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exam 3 patho
skin/burns, inflammation/immunity/infection; renal/bladder, neuro
| Question | Answer |
|---|---|
| scratching, swelling, infection and self-treatment may | alter appearance of skin |
| functions of skin | temp control, barrier protection, secretion/absorption, vitamin d, immunological surveillance, mirror for internal disease processes, indicator of general health |
| layers of skin | epidermis (outer), dermis (middle), hypodermis (inmost) |
| erythema | reddened skin |
| induration | hardening or thickening of skin, seen with positive tb skin tests |
| atrophy | thinning and loss of skin layers; in all tissues of body |
| bulla | large blister, in burns |
| telangiectasia | fine, irregular red lines produced by dilation of capillaries, think spider veins |
| pustule | papule filled w pus, think pimple |
| scale | fragment of dry skin, think peeling or flaking |
| scar | permanent replacement of normal skin w connective tissue, after cut heals |
| ulcer | loss of epidermal and dermal tissue, can occur outside skin tissue as stasis ulcer or in stomach tissue as peptic ulcer |
| lichenification | hardening or thickening of the skin w markings due to trauma, think little scabs from scratching too much |
| machule | defined, flat area of altered pigmentation, think freckle |
| nodule | solid lump greater than 0.5 cm in diameter, think knot on skin |
| papule | raised, well-defined lesion, less than 0.5 cm in diameter; think bug bite or cystic acne which is a bump under the skin but doesnt have pustule |
| plaque | raised, flat-topped lesion, greater than 2 cm, think eczema or psoriasis |
| vesicle | small blister, think herpes blister |
| wheals (urticaria) | transient pale, elevated papules w pink margins, think itchy allergic reaction |
| albinism | genetic disorder, lack of pigmentation |
| vitiligo | abnormalities in melanin production leading to discolored skin patches |
| melasma | appearance of dark macules on face, more common in brown-skinned women |
| lentigos | age spots |
| xerosis | dry skin, more easily bruised, damaged |
| pruritus | itching, various causes, treatment involves addressing underlying cause |
| telogen effluvium | dec growth vs rest cycle of hair, overall thinning of hair--> due to stress, nutritional deficiencies and chemical overprocessing |
| alopecia areata | sudden loss of hair in one area of scalp hair--> can reflect nutritional status or disease states |
| pitting | psoriasis |
| clubbing | chronic hypoxia |
| koilonychia (spooning) | liver and thyroid problem |
| infections | bacterial or fungal |
| paronychia | pain and swelling around paronychial fold |
| onychomycosis | fungal or yeast infection of nailfolds |
| onycholysis | infection that causes nail plate to separate from nail bed |
| hyperhidrosis | excessive sweat production, often palms, soles, axilla |
| anhidrosis | diminished sweat production |
| hidraclenitis suppurativa | clogging of apocrine glands |
| acne vulgaris | multifactoral inflammation of these glands |
| comedome | acne lesion, most common during puberty due to hormones, bacterial component (p. acnes) |
| acne rosacea | middle aged adults, rosacea=inflammatory process |
| birthmarks | present @ birth or develop during infancy |
| hemangiomas | benign tumors of blood vessels (30% of newborns) |
| port wine stains | permanent blood vessel abnormalities (0.5% population) |
| wood's light | uses uv light that causes bacterial or fungi to grow |
| skin scrapings | sample for suspected fungal lesions |
| patch testing | identify substances to which patient has developed an allergy |
| skin biopsy | performed to obtain tissue for microscopic examination |
| clinical photographs | document the nature and extent of skin condition |
| nevi (moles) | most common benign skin tumor, develop from melanocytes, irregular shape and varigated color |
| actinic keratosis | premalignant lesion, rough, scaly, red plaques |
| lentigos | premalignant skin lesion, brown spot (liver spots, age spots), benign but should be watched |
| malignant melanoma | most lethal form of skin cancer, originates in melanocytes, benign on surface but penetrates and metastasizes, uv plays role; diagnosed thru biopsy |
| malignant melanoma predictable stages | benign nevus, dysplastic nevus, radial growth phase of melanoma, vertical growth phase metastasis |
| most @ risk for malignant melanoma | fair skin, 50-100 moles, history of sunburn or indoor tanning |
| ABCDE of malignant melanoma | asymmetry, border, color, diameter, evolving |
| treatment of malignant melanoma | surgical removal of melanoma, staging, sentinel lymph node biopsy, chemotherapy |
| basal cell carcinoma | most common form of skin cancer, 90% skin cancer in US rarely metastasizes, begins as small, dome-shape bump, shiny, translucent texture, grow slowly and deeply; diagnosed thru biopsy |
| treatment of basal cell carcinoma | cured w surgery |
| squamous cell carcinoma | risk inc w age/uv exposure; appears red, crusted, or scaly patch, maybe non-healing ucler or firm, red nodule; may develop from actinic keratosis |
| diagnosis and treatment of squamous cell carcinoma | biopsy, treated if caught early, can invade and destroy surrounding tissue, those on lip, or ear are particularly aggressive; if untreated, can metastasize |
| candida albicans | yeast infections |
| superficial fungi | dermatophytes, tinea (ringworm)--> live on keratinized tissue, pruritus, lesions, cosmetic changes to skin, hair, nails can occur |
| invasive fungi can cause | septicemia |
| fungi skin infections diagnosed thru | microscopic exam and wood's light |
| shingles | painful vesicular eruption along the area of distribution of sensory nerves from one/more posterior ganglia; caused by herpes zoster and treated w antivirals |
| herpes simplex | type 1 occurs on mouth, type 2 occurs in genital area |
| human pailloma virus (hpv) | benign genital warts (or anywhere on body), risk of cervical, anal or rectal changes |
