Please make a handbook pdf for the below mentioned text,and explain in easy way if there is explanation needed for something for me as intern doctor. Shared Conversation Instant This shared conversation is generated by AI, for reference only. please write in English, to the point precise only useful exam points from this pdf for qualifications exam as doctor after internship. I am an intern doctor preparing for qualification exam. For above mentioned pdf you please cover all the parts of questions in your answer for example like disease definition, classification, clinical manifestations, diagnosis, severity stages , treatment and prevention in outpatient settings, medical rehabilitation, medical examination and tactics of a general practitioner Gp . COMPREHENSIVE EXAM POINTS: DERMATOLOGY, VENEREOLOGY, PHTHISIOLOGY, CLINICAL PHARMACOLOGY, EMERGENCY MEDICINE For Post-Internship Qualification Exam Based on the provided clinical materials 113. FUNGAL SKIN AND NAIL DISEASES (continued from previous document) Definition Infectious diseases caused by pathogenic fungi (dermatophytes, yeasts, molds). Most common: skin (mycoses) and nail (onychomycosis) involvement. Contagious, person-to-person. Common Pathogens Dermatophytes: Trichophyton rubrum, Trichophyton interdigitale Yeasts: Candida Molds Mixed fungal and fungal-bacterial flora Clinical Manifestations - Skin and Mucous Membranes Skin redness Itching, burning Skin eruptions Weeping (serous fluid exudation through micro-defects in epidermis) Small vesicles that may rupture with crust formation Skin peeling Pain in affected areas Mucous membrane plaques (e.g., white curd-like coating in oral cavity, vagina in candidiasis) Hair loss in affected areas Clinical Manifestations - Nails (Onychomycosis) Nail thickening Nail plate brittleness Nail shape distortion Loss of luster, color change (darkening, yellowing) Pain in nail area Systemic Manifestations (Primary/Endemic Mycoses) Depending on organ involvement (e.g., coccidioidomycosis - inhaled spores → lung involvement) Cough Fever Dyspnea Chest pain Diagnosis 1. PCR (polymerase chain reaction): Detection of fungal DNA in material (urogenital smear, biopsy, BAL, blood) Most specific and informative Blood detection: generalized forms (immunodeficiency) 2. IgG antibody detection: IgG synthesized after pathogen entry, persists long-term Marked elevation in systemic mycoses 3. Culture on media + antifungal sensitivity: Identifies fungus Selects most effective antifungal agents 4. Vaginal microbiocenosis analysis by PCR: Quantitative and qualitative composition of vaginal flora Optimal therapy selection 5. Additional tests (by severity/dissemination): CBC, urinalysis, CSF analysis Liver function tests, nitrogen metabolism, fluid-electrolyte status Treatment Antifungal drugs (injections, tablets, ointments, creams, topical solutions) Duration determined by physician Prevention Wear fresh underwear, change socks daily Avoid wet clothing (swimwear, sportswear) Personal hygiene, do not share towels, clothing, bedding, shoes Avoid tight shoes Dry hands and feet thoroughly after bathing Do not walk barefoot in gyms, pools Use antibiotics only as prescribed 114. PSORIASIS Definition Chronic non-infectious dermatosis, mainly affecting skin. Currently considered autoimmune. Characterized by red, excessively dry, raised patches (papules) that coalesce into plaques. These represent areas of chronic inflammation, excessive proliferation of lymphocytes, macrophages, keratinocytes, and angiogenesis. Stages of Psoriasis 1. Progressive stage: New eruptions appear Peripheral growth of existing lesions Bright pink peripheral growth rim around papules Clearly expressed Koebner phenomenon (psoriatic lesions at trauma sites) Clearly expressed psoriatic triad 2. Stationary stage: No new eruptions No peripheral growth Scaling uniformly covers plaque surface Koebner phenomenon may be absent Psoriatic triad present 3. Regressive stage: Reverse development of elements No new elements Scaling, hyperemia, infiltration disappear Spots begin to form Voronov's pseudo-atrophic rim: Narrow rim of anemic skin around papules/plaques Koebner phenomenon negative Psoriatic triad weakly expressed Skin normal Seasonal Forms Winter (most favorable) Summer (worsens with increased insolation) Undifferentiated (exacerbations not season-related) Severity Forms Mild: Psoriasis vulgaris Severe: 1. Psoriatic erythroderma: Erythema, infiltration, scaling over entire skin surface Primary or secondary (inadequate therapy, alcohol) Possible nail shedding, hair loss, fever, lymphadenopathy, general deterioration 2. Exudative psoriasis: Scales stick together into dense serous crusts (impede drug penetration) 3. Arthropathic psoriasis: May precede, accompany, or follow skin manifestations Often leads to disability Affects small joints (hands, feet) → elbows, knees → hip and spinal joints Stages of arthropathy: Stage 1: Arthralgia, no X-ray changes, no deformity Stage 2: Joint deformity, limited movement; X-ray: narrowed joint space, irregular joint surfaces, osteoporosis Stage 3: Ankylosis of affected joints 4. Pustular psoriasis: Primary or secondary Two types: generalized (Zumbusch), palmoplantar (Barber) Diagnosis 1. Psoriatic triad: Stearin spot phenomenon: from hyperkeratosis and parakeratosis Terminal film phenomenon: surface of stratum spinosum Spot bleeding (Polotebnov's blood dew, Auspitz phenomenon): papillomatosis (elongated papillae close to skin surface) 2. Koebner phenomenon (isomorphic reaction): Psoriatic lesions at irritation sites Treatment 1. Sedative therapy: Valerian, motherwort preparations Neuroleptics, tranquilizers Hypnosuggestive therapy Acupuncture 2. Comprehensive vitamin therapy (Hungarian regimen): B vitamins: B₁, B₆ alternated with B₁₂ (400 μg) Vitamin A (3.33% solution - 20 drops TID), vitamin E, "Aevit" (1 capsule BID for 1 month) Nicotinic acid (improves microcirculation) - 1 tab daily after meals (especially summer form - photodesensitizing) Folic acid - inhibits excessive erythropoiesis (2 tabs TID) 3. Calcium preparations 4. Immunotherapy: Immunomodulators: Levamisole (decaris): 1 tab (150 mg) once daily for 3 consecutive days, 4 days off; repeat 3-4 cycles; monitor WBC (stop if <3.5×10⁹/L) Pyrogenic drugs: Pyrogenal: induces fever response, activates immune system Biogenic stimulants: Aloe extract, placental extract, vitreous body, splenin, plasmol, gumizol, FIBS (1-2 ml daily) 5. Detoxification therapy: Hemodez, rheopolyglucin (400 ml IV q2d ×5 for widespread process) 6. Phosphodiesterase inhibitors (regulate cGMP/cAMP ratio): Methylxanthine derivatives: euphyllin, pentoxifylline, papaverine Cavinton (improves cerebral circulation) - improves skin condition, quality of life (2 weeks: 2 tabs 2-3x/day) 7. Local treatment (depends on stage): Progressive stage (irritation contraindicated): 2% salicylic ointment (keratolytic - removes scales) Stationary stage (accelerate infiltration resolution): Keratoplastic agents: ointments with tar, ichthyol, naphthalan, sulfur Active component concentration increased every 10 days from 3% to 10-15% Corticosteroid ointments: Apply to specific areas Do not use >1 month (side effects: striae, hirsutism) Avoid halogenated corticosteroids on face (use dexamethasone, prednisolone ointments, advantan) Children: use 1:1 with baby cream Combination ointments (hormone + salicylic acid): Lorinden A, diprosalic, betasalik, elocom Scalp: 5% sertolin ointment Steroid lotions: diprosalic, elocom Medicated shampoos: Skin-cap (zinc pyrithione), Friederm: Friederm-zinc, pH-balance, Friederm-tar - 2x/week for 4-6 weeks (therapeutic), then 1x/2 weeks (maintenance) Physiotherapy: UV: contraindicated in progressive stage and summer form General baths: 37°C, 20 minutes, q2d with sea salt, pine extract, herbal decoction, peat oxidate 8. Sanatorium treatment, sanitation of chronic infection foci, daily regimen, diet 115. SYPHILIS Definition Chronic systemic venereal infectious disease affecting skin, mucous membranes, internal organs, bones, nervous system with sequential stages, caused by Treponema pallidum. Clinical Manifestations Primary Syphilis Primary affect (chancre): Deep, usually painless, non-bleeding syphilitic ulcer with smooth sides, smooth base, regular round edges Firm (indurated) - not adherent to surrounding tissues, no tendency to enlarge or deepen Atypical forms: Indurative edema: Genital area; enlarged, discolored scrotum/clitoris/labia; painless; pressure leaves no indentation; skin congestive-cyanotic, paler centrally; duration 1-4 weeks; F>M Chancroid-panaritium: Medical workers; resembles typical panaritium; affects 1st-3rd fingers right hand; usually painful; may accompany genital chancre Chancre-amygdalitis: Oropharynx; unilateral