Final Exam Q

Question 1

1.Morphology of the skin and mucous membrane. Characteristics and functional significance of each layer.

Answer 1

The morphology of the skin and mucous membranes includes several layers:
—Skin:
1. Epidermis: The outermost layer, providing a waterproof barrier and creating our skin tone.
2. Dermis: Beneath the epidermis, containing tough connective tissue, hair follicles, and sweat glands.
3. Hypodermis: Deeper tissue made of fat and connective tissue that houses larger blood vessels and nerves. It provides insulation and padding.
Mucous Membranes:
- Found lining body cavities and internal passages, such as the nose, mouth, lungs, and digestive tract. They secrete mucus, which keeps the membranes moist and protects against infection.
—Functional Significance:
- Epidermis protects against external pathogens.
- Dermis supports skin flexibility and strength.
- Hypodermis acts as an insulator and shock absorber.

Question 2

2. Skin appendages. The structure of the sebaceous glands: varieties, functions.

Answer 2

Skin appendages include hair, nails, sweat glands, and sebaceous glands, each with specific functions.
Sebaceous Glands Structure and Functions:
- These are microscopic exocrine glands in the skin that secrete an oily or waxy substance called sebum, this coats and lubricates hair and skin.
- They are most often associated with hair follicles, discharging sebum into the follicular duct and onto the surface.
- Found everywhere except palms and soles.
Varieties of Sebaceous Glands:
1. Holocrine Sebaceous Glands: Common type, found throughout most of the body.
2. Specialized Sebaceous Glands: Such as Meibomian glands in the eyelids and others in the genital area.
Functions:
- Sebum moisturizes and waterproofs the skin and hair.
- Antimicrobial properties help inhibit the growth of certain bacteria on the skin.
- Acts as a barrier against external contaminants.

Question 3

3. Skin appendages. The structure of the sudoriferous (sweat) glands: varieties, functions.

Answer 3

Structure of Sudoriferous Glands:
- Eccrine Glands: The most numerous type, found all over the skin, especially on palms, soles, and forehead. They are coiled tubular glands that open directly onto the skin surface.
- Apocrine Glands: Found in specific areas like the armpits, groin, and around the nipples. They are larger than eccrine glands, and their ducts open into hair follicles.
Functions:
- Eccrine Sweat Glands: Secrete a clear, odorless fluid, primarily composed of water and salt. They help to cool the body through evaporation and regulate body temperature.
- Apocrine Sweat Glands: Produce a thicker fluid that creates body odor when decomposed by bacteria.

Question 4

4. Skin appendages. The structure of the hair follicle. General characteristics of hair types. Hair types and age characteristics of their growth.

Answer 4

Hair is another essential skin appendage, and hair follicles are the structures from which hair grows.
Structure of the Hair Follicle:
- Each follicle is a tubular sheath surrounding the lower part of the hair shaft, and is embedded within the skin.
- The follicle has several layers, with an outer dermal root sheath and an inner epithelial root sheath.
- The base of the follicle forms a bulb where hair originates in the dermis, adjoining the hair papilla filled with tiny blood vessels (capillaries) for nourishment.
General Characteristics of Hair Types:
1. Lanugo Hair: Fine, soft, usually unpigmented hair that covers the fetus and is usually shed before birth.
2. Vellus Hair: Thin, short, and lightly pigmented hair found on most of the body.
3. Terminal Hair: Longer, coarser, and usually more pigmented hair that develops with puberty due to hormonal changes; found on the scalp, eyebrows, legs, arms, and genital regions.
Hair Types and Age Characteristics of Their Growth:
- Infancy: Babies are born with soft, fine vellus hair and some lanugo, which is usually shed within a few weeks or months and replaced by vellus hair.
- Childhood: Most hair remains vellus until puberty.
- Puberty and Adult Age: Hormonal changes trigger the growth of terminal hair in areas such as the pubic region, under the arms, on the face for men, and on the limbs for both sexes.
- Aging: With age, some terminal hair may revert back to vellus hair, leading to thinning hair or baldness in some adults, particularly men.

Question 5

5. Skin appendages. The structure of the nail plate.

Answer 5

The nail plate is part of the nail system, which is an integral component of the skin appendages.
Structure of the Nail Plate:
- Keratin: The nail plate is composed mainly of keratin, which is a tough, protective protein. This gives nails their strength and resilience.
- Layers: It consists of several layers of dead, tightly packed cells.
- Free Edge: The part of the nail plate that extends beyond the finger or toe.
- Body: The main and visible part of the nail plate.
- Root: The part of the nail plate that is under the cuticle, embedded within the skin.
- Nail Bed: The skin beneath the nail plate.
- Lunula: The crescent-shaped whitish area of the bed of the nail. The lunula represents the visible part of the nail matrix, or root, where new nail growth occurs.
Functions:
- Protection: Nails protect the tips of fingers and toes from mechanical damage.
- Sensory Aid: They enhance fine-touch perception and manipulation of tiny objects.
- Support: Nails add rigidity to the ends of digits, aiding in their function.

Question 6

6. Skin functions; neuro-receptor, thermoregulatory, secretory-excretory, respiratory, resorptive, protective, immunological, pigment-forming.

Answer 6

The skin is a complex organ with several vital functions that contribute to the overall homeostasis and well-being of the body. Here is an outline of the key functions of the skin:
1. Neuro-receptor Function: The skin contains a vast network of nerve endings and receptors that detect touch, pressure, vibration, temperature, and pain sensations.
2. Thermoregulatory Function: The skin helps maintain body temperature through sweat production and the dilation or constriction of blood vessels. Eccrine sweat glands secrete sweat that evaporates from the skin surface, cooling the body.
3. Secretory-Excretory Function: The skin secretes sebum from sebaceous glands, which helps keep the skin and hair moisturized. It also excretes waste products like salts and small amounts of metabolic waste, alongside sweat.
4. Respiratory Function: While not a primary organ of respiration, the skin can absorb oxygen and expel carbon dioxide to a very small degree.
5. Resorptive Function: The skin can absorb substances from the environment, such as medications in transdermal patches, or harmful agents, highlighting the need for protective clothing and skin products.
6. Protective Function: The skin provides a physical barrier against mechanical injury, pathogenic organisms, and harmful radiation. The stratum corneum, the outermost layer, is critical in this barrier.
7. Immunological Function: Langerhans cells in the skin are part of the immune system and help detect and fight off pathogens. The skin acts as a first line of defense in the body’s immune response.
8. Pigment-forming Function: Melanocytes in the skin produce melanin, a pigment that protects against ultraviolet radiation damage and gives skin its color. Variations in melanin production are responsible for the wide variety of human skin tones.

Question 7

7. Primary morphological elements. Definition, characteristics, evolutionary paths, clinical examples: spot, papule, pustule, blister

Answer 7

1. Spot (Macule):
   - Definition: A macule is a flat, distinct area of skin that is visibly different in color from the surrounding skin and is not raised or depressed relative to the skin surface. It’s typically less than 1 cm in diameter.
   - Characteristics: The key characteristic of a macule is its color change, which could be red, brown, white, etc., without any alteration in texture or thickness of the skin.
2. Papule:
   - Definition: A papule is a small, raised, solid bump less than 1 cm in diameter on the skin. It emerges above the surface of the surrounding skin without producing any visible fluid.
   - Characteristics: It can be due to alterations in skin color or texture and may come in various shapes (round, oval) and colors (red, brown).
3. Pustule:
   - Definition: A pustule is a small, circumscribed, superficial skin elevation that is filled with purulent material (pus).
   - Characteristics: They can form as a result of infection, inflammation, or follicular reactions and usually indicate an infectious or inflammatory condition.
4. Blister (Vesicle/Bulla):
   - Definition: A blister represents a fluid-filled elevation of skin. A vesicle is smaller than 1 cm and filled with clear fluid, whereas a bulla is larger than 1 cm.

Question 8

8. Primary morphological elements. Definition, characteristics, evolutionary paths, clinical examples: tubercle, node, vesicle, bulla.

Answer 8

1. Tubercle:
   - Definition: A tubercle is a solid, rounded nodule greater than 0.5 cm in diameter, but generally smaller than 2 cm. It can extend into the dermis or subcutaneous tissue.
   - Characteristics: Tubercles may vary in color but are typically characterized by their elevation above the skin surface and can be felt as a firm lump.
   - Clinical Examples: Tuberculosis cutis, leprosy, syphilis, and some types of lipomas.
2. Node (Nodule):
   - Definition: A node or nodule is similar to a tubercle but is larger—typically greater than 2 cm in diameter. It extends deeper into the dermis and even into the subcutaneous tissue.
   - Characteristics: Nodes are larger and firmer than papules. They can be seen in various shapes and can affect deeper layers of the skin compared to papules and tubercles.
   - Clinical Examples: Cystic acne, erythema nodosum, rheumatoid nodules, and lipomas.
3. Vesicle:
   - Definition: A vesicle is a small, fluid-filled lesion (with clear serum) that is less than 1 cm in diameter. It arises from the outermost skin layer, the epidermis
   - Clinical Examples: Chickenpox, herpes simplex, contact dermatitis, and allergic eczema.
4. Bulla:
   - Definition: A bulla is a larger fluid-filled lesion than a vesicle, measuring more than 1cm in diameter.
   - Characteristics: Bullae can contain serum, blood, or pus, and they tend to form from a separation in the deep epidermal layers or between the epidermis and the dermis.
   - Clinical Examples: Blistering disorders like pemphigus vulgaris, bullous pemphigoid, large blisters from burns, and drug reactions

Question 9

9. Secondary morphological elements. Definition, characteristics, evolutionary paths, clinical examples: secondary spot, squama (scale), crust.

Answer 9

1. Secondary Spot:
   - Definition: A secondary spot (also known as a macule) is an area of altered color or texture that remains after an initial primary skin lesion has resolved. Unlike the primary spot, it’s often a result of healing processes.
   - Characteristics: These can include changes in pigmentation like hyperpigmentation or hypopigmentation and may vary in size.
   - Clinical Examples: Post-inflammatory hyperpigmentation or hypopigmentation after conditions like acne or eczema have healed.
2. Squama (Scale):
   - Definition: A squama, or scale, is a flake of dead epidermal cells that is abnormal in size, shape, or texture.
   - Characteristics: Scales can be fine and powdery, or they can be thick and adherent; they vary in size and in how easily they can be detached.
   - Clinical Examples: Psoriasis (silvery scales), tinea pedis (athlete’s foot, flaky skin), and seborrheic dermatitis (dandruff).
3. Crust:
   - Definition: A crust, or scab, forms when serum, pus, or blood dries out on the skin surface.
   - Characteristics: Crusts can range in color from yellow to brown to greenish-black, depending on their composition. They are typically seen on top of a break in the skin.
   - Clinical Examples: Impetigo (honey-colored crusts), scabs on abrasions or cuts, and the crusts following the rupture of herpes simplex blisters.

Question 10

10. Secondary morphological elements. Definition, characteristies, evolutionary paths, clinical examples: erosion, ulcer

Answer 10

Secondary morphological elements also encompass disruptions to the integrity of the skin surface, which are the result of factors such as the progression of a primary lesion, trauma, or infection. Erosion and ulcer are two such types of secondary lesions:
1. Erosion:
- Definition: An erosion is a loss of part or all of the epidermis (the skin’s outer layer) that occurs following the rupture of a vesicle or bulla, or due to trauma.
- Characteristics: Erosions are shallow depressions on the skin that are moist and do not bleed. They heal without scarring because they do not extend into the dermis.
- Evolutionary Paths: Erosions will typically heal by re-epithelialization, in which the skin cells migrate to close the wound. If they extend deeper, however, they may become ulcers.
- Clinical Examples: Ruptured chickenpox vesicles, abrasions, or areas of skin maceration.
2. Ulcer:
- Definition: An ulcer is a deeper loss of skin tissue that involves the epidermis and at least part of the dermis. It may extend down to subcutaneous tissue and muscle.
- Characteristics: Ulcers often have more clearly defined edges than erosions and may be painful. They frequently discharge pus or other fluids and are prone to bleeding. Because they extend deeper into the skin, they can heal with scarring.
- Evolutionary Paths: Healing of ulcers can be slow and typically involves granulation (formation of new tissue) and re-epithelialization. Large or chronic ulcers may require medical intervention to promote healing.
- Clinical Examples: Venous stasis ulcers on the lower legs, diabetic foot ulcers, and pressure ulcers (bedsores).

Question 11

11. Secondary morphological elements. Definition, characteristics, evolutionary paths, clinical examples: abrasion, fissure.

Answer 11

—In dermatology, secondary morphological elements arise from the modification or evolution of primary lesions. They might result from natural disease progression, healing, external trauma, or other pathological processes:
1. Abrasion:
- Definition: An abrasion is a superficial wound to the skin caused by friction or scraping that results in the loss of at least part of the epidermis.
- Characteristics: Abrasions are often raw and tender to the touch, may weep serous fluid, and usually have irregular borders. The base of an abrasion is often pink and moist.
- Evolutionary Paths: They heal by re-epithelialization, where new skin cells proliferate and migrate over the area. Abrasions typically heal without scarring unless they become infected or are very deep.
- Clinical Examples: Road rash from falls, scratches from rough surfaces, or skin injuries from athletic activities.
2. Fissure:
- Definition: A fissure is a linear loss of epidermis and dermis due to exaggerated skin tension or decreased skin elasticity.
- Characteristics: Fissures are characterized by sharply defined, nearly vertical walls that can be painful, especially if they are deep. They may bleed if the fissure extends into the capillaries.
- Evolutionary Paths: Healing occurs by slow granulation and epithelial bridge formation. If the skin is continually stressed or dry, fissures may persist or worsen.
- Clinical Examples: Cheilitis (fissures in the lips), athlete’s foot where the skin cracks between the toes, and anal fissures from constipation or inflammatory bowel disease.

Question 12

12. Secondary morphological elements. Definition, characteristics, evolutionary paths, clinical examples of scar, cicatricial atrophy.

Answer 12

-When talking about the body’s healing process, especially the skin, secondary morphological elements like scars and cicatricial atrophy are significant indicators of the skin’s history and the processes it has undergone following injury or disease.
1. Scar:
- Definition: A scar is a mark left on the skin or within body tissue where a wound, burn, or sore has not healed completely and fibrous connective tissue has developed.
- Characteristics: Scars may appear flat, lumpy, sunken, or colored and can vary significantly in their texture compared to surrounding skin. Initially, scars may be red or purple, becoming paler over time, and are generally non-painful.
- Clinical Examples: Surgical incisions, injuries that have penetrated through the dermis, healed wounds from acne or chickenpox, and healed areas of skin loss due to infection like a staphylococcal scalded skin syndrome.
2. Cicatricial Atrophy:
- Definition: Cicatricial atrophy refers to the skin’s appearance when there is a loss of tissue and the surrounding skin contracts, often following a destructive skin process or injury.
- Characteristics: The skin appears thin, flattened, and more translucent than normal. It may adhere more directly to underlying bone or muscle and often shows the signs of previous scarring processes.
- Clinical Examples: Skin damage from lupus, long-standing venous ulcers that have healed, and areas of skin recovery following severe acne or burns.

Question 13

13. Secondary morphological elements. Definition, characteristics, Evolutionary paths, clinical examples, lichenification, vegetation.

Answer 13

1. Lichenification:
   - Definition: Lichenification is the thickening of the skin with accentuation of normal skin markings that arises due to chronic rubbing or scratching.
   - Characteristics: The skin appears leathery and rough with exaggerated skin lines and often has a variable degree of pigmentation. It is usually associated with itching.
   - Clinical Examples: Common in chronic atopic dermatitis or eczema, and areas exposed to repeated mechanical trauma, like the ankles in chronic venous insufficiency or the back of the neck in patients who frequently rub that area.
2. Vegetation:
   - Definition: Vegetation refers to the pathological growth of tissue resulting in elevated plaques that are often broad at the base and exophytic (growing outward from the surface).
   - Characteristics: These lesions can look wart-like or cauliflower-like in appearance, with irregular or pebbly surfaces, which can be soft or firm and are typically secondary to chronic inflammation or infection.
   - Clinical Examples: Seen in immunocompromised patients like those with HPV-induced verrucous carcinoma or inflammatory diseases leading to hypertrophic granulation tissue.

Question 14

14. Pathohistological changes in the epidermis: hyperkeratosis, parakeratosis, acanthosis, granulosis, dyskeratosis, acantholysis. Characteristics, clinical examples.

Answer 14

1. Hyperkeratosis:
   - Characteristics: Thickening of the stratum corneum, often associated with an abnormality in the skin’s keratinization process.
   - Clinical Examples: Calluses from friction, psoriasis where excessive skin cell production leads to thick scale, and actinic keratosis from sun damage.
2. Parakeratosis:
   - Characteristics: Retention of the nuclei in the stratum corneum where normally the cells are anucleated, which indicates an abnormal keratinization process.
   - Clinical Examples: Psoriasis and zinc deficiency (acrodermatitis enteropathica).
3. Acanthosis:
   - Characteristics: Thickening of the stratum spinosum layer of the skin, which can be diffuse or focal.
   - Clinical Examples: Acanthosis nigricans, which is associated with insulin resistance, and epidermal nevus.
4. Granulosis:
   - Characteristics: Hypergranulosis is an increased granular layer thickness, while hypogranulosis means a thinner or absent layer.
   - Clinical Examples: Lichen planus typically shows hypergranulosis and wart virus infection shows granular layer changes.
5. Dyskeratosis:
   - Characteristics: Abnormal keratinization occurring prematurely within individual cells or groups of cells below the stratum corneum.
   - Clinical Examples: Disorders like Darier disease and actinic keratosis.
6. Acantholysis:
   - Characteristics: Loss of intercellular connections resulting in the breakdown of cellular cohesion within the epidermis.
   - Clinical Examples: Pemphigus vulgaris where autoantibodies attack desmogleins, the proteins that hold skin cells together, causing blistering and sores.

Question 15

15. Pathohistological changes in the epidermis. Types of serous inflammation in the epidermis: vacuolar, ballooning degeneration, spongiosis. Characteristics, clinical examples.

Answer 15

Vacuolar Degeneration (Interface Dermatitis):
- Characteristics: Damage at the dermoepidermal junction, where there is the formation of vacuoles (small cavities) around the basal keratinocytes.
- Clinical Examples: Lupus erythematosus and lichen planus can show vacuolar alteration.
Ballooning Degeneration:
- Characteristics: Characterized by keratinocytes swelling (ballooning), becoming large, pale, and roundish with eventual cell rupture.
- Clinical Examples: Viral infections such as herpes simplex and varicella-zoster virus exhibit this change.
Spongiosis:
- Characteristics: Inter-cellular edema in the epidermis leading to widened intercellular spaces and a spongy appearance of the skin.
- Clinical Examples: Commonly seen in acute eczema, contact dermatitis, and atopic dermatitis.

Question 16

16. Pathomorphological and histological changes in the dermis: acute and chronic inflammation, dermal edoma, papillomatosis, infectious granuloma.

Answer 16

Acute Inflammation:
- Characteristics: A rapid response to injury or infection characterized by the presence of edema and infiltration by neutrophils.
- Clinical Examples: Acute cellulitis or an acute flare of a chronic condition like psoriasis or eczema.
Chronic Inflammation:
- Characteristics: Long-standing inflammation characterized by lymphocytes, plasma cells, macrophages, and sometimes eosinophils and granuloma formation.
- Clinical Examples: Conditions like lupus erythematosus, scleroderma, and chronic dermatitis of various kinds.
Dermal Edema:
- Characteristics: Accumulation of fluid in the dermal interstitial tissue.
- Clinical Examples: Urticaria (hives) where there’s transient dermal edema along with dilated lymphatics.
Papillomatosis:
- Characteristics: Enlargement of the dermal papillae projecting above the skin surface that causes a rough texture.
- Clinical Examples: Seen in conditions such as verruca vulgaris (warts) where there is epithelial hyperplasia.
Infectious Granuloma:
- Characteristics: A type of chronic inflammation where there’s a formation of granulomas, which are small nodules of immune cells.
- Clinical Examples: Tuberculosis of the skin, leprosy, and deep fungal infections can result in granuloma formation.

Question 17

17. Methods of examination of the skin and mucous membranes in dermatology (dermatological tests in the diagnosis of certain skin diseases and diseases of the oral mucosa (psoriasis, lichen planus, pemphigus, tuberculosis, neurodermatitis, lupus crythematosus, etc.).

