Disease of the Annexa

Question 1

What is acne?

Answer 1

Acne is a chronic inflammatory disorder involving the follicles (pilosebaceous unit), therefore the sebaceous areas of the body, such as the face, thorax and back. It is a frequent disorder, which mostly occurs between 12-25y. At least more than 80% of young people present acne, however it doesn’t spare adults, for instance 15% of adult women are involved with acne. White people are more commonly affected by acne compared to Afro-Americans/Orientals.

Question 2

What are the typical skin lesions of acne?

Answer 2

Primary lesions : White or black heads (comedo), which are the dilation of the infundibulum of the follicle. The start of acne is the comedo, which is the plug of the opening of the follicle. There is a kind of occlusion of the opening of the follicle, which is the start of the inflammatory process of acne.

Then we have the papules and pustules. Pustules are characterized by a collection of neutrophils in the follicles. Papules instead are characterized by follicular cysts. When the follicle enlarges there is the formation of the papule and pustule.

Nodules occur when there is a rupture of the follicle and the inflammatory reaction increases. Comedo, nodules, pustules, and papules are the lesions that characterise acne.

Question 3

How is acne graded?

Answer 3

It is based on the severity of the acne.
Grade 1: Comedo, occasional papules. The comedo can be:
Open (blackhead2) : Dilation of the infundibulum of the hair with dilated orifice of dark colour filled with keratin, lipids, melanin, bacteria, and fungi. Closed comedo (whitehead) : Small follicular cysts filled with cornified cells and microorganisms with narrowed follicular ostium.

Grade 2 (moderate acne) :Papules, comedo, few pustules. Most of the lesions are comedo.

Grade 3 : Predominant pustules, nodules, abscesses. Represented by the development of many papules and pustules.

Grade 4 (nodulocystic) : Main cysts, abscesses, widespread scarring. Most severe type characterized by comedo, inflammatory lesions, and large cysts and nodules greater than 5mm in diameter. Also called nodulocystic acne, which may also cause cheloids.More frequent in males than females

Question 4

Pathogenesis and etiology of acne?

Answer 4

Acne is a multifactorial disease, whose etiopathogenesis includes:
Genetic factors, hormones, endogenous and exogenous factors like drugs, cosmetics, environmental toxicants, stress, nutrition like dairy products and food of high glycaemic load.

Epidemiological studies have shown that there is a relationship between the amino acid Leucine, found in dairy products, and the stimulation of sebum and the proliferation of the follicles, which is followed by the closing of the pore, eventually starting acne process.

1. Altered keratinisation of the follicle leading to the closing
   of the opening, which is represented by the comedo.
2. Excess of sebum produced by the sebaceous gland
   attached to the follicle, so the sebum cannot go out.
3. The Cutibacterium acnes acts on the sebum to stimulate the inflammatory response. It is a Gram+ anaerobic bacteria, a normal saprophyte of the skin, C. acnes prefers sebaceous follicles and uses lipids as the main source of energy, stimulating a massive inflammatory response.
4. Stimulates an inflammatory process, with the release of inflammatory mediators. Hydrolyses the sebum triglycerides into the proinflammatory free fatty acids, which have an inflammatory stimulus on the process, as they act as complement.

Question 5

Treatment for acne?

Answer 5

Derivatives of vitamin A.

Question 6

What is rosacea?

Answer 6

In the past it was called acne rosacea because it was thought that it had a relationship with acne, but they are 2 different processes. It is a chronic dermatosis with multiple clinical expressions, especially involving the mid face region. It is a typical disease of people with fare skin, blond hair, and blue/green eyes. The most affected age is 30 years old. Women are affected more often than man. Rosacea is a typical disease of people of Celtic origin.
Rosacea is divided into 4 stages:
1. Erythemato-telangiectatic : Centrofacial erythema, telegiectasia, flushing.
2. Papulo-pustular : Centrofacial erythema, variable number of red papules and pustules.
3. Phymatous : Skin thickening, tissue hypertrophy, sebaceous glands hyperplasia.
4. Ocular : Blepharitis, conjunctival redness, ocular dryness, pruritus and tearing.

It is not necessary to have all the steps, rosacea can also start with the phymatous stage. Usually, one step antedates the other but it is not mandatory.

Question 7

What is the erythemato-telangiectatic phase?

Answer 7

1. Transient congestive flushing : Transient redness, lasting a few minutes, with a sensation of warmth in the face. Triggers are emotional stress, alcohol, sun exposure, hot and spicy meals, abrupt transition from a cold to hot temperature. It only lasts a few minutes.
2. Erythrosis or Persistent telangiectatic redness : Not transient in this stage, it is a persistent dilatation of the face. Commonly named cuperose. Usually in the nose and cheeks.

