Low Back Pain

Introduction
• Low back pain (LBP) is extremely common and includes a wide range of symptoms involving the lumbosacral spine and pelvic girdle
• Characterized by duration or associated symptoms
• Duration
– Acute ( least than 6 weeks)
– Subacute ( 6 weeks to 3 months)
– Chronic (more than 3 months)
• Associated symptoms
– Localized/nonspecific “mechanical” LBP
– Back pain with lower extremity symptoms
– Systemic and visceral symptoms
• There isn't the specific cause for most patients with LBP. Most cases resolve in 4 to 6 weeks
• Rule out “red” flag symptoms are needed for immediate intervention
• System(s) affected: musculoskeletal, neurologic
• Synonym(s): lumbago, lumbar sprain/strain, low back syndrome.

Etiology and Pathophysiology
A clear etiology is not found in most patients. Age-related degenerative changes of the lumbosacral spine and atrophy of supporting musculature may contribute.

Risk Factors
• Age
• Activity (lifting, sudden twisting, bending)
• Obesity
• Sedentary lifestyle
• Physically strenuous work
• Psychosocial factors—anxiety, depression, stress
• Smoking

General Prevention
• Maintain normal weight
• Adequate physical fitness and activity
• Stress reduction
• Proper lifting technique and good posture
• Smoking cessation
• There isn't sufficient evidence to recommend for, or against routine preventive measures in adults.

Pleural Effusion

What is a pleural effusion?

Pleural effusion is a common clinical problem that can complicate many medical conditions. Breathlessness is the most common symptom of pleural effusion of any cause and the most common reason for pleural drainage.
It can pose a diagnostic dilemma to the treating physician because it may be related to disorders of the lung or pleura, or to a systemic disorder. Patients most commonly present with dyspnea, initially on exertion, predominantly dry cough, and pleuritic chest pain. To treat pleural effusion appropriately, it is important to determine its etiology. However, the etiology of pleural effusion remains unclear in nearly 20% of cases.
The diagnostic evaluation of pleural effusion includes chemical and microbiological studies, as well as cytological analysis, which can provide further information about the etiology of the disease process.
The physiological mechanisms underlying breathlessness in patients with a pleural effusion are unclear and likely to be multifactorial with patient-related and effusion-related factors contributing.

Primary headache

The cause of primary headache include :
1. Migraine
  - 10-20 % of the population
  - Peak at 25-55 yrs
2. Tension type
  - 30-78 % of the population
  - Peak at 30-39 yrs
3. Trigeminal autonomic cephalalgia
  - 1 %
4. Other

Criteria for diagnosis migraine
  - At least 5 attacks
  - 2 or more of the following
    + Unilateral
    + Pulsating
    + Moderate or severe
    + Aggravation by/or causing avoidance of routine physical activity
  - 1 or more of the following
    + Nausea and/or vomiting
    + Photophobia and phonophobia
  - Lasting 4-72 hours (untreated or unsuccessfully treated)

Criteria for diagnosis of tension type headache
  - 2 or more of the following
    + Bilateral
    + Pressing or tightening
    + Mild to moderate
    + Not aggravation by routine activity
  - Both
    + No nausea and vomiting
    + Photophobia or phonophobia
  - At least 10 episodes
  - 30 minutes to several days

ACNE VULGARIS

Introduction
Acne is a chronic dermatosis, frequently in adolescence and involve principle on the face. Usually it is the disorder the of the sebaceous unit, those chronic inflammatory dermatosis are presented as notable open/closed comedones, papules, pustules, or nodules.

Epidemiology
The prevalence in French is more than 70 % in adolescence [Vidal Reco 2018]. The predominant sex is male > female in adolescence but female > male in adult.

Physiopathology and etiology
There are 3 factors pathogenic involved in acne
- hypersecretion sebaceous androgenic dependent
- retention sebaceous related to hyperkeratosis of canal infundibulum follicular
- inflammation is related to colonization follicular sebaceous by Propionobacterium acnes. P. acnes promote proinflammation mediator lead to inflammation of follicle and dermis.
Genetic maybe associated in 50 % and if there exist family history, the acne may be more severe and occur earlier.
Androgens are produced by the adrenal gland, the gonads and also by the sebaceous gland, it plays in the role of the following:
- stimulating the growth and secretory function of sebaceous glands (produce sebum)
- dehydroepiandrosterone sulfate (DHEA-S)[androgen precursor] converted to testosterone via the action of several enzymes and then testosterone is converted to 5-alpha-dihydrotestosterone (DHT) via the action of type I 5-alpha reductase in the sebaceous gland.
- Both DHT and testosterone bind to receptor presented in the sebaceous glands and the outer root sheath keratinocytes of the follicular epithelium to get in its action. In this case, the men who are lacking androgen receptor do not produce sebum and do not develop acne.

Risk factors
- Overproduction of androgen can cause acne but in the majority case of acne, the androgen level is normal. The excess of androgen is presented in polycystic ovarian syndrome, congenital adrenal hyperplasia, and adrenal or ovarian tumors.
- External factor: include oily cosmetics, cocoa butter, scrubbing with soaps, detergents, and astringents may worsen the disorder by rupturing comedos, promoting the development of inflammatory lesions.
Turtlenecks, bra straps, shoulder pads, orthopedic casts, and sports helmets, hands against the skin and others may cause acne by occlusion of pilosebaceous follicles leads to the comedone formation.
- Diet: natural hormonal components of milk or other bioactive molecules in milk, ingestion of high glycemic loads could exacerbate acne. In these cases, insulin-like growth factor (IGF) may play a role in acne. There is the limitation of data about consumption of chocolate, zinc, omega-3 fatty acids, antioxidants, vitamin A, and dietary fiber to determine the roles in acne vulgaris.
- Stress: would be related to the severity of acne. Receptors for corticotropin-releasing hormone (CRH) are presented in sebaceous gland so the CRH system may participate in the occurrence of stress-exacerbated acne.
- Insulin resistance: it may increase the production of androgen and IGF.
- Obesity: rising BMI increased the risk for acne in females.
- Smoking maybe worsen the severity of acne,

