  
  Syphilitic Aneurysm 
  
  Caused by The spirochetes T. pallidum 
  
  Tertiary stage of syphilis can cause obliterative endarteritis of the involve small vessels in any part of the body, including the vasa vasorum of the aorta 
  
  This results in ischemic medial injury, leading to aneurysmal dilation of the aorta and aortic annulus, and eventually valvular insufficiency. 
  
  valvular insufficiency and massive volume overload lead to hypertrophy of the left ventricle. The greatly enlarged hearts are sometimes called "cor bovinum" (cow's heart).
  
  CLINICAL CONSEQUENCES
  
  1.  Rupture → massive potentially fatal hemorrhage 
  2. Obstruction of downstream vessel → tissue ischemic injury
  3. Embolism → from atheroma or mural thrombus 
  4. Impingement and compression on an adjacent structure 
  5. Presentation as an abdominal mass 

Hepatitis D virus—can only infect cells previously infected with hepatitis B. 
 Delta hepatitis (HDV) is associated with a 35-nm RNA virus composed of a delta antigen-bearing core surrounded by HBV's Ag coat;

HDV requires HBV for replication.

Delta hepatitis can cause quiescent HBV states to suddenly worsened . Its transmission is the same as that of HBV.
 
 Hepatitis E virus—a high mortality rate in infected pregnant women.

Hepatitis E (HEV) is caused by a single-stranded RNA virus. The disease is typically self-limited and does not evolve into chronic hepatitis; it may, however, be cholestatic.

Pregnant women may develop fulminant disease.

Transmission is by the fecal oral route.

HEV occurs mainly in India, Nepal, Pakistan, and Southeast Asia.