palatine tonsil enlargement without surface defect; protrudes into pharynx; pain/difficulty swallowing; malaise, fever (resembles tonsillitis but unilateral); unilateral regional adenitis Obligatory component: Regional lymphadenitis (enlarged, firm, painless, not adherent, "cold") "Decapitated syphilis": No primary affect (direct blood entry - transfusion) End of primary period: possible malaise, weakness, dizziness, fever Secondary Syphilis Generalized skin and mucous membrane lesions: Pale spotted rash ("Venus necklace") Multiple small hemorrhages into skin/mucous membranes Focal hair loss (to baldness) Generalized lymphadenitis (enlarged, firm, painless, "cold") Mild malaise, subfebrile temperature, weakness, upper respiratory catarrh (cough, nasal discharge) or conjunctivitis May be asymptomatic (no rash, no catarrh) → directly to chronic stage Duration: days to 1-2 weeks Early Neurosyphilis (first 2-3 years) Corresponds to secondary period Vascular and meningeal involvement Proliferative inflammation of meninges Intimal hyperplasia, miliary gummas around vessels Most common: Chronic syphilitic meningitis Pathognomonic: Argyll Robertson pupils (accommodation/convergence reflex preserved, light reflex impaired) Rare forms: early meningovascular syphilis, syphilitic neuritis/polyneuritis, meningoencephalitis Tertiary Syphilis Develops after latent period (months to 10-20+ years) in ~30% untreated Progressive destructive lesions: Aorta (syphilitic aortitis) Brain (general paresis) Spinal cord (tabes dorsalis) Large vessels (syphilitic endarteritis) Musculoskeletal system Skin/mucous membranes Gummas: Soft tissue tumors → fibrous scars Late Neurosyphilis (classification by Meritt, 1946) Form Frequency Asymptomatic neurosyphilis 31% Syphilitic meningitis 6% Meningovascular - cerebral 11% Meningovascular - spinal 3% General paresis 12% Tabes dorsalis 30% Taboparesis 3% Optic atrophy 3% Gummatous (brain/spinal cord) 1% Features: All forms develop long after infection; serology often negative. Latent syphilitic meningitis develops after ≥2 years; other forms require 10-15 years. Symptoms: paralyses, paresis, headache, impaired higher nervous activity, ↓logical thinking, ↓memory/attention. Diagnosis Based on: History (especially epidemiological) Clinical picture Laboratory confirmation (blood, CSF) Methods classification: Direct / Indirect Treponemal (specific) / Non-treponemal (non-specific) Screening / Confirmatory Instrumental / Non-instrumental Direct treponemal methods: Dark-field microscopy Rabbit inoculation Culture PCR Most common combination: Cardiolipin test + Treponemal ELISA Both positive → confirmed syphilis Both negative → no syphilis Cardiolipin negative, ELISA positive → past infection Cardiolipin positive, ELISA negative → repeat (may be due to HIV, hepatitis, pregnancy, etc.) Direct methods limitations: Dark-field: only fresh syphilis, no treatment monitoring Rabbit inoculation: expensive, slow Culture: extremely difficult PCR: effective only in primary/secondary, expensive Approved serological methods (Order №87, 2001): Micro-precipitation reaction (MOR) - screening Passive hemagglutination (RPHA) Immunofluorescence (RIF) Treponemal immobilization (RIBT) ELISA Note: No method is 100% sensitive (90-98%). Two different methods simultaneously provide highest reliability. Treatment T. pallidum remains highly sensitive to penicillin and derivatives (no penicillinase, no other resistance mechanisms) Main method: Long-term systematic penicillin derivatives in adequate doses Penicillin allergy or confirmed resistance: Tetracyclines (doxycycline) Cephalosporins (ceftriaxone) Macrolides (erythromycin, azithromycin) Neurosyphilis: Penicillins + endolumbar administration + pyrotherapy (↑BBB permeability) Alternatively: cephalosporins (cross BBB) Widespread tertiary syphilis (poor response to antibiotics, good general condition): Add bismuth derivatives (bismuthol) or arsenic derivatives (miarsenol, novarsenol) Note: Highly toxic, limited availability Mandatory: Treat all sexual partners Primary syphilis: All sexual contacts within last 3 months Secondary syphilis: All sexual contacts within last year 116. GONORRHEA AND TRICHOMONIASIS GONORRHEA Incubation Period 3-10 days (varies by strain virulence, host resistance, immune response, subtherapeutic antibiotics) Longer incubation → more indolent course Gonorrhea in Men Acute Urethritis (most common): Burning, pain (worse with urination) Purulent discharge (yellow-green, stains underwear) Exam: hyperemia, edema of urethral lips, free-flowing discharge Anterior urethritis: pain at urination onset Total urethritis: pain at end of urination; frequent urges, painful erections/ejaculations; possible bloody discharge, hemospermia, hematuria Urine: cloudy (pus), floating mucous flakes, purulent threads Two-glass test (Thompson): Anterior urethritis: first glass turbid (washes out pus), second glass clear Total urethritis: pyuria in both glasses Three-glass test: Pyuria in third glass → complications (prostatitis, vesiculitis) Subacute urethritis: Less severe symptoms Minimal pain Scanty discharge (often mucous, more noticeable morning - "morning drop") Minimal hyperemia/edema First glass urine may be clear but contains floating/sediment flakes Torpid urethritis: Often after acute/subacute stages May develop primarily Asymptomatic or minimal Only symptom: "stuck" urethral lips after sleep Urine usually clear Increasing frequency in recent years (epidemiologically unfavorable) Chronic urethritis: Oligosymptomatic (similar to torpid) Periodic exacerbations (alcohol, spicy/salty food, sexual excess) Urethroscopy: infiltrative/granulation changes, strictures Complications of Gonococcal Urethritis: Paraurethritis: Infection of paraurethral ducts (rudimentary structures) Inflammation similar to urethritis Hyperemia of orifice, purulent discharge (visible on pressure) Tortuous ducts → infiltrates, pus-filled swellings May cause relapse (gonococci isolated in ducts with low-dose antibiotics) Littreitis (inflammation of endourethral glands): Accompanies urethritis Urethroscopy: visible Gland blockage → palpable tender nodules (cysts) Pseudoabscesses (cherry stone-sized) → may rupture into urethra Painful urination, urine stream splitting Morgagni's lacunitis: Similar to littreitis Periurethritis/Cavernitis: Spread to periurethral tissue/cavernous body Palpable spindle-shaped/diffuse tender swelling Painful erections, penile curvature Rare: abscess → rupture into urethra or externally (fistulas) Tysonitis: Inflammation of Tyson's glands (beside frenulum) Palpable tender nodules Pressure → purulent discharge from ducts Possible abscess Colliculitis: Spread to seminal colliculus (with total urethritis) Pain radiating to penis, testes, lumbar, inner thighs Ejaculation disturbances (premature/delayed) May be asymptomatic (urethroscopy finding) Cowperitis (rare): Usually one bulbourethral gland If duct patent: asymptomatic If blocked: pulsating perineal pain (worse with defecation, movement, sitting) Forced position: lying on back, legs apart Fever to 40°C, possible urinary disturbance Painful nodule → infiltrate → abscess → may rupture through skin, urethra, rectum (chronic fistulas) May cause protracted course, relapse Prostatitis (most common complication): Infection from posterior urethra (protracted urethritis) Acute (rare) or chronic Acute prostatitis: Frequent urges, pulsating perineal/suprapubic pain (sometimes lumbar) Possible acute urinary retention Intoxication, malaise, fever to 39°C+ Rectal exam: enlarged, very tender prostate (one lobe) Purulent inflammation → abscess → emergency surgery Chronic prostatitis (more typical): May be minimally symptomatic Periodic urethral discharge, frequent urination, perineal discomfort (pressure pain radiating to testes/penis), lumbar pain (simulating radiculitis) Long-standing: neurotic states, sexual dysfunction (↓libido, erectile dysfunction, premature ejaculation) Asymptomatic common: diagnosis by rectal exam + prostatic secretion microscopy Forms by inflammation severity: Catarrhal: In ducts; asymptomatic; palpation/ultrasound normal; tender on rectal exam; diagnosis by leukocytosis in expressed secretion Follicular: Tender nodules on prostate surface (pseudoabscesses); long-standing → scarring, calculi Parenchymatous: Spread to interstitium; prostate enlarged, firm (palpation/ultrasound), central sulcus disappears; marked tenderness, dysuria, sexual dysfunction; ↓lecithin granules in secretion Vesiculitis (seminal vesicle inflammation): Usually with prostatitis; rare isolated Similar symptoms Diagnosis: rectal exam, ultrasound Pathognomonic: Painful ejaculation, hemospermia Epididymitis: Most serious complication Pathogen spreads from posterior urethra