Caleb - Unfinished Disorder Notes PDF

Disorders Integumentary, Skeletal, and Muscular Integumentary System Burns (a.vi) Treatment Allergens (a.vi) ? (see contact dermatitis) HPV (a.vi) "non-oncogenic" (wart-causing) "oncogenic" (cancer-causing) Most HPV infections (9 out of 10) go away by themselves within 2 years. But...

Disorders Integumentary, Skeletal, and Muscular Integumentary System Burns (a.vi) Treatment Allergens (a.vi) ? (see contact dermatitis) HPV (a.vi) "non-oncogenic" (wart-causing) "oncogenic" (cancer-causing) Most HPV infections (9 out of 10) go away by themselves within 2 years. But sometimes, HPV infections will last longer and can cause some cancers. HPV infections can cause cancers of the: ○ Cervix, vagina, and vulva ○ Penis ○ Anus ○ Back of the throat (called oropharyngeal cancer), including the base of the tongue and tonsils Cutaneous types cause “warts” on the hands and feet Cutaneous HPVs can cause warts on top of the skin in areas such as hands, feet, arms, and legs. These are common warts that are only on the skin. NOT the same as genital warts ○ Genital ones are “cauliflower-shaped” HPV (a.vi) Common wart treatments: ○ Topical (applied to the skin) chemicals – such as salicylic acid or lactic acid. ○ Cryotherapy – the warts are frozen with liquid nitrogen. It may take up to four months of regular cryotherapy to get rid of the warts. ○ Currettage and electrocautery – a surgical procedure performed under local anaesthesia. Wart curettage is a surgical procedure that involves removing a wart by scraping it off with a sharp knife or a small, spoon-shaped tool called a curette ○ Laser therapy – a laser is used to burn off the warts. Scarring may occur. Boils (a.vi) Furuncles (boils) are skin abscesses caused by staphylococcal infection, which involve a hair follicle and surrounding tissue. Furuncles are common on the neck, breasts, face, and buttocks. They are uncomfortable and may be painful when closely attached to underlying structures (eg, on the nose, ear, or fingers). Appearance is a nodule or pustule that discharges necrotic tissue and sanguineous pus. Treatment ○ Drainage ○ Often antibiotics effective against MRSA Carbuncles (a.vi) Carbuncles are clusters of furuncles connected subcutaneously, causing deeper suppuration and scarring. clusters of furuncles that are subcutaneously connected. They may be accompanied by fever. Treatment ○ Drainage ○ Often antibiotics effective against MRSA Athlete’s foot (a.vi) AKA Tinea pedis Fungal infection of the foot Signs and Symptoms: ○ Scaly, peeling or cracked skin between the toes ○ Itchiness, especially right after taking off shoes and socks ○ Inflamed skin that might appear reddish, purplish or grayish, depending on your skin color ○ Burning or stinging ○ Blisters Causes: contagious; damp socks and shoes and warm, humid conditions favor the organisms' growth. ○ Frequently wear enclosed footwear ○ Sweat heavily ○ Share mats, rugs, bed linens, clothes or shoes with someone who has a fungal infection ○ Walk barefoot in public areas where the infection can spread, such as locker rooms, saunas, swimming pools, communal baths and showers Treatment: prescription-strength cream or ointment, such as clotrimazole, econazole (Ecoza) or ciclopirox (Loprox) Impetigo (a.vi) superficial skin infection with crusting or bullae caused by streptococci, staphylococci, or both. Nonbullous - clusters of vesicles or pustules that rupture and develop a honey-colored crust (exudate from the lesion base) over the lesions. Smaller lesions may coalesce into larger crusted plaques. Bullous - vesicles typically enlarge rapidly to form bullae. The bullae burst and expose larger bases, which become covered with honey-colored varnish or crust. Treatment ○ Topical mupirocin, retapamulin, fusidic acid, or ozenoxacin ○ Sometimes oral antibiotics Hansen’s Disease (a.vi) AKA leprosy Mycobacterium leprae and Mycobacterium lepromatosis Spreads through droplets ○ you must have prolonged, close contact with someone with untreated Hansen's disease over many months to catch the disease Skin symptoms ○ Discolored or lighter patches of skin ○ Nodules on the skin ○ Thick, stiff, or dry skin ○ Painless ulcers on the soles of feet ○ Painless swelling or lumps on the face