| pressure ulcers | decubitis ulcers, bedsores; involve the breakdown of skin due to prolonged pressure, friction and shear, & insufficient blood supply especially over bony prominences |
| 4 stages of pressure ulcers | 1-skin red and closed/no blanching, 2-open skin (ulcer), painful, 3-extends into tissue, may see fat, not muscle, tendon or bone, 4-damage into muscle, bones, tendons |
| prevention of pressure ulcers | repositioning patients and skin moisture |
| venous stasis ulcers | diminished circulation in lower extremities; blood pools in veins, skin damage develops, slow healing |
| arterial ulcers | related to insufficient blood supply to extremities, painful, pale, cool to the touch, hairless skin, deep, red, yellow or black sores |
| neuropathic ulcers | ocur due to reduced blood supply to nerves (often related to diabetes)-loss of feeling; found on bottom of feet, reddish to brown-black, margins well-defined, punched out look, surrounding skin calloused |
| contact dermatitis | delayed hypersensitivity, inflammatory reaction of skin to physical, chemical, or biological agents (metal, chemicals, poison ivy) |
| irritant type contact dermatitis | response to nonallergic reaction |
| allergic type contact dermatitis | allergic reaction resulting from exposure to contact allergens |
| seborrheic dermatitis | inflammation due to excessive secretion of sebaceous glands, red lesions, dandruff |
| urticaria | hives, wheals, can be accompanied by angioedema; acute treated with antihistamines; chronic has autoimmune component |
| angioedema | swelling of eyes, face, lips, mucous membranes |
| inflammatory lesions | histamine released by mast cells, immunological, chemical, physical stimuli |
| 2 most common burn etiologies are | flame and scald |
| burns | thermal, chemical, electrical, radiation; all depend on temp of burning agent, duration of contact and thickness of skin |
| superficial | damage only to epidermal layer, vasodilation causes redness to skin; no blisters, healing in less than 1 week |
| superficial partial-thickness injuries | char epidermis and papillary dermis; edema and epidermal blisters; skin is wet, raw, pink or white; painful, will heal in 3-6 weeks, scarring may occur |
| deep partial-thickness injuries | thru epidermis and dermis; skin may be mottled, blistering |
| full-thickness injuries | damage to epidermis, dermis, hair follicles, and all underlying structures; nerve endings destroyed, so pain is rare; skin-white, black, brown, or red; significant edema in surrounding tissues |
| rule of nines | rapid, used pre-hospital & in emergent phase; body divided into 11 regions that represent 9% each of BSA, w perineum @ 1%; accurate for adults |
| lund and browder method | more precise method of estimating the extent of a burn; body is divided into smaller sections of tbsa and % |
| minor burn injury | partial thickness less than 15% tbsa, full-thickness less than 2% tbsa (excluding eyes and hands) |
| moderate burn injury | partial thickness 15-25% tbsa, full-thickness less than 10% (excluding special care areas) |
| major burn injury | partial thickness greater than 25% tbsa, full-thickness in children; all full thickness burns exceed 10%; all involve eyes, ears, face, hands, feet, perineum, or joints inhalational injury, electrical injury, concurrent trauma and poor-risk patients |
| zone of coagulation | deepest point of injury, most irreversible damage |
| zone of stasis | dec tissue perfusion, potentially reversible damage |
| zone of hyperemia | outer zone, reddened due to vasodilation, minimal tissue damage |
| normal organ function disrupted if | tbsa >30% |
| cell damage and death release vasoactive substances | inc vascular permeability, w fluid and protein shift from ICF to ECF; greatest 6-8 hrs post-injury; cell damage: leak of potassium into ecf inc risk hyperkalemia |
| hypotension, tachycardia, dec urine output | specific hypovolemic shock:burn shock; fluid resuscitation critical |
| hypermetabolic state | energy needs inc 50-100%, bmr 1.3x greater than normal on average; nutritional supplementation calculated as 25 kcalxbody weight (kg) + %tbsa |
| cardiovascular effects of burns | hemodynamic instability, fluid, sodium and protein losses: fluid loss causes dec in vascular volume, cardiac output and bp lactated ringer's is administered; systemic edema, hyponatremia, hyperkalemia |
| pulmonary effects of burns | upper airway injury; inhalation injury: related to carbon monoxide; airway edema: rapid progression, stridor (immediate intubation); patient is @ risk acute respiratory failure and distress |
| renal effects of burns | altered function as result of dec blood volume; impairment to immune system diminishes resistance to infection; loss of skin: inability to regulate body temp; gi complications: paralytic ileuus and curling's ulcer |
| immune system effects of burns | neg impact on immune function, reduction of complement system, Ig production, dec wbc production/function, dec t helper cells; inc infection risk; debridement=used to stimulate blood flow to area of injury, dec risk of incetion |
| if 35% tbsa, | dec blood flow to gi tract; secondary to hypovolemia, dec motility and nutrient absorption, paralytic ileus |
| to protect gastric mucosa | enteral feedings, proton pump inhibitors (ppis) and h2 blockers; help to prevent curling's ulcer (gastric ulcer in severely burned individuals) |
| priority of burn care | ABCDEF- airway, breathing, circulation, disability, exposure, fluid resusitation |
| infection/sepsis after burns | skin barrier broken, immunosuppression w suppressed t cell and macrophage function, dec circulation to injury, prolonged hospitalization staph aureus/mrsa, would infection turns into cellulitis, then necrotizing fascitis, to sepsis (blood stream) |
| adult respiratory distress syndrome (ards) | leading cause of death in severe burn injuries; risk inc when burn >40% tbsa or full-thickness burn >20% |