Question 8

What is the papulo-pustular phase?

Answer 8

Papules and pustules are generally located on the nose and cheekbones, more rarely on the forehead and chin. The development of papule and pustules are like acne, but without the comedo. This is the most important difference from acne. This is a disfiguring phase.

Question 9

What is the phymatous stage?

Answer 9

Tissue hypertrophy manifesting as thickened skin with irregular contours of the nose (rhinophyma). Common associated features include prominent sebaceous hyperplasia and oily skin.

Question 10

What is the ocular rosacea stage?

Answer 10

The most frequent manifestation is simple conjunctival hyperaemia. Blepharitis or chalazion is also common, while Keratitis and uveitis are rarer.

Question 11

Etiopathogenesis of rosacea?

Answer 11

The etiopathogenesis is not totally clear, there is a role of solar radiation, with damage of the connective tissue of the dermis, causing an immune reaction directed against the elastotic tissue, collagen VII and demodex folliculorum. Solar radiation damages both perivascular and vascular elastic tissue.
GI disorders play a role in rosacea/flushing :
• Gastritis.
• Hypochlorhydria.
• Alterations of the intestinal mucosa.
• Bacterial overgrowth syndrome of the small intestine.
• Lipid deficiency Helicobacter pylori also plays a role in rosacea.

Question 12

What are some differential diagnoses of rosacea?

Answer 12

Seborrheic dermatitis : Is one of the most frequent disorders of the outpatient consultation. It is a type of endogenous eczema. Occurs in the sebaceous areas.There are no papules and pustules. There are greasy scales around the nose, in the scalp, eyebrows. Sometimes the 2 process co-exist. They are different processes also
considering the pathogenesis.

2. Butterfly rush of SLE : In this case the butterfly rash is always the sign of a systemic involvement of SLE. The patients probably also have other types of problems, such as the presence of autoantibodies. There are not papules or pustules.
3. Acne : The difference is in the age of the patient and the absence of comedo.

Question 13

What is alopecia? How is it classified?

Answer 13

It is the limited or widespread lack of hair with possible atrophy or destruction of the hair follicle.

1. Scarring alopecia : Implies a permanent loss of hair. They cannot regrow.
   a. Congenital: ex. Aplasia Cutis. The baby is born with defect in the cap with a permanent loss of hair. It is probably due to a traumatic origin, even though sometimes there is no evidence
   of a traumatic process.
   b. Acquired
2. Non scarring alopecia like alopecia areata.

Question 14

Where can we see acquired scarring alopecia? What are the causes?

Answer 14

Lichen ruber planus, discoid chi runic LE, morphea, BCC, lymphoma.

Causes can be physical agents like radiation therapy for cancer, infectious, neoplastic, idiopathic and autoimmune.

Question 15

What are some acquired non scarring alopecias?

Answer 15

Monilethrix is a rare genodermatosis characterized by hypotrichiosis.

Alopecia areata is characterized by an autoimmune process against the follicles, shows coin shaped patches with rapid development. Can be totalis or subtotalis. The beard can also be involved.

Calvizea also known as baldness or more scientifically as androgenetic alopecia. It is a genetic disorder due to an altered response of the hard to androgens. Men are graded with the Hamilton score which looks at receding frontal hairline and bitemporal hairline. Women are graded by the Ludwig score which looks at hair loss in the crown.

Question 16

What is the pathogenesis of androgenetic alopecia?

Answer 16

The androgenetic alopecia is not a real loss of hair, it is due to a shortening of the hair cycles, with a progressive miniaturisation of the stem of the hairs. The hairs become very thin and then disappears. Due to genetics and androgens. There is not a loss of hair in baldness. If you see a bald scalp there is plenty of vellus. There is an increased frequency and longer duration of empty follicles.

Question 17

What is non scarring acquired alopecia telogen effluvium?

Answer 17

Temporary hair loss due to the excessive shedding of resting or telogen hair after some shock to the system.
The shock:
• Stressful event-
• Acute illness.
• Surgical intervention.
• Thyroid disease, iron deficiency, weight loss.
• Childbirth: postpartum hair loss All these are triggering events that can cause a telogen effluvium, in which people see a profuse loss of hairs, lasting some months, 3-4 months, after the stressful event stops, there is a total regrowth of the hair.

Question 18

What are scabies?