or earlobes ○ Loss of eyebrows or eyelashes Muscle weakness or paralysis, especially in the hands and feet Enlarged nerves, usually around the elbows, knees, and side of the neck Eye problems that may lead to blindness Hansen’s Disease (a.vi) AKA leprosy Diagnosis and treatment ○ skin biopsies Treatment: antibiotics Cellulitis (a.vi) Causes ○ Skin is broken/compromised ○ Staphylococcus aureus or Streptococcus pyogenes infection Streptococci cause diffuse, rapidly spreading infection because enzymes produced by the organism break down cellular components that would otherwise contain and localize the inflammation. Group B hemolytic streptococci Symptoms ○ lower extremities; unilateral (one side) ○ Redness, increased warmth, edema (swelling) ○ Fever, chills, tachycardia may precede cutaneous findings ○ Cellulitis with rapid spread of infection, rapidly increasing pain, hypotension, delirium, or skin sloughing, particularly with bullae and fevers, suggests life-threatening infection. Treatment: ○ Antibiotics Erysipelas (a.vi) Caused ○ Group A hemolytic streptococci Symptoms ○ shiny, raised, indurated, and tender plaques with distinct margins. ○ High fever, chills, and malaise Treatment ○ oral antibiotics Chickenpox and shingles (a.vi.) Chickenpox = Varicella zoster ○ transmitted by direct contact or inhalation of material from the skin lesions. ○ Symptoms: A pustular rash then develops on the face, progresses to the trunk, and then the extremities, although most form on the trunk ( Burst → scab Infectious until all pustules have scabbed over ○ Virus moves along sensory nerve cells towards spinal cord → lay dormant (latent) for many years; triggered by stress, aging, and weak/low immune system Reactivated: move along nerves of face and trunk → painful lesions in a condition known as shingles ○ Shingles can transmit CHICKENPOX to an individual (but not shingles) Chickenpox and shingles (a.vi.) Diagnosis ○ Rash? ○ Serological and PCR testing Tx: ○ Children → nothing ○ Shingles: Acyclovir (antiviral) Prevention: ○ Vaccination prevents chickenpox in children ○ Vaccination can prevent shingles in adults who already contracted chickenpox Psoriasis (a.vi) Scaling skin condition Symptoms: ○ Lesions with distinct edges ○ **silvery scales** ○ Pitting nails (microscope “dents” in the nails) Pathophysiology/Cause ○ Proliferation/rapid production of keratinocytes ○ Endothelial cells (lining of blood vessels) hyperproliferation messes up the structure of the capillaries in the dermis → erythema (redness) ○ Innate and adaptive immune responses occur Psoriasis (a.vi) Treatment: ○ topical treatments (eg, corticosteroids, vitamin D3 analogs, calcineurin inhibitors, tazarotene, roflumilast, tapinarof, emollients, salicylic acid, coal tar, anthralin) Corticosteroids = TOPICAL ONLY; reduce inflammation Vitamin D3 reduces keratinocyte proliferation Tazarotene - keratolytic effect ○ Phototherapy UVB light reduces DNA synthesis and can induce mild systemic immunosuppression psoralen plus ultraviolet A (PUVA) antiproliferative effect and also helps to normalize keratinocyte differentiation repeated treatments may increase the incidence of UV-induced skin cancer and melanoma ○ systemic medications (eg, methotrexate, oral retinoids, cyclosporine, other immunosuppressants [biologics or small molecules]). Methotrexate - interfere with the rapid proliferation of epidermal cells ***Dermatitis (a.vi) Atopic eczema ○ A primary genetic defect in skin barrier function (loss of function variants of the protein filaggrin) Filaggrin - an essential protein for the correct formation and function of the skin barrier ○ Symptoms: itchy papules and vesicle often weepy (exudative) Chronic lesions : dry scaly itchy patches can be erythematous in paler skin or grey/ brown in richly pigmented skin Chronic scratching/rubbing leads to lichenification ○ Treatment: General measures - avoid known exacerbating agents, frequent emollients/lotions Topical therapies – topical steroids for active areas; topical immunomodulators Oral therapies - antihistamines for symptomatic relief, antibiotics ***Dermatitis (a.vi) Contact Dermatitis ○ Irritant - acute toxic insult (e.g. exposure to acids) or by cumulative damage from irritants (e.g. water, soaps, detergents, solvents