| burns lead to ards | capillary hyperpermeability causes fluid to leak into alveoli, gas exchange impaired-tachypnea, nasal flaring, accessory muscle use, cough, hypotension, tachycardia, fever; mechanical ventilation needed |
| eschar | tough, elastic, dead, burned tissue, compromises circulation causes excessive build up, ischemic and infarction or area may occur |
| compartment syndrome | full thickness circumferential and near-circumferential skin burns |
| contractures | epithelial replacement not possible if skin is burned below certain level with deep dermal and full-thickness burns |
| hypertrophic scarring | scarring after burn injury w keloids |
| keloids | raised scar on skin |
| goal of inflammation | keep injury contained, prevent spread of injury, bring body's defenses to needed area |
| 3 phases of acute inflammation | inc vascular permeability, cellular chemotaxis, systemic response |
| vascular permeability | rubor (redness), tumor (swelling), calor (heat), dolor (pain), loss of function (function laesa); fluid, wbcs, platelets travel to injury |
| histamine and bradykinin | dilate vessels |
| cellular chemotaxis | chemotaxis, leukocytosis, leukemoid reaction, margination |
| chemotaxis | chemical signals attract wbcs and platelets |
| leukocytosis | inc # of leukocytes (>10,000) |
| leukemoid reaction | severe elevation in leukocytes (>50,000) |
| margination | wbcs line up along endothelium, release inflammatory mediators |
| granulocytes | neutrophils, eosinophils, basophils |
| neutrophils | 6-24 hrs, prep for repair of tissue damage |
| basophils | when organism enters body, cytokine and protease production |
| eosinophils | when immune system is activated, inflammatory mediators |
| agranuloyctes | monocytes and lymphocytes |
| monocytes | 24-48 hrs, boost immune response |
| lymphocytes | viral infections, inc blood flow |
| phagocytosis | respiratory burst releases free radicals that destroys microbes |
| mature neutrophils | segmented nuclei |
| immature neutrophils | known as bands |
| cytokines | released by wbcs, stimulate the liver to release acute phase proteins which facilitate wbc phagocytosis |
| chemokines | proteins that attract leukocytes to endothelium |
| systemic response | fever, lympphoadenopathy, anorexia, sleepiness, lethargy, anemia, weight loss |
| fever | >100.2 F |
| pyrogens | substances that cause fever; activate PGs to reset the hypothalamic temperature (regulating center) |
| higher temps | inc wbc efficiency |
| fever onset | shivering to inc temp |
| fever break | sweating to reduce temp |
| histamine | produced by basophils, platelets and mast cells; arteriolar vasodilation, large artery vasoconstriction, inc permeability of venules |
| prostaglandins | released from wbcs and cell membranes |
| TNF-alpha and interleukins | inflammatory signals produced by macrophages; induce fever, loss of appetite, and lethargy; promote weight loss and cachexia |
| outcomes of acute inflammation | complete resolution, healing by connective tissue (regernation of normal cells do not occur, excessive proliferation of connective tissue, fibrous scar tissue formed), chronic, persistetn inflammation (resolution does not occur, extensive tissue damage) |
| chronic inflammation | inflammation for weeks or months w no resolution or healing |
| persistent infection | tuberculosis, syphilis, viruses |
| hypersensitivity disorders | rheumatoid arthritis, systemic lupus erythematosus (sle) |
| exposure toxic agents | coal dust-anthracosis (black lung) |
| atherosclerosis | chronic inflammatory disease |
| granuloma formation | macrophages aggregate and are transformed into epithelial-like cells |
| differences bw chronic and acute inflammation | predominance of monocytes, lymphocytes, and macrophages; continual secretion of cytokines damages healthy tissues stimulating further info |
| host | human or animal colonized by pathogen |
| pathogen | microorganisms capable of causing infectious diseases |
| colonization | pathogen living in host |
| infection | invasion, colonization, and multiplication of pathogens |
| virulence | ability to produce disease |
| reservoir | pathogen source (person or inanimate object (fomite)) |
| vector | living being that can carry pathogen from reservoir to host (mosquito, tick, and flea) |
| epidemiology | study of disease distributions |
| incidence | number of new infection cases |
| prevalence | number of active ongoing infections |
| endemic | incidence and prevalence are stable |
| epidemic | abrupt inc in incidence in location |
| pandemic | global spread of disease |
| microbial flora | organisms that live in or on the human body that secrete nutrients and competitively inhibit harmful pathogens |
| microbial flora do not | cause infection/disease w/in normal area |
| opportunistic infection | infection caused by microorganisms that flourish bc host's immune system is weakened |
| skin | natural barrier due to thickness and low pH; harbors normal flora (staphylococcus, streptococcus, and candida) |
| respiratory tract | possible entry point for thousands of microorganisms; cilia, mucous secretions, specialized immune cell help reduce infections |
| gastrointestinal tract | contaminated food and drink, fecal-oral transmission; stomach pH, mucus, normal flora prevent infections |
| blood-blood transmission | blood transfusions, sharing of needles; also enter thru mucous membranes, eyes and skin (hence universal precautions) |
| maternal-fetal transmission | some pathogens can cross placental barrier; some thru childbirth; congenital infection passed from mother to child |
| incubation | microorganisms begin replication w/o identifiable symptoms; short as 24 hrs or 2-3 months |
| prodromal | initial symptoms appear, often vague and general |
| acute | full infectious disease sign and symptoms are present and immune system is fully engaged |
| convalescent | body containing the infection and progressively eliminating the pathogen; days, weeks, or months |
| resolution | pathogen eliminated from the body |