Answer 17

Physical Examination:
- Initial assessment through visual inspection and palpation of the skin and mucous membranes.
Dermoscopy:
- Non-invasive technique that uses magnification and lighting to evaluate pigmented skin lesions, particularly useful in diagnosing melanoma.
Patch Testing:
- Used to identify substances that a person is allergic to and can cause contact dermatitis.
KOH Preparation:
- A test where potassium hydroxide is used to dissolve skin cells, leaving fungal cells visible under a microscope, often used in fungal infections.
Tzanck Smear:
- A test that involves scraping the base of a blister to look for signs of certain blistering diseases like herpes simplex and varicella-zoster.
Biopsy:
- Involves taking a small sample of tissue for microscopic examination. Can be incisional, excisional, or a shave biopsy.
Wood’s Lamp Examination:
- Ultraviolet light used to highlight changes in the skin invisible to the naked eye, useful for diagnosing conditions like vitiligo or fungal infections.
Blood Tests:
- Includes complete blood count, autoimmune disease panels, antinuclear antibody tests, and other specific tests depending on the suspected condition.
Culture and Sensitivity:
- Identifying microbes causing infection and their antibiotic sensitivities, especially in cases of bacterial, fungal, or viral skin infections.
———————————————-
Psoriasis:
- Typically diagnosed by the physical presentation, a biopsy may be performed to confirm the diagnosis in uncertain cases.
Lichen Planus:
- Diagnosis usually through clinical presentation and history, but a biopsy with direct immunofluorescence can be helpful to confirm unclear cases.
Pemphigus:
- Direct immunofluorescence or Tzanck smear can be used for diagnosing, alongside a biopsy.
Cutaneous Tuberculosis:
- Skin biopsy along with staining (acid-fast bacillus stain), culture, or PCR testing for Mycobacterium tuberculosis
Neurodermatitis:
- Diagnosed clinically, but a skin biopsy might be performed to rule out other conditions.
Lupus Erythematosus:
- A combination of clinical presentation, blood tests for autoantibodies (ANA, anti-dsDNA), complement levels, and a skin biopsy with immunofluorescence is typically employed.

Question 18

19, Fundamentals of dermatosestherapy. General and local therapy. Keratoplastic agents in the external treatment of dermatoses, Mechanism of action, indications, method of application.

Answer 18

—-General Therapy:
- This includes systemic treatments such as oral medications, injections, or infusions that affect the entire body.
- Examples include antibiotics for bacterial infections, antifungals for fungal infections, biologic therapies for psoriasis, and oral corticosteroids for severe inflammatory conditions.
——–Local Therapy:
- Topical treatments applied directly to the skin.
- Examples include corticosteroid creams for inflammation, antifungal creams, moisturizers for dry skin conditions, and topical chemotherapy agents for certain skin cancers.
——————–
Keratoplastic Agents:
- These are topical agents that regulate keratinization and are used to treat skin conditions characterized by abnormal skin growth, scaling, or roughness.
- They work by modulating the process of keratinization, which helps to normalize the shedding of the stratum corneum, the outermost layer of the skin.
Mechanism of Action:
- Keratoplastic agents act by promoting the proliferation of basal epidermal cells or by modulating the cohesiveness of the corneocyte layer, often increasing the shedding of dead skin cells and smoothing the skin surface.
- Some agents have anti-inflammatory properties or can modulate the immune response.
Indications:
- Conditions characterized by hyperkeratosis such as psoriasis, ichthyosis, and keratosis pilaris.
- Disorders featuring abnormal desquamation like acne and seborrheic dermatitis.
Method of Application:
- Keratoplastic agents are typically applied topically in various formulations like creams, ointments, gels, lotions, or shampoos.
- The specific concentration and formulation, frequency of application, and duration of therapy depend on the problem being treated, the agent being used, and the individual patient’s response.
—Examples of keratoplastic agents include:
- Salicylic Acid
- Urea:
- Alpha-hydroxy Acids

Question 19

20. Fundamentals of dermatosestherapy. General and local therapy. General concepts of PUVA therapy.

Answer 19

General Therapy:
- This includes systemic treatments such as oral medications, injections, or infusions that affect the entire body.
- Examples include antibiotics for bacterial infections, antifungals for fungal infections, biologic therapies for psoriasis, and oral corticosteroids for severe inflammatory conditions.
Local Therapy:
- Topical treatments applied directly to the skin.
- Examples include corticosteroid creams for inflammation, antifungal creams, moisturizers for dry skin conditions, and topical chemotherapy agents for certain skin cancers.
PUVA (Psoralen + UVA):
- Psoralen is a photosensitizing agent that makes the skin more sensitive to ultraviolet light. It can be administered orally, topically, or even added to bathwater.
- UVA light penetrates deeper into the skin compared to UVB and, when used with psoralen, it can effectively treat certain skin disorders.
Mechanism of Action:
- Psoralen interacts with DNA when exposed to UVA light, which leads to an alteration in skin cell growth and a decrease in inflammation.
Indications:
- PUVA therapy is commonly indicated for conditions such as psoriasis, vitiligo, mycosis fungoides (a type of cutaneous T-cell lymphoma), and eczema.
- It is also used for other less common disorders that are responsive to phototherapy.
Procedure:
- For oral PUVA, patients ingest psoralen before UVA exposure, usually about 2 hours prior to the treatment.
- In bath or topical PUVA, the skin is soaked or covered with psoralen before UVA light exposure.

Question 20

21. Fundamentals of dermatosestherapy. General and local therapy. External dosage forms: lotions, pastes, ointments, creams, powders, lotion, emulsion. Definition. Method of application based on indications.

Answer 20

Lotions:
- Definition: Lotions are liquid preparations often prescribed for treating large or hairy areas of the body because they are easy to spread and less greasy.
- Application: They are typically applied with a cotton ball or pad, or directly with the hands, and are suitable for conditions like eczema or heat rash where a cooling, soothing effect is desired.
Pastes:
- Definition: Pastes are semi-solid preparations that contain a larger proportion of solid material, which makes them thicker and more absorbent than creams or ointments.
- Application: They are applied in a thin layer and are often used for their protective and absorbing properties in conditions like diaper rash or in areas where skin surfaces rub together.
Ointments:
- Definition: Ointments are thick, greasy formulations that are good for delivering active ingredients to the skin and are often used to treat dry, scaly skin conditions.
- Application: They are best applied in a thin layer to affected areas and are especially useful for bedtime application in conditions such as psoriasis or chronic eczema.
Creams:
- Definition: Creams are emulsions that are less greasy than ointments and can be absorbed quickly. They are usually favored for daytime use.
- Application: Applied by gently rubbing into the skin, they are effective for a wide range of conditions, including mild to moderate eczema and dermatitis.
Powders:
- Definition: Powders consist of fine particles and are used to reduce friction and absorb moisture.
- Application: They are dusted onto the skin and are often used in areas prone to moisture such as the feet, groin, and underarms, helping conditions like athlete’s foot and intertrigo.
Gel:
- Definition: Gels are typically alcohol-based, which allows them to dry quickly when applied to the skin. They are clear and non-greasy.
- Application: Applied in a thin layer, they are useful for hairy areas or on the scalp, and in conditions like acne or sunburn.
Emulsions:
- Definition: Emulsions are mixtures of oil and water that can be used as a base for creams or lotions.
- Application: The method of application would be similar to creams or lotions and can be suitable for conditions where both moisturizing and a cooling effect are desired.

Question 21

22. Pyoderma: Definition and classification.

Answer 21

—Classification of Pyoderma:
The classification of pyoderma generally takes into account the depth and severity of the infection. Here is a simplified classification:
1-Primary Pyoderma:
- Impetigo: Highly contagious, superficial skin infection often seen in children. It is characterized by honey-colored crusts on the face and extremities.
- Folliculitis: Infection of hair follicles, presenting as small, red, and sometimes painful bumps, often with a pus-filled top.
- Ecthyma: A more severe form of impetigo that penetrates deeper into the dermis, forming ulcers with a crust on top.
- Cellulitis: A diffuse inflammation of the skin that involves the deeper dermis and subcutaneous fat with areas of redness, swelling, and tenderness.
2-Secondary Pyoderma:
- Infection that occurs on top of a pre-existing skin condition such as atopic dermatitis, scabies, or wounds, which have been compromised and become infected.
————Classification by severity or course of the disease:
- Acute Pyoderma: Occurs suddenly and typically responds well to treatment.
- Chronic Pyoderma: Persistent and may be more difficult to treat, often due to antibiotic resistance or underlying conditions that compromise the skin, such as diabete

Question 22

23. Staphyloderma: acute and chronic forms (ostiofolliculitis, sycosis, furuncle, carbuncle, hydradenitis, etc.). Etiology, methods of diagnosis and treatment. Prevention methods in patients of different age groups.

Answer 22

—Staphyloderma refers to skin infections caused by Staphylococcus bacteria, particularly Staphylococcus aureus. These infections can be acute or chronic and range in severity from mild to potentially life-threatening. Here are descriptions of the conditions listed as well as the etiology, diagnostics, treatments, and prevention methods:
### Acute Forms:
Ostiofolliculitis:
- Definition: Infection of the hair follicle opening, presenting as small, pus-filled lesions.
- Etiology: Often due to Staphylococcus aureus infection.
- Diagnosis: Usually diagnosed based on clinical appearance; cultures may be taken if recurrent.
- Treatment: Topical antibacterial agents; good hygiene.
- Prevention: Regular washing with antibacterial soap; avoiding sharing personal items.
Sycosis:
- Definition: Deep infection of the hair follicles, often in the beard area, leading to pustules and abscesses.
- Etiology: Caused primarily by Staphylococcus aureus.
- Diagnosis: Clinical assessment; sometimes cultures are needed.
- Treatment: Topical and oral antibiotics.
- Prevention: Proper shaving techniques, skin cleansing.
Furuncle:
- Definition: Deep infection of a single hair follicle, creating a boil.
- Etiology: Most often caused by Staphylococcus aureus, entering through minor skin abrasions.
- Diagnosis: Clinical; may require incision and drainage, with cultures from the pus.
- Treatment: Warm compresses, incision and drainage if necessary, antibiotics.
- Prevention: Skin hygiene, avoiding manipulation of lesions.
Carbuncle:
- Definition: Larger, deeper infection than a furuncle involving a group of hair follicles.
- Etiology: Staphylococcus aureus infections.
- Diagnosis: Based on clinical signs; may require imaging to assess depth.
- Treatment: Incision and drainage, antibiotics.
- Prevention: As with furuncles, good skin hygiene and avoiding injury/abrasion to skin.
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### Chronic Forms:
Hydradenitis Suppurativa:
- Definition: A chronic condition involving the inflammation of sweat glands, leading to painful, deep abscesses and scars, commonly in the armpits and groin.
- Etiology: Linked to blockage of hair follicles and secondary infection, often with Staphylococcus aureus, stress, hormonal factors, and smoking may exacerbate the condition.
- Diagnosis: Clinical diagnosis; may need imaging to evaluate the extent.
- Treatment: Antibiotics for infection, anti-inflammatory medication, surgery in severe cases.
- Prevention: Weight management, smoking cessation, loose-fitting clothing to decrease friction, good hygiene.
### Methods of Diagnosis and Treatment:
Etiology:
- These conditions are predominantly caused by infection with the bacterium Staphylococcus aureus, which can invade through small breaks in the skin.
Diagnosis:
- Clinical examination is often sufficient for diagnosis.
- Culture of pus or drainage to identify the specific bacteria and its antibiotic sensitivity.
- Occasionally, blood tests or imaging studies are needed, particularly for more severe infections.
Treatment:
- Hygiene measures and warm compresses to promote drainage.
- Topical antiseptics or antibiotics for milder infections.
- Oral antibiotics for more significant infections, based on culture results when available.
Appropriate antibiotics, including oral antibiotics cephalexin, clindamycin, amoxicillin/clavulanate
- Incision and drainage may be required for abscesses.
- In cases of recurrent staph infections, nasal carriers of Staphylococcus aureus might be treated.
Prevention Methods:
- Good personal hygiene and regular handwashing.
- Avoid sharing personal items such as towels and razors.

Question 23

24. Streptoderma: acute and chronic forms (impetigo: streptococcal, bullous, slit-like, lichen simplex, impetigo of nail folds; streptococcal diaper rash; ecthyma: ordinary, terebrant; chronic superficial diffuse streptoderma). Etiology, methods of diagnosis and treatment. Prevention methods in patients of different age groups.

Answer 23

### Acute Forms:
Impetigo (Streptococcal):
- Definition: A highly contagious skin infection commonly seen in children, with small blisters or crusty lesions.
- Etiology: Mainly caused by Streptococcus pyogenes and sometimes by Staphylococcus aureus.
- Diagnosis: Visual examination, and confirmation may be done through bacterial cultures.
- Treatment: Topical antibiotics or oral antibiotics in more widespread cases.
- Prevention: Good hygiene, prompt treatment of cuts and scrapes, and avoiding direct contact with infected persons.
Bullous Impetigo:
- Definition: A form of impetigo characterized by larger blisters.
- Etiology: Usually caused by a toxin-producing strain of Staphylococcus aureus.
- Diagnosis: Clinical appearance, culture of blister fluid may be tested to confirm.
- Treatment: Removal of blister roofs, topical therapy, or oral antibiotics.
- Prevention: Similar to non-bullous impetigo; personal hygiene and avoiding sharing personal items.
Ecthyma:
- Definition: A more severe, ulcerated form of impetigo that extends to the dermis.
- Etiology: Caused by Streptococcus pyogenes, sometimes in combination with Staphylococcus aureus.
- Diagnosis: Based on the clinical presentation; cultures may be needed.
- Treatment: Oral antibiotics, appropriate wound care.
- Prevention: As with impetigo, maintaining good skin hygiene.
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### Chronic Forms:
Lichen Simplex:
- Definition: A skin condition due to chronic itching and scratching that leads to thickened skin.
- Etiology: Often secondary to conditions that cause itchiness, including bacterial infections.
- Diagnosis: Clinical evaluation, ruling out underlying infections.
- Treatment: Reduction of scratching, topical corticosteroids, treating any underlying infection.
- Prevention: Managing chronic conditions that lead to scratching, maintaining skin moisture.
Chronic Superficial Diffuse Streptoderma:
- Definition: A persistent infection of the skin by Streptococcus bacteria.
- Etiology: Chronic skin conditions that allow bacterial infiltration and growth.
- Diagnosis: Clinical signs and bacterial cultures.
- Treatment: Long-term antibiotics; treatment of underlying skin issues.
- Prevention: Controlling conditions such as eczema prevents skin breaches allowing bacterial entry. Regular follow-up with a dermatologist is suggested.
### Methods of Diagnosis and Treatment:
Etiology:
- Caused by streptococcal bacteria, predominantly Streptococcus pyogenes, and may coexist with Staphylococcus infections.
Diagnosis:
- Usually diagnosed from the clinical presentation.
- Bacterial cultures can identify the pathogen and help guide antibiotic therapy.
- For complicated cases, a skin biopsy might be indicated.
Treatment:
- Good wound care and hygiene.
- Topical antibacterial treatments for localized infection.
- Oral antibiotics for more extensive disease.
- In persistent or recurrent cases, a search for potential nasal carriers or environmental reservoirs.
Prevention Methods:
- Encouraging frequent handwashing, especially in children.
- Keeping fingernails short to minimize the risk of skin breakdown due to scratching.
- Avoiding close contact with those infected and not sharing personal items like towels

Question 24

25. Strepto-staphyloderma: acute and chronic forms. Etiology, methods of diagnosis and treatment. Prevention methods in patients of different age groups.

Answer 24

### Etiology:
- The cause is generally a co-infection with Streptococcus pyogenes and Staphylococcus aureus, which leads to a variety of skin lesions.
### Acute Forms:
- Manifest as quickly developing skin conditions, such as impetigo, wound infections, cellulitis, or abscesses.
### Chronic Forms:
- Chronic presentations can occur due to inadequate treatment, recurring exposure to the pathogens, or underlying comorbidities that compromise the immune system.
### Methods of Diagnosis:
- Clinical Examination: The appearance of the skin lesions gives a primary indication of infection.
- Microbial Cultures: Swabs from the lesions can help identify the specific bacteria causing the infection.
- Sensitivity Testing: Determines the appropriate antibiotics to combat the specific bacteria found in cultures.
- Blood Tests: May be done if systemic infection is suspected.
### Treatment:
Medications for such mixed infections might include:
- Penicillins: For example, Dicloxacillin may be used as it is effective against certain strains of both Staphylococcus and Streptococcus.
- Cephalosporins: Cephalexin (Keflex) can be an alternative if the sensitivity profile is appropriate.
- Clindamycin: Offers coverage against both types of bacteria and can be used in cases of allergies to other antibiotics.
- Combination Therapy: Sometimes, especially with resistant bacteria, a combination of drugs like a beta-lactam antibiotic with a macrolide may be effective.
The choice of medication should be guided by the result of sensitivity tests and clinical judgment.
### Prevention Methods:
- Hygiene: Regular handwashing and good skin care are fundamental.

Question 25

26. Scabies: etiology, epidemiology, clinical picture, diagnostics, differential diagnosties, principles and methods of treatment, prevention.

Answer 25

----Scabies is an itchy skin condition caused by a tiny burrowing mite called Sarcoptes scabiei. Here are the details regarding its etiology, epidemiology, clinical picture, and more. ### Etiology: - Caused by infestation with the mite Sarcoptes scabiei var. hominis. ### Epidemiology: - Scabies is common worldwide and affects people of all races and social classes. - Spread is usually by direct, prolonged skin-to-skin contact with an infested person and is common in crowded environments. ### Clinical Picture: - Presents with intense itching, especially at night. - Characteristic burrows in the webbing between fingers, on the wrists, elbows, buttocks, and genital area. - Secondary infections due to scratching are common. ### Diagnostics: - Diagnosis is primarily clinical, based on the appearance of burrows or the distribution of the rash and the itching pattern. - Microscopic examination of skin scrapings can confirm the presence of mites, eggs, or fecal matter (scybala). - Dermoscopy may also help visualize mites in burrows. ### Differential Diagnoses: - Includes atopic dermatitis, other ectoparasites like body lice, drug reactions, and more. ### Treatment: Medications typically used include: Topical Treatments: - Permethrin Cream (5%): The first-line treatment for scabies. Applied to the whole body from the neck down and washed off after 8–14 hours. - Crotamiton Cream or Lotion: An alternative that also has anti-pruritic properties. - Lindane: Less commonly used due to neurotoxicity risks, especially in children and pregnant women. - Ivermectin Lotion: Recently approved topical form for treatment of head lice and scabies. Oral Treatments: - Ivermectin: Used in cases where topical treatments are ineffective or not feasible. Dosage is typically determined by body weight. Supportive Treatments: - Antihistamines: To help with itching. - Antibiotics: If secondary bacterial skin infection occurs. ### Prevention: - Good personal hygiene and prompt treatment of infected individuals and their close contacts. - Washing clothing, bedding, and towels in hot water and drying them on a hot cycle or sealing them in a bag for at least 72 hours to kill mites.

Question 26

27. Pediculosis: etiology, epidemiology, clinical picturo, diagnostics, differential diagnostics, principles and methods of treatment, prevention.

Answer 26

Pediculosis refers to an infestation with lice, parasitic insects that feed on human blood. There are three types of lice that infest humans: head lice (Pediculus humanus capitis), body lice (Pediculus humanus corporis), and pubic lice ('crabs'), or Pthirus pubis. ### Etiology: - Infestations occur from direct contact with an infested person or through contact with infested personal items. ### Epidemiology: - Common worldwide and seen in all socioeconomic groups, often in crowded settings. - Head lice infestations are especially common among school children aged 3-11 years. ### Clinical Picture: - Head Lice: Signs include itching of the scalp, red bites, and possibly a rash from scratching. Lice and nits (eggs) may be seen on the hair shafts. - Body Lice: More associated with social distress and signs may include itching, rash, and long-term infestations can lead to thickened and darkened skin, especially around the waist, groin, and upper thighs. - Pubic Lice: Presents with itching in the genital area, with visible lice or nits on pubic hair. ### Diagnostics: - Visual inspection for nits, nymphs, or adult lice is common. - Wet combing can be used to catch lice on the comb. - For pubic lice, a magnifying glass may be necessary due to their smaller size. ### Differential Diagnostics: - Dandruff, hair casts, folliculitis, eczema, or scabies should be considered. ### Treatment: The following medications are used to treat lice infestations: Topical Treatments: - Permethrin Lotion/Cream (1% for head lice, 5% for body lice): Applied to affected areas and left on for a specified amount of time before rinsing off. - Malathion Lotion (0.5%): Applied to the hair, left to dry naturally, and washed off after 8-12 hours. - Pyrethrins with Piperonyl Butoxide: Applied to the hair and washed off after 10 minutes. - Benzyl Alcohol Lotion: Applied to the hair and washed off after 10 minutes. It asphyxiates lice but doesn't kill eggs, so repeat treatment is usually necessary. - Ivermectin Lotion: Applied to dry hair and rinsed off after 10 minutes. Oral Treatments: - Oral Ivermectin: Given twice, 7-10 days apart, when topical therapy is unsuccessful. Removal Methods: - Manual removal of nits with a fine-toothed nit comb is important for the successful elimination of head lice. ### Prevention: - Avoiding close head-to-head contact.