and diluted acids or alkalis). ○ Allergic - type IV (cell-mediated or delayed) hypersensitivity; 1st contact causes no problems but each next contact causes more and more symptoms nickel, chromate, rubber and fragrances. ○ Symptoms: Irritant: well demarcated rash with a glazed surface, but there may be redness, itching, swelling, blistering and scaling of the damaged area. Allergic - redness, blistering, edema (swelling), dryness, crusting, ○ Treatment: Avoidance of irritants and allergens Emollients Topical corticosteroids Oral steroids Alitretinoin (Toctino) as an oral treatment for adult severe chronic hand eczema that has not responded to potent topical corticosteroids ***Dermatitis (a.vi) Varicose/stasis dermatitis/eczema ○ Increased pressure in the legs ○ Signs and symptoms: skin becomes thin, fragile, shiny, inflamed, itchy and flaky exudating areas around the ankles Eczema all the way around the leg or in patches Purpura (purple patches) haemosiderosis (causing brown staining) ○ Treatment: Graduated compression stockings/socks Avoidance of standing for long periods Regular exercise Elevation of legs Weight loss Surgery for varicose veins ***Dermatitis (a.vi) DISHYDROTIC eczema ○ aggravated by heat and stress or could be the result of contact with irritants or allergens. ○ Signs and symptoms: tiny blisters (vesicles) appear deep in the skin of the palms, fingers, instep or toes. INTENSE ITCHING peeling, blistering ○ Treatment: Emollients Topical corticosteroids Antibiotics if infected Systemic immunosuppressive drugs or light therapy for severe cases Melanoma (a.vi) Basal cell carcinoma (a.vi) Squamous cell carcinoma (a.vi) Kaposi’s sarcoma (a.vi) Merkel cell carcinoma (a.vi) *Rosacea (a.ix) chronic inflammatory disorder characterized by facial flushing, telangiectasias, erythema, papules, pustules, and, in severe cases, phymatous changes such as rhinophyma ○ telangiectases - small, permanently enlarged blood vessels that appear as red spots on the skin or mucous membranes limited to the face and scalp 4 stages ○ Pre-rosacea: flushing and blushing, often accompanied by uncomfortable stinging ○ Vascular: develop facial erythema and edema with multiple telangiectases ○ Inflammatory: sterile papules and pustules ○ late phase: phymatous changes (skin to thicken and scar, resulting in a bumpy, swollen, and sometimes discolored appearance) Triggers: sun exposure, emotional stress, cold or hot weather, alcohol, spicy foods, exercise, wind, cosmetics, and hot baths or hot drinks. *Rosacea (a.ix) Causes: ○ A condition that affects your blood vessels, immune or nervous system. ○ Microscopic skin mites (Demodex): Your body has a natural, microscopic mite that lives on your nose and cheeks. Having too many of these mites causes symptoms of rosacea. ○ An infection: The H. pylori bacteria can cause an infection. Studies suggest that people who had this infection can develop rosacea. ○ A protein malfunctioning: The cathelicidin protein protects your skin from infection. If the protein isn’t working as it should, you’ll experience symptoms of rosacea. Treatment ○ Avoidance of triggers ○ Consideration of topical or oral antibiotics or topical azelaic acid or ivermectin ○ topical brimonidine or oxymetazoline and sometimes oral beta blockers ○ For rhinophyma, consideration of dermabrasion, laser ablation, and tissue excision Vitiligo (a.ix) Bullous pemphigoid (a.ix) specific inflammatory reaction Detachment of epidermis from dermis subepidermal vesiculation IgG and C3 ○ IgG - highest opsonization and neutralization activities Opsonization “coating” ○ The binding of the IgG antibodies to the basement membrane zone leads to the complement cascade→ inflammation ○ Complement fragments induce mast cell degranulation and attract neutrophils Degranulation → releases histamines (causes inflammation) + enzymes Bullous pemphigoid (a.ix) large, tense blisters on arms, legs, and trunk Pruritus = itching Treatment ○ Corticosteroids → reduce inflammation Oral or ointment Erythema multiforme (a.ix) acute, recurring, inflammatory disorder of the skin and mucous membranes deposition of C3, IgM, and fibrinogen CAUSES: ○ Herpes simplex viral infection and reactions to medications T-cell–mediated cytolytic reaction