| stages of infection | incubation, prodromal, acute, convalescent, resolution |
| gram stain | most common clinical microbiology stain, results based on cell wall of bacteria |
| gram pos | thick peptidoglycan cell wall; purple |
| gram neg | thin cell wall; red |
| best prevention for infection | hand washing |
| disinfecting equipment bw patients | stethoscopes |
| vaccines are most efficient method of | controlling contagious diseases |
| treatment of infectious diseases | antimicrobial agents, immunological boosting agents, surgical removal of infected tissues |
| staphylococcal | gram-pos, part of normal flora |
| s. aureus | colonizes skin, vagina, nares and oropharynx; most virulent staph infection bc of toxins and proteases, leading cause of health-care associated infections; antibiotic resistance mrsa and vrsa |
| streptococcal | gram pos, strains cause infections in humans |
| s. pyogenes | gabhs (group a beta hemolytic streptococcus) |
| pseudomonas aeruginosa | gram neg, most common pathogen isolated from patients hospitalized for 1 week +; can infect many systems, may be life threatening |
| bacterial meningitis | fatal, more severe than viral; fever, nuchal rigidity, headache, and photophobia common signs |
| kernigs sign | extending leg up in laying down position; associated with bacterial meningitis |
| brudzinskis sign | moving knees and neck up, associated with bacterial meningitis |
| lumbar puncture is needed for diagnosis of | bacterial meningitis |
| eschericia coli (e coli) | lives in intestines of healthy cattle, undercooked meat means of transmission; common cause of utis in women |
| hemolytic uremic syndrome | small blood vessels in kidneys become damages and inflamed, from diarrheal illness w e coli |
| clostridium difficile | prolonged antibiotic use that distorts normal flora of gi tract enables overgrowth |
| lyme disease | bariela burgorferi, deer tick transmits, erythemia migrens may be present, arthritis and nerve involvement may develop, difficult to diagnose |
| viruses are | acellular, use host cell's metabolic processes; have either dna or rna surrounded by protein coat; can cause acute/chronic/latent infections or cancer cell growth |
| common cold | adults 3-4 colds per year, rhinovirus, adenovirus, coronavirus; direct contact or droplet |
| influenza virus | a, b, or c types; annual outbreaks, high mutation rate leads to seasonal vaccine, abrupt onset of symptoms may last 2+ weeks |
| epstein barr virus (ebv) | cause of mononucleosis; more than 90% of population infeted, may not develop into mono; pharyngitis, severe fatigue, lymphadenopathy, and splenomegaly present; spread thru saliva |
| herpes simplex virus (hsv) | 2 forms HSV-1 (cold sores) and HSV-2 (genital infection) |
| acute herpes | vesicular lesions w active viral particles |
| latent herpes | reactivations often occurs during times of stress |
| varicella zoster | causes chickenpox (vaccine available); rash first appears on scalp and progresses over body |
| shingles | reactivation of varicella zoster; remains dormant along nerves (vaccine available) |
| poliomyelitis | fecal-oral route transmission; virus damages motor neurons; abortive, aseptic meningitis, and paralytic; vaccines available; symptoms: muscle loss, fatigue, slow progression |
| fungi | mold-like organisms; mycoses=fungal infections |
| dermatophytes | tinea (ringworm), superficial infections involving the skin, hair, or nails |
| candida | part of normal flora, pathogenic when it overgrows |
| thrush | oropharyngeal candidiasis |
| vulvovaginal candidiasis | yeast infection |
| candida albicans | can cause fatal disseminated infection, especially in immunocompromised |
| protists | protozoa, giardiasis and malaria |
| helminths | worms that cause infection; eneteroblasis (pinworms), ascariasis (roundworm), hookworm, tapeworm; more prevalent in tropical areas |
| insects | directly cause disease or severe as vector |
| malaria | plasmodium protozoan, transmitted by anopheles mosquito; destroys rbcs, affects liver and spleen; malaria prophylaxis; jaundice, chills, hemolytic anemia, hepatomegaly, splenomegaly |
| toxoplasmosis | toxoplasma gondii protozoan, cysts present in cat feces, pregnant women and immunocompromised @ risk; can be transmitted to fetus and cause encephalitis |
| prions | crutzfeldt-jaokb disease (cjd); fatal degenerative neurological disease, spongiform appearance of brain; bovine spongiform encephalopathy: mad cow disease, spread via meat and bone meal fed to cattle |
| antigens | non-self substances, target of immune response |
| immunodeficiency | weakened immune system |
| autoimmunity | attack self cells |
| hypersensitivity | overreactive immune system |
| immunocompetence | ability to protect oneself due to strong immune system |
| innate immunity | nonspecific, 1st level of defense; physical and chemical barriers (skin, pH of gi tract, enzymes in tears) |
| monocyte | macrophage arise from monocytes; migrate to tissues, phagocytize, release cytokines, present antigens; secretory products like hydrolytic enzymes, tnf-alpha, interleukins |
| cytokines | chemical signals produced by wbc; regulate, coordinate immune system; inflammation regulation |
| natural killer cells | granular lymphocytes, destroy tumor cells and virus-infected cells |
| adaptive immunity | 2nd line of defense; slower to respond and dependent on innate immune system |
| toll-like receptors | help activate immune response |
| acquired immunity | specific/memory response |
| major histocompatibility complex (mhc) | aka (hla) human leukocyte antigen |
| t cells | cell-mediated immunity |
| b cells | antibody-mediated immunity (humoral immunity) |
| cd4 cells | helper t cells; damaged by hiv |
| cd8 cells | cytotoxic t cell |
| antigen presenting cells (apc) | macrophages and dendritic cells; present antigens to lymphocytes to activate t cells; derived from bone marrow precursors |
| plasma cells | antigens activate a specific b cell; activated b cell becomes plasma cell that produces antibodies (immunoglobulins) (antibody-mediated or humoral immunity) |