Question 27

28. Classification of mycoses. Pathogens. Epidemiology of skin mycoses.

Answer 27

Classification of Mycoses: 1. Superficial Mycoses: - These are limited to the outermost layers of the skin and hair. - Pathogens include: Malassezia species; causes conditions like pityriasis versicolor. 2. Cutaneous Mycoses: - These affect the skin, hair, and nails, and are caused primarily by dermatophytes. - Pathogens include: - Trichophyton spp. - Conditions include ringworm (tinea), athlete's foot (tinea pedis), and nail fungus (onychomycosis). 3. Subcutaneous Mycoses: - These involve the deeper layers of the skin up to the subcutaneous tissue. - Pathogens include: - Sporothrix schenckii causing sporotrichosis. 4. Systemic Mycoses: - These can affect any part of the body and are typically acquired via inhalation. - Pathogens include: - Histoplasma capsulatum causing histoplasmosis. - Coccidioides spp. causing coccidioidomycosis. - Blastomyces dermatitidis causing blastomycosis. 5. Opportunistic Mycoses: - These occur primarily in people with weakened immune systems. - Pathogens include: - Candida spp. causing candidiasis. - Aspergillus spp. causing aspergillosis. - Cryptococcus neoformans causing cryptococcosis. - Pneumocystis jirovecii causing pneumocystis pneumonia. ### Epidemiology of Skin Mycoses: - Dermatophyte Infections (Dermatophytoses): - These are among the most common skin mycoses globally. - They are highly contagious and can spread through direct contact with infected individuals or animals, or indirectly through contaminated objects. - Factors like humidity, high temperatures, and crowded living conditions can increase the risk of transmission. - Candidiasis: - It's caused by Candida species, typically Candida albicans, although other species can also be responsible. - These yeasts are normal flora in many individuals but can cause infection if the skin's microbial environment is disrupted or the immune system is compromised. - Risk factors include antibiotic use, diabetes, and conditions that affect skin integrity. - Pityriasis Versicolor: - Caused by Malassezia yeasts that normally reside on the skin surface. - Overgrowth can occur due to changes in the skin environment, like increased oiliness or moisture, leading to patches of discolored and flaky skin. - More common in warm, humid climates.

Question 28

29. Keratomycosis (pityriasis versicolor): etiology, pathogenesis, clinical picture,diagnostics, differential diagnosties, principles of treatment, prevention.

Answer 28

Keratomycosis, also known as pityriasis versicolor, is a common superficial fungal infection of the skin. Let's break down your query into specific sections: ### Etiology: Pityriasis versicolor is primarily caused by the yeast Malassezia, a genus of fungi that normally resides on the skin's surface. The specific species involved include Malassezia globosa, Malassezia furfur, and others within this genus. ### Pathogenesis: The pathogenesis of pityriasis versicolor involves an overgrowth of the Malassezia yeasts on the skin. Factors that can contribute to this overgrowth include: - Warm and humid environments - Excessive sweating - Oily skin - Immune system changes - Hormonal variations These yeasts produce azelaic acid and other substances that disrupt melanin synthesis, leading to either hyperpigmented or hypopigmented patches on the skin, which is characteristic of the condition. ### Clinical Picture: The typical clinical presentation of pityriasis versicolor includes: - Patches of skin that appear lighter or darker than the surrounding areas - Fine scaling of the skin (flaking) - Mild itching (pruritus), particularly in warm environments - Most commonly affects the back, chest, neck, and upper arms The color of the patches may range from white to pink or brown, depending on the individual's skin tone and the extent of exposure to sunlight, as the affected areas often do not tan normally. ### Diagnostics: Diagnosis of pityriasis versicolor primarily involves the clinical assessment and may include: - Wood's Lamp Examination: Under ultraviolet light, the patches may show a yellow to yellow-green fluorescence. - KOH (Potassium Hydroxide) Preparation: Skin scrapings are examined microscopically after treatment with KOH to reveal the characteristic "spaghetti and meatballs" appearance of Malassezia cells and hyphae. - Skin Biopsy: Rarely needed, but can be performed in atypical cases. - Culture: Not typically performed due to the ubiquity of the Malassezia species on normal skin. ---Treatment of pityriasis versicolor typically involves topical antifungals like ketoconazole, selenium sulfide, or terbinafine.

Question 29

30. Denmatophytosis. Epidermophytosis of large folds: etiology, pathogenesis, clinical picture, diagnostics, differential diagnostics, principles of treatment, prevention.

Answer 29

Dermatophytosis or Epidermophytosis, particularly of the large skin folds, is commonly referred to as Tinea cruris. It's a type of fungal infection affecting the groin, inner thighs, and buttocks (large folds of the skin). Here's a comprehensive overview: ### Etiology: The most common causative fungi of tinea cruris are dermatophytes, which are mold-like fungi that feed on the keratin in skin: - Trichophyton rubrum - Trichophyton mentagrophytes - Epidermophyton floccosum ### Pathogenesis: Dermatophytes thrive in warm, moist environments. They invade the stratum corneum of the skin and proliferate, causing infection. The infection is more common in males and is often associated with: - Sweat retention and friction - Wearing tight clothing that does not allow the skin to breathe - Hot, humid climates - Obesity, which can create large skin folds prone to moisture accumulation ### Clinical Picture: Clinical manifestations of tinea cruris include: - Itching and burning in the groin, thigh skin folds, and buttocks - A red, raised rash with a clear center, which may blister and ooze - Changes in skin color - Sharp borders, often more red around the edges ### Diagnostics: Diagnosis usually involves clinical examination and can be confirmed by: - KOH Exam: A microscopic examination of a skin scraping treated with KOH to identify the fungus. - Fungal Culture: May be used to identify the exact species of dermatophyte. ### Differential Diagnostics: Tinea cruris should be differentiated from other conditions like: - Candidiasis - Intertrigo - Erythrasma - Psoriasis - Seborrheic dermatitis - Inverse lichen planus ### Principles of Treatment: Treatment generally involves: - Topical antifungal agents like: - Imidazoles: e.g., clotrimazole, ketoconazole, or miconazole - Allylamines: e.g., terbinafine - Azoles: e.g., econazole, oxiconazole, or sulconazole ### Prevention: Preventive measures include: - Maintaining proper hygiene - Drying the groin area thoroughly after showering

Question 30

31. Dermatophylosis, Epidermophytosis of the feet: etiology, pathogenesis, clinical picture, diagnostics, differential diagnosties, principles of treatment, prevention.

Answer 30

Dermatophytosis of the feet, commonly known as Tinea pedis or athlete's foot, is a fungal infection of the skin on the feet. Here's a detailed insight: ### Etiology: Tinea pedis is caused by several types of dermatophyte fungi, including: - Trichophyton rubrum - Trichophyton mentagrophytes - Epidermophyton floccosum ### Pathogenesis: The infection occurs when the dermatophytes invade the keratin layer of the epidermis. Conditions that favor the growth of these fungi include: - Warm, moist environments like sweaty shoes - Public showers or locker rooms where the infection can spread from person to person - Occlusive footwear - Minor skin or nail injuries ### Clinical Picture: Clinical manifestations include: - Itching, stinging, and burning between the toes or on the soles of the feet - Peeling and cracking skin, especially between the toes and on the soles - Dryness and scaling on the sides or bottoms of the feet - Blisters and ulcers in severe cases ### Diagnostics: Diagnosis is based on the clinical presentation and confirmed with laboratory tests like: - KOH Exam: Skin scrapings examined under a microscope after being treated with potassium hydroxide reveal dermatophyte fungi. - Fungal Culture: Identifies the species of the dermatophyte. - Skin Biopsy with PAS Stain: Rarely necessary but used to rule out other conditions. ### Differential Diagnostics: Differential diagnosis may include: - Eczema - Psoriasis - Dyshidrosis - Contact dermatitis - Scabies ### Principles of Treatment: Treatment typically involves: - Topical antifungal medications are first-line treatments and include: - Imidazole Creams: e.g., clotrimazole or miconazole - Allylamines: e.g., terbinafine - Azoles: e.g., ketoconazole ### Prevention: Preventive tips include: - Washing feet daily and drying thoroughly, especially between the toes - Changing socks at least once a day or more often if sweating heavily

Question 31

32. Demnatophylosis Rubromycosis, Etiology, pathogenesis, clinical picture, diagnostics, differential diagnostics, principles of treatment, prevention.

Answer 31

Dermatophytosis, known when caused by Trichophyton rubrum as Rubromycosis, is a fungal infection affecting various parts of the body like the foot (tinea pedis), groin (tinea cruris), nails (onychomycosis), and other regions. Specific to T. rubrum, it results in chronic and often recalcitrant infections. ### Etiology: Rubromycosis is caused by the dermatophyte fungus Trichophyton rubrum. This fungus is one of the most common dermatophytes responsible for a broad range of skin and nail infections. ### Pathogenesis: T. rubrum can invade keratinized tissues, such as the stratum corneum of the skin, nails, and hair. It produces enzymes that degrade keratin, allowing the fungus to spread. Factors contributing to infection include: - Warm, moist conditions - Compromised immune system - Minor skin trauma - Genetic susceptibility - Poor circulation ### Clinical Picture: Clinical manifestations depend on the infection site and typically include: - Tinea Pedis: Itchy, scaling skin between the toes or on the soles; may also have blisters. - Tinea Cruris: Red-brown rash with sharp edges in the groin area. - Onychomycosis: Thickened, discolored, and sometimes painful nails. - Tinea Corporis: Ring-like red, itchy patches on the body. - Tinea Manuum: Scaling on the palms and fingers. ### Diagnostics: Diagnostic methods involve: - Direct Microscopy with KOH: Skin scrapings or nail clippings are treated with potassium hydroxide to reveal fungal elements. - Fungal Culture: Can confirm the diagnosis and identify the fungal species. - Wood's Lamp Examination: Not typically helpful for T. rubrum infections. ### Differential Diagnostics: Conditions that might be confused with rubromycosis include: - Eczema - Psoriasis ### Principles of Treatment: Treatment involves: - Topical Antifungals: Especially for skin infections, including imidazoles (e.g., clotrimazole, ketoconazole) and allylamines (e.g., terbinafine). - Oral Antifungals: Often necessary for nail infections and extensive skin involvement; medications include terbinafine, itraconazole, and fluconazole. - Proper skin and nail care to reduce moisture and prevent reinfection. ### Prevention: Preventive measures include: - Maintaining good skin hygiene - Keeping affected areas clean and dry

Question 32

33. Dermatophytosis. Microsporia (superficial and chronic, infiltrative-suppurative forms): pathogens, source, transmission routes, clinical picture, diagnostics, differential diagnostics, principles of treatment, prevention.

Answer 32

**Dermatophytosis**, particularly when referred to as **microsporia**, is a fungal infection typically affecting the scalp or body with different forms, including superficial, chronic, and infiltrative-suppurative forms. Here is an overview: ### Pathogens: - *Microsporum canis* - *Microsporum audouinii* - *Microsporum gypseum* ### Source: - Infected animals (especially for *M. canis*) - Infected individuals - Fomites like clothing, brushes, and combs - Contaminated soil ### Transmission Routes: - Direct contact with infected persons or animals - Indirect contact through fomites - Contact with spores in the environment ### Clinical Picture: - Superficial: scale and hair breakage - Chronic: less inflammation, adults more often affected - Infiltrative-suppurative: kerion formation with nodules and potential pus ### Diagnostics: - **Wood's Lamp**: can reveal fluorescence - **Microscopy with KOH**: detects fungal spores/hyphae - **Culture**: identifies specific pathogen ### Differential Diagnostics: - Other dermatophytoses (e.g., tinea capitis) - Seborrheic dermatitis - Scalp psoriasis - Bacterial folliculitis - Alopecia areata ### Principles of Treatment: For successful management of microsporia, the following treatments are usually applied: #### Superficial Microsporia - **Topical Antifungals**: such as - Miconazole - Clotrimazole - Terbinafine

Question 33

34. Dermatophytosis. Trichophytosis (superficial and chronic, infiltrative-suppurative forms): pathogens, source, transmission routes, clinical picturo, diagnostics, differential diagnostics, principles of treatment, prevention.

Answer 33

Dermatophytosis, when caused by Trichophyton species, is referred to as trichophytosis. It's another type of fungal infection of the skin, hair, or nails and can present in various forms, including superficial, chronic, and infiltrative-suppurative. Let's break down this infection: ### Pathogens: - Trichophyton tonsurans - Trichophyton rubrum - Trichophyton verrucosum - Trichophyton mentagrophytes ### Source: - Direct skin-to-skin contact with infected individuals - Contact with animals, especially with T. verrucosum - Contaminated items such as clothing, towels, and hairbrushes - Soil, in fewer cases ### Transmission Routes: - Human to human - Animal to human - Fomites (contaminated items) - Sometimes from soil to human ### Clinical Picture: - Superficial Form: Scaling, itching, and ring-like lesions on the skin; may also see brittle hair over the infected area. - Chronic Form: Less inflammatory reaction, might present as more widespread, scaly patches, common in adults. - Infiltrative-Suppurative Forms (Kerion): Painful, purulent, swollen lesions, usually on the scalp; can lead to scarring and hair loss if not treated. ### Diagnostics: - Wood's Lamp Examination: Some species show fluorescence. - Microscopy with KOH Solution: Observing fungal elements in skin or hair samples. - Fungal Culture: Definitive identification of the fungus. - Histopathology: Skin biopsy stained with PAS (Periodic Acid-Schiff) can be used sometimes. ### Differential Diagnostics: - Seborrheic dermatitis - Psoriasis - Scalp folliculitis - Impetigo ### Principles of Treatment: #### Superficial Form - Topical Antifungals: - Terbinafine - Clotrimazole - Ketoconazole - Miconazole - Hygiene: Regular washing, not sharing personal items. #### Chronic Form - Oral Antifungals: Required for hair or nail involvement: - Griseofulvin - Terbinafine - Itraconazole - Fluconazole

Question 34

35, Dermatophytosis. Favus (superficial and chronic, infiltrative-suppurative forms): pathogens, source, trasmission routes, clinical picture, diagnostics, di ferential diagnostics, principles of treatment, prevention.

Answer 34

Dermatophytosis known as Favus is a chronic form of tinea capitis mainly caused by the fungus Trichophyton schoenleinii. Favus is recognized for its distinctive scutula lesions, which are crust-like structures on the scalp, and can lead to scarring and permanent hair loss if not treated adequately. Let's explore Favus in detail: ### Pathogens: The primary pathogen responsible for Favus is Trichophyton schoenleinii. ### Source: The source is primarily human-to-human transmission, although the fungus can also live in soil and be transferred to humans indirectly. ### Transmission Routes: - Direct contact with infected individuals - Contact with contaminated objects, such as combs, hats, or bedding - Rarely, from soil ### Clinical Picture: Favus is characterized by: - Yellow, cup-shaped crusts (scutula) on the scalp - Hair loss at the lesion sites - A distinctive mousy odor - Without treatment, can lead to scarring and permanent alopecia ### Diagnostics: - Clinical Examination: The presence of scutula is highly indicative of Favus. - Microscopy with KOH Solution: Observation of fungal hyphae and spores from the crusts. - Fungal Culture: To confirm the specific species of fungus. - Wood's Lamp Examination: May show a pale green fluorescence. ### Differential Diagnostics: - Scalp psoriasis - Seborrheic dermatitis - Bacterial infections, such as impetigo - Other forms of dermatophytosis (tinea capitis) ### Principles of Treatment: For Favus, the following treatments are commonly employed: #### Superficial and Chronic Forms - Oral Antifungals: Given the chronic nature and potential for scarring and alopecia, oral antifungals are essential: - Griseofulvin (traditional choice) - Terbinafine - Itraconazole - Fluconazole - Topical Antifungals: For adjunct treatment ### Prevention: - Early diagnosis and treatment are crucial to prevent the spread and complications of Favus. - Avoid sharing personal items like combs, hats, or hairbrushes. - Good personal hygiene and regular washing of hair and scalp.

Question 35

36, Candidiasis: classification, etiology, pathogenesis, classification, clinical picture, diagnosties, differential diagnosties, principles of treatment, prevention.

Answer 35

Candidiasis is an infection caused by fungi of the genus Candida, with Candida albicans being the most common culprit. Candidiasis can affect various parts of the body, leading to a range of clinical manifestations. Below you can find a detailed breakdown: ### Classification: - Oral Candidiasis (Thrush) - Vulvovaginal Candidiasis (VVC) - Invasive Candidiasis (including candidemia) - Cutaneous Candidiasis - Chronic Mucocutaneous Candidiasis ### Etiology: Most candidiasis infections are caused by Candida albicans, but other species such as Candida glabrata, Candida parapsilosis, and Candida tropicalis may also be involved. ### Pathogenesis: - Disruption of normal flora (e.g., antibiotic use) - Moist and warm environment - Weakened immune system - Hormonal changes (e.g., pregnancy) - Diabetes mellitus - Use of corticosteroids or immunosuppressive therapy ### Clinical Picture: Oral Candidiasis: White creamy patches on the tongue or oral mucosa, which can be wiped off to reveal a red base. Vulvovaginal Candidiasis: Vaginal itching, redness, swelling, and a thick, white discharge resembling cottage cheese. Invasive Candidiasis: Fever, chills, and a variety of symptoms depending on infected organs, often occurring in hospital settings. Cutaneous Candidiasis: Red rashes with well-defined borders, often found in folds such as under the breasts, groins, or between fingers. Chronic Mucocutaneous Candidiasis: Persistent candidal infections on the skin, nails, and mucous membranes. ### Diagnostics: - Clinical examination - Microscopy: KOH smear shows yeast and pseudohyphae. - Culture: Identification of Candida species. - Biopsy: In case of chronic or invasive infections. - Blood tests: For invasive candidiasis (e.g., blood cultures). ### Differential Diagnostics: - Bacterial infections (e.g., Streptococcal pharyngitis) - Other fungal infections (e.g., dermatophytosis) - Herpes simplex virus - Lichen planus ### Principles of Treatment: Topical Antifungals (for localized infections): - Clotrimazole - Nystatin - Miconazole Oral Antifungals (for severe or esophageal candidiasis, and VVC): - Fluconazole - Itraconazole

Question 36

37. Mucosal candidiasis: eriology, pathogenesis, classification, elinical picture, diagnosties. diffrantial diagnosties, principles of treatment, prevention

Answer 36

Mucosal Candidiasis: ### Etiology: Mainly caused by Candida albicans, but other Candida species like C. glabrata or C. tropicalis can also be involved. ### Pathogenesis: Occurs when the balance of normal mucosal flora is disrupted or the immune system is compromised, leading to overgrowth of Candida. Common contributing factors: - Antibiotic use - Immunodeficiency (e.g., HIV) - Diabetes - Corticosteroid therapy - Pregnancy ### Classification: - Oral Candidiasis: Including thrush and angular cheilitis - Oesophageal Candidiasis - Vulvovaginal Candidiasis - Candidal Balanitis - Candidal Diaper Rash - Chronic Mucocutaneous Candidiasis ### Clinical Picture: Varies depending on site: - Oral: White patches, redness, soreness - Esophageal: Dysphagia, pain on swallowing - Vulvovaginal: Itching, discharge, inflammation - Balanitis: Erythema, itching, scaling on the penis - Diaper Rash: Bright red rash with satellite lesions ### Diagnostics: - Clinical examination - KOH smear or fungal culture - Biopsy (for refractory cases) - Endoscopy (for esophageal candidiasis) ### Differential Diagnostics: - Bacterial infections - Lichen planus - Gastroesophageal reflux disease (GERD) - Herpes simplex virus (HSV) infections ### Principles of Treatment: Localized candidiasis: - Topical antifungals (nystatin or azole creams) Moderate to severe or oropharyngeal/esophageal candidiasis: - Systemic therapy with fluconazole or other azoles - Amphotericin B for refractory cases ### Prevention: - Good oral hygiene - Control of diabetes - Appropriate antibiotic use

Question 37

38. Candidiasis of large folds: etielogy, pathogenesis, classification, clinical picture, diagnostics, difTerential diagnosties, principles of tratment, preventon.