Diagnosis
History: duration, medications, cleaning products, stress, smoking, exposures, diet, and family history have to be asked. Females may worsen 1 week before menses.
Physical exam: the present of closed comedones (whiteheads), open comedones (blackheads), nodules or papules, pustules (“cysts”), scaring and post inflammatory lesions: ice pick, rolling, boxcar, atrophic macules, hypertrophic, depressed, sinus tracts; in face, neck, chest, upper back, and upper arms. Usually, acne vulgaris affects those areas of the body that have the largest hormonally-responsive sebaceous glands.
Classification: there isn’t a universal classification system for acne vulgaris. American Academy of Dermatology in 1990 classified acne into 4 grads : Mild: few papules/pustules, no nodules; Moderate: some papules/pustules, few nodules; Severe: numerous papules/pustules, many nodules; and Very severe: acne conglobata, acne fulminans, acne inversa.

There are 3 types of basic lesion: hyperseborrhoea (oily appearance, greasy to the touch, predominant on the nose, forehead, cheeks and upper thoracic region), retinal lesions (comedones, micro and macro-cysts), and inflammatory lesions (papules, pustules, nodules).

Differential diagnosis Many disorders may present with acneiform eruptions which have similar features but are unrelated to acne vulgaris.
Rosacea: the feature of rosacea include erythema, telangiectasias, and papules or pustules on the central face. Acne vulgaris is the absence of telangiectasias. Acne cosmetica: caused by an irritant reaction to cosmetic ingredient; especially heavy oil-based hair products. Papules or pustules may occur within hours after the application, commonly on the forehead.
Drug-induced acne: commonly steroid, characterized by the presence of monomorphous inflammatory popular eruption.
Perioral dermatitis or periorificial dermatitis: the presence of small, grouped, erythematous papules in a perioral (or perinasal, periorbital), a rim of skin around the vermilion border of the lip.
Sebaceous hyperplasia: it is the enlargement of sebaceous glands, which umbilicated yellowish papules and found on the forehead and cheeks.
Pseudofolliculitis barbae and acne keloidalis nuchae: most common in African origin, it’s related to the configuration of the hair follicle. A foreign body inflammatory reaction caused by short shaved or clipped hairs curl back toward the skin, penetrate the skin. After lesion papule and pustule heal, it may result in keloidal scarring.
Folliculitis: there aren’t comedos, and lesions are usually monomorphous.
Keratosis pilaris: it caused by keratotic follicular plugging, characterized by the presence of small follicular papules on the extensor surfaces of the upper arm of thighs, erythema also may be present.
Favre-Racouchot syndrome: resulted from cutaneous photodamage (sun damage), characterized by open and closed comedos on the damaged area, mostly on the lateral upper cheeks and seen in middle and older aged.
Nevus comedonicus: linear arrangement comedos in childhood.
Adnexal tumors: flesh-colored facial papules seen in trichoepitheliomas, trichodiscomas or fibrofolliculomas.
Hidradenitis suppurativa: characterized by the recurrent, inflamed nodules and abscesses of intertriginous skin areas, such as the axilla, groin, perianal, perineal, and inframammary regions. The comedones, sinus tracts, and scarring also present. It is a chronic inflammation of the skin.
Steatocystoma multiplex: the presence of multiple yellow or skin-colored sebum-filled cysts on the trunk, upper arms, or chest.
Tuberous sclerosis: presented as the persistent 1 to 3 mm pink or red papules on the nose and medial cheeks.
Occupational acne or chloracne: comedos, inflammatory papules, pustules, nodules, or cysts can occur after exposure to chemicals include insoluble cutting oils, coal, hydrocarbons. The comedone are large and monomorphic, mostly affect on the face, neck, postauricular skin, axillae, and scrotum.
Tropical acne: presented large inflammatory nodule on the trunk and buttocks. It’s related to environmental temperature.
Radiation acne: radiation can induce follicular hyperkeratotic plugs.
Apert syndrome: it could be presented of an acneiform eruption on the arms, buttock, and thigh.

TREATMENT
• Comedonal (grade 1): keratinolytic agent (see as follows for specific agents)
• Mild inflammatory acne (grade 2): benzoyl peroxide or topical retinoid or benzoyl peroxide +/− topical antibiotic +/− topical retinoid
• Moderate inflammatory acne (grade 3): Add systemic antibiotic to grade 2 regimen.
• Severe inflammatory acne (grade 4): as in grade 3, or isotretinoin
• Topical retinoid plus a topical antimicrobial agent is first-line treatment for more than mild disease.
• Topical retinoid + antibiotic (topical or PO) is better than either alone for mild/moderate acne.
• Topical retinoids are first-line agents for maintenance. Avoid long-term antibiotics for maintenance.
• Avoid topical antibiotics as monotherapy.
• Recommended vehicle type
– Dry or sensitive skin: cream, lotion, or ointment
– Oily skin, humid weather: gel, solution, or wash
– Hair-bearing areas: lotion, hydrogel, or foam
• Apply topical agents to entire affected area, not just visible lesions.
• Mild soap daily to control oiliness; avoid abrasives.
• Avoid drying agents with keratinolytic agents.
• Gentle cleanser and noncomedogenic moisturizer help decrease irritation.
• Oil-free, noncomedogenic sunscreens
• Stress management if acne flares with stress


Source :
UpToDate 2018
Vidal Recos 2018
5-Minute Clinical Consult 2018