via vas deferens (antipersitalsis from seminal colliculus irritation; also lympho-/hematogenous) Contributing: heavy lifting, physical exertion, sexual excess, trauma, alcohol Mixed infections (chlamydia, trichomonas) often present Usually unilateral; acute onset Sudden pain in epididymis/groin (worse with movement, touch) Rapid fever to 40°C, intoxication Scrotal skin hyperemic, edematous, tense Palpation: enlarged epididymis surrounding testis, bumpy, firm Often spreads to testis → orchiepididymitis (conglomerate, cannot differentiate testis/epididymis) Spread to tunica vaginalis → exudate → fluctuant mass (acute periorchitis) Spontaneous resolution possible (by week 2 without treatment) Without treatment: abscess, sepsis; abscess rupture → purulent fistulas Chronic epididymitis (less typical): mild pain, slight swelling, general condition normal, subfebrile; late presentation → marked inflammatory changes Consequences: Scarring in vas deferens → azoospermia, infertility (especially bilateral); immunological infertility (sperm components absorbed → anti-sperm antibodies) Balanoposthitis: Men with long, narrow foreskin Multiple erosions/ulcerations on glans and inner prepuce, perifocal inflammation May cause phimosis Urethral strictures: Result of chronic littreitis, morganitis, periurethritis Infiltrate → fibroblast replacement → dense fibrous tissue Narrow, rigid orifice with non-distensible walls Single/multiple, varying length (often bulbar part) Symptoms depend on severity Typical: slow bladder emptying, thin weak stream Severe: surgery required Gonorrhea in Women Features: Multifocal urinary tract involvement Women more easily infected than men Often oligo-/asymptomatic (anatomical features) - epidemiologically unfavorable Classification (by anatomical extent): Lower tract: urethritis, cervicitis, bartholinitis, vestibulitis, vulvitis, vaginitis Upper tract (ascending): endometritis, salpingitis, oophoritis, pelvioperitonitis By duration: Fresh (acute, subacute, torpid) - <2 months Chronic Disseminated forms (more common in women): Gonococcal sepsis Endo-/myocarditis, hepatitis (perihepatitis), arthritis, meningitis, disseminated skin lesions Urethritis (30-50%): Early symptom Pain, burning at urination onset Exam: hyperemia, edema of urethral orifice, mucopurulent discharge (more on massage) Spread → urethrocystitis: frequent painful urination Chronic: minimal/absent symptoms; palpation through vaginal wall may reveal cord-like infiltration Vestibulitis, vaginitis, vulvovaginitis (rare): Pregnant, infantile, menopausal women Acute: diffuse hyperemia, edema of vaginal mucosa and vestibule; reddened crypt depressions May ulcerate → pain (especially with urination, walking), fever, inguinal lymphadenitis Vulvovaginitis usually with secondary infection (staph, enterobacteria) Bartholinitis (inflammation of Bartholin's glands): Degree varies by gland involvement Begins with duct orifice inflammation: hyperemic spot with dark-red center Pressure → drop of turbid mucus Duct closure → mobile tender cyst (pseudoabscess) Often spontaneous rupture after days Spread to surrounding tissues → tender infiltrate (to egg-size), intoxication, malaise, fever Marked edema, hyperemia, bulging toward vestibule Abscess → surgical indication Endocervicitis, cervicitis (most common primary manifestation): Purulent-mucous vaginal discharge, sometimes lower abdominal pulling pain Often asymptomatic (long unrecognized) Exam: hyperemia, edema of vaginal cervix; purulent plug in canal; erosion with epithelial ectopia around external os; mucopurulent discharge in posterior fornix Sometimes: vesicles with turbid contents Chronic: often asymptomatic; mild inflammatory changes; late presentation (incidental finding or contact tracing) Ascending Gonorrhea: Facilitated by: childbirth, abortion, menstruation, sexual activity Menstruation: external os open, mucous plug loose Risk increases with chronicity Endometritis (first stage): Intoxication: fever, chills, tachycardia, nausea, vomiting Severe cramping lower abdominal pain (worse with movement) → bed rest Some cases: milder (normal temperature, dull pain, spotting) Acute course more common in young nulliparous (narrow internal os → impaired drainage) Severe: spread to myometrium → metroendometritis; uterus enlarged, very tender, profuse spotting, peritoneal irritation Myometrial abscesses → pulsating pain, marked intoxication, blood changes Chronic: less severe; menstrual cycle disturbances; uterus slightly enlarged, tender, patent cervical canal Salpingitis (fallopian tube inflammation): Sudden lower abdominal pain (worse with movement, urination, defecation), nausea, fever Acute: bimanual exam impossible (marked tenderness) Indolent onset possible (mild pain, iliac region, menstrual cycle disturbances) Palpation: "cords" in adnexal area, variably tender Intratubal inflammation → adhesions, partial/complete occlusion Perifocal inflammation (periadnexitis) → purulent-fibrinous plaques on peritoneum → adhesions, dense adhesions deforming tubes, adhering to adjacent organs → infertility, ectopic pregnancy Oophoritis: Infection from tubal ampulla to ovary surface (also hematogenous/lymphogenous) Ovary enlarged, cysts form Symptoms similar to salpingitis, but pain may be lumbar/abdominal Irregular, heavy uterine bleeding Spread to vesicular follicles → pseudoabscesses, pyovarium → diffuse lower abdominal/lumbar pain radiating to groin/lower limbs, peritoneal irritation, intoxication Pelvioperitonitis: Follows uterine/adnexal involvement → spread to pelvic peritoneum High fibrin content in exudate → numerous adhesions in recto-uterine pouch and pelvis (limits spread) Severe lower abdominal pain, vomiting, flatulence, stool retention, intoxication, abdominal wall rigidity, positive Shchetkin-Blumberg sign Chronic: numerous adhesions → altered position of uterus, ovaries, tubes Note: Often discrepancy between marked ESR elevation and normal/relatively low leukocytosis in ascending forms. Diagnosis of Gonorrhea Clinical: History (epidemiological investigation - source, contacts) Physical exam: genital area, skin, visible mucosa, perianal area (exclude other STDs) Palpation of all lymph nodes Women: standard gynecologic exam (abdomen, urethra, vestibular glands, uterus, adnexa) Men: palpation of urethra, scrotal contents; if no active inflammation, prostate exam (rectal), 2- or 3-glass urine test Urethroscopy: after treatment (for soft/hard infiltrate) Laboratory confirmation required: Microscopy: Fixed stained smears Preliminary: simple stains (1% methylene blue) for rapid screening Differentiation: Gram stain Criterion: Gram-negative diplococci, predominantly intracellular (incomplete phagocytosis) Limitations: Ineffective in chronic/torpid forms; not for extragenital infections, pre-pubertal girls, postmenopausal women (non-pathogenic Neisseria possible) Less sensitive in women than men → not recommended as sole diagnostic in women Culture: Main method for: girls, women (especially postmenopausal), extragenital specimens Supplementary in men Media: enriched (serum, ascitic agar, chocolate agar) Conditions: increased humidity, CO₂, 35-37°C Differentiate from: meningococcus, other non-pathogenic Neisseria, gram-negative cocci (oxidase test, sugar fermentation, RIF) Nucleic acid amplification (PCR): No significant advantage over traditional methods (sensitivity/specificity) More expensive, labor-intensive Provocation methods (for chronic, torpid forms, test of cure): Biological: gonococcal vaccine, pyrogenal, plasmol IM Chemical: urethral instillations, mucosal swabbing with 0.5% AgNO₃, Lugol's solution Mechanical: sterile metal bougie, urethral massage Alimentary: salty/spicy food, mild alcohol Physiotherapeutic: pelvic heating (inductothermy) Physiological: during menstruation (women) Often combined Material collection on days 2,3,4 post-provocation Reporting: Medical record of venereal disease patient Notification form (0/89-у) to regional hygiene center for registration Treatment of Gonorrhea Antibiotics: Drug Dosage Course Benzylpenicillin IM First 600,000 U, then 400,000 U q3h Fresh acute/subacute: 6.6 million U; Chronic/torpid/complicated: 9.8-13 million U Ampicillin PO 0.5 g q4h 6.0-12.0 g Augmentin PO 0.375 g q8h 3-5 days (to 1.875 g) Erythromycin PO 0.5 g QID 10-14 g Doxycycline PO 0.2 g q12h 1.0-2.0 g Immunotherapy (adjuvant - chronic/torpid/complicated): Specific: Gonococcal vaccine IM in increasing doses Start: 200-300 million microbial bodies Increase by 200 million each dose Total: 6-8 injections Monitor tolerance Non-specific: Pyrogenal Immunomodulators Biostimulants Adaptogens Local therapy: For marked infiltrative/granulomatous changes on urethroscopy Urethral irrigation: KMnO₄ 1:6000-1:5000 Chlorhexidine 