ilovepdf_merged (1).pdf

Nonspeci ic infection f a a Prof H yder M. Abduln bi Syphylis Infection caused by Treponema pallidum ( spirochete bacteria) —corksrew motion Transmitted usually by sexual contact, direct contact, mother to fetus Spirochete bacteria Classi ication of syphilis 1. Early (one year) A. Primary...

Nonspeci ic infection f a a Prof H yder M. Abduln bi Syphylis Infection caused by Treponema pallidum ( spirochete bacteria) —corksrew motion Transmitted usually by sexual contact, direct contact, mother to fetus Spirochete bacteria Classi ication of syphilis 1. Early (one year) A. Primary B. Secondary C. Early latent 2. Late (after one year) A. Late latent f B. Tertiary syphilis Primary syphilis Primary chancre Painless, usually single,erythematous papule —— ulcerate —— spontaneous healing Site —— usually genitalia anal, mouth, tongue Secondary syphylis 2–12 weeks after the primary chancre Symptoms Fever, headache, malaise, sore throat, cutaneous rash ( macule)—- pustule , adenopathy Usually disappear without treatment ——- latent Macular rash secondary syphilis Tertiary syphilis 1— 20 years after acute infection Charecterized by gumma formation ( granulomatous in lammatory destructive process) Non cancerous gummy or rubbery masses that ulcerate f giving a central necrosis The main parts affected are Neurosyohilis——- insanity Cardiosyphilis ——— valve ibrosis, aneurysm f Gummas ( skin, bone,liver and others) Diagnosis Serological tests VDRL and RPR and Wasserman test Antigen antibody reaction (Vinereal disease research lab test) ( rapid plasma reagin ) Treatment Penicillin Anthrax Organism Bacillus anthracis Anthracos means coal Transmission 1. Contact with animal tissues dying of the disease ( cattle skin, sheep, pigs, horses , others 2. Biting lies 3. Contact with contaminated hair, wool, skin and hides (drum, brushes, rugs) f 4. Contact with soil 5. Inhalation of spores ( tanning hides and wool processing) 6. Intestinal or oropharngeal ( ingestion of undercooked contaminated meat ) 7. Accidental ( laboratory workers ) Tanning Wool processing Spores Clinical manifestation 95-99% are cutaneous anthrax —— gelatinous edema ( papule, vesicle, malignant pustule, necrotic ulcer ) (black) 80- 90 % heal spontaneously 20% progress to septicemia Respir tory nthr x Require very high dose of spores ( biotrrrorism aerosol) Severe respiratory infection, fever and chest pain Haemorrhagic mediastinitus Progress rapidly to septicemia a a a Mortality rate very high ( more than 95% ) Aerosol Biological war Haemorrhagic mediastinitis Anthrax meningitis ( a complication of septicemia ) —— Subarachnoid haemorrhage Treatment Penicillin Tetracycline, erythromycin f Cipro loxacine Vaccination Tetanus Acute bacteria, infection Clostridium tetani. ——- neurotoxin ( tetanospasmine ) ——Prolonged skeletal muscle contraction Also called lockjaw Clostridium tetani Transmission Direct contamination of a wound Skin abrasion, punctured wound, animal bite, aseptic abortion, unsterile surgery, unsterile cutting of umbilical cord Spores found in the intestine of horses, sheeps, cats,dogs, rats, chickens Neonatal tetanus f A signi icant health problem Not from person to person Spores enter damaged tissue ——— transform to rod shaped bacteria ——- neurotoxin ( tetanospasmine ) ——interferes with neurotransmission ——— result to uncontrolled spasms and contractions Opisthotonos position Risus sardonicus Trismus ( lockjaw) Dysphagia Asphyxia Opisthotonos Risus sardonicus V for vendetta Jocker Treatment Injection of tetanus toxoid intramuscularly Local wound care Incision and drainage of pus Debridement Wound should be open Control of spasm ——- diazepam injection Paralyze and ventilate Antibiotics Isolation in a quit dark room Oxygen Complication 1. Acute asphyxia 2. Respiratory arrest 3. Vertebral fracture 4. Laceration of tongue, lips, buccal cavity Tetanus is a vaccine preventable disease Surgical immunity a a Prof. H yder M. Abduln bi Innate Adabtive Born ready baby I’m always ready