IMID 2 EXAM 1

• Acute utricaria


  less than 6 weeks

  type 1 hypersensitivity response to allergens may lead to anaphylactic shock
• Uriticaria


  caused by IgE and non IgE mediated release of histamine and other inflammatory mediators from mast cells and basophils

  -classified based on duration

  
• immunopathogenesis of psoriasis

  triggered by trauma induces the production of LL-37 by keratinocytes which gets recognized by TLR9 and activates pDC and induces IFN-a production to activate mDC that releases IL-23 and IL-12 which activates t helper cells Th17 ( IL-23) which then secretes IL-22 which starts Keratinocyte proliferation as well as IL-17 and Th1 ( IL-12) that releases iFN-y and TNF-a which along w IL-17 are involved in inflammatory response.

  -Epidermis- thickened scaly

  Dermis- enlarged capillaries
• Risk factors of Psoriasis

  genetic predisposition, living in cold climates, stress, infection ,skin injuries, smoking

  10-15% develop psoriatic arthritis ( joint pain and inflammation)
• Psoriasis

  chronic inflammatory skin condition w hyperplasia of epidermis ( acanthosis)

  - scaly erythematous demarcated skin plaques (itchy flaky skin)

  - Auspitz sign- pinpointing bleeding when removing scales
• CCR4, CCR8, CCR10

  UV-catalyzed Vitamin D stimulates T cell migration by inducing _____which binds w CC227 and reacts w chemokines which helps w migration
• CLA (cutaneous lymphocyte antigen)


  formed when IL-12 secreted from activated DC induces T cell expression of ____ which binds to E selectin ( rich on dermal venule)
• Skin homing molecules

  CLA, CCR4, CCR8, CCR10
• IEL t cells (intraepidermal)


  mostly CD8+ (restricted)

  direct killing of pathogens
• IL-17 and Il-22 in skin

  induce defensin and LL-37 secretion by keratinocytes and epidermal cell proliferations
• Th1 and Th17 in Skin

  important for defense against intracellular and extracellular microbes
• Dermal T cells

  CD4+ and CD8+ express markers of typical activated or memory cells

  Th1, Th2 Th17 and Treg
• Langerhans cells


  tissue specific epidermal dendritic cells

  -langerin -antigencapture receptor that forms birbeck granules
• Keratinocytes


  provide innate immunity barrier by acting as innate immune cells and express most of the TLRs and NLRS and secrete antimicrobial peptides ( AMPs; B-defensins and cathelicidin LL-37) produce proinflammatory cytokines ( TNF-a IL-6, IL-1 and Il-33) and CCL27 to recruit CCR10+ lymphocytes to regulate cutaneous immunity
• dermis layer of skin


  contains t cells, macrophages, dendritic cells, and mast cells
• epidermis layer of skin


  contains keratinocytes, Langerhans cells, intraepithelial lymphocytes
• cellular components of cutaneous immunity


  skin

  promotes local response
• clue cells


  hallmark of bacteria vaginosis

  
• bacterial vaginosis

  shift in vagina microbiome by dybiosis of normal flora lactobacillus dominant flora to polymicrobial flora including gardnerella vaginalis

  - abnormal vaginal order (fishy) and thin grey white discharge that contain clue cells, elevated pH

  - may be asymptomatic
• microbiome of vagina

  lactobacillus, bacterial vaginosis
• gut microbiome influence on health

  composition and manipulation leads to development and prevention of human diseases

  - cardiovascular health , metabolism, autoimmunity, neurodegenerative disease and mood disorder
• gut microbiota


  large intestine and colon have the highest density of microbiota due to an anaerobic environment

  Bacteroidetes( most abundant) - bacteriodes spp.

  potential pathogens can cause GI problems and disease
• breath test of h.pylori

  if present urease activity generates ¹³CO₂ or ¹⁴CO₂ that is detected in expelled breath - in vivo
• lab diagnosis of H.pylori

  silver staining ( warthin- starry or GMS)

  tests to detect urease activity

  
• CagA


  interferes w host cell signaling
• Ex of cytokines that are released from H.pylori

  vaculoting cytokine - associated w gene A protein (cagA) which is directly associated w gastric diseases by type 4 secretion system and induces tissue damage and inflamation
• pathology of h. pylori

  acid from H. pylori creates urease to neutralize acid to go through mucus since mucus is impermeable to acid the flagella move through the mucus and mucinase damages the mucus to allow bacteria to penetrate and releases cytokines to cause tissue inflammation and damage
• helicobacter pylori ( h. pylori)

  gram negative curved rod that is motile w multiple flagella , grows microaerophilic environment and produces low amount of superoxide dismutase and catalysts, often carried asymptomatically

  causes - gastritis, peptic ulcer, and gastric carcinoma
• microbiota in stomach

  Helicobacter pylori
• treatment and prevention of dental caries

  drilling and filling, restricting dietary sucrose, fluoride, tooth brushing and flossing
• pathogenesis of dental carries

  dietary sucrose presents leading to dental plaque formation which produces S. mutans producing glucose which polymerizes glucan creating matrix for biofilm formation and fructose that ferments lactic acid and with the addition of proteolytic enzymes it demineralizes the enamel
• Streptococcus mutans

  gram-positive aerotolerant anaerobe that do not produce catalase that synthesizes glucan from sucrose to form biofilm and ferments sugar to produce lactic acid that decalcifies tooth leading to dental caries

  - acid tolerant; apart of Streptococcus Viridians
• dental caries


  most common infectious diseases in developed countries that causes discoloration and tooth break while chewing resulting in severe throbbing pain
• erythrocin


  dye to show dental plaque
• dental plaque


  bacteria growing together in a biofilm on tooth surface composed from normal flora in mouth that protects from hazards
• Mouth pathogens

  Viridans Streptococci ( Streptococcus mutans)- dental carries

  Anerobes ( porphyromonas gingivalis) - gingivitis and periodontal disease (o2 low)

  Candida ( candida albicans) - oral thrush
• treatment of acne

  combination antiinflamamtory and antibiotics
• Pathogenesis of acne


  puberty increases androgenic hormones that increases sebum production and increased keratinization and desquamation that leads to blockage of ducts causing the acne to multiply and sebum generates FAs, peptides contributing to inflammation
• cutibacterium acnes


  gram positive bacillus rod shaped anaerobic that colonizes sebaceous glands and uses sebum as carbon source

  -stained purple

  
• sebaceous gland


  innate immune system that produces antimicrobial peptides and lipids ; anaerobic