0.05% Furacillin 1:5000 Boric acid 2% Copper sulfate 0.5% Women: baths with 3-5% protargol/collargol, 1-3% AgNO₃, 1% povidone-iodine; vaginal suppositories (betadine 0.2 g, chlorquinaldol) TRICHOMONIASIS Clinical Manifestations Women: Asymptomatic to profuse yellow-green frothy vaginal discharge Vulvar/perineal sensitivity Dyspareunia, dysuria Asymptomatic infection may become symptomatic at any time (vulvar/perineal inflammation, labial edema) Vaginal walls and cervix: patchy, raspberry-red spots Possible urethritis, cystitis Men: Usually asymptomatic Occasionally: urethritis with discharge (temporary, frothy, purulent) Dysuria, frequency (especially morning) Usually mild, minimal irritation, sometimes moisture at urethra/under foreskin Epididymitis and prostatitis rare Diagnosis Women: Point-of-care tests: Direct microscopic exam of vaginal discharge Immunochromatographic strip test pH measurement Wet mount preparation: With KOH (fishy odor - amines from trichomonas or bacterial vaginosis) With saline (examine ASAP - trichomonads become immobile within minutes) Trichomonads: Pear-shaped with flagella, often motile, 7-10 mm (size of WBC, sometimes to 25 mm); numerous neutrophils present Often diagnosed on Pap smear Men: Urine culture or urethral swab (only validated test) Microscopy insensitive NAATs and strip tests not well studied; epidemiological studies suggest urethral swabs better than urine for NAAT Rule out other STDs (gonorrhea, chlamydia) Treatment Women: Metronidazole 2 g single dose or tinidazole 2 g single dose (cure ≤95% if partners treated simultaneously) Men: Metronidazole 500 mg PO BID for 5-7 days (efficacy of single-dose less studied) Persistent infection (reinfection excluded): Retry metronidazole/tinidazole 2 g single dose OR metronidazole 500 mg BID ×7 days If still ineffective: metronidazole/tinidazole 2 g once daily ×5 days Side effects: Metronidazole: leukopenia, disulfiram-like reaction with alcohol, Candida superinfection Relatively safe in early pregnancy (though cautious); safe after 1st trimester Tinidazole: not safe in pregnancy, not used Partner treatment: Examine and treat sexual partners (tinidazole 2 g single dose or metronidazole 500 mg BID ×5 days) Screen for other STDs If compliance concerns, treat partners without confirmation 117. TUBERCULOSIS - LABORATORY DIAGNOSIS AND SPECIMEN COLLECTION Importance of Microbiological Studies Identify epidemically dangerous patients (bacterial excretors) Verify TB diagnosis Determine drug sensitivity of MBT Assess treatment efficacy and prognosis Control TB spread Specimen Types Sputum (most common) Bronchial washings Gastric washings (especially children who swallow sputum) Pleural fluid CSF, pericardial, synovial, ascitic fluid Menstrual blood Surgical specimens: lung, pleura, lymph nodes Sputum Collection Morning specimen Patient brushes teeth and rinses mouth Collect 3-5 ml in sterile container (less acceptable) If no sputum: aerosol induction with 5-15% NaCl in 1% NaHCO₃ Collect in designated room (prevent airborne spread) If negative: examine daily for 3 consecutive days Microscopy Ziehl-Neelsen stain: Acid-fast bacilli → red Background and non-acid-fast organisms → blue Limitations: Early disease: low bacterial load (<10⁴/ml) → may be negative Cannot differentiate M. tuberculosis from non-tuberculous mycobacteria Fluorescence microscopy: Fluorochrome stains Culture Sensitivity: Detects 20-100 organisms/ml Standard medium: Löwenstein-Jensen (egg-based) First colonies: 4-8 weeks Total time: ~3 months Radiometric methods: Faster results Molecular-Biological Methods PCR (polymerase chain reaction): Amplifies specific M. tuberculosis DNA segment Material: sputum, bronchial contents Highly sensitive, specific, rapid Requires special test systems and laboratories QuantiFERON-TB Gold (IGRA): Measures immune response to specific M. tuberculosis antigens High specificity (antigens absent in BCG and most other mycobacteria) Assesses IFN-γ production by sensitized lymphocytes in whole blood culture (20-24h) Positive: certain IFN-γ concentration with M. tuberculosis antigens No repeat visit needed Can be repeated at short intervals Limitations: Not informative first weeks post-infection (time needed for immune response) Requires venous blood Russian test systems: Measure IFN-γ induction by specific TB antigens in vitro "Tuberculosis Infection-INTERFERON-gamma" system uses both M. tuberculosis antigens and tuberculin → differentiates infectious from post-vaccination allergy DIASKINTEST: Recombinant protein (ESAT6 + CFP10 antigens) Present only in virulent M. tuberculosis and M. bovis 0.1 ml contains 0.25 mg recombinant protein Sensitivity comparable to Mantoux with 2 TU PPD-L Specificity significantly higher Industrial production available ELISA: Antigen-antibody reaction Confirms TB etiology, assesses activity, treatment efficacy Detects antibodies to MBT using tuberculin (erythrocyte antigenic diagnosticum) Sensitivity: 60-70% Specificity: ~90% 118. OBLIGATORY DIAGNOSTIC MINIMUM FOR SUSPECTED TB (GP TO TB DISPENSARY) Obligatory Diagnostic Minimum (ODM) 1. Targeted history and complaints analysis 2. Physical examination of respiratory system 3. Radiological studies: Large-frame fluorography Chest X-ray in 2 projections CT scan 4. Sputum (bronchial washings) examination for MBT: 3x immersion or fluorescence microscopy (Ziehl-Neelsen: MBT red, background blue) Culture (Löwenstein-Jensen medium) 5. Mantoux test with 2 TU PPD-L: Technique: Draw 0.2 ml tuberculin into syringe, expel 0.1 ml (final volume 0.1 ml = 2 TU) Inner surface middle third forearm, treat with 70% ethanol, dry Insert needle bevel-up into upper skin layers parallel to surface, inject 0.1 ml Correct: white papule 7-8 mm diameter Reading at 72 hours: Measure infiltrate (papule) perpendicular to forearm axis with transparent ruler Interpretation: Result Criteria Negative No infiltrate or hyperemia Doubtful Infiltrate 2-4 mm OR only hyperemia any size Positive Infiltrate ≥5 mm Hyperergic Children/adolescents: ≥17 mm; Adults: ≥21 mm; OR vesicle, lymphangitis, regional lymphadenitis regardless of size Note: Negative Mantoux may represent: True anergy (not infected with MBT) False anergy (severe progressive TB, concomitant oncopathology, severe immunodeficiency from various infections) To differentiate: Mantoux with 100 TU PPD-L → if negative → not infected 6. Clinical blood and urine analysis Additional Diagnostic Methods (ADM) Group 1 - Non-invasive a) Repeat sputum examination for MBT with flotation method: After shaking aqueous suspension with hydrocarbon, MBT float with foam Creamy ring collected for microscopy Then determine virulence and antibiotic sensitivity Virulence determination methods: Method Finding Colony type R-rough = highly virulent; S-smooth = low virulence Cord factor Present in highly virulent strains Catalase activity Higher = more virulent Animal bioassay Guinea pig dies faster with more virulent MBT b) Tomography of lungs and mediastinum c) Advanced tuberculin diagnosis (threshold sensitivity determination) d) Immunogram e) Chemistry: Proteinogram, CRP Group 2 - Invasive Bronchoscopy with catheter biopsy, brush biopsy, direct biopsy of bronchial mucosa/pathology Transthoracic aspiration or open lung biopsy Pleural puncture biopsy Peripheral lymph node puncture Prescalene fat pad biopsy Mediastinoscopy, pleuroscopy Main Imaging Methods in TB Fluorography (film, digital) Chest X-ray Fluoroscopy CT MRI General and selective angiopulmonography, bronchial arteriography Non-directed and directed bronchography Pleurography, fistulography Ultrasound (pleural fluid level, lymph node status) Radioisotope studies PET 119. RISK GROUPS FOR TUBERCULOSIS - GP ROLE Social Risk Groups Drug addicts Homeless Prisoners/ex-prisoners HIV-infected Chronic alcoholics Unemployed Migrants from high-incidence regions Medical Risk Factors (Health-Related) Chronic respiratory diseases: Chronic inflammatory lung diseases Repeated atypical pneumonias Recurrent upper respiratory tract infections History of exudative pleurisy Occupational lung diseases GI diseases: Peptic ulcer (gastric/duodenal) Gastric surgery Metabolic/Endocrine: Diabetes mellitus Chronic adrenal insufficiency Other: Long-term hormone therapy Radiation-exposed individuals Treated TB patients (removed from register) VPI, HIV, drug addiction, alcohol, prison term Note: 90% of newly diagnosed TB cases are from risk groups Epidemiology Risk Groups (Dispensary Observation) Contacts with open TB patients Newly infected children/adolescents (conversion) Cured TB patients with large post-TB changes Individuals with hyperergic tuberculin tests Factors Increasing TB Risk HIV (most significant worldwide) Smoking (especially >20 cigarettes/day) - increases