Answer 37

Candidiasis of Large Folds (Intertrigo): ### Etiology: Infection with Candida species, most commonly Candida albicans. ### Pathogenesis: Overgrowth of Candida in warm, moist, and friction-prone areas of large skin folds due to disturbed local microenvironment, impaired immunity, or increased skin pH. ### Classification: - Inframammary Candidiasis - Intertriginous Candidiasis (involving other skin fold areas) ### Clinical Picture: Bright red rashes with a distinct edge, possible oozing, satellite pustules, and discomfort or itching. ### Diagnostics: - Clinical examination - KOH smear showing pseudohyphae and/or yeast cells - Culture may be used to identify species ### Differential Diagnostics: - Psoriasis - Erythrasma due to Corynebacterium - Tinea infections - Seborrheic dermatitis ### Principles of Treatment: - Keeping the affected area dry and clean - Topical antifungals like clotrimazole, miconazole, or nystatin - Severe cases may require oral antifungals (fluconazole) ### Prevention: - Regular changing of clothes to keep skin dry - Using absorbent powders in susceptible individuals - Weight loss to reduce skin folds

Question 38

39. Onychomycosis, Pathogens, elinical pieture, diagnosties, differential diagnosties, basic principles of treatment.

Answer 38

Onychomycosis: ### Pathogens: Mostly caused by dermatophytes (e.g., Trichophyton rubrum), nondermatophytic molds, and yeasts (Candida species). ### Clinical Picture: Thickening of the nail, discoloration, subungual debris, and possible separation of the nail from the nail bed (onycholysis). ### Diagnostics: - Visual inspection - KOH preparation to view fungi - Nail clippings for culture and histological examination using PAS (Periodic Acid-Schiff) staining ### Differential Diagnostics: - Psoriasis - Lichen planus - Traumatic nail dystrophy - Nail bed tumors ### Basic principles of Treatment: - Oral antifungal agents: terbinafine, itraconazole, fluconazole - Topical treatments: ciclopirox, efinaconazole, amorolfine nail lacquers - Mechanical debridement of the affected nail(s) - Photodynamic therapy and laser treatments in some resistant cases ### Prevention: - Good foot hygiene - Keeping nails short and dry - Wearing breathable shoes and socks

Question 39

41. Dermatitis: simple contact, allergie, General characteristies, differential diagnostics, principles of trealment.

Answer 39

Dermatitis: ### Simple Contact Dermatitis: General Characteristics: Caused by direct skin contact with irritants like soaps, chemicals, or detergents leading to non-allergic irritation of the skin. ### Allergic Contact Dermatitis: General Characteristics: An immune-mediated response where the skin develops a rash after exposure to an allergen, which is a substance the person's immune system recognizes as foreign. ### Differential Diagnostics: - Psoriasis - Atopic dermatitis - Seborrheic dermatitis - Urticaria - Infections - Photodermatitis ### Principles of Treatment: - Identification and avoidance of the irritant or allergen - Topical steroids like hydrocortisone for inflammation and itching

Question 40

42, Toxidermia (fixed erythema, Lyell's discase, Stevens-Johnson syndrome, ete.): definition, etiopathogenesis, clinical picture, principles of treatment, prevention.

Answer 40

Toxidermia: ### Definition: Toxidermia refers to skin manifestations resulting from a systemic reaction to drugs or toxins. ### Etiopathogenesis: Drug-induced toxidermia is caused by adverse reactions to medications, which may be dose-dependent or idiosyncratic. ### Clinical Picture: - Fixed Drug Eruption: Singular or multiple round, red or purple patches that recur at the same site upon re-exposure to a drug. - Toxic Epidermal Necrolysis (Lyell's Disease): Severe, life-threatening condition with widespread skin peeling and mucosal involvement. - Stevens-Johnson Syndrome (SJS): A milder form of TEN with less than 10% body surface area involvement but with similar systemic symptoms. ### Principles of Treatment: - Immediate discontinuation of the suspected drug - Supportive care and monitoring in a hospital setting, potentially including intensive care for severe cases - Fluid and electrolyte balance maintenance - Wound care for skin lesions - Analgesics for pain management - Corticosteroids may be used in early stages of SJS but are controversial in TEN - Immunosuppressants like cyclosporine or IVIG (intravenous immunoglobulin) may be considered in certain case ### Prevention: - Avoiding known drug allergies - Use of alert bracelets or carrying cards with drug allergy information - Slow trial doses for medications when a history of drug reactions exists

Question 41

43. Unicaria: classification, etiopathogenests, clinical picture, treatment principles, relapse prevention. Quincke's clemas ctiopathogenesis, clinical picture, lintaid

Answer 41

Urticaria (Hives): ### Classification: 1. Acute Urticaria: Lasts less than six weeks. Causes can include certain foods, medications, infections, insect stings, or stress. 2. Chronic Urticaria: Persists for longer than six weeks and often has no identifiable cause. ### Etiopathogenesis: Triggered by histamine release from skin mast cells and basophils, often due to allergies, but can also be caused by factors such as infection, stress, or temperature extremes. ### Clinical Picture: Presents as red, raised, itchy welts that vary in size and can migrate and coalesce on any part of the skin. ### Treatment Principles: 1. Antihistamines: Such as cetirizine, loratadine, fexofenadine. 2. Corticosteroids: Short courses of oral steroids for severe acute urticaria. 3. Leukotriene Receptor Antagonists: Montelukast may be useful in combination with antihistamines. 4. Omalizumab: For chronic spontaneous urticaria unresponsive to antihistamines. ### Relapse Prevention: Patient education to identify and avoid triggers, long-term management with the lowest effective dose of medication, and regular follow-up. ### Quincke's Edema (Angioedema) Etiopathogenesis and Clinical Picture: - Etiopathogenesis: Often occurs in conjunction with urticaria; hereditary angioedema is due to C1 inhibitor deficiency. Can be triggered by medications (ACE inhibitors), allergens, and unknown causes. - Clinical Picture: Sudden onset of swelling in the deeper layers of the skin, typically around the eyes and lips, and sometimes the genitals, hands, and feet. ### Treatment: 1. Antihistamines: If associated with urticaria. 2. Corticosteroids and Antihistamines: For acute attacks. 3. C1 Inhibitor Concentrate: For hereditary angioedema episodes. 4. Fresh Frozen Plasma: Can be used in acute hereditary angioedema.

Question 42

44. Skin itching: etiopathogenesis, diagnosties, differential diagnosties, treatment

Answer 42

Skin Itching (Pruritus): ### Etiopathogenesis: 1. Dry Skin: Common, especially in older age. 2. Dermatological Conditions: Eczema, psoriasis, hives. 3. Systemic Diseases: Liver disease, kidney failure, thyroid disorders. 4. Allergic Reactions: To drugs, food, or other allergens. 5. Parasitic Infections: Such as scabies. ### Diagnostics: 1. Thorough medical history and physical examination. 2. Blood tests to check liver, kidney, and thyroid function, and possibly blood cell counts. 3. Skin tests for allergies. 4. Biopsy of skin lesions if present. ### Differential Diagnostics: 1. Differentiating from conditions that primarily cause skin lesions like psoriasis or eczema. 2. Systemic causes such as liver or kidney disease. 3. Neurologic conditions that cause itching without rash. ### Treatment: 1. Moisturizers: For dry skin. 2. Topical Corticosteroids: For dermatologic causes like eczema. 3. Antihistamines: Such as cetirizine or diphenhydramine, for allergic reactions. 4. Phototherapy: For systemic and severe dermatological causes.

Question 43

45. Alepic dermatitis: definition, etiopathogenesis, clinical characteristies of the stages of the process, diagnusties, differential diagnosties, principles of therapy and prevention.

Answer 43

Atopic Dermatitis (Eczema): ### Definition: A chronic, inflammatory skin condition characterized by red, itchy, and sometimes oozing rashes. ### Etiopathogenesis: 1. Genetic predisposition. 2. Impaired skin barrier function. 3. Immune system dysregulation. 4. Environmental factors, such as allergens or irritants. 5. Stress can exacerbate the condition. ### Clinical Characteristics of the Stages: 1. Acute: Erythema (redness), vesicles (small blisters), weeping, and pruritus (itching). 2. Subacute: Scaling, erythema, and less weeping. 3. Chronic: Lichenification (thickened skin), scaling, and fibrotic papules. ### Diagnostics: 1. Medical history evaluation. 2. Physical examination and assessment of skin. 3. Blood tests for allergens, including IgE levels. 4. Skin patch testing for environmental allergens. ### Differential Diagnostics: 1. Psoriasis. 2. Seborrheic dermatitis. 3. Contact dermatitis. 4. Skin infections such as scabies or fungal infections. ### Principles of Therapy: 1. Skin Care: Regular use of emollients and moisturizers to improve skin barrier function. 2. Topical Corticosteroids: For flare management and to reduce inflammation. 3. Topical Calcineurin Inhibitors: Tacrolimus and pimecrolimus for inflammation without the side effects of steroids. 4. Systemic Therapies: For severe cases, systemic corticosteroids or newer agents like dupilumab may be used.

Question 44

46. Eczema: clioputhogenesis, classification, clinical features, diagnustics, differential diugnostics, principles of general and local ucatment.

Answer 44

Eczema (Dermatitis): ### Cliopathogenesis: A combination of genetic, environmental, and immunological factors causing inflammation and barrier dysfunction of the skin. ### Classification: 1. Atopic Dermatitis: Typically begins in childhood, often associated with asthma and allergic rhinitis. 2. Contact Dermatitis: A result of skin contact with allergens or irritants. 3. Dyshidrotic Eczema: Small fluid-filled blisters on hands and feet. 4. Nummular Eczema: Round patches of irritated skin that can be crusted, scaling, and itchy. 5. Seborrheic Dermatitis: Oily, scaly yellowish patches of skin, often on the scalp and face. ### Clinical Features: - Itchiness. - Red to brownish-gray patches. - Small, raised bumps, which may leak fluid when scratched. - Thickened, cracked, or scaly skin. - Sensitive and swollen skin from scratching. ### Diagnostics: 1. Medical history and physical exam. 2. Skin biopsy (rarely needed). 3. Patch testing for contact dermatitis. ### Differential Diagnostics: 1. Psoriasis. 2. Scabies. 3. Fungal infections. 4. Lichen planus. ### Principles of General Treatment: 1. Anti-Inflammatory Medications: Systemic corticosteroids for severe flares. 2. Immunosuppressants: Cyclosporine, methotrexate, or mycophenolate mofetil in chronic cases ### Principles of Local Treatment: 1. Topical Corticosteroids: Varying potencies based on severity and location of eczema. 2. Topical Calcineurin Inhibitors: Such as tacrolimus or pimecrolimus. 3. Moisturizers: To hydrate and repair skin barrier. 4. Topical Antibiotics: If secondary infection is present.

Question 45

47. Scabies: etiopathogenesis, classification, clinical picture, diagnostics, differential diagnostics, principles of treatment, prevention.

Answer 45

Scabies: ### Etiopathogenesis: Caused by the mite Sarcoptes scabiei, an obligate parasite that burrows into the skin to lay eggs, causing intense itching. ### Classification: 1. Typical Scabies: Common infestations characterized by burrows and papular rash. 2. Norwegian (Crusted) Scabies: Severe form with thick crusts, seen in immunocompromised individuals. 3. Nodular Scabies: Persistent nodules occur, particularly in the groin or axillary regions. ### Clinical Picture: - Intense itching, especially at night. - Pimple-like irritations or a rash. - Scales or blisters. - Sores caused by scratching. - Linear burrows into the skin. ### Diagnostics: 1. Clinical evaluation of skin lesions. 2. Microscopic examination of skin scrapings for mites, eggs, or fecal matter. 3. Dermoscopy can aid in identifying burrows. ### Differential Diagnostics: 1. Eczema. 2. Psoriasis. 3. Folliculitis. 4. Atopic dermatitis. ### Principles of Treatment: 1. Topical Permethrin: First-line treatment to be applied to the whole body. 2. Ivermectin: Oral medication for severe cases or for those who didn't respond to topical treatment. 3. Lindane: An alternative treatment, although neurotoxicity restricts its use.

Question 46

48. Psoriasis, etiopathogenesis, clinical varieties, diagnostic phenomena, diagnostics, differential diagnostics, fundamentals of therapy.

Answer 46

Psoriasis: ### Etiopathogenesis: A chronic autoimmune condition characterized by rapid skin cell growth. Results from a combination of genetic predispositions and environmental factors. Triggers may include infections, stress, and certain medications. ### Clinical Varieties: 1. Plaque Psoriasis: Most common, with raised, red patches covered with a silvery white buildup of dead skin cells. 2. Guttate Psoriasis: Characterized by small, dot-like lesions. 3. Inverse Psoriasis: Shows up in skin folds (armpits, groin, under breasts) as red and may be smooth and shiny. 4. Pustular Psoriasis: White pustules surrounded by red skin. 5. Erythrodermic Psoriasis: Intense redness covering large areas. ### Diagnostic Phenomena: - Auspitz Sign: Removal of scaling reveals pinpoint bleeding. - Koebner Phenomenon: Psoriatic skin lesions appear at sites of physical trauma. ### Diagnostics: 1. Clinical examination of the lesions. 2. Skin biopsy to distinguish from other skin diseases. ### Differential Diagnostics: 1. Eczema. 2. Seborrheic dermatitis. 3. Lichen planus. 4. Cutaneous lupus erythematosus. ### Fundamentals of Therapy: - Topical Treatments: Including corticosteroids, vitamin D analogues (calcipotriene), and retinoids. - Phototherapy: UVB light therapy for skin lesions. - Systemic Medications: Include methotrexate, cyclosporine, and acitretin for severe cases. - Biologic Agents: Such as etanercept, adalimumab, and ustekinumab, target specific parts of the immune system

Question 47

49. Lichen planus: etiopathogenesis, clinical varieties, lesions of the oral mucosa, diagnosties, differential diagnosties, basies of therapy.

Answer 47

Lichen Planus: ### Etiopathogenesis: An inflammatory condition of unknown origin, thought to be an autoimmune response. Possible triggers include medications, infections, allergens, or stress. ### Clinical Varieties: 1. Cutaneous Lichen Planus: Classic purple, polygonal, flat-topped papules, most commonly on wrist and ankles. 2. Oral Lichen Planus: White streaks and patches on oral mucosa; may cause pain or burning. 3. Genital Lichen Planus: Erosions or papules in the genital area. 4. Lichen Planopilaris: Affects hair follicles, leading to hair loss. 5. Lichen Planus Pigmentosus: Brownish patches on the face, neck, or limbs. 6. Nail Lichen Planus: Affects nails, leading to ridges, thinning, and can result in nail loss. ### Lesions of the Oral Mucosa: - Wickham's striae: White, lacy pattern overlaying the mucosal lesions. - Painful erosions or ulcers in more severe cases. - Burning sensation or discomfort. ### Diagnostics: 1. Clinical assessment of characteristic lesions. 2. Skin biopsy may be performed to confirm diagnosis. ### Differential Diagnostics: 1. Psoriasis. 2. Eczema. 3. Candidiasis (for oral lesions). 4. Squamous cell carcinoma (for persistent oral lesions). ### Basics of Therapy: 1. Topical Corticosteroids: First-line treatment, reduces inflammation and symptoms. 2. Oral Corticosteroids: For severe or widespread cases. 3. Topical Calcineurin Inhibitors: Such as tacrolimus or pimecrolimus may be used, especially for oral lichen planus. 4. Antihistamines: May help control itching.

Question 48

50. Gibert's disease (pityriasisosen) etiology, pathogenesis, diagnostics, differential diagnosties. treatment.

Answer 48

Gilbert's Disease (Often confused but should be Pityriasis Rosea): ### Etiology: The exact cause of Pityriasis Rosea is unknown, but it's believed to be associated with viral infections, especially of the human herpesvirus (HHV-6 and HHV-7). ### Pathogenesis: The disease usually begins with a single, large round or oval patch (herald patch) followed by the appearance of numerous smaller lesions. These lesions spread along the lines of skin cleavage, creating a characteristic "Christmas tree" pattern on the back. ### Diagnostics: 1. Clinical examination of characteristic rash. 2. Rule out other conditions with similar presentations through tests if necessary (like syphilis with RPR/VDRL tests). ### Differential Diagnostics: 1. Tinea corporis (fungal infection). 2. Secondary syphilis. 3. Eczema. 4. Drug rashes. ### Treatment: Pityriasis Rosea typically resolves without treatment within 6 to 8 weeks. No specific medication is required. Treatments focus on relieving symptoms: 1. Topical Steroids: For itch relief. 2. Antihistamines: Like cetirizine or loratadine to reduce itching. 3. Calamine Lotion: To soothe itching. 4. UVB Light Therapy: Can be used in severe cases to hasten the resolution of lesions.

Question 49

51. Etythema multiforme exudative: etiopathogenesis, clinical picture, diagnostics, differential diagnostics, treatment, prevention of recurrence.

Answer 49

Erythema Multiforme Exudative: ### Etiopathogenesis: Triggered by infections (especially herpes simplex virus), certain medications (sulfonamides, NSAIDs, anticonvulsants), or other factors. ### Clinical Picture: Symmetrical red, pink, or purplish spots, blisters, or patches on the skin, often with target or "bullseye" appearance, primarily on the limbs and trunk. ### Diagnostics: 1. Clinical assessment. 2. Skin biopsy for confirmation. 3. Blood tests to identify underlying causes. ### Differential Diagnostics: - Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis - Pityriasis Rosea - Drug eruptions - Viral exanthems ### Treatment: 1. Identify and remove trigger: Discontinue causative drugs or treat underlying infections. 2. Topical Steroids: For localized mild symptoms. 3. Systemic Steroids: Prednisone for severe cases

Question 50

52. Lupus erythematosus: etiopathogenesis, classification, clinical picture, lesions of the oral mucosa, diagnostics, treatment, clinical examination.

Answer 50

Lupus Erythematosus: ### Etiopathogenesis Autoimmune disorder with genetic, environmental, hormonal, and immunological factors. ### Classification 1. Systemic Lupus Erythematosus (SLE) 2. Cutaneous Lupus Erythematosus (CLE), including: - Acute Cutaneous LE - Subacute Cutaneous LE - Chronic Cutaneous LE (Discoid Lupus Erythematosus - DLE) ### Clinical Picture - Fatigue, fever, joint pain, skin lesions. - Discoid rash, malar rash, photosensitivity. ### Lesions of the Oral Mucosa Painless ulcers, usually observed on the palate. ### Diagnostics - ANA test - Anti-dsDNA - Anti-Sm antibodies - CBC, ESR, renal and liver function tests. ### Treatment 1. NSAIDs: For joint pain. 2. Antimalarials: Hydroxychloroquine for skin and joint issues. 3. Corticosteroids: Prednisone for severe cases. 4. Immunosuppressants: Methotrexate, azathioprine, mycophenolate mofetil.

Question 51

53. Scleroderma: etiopathogenesis, clinical varieties, diagnosis, differential diagnosis, treatment, elinical exurination.

Answer 51

Scleroderma is a chronic connective tissue disease. Here's a brief summary: Etiopathogenesis: The exact cause is unknown, but involves immune system activation leading to collagen deposition in skin and organs. Genetic factors, environmental exposure, and vascular abnormalities are involved. Clinical varieties: There are two main types: 1. Localized scleroderma - affects only the skin. 2. Systemic sclerosis - affects the skin and internal organs. Diagnosis: Based on clinical findings, skin biopsy, and blood tests for specific antibodies. Differential diagnosis: Dermatomyositis, lupus erythematosus, rheumatoid arthritis, etc Treatment: Focuses on managing symptoms and preventing complications. Medications include: - Immunosuppressants (e.g., cyclophosphamide, mycophenolate mofetil) - Vasodilators (e.g., calcium channel blockers) - Anti-fibrotic agents (e.g., nintedanib) - Prostacyclin analogues for pulmonary arterial hypertension (e.g., iloprost) - Endothelin receptor antagonists (e.g., bosentan) Clinical examination: Involves checking skin tightness, Raynaud's phenomenon, joint mobility, and organ function assessments.

Question 52

54. True pemphigus: etiopathogenesis, varieties, clinical pieture, lesions of the oral mucosa, diagnostics, differential diagnostics, treatment, clinical examination.

Answer 52

-True pemphigus (pemphigus vulgaris) involves the production of antibodies against desmogleins, which are key proteins for cell adhesion in the skin and mucous membranes, causing blistering. -Varieties include pemphigus vulgaris, pemphigus foliaceus, and paraneoplastic pemphigus, each with distinct clinical manifestations and severity. -Clinically, it presents with painful mucosal erosions, often initially in the oral mucosa, and can progress to skin blisters. -Diagnosis is based on clinical examination, histopathology, and direct immunofluorescence of skin or mucosal biopsies, showing intercellular IgG deposits. -Differential diagnosis includes bullous pemphigoid, mucous membrane pemphigoid, erosive lichen planus, and epidermolysis bullosa acquisita. -Treatment involves systemic corticosteroids (e.g., prednisone), immunosuppressants (e.g., azathioprine, mycophenolate mofetil), rituximab, and IVIG for severe cases.

Question 53

55. Duhring's dermatitis herpetiformis; stiopathogenesis,clinical picture, lesions of the oral mucosa, diagnosties, differential diagnosties, treatment, medical examination.

