Inflammatory Skin Conditions PDF

Inflammatory skin conditions Acne (Acne vulgaris) - Pathogenesis- caused by hyperseborrhea (increase sebum production) and abnormal follicular keratinization (small plug forms blocking pores). - Androgens and anabolic steroids increase sebum production- diet and stress can also...

Inflammatory skin conditions Acne (Acne vulgaris) - Pathogenesis- caused by hyperseborrhea (increase sebum production) and abnormal follicular keratinization (small plug forms blocking pores). - Androgens and anabolic steroids increase sebum production- diet and stress can also modulate production - Estrogen decreases sebum production by lowering androgen production - Can cause bacterial proliferation and inflammation as commensal bacteria can be trapped Atopic dermatitis (eczema) - Chronic allergic hypersensitivity disease and immune dysfunction- mediated by TH2 - Appears dry, red, cracked, itching, and weeping skin - Associated with other atopic conditions eg. asthma - Pathogenesis: 1. Acute- allergens enter damaged skin causing release of inflammatory mediators from granulocytes 2. Chronic- driven by cytokines released by T cells (causes inflammatory response) + keratinocyte dysfunction (causes lichenification-skin thickening) Contact Dermatitis 1. Irritant Contact Dermatitis - Physical or chemical agents causes direct irritation/injury - Eg. Nappy rash is caused by irritants of ammonia in urine, proteolytic enzymes in faeces, friction, and damp environment. 2. Allergic Contact Dermatitis - Immune response to small organic and inorganic allergens that can penetrate the skin - Mediated by T cell response 3. Protein contact Dermatitis - Immune response to large protein allergens which can not penetrate intact skin Cellulitis - Acute bacterial infection of the skin involving deep dermis and subcutaneous fat - Commonly caused by Streptococcus Pyogenes or Staph Aureus- must gain entry through a wound - Symptoms: ill defined lesions, red, painful, swollen, +/- systemic symptoms- fever,chills - Complications it can lead to: 1. Toxic Shock Syndrome 2. Necrotising Fasciitis Urticaria - Causes itchy wheals (hives) and/or dermal swelling (angioedema) - Can be acute (allergic, one-off) or chronic (thought to have an autoimmune component) - Pathogenesis- stimuli/trigger causes mast cell degranulation leading to release of histamine and other mediators, resulting in weals and blisters to develop Psoriasis - Excessive proliferation and differentiation of keratinocytes - Chronic - Pathogenesis- Stimuli/trigger damages keratinocytes which go to the lymph node and activates T cells. This leads to a release in cytokines which activate keratinocytes and inflammatory mediators (neutrophils, mast cells, macrophages) causing dermal hyperplasia and impairing keratinocyte differentiation- leading to plaque formation.. - Lesions appear variable, sharp, red, scaly, pustules (pus filled bumps) Infectious skin conditions Fungal: 1. Tinea Pedis (Athlete’s foot) - Caused by T. rubrum, T.mentagrophytes, Epidermophyton floccosum - Not infectious - Grows in warm (sweaty), moist environments - Chronic, recurrent disease - More common in patients that are immune deficient and have poor circulation - Presentation is variable- dry, scaly, red, itchy, blistering ,onychomycosis (nail infection) 2. Tinea Corpis (Ringworm) - Often zoonotic - Can be acute or chronic - Appears as inflamed red patches with white healing middle- itchy - Distinguished by using Wood’s light (fungi will glow) 3. Tinea Capitis (Scalp infection) - Scalp appears inflamed, may cause hair loss - Common in school age children - Caused by M. Canis - Transmissible via spores on hairbrush and clothing Viral: 1. Warts (Verruca Vulgaris) - Cutaneous tumours (benign) - Caused by human papillomavirus (HPV) - Human-human transmission, with long incubation time - Can be auto-inoculated - Must be referred if patient is elderly or immunocompromised if they have atypical warts (not normal) 2. Cold sores - Caused by Herpes simplex virus Type 1 (HPV1) - Remains latent and can be reactivated in the trigeminal nerve - Appears as red bumps, blisters, crusts and drops off within 7-10 days - HPV1 can be reactivated by: sunlight, fever, menstruation, immune suppression 3. Chickenpox - Caused by Varicella-zoster virus (VZV) - Transmitted person-person via airborne route- vesicles shed from skin - Highly contagious but self-limiting - Can be reactivated by Herpes zoster - 14-16 