Answer 18

It is a parasitosis. It is due to a mite sarcoptes scabei hominis, which is a mandatory human parasitosis. It is an infection diffused all over the world, there are no areas spared by scabies. It is a very contagious disease, passed on by a close contact with affected people. The sarcoptes scabies don’t fly, and therefore you need a close contact, such as sleeping together with someone infected. An indirect contact is possible such as via beds and sheets. In the skin the mite creates tunnels in the superficial part of the skin (epidermis), where there is the production of eggs. The females produce tunnels in the skin, 2-3 mm per day. They produce 1-3 eggs/day. People tends to search consultation for the itch. It is an incredible itch that worsens at night because heat in the bed stimulates females to have a strong activity to create the tunnel, so people cannot sleep.

Question 19

Clinical appearance of scabies?

Answer 19

Track-like burrows are the tunnels that females create for the eggs and are pathognomonic for the disease. You can look for the burrows between the digits and on the wrists. If you look with a dermatoscope, you can see the burrows created by the females to put inside the eggs. Main sites of involvement : hands, axillae, trunk, genitalia, gluteal region and feet
If the scabies is not treated there is a widespread rash. It is mainly due to the antigens of the mites, eggs and due to the scratch of the patient. The rash is made by papules and excoriations made by the patient itself.

Question 20

How to diagnose scabies? Treatment?

Answer 20

1. Find the burrows (where there is the mite).
2. Obtain a skin scraping of the burrow à put it on a slide and you can see the parasite Examine under a microscope for mites, eggs, or mite faecal matter (scybala). Treated with antihistamines, anti inflammatory agents, permethrin which is an insecticide.

Question 21

What is pediculosis?

Answer 21

They are insects, hematophagy, obligate parasites of humans. We can see the pediculus with the naked eye. Types:
• Pediculus pubis/ pediculus pubis: looks like a crab; larger body.
• Pediculus capitis.
• Pediculus corporis.

Question 22

What is pediculus capitis?

Answer 22

It is diffused all over the world and is a typical disease of children. The parasitosis is taken by a direct or indirect contact, such as the comb or the caps that the children share. Head-to-head contact with an already infected person is the most common way to get head lice.

The pediculus capitis life cycle:
1. Egg (called nits): attached to the hairs; it is cemented. 4 to 10 nits a day.
2. Nymph.
3. Adults.
Main symptoms are itch, scratching lesions and possible papules and vesicles.
DDX : Dandruff.

Treatment si permetrine, malathion and benzil benzoato.

Question 23

What is pediculus corporis?

Answer 23

It is the less frequent and the less important. It is a body louse, roughly 3mm in length. It is a disease of the homeless and the people with poor hygiene. The insect bites the host, they suck the blood and then it lives on the clothes. It can be a vector of epidemic typhus, relapsing fever of other infectious diseases. It is characterised by itch, macules, and papules. It is a chronic body lice infestation which causes thickening and discoloration of skin. It is also known as “vagabond disease”.

Question 24

What is pediculosis pubis?

Answer 24

It is a Crab louse. It is a sexual transmitted disease or indirect contact. The itching is the chief complain of patients, in addition to small red or blue spots, which represent the bits of the lice on the pubic area. The diagnosis is made by the identification of the lice and nits because the process is the same. The nits are cemented on the hairs of the pubis. Also called crabs and they have a larger body.

Question 25

What is cutaneous vasculitis?

Answer 25

A group of conditions characterised by acute, relapsing, or chronic inflammatory damage to small or medium-sized blood vessels in the skin resulting in downstream ischemic tissue damage. Cutaneous vasculitis can occur as : Single organ involvement, in the setting of systemic involvement for example, the kidney, the GI tract and so on.

Manifestations include palpable purport which is a hemorrhagic papule caused by RBC e travasati on, nodules, livedo reticularis which is a network of hemorrhagic lesions sometimes seen in PAN, and urticaria lesion.

They can affect small, medium or large vessels and can be caused by infections, tumors, autoimmune disorder or drugs.

IgM and IgG vasculitis are the most common characterized by the deposition of immunoglobulins.

Diagnosis includes a good clinical-pathologic correlation (histopathology and DIF), organs involved, the size of affected blood vessels, imaging, and laboratory findings (ANCA).

Question 26

What is allergology?

Answer 26

It is a subspecialty of dermatology, which treats dermatitis/eczema5. It is a group of disorders in the which the skin becomes inflamed and forms erythema, vesicles (main lesions), and blisters, and becomes crusty, thick, and scaly, causing burning and itching.