| activated b cells also form | memory cell; that has quicker and stronger response |
| immunoglobulins | produced by b cells; bind to specific antigens |
| primary response | first exposure to antigen, lag time before Ig levels inc, IgM first antibody |
| secondary response | any exposure after first, amnetic response, IgG levels inc rapidly (memory cell response), antigen neutralized before disease signs and symptoms |
| IgD | hypersensitivity reactions; attached to surface of b cells and in skin, gi, respiratory tract; bind to basophils and mast cells |
| IgM | macroglobulin-largest Ig; found throughout bloodstream, present in early infection |
| IgG | long-term immunity; most abundant Ig in bloodstream, present late in disease/recovery and long after, moves across maternal-fetal barrier |
| IgA | protects mucous membranes of gi, gu, and pulmonary systems; found in saliva, secretions, breast milk, gi, tears |
| IgE | produced in response to allergies and parasitic infections; found on mast cells in pulmonary and gi tracts, skin and mucous membranes |
| active acquired | exposure to antigen thru illness or vaccination; immune system activated and memory cells produced |
| passive acquired | individual receives premade antibodies; immediate immunity, but short-term; antibodies transferred in breast milk |
| vaccines | specific formulation that contains a weakened, nondisease-producing pathogen; exposes body to antigen |
| vaccines stimulate | immune response and produce memory cells w/o disease contraction |
| booster | additional dose of vaccine to stimulate the immune system's antigenic memory |
| toxoid | vaccine produced against toxin-producing bacteria (tetanus toxoid) |
| anergy panel | test of immunocompetence where inject common antigens (mumps, candida) intradermally; patient should have positive skin reaction, lacks response may indicate immune deficiency |
| antibody titers | antibody screening tests indicating presence and level of antibodies; can indicate immunity |
| allergy test | skin test to measure reaction to allergen by scratching or injecting small amount of antigen into skin (IgE) |
| serology testing | measures IgE levels in response to antigens |
| overreaction | hypersensitivity and 4 types |
| underreaction | immunodeficiency |
| primary immunodeficiency (congenital) | present @ birth |
| secondary immunodeficiency (acquired) | develops due to infection, chemotherapy, immunosuppressive drugs |
| type 1 hypersensitivity (immediate) | allergy, atopic disorder; process: antigen (allergen) interacts with apc, b cells are activated and produce IgEs, IgEs bind to mast cells, cause degranulation, histamine induce allergy symptoms |
| degranulation | release of histamine from mast cells |
| allergic rhinitis | allergen causes release of histamines, prostaglandins, leukotrienes; mucous hypersecretion, bronchiole constriction, pale nasal mucosa, watery eyes, sneezing, rhinorrhea, cough, bronchospasm |
| most common food allergies | milk, eggs, peanuts, wheat, barley, rye, oats, tree nuts, walnuts, almonds, pecans, fish, soy, shellfish |
| anaphylaxis | severe, overwhelming allergic response (urticaria, bronchoconstriction, laryngeal edema, angioedema); death can occur, medical emergency |
| angioedema | swelling of facial area |
| epipen (epinephrine) | used to counteract response until medical help can be obtained |
| type 2 hypersensitivity (cytotoxic) | Igs attack antigens on cell surface, antibody-mediated cell lysis results; blood transfusion reaction-hemolytic transfusion reaction |
| type 3 hypersensitivity (immune complex) | antigen-antibody complex deposited in tissues; tissue damage results, may be systemic (lupus) or localized (rheumatoid arthritis) |
| type 4 hypersensitivity (delayed) | t cell mediated, previous exposure to antigen primes t cells; t cell attack does not occur until days after initial exposure (delayed); mantoux test for tb; poison ivy or transplant rejection |
| autoimmune disorder | attacks self cells, t cell or Ig-mediated (autoantibodies), organ-specific or systemic |
| molecular mimicry | body's antigens resemble infectious agent, immune system mistakenly attacks body's cells (rheumatic fever) |
| systemic lupus erythematosus (sle) | mulisystem disease; antinuclear antibodies present, antibody complexes deposited in tissues, chronic disease w remission and exacerbations |
| systemic lupus erythematosus shows | skin rash (butterfly rash across cheeks), joint inflammation, kidney damage, vasculitis, raynaud's phenomenon |
| systemic lupus erythematosus people are | genetically predisposed, environmental factors (ebv infection), hormonal component; diagnosis on history, physical exam, and lab results |
| ana elevated in 95% of lupus cases | ana elevation not specific to lupus |
| rheumatoid arthritis (ra) | chronic joint inflammation (affect multiple tissues) |
| rheumatoid arthritis risks | genetic factors, environmental factors (infections), hormonal influence (women more likely to develop ra) |
| symptoms of ra | symmetrical, tender, swollen joints in fingers, wrists, knees, and hips; painful stiff joints for 30+ mins |
| diagnosis of ra | set of specific criteria (acr), rheumatoid fever, esr, c-rp elevation, swan neck, and boutonniere derformities |
| sarcoidosis | chronic, multi-system disorder; accumulation of t cells, macrophages in organs; chronic inflammaation causes granulomas, in lung, skin, eyes; erythema nodosum: tender, erythematous nodules on anterior legs |
| diagnosis of sarcoidosis | chest xray reveals bilateral hilar lymphadenopathy, no diagnostic blood tests; biopsy of sarcoid lesion |
| human immunodeficiency virus (hiv) | virus that infects cd4 cells (t helper); 3 stages-->acute, chronic, aids |
| routes of hiv transmission | sexual activity, semen and vaginal secretions, blood, transplacental, breast milk, organ transplants, saliva (in open mouth wounds) |