day incubation period- first phase is prodromal (fever, malaise, fatigue) then the rash - Appears as red bumps, fluid filled blisters which can rupture and scab Bacterial: 1. Hair follicle infections - Generally caused by S. Aureus, but can be fungal - Grows in moist and warm environments eg. groin, arm pits, scalp  - Often occurs with acne or after waxing/shaving - 3 types: 1. Folliculitis- localised, small inflamed pustules, itchy or painful 2. Boils (furunculosis)- more severe, deeper infection of one or more follicles, bigger lesions, has a central yellow plug 3. Carbuncle- great amount of necrosis and bacteria (pus), systemic symptoms, must be drained 2. Impetigo - Superficial infection of the epidermis - Caused by Staph. Aureus or Strep. Pyogenes - Highly infectious - No systemic symptoms- resolves without scarring - Transmitted person to person - Can be autoinoculated - Complications (if spread systemically)- Glomerulonephritis or Scarlet fever - 2 types: 1. Nonbullous (impetigo contagiosa- honey-coloured crust, highly contagious, often around the nose and mouth 2. Bullous- fluid filled blister- burst and crust, less contagious, occurs in armpits and neck folds (moist areas) 3. Clostridial skin infection - Bacteria are gram positive, anaerobic (lies deep), rod shape, spore forming and toxin producing - Caused by 2 bacteria: 1. C. tetani - Early symptoms- tissue infection, weakness, stiffness, cramps - Late symptoms- spasms, seizures - Produces tetanus toxin- binds to nerve endings and prevents release of GABA (neurotransmitter) and glycine- causes symptoms 2. C. perfringens - Necrotising disease - Produces α-toxin - Early symptoms- Pale skin, fluid filled blisters, discharge, gas production - Late symptoms (systemic)- severe pain, tachycardia -> progresses to hypotension and organ failure 4. Leprosy - Chronic - Minimally contagious - Caused by Mycobacterium Leprae - Long incubation time - 2 types: 1. Tuberculoid Leprosy - Non-infectious - Paucibacillary - Appears small, defined, dry, scaly lesions, slow growing, may cause hair loss - Causes some systemic nerve damage 2. Lepromatous Leprosy - Progressive - Contagious - Multibacillary - Causes systemic nerve damage but is slow to develop Mouth conditions Cold sores (Aciclovir, Valaciclovir (prodrug of aciclovir) ,Famiclovir, Cold sore patches) - Caused by Herpes simplex virus Type 1 (HPV1) - Remains latent and can be reactivated in the trigeminal nerve - Appears as red bumps, blisters, crusts and drops off within 7-10 days - HPV1 can be reactivated by: sunlight, fever, menstruation, immune suppression Mouth Ulcers (minor aphthous ulcers) (Benzydamine, Triamcinolone, Lignocaine) - It is when there is damage to the epithelium and its underlying tissue in the mouth - Not contagious - Usually painful - Heals within 1-2 weeks - Triggers include physical injury, nutritional deficiency, stress, and anxiety - If it is persistent and painless, it must be referred. Oral Candidiasis (Miconazole, Nystatin) - Fungal infection in the mouth caused by yeast Candida albicans (commensal in mouth flora) - Common in babies and older people - Common trigger is through the use of antibiotics - Risk factors include: immunocompromised, dry mouth (xerostomia, uncontrolled diabetes, regular inhaled corticosteroid therapy - If recurrent, it must be referred for further investigation Angular Cheilitis (Miconazole +/or antifungal hydrocortisone, Hydrogen peroxide, Lip balm, nutritional advice) - Inflammatory condition affecting the corners of the mouth - Does not itch or crust - Area is soggy, soft, and slow to heal due to the movement of the mouth - Lesions can sometimes become infected with bacteria (impetigo), fungus, and virus - Made worse by licking the lips - Risk factors includes: oral thrush, poor nutrition, poor fitting dentures, systemic illness (IBD, UC, CD), atopic dermatitis (eczema), genetic predisposition (down syndrome), oral retinoid treatment Dry mouth (Xerostomia) (Pilocarpine- stimulates large amount of saliva and sweat) - Variety of causes: dehydration, sleeping with mouth open, Sjögren's syndrome, adverse effects of drugs, and following radiotherapy to the head and neck - Predisposed to: mouth infections (eg. oral thrush), dental caries, difficulty- eating, swallowing, talking - Dentist is best on diagnosis, management, and monitoring for this condition Ear and Eye infections Conjunctivitis - 3 types: 1. Bacterial (Treatment- Chloramphenicol, Propamidine ): affects both eyes but one is often affected first by 24-48 hours, discharge is thick and yellow, pain is sore and gritty, has no associated symptoms 2. Viral: affects both eyes, discharge is clear and watery, pain is sore and gritty, associated with cold symptoms (eg. sore throat) 3. Allergic (Treatment- Antihistamines, Mast cell stabilisers): affects both eyes, discharge is clear and watery, itchy, associated with rhinitis or history of atopy Dry Eye - Caused by deficiency or dysfunction of the tear film that keeps the eye moist and lubricated - More common in women than men - Symptoms include: feeling of dryness, grittiness, or mild pain/burning in both eyes - Otitis Externa - Inflammation of the external auditory meatus (EAM) - Can be caused by water, humidity, heat, and moisture making the EAM more prone to infection - Ear Wax Implication - When there is a build up of ear wax - Common in patients that are: elderly, have narrow ear canal, learning difficulties, and fitted hearing aids - Symptoms include: gradual hearing loss and ear discomfort - Refer if there is any itching, tinnitus, dizziness, systemic symptoms (eg. fever), associated trauma, and foreign objects in the EAM Infestations + Insects Scabies - Spread of scabies mite through skin-skin contact with a person who has scabies or through shared bedding or clothing - Symptoms itchiness, red bumps, rash- starting 3-6 weeks after infestation Head lice - Small insects which can live on human scalp/ hair and feed by sucking blood from the scalp - Transmitted person-person from someone who has head lice already Insect bites - Insect pierces the skin to feed on blood - Symptoms of intense itching, redness, or blistering - Eg. Mosquitos, bed bugs, sandflies Insect stings - Insect or vertebrae injects toxin and painful poison (venom) through its stinger - Symptoms of pain, redness, swelling in the area - Eg. bees, wasps, spiders, jellyfish GI conditions Inflammatory Bowel Disease: - Pathogenesis: believed to be caused by dysbiosis (decrease in peacekeeping bacteria) of the microbiota along with genetics that impacts barrier function and immune system. - Proinflammatory response governed by Th17, anti inflammatory response governed by Treg cells - Onset is within 15-40 years of age - Idiopathic - 2 types: 1. Ulcerative Colitis - Pathogenesis: Trigger causes APC to present antigen to T(helper) cells which secrete IL4 and produces TH2 cells- recurites cell adhesion molecules (integrins) which are important in infiltration of leukocytes eg. lymphocytes, monocytes leading to an immune response - Smoking and appendectomy (removal of appendix) is a protective factor - Inflammation affects the colon only - Continuous inflammation from the rectum to the proximal parts of the colon - Inflammation is superficial - Symptoms: diarrhoea (bloody), abdominal cramping, anaemia, weight loss, and fatigue - Complications: severe bleeding, toxic megacolon, rupture of the bowel, and colon cancer - Smoking is a protective factor 2. Crohn’s Disease - Pathogenesis: Trigger causes APC to present antigen to T(helper) cells which secrete IL-12 and IL-18 and causes production of TH1 cells- releasing TNF-α and INFγ leading to recruitment of macrophages who in turn positively regulates Th1 Cells via. secretion of INFγ and TNFα - Inflammation affects distal ileum and colon - Discontinuous patchy gut inflammation with skip lesions - Transmural (affects all layers of the bowel) - Smoking is risk factor - Symptoms: diarrhoea, abdominal cramping, fever, anaemia, weight loss, and fatigue - Complications: stenosis, abscess formation, fistulas, and colon cancer Coeliac Disease - Inflammatory disease in the small intestine triggered by gluten - Gluten is difficult to digest due to how it is broken down into gliadins and glutenins which has high proline and glutamine content - Genetic influence/ dysfunction in MHC class-II (HLA-DQ2, or DQ8) which presents epitopes of gluten to T-cells more greatly - Pathophysiology: Mucosal permeability is impacted (decreased barrier function) and allows gluten peptides to enter. Tissue transglutaminase 2 (TTG) then deamidates this and are sensed by APC which present HLA-DQ2,DQ8 to T-cells- leading to inflammation - Characterised by damage to the villi and nutrient malabsorption - Symptoms of diarrhoea, nausea and vomiting. Malnutrition symptoms include fatigue, anaemia, and joint/bone pain and depression Gastric acid secretion Process: - Parietal cells- contain proton pump (H+/K+ ATPase) which secrete H+ and Cl- separately (produce acid) - Chief cells- produce pepsinogen which gets converted into pepsin in the present of HCl- important for breaking down protein in food - Goblet cells- produce mucin (mucus)- provides protection - 3 phases: 1. Cephalic: Stimuli (sight, smell, taste, or thought of food) is processed by the brain and activates enteric neurons via parasympathetic preganglionic neurons which travel down the vagus nerve (efferent). As a result, acid will be prepared and ready to break down food. 2. Gastric: Food stretches the walls of the stomach and is sensed by mechanoreceptors which activates a neural reflex to stimulate acid secretion. Peptides and amino acids in food also stimulate G cells to secrete gastrin to further produce acid. 3. Intestinal: Munched up food (chyme) enters the duodenum, where it activates a negative feedback system from which somatostatin (SST) is released from antral D cells, which inhibit gastric acid secretion. Peptic Ulcer Disease - A sore that develops when pepsin and bile overwhelm defensive factors of the gastrointestinal mucosa - Symptoms: burning stomach pain (dyspepsia/ indigestion), nausea, belching/bloated - Main causative factor is the presence of H.pylori which 1. Breaks down the protective mucous layer via exotoxins, inflammatory mediators, proteases, etc…, that the bacteria produces 2. Increases gastric secretion - Other causative factors: smoking, excess alcohol, genes, and NSAID use - Red flags: vomiting blood/ coffee grounds, black or tarry stools, unexpected weight loss, severe +sharp sudden pain - Diagnosed by 1. Faecal antigen test, widely available in NZ, can’t be used in patients who have taken PPI or antibiotics 2. Urea breath test- non invasive, is expensive and unfunded 3. Biopsy (endoscopy)- accurate as it provides material and can be used to test cultures, very invasive GORD (Gastro Oesophageal Reflux Disease) - Reflux of gastric acid into the oesophagus - Chronic - Symptoms: heartburn (dyspepsia), belching/ bloated, acid taste - Can develop to oesophagitis - Red flags: >50 yrs (risk of gastric cancer), severe and persistent dyspepsia, signs and symptoms of GI bleeding Zollinger's-Ellison Syndrome - Is when there are pancreatic or duodenal gastrinomas that stimulate large production of acid which damages the gut mucosa- leading to severe gastroduodenal ulceration and hypochlorhydria (low pH) Haemorrhoids - Occurs when vascular-rich connective tissue becomes engorged or swollen - Common among elderly - More common in men than women - Categorised as either: 1. Internal: inside rectum, usually not painful 2. External: visible and felt around the anus (firm grape) - Multifactorial (caused by multiple factors): 1. Anatomical: degeneration of elastic connective tissue due to ageing 2. Physiological: heavy lifting, obesity, childbirth, chronic diarrhoea 3. Mechanical: straining and prolonged sitting which interferes with blood flow to and from rectal area - Symptoms of external haemorrhoids: bright red blood seen when wiping, uncomfortable feeling of fullness in the anus, irritation and itching, extra skin + small lump around the anus - Internal haemorrhoids are asymptomatic - Red flags: symptoms lasts longer than 3 weeks, sharp stabbing pain, large volume of blood, people >50yrs complaining of change in bowel habit (must rule out carcinoma) Threadworms  - Belongs to the Phylum Nematoda - Small, thin, white worms between 2 mm and 13mm long - Lives in the bowel - Transmitted via self infection (ingestion of eggs) or human to human via contaminated clothes and bed linen - Symptoms include: itchy anal region (worst at night), teeth grinding, bed wetting, insomnia (due to disturbed sleep), loss of appetite, abdominal pain (mostly asymptomatic) - Red flags are: pregnant/ breast feeding women, 50%) Enveloped? Not Yes Yes Constipation - Infrequent defecation 50yrs Diarrhoea - An increase in frequency of stool, looseness of stool or both, compared to the person’s usual bowel habit - 3 types: 1. Osmotic- something in bowel is drawing water from the body into the bowel 2. Secretory- body is releasing water into the bowel when it is not supposed to 3. Exudative- presence of pus and blood in the stool eg. IBD - Common causes can be: viral and bacterial infections, medications (ADR), medical conditions (IBD or Coeliac), allergies, intolerance, radiation therapy, anxiety or stress - Vulnerable patients: elderly and children (prone to dehydration) - Red flags: >10 runny bowel motions in one day, blood or mucus in bowel motions, signs of severe dehydration, overseas travel, or possible medication cause Vomiting - Regulated by 2 components: 1. Chemoreceptor Trigger Zone (CTZ): lies close to the BBB and is relatively permeable therefore circulating mediators can act directly- this means it can receive input from drugs and hormones and can communicate with the vomiting centre. This also regulates motion sickness 2. Vomiting centre: - Sends signals to: 1. Vagus nerve- acts on oesophagus, stomach, duodenum 2. Phrenic nerve- acts on diaphragm 3. Spinal nerve- acts on abdominal rectus, intercostals - 3 factors can trigger vomiting: 1. Emetic stimuli: chemicals or drugs in blood or neuronal input from the GIT, labyrinth and CNS - Emetic factors: Chemotherapy, digoxin, opioids, NSAIDs, antibiotics - Other: Odour, smell, noxious stimuli (visual or physical) - Motion sickness 2. Pathways and mediators: Impulses from CTZ and other CNS centres are relayed to the vomiting centre. Mediators include chemical transmitters eg. histamine 3. Enkephalins: might at on delta (CTZ) or mu (vomiting centre) opioid receptors + endocannabinoids - Red flags: 1. Long duration/length 2. Elderly and infant patients 3. Possible medication cause 4. Recent overseas travel Food poisoning - It is when there is ingestion of a large number of bacteria + bacterial toxins in food - NOT an infection - Rapid onset with short duration (24hrs) - Causes violent diarrhoea, vomiting, cramps, but no fever - Caused by pathogens: 1. Staph. A 2. Clostridium Perfringens + Botulinum 3. Vibrio parahaemolyticus + Vulnificus- (Marine bacteria) GI Infections - Long incubation (days) - Long disease progression - Systemic (causes fever) - Main symptom is diarrhoea - Caused by: 1. Campylobacter Jejuni 2. Yersiniosis 3. Shigella 4. Listeriosis 5. Salmonella 6. E. Coli: - ETEC (enterotoxigenic): travellers diarrhoea - EPEC (enteropathogenic): infant diarrhoea - EHEC/ STEC (enterohaemorrhagic): causes bloody diarrhoea - EIEC (enteroinvasive) - EAEC (enteroaggregative) Antibiotic Associated Diarrhoea - Caused by removal of normal microflora and proliferation of pathogens - Common drug adverse event - No damage to the GIT MSK conditions Osteoarthritis - Chronic joint disease that leads to destruction and immobility of joints - 2 types: 1. Primary- most common, no predisposing factors 2. Secondary- pathologically the same as primary, caused by- obesity, diabetes, RA - Common in patients >55 years old - Risk factors include: age, gender, obesity, injury, occupation (heavy lifting), injury, and muscle weakness - Non-symmetric - Morning stiffness 60 mins - Worsens with inactivity, improves with activity - Pathogenesis 1. Exposure to genetically susceptible host to an unknown antigen 2. APC activate T cells (MHC II- CD4+ T) which leads to the activation of B cells 3. Proinflammatory cytokines are released eg. TNF-α by macrophages - leading to joint inflammation  4. Proinflammatory cytokines cause macrophages and fibroblasts to release matrix metalloproteinases (MMPs) which degrade cartilage 5. Proinflammatory cytokines cause fibroblasts to release RANKL which activates osteoclast and lead to bone destruction 6. Pannus is formed which defined as a hypertrophied synovial tissue with inflammatory cells, cytokines and fibroblasts growing over articular cartilage causing erosion Gout - Caused by deposition of monosodium urate acid crystals in joint spaces or surrounding tissue- due to raised total body uric acid concentration - Factors: increased in uric acid production (10%) or decreased renal clearance (10%) - Genetic influence: GLUT9 polymorphism- increase GLUT9 transporter which absorbs more uric acid, common among Maori and Pasifika - Acute attack lasts 2-5 days - Chronic (life long) - Symptoms: intense pain, erythema, and joint swelling (inflammation)- LOCALISED - Complications: tophi, kidney stones, joint + kidney damage if untreated - More common amongst men than women - Non-symmetrical - No morning stiffness - Often affects the first metatarsophalangeal joint of big toe Pseudo Gout (CPPD)  - Arthritis caused by the accumulation of calcium pyrophosphate crystals - Symptoms of fever and chills - NO TREATMENT Osteomyelitis - Infection of the bone - Can be acute or chronic - Risk factors: 1. Use of indwelling catheter and IV drugs 2. Poor vascularity eg. poorly controlled diabetes, PVD (Peripheral Vascular Disease) 3. Immunocompromised 4. Sickle cell disease 5. 