to HSV DNA fragments present in keratinocytes ○ vacuolated keratinocytes (full of holes) in the basal layer of the epidermis ○ CD4 and CD8 T lymphocytes ○ After this recruitment, keratinocytes are injured and killed by the combined negative influences of cytotoxicity and cytokines, such as interferon-y and TNE Symptoms: ○ RED macules, papules, wheals, vesicles, bullae, or a combination on the distal extremities (often including palms and soles) and face ○ “bull’s eye” lesion Treatment: ○ Antivirals to treat the HSV ○ Antihistamines Stevens-Johnson syndrome (a.ix) expressed in children and young adults altered medication metabolism (body cannot break down medications correctly/completely) Symptoms: ○ malaise, fever, headache, cough, and keratoconjunctivitis ○ Macules in target configuration on the face, neck, and upper trunk. ○ Merge into large flaccid bullae ○ large sheets of epithelium slide off the entire body at pressure points (Nikolsky sign), exposing weepy, painful, and erythematous skin. triggers a T-cell–mediated cytotoxic reaction ○ Cytotoxic → cytotoxic T-cells (killers) → release granulysin → keratinocyte death Treatment ○ Cyclosporine - inhibits CD8 cells ○ Plasmapheresis can remove reactive drug metabolites or antibodies and can be considered. ○ Early high-dose IVIG ***Erythema nodosum (a.ix) Type of panniculitis, which is inflammation of the subcutaneous fat Causes ○ Streptococcal infections Or other bacteria, fungi, or viral infections ○ Sarcoidosis ○ Inflammatory bowel disease Signs and Symptoms ○ purple, tender nodules or plaques on anterior/front of the lower legs Diagnosis ○ incisional wedge biopsy of a nodule Treatment ○ Anti-inflammatory medications (but not corticosteroids) ○ bed rest, elevation, cool compresses ○ Potassium iodide **Alopecia (a.ix) loss of hair from the body ○ Scarring alopecia is the result of active destruction of the hair follicle. ○ Nonscarring alopecia results from processes that reduce or slow hair growth without irreparably damaging the hair follicle. Causes: Androgenetic alopecia ○ androgen-dependent hereditary disorder in which dihydrotestosterone plays a major role. Treatment ○ Minoxidil ○ Finasteride - inhibits 5-alpha-reductase enzyme, blocking conversion of testosterone to dihydrotestosterone ○ Dutasteride - inhibits 5-alpha-reductase enzyme as well ○ Low-level laser light therapy - promotes hair growth ○ Autologous platelet-rich plasma - ontain growth factors that promote hair follicle growth and maintenance ○ Albinism (a.x) ***Xeroderma pigmentosum (a.x) the skin and tissue covering the eye to be extremely sensitive to ultraviolet (UV) light Causes: ○ Genetic ○ the body does not fix the damage to DNA done by UV light from the sun ○ the skin gets very thin and patches of varying color (splotchy pigmentation) appear Signs and symptoms ○ Sunburn that does not heal ○ Blistering after just a little bit of sun exposure ○ Spider-like blood vessels under the skin ○ Patches of discolored skin that get worse, resembling severe aging ○ Crusting, scaling of the skin ○ Oozing raw skin surface ○ Discomfort when being in bright light (photophobia) ***Xeroderma pigmentosum (a.x) Diagnosis ○ Skin biopsy in which skin cells are studied in the laboratory ○ DNA testing for the problem gene Treatment ○ total protection from sunlight, sunlight from windows, and from fluorescent bulbs High SPF sunscreen Sunglasses Long sleeved shirts and long pants ○ retinoid cream (to prevent skin cancers) acanthosis nigricans associated with cancer can be of rapid onset and particularly widespread. Acquired ichthyosis or pruritus without a clearly associated dermatitis may indicate occult cancer, often lymphoma. GI cancer Polycystic ovarian syndrome Diabetes Mellitus Calluses and Corns Corns consist of a sharply circumscribed keratinous plug, pea-sized or slightly larger, which extends through most of the underlying dermis. An underlying adventitial bursitis may develop. Hard corns occur over prominent bony protuberances, especially on the toes and plantar surface. Soft corns occur between the toes. Most corns result from poorly fitting footwear, but small seed-sized corns on non–weight-bearing aspects of the soles and palms may represent inherited keratosis punctata. Corns