risk 2-4× Diabetes mellitus Chronic non-specific lung diseases Repeated pneumonias Mental illness Pneumoconiosis Severe operations/trauma Peptic ulcer Pregnancy/childbirth Alcoholism, drug addiction Imprisonment Diseases requiring long-term hormone/cytostatic therapy Congenital/acquired immunodeficiencies Currently highest risk: Children/adolescents (not infected, not BCG-vaccinated) Adults: endogenous reactivation of post-TB changes GP Tactics 1. Suspect TB in patients with characteristic complaints, ensure timely investigation 2. Investigate according to algorithm: History and physical exam Ensure quality diagnostic material collection (usually sputum) Transfer sputum to microscopy centers (Level 1 labs) Perform X-ray If lung inflammation changes + negative TB tests → non-specific broad-spectrum antibiotics trial, then repeat tests Refer suspected TB to TB specialist service for confirmation and treatment Implement infection control measures 3. Monitor high-risk groups: Ensure X-ray/fluorography and/or microbiologic studies according to regulations If TB detected on routine screening → refer to TB specialists 4. Perform routine tuberculin diagnosis in children → refer to TB pediatrician as needed 5. Patient education when referring to TB facilities: Explain TB is curable with regular medication and adequate duration Emphasize importance of family/contact screening 6. Assist TB service in contact investigation (including children <17) Active TB Detection in Adults Method: X-ray/fluorography (RFO) Urban: by territorial-production principle Small towns: by territorial principle Rural: mobile X-ray units, nearest healthcare facilities Occupational hazards: according to regulations If pathology detected: call for further investigation within 48 hours Includes: X-ray complex, tomography, CT as indicated Radiologists monitor follow-up (≤14 days from RFO) Treating physician refers to TB facility within 3 days of suspicion, monitors follow-up Results (final clinical-radiological diagnosis) entered into RFO card (form 052/у) 120. SARCOIDOSIS Definition Systemic benign disease of unknown etiology, characterized by productive tissue reactions with epithelioid cell granuloma formation without caseation, resulting in resolution or interstitial fibrosis. Clinical-Radiological Forms Intrathoracic lymph node sarcoidosis Intrathoracic lymph node and lung sarcoidosis Pulmonary sarcoidosis Respiratory sarcoidosis with other organ involvement Generalized sarcoidosis with respiratory involvement International Staging Stage Description I (Mediastinal) Bilateral enlargement of bronchopulmonary nodes (rarely other groups) to 3-5 cm, clear polycyclic contours; no periadenitis, lung changes, mediastinal compression II (Mediastinal-pulmonary) Combined intrathoracic node and lung involvement (diffuse-interstitial or focal) III (Pulmonary) Marked lung changes: dense dissemination in middle zones on pneumosclerosis/emphysema background; progression → entire lung involvement IV Pulmonary fibrosis with "honeycomb lung" signs Clinical Picture Epidemiology: Mainly women 20-40 years Onset types: Asymptomatic (incidental on fluorography) Gradual: weakness, night sweats, dry cough, interscapular pain, progressive dyspnea Acute: brief fever, arthralgia, chest pain, dry cough Acute onset syndromes: Löfgren's syndrome: Mediastinal lymphadenopathy, fever, erythema nodosum, arthralgia, ↑ESR Heerfordt-Waldenström syndrome: Mediastinal lymphadenopathy, fever, parotitis, anterior uveitis, facial nerve palsy Course: Primary-chronic (most common): Lungs first, then other organs; 50% spontaneous recovery Secondary-chronic: Transformation from acute; unfavorable prognosis Intrathoracic lymph node involvement: Hilar bronchopulmonary, tracheobronchial, paratracheal nodes >1.5 cm (mediastinal lymphadenopathy) Peripheral nodes (cervical, supraclavicular): painless, not adherent, firm-elastic, never ulcerate/suppurate/rupture/fistulize Bronchopulmonary involvement: Lungs: Dry or minimally productive cough (small mucous sputum) Chest pain Progressive dyspnea Fibrosis/emphysema → significantly diminished vesicular breathing Bronchi: Minimally productive cough Scattered dry, rarely fine crackles Bronchoscopy: vessel ectasia (pathognomonic) Pleura: Dry or exudative pleurisy (lymphocytes in exudate) GI involvement: Parotid enlargement/tenderness Liver: right hypochondrial heaviness, dry mouth, bitter taste; liver enlarged, firm, smooth Spleen: May progress to hypersplenism (leukopenia, thrombocytopenia, hemolytic anemia) Heart: Sarcoid infiltration, granulomatosis, myocardial fibrosis Dyspnea, exertional chest pain, palpitations, arrhythmias Left border enlargement, muffled tones, apical systolic murmur, heart failure signs Musculoskeletal: Mild bone pain (osteoporosis) Reversible aseptic arthritis of large joints (mainly pain) Nervous system: Peripheral neuropathy: ↓sensation in lower legs/feet, ↓muscle strength Sarcoid meningitis Spinal cord involvement → peripheral paralysis Skin: Erythema nodosum: Painful red nodules in subcutaneous tissue of thighs, lower legs, extensor forearms; skin color changes red → yellow-green Granulomatous sarcoidosis: Small/large erythematous plaques on dorsum of hands/feet, face, old scars Darier-Roussy sarcoid: Dense painless spherical nodules 1-3 cm in subcutaneous tissue, no skin changes Eyes: Anterior/posterior uveitis, conjunctivitis, corneal opacities, cataract, glaucoma Diagnosis of Respiratory Sarcoidosis 1. Imaging (X-ray, tomography - direct and lateral): Intrathoracic adenopathy: Bilateral widening of mediastinum and lung roots; nodes as large conglomerates, clear contours, round/oval Dissemination: Scattered granuloma shadows (miliary to 0.7-1.0 cm), denser near interlobar pleura, axillary zones Infiltration: Pneumonic changes (alveolitis) may obscure lung fields and granulomas Interstitial changes: Fine reticular deformation → diffuse fibrosis and emphysema 2. Radioisotope scanning (⁶⁷Ga citrate): Accumulates in affected nodes, lungs, other organs 3. Fiberoptic bronchoscopy with biopsy: Non-caseating granulomas 4. Mediastinoscopy, thoracoscopy, open lung biopsy: When other methods fail 5. Laboratory: CBC: Eosinophilia, absolute lymphopenia Chemistry: ↑ACE (correlates with activity), ↑lysozyme Immunogram: Fluctuating NK activity, ↓leukocyte phagocytosis, ↑B-lymphocytes, ↑immunoglobulins, ↑CIC Kveim test: 0.15-0.2 ml standard sarcoid antigen intradermally → after 3-4 weeks excise injection site (with subcutaneous fat) → histology; positive = typical sarcoid granuloma Mantoux test (2 TU PPD-L): Negative Treatment Indications for corticosteroids: Extrapulmonary manifestations Vision deterioration Myocardial involvement CNS involvement Progressive course Recurrence with marked symptoms, impaired PFT Hypercalcemia, hypercalciuria Corticosteroid regimens: Continuous: Prednisolone 15-20 mg/day initially → from month 2 reduce to maintenance 5-10 mg/day for 6-36 months Intermittent: Prednisolone 25-30 mg every other day, taper by ¼ tablet every 7 days to 7.5 mg/day by 6 months Inhaled: For bronchial mucosal involvement, obstruction: fluticasone, budesonide If corticosteroids ineffective: Cytostatics: Methotrexate 10-25 mg/week Azathioprine 100-150 mg/day Cyclophosphamide 50-150 mg/day Skin/mucosal involvement: Delagil 750 mg/day Plaquenil 200-400 mg/day for 5-6 months Interstitial fibrosis (if GCS ineffective): Interferon gamma-1b 100 mg SC daily ×6 months Anticytokine therapy: Pentoxifylline 25 mg/kg ×6 months (inhibits TNFα production by alveolar macrophages) Antioxidant complexes ×2 months 121. FRACTURES, DISLOCATIONS, CONTUSIONS, SPRAINS DISLOCATIONS Definition Persistent displacement of articular surfaces of bones, accompanied by joint capsule damage. Signs Change in joint shape Uncharacteristic limb position Pain Springy fixation (resistance when attempting to restore physiological position) Impaired joint function Most Common: Traumatic Dislocation From excessive joint movement (strong blow, fall) Usually accompanied by joint capsule rupture, joint surface separation Attempts to reduce cause severe pain and springy resistance May be complicated by fractures (fracture-dislocation) Emergency Care 1. Immobilize in current position: Use transport splints, special bandages, or any available materials Upper limb: sling, ends tied around neck Lower limb: splints/boards under and beside limb, bandage to limb Finger: immobilize entire hand on flat firm surface Layer of cotton between splint and limb at joints Mandible: sling bandage (crossed ends tied at occiput) 2. Hospitalize for reduction FRACTURES Definition Bone injury with disruption of continuity (closed - no skin damage; open - skin damage). Includes hairline fractures. Signs Deformity at fracture