Answer 53

-Dermatitis herpetiformis, also known as Duhring's disease, is a chronic skin condition characterized by blistering, extremely itchy skin. It is considered to be related to celiac disease and is a result of the body's immune response to gluten. Here's a short overview: -Pathogenesis: It's thought to be an autoimmune disease linked to gluten sensitivity. Immunoglobulin A (IgA) antibodies are deposited in the skin. -Clinical Picture: Presents as clusters of itchy blisters and bumps, mainly on the elbows, knees, back, and buttocks. -Lesions of the Oral Mucosa: Although rare, some patients might have oral manifestations including blistering and ulcerations. -Diagnostics: Mainly clinical examination supported by skin biopsy showing granular IgA deposits in dermal papillae and direct immunofluorescence. Blood tests may show antibodies associated with celiac disease. -Differential Diagnostics: Must be distinguished from other blistering skin conditions like bullous pemphigoid or pemphigus vulgaris. -Treatment: A gluten-free diet is key to managing the condition. Medications include Dapsone or sulfapyridine to control the skin symptoms. For those intolerant to Dapsone, a gluten-free diet becomes even more essential. =Medical Examination: Regular follow-ups to monitor the skin condition and adherence to a gluten-free diet. Blood tests to check for antibodies and liver function tests due to medication side effects may be needed. =Medications: Dapsone is the primary medication used.

Question 54

56. Scarring pemphigoid, Etiology, pathogenesis, clinical picture, diagnostics, differential diagnostics, treatment.

Answer 54

-Scarring pemphigoid (also known as mucous membrane pemphigoid) is a rare chronic autoimmune disorder affecting mucous membranes and the skin, causing blistering and scarring. -Etiology: The exact cause is unknown, but it involves the immune system producing antibodies against components of the epithelial basement membrane zone. -Pathogenesis: Antibodies target proteins such as BP180 and BP230 in the basement membrane, leading to inflammation, blister formation, and subsequent scarring. -Clinical Picture: It presents with blisters, erosions, and scarring predominantly affecting mucous membranes (mouth, eyes, nose, throat, genitals) and sometimes the skin. Scarring can lead to serious complications like blindness or airway obstruction. -Diagnostics: Diagnosis is based on clinical findings, histopathology (biopsy showing subepidermal blistering), and direct immunofluorescence of a biopsy showing linear deposition of IgG and/or C3 at the basement membrane zone -Differential Diagnostics: Differentiated from other blistering diseases like bullous pemphigoid (less scarring and generally doesn’t involve mucous membranes as extensively), epidermolysis bullosa acquisita, and Steven-Johnson syndrome/toxic epidermal necrolysis. --Treatment: The goal is to reduce symptoms, prevent complications, and halt disease progression. Treatment options include: - Topical Corticosteroids: For mild cases. - Systemic Corticosteroids: For more severe cases; prednisone is commonly used. - Immunosuppressive Agents: Such as azathioprine, mycophenolate mofetil, and cyclophosphamide, to reduce corticosteroid dosage and manage refractory cases. - Dapsone and rituximab have also been used in some cases.

Question 55

57. Viral denmatoses (herpes simplex, herpes zoster , warts, molluscumcontagiosum, papillomas, genital warts): etiology, pathogenesis, general characicristics, diagnostics, differential diagnostics, treatment principles, prevention issues.

Answer 55

Viral dermatoses are skin conditions caused by viruses, including herpes simplex, herpes zoster, warts, molluscum contagiosum, and papillomas. Etiology: - Herpes simplex: Caused by HSV-1 and HSV-2. - Herpes zoster: Due to reactivation of the varicella zoster virus. - Warts (including genital warts): Caused by human papillomavirus (HPV). - Molluscum contagiosum: Caused by the molluscum contagiosum virus (MCV), a poxvirus. - Papillomas: Result from HPV infection. Pathogenesis: Viral invasion and replication within skin cells or mucosa, followed by host immune response, leading to clinical manifestations. General Characteristics: - Herpes simplex: Grouped vesicles on an erythematous base, painful, can recur. - Herpes zoster: Painful rash in a dermatomal distribution, vesicles. - Warts: Rough, skin-colored papules, can be anywhere on the body. - Molluscum contagiosum: Pearly, dome-shaped nodules with central umbilication. - Papillomas/Genital warts: Soft, skin-colored, can be extensive, found in the anogenital area. Diagnostics: Clinical examination, viral culture, PCR, and histology for definitive diagnosis Differential Diagnostics: Differentiate from other skin conditions based on location, appearance, and patient history. Treatment Principles: - Antivirals: Acyclovir, valacyclovir for herpes simplex and zoster. - Immunomodulators: Imiquimod for warts and genital warts. - Physical Removal: Cryotherapy, surgical removal, or laser therapy for warts, molluscum, and papillomas.

Question 56

58, Herpes simplex. Etiology and pathogenesis. Types of pathogen and their characteristics. Clinical manifestations, Diagnosties, differential diagnosties, treatment. Prevention.

Answer 56

Herpes simplex is caused by two types of viruses: HSV-1 (typically causes oral herpes) and HSV-2 (usually genital herpes). Both types share similar characteristics such as a double-stranded DNA structure, and both can cause infections in oral and genital areas. Etiology and Pathogenesis: Infection occurs through direct contact with an infected individual. The virus enters the body through mucosal surfaces or breaks in the skin, then travels to the sensory neurons where it can remain latent until reactivated. Types of Pathogen and Characteristics: - HSV-1: Commonly associated with oral lesions such as cold sores. - HSV-2: Commonly associated with genital lesions. Clinical Manifestations: - Oral Herpes (HSV-1): Cold sores or fever blisters on or near the mouth. - Genital Herpes (HSV-2): Blisters and sores in the genital area. Both types can also cause symptoms like itching, pain, and discomfort. Diagnostics: - Physical examination. - PCR tests for virus detection. - Serological tests to identify antibodies. Differential Diagnostics: - Aphthous ulcers - Syphilis - Chancroid Treatment: - Antiviral medications such as Acyclovir, Valacyclovir, and Famciclovir to reduce severity and frequency of episodes. Prevention: - Avoiding direct contact with sores, - Using protection during sexual activity,

Question 57

59. Herpes zoster. Etiology and pathogenesis. Characteristics of the pathogen, Clinical manifestations. Diagnosties, differentin diagnosties, treatment. Prevention

Answer 57

-Herpes zoster, commonly known as shingles, is caused by the reactivation of the varicella-zoster virus (VZV), the same virus that causes chickenpox. After a person recovers from chickenpox, the virus can remain dormant in the nervous system for years before reactivating as shingles. -Etiology and Pathogenesis: The primary risk factor for VZV reactivation is weakened immunity due to age, stress, or immunosuppression. The virus travels along nerve fibers, causing inflammation and the characteristic painful rash of shingles. -Characteristics of the Pathogen: VZV is a DNA virus that belongs to the herpesvirus family. -Clinical Manifestations: Shingles is marked by a painful, blistering skin rash, usually appearing on one side of the body or face. Other symptoms may include fever, headache, and fatigue. -Diagnostics: Diagnosis is mainly clinical, based on the distinctive appearance of the rash. Laboratory tests (e.g., PCR, direct fluorescent antibody staining) can confirm the diagnosis. -Differential Diagnostics: Shingles must be differentiated from conditions like herpes simplex, impetigo, contact dermatitis, and insect bites. --Treatment: - Antiviral medications (e.g., acyclovir, valacyclovir, and famciclovir) can shorten the duration and severity of the outbreak if started early. - Pain management might include NSAIDs, narcotic pain medication, and nerve block injections. - Calamine lotion and oatmeal baths can help relieve itching.

Question 58

60. Warts, Classification, Etiology and pathogenesis, Clinical manifestations. Diagnosties, differential diagnostics, treatments, Prevention.

Answer 58

--Warts are non-cancerous skin growths caused by the human papillomavirus (HPV) infection. There are more than 100 types of HPV, and different types affect different parts of the body. -Classification: 1. Common warts (Verruca vulgaris): Typically appear on the hands. 2. Plantar warts (Verruca plantaris): Found on the soles of the feet. 3. Flat warts (Verruca plana): Smaller and smoother, appearing on the face, neck, or legs. 4. Filiform warts: Finger-like warts on the face and neck. 5. Periungual warts: Around or under the nails. --Etiology and Pathogenesis: Warts are caused by HPV infection. The virus enters the body through small cuts or breaks in the skin, leading to rapid cell growth on the outer skin layer. Not everyone who comes into contact with HPV will develop warts; immune system strength plays a significant role. --Clinical Manifestations: Warts are characterized by small, fleshy bumps on the skin or mucous membranes. The appearance can vary depending on the type, but they may be grainy, flesh-colored, and rough to the touch. --Diagnostics: Warts are usually diagnosed based on their appearance. In uncertain cases, a biopsy or other tests might be performed to exclude other conditions. --Differential Diagnostics: Other skin conditions that might be confused with warts include corns, calluses, molluscum contagiosum, skin tags, and certain types of skin cancer. --Treatments: - Salicylic acid: Topical treatments that gradually peel away the infected skin. - Cryotherapy: Freezing the wart with liquid nitrogen. - Surgical removal: Cutting away the wart, generally used for persistent warts.

Question 59

61, Papillomas, Classification, Etiology and pathogenesis, Clínical manifestations, diagnosties, differential diagnostics, treatment. Prevention.

Answer 59

--Papillomas are noncancerous tumors caused by the human papillomavirus (HPV). Let's break down your request concisely: --Classification: There are many types, including cutaneous and mucosal papillomas, based on the affected site. --Etiology and Pathogenesis: Caused by HPV infection. The virus triggers cell proliferation, leading to tumor formation. --Clinical Manifestations: Appear as small, cauliflower-like growths on the skin or mucous membranes. Their location can range from the skin, genital area, to the respiratory tract. --Diagnostics: Visual examination, HPV testing, and biopsy. --Differential Diagnostics: Differentiate from warts, benign skin lesions, and in some cases, malignant tumors. --Treatment: - Topical treatments include salicylic acid and imiquimod. - Surgical options like cryotherapy, laser therapy, and excision. - Preventive vaccines against HPV, such as Gardasil and Cervarix. Prevention: HPV vaccination is the primary prevention method. Safe sexual practices and regular screenings can also help prevent infection or early detection.

Question 60

62. Molluscumcontagiosum. Classification Biology and pathogenesis, Clinical manifestations. diagnostics, differential diagnostics, treatment. Prevention

Answer 60

--Molluscum contagiosum is caused by a poxvirus and leads to benign, usually self-limited skin lesions. - Classification/Biology: It's a viral infection classified under Poxviridae. The virus infects the skin's epidermal layer, inducing cell proliferation - Pathogenesis: The virus enters through small breaks in the skin or mucous membrane, leading to localized infection. - Clinical Manifestations: Presents as small, firm, painless papules, usually with a central dimple. They can occur anywhere on the body but are most commonly seen on the trunk, limbs, and genital area. - Diagnostics: Primarily clinical based on the appearance of lesions. A skin biopsy can confirm the diagnosis if uncertain. - Differential Diagnostics: Includes conditions like warts, basal cell carcinoma, and keratoacanthoma. - Treatment: Often not necessary as lesions can resolve spontaneously. For persistent cases, treatment options include cryotherapy, curettage, and topical agents. - Prevention: Minimizing direct skin-to-skin contact and avoiding sharing personal items. - Medications: Imiquimod cream, Cantharidin, and Potassium hydroxide solution are common treatments.

Question 61

63. The main criteria for the diagnosis of herpes simplex and herpes zoster.

Answer 61

For Herpes Simplex (HSV): 1. Clinical Presentation: HSV typically presents as painful blisters or ulcers on the skin, lips, oral mucosa, or genitals. HSV-1 often affects the oral area, while HSV-2 typically involves the genital area, although crossover can occur. 2. Viral Culture: Taking a swab from the base of a fresh lesion to grow the virus in culture is a traditional method. 3. Polymerase Chain Reaction (PCR) Test: A more sensitive method that detects HSV DNA in a sample from a lesion, blood, or other body fluids. 4. Serological Tests: Antibody tests can identify past exposure but are not always useful for diagnosing an active infection. ### For Herpes Zoster (Shingles): 1. Clinical Presentation: HZV is characterized by a painful, unilateral rash that presents in a dermatomal distribution. It often starts with pain or tingling before the rash appears and can be accompanied by fever, headache, and fatigue. 2. Tzanck Smear: A microscopic examination of scraped cells from the base of the lesion can show multinucleated giant cells common in herpesvirus infections but does not differentiate between HSV and VZV. 3. Direct Fluorescent Antibody (DFA): A test that can be used to detect VZV from scrapings from the base of the rash. 4. PCR Test: Can detect VZV DNA from lesions and is more specific than a Tzanck smear or DFA.

Question 62

64, Condylomaacuminate. Eriology and pathogenesis. Clinical manifestations, diagnosties, differential diagnostics, treatment. Prevention.

Answer 62

Condyloma acuminata, also known as genital warts, are primarily caused by the Human Papillomavirus (HPV), particularly strains 6 and 11. Etiology and Pathogenesis: The virus is transmitted through sexual contact, leading to epithelial cell infections. The incubation period varies, and the virus can remain latent, making it sometimes challenging to identify the source of infection. Clinical Manifestations: Appear as small, flesh-colored to white, projections on genital and anal areas. They might be singular or multiply to form a cauliform mass. Diagnostics: Diagnosis is mainly clinical, through visual inspection. Biopsy or HPV typing may be required for uncertain cases or differential diagnostics. Differential Diagnostics: Must be differentiated from other sexually transmitted infections (STIs) and benign/malignant lesions, like molluscum contagiosum or squamous cell carcinoma. Treatment: Several treatments exist, including topical agents and surgical options: - Topical agents: Imiquimod, Podophyllotoxin, and Trichloroacetic acid. - Surgical options: Cryotherapy, Laser therapy, Electrocautery, or Surgical excision. Prevention: HPV vaccines (Gardasil and Cervarix) can prevent strains of HPV that cause genital warts and cervical cancer. Additionally, safe sex practices and regular screenings play crucial roles.

Question 63

65. Vasculitis of the skin: etiology and pathogenesis, classification, clinical manifestations, principles of therapy, prevention.

Answer 63

--Vasculitis of the skin is characterized by inflammation of the blood vessels, leading to various symptoms and complications. --Etiology and Pathogenesis: Can result from autoimmune responses, infections, medications, or diseases like rheumatoid arthritis and SLE. It involves immune-mediated inflammation leading to vessel damage. --Classification: Primarily classified based on the size of affected vessels and includes: - Large vessel vasculitis (e.g., Giant cell arteritis) - Medium vessel vasculitis (e.g., Polyarteritis nodosa) - Small vessel vasculitis (e.g., Cutaneous leukocytoclastic angiitis) --Clinical Manifestations: Manifestations include palpable purpura, ulcers, digital gangrene, and livedo reticularis. Symptoms vary according to the type and severity of vasculitis. Principles of Therapy: --Treatment aims at reducing inflammation and controlling the immune system. It includes: - Corticosteroids (e.g., Prednisone) to reduce inflammation. - Immunosuppressants (e.g., Cyclophosphamide, Azathioprine) for severe cases. - Biological agents (e.g., Rituximab) in certain types. --Prevention: Involves managing underlying conditions, avoiding triggers,

Question 64

66. Vasculitis of the skin: benign pigmentary vasculitis of Schimberg. Etiology and pathogenesis, classification, clinical manifestations, Diagnostics, differential diagnostics, treatment. Prevention.

Answer 64

--Etiology and Pathogenesis: Benign pigmentary vasculitis of Schamberg, also known as Schamberg's disease, is a form of capillaritis. Although its exact cause is unknown, it's believed to involve an immune response that leads to leaking of blood vessels, resulting in pigmentation. Factors like medications, viral infections, or other immune-mediated conditions may play a role. --Classification: Schamberg's disease falls under pigmented purpuric dermatoses, characterized by petechiae, purpura, and brown pigmentation. --Clinical Manifestations: Presents as reddish-brown patches, often with "cayenne pepper" spots due to leakage of red blood cells and hemosiderin deposition, primarily on the lower legs. --Diagnostics: Diagnosis is mainly clinical, supported by dermatoscopy. Skin biopsy can confirm the diagnosis showing hemosiderin deposition and perivascular lymphocytic infiltration. --Differential Diagnostics: Needs to be differentiated from other causes of pigmented purpuric dermatoses and conditions causing leg pigmentation. --Treatment: Treatment is often not necessary as the condition is benign but can include: - Topical steroids to reduce inflammation (e.g., Hydrocortisone). - Leg elevation and compression garments to reduce venous pressure. - Occasionally, systemic medications like pentoxifylline or bioflavonoids may be used to improve microcirculation. --Prevention: There is no specific prevention, but managing risk factors like avoiding certain medications or controlling underlying conditions may help reduce risk.

Question 65

67. Vasculitis of the skin: hemonhagic vasculitis of Shonlein-Genoch. Etiology and pathogenesis, classification, clinical manifestations, Diagnostics, differential diagnostics, treatment. Prevention.

Answer 65

-Etiology and Pathogenesis: Henoch-Schönlein Purpura (HSP), also known as IgA vasculitis, is caused by the deposition of IgA immune complexes in the small vessels' walls. It's often preceded by an upper respiratory tract infection. The exact cause is unknown but involves an abnormal immune response. -Classification: HSP is classified as a small vessel vasculitis. --Clinical Manifestations: Characterized by a tetrad of symptoms: palpable purpura (especially on the lower limbs and buttocks), arthritis or arthralgias, abdominal pain, and kidney involvement (hematuria and/or proteinuria). -Diagnostics: Diagnosis is largely clinical but can be supported by elevated IgA levels, skin or renal biopsy showing IgA deposits, and abdominal ultrasound for gastrointestinal involvement. -Differential Diagnostics: Needs differentiation from other causes of vasculitis, including infections, other systemic vasculitides, and coagulation disorders. -Treatment: - Corticosteroids, (e.g., Prednisone) to reduce inflammation. - Symptomatic treatment for joint, abdominal pain, and other symptoms. - Severe cases may require immunosuppressants like cyclophosphamide or azathioprine. - ACE inhibitors for significant renal involvement.

Question 66

68, Skin vasculitis: allergies vasculitis. Etiology and pathogenesis, classication, clinical manifestations, Diagnostics, differential diagnostics, treatment. Prevention.

Answer 66

--Allergic vasculitis, also known as hypersensitivity vasculitis, is a condition where there's inflammation of the blood vessels due to an allergic reaction. --Etiology and Pathogenesis: Often triggered by a reaction to a medication, infection, or another underlying condition. It involves an immune response that results in inflammation of blood vessels. --Classification: Classified based on the size of affected vessels and can be categorized under cutaneous small-vessel vasculitis. --Clinical Manifestations: Skin lesions are the most common, including palpable purpura, often on the legs. Other symptoms may depend on organ involvement. --Diagnostics: Diagnosis is made via patient history, physical exam, blood tests, skin biopsy, and sometimes imaging tests to assess organ involvement. --Differential Diagnostics: Needs to be distinguished from other types of vasculitis and conditions that cause similar skin lesions like infections or clotting disorders. --Treatment: Mainly involves removing the offending agent if known, and management of symptoms. Medications include: - Corticosteroids (e.g., prednisone) to reduce inflammation. - Immunosuppressive drugs (e.g., azathioprine, cyclophosphamide) for severe cases. - Antihistamines and nonsteroidal anti-inflammatory drugs (NSAIDs) may also be used to relieve symptoms. Prevention: Involves avoiding known triggering agents when possible. Regular monitoring and management of underlying conditions that could contribute to vasculitis flare-ups are also beneficial.

Question 67

69. Skin vasculitis: nodular necrotic vasculitis. Etiology and pathogenesis, classification, clinical manifestations. Diagnostics, differential diagnostics, treatment. Prevention.

Answer 67

--Nodular necrotic vasculitis is a form of cutaneous vasculitis. Its etiology can be linked to infections, autoimmune disorders, or medications, with a pathogenesis involving an immune response that damages blood vessels. It belongs to a broader classification of vasculitis’s affecting the skin, categorized based on the size of the affected vessels and the organs involved. --Clinically, it presents with painful, necrotic nodules predominantly on the lower legs. Diagnosis is primarily clinical, supported by skin biopsy. Differential diagnosis includes other types of vasculitis, infections, and thrombotic disorders. ---Treatment involves addressing the underlying cause, if known, and may include: - Corticosteroids: prednisone - Immunosuppressants: azathioprine, methotrexate - Anticoagulants: in cases associated with thrombosis - Antibiotics: if an infection is present Prevention focuses on managing underlying conditions and avoiding known triggers.

Question 68

70, Skin vasculitis: erythema nodosum. Etiology and pathogenesis, classification, clinical manifestations. Diagnosties, differential diagnostics, treatment. Prevention.