to learn and remember f Require activation Immediately act on pathogen React to a speci ic pathogen They do not require activation Form memory cells to protect from future attack Innate immune response 1. Physical barriers 2. Chemical barriers 3. Complement f 4. In lammation Physical barriers Skin and mucous membrane Sneezing Coughing Urination Running nose Chemical barriers Saliva Sweat Stomach acid In lammatiin Increase blood low Increase permeability f f ( red, hot, swelling, pain, loss of function ) Complement Proteins produced by the liver When triggered make a complex ( membrane attack complex) ——- punch holes in the microorganism cell membrane and make them more delicious for phagocytisis and antibody attack Complement structure Cells involved in innate immunity Neutrophil —— secrets bleach and peroxides Basophils ——- Base loving , contain granules —— secret histamine Mast cells ——— found in the body tissue —— secret histamine Eiosinoohil ———- acid loving ——— against parasite Basophil found in the blood stream Mast cells found in the body tissues Both have plenty of granules containing histamine More in mast cells Basophil and mast cells Macrophage——- big eaters Dendritic cell ——- antigen presenting cells Natural killer cell ——- basically lymphocytes that do not require activation kill cancer cells and viruses Dendritic cell Present microorganism antigen fragment to T and B lymphocytes Origin of Leukocytes Bone marrow Adaptive immunity Activated by the helper T lymphocyte which are activated by antigen presenting cells ( dendritic cell ) This will stimulate cytotoxic T lymphocyte (directly destroy enemies ). And stimulate B lymphocytes to get much bigger —called plasma cells———- antibodies IgG IgM IgE IgA Activation of T lymphocyte and B lymphocyte produce memory T cells and memory B cells They circulate in your blood for the rest of your life protecting against whatever microorganism f that made you sick for the irst time Hypersensitivity Types I —-IV Each varying in severity from mild to lifethreatening Excessive activation of immune system Hypersensitivty type I Appears within minutes of exposure to antigen Interaction of antigen, IgE and tissue mast cells Previous exposure to antigen is necessary Mast cells have speci ic IgE receptors f IgE bind to receptors Mast cell degranulation ——- release of intracellular contents Histamine, heparin, proteases and other substances These mediators cause immediate response Vasodilation Increased vascular permeability Bronchospasm Neutrophil and eosinophil chemotaxis Examples of type I hypersensitivty Allergic rhinitis Asthma atopy) Eczema Urticaria Systemic anaphylaxis (Atopic people who suffer From Allergic rhinitis Eczema Urticaria Asthma Type II Hypersensitivity Antibody mediated immune reaction where antibodies IgG and IgM are directed against cellular or extracellular matrix antigen ( cytotoxic) ——— cellular destruction, functional loss, or tissue damage Examples Blood transfusion reaction Anemia Tissue transplant rejection Some platelet disorders Examples Kidney transplant Type III Hypersensitivity Abnormal immune response mediated by the formation of Antigen- antibody aggregates called immune complexes that precipitate in various tissues such as skin, joints, glomeruli And trigger the classical complement pathway Examples Drug induced serum sickness Farmer’s lung( hypersensitivity pneumonitis) ( hay and straw) Systemic lupus erythematosus Farmer’s lung Serum sickness Systemic lupus erytheromatosus Type IV hypersensitivity Hypersensitivity mediated by T cells that produce in lammatory reaction against f exogenous and endogenous antigens Examples Contact dermatitis from chemicals, poisons, topical creams Autoimmune diseases When the immune system attack your body instead of protecting it Cause unknown Examples Type I diabetes Rheumatoid arthritis Psoriasis Multiple sclerosis Graves’ disease Immunode iciency A state where the immune system fail to ight f f infections or cancer Causes Acquired ( secondary) due to extrinsic factors that affect the immune system HIV infection Environmental factor Nutrition Primary Genetic ( SCID ) f Severe combined immunode iciency Bubble boy Bubble boy Wound wound healing and scars By Prof. HAYDER M. ABDULNABI Wound • • • • • • • • • Break down or discontinuity in the integrity of an epithelium ( cellular ) surface down to deeper structures, and can beOpen (exposed) or. Closed ( not exposed ) Open wound types— A. PENETRATING 1. Puncture and wound cutting 2. Surgical wound (incision) 3. Burn ( thermal, chemical, electrical 5. Bite and stings 6. Gunshot , other high velocity projectile • • • B. BLUNT TRAUMA 1. Abrasion- Top layer of skin only removed by for example sliding over a rough surface 2. Laceration- Irregular shape tears from trauma • Abrasion Laceration 2. Blister- clear uid lled pocket under the skin 3. Seroma- uid lled area under the skin commonly after blunt trauma or surgery 4. Hematoma- blood lled area under the skin due to blood vessel injury fi fi 5. Crush injury- force over a long period of time fi • • 1. contusion- blunt trauma cause pressure to the skin and/ or underlying tissue fl • • C. CLOSED WOUND fl • • Hematoma Contusion Blister Seroma Crush injury Wound classi ication based on depth Super cial Partial thickness Full thickness f Deep fi • • • • Wound healing • A mechanism where the body attempts to restore the integrity of the injured part F ctors ffecting wound he ling Site of the wound Structures involved Mechanism- crush or incision Contamination- foreign body, bacteria Vascular insu ciency- athero sclerosis, diabetes Pressure Malnutrition a a Medication—steroids, chemotherapy ffi a • • • • • • • • Wound healing • • • • It constitute three phases 1– Clot formation 2–. In ammatory phase—- cellular cleaning by macrophages 3— proliferative phase—- 3rd day to 3rd week—- broblast lay down collagen (granulation tissue ) , re epithelializatiin • fi fl 4– remodeling phase— maturation of collagen— increase tensile strength— maximum at 12th week ( contraction ) Phase 1 Clot formation Phase 2 Phase 3 Phase 4 Types of wound closure • • • 1– primary intention closure— wound edges opposed— minimal scar 2.-Secondary intention—contaminated wounds, untidy — more collagen , big granulation tissue— poor scar 3-Tertiary intention (delayed primary)—- wound left open and opposed after few days • Healing by 2nd intention Gr nul tion tissue • • The main part of 2ndary healing is granulation Granulation tissue is formed of broblast and new blood vessels( revascularization ) fi It is deep red, granular, very fragile and easy to bleed a a • Granulation tissue Surgical wound classi ication • • • Class I. Clean. Simple open wound, surgical incisions ( where alimentary, urinary, genital tract are not entered) —- example operation of thyroid, breast. ClassII. Clean- contaminated— incisions involving alimentary, genital, urinary where contamination is minimal ClassIII. contaminated— gastrointestinal tract operation ClassIV. dirty/ infected —- where infection present before applying the incision— ruptured appx, ruptured gall bladder, ruptured colon, diabetic foot f • Managing wounds • • • • Cleaning Debridement Skin closure without tension All the above with careful tissue handling and meticulous technique Cleaning Debridement Skin closure Scar types • • • Atrophic Hypertrophic Keloid • • • Atrophic scar pale, at, and stretched— area of tension Easily traumatized ( epidermis and dermis are attened Solution is excision and resuturing fl fl • • • • Hypertophic scar Excessive scar tissue — does not extend beyond the boundary of the original wound or incision Results from prolonged inl amatory phase of wound healing Or from unfavourable site of wound or incision ( across lines of of skin tension fl • • • • • Keloid Scar that extend beyond the area of the original wound Pink, red, skin-coloured, or darker than the surrounding skin, hard or rubbery, shiny and hairless It may occur even after an acne spot or ear piercing THANK YOU