Ichthyosis vulgaris is a genetic disease characterized by increased cohesiveness of the cells in the stratum corneum, resulting up in a piling up stratum corneum (scales like a fish).

Congenital heart defect
Congenital heart defects can be broadly categorised into two groups,
o    acyanotic heart defects ('pink' babies) :

 An acyanotic heart defect is any heart defect of a group of structural congenital heart defects,  approximately 75% of all congenital heart defects.
 It can be subdivided into two groups depending on whether there is shunting of the blood from the left vasculature to the right (left to right shunt) or no shunting at all.

Left to right shunting heart defects include 
- ventricular septal defect or VSD (30% of all congenital heart defects),
- persistent ductus arteriosus or PDA, 
- atrial septal defect or ASD, 
- atrioventricular septal defect or AVSD.

Acyanotic heart defects without shunting include 
- pulmonary stenosis, a narrowing of the pulmonary valve, 
- aortic stenosis 
- coarctation of the aorta.

cyanotic heart defects ('blue' babies). 
obstructive heart defects

 cyanotic heart defect is a group-type of congenital heart defect. These defects account for about 25% of all congenital heart defects. The patient appears blue, or cyanotic, due to deoxygenated blood in the systemic circulation. This occurs due to either a right to left or a bidirectional shunt, allowing significant proportions of the blood to bypass the pulmonary vascular bed; or lack of normal shunting, preventing oxygenated blood from exiting the cardiac-pulmonary system (as with transposition of the great arteries).

Defects in this group include 
hypoplastic left heart syndrome,
tetralogy of Fallot, 
transposition of the great arteries, 
tricuspid atresia, 
pulmonary atresia, 
persistent truncus arteriosus.
 

Polycystic kidney disease

Characterized by the formation of cysts and partial replacement of renal parenchyma.
Genetic transmission: autosomal dominant.
Clinical manifestations:

 hypertension, hematuria, palpable renal masses, and progression to renal failure. Commonly associated with berry
aneurysms. 

OEDEMA

 Excessive accumulation of fluid in the extra vascular compartment (intersttitial tissues). This includes ascites (peritoneal sac), hydrothorax (pleural cavity) hydropericardium (pericardial space) and anasarca (generalised)

Factors which tend to accumulate interstitial fluid are:

- Intravascular hydrostatic pressure

- Interstitial osmotic pressure.

- Defective lymphatic drainage.

- Increased capillary permeability.

Factors that draw fluid into circulation are:

- Tissue hydrostatic-pressure (tissue tension).

- Plasma osmotic pressure,

Oedema fluid can be of 2 types:

A. Exudate.

It is formed due to increased capillary permeability as in inflammation.

B. Transudate

Caused by alterations of hydrostatic and osmotic pressures.

Local Oedema

1. Inflammatory oedema. Mechanisms are.

- Increased capillary permeability.

- Increased vascular hydrostatic pressure.

- Increased tissue osmotic pressure.

2.Hypersensitivity reactions especially types I and III

3. Venous obstruction :

- Thrombosis.

- Pressure from outside as in pregnancy, tourniquets.

4. Lymphatic obstruction:

- Elephantiasis in fillariasis

- Malignancies (Peau de orange in breast cancer).

Generalized Oedema

1.         Cardiac oedema

Factors :Venous pressure increased.

2. Renal oedema

- Acute glomerulonephritis

- Nephrotic syndrome

3. Nutritional (hypoproteinaemic) oedema. it is seen in

- Starvation and Kwashiorkor

- Protein losing enteropathy

4.  Hepatic oedema (predominantly ascites)

Factors:

- Fall in plasma protein synthesis

- Raised regional lymphatic and portal venous pressure

5. Oedema due to adrenal corticoids

As in Cushing's Syndrome

Pulmonary oedema

- Left heart failure and mitral stenosis.

- Rapid flv infusion specially in a patient of heart failure.

Psoriasis
1. Characterized by skin lesions that appear as scaly, white plaques.
2. Caused by rapid proliferation of the epidermis.
3. Autoimmune pathogenesis; exact mechanism is unclear.

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).