| high risk individuals for hiv | participate in unsafe sex, gay sex, iv drug abusers |
| hiv-1 more common in us | hiv-2 more common in w africa |
| retrovirus | rna virus, reverse transcriptase: enzyme converts hiv rna into dina; virus gives genetic instruction to the host and host uses dna to make more viruses in body |
| hiv targets cells | that express cd4 receptors and chemokine receptors, ccrs or cxcr4 |
| ccrs receptor | on surface of t cells, needed for hiv attachment to t cell |
| infected cd4 cells | unable to carry out normal functions (adaptive immunity compromised) |
| acute retroviral syndrome of hiv | occurs in first 28 days, flu like symptoms: fever, headache, fatigue, pharyngitis, gi symptoms, lymphadenopathy, arthralgias, and myalgias; asymptomatic early on |
| late-stage symptoms of hiv | fever, night sweats, weight loss, opportunistic infections; high levels of antibodies |
| normal cd4 range | 800-1200 cell/ml |
| <500 cd4 cells | inc opportunistic infection risk |
| <200 cd4 cells | lead to aids classification |
| diagnosis of hiv | hiv rna assay (earliest detection): measures # viruses in bloodstream; inversion of cd4:cd8 ratio (1:2 in hiv); |
| seroconversion | antibody negative to antibody positive; detectable antibodies (2 weeks-6 months); ELISA must be confirmed |
| most accurate measurement of immune system impairment | cd4 levels when fall below 200 (aids) |
| complications of hiv | opportunistic infections: pneumocystic pneumonia, tb; malignancies: kaposi sarcoma, non-hodgkins lymphoma; aids |
| kaposi sarcoma | cancer lesion in soft tissues (bump) |
| kidney functions | filtration, secretion, acid/base balance, blood pressure regulation, rbc formation, drug metabolism, hormone metabolism, vitamin d synthesis, and glucose homeostasis |
| kidneys receive | 1/3 of cardiac output |
| glomerular filtration rate (gfr) | renal blood filtered per unit of time, 90-120 ml/min; directly related to renal perfusion, dec renal perfusion=dec gfr |
| gfr peak @ 30 | dec to 70ml/min @ 70 |
| nephron | functional unity of kidney |
| nephron functions | filtration, reabsorption, and secretion |
| end product of nephrons | urine |
| bowman's capsule and glomerulus form | renal corpuscle |
| endothelium of glomerulus and capsule membrane contain filtration slits | allow water and substrate to filter out water and substances from blood |
| glomerular capillaries | specialized capillaries, blood enters thru afferent arteriole, leaves thru efferent arteriole; high hydrostatic pressure causes filtration of blood |
| proximal tubule | segment following bowmans capsule, reabsorbs majority of filtrate |
| loop of henle | begins to concentrate filtered fluid, urea |
| urea | waste product enters loop of henle |
| distal tubule | under influence of aldosterone, absorbs water and sodium |
| collecting ducts | under influence of adh, additional water reabsorbed |
| glomerulus releases | renin and erythropoietin |
| acid-base balance | excrete/reabsorb H+ ion and bicarbonate as needed |
| waste elimination | urea, uric acid, creatinine (Cr), drug metabolites |
| secretory function | erythropoietin (epo) and renin |
| erythropoietin | increases rbcs in response to hypoxia |
| renin | released in response to low bp or perfusion; activate raas (renin-angiotensin-aldosterone) |
| vitamin d synthesis and calcium balance | kidney activates vitamin d, important in calcium absorption |
| glucose homeostasis | renal threshold to reabsorb glucose (bg of 180 mg/dl), kidneys degrade insulin, gluconeogenesis; can lead to glucose being pushed into urine (diuresis) |
| polydyspia | very thirsty |
| polyphasia | cannot stop eating |
| polyurea | constant peeing |
| kindey dysfunction consequences | insufficient filtration and waste buildup, unconcentrated urine, toxin build up:destruction of blood cells, confusion, excess renin secreted raising bp, dec erythropoietin (dec rbc), a/b unbalanced, excess K+ not secreted, dec vitamin d, dec ca absorption |
| kidneys are susceptible to | ischemic injury |
| high pressure is required to | push fluid thru kidneys and urinary system |
| nephrons are harmed by | toxins |
| uropathy | obstruction of urine flow; can cause fluid backup which damages renal pelvis |
| symptoms w kidney damage | cva tenderness, hematura, proteinuria, tea-colored urine |
| costovertebral angle (cva) tenderness | pain where kidneys are, hit on back causes lots of pain |
| ensephylopoly | toxin build up |
| abdominal tenderness | pressure; red/swollen/heat/pain/not functional |
| hematuria | blood in urine, not filtering correctly; urine is pink or red, sign of renal calculi or infection |
| proteinuria | microalbuminuria, protein in urine; looks foamy |
| tea-colored urine | bilirubin (built up rbc) in urine; brown color |
| kidney stones from too much | calcium in kidneys |
| oliguria | low urine output <400ml per day |
| anuria | no urine output (kidney failure) |
| diagnosis of urinalysis | pH 4.6-8, specific gravity, uncontrolled diabetes, ketones, leukocyte esterase, nitrite, protein, bilirubin, urobilinogen, crystals (urolithiasis), casts |
| specific gravity | measures particles in urine-electrolyes and osmolarity (1.005-1.030) |
| ketones | fasting starvation or uncontrolled diabetes |
| leukocyte esterase (wbcs) and nitrite | uti or asymptomatic bacteriuria |
| protein | pos can indicate inflammation, htn, glomerular injury |
| bilirubin | liver disorders, excess hemolysis |
| urobilinogen | liver disease-none indicates liver not working |
| other diagnostics of urinalysis | nephrotic syndrome, dehydration, vigorous exercise, diuretics, tubular necrosis, autoimmune disorders, pyelonephritis, other kidney diseases |
| urine culture | reveals presence or absence of bacteria |
| clean-catch samples | cultures w >100,000 cfu of one type of bacteria usually indicative of infection |
| samples collected w minimal contamination (catheter) | 1,000-100,000 cfu; can be considered significant |
| urea | composite of nitrogenous waste that needs to be excreted; waste product |