site Inability to move limb Limb shortening Creaking of bone fragments under skin Pain on axial percussion (along bone) Pelvic fracture: unable to lift leg from surface Open Fracture Recognition Bone fragments visible in wound Closed Fracture Diagnosis Signs may mimic contusion (pain, swelling, hematoma, inability to move) Key differentiating signs: Creaking at fracture site Pain on axial loading (gentle percussion along limb axis → sharp pain at fracture site) Emergency Care Closed fractures: Immobilize limb in position Splints, auxiliary devices Femur/humerus: Immobilize 3 joints (ankle, knee, hip OR wrist, elbow, shoulder) Other: Immobilize 2 joints (above and below fracture) Never attempt to realign fragments (may cause bleeding) Open fractures: Stop bleeding: Pulsating stream (arterial): tourniquet above wound Even stream: pressure dressing Aseptic dressing on wound Immobilize (2 joints above and below; femur/humerus: 3 joints) Note: Splint never on bare skin (clothing or cotton underneath) Open or closed (with displacement) fractures of large bones → urgent hospitalization for reduction If >2 hours without reduction → risk of fat embolism (death/disability) HAIRLINE FRACTURE Definition Partial bone integrity disruption from load exceeding strength of affected skeletal area. Locations Skull, spine, sternum, ribs, upper/lower limbs After trauma, blow May relate to age-related bone density changes, musculoskeletal diseases Symptoms Intense pain (various character) with movement/palpation Stiffness (patient avoids movement, assumes least painful position) Swelling over injury site If vessels damaged: hematoma (cyanotic, red, burgundy) Additional symptoms by location: Ribs: impaired breathing, dyspnea, tachycardia, pale skin Skull: possible LOC to coma, sensory disturbances, paralysis, nausea, vomiting, headache, vision loss CONTUSION Definition Closed tissue/organ injury without significant structural disruption. Most often superficial tissues (skin, subcutaneous fat, muscles, periosteum). Soft tissues pressed against bones at impact. Mechanism Blunt object impact Blast/gunshot trauma: local + "hydrodynamic shock" (damage distant from impact point) Signs Varying pain intensity Continued deep bleeding → compression of adjacent tissues → increasing pain, dysfunction Hemorrhage at site → bruise (blue-purple → green → yellow) Emergency Care Immediate cold (reduces pain, limits bleeding): towel in ice water, ice pack Apply Lemakol or Bepanthen cream After 3 hours: pressure bandage (not too tight, maintain circulation) for 2 days SPRAIN Signs Sharp pain at injury site (worse with joint movement, pressure on injured ligament) Due to rupture of small nerve fibers innervating ligament May cause numbness Swelling of injured limb (over injured joint, rapidly increasing) Redness, increased skin temperature (aseptic inflammation) Limited movement: Disrupted joint architecture Reflex muscle spasm (protects limb) Ankle sprain: difficult/painful to stand; shoulder: difficult to raise arm Hematoma (from ruptured small vessels) May not always form (unlike complete rupture) May be subcutaneous (rarely intermuscular, very rarely intra-articular) May appear immediately or develop over 2-3 days Popping sound at injury (more common in complete rupture; may occur in sprain) Differential Diagnosis (vs Fracture) Fracture: shortening, deformity, axis disturbance Diagnosis MRI of injured joint Ultrasound of joint and surrounding soft tissues X-ray (excludes fracture, indirect signs of sprain) Treatment Goals Eliminate pain Reduce swelling Restore mobility Analgesia/anti-inflammatory: NSAIDs (gels, ointments, creams - local; tablets, suppositories, powders, injections - systemic) Duration: 6-8 days (sufficient for inflammation; longer → side effects) Reduce swelling: Ice wrapped in towel, 10-15 min q3-4h Elevate injured limb first days Large hematoma: Topical direct anticoagulants (creams/ointments) - faster resolution, normalize microcirculation, prevent venous thrombosis Contraindications: bleeding tendency, broken skin, skin diseases at application site Immobilization: Orthosis (rigid or semi-rigid with side plates) or elastic bandage Immobilize joint in anatomically correct position Not too tight (impaired circulation, increased swelling) Duration: 1-4 weeks (individualized) 122. BURNS AND FROSTBITE BURNS Definition Tissue damage from local high temperature, chemical agents, electric current, or ionizing radiation. Types by Etiology Thermal Chemical Radiation Electrical Thermal Burn Pathophysiology Heat transfer to tissues: Convection: hot gas/steam (very dangerous) Conduction: direct contact with heated object/liquid Radiation: thermal (infrared) radiation Cell protein denaturation: at 60-70°C <60°C: Wet (colliquative) necrosis >60°C: Dry (coagulation) necrosis Combinations present (uneven tissue heating) Infrared radiation: penetrates to 5 mm, heats to 50-60°C Severity Determinants Burn surface area Depth of skin and underlying tissue damage Classification Vishnevsky classification: Degree Depth I Stratum corneum and granular layer II All epidermal layers, sometimes basal keratinocytes IIIa Entire epidermis + superficial dermis; skin appendages partially preserved IIIb Full-thickness skin necrosis; possible subcutaneous fat involvement IV Necrosis of skin, subcutaneous fat, and deeper structures (muscles, tendons, bones, joints) ICD-10: I: Hyperemia II: Thin-walled blisters, superficial dermal injury III: Total dermal and underlying tissue damage Burn Notation (Dzhanelidze Formula) Etiology = (Area% [deep%]) / Degree Localization Example: Thermal burn = (10% (5%) / II-III) head, neck Clinical Presentation by Degree I Degree: Redness, edema Burning, pain (worse on touch) Pressure → skin pales 2-4 days: pain, hyperemia, edema resolve → regeneration + desquamation II Degree: More marked pain, burning, edema Thin-walled blisters (minutes post-burn) on edematous, hyperemic skin Fluid: plasma-like, extracellular matrix components Blisters enlarge over time; may appear day 1-2 After removal/rupture: exposed basal layer (pale pink), very tender (receptors preserved) Healing: 2 weeks (spontaneous regeneration from germinal layer) New epidermis: pink, increased pain sensitivity, vulnerability (no stratum corneum) Redness/hyperpigmentation may persist weeks IIIa Degree: Variable presentation Type 1: Thick-walled blisters (full-thickness detached epidermis) Large, tense, often confluent Jelly-like exudate (deep yellow or bloody) After rupture: wound surface with alternating gray/white and pink areas Pain sensation preserved or markedly reduced in some areas Type 2: Dead epidermis fixed to partially necrotic dermis Wound surface: brownish or "chocolate" color No capillary pulse, no pain 3-5 days: thin necrotic eschar forms Dry necrosis: parchment-like Wet necrosis: gray moist fibrin film Granulation under eschar Week 2: necrotic tissue sloughing Healing: 3-6 weeks (spontaneous from preserved skin appendages - island epithelization) Slower healing with fewer epithelial islands → disfiguring scars Diagnosis difficult early; confirmed by dynamic observation (epithelial islands on granulation) IIIb Degree: Full-thickness skin necrosis; ± subcutaneous fat Hot liquids: gray-white, soft/doughy eschar Flame/hot metal: dense, dry, dark brown/black eschar Vascular pattern (venous thrombosis) indicates deep injury Moderate edema, narrow hyperemic rim around eschar Prolonged hot liquid exposure: hemorrhagic blisters possible; base: dull, dry, pale, insensate dermis with punctate hemorrhages Wet necrosis → inflammation spreads to intact tissues Suppuration + proliferation Eschar separation 2 weeks earlier than dry necrosis Wound covered with granulations No spontaneous healing (skin appendages destroyed) Healing by scar contraction and marginal epithelization → requires skin grafting Spontaneous healing possible only if diameter ≤1.5-2.0 cm (marginal epithelization) Special form: "Skin fixation" from distant infrared burns First 2-3 days: burned skin paler, cooler than surrounding No "vascular play," narrow hyperemic/edematous rim 3-4 days: dry eschar forms Differential diagnosis IIIa vs IIIb: Needle test: no pain in IIIb Alcohol test: no pain in IIIb Hair pull test: no pain in IIIb Skin thermometry: IIIa 1.5-2.5°C warmer than IIIb (impaired circulation in deep burns) IV Degree: Flame/hot metal Necrosis of skin, subcutaneous fat, and deeper structures (muscles, tendons, bones, joints) Possible limb segment/full limb charring Burn surface: dense, thick, dark brown/black eschar, multiple cracks exposing necrotic muscles/tendons/bones Thrombosed veins visible No tactile/pain sensation, tendon/muscle/joint function absent Depth often only determinable days after injury Determining Burn