Answer 68

--Etiology and Pathogenesis Erythema nodosum is considered a reactive condition, potentially triggered by a variety of factors. These can include infections (such as streptococcal infections, tuberculosis), medications (sulfonamides, oral contraceptives), and other conditions like sarcoidosis, inflammatory bowel diseases (Crohn's disease and ulcerative colitis), and cancers. --Classification Erythema nodosum is primarily classified based on its duration (acute, subacute, or chronic) and potential causes (infectious, drug-induced, associated with systemic diseases, or idiopathic when the cause is unknown). --Clinical Manifestations Patients often present with tender, red nodules, mostly located on the shins. These nodules can be painful. Other symptoms might include fever, joint pain, and swelling, indicating an underlying systemic issue. --Diagnostics The diagnosis is mostly clinical, based on the appearance of the characteristic nodules. However, to identify an underlying cause, blood tests (like a complete blood count, erythrocyte sedimentation rate, and C-reactive protein), throat cultures, chest X-rays, and specific tests for suspected causes (e.g., tuberculin test for tuberculosis) might be performed. --Differential Diagnostics It's essential to differentiate erythema nodosum from other types of panniculitis (inflammation of subcutaneous fat), such as erythema induratum, nodular vasculitis, or infections like cellulitis. --Treatment Treatment of erythema nodosum focuses on relieving symptoms and addressing the underlying cause, if known. NSAIDs (nonsteroidal anti-inflammatory drugs) are commonly used to manage the pain and inflammation. Corticosteroids may be considered in severe cases. The condition often resolves within 3-6 weeks, but treatment of the underlying cause is crucial to prevent recurrence.

Question 69

71. Schorhea: etiology and pathogenesis, classification, clinical manifestations, complications, basis principles of therapy and prevention.

Answer 69

--Schorhea appears to be a misspelling or potentially incorrect term. The context suggests you might be referring to "seborrhea" or "seborrheic dermatitis," a common skin condition. If that’s the case, here's a concise overview: --Etiology and Pathogenesis: Seborrheic dermatitis is linked to the overproduction of sebum and the presence of Malassezia yeast. Genetic, environmental, and health-related factors, such as stress and certain medical conditions, can contribute to its development. --Classification: - Infantile seborrheic dermatitis, occurring in infants and usually clearing up on its own. - Adult seborrheic dermatitis, which can be chronic and requires management. --Clinical Manifestations: - Scalp: Dandruff or thick crusts. - Face and body: Reddish, oily skin lesions with yellowish scales --Complications: - Secondary bacterial or fungal infections. - Psychosocial distress due to appearance. --Therapy: - Medicated shampoos (containing ketoconazole, ciclopirox, selenium sulfide, or coal tar). - Topical antifungals (ketoconazole cream). - Topical corticosteroids for inflammation. - Calcineurin inhibitors for inflammation without the side effects of steroids. --Prevention: - Regular use of medicated shampoos. - Managing stress.

Question 70

72. Blackheads (Acne), Classification. Etiology and pathogenesis, clinical manifestations, complications, basic principles of therapy and prevention.

Answer 70

--Blackheads (Open Comedones), Part of Acne Vulgaris ----Classification: - Grade 1: Mild, mostly non-inflammatory (blackheads and whiteheads). Etiology and Pathogenesis: - Caused by clogged hair follicles with oil (sebum) and dead skin cells. Hormonal changes, certain medications, and diet can contribute. --Clinical Manifestations: - Small, dark lesions on the skin, often seen on the face, neck, chest, and back. --Complications: - If untreated, can lead to inflammatory acne, skin infections. ---Therapy: - Topical Retinoids (e.g., adapalene) to prevent clogging. - Salicylic Acid to exfoliate and unclog pores. - Benzoyl Peroxide to kill bacteria and reduce inflammation. --Prevention: - Regular cleansing, avoiding comedogenic products, and using non-oily skin care products.

Question 71

73. Acne vulgaris. Etiology and pathogenesis, classification, clinical manifestations, complications, basic principles of therapy and prevention.

Answer 71

-Acne vulgaris is a common skin condition caused by blocked hair follicles and oil (sebaceous) glands of the skin, primarily due to an excess of oil, dead skin cells, and bacteria. Its etiology involves hormonal changes, diet, stress, and certain medications. -Classification ranges from mild, moderate to severe, based on the type and number of lesions: comedones (blackheads and whiteheads), papules, pustules, nodules, and cysts. -Clinical manifestations include the appearance of these lesions primarily on the face, chest, and back. -Complications can involve scarring and hyperpigmentation. -Basic principles of therapy include topical treatments like retinoids, benzoyl peroxide, and antibiotics; systemic treatments like oral antibiotics, isotretinoin for severe cases, and hormonal therapies. Prevention focuses on regular skin cleansing, avoiding known triggers, and proper medication use. --Name of medication for a short answer: Isotretinoin (for severe cases), Benzoyl Peroxide, and Topical Retinoids are among the common choices.

Question 72

74. Rosacca, Etiology and pathogenesis, classification, clinical manifestations, complications, basic principles of therapy and prevention.

Answer 72

Rosacea, a chronic skin condition, involves facial redness, swelling, and sometimes acne-like breakouts. The etiology is not fully understood but may involve genetic, environmental, vascular, and inflammatory factors. Rosacea's classification includes four subtypes: Erythematotelangiectatic, Papulopustular, Phymatous, and Ocular. Clinical manifestations include persistent redness, visible blood vessels, and acne-like breakouts. Complications can involve ocular issues like dry eyes and vision problems, and in severe cases, a thickening of the skin, particularly on the nose (rhinophyma). For therapy and prevention, treatment varies based on subtype and severity, but can include: - Topical treatments: Metronidazole, Azelaic acid, Ivermectin - Oral antibiotics: Doxycycline, Minocycline (for more severe cases) - Isotretinoin: For severe cases, particularly those not responding to other treatments (use is much more cautious due to its potential side effects) - Laser and light therapy: To reduce redness and visible blood vessels Preventive measures include avoiding known triggers (e.g., hot drinks, spicy foods, alcohol),using sun protection, and gentle skin care routines.

Question 73

75. Alopecia, Etiology and pathogenesis, classification, clinical manifestations, complications, basic principles of therapy and prevention.

Answer 73

Alopecia refers to hair loss, which can stem from various causes. - Etiology and Pathogenesis: Causes range from genetic factors, autoimmune diseases (alopecia areata), hormonal changes (e.g., postpartum, menopause), medical conditions (thyroid disorders, iron deficiency), medications, and stress. - Classification: Types include androgenetic alopecia (pattern hair loss), alopecia areata (patchy hair loss), alopecia totalis (total scalp hair loss), alopecia universalis (body hair loss), and telogen effluvium (temporary hair shedding). - Clinical Manifestations: Symptoms vary with type but can include thinning hair, bald patches, or complete loss of hair on the scalp or body. - Complications: Psychological distress is a common complication, including reduced self-esteem and anxiety. - Basic Principles of Therapy and Prevention: - For androgenetic alopecia: Minoxidil (topical), Finasteride (oral, for men), Minoxidil and Finasteride (for androgenetic alopecia) - For alopecia areata: Corticosteroids (topical, intralesional, or systemic), Corticosteroids (for alopecia areata, in various forms) - Other treatments might include immunotherapy, Immunotherapy (for severe cases), and light therapy. - Preventive measures focus on managing underlying conditions and stress.

Question 74

76. Alopecia arcata (Celsus" vitiligo), Friology and pathogenosis, classification, clinical manifestations, complications, basic principles of therapy and prevention.\

Answer 74

Alopecia Areata - Etiology and Pathogenesis: An autoimmune condition leading to patchy hair loss. - Classification: Ranges from alopecia areata (patches of hair loss), totalis (total scalp hair loss), to universalis (complete body hair loss). - Clinical Manifestations: Sudden hair loss in patches. - Complications: Psychological impact, including anxiety and depression. - Therapy and Prevention: Corticosteroids (topical, intralesional, oral), topical immunotherapy. Medication: Minoxidil may also be used to stimulate hair growth.

Question 75

77. Telogen alopecia (lelogen effuvium). Etiology and pathogenesis, classification, clinical manifestations, complications, basic principles of therapy and prevention.

Answer 75

-------Telogen alopecia, also known as Telogen Effluvium, involves temporary hair shedding due to a change in the number of hair follicles cycling in the growth phase. - Etiology and Pathogenesis: Often triggered by a significant stressor such as severe illness, major surgery, severe psychological stress, extreme weight loss, change in diet, certain medications, childbirth, or severe trauma. The stress causes hair follicles to prematurely enter the telogen phase, leading to increased hair shedding. - Classification: Can be acute or chronic. Acute telogen effluvium occurs suddenly and may resolve spontaneously within six months. Chronic telogen effluvium lasts longer than six months. - Clinical Manifestations: Diffuse hair thinning across the scalp without distinct patches. The individual may notice more hair falling out during washing, brushing, or gentle pulling - Complications: Psychological distress, including lowered self-esteem and anxiety. - Basic Principles of Therapy and Prevention: Identifying and removing the underlying cause is essential. Nutritional support, management of stress, and sometimes counseling for psychological support. Ensuring a balanced diet and avoiding harsh hair treatments can help prevent some cases.

Question 76

78. Anagenie alopecia, Etiology and pathogenesis, classification, clinical manifestations, complications, basic principles of therapy and prevention.

Answer 76

- Etiology and Pathogenesis: Caused by an interruption of the mitotic or metabolic activity of hair follicles due to an insult, most commonly chemotherapy or radiation therapy. These treatments can harm rapidly dividing hair matrix cells, leading to hair loss. - Classification: Typically, it's not classified as it is a direct consequence of the underlying treatment. However, severity can vary based on the specific causative agent. - Clinical Manifestations: Rapid hair loss occurring within days to weeks of the causative treatment. Affects not only the scalp but also other body hair. - Complications: Psychological distress is a significant complication, affecting the individual's self-image and potentially leading to anxiety or depression. - Basic Principles of Therapy and Prevention: The main approach is supportive care. The use of cooling caps during chemotherapy sessions may reduce the risk.

Question 77

79. Skin diseases associated with impaired pigment metabolism (hyperchromia and hypochromia). Etiology and pathogenesis, classification, clinical manifestations, complications, basic principles of therapy and prevention.

Answer 77

--Skin diseases that involve altered pigment metabolism, manifesting as either hyperchromia (increased pigmentation) or hypochromia (reduced pigmentation), result from various causes and mechanisms. --Etiology and Pathogenesis: These conditions might be caused by genetic factors (like albinism), autoimmune processes (as in vitiligo), or environmental factors (such as sun exposure leading to melasma). The pathogenesis often involves the melanocytes, which are responsible for producing melanin. --Classification: They can be broadly classified based on whether they cause hyperpigmentation (melasma, post-inflammatory hyperpigmentation) or hypopigmentation (vitiligo, albinism, and post-inflammatory hypopigmentation) --Clinical Manifestations: Manifestations vary widely, from patches of altered skin color (white patches in vitiligo, dark patches in melasma) to the entire skin (as in albinism). --Complications: Complications can include psychosocial impact, increased risk of sunburn or skin cancer (particularly in conditions causing hypopigmentation), and secondary infections. --Basic Principles of Therapy and Prevention: Treatment focuses on managing symptoms and might include topical agents (like corticosteroids for anti-inflammatory effects), procedures (such as laser therapy), and strict sun protection

Question 78

80. Vitiligo, Etiology and pathogenesis, classification, clinical manifestations, complications, basic principles of therapy and prevention.

Answer 78

--Vitiligo is a skin condition characterized by the loss of skin pigment, leading to white patches on various parts of the body. --Etiology and Pathogenesis: The exact cause is unknown, but it's believed to involve an autoimmune response where the body's immune system attacks and destroys the melanocytes, the cells responsible for producing melanin. Genetic factors, oxidative stress, and environmental factors may also contribute. --Classification: Vitiligo can be classified into two main types: segmental (affecting one side or part of the body and usually stops progressing after a year or two) and non-segmental (the most common type, symmetrical, and can progress). --Clinical Manifestations: It presents as well-defined white patches on the skin that may spread. These patches are more common on areas exposed to the sun, around body openings, and on injuries or pressure points. --Complications: The primary complications include psychological and emotional distress, sunburn, and an increased risk of skin cancer. --Basic Principles of Therapy and Prevention: There is no cure for vitiligo, but treatments aim to restore color to the affected skin and include topical corticosteroids, phototherapy, and, in some cases, surgery (like skin grafting). For prevention, protecting the skin from the sun using high-SPF sunscreen and covering up are recommended to prevent burns and potential worsening of vitiligo. Psychological support may also be beneficial for affected individuals.

Question 79

81. Neoplasms of the skin. Benign pigmented neoplasms of the skin. Classification of neoplasms. Tactics of a dermatologist.

Answer 79

--Neoplasms of the skin can broadly be classified into benign, premalignant, and malignant. Benign pigmented neoplasms include conditions like nevi (moles), seborrheic keratosis, and lentigo. --The classification of skin neoplasms is primarily based on their histological appearance and their potential for malignancy. -- A dermatologist's tactics in managing these conditions involve diagnosis through clinical examination and, if necessary, biopsy, followed by an appropriate treatment plan which could include monitoring, surgical removal, or other therapeutic interventions depending on the nature and severity of the neoplasm.

Question 80

82. Neoplasms of the skin. Seborrheic keratosis. Lezer-Trell syndrome. Tactics of a dermatologist.

Answer 80

--Seborrheic keratosis is a common, benign skin growth often seen in older adults. Leser-Trélat syndrome is a rare condition potentially indicating an underlying malignancy, : characterized by the sudden appearance of multiple seborrheic keratoses. ---A dermatologist's tactics for managing seborrheic keratosis usually involve reassurance and observation, as they are benign. However, if the growths are cosmetically concerning or cause symptoms, they can be removed through cryotherapy, curettage, or laser therapy. In the case of Leser-Trélat syndrome, the dermatologist would focus on identifying and managing the underlying malignancy, in addition to addressing the skin manifestations.

Question 81

83, Dermatological parancoplastic syndromes. Definition. Obligate and Optional dermatological parancoplastie syndromes. Tactics of a physician

Answer 81

--Dermatological paraneoplastic syndromes are a group of conditions that arise from the systemic effects of cancer, but are not due to the direct local effects of tumor cells. These syndromes are seen in patients with malignancies and can manifest before, after, or at the time of diagnosis of the cancer. There are two main types: 1. Obligate Dermatological Paraneoplastic Syndromes: These are strongly associated with malignancies. The presence of obligate syndromes often indicates an underlying, undiagnosed cancer. Examples include Acanthosis nigricans maligna and paraneoplastic pemphigus. 2. Facultative (Optional) Dermatological Paraneoplastic Syndromes: These may occur in patients with malignancies but can also be seen in the absence of cancer. They are not as strongly predictive of an underlying malignancy as obligate syndromes. Examples include generalized pruritus and erythema gyratum repens. Tactics of a Physician: The main tactics involve a high index of suspicion for underlying malignancy in patients presenting with dermatological conditions that match paraneoplastic syndromes. This includes detailed patient history, physical examination, appropriate screening for suspected cancers, and multidisciplinary team involvement for comprehensive management of both the skin manifestations and the underlying malignancy.

Question 82

84. Melanoma, Clinical manifestations, Diagnostics. Differential diagnostics, Treatment.

Answer 82

---Melanoma is a type of skin cancer developing from melanocytes, cells that produce the pigment melanin. Clinical Manifestations: - Change in an existing mole or the development of a new pigmented or unusual-looking growth on your skin. - Asymmetry, Border irregularity, Color variegation, Diameter over 6mm, Evolving size, shape or color. Diagnostics: - Skin examination. - Biopsy of suspicious skin lesions (excisional, incisional, or punch biopsy). Differential Diagnostics: - Basal cell carcinoma. - Squamous cell carcinoma. - Nevus (benign mole). - Seborrheic keratosis. Treatment: - Surgical removal of the melanoma. - For advanced melanoma: targeted therapy (e.g., BRAF inhibitors such as Vemurafenib or Dabrafenib), immunotherapy (e.g., CTLA-4 inhibitor Ipilimumab, PD-1 inhibitors Pembrolizumab or Nivolumab), and in some cases, chemotherapy.

Question 83

85. Basalioma Clinical manifestations Diagnostics, Differential diagnostics. Treatment.

Answer 83

--Basalioma, also known as Basal Cell Carcinoma (BCC), is the most common type of skin cancer, originating from the basal cells in the epidermis. Clinical Manifestations: - Appearance of a pearly or waxy bump, often on sun-exposed areas like the face and neck. - Flat, flesh-colored or brown scar-like lesion. - Bleeding or scabbing sore that heals and returns. Diagnostics: - Physical examination. - Skin biopsy (e.g., shave biopsy, punch biopsy, or excisional biopsy) for definitive diagnosis. Differential Diagnostics: - Squamous cell carcinoma. - Melanoma. - Seborrheic keratosis. - Actinic keratosis. Treatment: - Surgical options include excisional surgery, Mohs surgery (for high-risk areas), and curettage and electrodessication. - For superficial BCC, topical treatments such as Imiquimod cream or 5-Fluorouracil cream can be effective. - Radiation therapy may be considered for individuals who cannot undergo surgery. - Advanced or metastatic BCC might be treated with targeted therapy drugs like Vismodegib or Sonidegib.

Question 84

86. Squamous cell skin cancer. Clinical manifestations. Diagnostics. Differential diagnostics. Treatment.

Answer 84

--Squamous cell skin cancer is a type of skin cancer that begins in the squamous cells. --Clinical manifestations: It may appear as a firm red nodule, a flat lesion with a scaly crust, or a new ulceration or growth on pre-existing chronic wounds or in scar areas. --Diagnostics: Diagnosis primarily involves physical examination and biopsy of the lesion. --Differential diagnostics: It should be differentiated from basal cell carcinoma, actinic keratosis, and malignant melanoma among other conditions. --Treatment: Treatment options include surgical removal (excision), Mohs surgery, cryotherapy, and radiation. Medications may involve chemotherapy creams for superficial cases (e.g., 5-fluorouracil, imiquimod). Always consult healthcare professionals for accurate diagnosis and appropriate treatment.

Question 85

87. skin diseases associated with impaired metabolism of vitamins (A. C. PP. group B).

Answer 85

---Skin diseases linked to impaired metabolism or deficiency of vitamins include conditions related to deficiencies in Vitamin A, Vitamin C, Niacin (Vitamin PP), and the B-group vitamins. Here's a brief overview: --Vitamin A deficiency: It can lead to xerosis cutis (dry skin), which may progress to hyperkeratosis (thickening of the stratum corneum) or follicular hyperkeratosis (bumps on the skin). Night blindness and an increased risk of infections are also associated with Vitamin A deficiency. -Vitamin C deficiency (Scurvy): Symptoms include rough, dry, and scaly skin; gingival swelling; bleeding gums; and petechiae (small red spots caused by bleeding into the skin), and easy bruising. Vitamin C is crucial for the synthesis of collagen, and its deficiency impairs the healing of wounds. -Niacin (Vitamin PP/B3) deficiency (Pellagra): Characterized by the '3 Ds': Dermatitis, Diarrhea, and Dementia. Dermatitis may present as a bilateral symmetrical rash on sun-exposed areas (pellagrous dermatitis), which is rough, red, and may become pigmented and scaly. --Group B Vitamins deficiency: Deficiencies can manifest in various ways, such as: - Vitamin B2 (Riboflavin) deficiency: Can cause angular cheilitis (cracks at the corners of the mouth), cheilosis (swollen, cracked lips), and seborrheic dermatitis. - Vitamin B6 (Pyridoxine) deficiency: May lead to seborrheic dermatitis, glossitis (inflamed tongue), and cheilosis. - Vitamin B12 deficiency: Can result in hyperpigmentation of the skin, especially on the hands and feet, angular cheilitis, and glossitis.

Question 86

88. Cheilitis (own and symptomatic) General characteristics.

Answer 86

--Cheilitis refers to the inflammation of the lips and can appear in various forms, either as a primary condition (own cheilitis) or as a symptom of underlying issues (symptomatic cheilitis). General Characteristics: - Signs and Symptoms: Chapped lips, redness, dryness, scaling, swelling, cracks at the corners of the mouth (angular cheilitis), and pain or burning sensation. - Own Cheilitis: Can be due to various factors including environmental (such as wind, sun exposure), irritant contact dermatitis, allergic contact dermatitis, or infection. - Symptomatic Cheilitis: Occurs as a manifestation of systemic conditions including nutritional deficiencies (e.g., B vitamins, iron), gastrointestinal diseases (e.g., Crohn's disease), or as a side effect of medications. - Management: Involves identifying and treating the underlying cause, protecting lips from excessive moisture loss or environmental damage, and using topical emollients or anti-inflammatory agents as needed.

Question 87

89. Precancerous diseases of the red border of the lips and oral mucosa (Bowen's discasc, hyperkeratosis of the lips, cheilitis, leukoplakia, cutaneous horn, keratoacanthoma).