may be painful or tender when pressure is applied. A bursa or fluid-filled pocket sometimes forms beneath a corn. Calluses lack a central plug and have a more even appearance. They usually occur on the hands or feet but may occur elsewhere, especially in a person whose occupation entails repeated trauma to a particular area (eg, the mandible and clavicle of a violinist). Calluses are usually asymptomatic but, if friction is extreme, may become thick and irritated, causing mild burning discomfort. Calluses and Corns Treatment ○ Manual removal A nail file, emery board, or pumice stone used immediately after bathing is often a practical way to manually remove hyperkeratotic tissue. ○ Keratolytics (eg, 17% salicylic acid in collodion, 40% salicylic acid plasters, 40% urea) can also be used, taking care to avoid applying the agents to normal skin. Normal skin may be protected by covering it with petrolatum before application of the keratolytic. ○ Biomechanics soft, well-fitting shoes are important; roomy toe box so that toes can move freely in the shoe. Pads or rings of suitable shapes and sizes, moleskin or foam-rubber protective bandages, arch inserts (orthotics), or metatarsal plates or bars may help redistribute the pressure. ○ Birthmarks Types ○ Vascular birthmarks happen when blood vessels don't form correctly. Either there are too many of them or they're wider than usual. Macular stain = salmon stain; faint red marks sometimes more visible when child cries Hemangiomas Superficial (strawberry) = raised, bright red Deep = blue (dermis) Port wine stains = like wine was spilled on an area of the body, most often on the face, neck, arms, or legs darken over time, and can thicken and feel like pebbles in middle adulthood unless treated. They never go away on their own. ○ Pigmented birthmarks are caused by an overgrowth of the cells that create pigment (color) in skin. Cafe au lait - color of coffee with milk; anywhere on the body; sometimes increase in number as a child gets older; one by itself = not a problem Birthmarks Types ○ Pigmented birthmarks (cont’d) Mongolian spots - flat, bluish-gray patches are often found on the lower back or buttocks. They are most common on darker skin, such as on children of Asian, American Indian, African, Hispanic, and Southern European descent. They usually fade — often completely — by school age without treatment. Hemangiomas ○ Cause: unknown ○ Use topical treatments and wound care for ulcerated lesions and to help prevent scarring, bleeding, and pain. ○ Unless complications are life threatening or vital organs are compromised, avoid surgery. Muscular System myasthenia gravis Cause: autoimmune response to the acetylcholine receptors on skeletal muscle cells (body thinks that the acetylcholine receptors are foreign and therefore makes antibodies against them; when the antibodies bind to the receptors, they block the acetylcholine from binding to the receptors→ the muscle never receives the signal to contract) Signs and symptoms ○ Ptosis - drooping eyelid ○ Diplopia - double vision ○ Muscle weakness after use of the affected muscle myasthenia gravis Treatment ○ Anticholinesterase medications to relieve symptoms Breaks down the enzyme acetylcholinesterase → acetylcholine remains in the cleft for longer ○ Immunosuppressants (eg, corticosteroids) ○ IV immune globulin [IVIG] or plasma exchange IVIG = putting “dummy” antibodies into the blood to “trick” the immune system into detectung high levels of antibodies and therefor slowing/stopping the production of more Plasma exchange = taking out all substances from the plasma except RBC and platelets (which means antibodies will also be removed) ○ Sometimes thymectomy ○ Supportive care Lambert-Eaton myasthenic syndrome Cause: the immune system attacks the calcium channels on nerve endings that are required to trigger the release of chemicals (acetylcholine). With fewer calcium channels, the nerve ending releases less acetylcholine. ○ In about 50 to 60 percent of cases - underlying disease; small cell lung cancer. ○ the body's attempt to fight the cancer inadvertently causes it to attack nerve endings because cancer cells share some of the same proteins as nerve endings. Signs and symptoms: ○ weakness in the upper legs and