| azotemia | increase BUN in blood |
| blood urea nitrogen (BUN) 6-24 mg/dl | increased when dec gfr, dehydration, extremely muscular persons, high protein diet |
| uremia | extremely high levels of urea and other nitrogenous wastes; worsening of chronic failure |
| creatinine | product of muscle breakdown that is excreted completely; measures kidney filtration |
| high serum creatinine | kidney dysfunction |
| creatine clearance | used to assess gfr, collected by blood sample and 24 hr urine |
| decreased creatinine clearance | decreased gfr and impaired renal function |
| serum creatinine is better measure of kidney function than | bun |
| BUN good measure of | dehydration, high protein intake, and high muscle breakdown |
| diagnosis of kidney dysfunction | renal ultrasound, iv pyelography, ct scan, mri |
| urosepsis | complication of uti w bacteremia |
| diuresis | large unconcentrated urine outflow |
| neurogenic bladder | spinal cord disorders |
| hydronephrosis | urine back up into kidney |
| acute kidney injury (aki) or acute renal failure | abrupt insult to the kidney: rapid dec kidney function (w intervention, normal function restored) |
| signs of aki | azotemia, elevated cr, fluid retention |
| classifications of aki | prerenal, intrarenal, postrenal |
| prerenal (most common) | decreased blood flow and perfusion to kidney |
| intrarenal | injury to kidney from medications or infections |
| postrenal | obstruction of urine outflow from kidneys |
| prerenal dysfunction | reduced cardiac output or severe hypovolemia (low blood vol), shock, large blood loss from body (hemorrhage from ischemia) |
| prolonged renal hypoperfusion | acute tubular necrosis-damage to nephron tubule epithelial cells |
| atn | cell slough off tubules-block lumen and urine formation; worsens injury (intrarenal); if not revered renal failure |
| intrarenal dysfunction | trauma to kidney (pyelonephritis, autoimmune (lupus); infection of kidney (post-streptococcal glomerulonephritis); nephrotoxic drugs (nsaids, ace inhibitors, angiotensin-receptor blockers, statins, antibiotics) |
| postrenal dysfunction | hydronephrosis (urine backup into kidney); example: kidney stone, prostate gland hyperplasia, neurogenic bladder |
| aki phases | initial insult, oliguria, diuresis, recovery |
| initial insult | prerenal, intrarenal, or postrenal condition that disrupts kidney function |
| oliguria | low gfr, lack of urine output, fluid overload |
| diuresis | large unconcentrated urine outflow; kidney is not concentrating urine properly |
| recovery | healthy nephrons take over function of damaged nephrons; kidney function resumes |
| acute tubular necrosis (atn) | ischemia and hypoxia damage to nephron, common cause of aki, can lead to renal failure |
| acute glomerulonephritis (agn) or nephritic syndrome | triggers inflammation that damages the membranes of the glomerulus; autoimmune or post-streptococcal disorder; can progress to esrd; antigen-antibody reaction damages glomeruli leading to hyperpermeability |
| damaged glomeruli leads to | protein loss, edema (periorbital), oliguria, hypervolemia, psgn: 7-21 days post strep; dark urine: rbcs |
| diagnosis of nephritic syndrome | elevated serum Cr and BUN; low serum albuminia; urinalysis: protein, wbcs, blood; antibodies to streptococcal bacteria present |
| treatment of nephritic syndrome | antibiotics, dietary modifications, diuretics |
| nephrotic syndrome | glomerular damage resulting in proteinuria and edema; commonly caused by diabetes mellitus, amyloidosis, and lupus |
| nephrotic syndrome is | massive albuminuria (facial edema), hematuria, htn, oliguria; hyperlipidemia=lipid synthesis by liver inc as liver inc albumin synthesis to compensate for urinary loss |
| treatment of nephrotic syndrome | adequate liquid, dietary modification, may become renal failure |
| renal calculi | stones (calculi) in kidneys; presentation depends on location; kidneys secrete stone-inhibitors |
| urolithiasis | stone travels to ureter |
| cystolithiasis | vesical calculi in bladder |
| risks for renal calculi | genetics, diet, metabolic abnormalities, dehydration, excess ca intake, hyperparathyroidism, gout, hyperuricemia, immobility, uti, urinary stasis |
| calcium renal calculi | most common kind; hypercalcemia |
| struvite renal calculi | magnesium and ammonium phosphate; occurs in proteus uti; patients with spinal cord injuries more @ risk |
| uric acid renal calculi | foods high in purines; gout |
| cystine renal calculi | rare, disorder of cystine metabolism |
| symptoms of urolithiasis | cva pain, abdominal pain, spasms of ureter; pain in waves lasting 20-60 mins; nausea, vomiting, fever, hematuria, pyuria, crystalluria, painful urination, writing to control pain, hydronephrosis |
| diagnosis of calculi | hematuria and crystalluria, ultrasound, ct scan, collection of stone and stone analysis |
| treatment of calculi | hydration greater than 3L/day, pain meds, diuretic, lithotripsy |
| pyelonephritis | infection of renal pelvis; ascends into uti; stasis of urine plays role |
| factors affecting pyelonephritis | obstructive uropathy, vesicoureteral reflux (anatomical abnormality), neurogenic bladder, urological instrumentation, pregnancy |
| symptoms of pyelonephritis | fever, abdominal or cva tenderness, flank pain, nausea, vomiting, chills, dysuria, urinary frequency, microscopic hematuria, pyuria, leukocyte esterase test of urine |
| pyuria | wbcs in urine |
| diagnosis of pyelonephritis | urine cultures (e coli, s saprophyticus, p mirabilis); dipstick urinalysis (pyuria, + leukocyte esterase); contrast-enhanced helical/spiral computed tomography, ct scan (kidney, ureters, bladder), ultrasound |
| polycystic kidney disease (pkd) | genetic disorder; kindey and other organs affected; cysts formation impair renal function; 6-8% of patients on dialysis in us |
| most common form of pkd | autosomal dominant pkd (recessive exists) |
| pkd symptoms | fluid-filled cysts in kidneys; pain, renal calculi, cva, inc bp (if cysts place pressure on kidney blood vessels, activating raas) |