Answer 87

Precancerous conditions affecting the red border of the lips and oral mucosa are critical to recognize for early intervention and prevention of progression to cancer. These conditions include: 1. Bowen's Disease: A form of squamous cell carcinoma in situ characterized by a persistent, scaly patch on the skin or mucous membranes, which may evolve into invasive squamous cell carcinoma if left untreated. 2. Hyperkeratosis of the Lips: A condition marked by thickening of the outer layer of the lips due to excessive production of keratin. While not cancerous on its own, it can be a reaction to a chronic irritant or trauma and may coexist with other precancerous conditions. 3. Cheilitis: Inflammation of the lips. Certain forms like actinic cheilitis (caused by long-term sun exposure) can become precancerous, leading to lip cancer if unaddressed. 4. Leukoplakia: A white patch or plaque that develops on the oral mucosa, which cannot be rubbed off. It's often associated with tobacco use, and a percentage of leukoplakia cases may transform into oral cancer. 5. Cutaneous Horn: A protuberant growth that looks like a horn, the base of which can sometimes be precancerous or cancerous, necessitating examination and often biopsy to rule out malignancy. 6. Keratoacanthoma: A rapid-growing, but usually self-regressing skin lesion, that mimics squamous cell carcinoma. Despite its tendency to regress, it can be difficult to distinguish from malignancies clinically and histologically, often warranting excision to confirm the diagnosis and prevent potential malignant transformation.

Question 88

103. False positive and false negative reactions in syphilis.

Answer 88

---False positive and false negative reactions in syphilis testing refer to incorrect test results that do not accurately reflect the presence or absence of the syphilis infection. --A false positive result occurs when a test indicates that a person has syphilis when they do not actually have the infection. This can happen due to the presence of other conditions or factors that interfere with the test, leading to a positive reaction despite the absence of syphilis. --On the other hand, a false negative result occurs when a test fails to detect syphilis in a person who is actually infected. This might happen in the early stages of infection when antibodies to the syphilis bacteria (Treponema pallidum) have not yet reached detectable levels, or if there's a problem with the test procedure itself. --Both false positives and false negatives can complicate the diagnosis and treatment of syphilis, underlining the importance of confirmatory testing and clinical judgment in the management of potential syphilis cases.

Question 89

104.Neurosyphilis: early and late. Etiopathogenesis, diagnostics, classification.

Answer 89

---Neurosyphilis is a complex and serious manifestation of syphilis, an infection caused by the bacterium Treponema pallidum. It typically occurs when the infection goes untreated for an extended period, allowing the bacterium to invade the central nervous system (CNS). Neurosyphilis can manifest at any stage of syphilis, with varying symptoms based on the stage and specific form of the condition. The classification and stages of neurosyphilis include: ### Enteropathogenesis: The bacterium Treponema pallidum enters the body through mucous membranes or small breaks in the skin, primarily during sexual contact. Over time, without appropriate treatment, it can spread through the bloodstream and lymphatic system, eventually crossing the blood-brain barrier to infect the central nervous system. This process can happen early during the infection but symptoms of neurosyphilis might not appear until much later, hence the term "late." ### Diagnostics: Diagnosing neurosyphilis requires a combination of clinical examination, serologic tests, and analysis of cerebrospinal fluid (CSF). Serologic tests might include the Venereal Disease Research Laboratory (VDRL) test, the Fluorescent Treponemal Antibody Absorption (FTA-ABS) test, and others specific to Treponema antibodies. The definitive diagnosis often rests upon abnormalities in the cerebrospinal fluid obtained through lumbar puncture, showing signs of infection and immune response in the CNS. ### Classification: 1. Asymptomatic Neurosyphilis: The presence of Treponema pallidum in the CNS without any symptoms. 2. Meningovascular Neurosyphilis: Involves inflammation of the blood vessels in the brain and spinal cord, which can lead to stroke-like symptoms. 3. General Paresis: Affects the brain, leading to gradual cognitive decline, mood changes, and motor dysfunction. 4. Tabes Dorsalis: Typically a late-manifestation featuring demyelination of the dorsal columns and dorsal roots of the spinal cord, leading to severe pain, instability, and sensory deficits. 5. Gummatous Neurosyphilis: Characterized by the formation of gummas, which are soft, tumor-like growths in the CNS, though this form is rare. Early detection and treatment of syphilis can prevent the development of neurosyphilis. Treatment usually involves high doses of intravenous penicillin over an extended period to ensure the bacteria are eradicated from the CNS. It's important for indivi

Question 90

106, Syphilis of the osteoarticular apparatus.

Answer 90

Syphilis of the osteoarticular apparatus refers to the manifestation of syphilis in the bones and joints, a condition more commonly associated with the tertiary stage of syphilis infection. This condition can cause a wide range of symptoms, from mild to severe, and can affect almost any bone or joint in the body. The most commonly affected areas include the long bones, skull, spine, and sternum. ### Symptoms Symptoms of osteoarticular syphilis might include - Pain: This can be localized to the affected bone or joint, varying in intensity and often worsening at night. - Swelling: The areas around the affected bones or joints might appear swollen or inflamed. - Lesions: In some cases, gummatous lesions (soft, non-cancerous growths) can form on the bones or within the bone structure, leading to deformities or bone destruction. - Joint Effusion: Accumulation of fluid in joint spaces, leading to swollen joints. - Limited Mobility: Affected joints may have a reduced range of motion. ### Diagnostics Diagnosing syphilis of the osteoarticular apparatus involves a combination of: - Serological Tests: Blood tests that look for antibodies to the syphilis bacteria can confirm a syphilis infection. - Radiological Examinations: X-rays, MRI, or CT scans can help visualize bone lesions, areas of bone destruction, or changes in the joints associated with syphilis. - Bone Biopsy: In some cases, a biopsy of the affected bone might be conducted to distinguish syphilis from other bone diseases. ### Differential Diagnostics Differential diagnosis is crucial to distinguish syphilis of the osteoarticular apparatus from other conditions that can cause similar symptoms, such as - Tuberculosis of the bones and joints. - Osteomyelitis caused by other bacterial infections. - Rheumatoid arthritis or other inflammatory joint diseases. - Malignancies affecting the bones. ### Treatment The treatment for syphilis of the osteoarticular apparatus typically involves antibiotics, with penicillin being the most commonly used antibiotic

Question 91

108. Syphilis of the fetus and placenta, Diagnostics, differential diagnostics .

Answer 91

---Diagnosing syphilis in the fetus and placenta primarily revolves around detecting the bacterium Treponema pallidum, which causes the infection. Here’s a brief overview of the diagnostics and differential diagnostics involved: ### Diagnostics: 1. Serologic Testing: Pregnant women are typically screened for syphilis using non-treponemal tests (VDRL, RPR) followed by confirmatory treponemal tests (FTA-ABS, EIA for T. pallidum). These tests are also used to evaluate the baby if congenital syphilis is suspected. 2. Ultrasound: Prenatal ultrasounds may show signs consistent with congenital syphilis in the fetus, including hepatomegaly, hydrops fetalis, and placental thickening. 3. Direct Detection: PCR (Polymerase Chain Reaction) can directly detect T. pallidum DNA in amniotic fluid, placental tissue, or lesion samples from the newborn. 4. Pathological Examination of the Placenta: Examination of the placenta and umbilical cord can provide definitive signs of syphilis infection, such as specific types of inflammation or T. pallidum detected via special staining techniques. ### Differential Diagnostics: It’s essential to distinguish syphilis from other conditions that may present similarly in the fetus or placenta: 1. Other Infections: Congenital infections like toxoplasmosis, rubella, cytomegalovirus (CMV), and herpes (TORCH infections) can show overlapping signs and should be ruled out. 2. Non-infectious Conditions: Conditions like immune thrombocytopenia, fetal anemia, or structural anomalies may mimic some signs seen in congenital syphilis and require differentiation through screening and diagnostic evaluations. Diagnosis is critical for starting appropriate treatment and managing the pregnancy effectively to reduce risks to the fetus. If you have any more specific questions or need further details, feel free to ask.

Question 92

109. general pathology of early congenital syphilis. Diagnostics, differential diagnostics

Answer 92

---General Pathology: - Skin Lesions: These can include a rash which may cover the entire body, including the palms of the hands and soles of the feet. - Skeletal Abnormalities: Such as osteochondritis and periostitis, leading to pain and swelling in the bones. - Hepatosplenomegaly: Enlargement of the liver and spleen. - Neurosyphilis: Infection of the central nervous system, potentially causing seizures and other neurological issues. - Rhinitis: Often referred to as "snuffles," this presents as a persistent, runny nose. - Anemia: A common finding due to various factors including splenic sequestration. Diagnostics: - Serological Tests: These tests look for antibodies against the syphilis bacteria. Testing should include both nontreponemal tests (such as the VDRL or RPR tests) and treponemal tests (such as the FTA-ABS or TPHA tests). - Direct Tests: Methods like dark-field microscopy can directly visualize spirochetes from samples taken from lesions or other affected tissues. - PCR (Polymerase Chain Reaction): This method can detect syphilis DNA in samples, offering a direct evidence of infection. Differential Diagnostics: - Other infections that can present with similar systemic symptoms need to be considered and ruled out. Such infections include, but are not limited to, rubella, cytomegalovirus (CMV), toxoplasmosis, and Herpes. - Neonatal lupus erythematosus can also mimic some features of congenital syphilis, especially cutaneous manifestations. - Hematologic conditions leading to anemia or hepatosplenomegaly may also need consideration.

Question 93

110. General pathology of late congenital syphilis. Diagnosties, differential diagnostics

Answer 93

--General Pathology: The pathology of congenital syphilis can be divided into early and late manifestations. Early symptoms are typically noticeable at birth or within the first few weeks of life and include skin rashes, fever, swollen liver and spleen, jaundice, anemia, and various other symptoms. If untreated, the disease can progress to more severe complications such as bone deformation, deafness, and neurological issues. Late congenital syphilis, also known as lute congenital syphilis, may not become apparent until the age of 2 or later. It primarily affects the bones, teeth, eyes, and skin, potentially leading to deformities and functional impairments. The most characteristic signs include Hutchinson's teeth (notched, widely spaced teeth), mulberry molars, saddle nose (collapse of the bony part of the nose), and saber shins (anterior bowing of the shins). --Diagnostics: Diagnosis of congenital syphilis involves several steps, often including both physical exams and diagnostic tests. Blood tests of the infant, including non-treponemal tests such as VDRL or RPR, and treponemal tests like FTA-ABS, are critical for identifying the disease. Examination of placental tissue and umbilical cord using special staining techniques can also be employed. In late congenital syphilis, radiographs may show characteristic skeletal abnormalities. --Differential Diagnostics: Differentiating congenital syphilis from other conditions can be challenging due to the broad spectrum of symptoms. Conditions with similar presentations include other congenital infections (such as those from the TORCH complex - Toxoplasmosis, Other (like HIV), Rubella, Cytomegalovirus (CMV), Herpes simplex), neonatal sepsis, and inherited metabolic disorders. A thorough diagnostic workup, considering the mother's serology and the infant's clinical signs, symptoms, and available laboratory tests, is essential for accurate diagnosis.

Question 94

111. Serodiagnosis of syphilis. Treponemal and non-treponemal tests. Clinical significance of scrarcactions to syphilis.

Answer 94

-Treponemal tests, such as the Treponema pallidum particle agglutination assay (TPPA) and the fluorescent treponemal antibody absorption (FTA-ABS) test, detect antibodies that specifically react with T. pallidum. These tests are highly specific and are used to confirm a diagnosis of syphilis. -Non-treponemal tests, such as the Venereal Disease Research Laboratory (VDRL) test and the Rapid Plasma Reagin (RPR) test, detect antibodies that react with substances released by damaged host cells as well as T. pallidum. These tests are less specific than treponemal tests and are used for screening purposes. A positive result on a non-treponemal test should be confirmed with a treponemal test. -Scrarcactions to syphilis, or the presence of scars or marks left by syphilis infections in the past, may have clinical significance. Scarring can occur in the skin, mucous membranes, or internal organs as a result of untreated or inadequately treated syphilis infections. Scarring in the skin may present as gummatous lesions, which are soft, tumor-like growths that can ulcerate and leave behind disfiguring scars. Scarring in the mucous membranes can lead to complications such as syphilitic rhinitis or syphilitic glossitis. Scarring in internal organs, such as the heart or brain, can lead to serious complications such as cardiovascular syphilis or neurosyphilis.

Question 95

112. Liquodiagnosties of syphilis, indications for spinal puncture.

Answer 95

--Liquodiagnosis of syphilis refers to the diagnosis of neurosyphilis, for which indications include neurological, psychiatric symptoms, and evidence of active syphilis with a higher risk of CNS involvement. A spinal puncture (lumbar puncture) is performed to obtain cerebrospinal fluid (CSF) for analysis, which can include VDRL testing, amongst other assessments, to diagnose syphilis affecting the central nervous system (CNS). This procedure is particularly important in individuals with syphilis who show signs of neurological or ophthalmic involvement, as it can guide the necessity and adequacy of treatment.

Question 96

113. Specific, prophylactic, preventive and trial ant syphilitic treatment

Answer 96

Specific Treatment The specific treatment for syphilis primarily involves antibiotic therapy: - **Penicillin G** is the preferred treatment for all stages of syphilis. The form of penicillin (e.g., benzathine, aqueous procaine, or aqueous crystalline), dosage, and duration of treatment depend on the stage and clinical manifestations of the disease. - For **primary, secondary, and early latent syphilis**, a single intramuscular injection of benzathine penicillin G is often sufficient. - For **late latent syphilis or syphilis of an unknown duration**, treatment may involve three doses of benzathine penicillin G administered at one-week intervals. - **Neurosyphilis**, including ocular syphilis, requires more aggressive treatment, usually with intravenous aqueous crystalline penicillin G for 10 to 14 days. ### Prophylactic and Preventive Treatment - **Condom use** during sexual activity reduces the risk of transmitting or acquiring syphilis. - **Regular screening and early treatment** of sexually active individuals, especially those in high-risk groups, help prevent the spread of syphilis. - Following exposure, individuals identified as close contacts of someone with infectious syphilis may receive **prophylactic treatment** with benzathine penicillin G, even if their tests are negative, to prevent the development of the disease ### Trial Antisyphilitic Treatment - Trial treatments may be considered in cases where the diagnosis is uncertain, particularly in latent syphilis where symptoms are not present, and serological tests are inconclusive. - A "trial treatment" might involve administering a standard course of penicillin and observing for a response, such as a decline in non-treponemal test titers, to help confirm a diagnosis. However, this approach is less common today due to the availability of more specific treponemal testing. ### Concerns and Considerations - **Penicillin Allergy**: For individuals allergic to penicillin, doxycycline or another appropriate alternative may be used, except in cases of pregnant women and neurosyphilis

Question 97

114 medical examination and criteria syphilis for the cure of syphilis - clinical and serological control

Answer 97

Clinical Control - **Resolution of Symptoms**: For primary and secondary syphilis, clinical cure is often indicated by the resolution of symptoms, such as the healing of chancre in primary syphilis and the disappearance of rashes in secondary syphilis. - **Neurosyphilis Assessment**: In cases of neurosyphilis, clinical evaluations might include neurologic exams to assess the resolution of symptoms like meningitis or vision issues. Improvement or stabilization in these symptoms is a good sign, though some neurologic sequelae may be permanent. ### Serological Control Serological tests play a critical role in monitoring the response to therapy and are categorized into non-treponemal tests (e.g., Venereal Disease Research Laboratory [VDRL] test, Rapid Plasma Reagin [RPR] test) and treponemal tests (e.g., fluorescent treponemal antibody absorbed [FTA-ABS] test, T. pallidum particle agglutination assay [TP-PA]). - **Non-treponemal Tests**: These tests are quantitative and are primarily used for screening and evaluating treatment response. A fourfold decrease in titer (e.g., from 1:32 to 1:8) within 6 to 12 months after therapy for early syphilis, or within 12 to 24 months for late latent syphilis, is indicative of an appropriate response to treatment. In some cases, these titers may eventually become nonreactive. - **Treponemal Tests**: These tests typically remain positive for life, regardless of treatment or disease activity, and are not used to judge treatment success. However, a newer test known as the treponemal test for therapy monitoring (TTTM) has been developed to gauge the response to therapy, showing promising results in recent studies. ### Criteria for Cure or Adequate Response to Therapy - **Primary and Secondary Syphilis**: Resolution of signs and symptoms of disease plus a fourfold decrease in non-treponemal test titers within an appropriate timeframe after treatment. - **Late Latent Syphilis**: Due to the absence of clinical symptoms, serological response is critical, with a fourfold decrease in titer indicating treatment efficacy. - **Neurosyphilis**: Clinical improvement (for those with initial symptoms) and a decrease in CSF (Cerebrospinal Fluid) cell count and protein levels, along with non-treponemal titers in CSF, are used to assess treatment response. Serological tests might not return to nonreactive levels, but stabilization or reduction in titers is considered a positive outcome.

Question 98

115. Prevention of syphilis: public and individual.

Answer 98

Preventing syphilis involves both public health strategies and individual actions: 1. Public Health Strategies: - Educate the public on syphilis and safe sex practices. - Promote regular screening and early detection, especially in high-risk groups. - Ensure access to affordable health services for testing and treatment. - Implement partner notification and treatment programs. - Maintain surveillance to manage outbreaks. 2. Individual Prevention Methods: - Use condoms consistently during sexual activity. - Get tested regularly for STIs. - Communicate openly with sexual partners about STI testing and histories. - Limit the number of sexual partners. - Avoid sharing needles if using injectable drugs. - Adhere to treatment if diagnosed with syphilis. Both approaches are critical for effectively preventing the spread of syphilis.

Question 99

116, HIV infection enteropathogenesis, epidemiology, pathogen characteristics, immune disorders, laboratory diagnostics.

Answer 99

HIV infection involves a complex interplay of virus-host interactions, leading to a wide range of clinical manifestations and complications. Here's a brief overview based on the key points you've asked for: 1. Enteropathogenesis: HIV infection can cause HIV enteropathy, which is characterized by chronic diarrhea, malabsorption of nutrients, and weight loss. The virus directly infects the epithelial cells and immune cells in the gut, leading to a disruption of the gut epithelial barrier, immune dysregulation, and microbial translocation across the gut lining. 2. Epidemiology: The global HIV epidemic continues to represent a significant public health issue. According to UNAIDS, there were approximately 38 million people living with HIV worldwide at the end of 2019. Sub-Saharan Africa remains the most affected region. Efforts in prevention, testing, and treatment have seen some regions experience a decline in new infections and improvements in the lives of those living with HIV. 3. Pathogen Characteristics: HIV is a retrovirus that belongs to the family Retroviridae, genus Lentivirus. There are two main types: HIV-1, which is more prevalent and responsible for the global pandemic, and HIV-2, which is less transmissible and primarily found in West Africa. HIV targets the CD4+ T cells, which are crucial for the immune response, leading to a gradual decline in immune function. 4. Immune Disorders: HIV primarily causes immunodeficiency, making the individual susceptible to a wide range of opportunistic infections and cancers that a healthy immune system would usually control. The virus induces a state of chronic inflammation and immune activation, even in individuals who are receiving antiretroviral therapy (ART) and have undetectable viral loads. 5. Laboratory Diagnostics: Diagnosis of HIV infection primarily relies on the detection of antibodies against the virus, antigens such as p24, or the viral RNA itself. The initial screening is often done with rapid antibody tests or enzyme-linked immunosorbent assay (ELISA), followed by confirmatory tests like Western blot or PCR-based viral load tests. Monitoring of the disease and treatment efficacy involves CD4+ T cell counts and viral load testing.

Question 100

117. HIV infection: classification, clinical picture, skin and mucous membrane lesions, treatment, prevention.

Answer 100

HIV infection can be classified and managed through various stages, each presenting distinct clinical features, treatment approaches, and preventive measures. Below is a structured overview: 1. Classification of HIV Infection: - Acute HIV Infection: Often asymptomatic or marked by flu-like symptoms, occurs 2-4 weeks post-infection. - Chronic HIV Infection: The virus remains in the body, potentially causing mild symptoms or none at all for many years. - AIDS (Acquired Immunodeficiency Syndrome): The most advanced stage, characterized by a critically weakened immune system and the occurrence of opportunistic infections or cancers. 2. Clinical Picture: - Acute infection may cause fever, rash, sore throat, swollen lymph nodes, fatigue, and muscle aches. - Chronic infection may progress asymptotically until it transitions to AIDS. - AIDS symptoms include weight loss, fever or night sweats, extreme and unexplained tiredness, prolonged swelling of the lymph glands, prolonged diarrhea, and sores of the skin, mouth, and nose. 3. Skin and Mucous Membrane Lesions: - Kaposi's Sarcoma: A cancer forming purplish or dark spots on the skin or mucous membranes. - Oral Thrush: A yeast infection leading to white patches in the mouth. - Herpes Simplex and Herpes Zoster: Viral infections causing painful sores. 4. Treatment: The cornerstone of HIV treatment is Antiretroviral Therapy (ART), which doesn't cure HIV but controls virus replication, thereby helping maintain the immune system's function. - Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs): Tenofovir, Emtricitabine. - Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs): Efavirenz, Nevirapine. - Protease Inhibitors (PIs): Atazanavir, Lopinavir/Ritonavir. - Integrase Strand Transfer Inhibitors (INSTIs): Dolutegravir, Raltegravir. - Entry Inhibitors: Enfuvirtide.