hips, leading to difficulty walking, and weakness in the upper arms and shoulders ○ weakness of the eye muscles and those involved in talking, swallowing, and chewing ○ autonomic (involuntary) nervous system dysfunction (dry mouth is the most common symptom) Lambert-Eaton myasthenic syndrome Treatment ○ Potassium channel blockers Potassium channel blockers allow the electrical activity that passes through the neuromuscular junction to continue for a longer period, thereby increasing calcium influx into the nerve ending and the release of acetylcholine. ○ Cholinesterase inhibitors ○ intravenous immunoglobulin (IVIG) and plasma exchange LAB TEST: Erythrocyte Sedimentation Rate Erythrocyte sedimentation rate (ESR) is a blood test. It measures how quickly erythrocytes, or red blood cells, separate from a blood sample that has been treated so the blood will not clot. During this test, a small amount of your blood will be put in an upright tube. A lab specialist will measure the rate that your red blood cells settle toward the bottom of the tube after 1 hour. If you have a condition that causes inflammation or cell damage, your red blood cells tend to clump together. This makes them heavier, so they settle faster. The faster your red blood cells settle and fall, the higher your ESR. A high ESR tells your healthcare provider that you may have an active disease process in your body. C-reactive protein C-reactive protein (CRP) is produced by the liver. The level of CRP rises when there is inflammation in the body. It is one of a group of proteins, called acute phase reactants that go up in response to inflammation. The levels of acute phase reactants increase in response to certain inflammatory proteins called cytokines. These proteins are produced by white blood cells during inflammation. polymyalgia rheumatica Associated with giant cell arteritis ○ Giant cell arteritis - autoimmune disorder in which macrophages and T-cells migrate to the walls of arteries and form giant cells → causes inflammation of artery wall Signs and symptoms ○ bilateral proximal aching of the shoulder and hip girdle muscles and the back (upper and lower) and neck muscles ○ Morning stiffness, sometimes severe ○ Shoulder symptoms reflect proximal bursitis Treatment ○ Prednisone - corticosteroids; As symptoms subside, corticosteroids are tapered to the lowest clinically effective dose ○ Interleukin (IL)-6 inhibitor polymyositis Causes: idiopathic inflammatory myopathies; inflammatory cells of the immune system directly attack muscle fibers Signs and symptoms ○ Bilateral proximal weakness of shoulders, upper arms, hips, thighs and neck muscles ○ trouble extending their knees, stepping down or climbing stairs, or experience increasing difficulty in activities such as getting up from a chair, carrying groceries, lifting a gallon of milk, or picking up their children Treatment ○ Immunosuppressants: Glucocorticoids (Prednisone) dermatomyositis Causes: humoral mediated attack directed against the muscle capillaries and the endothelium of arterioles ○ Complement proteins get activated (when they’re not supposed to) and form the MAC (membrane attack complex) on the artery walls; deposits on vascular walls and causes inflammation ○ Lack of O2 → atrophy of muscle fibers, esp the ones most remote and far away from the vascular supply Signs and symptoms: ○ A reddish or purplish rash (heliotrope eruption) on the upper eyelids, nose, cheeks, forehead or scalp (flakiness is not uncommon). shoulders and upper back, resembling a shawl V-shape on chest ○ Muscle weakness dermatomyositis Treatment ○ Glucocorticoids, particularly prednisone ○ Intravenous immunoglobulin (IVIG) botulism Cause: ○ Clostridium botulinum releases a toxin that IRREVERSIBLY blocks the release of acetylcholine in neuromuscular junctions. ○ Foodborne botulism - homemade foods that have been improperly canned, preserved, or fermented; toxin has been made BEFORE ingestion ○ Infant botulism - botulism endospores are consumed; toxin is made AFTER ingestion ○ Wound botulism - if the spores get into a wound ○ Iatrogenic - too much botulinum toxin is injected for cosmetic reasons Signs and symptoms ○ Dry mouth ○ Blurred or double vision ○ Drooping eyelids ○ Slurred speech ○ Dysphagia ○ Muscles of respiration and of the extremities and trunk progressively weaken in a descending pattern. botulism Treatment: ○ ANTITOXIN Antitoxin does not inactivate toxin that is already bound at the neuromuscular junction; therefore, preexisting neurologic impairment cannot be reversed rapidly. antitoxin may slow or halt tetanus Clostridium tetani ○ peripheral nerve endings, binds there irreversibly, then travels retrograde along the axons and synapses, and ultimately enters the central nervous system (CNS). ○ unopposed muscle stimulation by acetylcholine ○ Once bound, the toxin cannot be neutralized. ○ Spores of Clostridium tetani are common in the environment, including soil, dust, and manure. ○ The spores can get into someone's body through broken skin, usually through injuries. ○ Wounds contaminated with dirt, feces (poop), or saliva (spit) ○ Puncture wounds (wounds caused by an object, like a nail or needle) Signs and symptoms: ○ Jaw stiffness (most frequent) ○ Difficulty swallowing ○ Restlessness and Irritability ○ Stiff neck, arms, or legs ○ Arching of the back (opisthotonos) ○ Headache ○ Sore throat ○ Tonic spasms tetanus Treatment ○ Prevent further toxin release by debriding the wound and giving an antibiotic. ○ Neutralize unbound toxin outside the CNS with TIG. human-derived antitoxin ○ Immunize using tetanus toxoid, taking care to inject it into a different body site than the antitoxin. ○ Minimize the effect of toxin already in the CNS. ○ Benzodiazepines Block reuptake of an endogenous inhibiting neurotransmitter, gamma-aminobutyric acid (GABA) GABA inhibits action potentials (makes an action potential more difficult) Blocking the reuptake means that GABA stays in the synaptic cleft longer → binds to receptors on the muscle cells more frequently → makes it more, and more, and more difficult for an action potential to occur → prevent muscle contraction poliomyelitis Cause ○ poliovirus, is a primarily intestinal disease that, in a small percentage of cases, proceeds to the nervous system, causing paralysis and, potentially, death. ○ 1. Mouth; 2.Replicates in pharynx and GI tract; 3. High virus amounts in pharynx and stool; 4. Low virus in pharynx, but still high in stool; 5. Enters lymph, then blood, then enters CNS; 6. Anterior horns of spinal cord (motor neurons), brain stem, or motor cortex ○ cell destruction and leads to flaccid paralysis Signs and symptoms ○ Most (70 to 75%) poliovirus infections cause no symptoms ○ Minor infection: 1 to 3 days of slight fever, malaise, headache, sore throat, and vomiting, which develop 3 to 5 days after exposure ○ Poliovirus aseptic meningitis without paralysis: Patients typically have a stiff neck and/or back and headache that appear after several days of prodrome similar to minor infections. Last 2-10 days. ○ Paralytic - aseptic meningitis + hyperesthesias, paresthesias, muscle spasm, dysphagia, dysphonia, poliomyelitis Treatment ○ supportive and includes rest, analgesics, and antipyretics as needed. ○ Specific antiviral therapy is not available. ○ Avoid complications of bed rest (eg, deep venous thrombosis, atelectasis, urinary tract infection) and prolonged immobility ○ Mechanical ventilation if necessary fibromyalgia increased sensitivity to touch, the absence of systemic or localized inflammation, fatigue, and sleep disturbances. Symptoms: generalized aching (sometimes severe); widespread tenderness of muscles, areas around tendon insertions, and adjacent soft tissues; muscle stiffness; fatigue; mental cloudiness; poor sleep Causes ○ increased muscle tenderness in fibromyalgia is a result of generalized pain intolerance that is possibly related to functional abnormalities within the CNS Risk factors ○ viral illnesses, physical traumas, or emotional trauma. Certain rheumatic diseases, such as RA and systemic lupus erythematosus (SLE) fibromyalgia Treatment ○ Stretching and aerobic exercise, local heat, and massage ○ Stress management ○ Medications such as tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, GABA-ergic agents, or cyclobenzaprine ○ Nonopioid analgesics (over-the-counter pain medications such as Advil, aspirin, Aleve, Tylenol, etc) ○ Capsaicin, biofeedback, massage, hypnotherapy, chiropractic interventions, chronic fatigue