Area and Depth "Palm rule" (Glumov, 1953): Palm surface area ≈1% body surface (women 1%, men 1.1-1.2%) Count number of patient's palms fitting on burn surface More precise: 0.78% of total body surface (Grazer et al., 1997) - correct for accuracy "Rule of nines" (Wallace, 1951) - adults only: Area % Head and neck 9 Each upper limb 9 Each lower limb 18 Anterior trunk 18 Posterior trunk 18 Perineum/genitalia 1 Postnikov method (1949): Cover burn with sterile cellophane sheets Outline contours of each degree with colored markers Place millimeter grid over sheets, calculate area in cm² Vilyavin method (1956): Outline and color each degree on history insert (silhouette front/back, height 17 cm = 1:10 scale of average adult) Use millimeter grid to determine area in mm² on drawing = cm² on body First Aid at Scene Remove from danger zone Extinguish burning clothing or remove clothing soaked with hot liquid (do not remove all clothing, especially in cold weather - cooling precipitates shock) If burned in enclosed space: move to fresh air, loosen collar, remove tie Restore airway patency (remove mucus/vomit, prevent tongue retraction) If no spontaneous breathing: artificial ventilation Cool burned areas with water or cold objects If general overheating: moisten skin with cold water, loosen clothing (warm weather only), apply ice/cold compresses to head Do not manipulate burn surface (may increase pain, worsen condition) Cut around clothing adherent to burn, apply dry aseptic (preferably cotton-gauze) dressing In extreme case, leave burned area uncovered for few hours If extensive burns: administer analgesics Limb burns: transport immobilization Hand burns: remove rings (prevent finger ischemia from developing edema) Local Treatment Primary wound care: Clean skin around burn with 0.25% ammonia solution, 3-4% boric acid, benzine, or warm soapy water Treat with alcohol Remove clothing remnants, foreign bodies, detached epidermis Incise tense large blisters, release contents Leave small/medium blisters intact Do not remove coagulated fibrin from blister base (healing occurs under it) Clean heavily contaminated areas with 3% H₂O₂ or antiseptic solutions Dry with sterile wipes Usually after premedication (promedol 1-2 ml 1% or omnopon) Closed method (most common): Isolates burned surface Optimal conditions for topical medication Allows active patient behavior even with significant burns Disadvantages: labor-intensive, high material consumption, painful dressings New dressing materials with antiseptic, anti-inflammatory, hemostatic, absorbent, enzymatic, non-adherent, wound-healing properties Biological/synthetic wound covers: allogeneic skin, dermal preparations, amniotic membrane, "Folyderm," "Biobrane," "Sipsusderm," "Omyderm" (protective, absorbent, therapeutic) Open method: Drying necrotic tissue to prevent microbial growth Treat with protein-coagulating agents: weak KMnO₄, tannin, 0.5% AgNO₃ Hyperosmolar agents: glycerin, polyethylene oxide Note: Eschar dehydration may slightly deepen wound (partial necrosis of paranecrotic zone) Technical devices: infrared emitters, fans, aerotherapy units, fluidized beds, light units Surgical treatment (for deep burns IIIb, IV): Early necrotomy Necrectomy Autodermoplasty Limb amputation Reconstructive surgery FROSTBITE Definition Tissue damage from low temperatures. Usually affects peripheral areas: fingers/toes, ears, nose. Pathogenesis Initial: cold sensation → numbness → anesthesia (pain then all sensation lost) Anesthesia makes continued cold exposure unnoticed → often causes severe irreversible damage Direct cold damage: At tissue temperature ≤ -40°C → structural disorganization, necrosis If > -40°C: Vascular disorders cause secondary necrosis: Vasoconstriction Slowed blood flow Increased blood viscosity Increased vascular permeability (protein) Stasis → after warming: intravascular thrombosis (paralysis of anticoagulant system) Impaired microcirculation and transcapillary exchange → severe regional hypoxia → necrosis Hormonal: ↑adrenaline-like substances → sustained angiospasm Sympathetic nervous system: Symmetry of damage; contralateral limb also has metabolic changes (lesser degree) Reflex: Circulatory disorders → autonomic disturbances → pathological changes in distant organs (respiratory, GI, peripheral nerves, bones) Early (hours-days): Salt/water imbalance Acid-base disturbances Leukocytosis, left shift Fever Wet necrosis → possible intoxication Functional vascular changes → morphological changes: phlebitis, endo-/meso-/periarteritis; later: endothelial hyperplasia, muscle layer thickening, obliteration Clinical Course Pre-reactive period (from cold exposure to beginning of warming/circulation restoration): Minimal symptoms Mild tingling, slight pain, burning, paresthesias Then numbness Skin: pale, sometimes cyanotic, cold Sensation decreased or absent (by depth) Usually no edema Capillary response decreased or absent Possible skin pattern smoothing, absent active movements in nearby joints Degree of damage impossible to predict Reactive period (begins with warming/circulation restoration): Early reactive (first 12h): microcirculatory disturbances, vessel wall changes, hypercoagulation, thrombosis Late reactive: necrotic changes, infectious complications Classification by Severity I Degree (short exposure): Reversible circulatory disturbances Skin pale, slightly edematous Sensation sharply decreased or absent before warming After warming: burning pain, itching, paresthesias, moderate edema, cyanosis or marbling Skin warm, active joint movements Resolves in 5-7 days; sometimes scaling Long-term increased sensitivity to cold II Degree: Necrosis of superficial skin layers (including papillary layer elements) After warming: purplish-cyanotic color Rapid edema spreading beyond injury Blisters 1-2 days (sometimes 3-5 days) with clear/white fluid Blister base: pink, tender Fever, chills, poor appetite/sleep Days 7-8: blisters shrink, necrotic layers slough, circulation slowly restores Long-term sensory disturbances, pain possible Possible nail loss (regrow later) Healing: 2-4 weeks, no granulation/scarring Skin remains cyanotic, hyposensitive, very cold-sensitive III Degree: Necrosis of all skin layers + partial subcutaneous fat After sloughing: granulation → scarring in 1-1.5 months Marked pain, capillary response absent, all sensation absent Hemorrhagic blisters (sometimes large, confluent, circumferential) Base: purplish-cyanotic, painless/minimally tender Inflammatory rim around necrosis Marked edema spreading proximally Peripheral pulse decreased Nails painlessly shed, usually not regrow; if regrow, deformed Necrotic tissue sloughing: 2-3 weeks End of first month: possible osteoporosis on X-ray IV Degree: Necrosis of all tissues (including bone, joints) After warming: affected part remains cold, absolutely insensate Early: cyanosis, sometimes marbling; no capillary pulse Possible hemorrhagic blisters (often flaccid, ichorous fluid) Blister base: purplish-cyanotic, dull, "dry," painless Peripheral arterial pulse decreased/absent Marked edema spreading proximally, severe pain Clear demarcation line: 10-17 days Affected zone quickly blackens, begins mummification Necrotic tissue sloughing: 1.5-2 months Wound healing: very slow, indolent Severe general condition, dystrophic organ changes Pain and intoxication exhaust patient, blood changes First Aid Stop cold exposure Massage frostbitten limb from periphery to center (hand or soft wool cloth) until warm and pink Do not rub with snow or alcohol (damages skin → infection, deeper injury) Apply cotton-gauze insulating bandage Warm affected limb (apply heating pads around shoulders/thighs) Warm both limbs even if only one affected (nervous system role) Immobilize frostbitten limb segments with standard splints or available materials Give hot drink, may give small amount of alcohol Treatment Goals: Restore impaired circulation Prevent/treat infectious complications Conservative vs Surgical Pre-reactive period: Persistent vasospasm, ↑viscosity, aggregation Intra-arterial/intravenous infusions: Metabolic normalizers Antispasmodics: papaverine, euphyllin Antiplatelets: aspirin, pentoxifylline, dipyridamole Anticoagulants: heparin Vasodilators: nicotinic acid, xanthinol nicotinate Analgesics Reactive period: Necrosis, intoxication, purulent complications Detoxification drugs Blood components Immunological, anti-inflammatory, analgesic, antihistamine drugs Antibiotics Parenteral nutrition Treat acidosis Local treatment: Primary wound care: Treat skin with alcohol Open blisters, remove contents, detached epidermis Apply antiseptic dressing Surgical treatment: Necrotomy: incising necrotic tissue (≤3 days) Necrectomy: Early (day 1): for gangrene, sepsis threat Delayed (15-30 days post-injury) Amputation: proximal to demarcation line Reconstructive surgery 123. CLINICAL PHARMACOLOGY - PENICILLINS General Characteristics β-lactam antibiotics Bactericidal Low toxicity Broad spectrum Acid-resistant Possible cross-allergy with other β-lactams Time-dependent Classification Natural: Benzylpenicillin (Na, K, procaine salts) Benzathine benzylpenicillin (bicillin-1,3,5) Phenoxymethylpenicillin Semi-synthetic: Antistaphylococcal: oxacillin, flucloxacillin, cloxacillin Extended spectrum (aminopenicillins): ampicillin, amoxicillin Antipseudomonal: Carboxypenicillins: carbenicillin Ureidopenicillins: azlocillin, piperacillin Inhibitor-protected: Amoxicillin/clavulanate Amoxicillin/sulbactam Ampicillin/sulbactam Combination: ampicillin + oxacillin Natural Penicillins Spectrum: Gram+ cocci, Gram- cocci, some anaerobes, spirochetes Pharmacokinetics: Destroyed in stomach acid → IV/IM only Na/K salts: distribute widely (except CSF, prostate, eye), excreted renally T½ = 30 min Phenoxymethylpenicillin: 60% stable orally, does not achieve high blood levels (not for severe infections) Prolonged-release (benzathine benzylpenicillin - 3-4 weeks; procaine penicillin - 24h): IM only, slow absorption, do not cross BBB Indications: Na/K salts: streptococcal infections (tonsillopharyngitis, erysipelas, scarlet fever), community-acquired pneumococcal infections, meningitis, bacterial endocarditis, syphilis, leptospirosis, anthrax, clostridial infections (tetanus) Phenoxymethylpenicillin: streptococcal infections, rheumatic fever prophylaxis, pneumococcal infections Prolonged-release: tonsillopharyngitis, syphilis, rheumatic fever prophylaxis Adverse effects: Allergic reactions High doses: tremor, seizures Nausea Interactions: Synergy: aminoglycosides (physicochemical incompatibility) Antagonism: sulfonamides High-dose K-benzylpenicillin + K-sparing diuretics/K⁺ supplements/ACE inhibitors → hyperkalemia risk Antipseudomonal penicillins + anticoagulants/antiplatelets → bleeding risk sulfonamides → ↓bactericidal effect Antistaphylococcal Penicillins Spectrum: Penicillinase-resistant → active against PRSA; otherwise similar to natural penicillins Pharmacokinetics: Oral bioavailability 20-30% Renal and biliary excretion T½ = 30 min Indications: Staphylococcal infections (except MRSA) Adverse effects: Allergy Vomiting, dyspepsia ↓Hb, neutropenia Extended-Spectrum (Aminopenicillins) Ampicillin: Active against some aerobic Gram- enterobacteria (E. coli, Salmonella, Shigella) Fasting bioavailability 30-40% (lower after meals) Poor BBB penetration Renal + biliary excretion T½ = 1 h allopurinol → ↑risk of "ampicillin rash" Amoxicillin: More active against pneumococcus, H. pylori GI absorption 2× better than ampicillin Bioavailability 75% (food-independent) High, sustained blood and bronchopulmonary secretion levels Secreted in gastric juice Renal excretion (high urine concentrations) T½ = 1 h Indications: Ampicillin: otitis, sinusitis, community-acquired pneumonia, meningitis, bacterial endocarditis, salmonellosis, shigellosis, biliary tract infections Amoxicillin: otitis, sinusitis, chronic bronchitis, community-acquired pneumonia, H. pylori eradication Adverse effects: Diarrhea Rash Antipseudomonal Penicillins Currently used only if other antipseudomonal agents unavailable Carboxypenicillins: Active against Proteus, Enterobacteria Ureidopenicillins: More active against Pseudomonas Pharmacokinetics: Parenteral only Poor BBB penetration Renal excretion T½ = 1 h Adverse effects: Platelet aggregation inhibition Hypernatremia Hypokalemia Carbenicillin: neurotoxicity Inhibitor-Protected Penicillins Rationale: Main resistance mechanism to β-lactams = β-lactamase production Amoxicillin + Clavulanic acid: Well absorbed orally Bioavailability food-independent Distributes widely (lungs, pleural fluid, middle ear, sinuses) Poor BBB and prostate penetration Renal excretion Indications: Otitis, sinusitis, bronchitis Intra-abdominal/pelvic infections Skin/soft tissue infections Bone/joint infections Biliary/urinary tract infections Adverse effects: ↑Transaminases Fever Nausea, vomiting Ticarcillin + Clavulanic acid: May cause electrolyte disturbances 124. CLINICAL PHARMACOLOGY - CEPHALOSPORINS General Characteristics β-lactam antibiotics Bactericidal Time-dependent Low toxicity Wide therapeutic index Cross-allergy with penicillins (5-10%) Avoid in alcohol (disulfiram-like reaction with certain cephalosporins) Classification by Generation 1st Generation Drugs: Cefazolin (parenteral), Cephalexin (oral) Spectrum: Gram+ cocci (except MRSA, enterococci) Streptococci, staphylococci (including PRSA) Resistant: MRSA, enterococci, Listeria, most H. influenzae, most Enterobacteriaceae Pharmacokinetics: Cefazolin: distributes widely, poor BBB/prostate; stable blood/urine levels with BID-TID dosing; T½ ~2h; 80% renal, partial biliary excretion Cephalexin: 95% oral absorption; highest levels in bone, pleural fluid, bile, urine; T½ = 1h Indications: Streptococcal/staphylococcal skin/soft tissue infections Bone/joint infections Perioperative prophylaxis 2nd Generation Drugs: Cefuroxime (parenteral) Cefoxitin Cefaclor (oral) Cefuroxime axetil (oral prodrug) Spectrum: Higher activity against Gram-: H. influenzae, M. catarrhalis, some Klebsiella, Proteus Cefuroxime: Good tissue penetration, crosses BBB with meningeal inflammation Renal excretion T½ = 1.5h Indications: Otitis media, sinusitis, acute exacerbation chronic bronchitis Community-acquired pneumonia Skin/soft tissue, bone/joint, UTI Sepsis Perioperative prophylaxis Cefuroxime axetil: Prodrug, bioavailability 50-70% (increased with food) Hydrolyzed to cefuroxime during absorption Renal excretion T½ = 1.5h Same indications (except prophylaxis) Step therapy effective: parenteral → oral Cefaclor: Less active against pneumococcus, H. influenzae than cefuroxime Bioavailability 90-95% T½ = 0.5-1h Same oral indications as cefuroxime, but ineffective in otitis media (does not reach therapeutic middle ear levels) 3rd Generation Parenteral: Cefotaxime Ceftriaxone Ceftazidime (antipseudomonal) Cefoperazone (antipseudomonal) Oral: Cefixime Spectrum: Highly active against Gram- Enterobacteriaceae (including nosocomial polyresistant strains) Ceftazidime, cefoperazone: active against Pseudomonas Severe/mixed infections: combine with aminoglycosides (2-3 gen), metronidazole, vancomycin Cefotaxime: Active against streptococci, penicillin-resistant pneumococci Less anti-staphylococcal activity than 1-2 gen Highly active against gonococci, meningococci, H. influenzae, M. catarrhalis, many Gram- Enterobacteriaceae Ceftriaxone: Similar spectrum to cefotaxime Longest T½ (5-7h) → once daily dosing (meningitis: BID) High protein binding (caution in newborns - bilirubin displacement) Renal + biliary excretion (no dose adjustment in renal failure) May form calcium salt in bile (pseudolithiasis) → avoid in biliary infections Ceftazidime: Active against Pseudomonas (superior to aminoglycosides, ciprofloxacin) Less active against Gram+ cocci T½ = 2h Cefixime (oral): More active against Gram- (H. influenzae, M. catarrhalis, gonococci, Enterobacteriaceae) than 2nd gen oral Good anti-streptococcal, less anti-pneumococcal/staphylococcal than cefuroxime Bioavailability 50% Renal + partial biliary excretion T½ = 3-4h Indications (3rd gen): Severe sinusitis, community/nosocomial pneumonia Severe UTI, skin/soft tissue, bone/joint infections Intestinal infections (shigellosis, salmonellosis) Intra-abdominal/pelvic infections Meningitis, sepsis, gonorrhea Ceftriaxone also: acute otitis media, bacterial endocarditis, Lyme disease Ceftazidime: Pseudomonas infections (including meningitis), nosocomial pneumonia, severe UTI, intra-abdominal/pelvic infections (+ anti-anaerobic) Cefixime: acute exacerbation chronic bronchitis (H. influenzae, M. catarrhalis), UTI, shigellosis, gonorrhea, step therapy after parenteral 3-4 gen 4th Generation Drug: Cefepime Spectrum: More resistant to β-lactamases from nosocomial Enterobacteriaceae More active against Gram+ cocci than 3rd gen Antipseudomonal activity Active against streptococci, staphylococci (except MRSA), meningococci, Pseudomonas Highly active against Enterobacteriaceae Pharmacokinetics: Crosses BBB T½ ~2h Indications: Severe, mainly nosocomial infections: Pneumonia, UTI Intra-abdominal/pelvic infections (+ metronidazole) Skin/soft tissue, bone/joint Sepsis Combination Preparations Cefoperazone + Sulbactam (β-lactamase inhibitor): More active than cefoperazone against β-lactamase-producing organisms (many Gram- Enterobacteriaceae, Acinetobacter) Unique: Active against non-spore-forming anaerobes → monotherapy possible for intra-abdominal/pelvic infections

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