Question 101

118. Gonorrhea: classification, etiopathogenesis, pathogen characteristics, forms of survival of gonococcus, laboratory diagnostics of gonorrhea, treatment

Answer 101

Gonorrhea is a sexually transmitted infection caused by the bacterium Neisseria gonorrhoeae. Here's a brief overview covering the key aspects: 1. Classification: It's classified as a sexually transmitted infection (STI). 2. Enteropathogenesis: Not typically associated with enteropathogenesis; it infects mucous membranes including the reproductive tract, mouth, throat, eyes, and anus. 3. Pathogen Characteristics: - Gram-negative bacteria. - Diplococci shape. - Does not form spores. - Requires moist, warm environments to survive 4. Forms of Survival of Gonococcus: It survives within human hosts, particularly in the mucous membranes of the urogenital tract, throat, and eyes. Outside the body, the bacterium quickly dies and cannot survive for long on surfaces. 5. Laboratory Diagnostics of Gonorrhea: - Nucleic Acid Amplification Tests (NAATs) are the most common and sensitive. - Culture methods for growing the bacterium from swab samples. - Gram staining can be used but is less commonly applied due to its lower sensitivity. 6. Treatment: - The current CDC recommendation is a dual therapy with - Ceftriaxone (an injectable cephalosporin) 500 mg, single dose. - Doxycycline (a tetracycline antibiotic) 100 mg, orally twice a day for 7 days.

Question 102

119. Torpid gonorrhea. Etiopathogenesis, features of diagnostics, complications, principles of treatment

Answer 102

--Torpid gonorrhea refers to a form of gonococcal infection that progresses slowly and with mild symptoms, often leading to delayed diagnosis and treatment. Here’s a concise overview of its etiopathogenesis, diagnostics, complications, and treatment principles: 1. Etiopathogenesis: - Caused by the bacterium Neisseria gonorrhoeae, similar to other forms of gonorrhea. - The torpid nature suggests a less aggressive interaction between the pathogen and the host’s immune response, or a partial immunity that limits the severity of symptoms without fully eradicating the infection. - Factors contributing may include specific strains of the bacterium, host genetics, previous exposure to the pathogen, or partial treatment. 2. Features of Diagnostics: - Diagnosis can be challenging due to the mild or absent symptoms. - Nucleic Acid Amplification Tests (NAATs) are recommended for their high sensitivity and specificity. Cultures can also confirm the diagnosis and allow for antibiotic susceptibility testing. - Because symptoms might be mild or overlooked, a high index of suspicion is necessary, especially in individuals with known exposure or those at higher risk for STIs. 3. Complications: - If untreated, even torpid gonorrhea can lead to serious complications. In women, pelvic inflammatory disease (PID), infertility, and ectopic pregnancy are concerns. In men, potential complications include epididymitis and infertility. - Disseminated gonococcal infection (DGI) can occur, affecting joints and, in rare cases, the heart or meninges. 4. Principles of Treatment: - Treatment does not differ significantly from other forms of gonorrhea, aimed at eradicating the infection and preventing complications. - The recommended treatment is a dual therapy with Ceftriaxone 500 mg IM as a single dose plus Doxycycline 100 mg orally twice a day for 7 days. - All sexual partners should be notified, tested, and treated if necessary to prevent reinfection and further transmission. - Follow-up testing to confirm the eradication of the infection is advised, usually 2 weeks post-treatment.

Question 103

120. Extragenital gonorrhea, Etiopathogenesis, features of diagnostics, differential diagnostics, complications, principles of treatment.

Answer 103

Extragenital gonorrhea refers to infection with Neisseria gonorrhoeae that affects parts of the body other than the genitals, such as the rectum, throat, and eyes. Enteropathogenesis: Not applicable to extragenital gonorrhea, as this term relates to pathogens affecting the gastrointestinal tract, whereas extragenital gonorrhea involves other non-genital sites. Features of Diagnostics: - Utilizes Nucleic Acid Amplification Tests (NAATs) for high sensitivity and specificity. - Cultures from the affected sites can be used for diagnosis and antibiotic susceptibility testing. Differential Diagnostics: - Chlamydia, especially since it can co-infect with gonorrhea. - Other causes of pharyngitis, proctitis, or conjunctivitis, depending on the site affected. Complications: - Can include dissemination to joints (arthritis), and in the case of ocular infection, can lead to conjunctivitis or more severe eye damage if untreated. Principles of Treatment: - Dual therapy with Ceftriaxone 500 mg IM as a single dose and Doxycycline 100 mg orally twice a day for 7 days is recommended, similar to genital gonorrhea. - Important to test and treat for chlamydia, as co-infection is common. - Partners should be notified, tested, and treated if necessary.

Question 104

121, Disseminated gonorrhea, Etiopathogenesis, features of diagnostics, differential diagnostics. complications, principles of treatment .

Answer 104

--Disseminated gonorrhea is a systemic infection caused by the bacterium Neisseria gonorrhoeae. It occurs when the bacterium spreads from the site of initial infection, often the genitals, to other parts of the body. --Etiopathogenesis: The condition results from bacteremia, where the bacteria enter the bloodstream and spread throughout the body, leading to infection in joints, skin, heart, or the central nervous system. Features of diagnostics: Diagnosis can involve cultures from the affected sites, polymerase chain reaction (PCR) tests, and blood tests to identify the bacteria. Symptoms may include fever, skin rash, and arthralgia (joint pain). --Differential diagnostics: Consideration should be given to other causes of arthritis, dermatitis, or systemic infections. Distinguishing it from conditions like reactive arthritis, rheumatoid arthritis, or infections caused by other bacteria is crucial. --Complications: Disseminated gonorrhea can lead to septic arthritis, tenosynovitis, and dermatitis. In severe cases, it can cause endocarditis or meningitis. --Principles of treatment: Treatment involves the use of antibiotic therapy, often starting with a cephalosporin administered intravenously or intramuscularly, followed by oral antibiotics. Supportive care for symptom management, such as pain relief, may also be necessary. Close follow-up and testing of sexual partners are also key components of management.

Question 105

122. Gonorrhea: diagnostic, differential diagnostics, principles of treatment, criteria for cure.

Answer 105

--Diagnostic: Gonorrhea is primarily diagnosed through nucleic acid amplification tests (NAATs) from samples collected from the site of infection (urethra, cervix, rectum, throat). Culture tests can also be used, especially for antibiotic susceptibility testing. --Differential Diagnostics: It involves differentiating gonorrhea from other sexually transmitted infections (STIs) like Chlamydia, Trichomoniasis, and Syphilis, based on symptoms, cultures, and specific STI tests. --Principles of Treatment: The current guideline recommends dual therapy with ceftriaxone (an injectable cephalosporin) and azithromycin (an oral macrolide), even though ceftriaxone alone has high efficacy, to cover potential co-infection with Chlamydia trachomatis and mitigate antibiotic resistance. --Criteria for Cure: Cure is typically assessed by resolution of symptoms and a negative test of cure (TOC) where applicable, usually with NAAT, 3-4 weeks after completing treatment, especially in cases of pharyngeal gonorrhea. For patients with uncomplicated urogenital gonorrhea, a TOC is not routinely recommended unless symptoms persist or reinfection is suspected.

Question 106

123. Trichomoniasis. Etiopathogenesis, characteristics of the pathogen, clinical picture, laboratory diagnostics, principles of treatment, criterion of cure.

Answer 106

--Etiopathogenesis: Trichomoniasis is caused by the protozoan parasite Trichomonas vaginalis. It is transmitted primarily through sexual contact. The parasite infects the urogenital tract, leading to infection --Characteristics of the Pathogen: Trichomonas vaginalis is a flagellated protozoan parasite. It is pear-shaped and possesses five flagella and a undulating membrane which aid in its mobility and adherence to the urogenital mucosa. --Clinical Picture: Symptoms include itching, burning, redness, or soreness of the genitals, discomfort with urination, and a foul-smelling, green or yellow vaginal discharge in women. Men often are asymptomatic but may experience irritation inside the penis, mild discharge, or slight burning after urination or ejaculation. --Laboratory Diagnostics: Diagnosis is primarily made by microscopic identification of the motile trichomonads from a wet mount of vaginal, urethral, or prostate secretions. Nucleic acid amplification tests (NAATs) are also highly sensitive and specific for T. vaginalis detection in both symptomatic and asymptomatic individuals. --Principles of Treatment: The recommended treatment is a single dose of metronidazole or tinidazole, orally. These are effective in eradicating the infection and can be taken by both pregnant and non-pregnant individuals. --Criterion of Cure: Cure is assessed based on the resolution of symptoms and, if performed, a negative test of cure (TOC) at least 3 weeks post-treatment. Testing for cure is not routinely recommended unless symptoms persist, but it may be considered in high-risk populations or in cases of recurrent symptoms.

Question 107

124. Chlamydia. Etiopathogenesis, characteristics of the pathogen, clinical picture, laboratory diagnostics, principles of treatment, criterion of cure

Answer 107

-Etiopathogenesis: Chlamydia is caused by the bacterium Chlamydia trachomatis, transmitted through sexual contact. It infects the mucous membranes of the urogenital tract, eyes, and respiratory tract. -Characteristics of the Pathogen: C. trachomatis is an obligate intracellular bacterium that exists in two forms: the infectious elementary body (EB) and the non-infectious, replicative reticulate body (RB). It's unique in its ability to cause persistent infections by evading host immune responses. -Clinical Picture: Many individuals are asymptomatic. When symptoms occur, they may include genital discharge, burning during urination, and in women, abdominal pain, bleeding between periods, and pain during sex. Untreated chlamydia can lead to serious reproductive health complications, like pelvic inflammatory disease (PID). -Laboratory Diagnostics: Diagnosis is primarily made using nucleic acid amplification tests (NAATs) on urine samples or swabs from the cervix or urethra, which are highly sensitive and specific for detecting C. trachomatis DNA --Principles of Treatment: The standard treatment includes a single dose of azithromycin or a week of doxycycline taken orally. Other antibiotics like erythromycin, levofloxacin, or ofloxacin are alternatives, especially for those who are pregnant or intolerant to the first-line treatments. -Criterion of Cure: Cure is assessed based on the resolution of symptoms. A test of cure (TOC) is recommended for pregnant women, 3-4 weeks post-treatment, to ensure eradication of the infection. For others, a TOC is not routinely recommended unless symptoms persist or reinfection is suspected.

Question 108

125, Ureamycoplasma infection, Etiopathogenesis, characteristics of the pathogen, clinical picture, laboratory diagnostics, principles of treatment, criterion of cure.

Answer 108

-Ureaplasma infection is caused by Ureaplasma, a type of bacteria that can infect the urinary and genital tracts. It is commonly spread through sexual contact but can also be transmitted from mother to baby during childbirth. -The pathogen, Ureaplasma, is a small, parasitic bacterium that lacks a cell wall. It can colonize the mucosal surfaces of the genitourinary tract and cause infection in susceptible individuals. -Clinical symptoms of Ureaplasma infection can vary and may include urethritis, pelvic inflammatory disease, and urinary tract infections. Laboratory diagnostics typically involve testing samples of bodily fluids, such as urine or genital swabs, for the presence of Ureaplasma DNA or antigens. -Treatment of Ureaplasma infection usually involves antibiotics such as azithromycin or doxycycline. The duration of treatment can vary depending on the severity of the infection and the patient's response to therapy. -Criterion of cure for Ureaplasma infection is typically based on the resolution of symptoms and the absence of detectable levels of the pathogen in follow-up laboratory tests. It is important to complete the full course of antibiotic treatment as prescribed by a healthcare provider to ensure successful eradication of the infection.

Question 109

126, Bacterial vaginosis. enteropathogenesis, characteristics of the pathogen, clinical picture, laboratory diagnostics, principles of treatment, criteria of cure,

Answer 109

-Bacterial vaginosis is a common vaginal infection caused by an imbalance of the normal bacterial flora in the vagina. The primary pathogen associated with bacterial vaginosis is Gardnerella vaginalis, although other organisms can also be involved. -Characteristics of Gardnerella vaginalis include being a gram-variable anaerobic bacterium. It is often found in high numbers in cases of bacterial vaginosis. -Clinically, bacterial vaginosis is characterized by a thin, greyish-white vaginal discharge with a fishy odor. Women may also experience vaginal itching or burning. -Laboratory diagnostics for bacterial vaginosis typically involve examining a sample of vaginal discharge under a microscope to look for high numbers of clue cells, a sign of the condition. -Treatment for bacterial vaginosis usually involves antibiotics such as metronidazole or clindamycin, either in oral or topical form. It is important to complete the full course of antibiotics to ensure the infection is fully cleared. -Criteria for cure of bacterial vaginosis include resolution of symptoms such as discharge and odor, as well as normalization of the vaginal pH and absence of clue cells on microscopic examination. Follow-up testing may be recommended in some cases to confirm cure.

Question 110

127. Reiter's disease. Etiopathogeneses is, characteristics of the pathogen, clinical picture, laboratory diagnostics, principles of treatment, criterion of cure.

Answer 110

-Reiter's disease, also known as reactive arthritis, is a type of inflammatory arthritis that typically occurs after an infection in another part of the body. The exact cause of Reiter's disease is not fully understood, but it is believed to be triggered by an infection, usually a bacterial infection such as Chlamydia trachomatis or gastrointestinal infections. -Characteristics of the pathogen: The pathogen responsible for triggering Reiter's disease is usually a bacteria, most commonly Chlamydia trachomatis. The immune system's response to the infection can lead to inflammation in the joints, eyes, and urinary tract. -Clinical picture: Symptoms of Reiter's disease can include joint pain, swelling, and stiffness, especially in the knees, ankles, and feet. Other common symptoms may include eye inflammation (conjunctivitis), urinary symptoms, skin rashes, and mouth ulcers. -Laboratory diagnostics: Diagnosis of Reiter's disease is based on a combination of clinical symptoms, medical history, physical examination, and laboratory tests. Blood tests may show signs of inflammation, and tests for specific pathogens like Chlamydia may be performed. -Principles of treatment: Treatment for Reiter's disease aims to reduce inflammation and manage symptoms. This may include nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce pain and swelling, corticosteroids for more severe inflammation, and antibiotics if an underlying infection is present. -Criterion of cure: The criterion for cure in Reiter's disease is the resolution of symptoms and inflammation. Patients may need ongoing monitoring and treatment to manage symptoms and prevent flare-ups.

Question 111

128. Urogenital candidiasis. Etiopathogenesis, characteristics of the pathogen, clinical picture, laboratory diagnostics, principles of treatment, criterion of cure.

Answer 111

---Urogenital candidiasis, commonly known as a yeast infection, is caused by the overgrowth of the fungus Candida, most often Candida albicans, in the urogenital tract. -Enteropathogenesis: Urogenital candidiasis occurs when there is an imbalance in the normal flora of the urogenital tract, allowing Candida to proliferate. Factors such as antibiotic use, pregnancy, diabetes, and weakened immune system can contribute to this imbalance. -Characteristics of the pathogen: Candida albicans is a type of fungus that is normally present in small amounts in the body. When conditions favor its growth, it can cause infection in the urogenital tract. -Clinical picture: Symptoms of urogenital candidiasis may include itching, burning, and abnormal discharge in the genital area. In men, symptoms may include redness and itching at the tip of the penis. -Laboratory diagnostics: Diagnosis is usually based on symptoms and examination. In some cases, a swab or sample from the affected area may be taken and examined under a microscope or cultured to confirm the presence of Candida. -Principles of treatment: Treatment typically involves antifungal medications, such as topical or oral azoles, to eliminate the Candida overgrowth. Avoiding irritants and maintaining good hygiene can also help manage symptoms. -Criterion of cure: The criterion for cure is the resolution of symptoms and the absence of signs of infection. Recurrent infections may require further evaluation and management to prevent future episodes.

Question 112

129. Genital herpes. Etiopathogenesis, characteristics of the pathogen, clinical picture, laboratory diagnostics, principles of treatment, criterion of cure

Answer 112

-Etiopathogenesis: Genital herpes is caused by the herpes simplex virus (HSV-1 or HSV-2) and is typically transmitted through sexual contact. -Characteristics of the pathogen: Herpes simplex virus is a DNA virus that can establish lifelong latent infection in nerve cells. -Clinical picture: Symptoms include painful blisters or sores in the genital area, along with flu-like symptoms such as fever and swollen lymph nodes -Laboratory diagnostics: Diagnosis is often confirmed through viral culture, PCR testing, or blood tests to detect antibodies against the virus. -Principles of treatment: Antiviral medications such as acyclovir, valacyclovir, or famciclovir can help manage symptoms and reduce the frequency of outbreaks. -Criterion of cure: There is no cure for genital herpes, as the virus remains in the body after initial infection. Treatment aims to alleviate symptoms and prevent recurrent outbreaks.

Question 113

130. Genital warts (HPV infection). Etiopathogenesis, characteristics of the pathogen, clinical picture, laboratory diagnostics, principles of treatment, criterion of cure.

Answer 113

-Etiopathogenesis: Genital warts are caused by the human papillomavirus (HPV), specifically types 6 and 11. HPV is a sexually transmitted infection and can be spread through skin-to-skin contact. -Characteristics of the pathogen: HPV is a DNA virus that infects the skin and mucous membranes. It can cause various types of warts, including genital warts. Clinical picture: Genital warts appear as small, flesh-colored or gray swellings in the genital or anal area. They can occur singly or in clusters and may be raised or flat. In some cases, they may cause itching, burning, or discomfort. -Laboratory diagnostics: Diagnosis of genital warts is usually based on visual inspection. In some cases, a biopsy may be performed to confirm the diagnosis, especially if there are atypical features or if the warts do not respond to standard treatments. -Principles of treatment: Treatment options for genital warts include topical medications (such as imiquimod or podophyllotoxin) that can be applied to the warts, or procedures such as cryotherapy (freezing the warts), laser therapy, or surgical removal. HPV vaccination can also help prevent future infections. -Criterion of cure: While treatment can remove visible warts, HPV infection itself cannot be completely cured. The virus may remain in the body even after treatment, and recurrence of warts is possible. However, the immune system can often control the virus, leading to long periods without symptoms. Regular monitoring and follow-up with healthcare providers are important for managing HPV infections.

Question 114

131. Tropical treponematoses (Yaws, Pinta, Bejel): general characteristics, diagnostics.

Answer 114

Tropical treponematoses are a group of infectious diseases caused by Treponema pallidum subspecies that primarily affect populations in tropical and subtropical regions. The three main diseases in this group are yaws, pinta, and bejel. Here are the general characteristics and diagnostics for each of these diseases: -----Yaws: General characteristics: Yaws is a chronic, non-venereal disease that primarily affects the skin, bones, and cartilage. It is transmitted through direct contact with the fluid from skin lesions of an infected person. Yaws is most common in children living in rural, tropical areas. Diagnostics: Diagnosis of yaws is usually based on clinical examination and the presence of characteristic lesions. Laboratory tests such as dark-field microscopy or serological tests (e.g., rapid plasma reagin test or treponemal-specific tests) can help confirm the diagnosis. ------Pinta: General characteristics: Pinta is a chronic skin disease caused by Treponema carateum. It is characterized by skin discoloration and thickening of the skin. Pinta is transmitted through direct contact with an infected person. Diagnostics: Diagnosis of pinta is primarily based on clinical examination and the appearance of characteristic skin lesions. Laboratory tests such as dark-field microscopy or serological tests can be used to confirm the diagnosis. ------Bejel (Endemic syphilis): General characteristics: Bejel is a chronic, non-venereal disease caused by Treponema pallidum subsp. endemicum. It primarily affects the skin, mucous membranes, and bones. Bejel is transmitted through direct contact with an infected person or through contaminated utensils. Diagnostics: Diagnosis of bejel is similar to that of other treponemal infections and involves clinical examination and laboratory tests such as dark-field microscopy or serological tests. ----In general, the diagnosis of tropical treponematoses involves a combination of clinical evaluation, laboratory tests to detect the presence of the treponemal bacterium, and serological tests to detect specific antibodies. Treatment typically involves antibiotics such as penicillin or doxycycline, depending on the specific disease and its stage.