80yrs 3. Diabetes 4. Prosthetic joints 5. Recent joint surgery 6. Prior intra articular corticosteroid injection 7. Alcoholism 8. IV drug use - Symptoms: 1. Swelling, tenderness, pain, warmth, restricted movement 2. Single joint involved 3. Febrile (symptoms of fever)- less common in elderly Reactive arthritis - An arthritis that develops soon after or during an infection somewhere else in the body - Common among 20-50yrs men - Pathogens: gram negative bacteria - Symptoms: 1. Musculoskeletal - Peripheral arthritis: often in knees, some polyarthritis in small joints - Enthesitis: Inflammation of ligaments and tendons of the joint capsule - Dactylitis: Sausage digits (swelling in toes), common if chlamydia induced - Back pain 2. Extra articular - Ocular: conjunctivitis - GI: diarrhoea - Oral lesions- ulcers - Skin changes - Nail changes similar to psoriasis - Cardiac issues (rare): valve disease - Dysuria Osteoporosis - A progressive skeletal disorder characterised by low bone density, impaired bone architecture, and compromised bone strength leading to an increased risk of bone fractures - Most common amongst postmenopausal woman- as oestrogen levels drop (>65yrs), older men (75yrs), and those taking long term oral corticosteroids (glucocorticoids) - Regulators: 1. Oestrogen: - increases osteoblast proliferation - inhibit apoptosis (cell death) - augments production of TGF-beta (responsible for bone formation and resorption) 2. Parathyroid hormone is a regulator calcium: - Mobilises calcium from bone - Promote reabsorption of calcium by kidneys (reduce excretion) - Stimulates synthesis of calcitriol which increases calcium absorption from the intestines - Promotes excretion of phosphate 3. Calcitonin: - Inhibits bone resorption by binding to osteoclasts and inhibiting their action - Decreases reabsorption of calcium and phosphate in proximal tubules 4. Vitamin D: - 2 sources: 1. Sunlight (ergocalciferol) 2. Diet (colecalciferol -> calcifediol in liver -> calcitriol (most potent product) in kidney - Promotes maturation and activity of osteoclast - Promotes bone formation 5. Glucocorticoids - Required for osteoblast differentiation but excess can inhibit it - May stimulate osteoclast activity 6. Thyroxine - Stimulates osteoclast activity which reduces bone density and liberates calcium  - DEXA scan is gold standard for diagnosing- assess bone density - T score -1.0 - Complications: more fractures in the future, chronic pain, immobility, loss of independence, reduce QoL. Pain - Defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage - 4 categories: 1. Acute- short period 3 months, pain does not go away after injury or illness 3. Cancer- caused by tumour- cancer grows and spreads causing pain on surrounding tissue eg. nerves bones, spinal cord, organs 4. Phantom- pain comes from a body part that is no longer there - 2 sources of pain: 1. Somatic- act on skin, muscles, connective tissue, bone, and joints 2. Visceral- act on intestines - 4 types of pain: 1. Nociceptive (tissue damage) - Visceral pain described as cramping, squeezing, pressure - Somatic pain described as aching, deep, dull, gnawing- well localised 2. Neuropathic - Abnormal sensations caused by either: 1. Hyperaesthesia- increased sensitivity to stimuli 2. Hyperalgesia- increased response to stimulus that is normally painful 3. Allodynia- pain caused by a stimuli that is not normally painful  - Pain described as neuralgia (shooting, sharp), paresthesia (tingling, pins and needles), and tightness 3. Mixed category 4. Central pain - Processes: 1. Transduction: eg. something has broken skin or tissue where nociceptors pick this up and use fibres to send signals (action potential) to the dorsal spinal cord via A (fast) and C (slow) fibres 2. Transmission: Excitatory neurotransmitters are activated which continues the action potential towards the brain 3. Perception: Action potential has arrived in the brain where the: - Limbic system: makes you think how to feel about pain - Sensory cortex: decides location of pain, type, and intensity (how sore) - Thalamus: might activates motor response to move away from the pain 4. Modulation: neurotransmitters (eg. endorphins and enkephalins) are sent via the efferent pathway to the spinal cord and blocks the afferent pathway from being from being transmitted (prevents step 3 from occurring)