syndrome Causes ○ Unknown ○ no allergic markers and no immunosuppression ○ COVID-19 infections: in some patients, COVID-19 seems to trigger typical CFS ○ low levels of IgG, abnormal IgG, decreased lymphocytic proliferation, low interferon-gamma levels in response to mitogens, poor cytotoxicity of natural killer cells ○ Recent studies have identified some genetic markers that might predispose to CFS. Signs and symptoms ○ initial viral-like illness with swollen lymph nodes, extreme fatigue, fever, and upper respiratory symptoms. ○ initial syndrome triggers severe fatigue worsens with exertion; REST DOES NOT FIX ○ Brain fog, excessive sleeping, sleep disturbances, unrefreshing sleep chronic fatigue syndrome Treatment ○ Acknowledgment of patient's symptoms ○ Sometimes cognitive-behavioral therapy ○ Sometimes graded exercise, limited to avoid a setback ○ Medications for depression, sleep, or pain if indicated Carpal Tunnel Syndrome Causes: ○ Carpal tunnel syndrome occurs when the tunnel becomes narrowed or when the tissue surrounding the flexor tendons (known as synovium) swells, putting pressure on the median nerve and reducing its blood supply. ○ This abnormal pressure on the nerve can result in numbness, tingling, pain, and weakness in the hand. ○ Activities or jobs that require repetitive flexion and extension of the wrist may contribute, but rarely. Most cases are idiopathic. ○ Risk factors include rheumatoid arthritis, diabetes mellitus, hypothyroidism, acromegaly Signs and symptoms ○ Numbness, tingling, burning, and pain - severe enough to wake people up at night ○ Occasional shock-like sensations that radiate to the thumb and index, middle, and ring fingers ○ Pain or tingling that may travel up the forearm toward the shoulder ○ Weakness and clumsiness in the hand — this may make it difficult to perform fine movements such as buttoning your clothes Carpal Tunnel Syndrome Treatment ○ Splint or brace (night and/or day) ○ Over the counter pain medications (ibuprofen or naproxen) ○ Activity changes - ergonomic corrections in holding wrist/hands ○ Steroid injections - temporary relief ○ Surgical treatment - carpal tunnel release by cutting the ligament that forms the roof of the tunnel (transverse carpal ligament) strains and sprains Strain (t = tendon) - tear in the tendons Sprains tear in a ligament Complete separation of tendon or ligament = avulsion Symptoms: ○ Tenderness, swelling, hematoma (bruising) Causes: ○ Inadequate equipment or training, inadequate warming up techniques, not allowing minor injuries to heal, excessive use and abuse Treatment: splints, RICE (Rest, Ice, Compression, Elevation) rhabdomyolysis Summary: breakdown of muscle tissue that can lead to severe organ damage/kidney failure Cause: ○ Mechanical trauma or muscle ischemia (eg, crush injuries, electric shocks, seizures, or compartment syndrome) Pathophysiology(HOW): ○ Destruction of skeletal muscle tissue leads to release of the intracellular components of myocytes into the plasma, including creatine kinase (CK), myoglobin, and various electrolytes. Myoglobinuria and electrolyte abnormalities cause end-organ complications, including acute kidney injury. Symptoms: ○ muscle pain, weakness, and reddish-brown urine Treatment: depends on the cause, depends on the damage done Duchenne muscular dystrophy Summary: lack of a muscular protein, dystrophin (which connects actin to sarcolemma), causes muscle degeneration and necrosis of muscle cells Signs and symptoms: ○ Around 3 years of age → muscle weakness and regression; waddling gait; Gower’s maneuver; weakness spreads to shoulder girdle ○ difficulty running, jumping, climbing stairs, and rising from the floor ○ Firm pseudohypertrophy (fatty and fibrous replacement of certain enlarged muscle groups, notably the calves) develops. ○ Most children need to use a wheelchair by age 12, and, if they are unsupported by mechanical ventilation, most die of respiratory complications by age 20. Treatment ○ Gentle (ie, submaximal) active exercise is encouraged for as long as possible to avoid disuse atrophy or complications of inactivity. Passive exercises may extend the period of ambulation. ○ Corrective surgery is sometimes needed, particularly for scoliosis ○ Corticosteroids ○ Gene therapy