Question 27

What is the difference between acute and chronic dermatitis?

Answer 27

Acute : Eczema is characterised by the development of real vesicles. It is an itchy condition.

Chronic : less vesicles are present, and the skin looks more dry. There is a thickened plaque. There is less exudate.

Question 28

How is eczema?

Answer 28

Endogenous : Atopic dermatitis, seborrheic dermatitis, eczema nummulare, eczema disidrosico.

Exogenous : Irritant contact dermatitis (dermatite irritative da contatto) or allergic contact dermatitis (dermatite allergica da contatto).

Question 29

What is atopic dermatitis?

Answer 29

Typically, but not exclusive disease of paediatric age, characterised by an itchy dermatitis with a chronic relapsing evolution and peculiar topographical characteristics. It has a peculiar involvement of some body areas. It is associated with:
• Asthma
• Rhinitis
• Conjunctivitis Often.
It is associated with aero allergens or food allergens. 75% manifest atopic dermatitis in the first year of life. There is equal prevalence in both sexes. Etiology is related to genetics, environmental factors and other non immunological factors.

Question 30

What is the pathogenesis of atopic dermatitis?

Answer 30

For pathogenesis we have 2 main causes : An immunological dysfunction and a dysfunction of the skin barrier. In atopic skin we have a skin barrier damage in the skin, lipids are intercellular, so we have a strong penetration of foreign substances that can cause the immunological reaction of the body in a genetic predisposition.
It is due to a deficit of filaggrin, that, in a physiological condition, drives the correct differentiation of the epidermis, ensuring the correct barrier composition. If filaggrin is not functioning, there is barrier damage. T lymphocytes react to the antigens causing the immune response. IL4 and IL13 are important.

Question 31

What is nummular eczema?

Answer 31

It is an endogenous eczema that has always been considered idiopathic. It is considered as the atopic dermatitis in adults. It is characterised by coin shaped lesions in the upper part of the leg. We have criteria to make diagnosis of atopic dermatitis. The major criteria are:
• Chronicity of the disease.
• History of atopy.
• Involvement of face and flexures.
• Itching.

Question 32

What is contact dermatitis?

Answer 32

It is the exogenous type of dermatitis which is divided into :

Irritant contact dermatitis : Irritation coming from substances, such as : water, disinfectants, detergents, and soluble oils.

Allergic contact dermatitis : Classic presentation of a T cell-mediated, delayed type hypersensitivity response to exogenous agents
The material is called an allergen. Ex. Nickel.

Patch test is used.

Question 33

Epidemiology of sexually transmitted diseases?

Answer 33

STD control is a priority of the WHO. Every year in the world there more than 448 million new cases. 1/3 of cases concerns minors under 25y, 1/10 has HIV co-infection.

The most common STD are :
Considering viral origin ; Condylomata, HPV and Herpes.
Bacterial.
Urethritis.
Syphilis.

Question 34

What is syphilis? What are the phases?

Answer 34

It is caused by the bacterium, treponema pallidum. Risk factored include engaging in unprotected sex, multiple sex partners and infection with HIV.

Primary syphilis : Infection develops 2-3 weeks after the exposure.
The disease starts as a painless sore, typically on your genitals, rectum, or mouth. Syphiloma: single firm painless ulcer tending to
spontaneous resolution in about 1 month, at the site of penetration of treponema. It is associated to a loco-regional aphlegmatic
lymphadenopathy primary complex, 1/3 heal spontaneously.

Secondary syphilis is the spreading of the bacterium all over the body. Systemic phase of the disease from 1-6 months after the sore.
Fever, malaise, bone, and joint pain, diffuse lymphadenomegaly involvement of all internal organs (often asymptomatic). Diffused lesions of the skin (roseoles, then papules) and mucous membrane (mucous plaques and flat condylomas) asymptomatic. It is a non-itchy rash with reddish-brown (copper like) papules on the trunk and frequently affects palms and soles.

Tertiary syphilis : Very rare; 20-40y after the first disease. Cardiovascular aneurysm of the aorta. Neurological involvement. Gumma is a solitary granulomatous lesion with central necrosis on the skin and bone.

Question 35

What is latent syphilis? How is syphilis treated?

Answer 35

Early latent : First 2 years. Patient is very infectious. Syphilis infection can pass to sexual partners. Infection can pass from pregnant woman to foetus.

Late latent : After 2 years. Transmission of syphilis occurs only in specific circumstances. Patient is non-infectious to sexual partners. Infection can still pass from pregnant woman to foetus. Serological tests are positive.

Penicillins are used.