| diagnosis of pkd | ultrasound and ct scan |
| chronic renal failure (crf) | irreversible and progressive w gradual onset; 90-95% of nephrons affected; progresses to esrd; hemodialysis or kidney transplant needed; dm, htn, glomerulonephritis, and pkd are leading causes |
| stage 1 of crf | kidney damage w normal or inc gfr (>90ml/min) |
| stage 2 of crf | mild reduction in gfr (60-89ml/min) |
| stage 3 of crf | moderate reduction in grf (30-59ml/min); symptoms become apparent; serum cr and bun inc |
| stage 4 of crf | severe reduction in gfr (15-29 ml/min) |
| stage 5 of crf | kidney failure (grf <15ml/min); transplant or dialysis needed |
| complications of crf | uremic encephalopathy, proteinuria, hypoalbuminemia, edema, fluid overload, oliguria, electrolyte imbalances, hemolysis, thrombocytopenia, anemia, dec vitamin d, htn, metabolic acidosis, hyperkalemia, hypocalcemia, hyperphosphatemia, hyperparathyroidism |
| crf diagnosis | cbc, bun, cr serum levels, urinalysis, albumin levels; renal imaging studies |
| crf treatment | fluid and electrolyte management, along w bp management; gfr <10-20ml/min- dialysis, kidney transplant |
| urological disorders affect | ureter, bladder, urethra, and prostate |
| obstructive uropathy (blockage) leads to hydronephrosis | fluid buildup in kidneys |
| lower utis | more common in women |
| urolithiasis | stones |
| adequate urine volume and unimpeded urine flow | essential for kidney health |
| detrusor | major muscle in bladder |
| bladder is innervated by | sympathetic-relax detrusor, tighten internal sphincter; parasympathetic-contract detrusor, relax internal sphincter |
| bladder hold | 300-400ml urine |
| micturition reflux (urination) | stretch of bladder walls send signals to spinal cord, activation of parasympathetic system, cerebral cortex: voluntary control of voiding |
| prolonged obstruction results in | inc hydrostatic pressure in nephrons dec gfr |
| hydronephrosis | dilation of renal calyces and pelvis due to obstruction; acute is reversible |
| hydroureter | dilation of ureter due to obstruction |
| in children dilation of structures can be from | anatomic abnormalities like vesicoureteral reflux, urethral stricture, stenosis |
| lower utis | most commonly caused by e coli, originating from bowel; proteus, pseudomonas, and klebsiella; proteus more common w catheterization or urinary instrumentation |
| healthy urinary tract | only has bacteria in urethral opening |
| stagnant urine inc infection risk for | lower utis |
| female risks for lower utis | improper perineal hygiene, tight/restrictive clothing, chronic dehydration, diabetes, use of irritating bath products, sex, urinary catheterization, use of contraceptive diaphragms and spermicides, pregnancy |
| male risks for lower utis | chronic dehydration, diabetes, bph which obstructs free flow of urine, bladder cancer, urinary catheterization |
| hospital-acquired uti | catheterization, multi-drug resistant pathogens, polymicrobial infection |
| symptoms of lower utis | inc frequency, dysuria, and urgency, hematuria, fever not present |
| diagnosis of lower utis | urinalysis-rbcs, +leukocyte esterase (wbcs), nitrates (bacteria); urine culture->100,000 cfu |
| urosepsis | serious complication of uti, bacteremia with bacterial endotoxins; acute, severe illness (fever, chills, confusion, disorientation, hypotension); elder, catheterized, immunocompromised @ risk |
| asymptomatic bacteriuria (asb) | 2 consecutive urine cultures >100,000 cfu bacteria; patient lacks uti symptoms; treatment w antibiotics doesnt help outcomes |
| stress incontinence | most common, women more @ risk due to loss of muscle support in pelvic floor; childbirth, abdominopelvic surgery, low estrogen (menopause) contributes to weakness of pelvic floor |
| overactive bladdre (oab) | detrusor muscle overactivity |
| overflow incontinence | chronic overdistention and urinary retention in bladder, detrusor muscle loses strength and elasticity, bph most frequent cause in men |
| functional incontinence | inability to hold urine (stroke, delirium) |
| risk factors urinary incontinence | inc age, pregnancy, childbirth, obesity, diabetes, stroke, neurological impairment, prostate disease and its treatments |
| diagnosis of urinary incontinence | x ray of kidney, ureter, bladder; ultrasound, ct scan, ivp, urodynamic testing, cystoscopy may be necessary, measurement of postvoid residual volume in bladder, simple urinary cough test, cotton swab test |
| simple urinary cough test | patient asked to forcefully cough with a full bladder in standing position |
| cotton swab test | assesses mobility and strength of bladder sphincter, sterile cotton swab lubricated with lidocaine and inserted transurethrally into bladder, patient asked to cough, angle of cotton swab can indicate stress incontinence |
| cystitis | bladder inflammation |
| stroke | 5th leading cause of death in us; results in paralysis on one side of body; risk for afr amer is greater |
| central nervous system | brain and spinal cord |
| peripheral nervous system | cranial and spinal nerves |
| spinal cord | motor neurons descend/sensory neurons ascend |
| upper neurons | within brain |
| lower neurons | spinal cord |
| corticospinal tract | upper neurons that descend into spinal cord |
| contralateral | cross over (80%) |
| ipsilateral | remain on same side (20%) |
| decussation | brainstem area of crossover |
| cerebral injury | presentation often on opposite side of body |
| cerebrum | upper most region of brain, right and left hemisphere, corpus callosum (connection) |
| diencephalon | thalamus and hypothalamus, relays sensory info and controls many autonomic functions |
| categorical hemisphere | language, sequential-analytic; L hemisphere in most |
| representational hemisphere | face recognition, music, visual-spatial; R hemisphere in most |
| aphasia | difficult to speak or understand language |
| broca's area | speak language; expressive aphasia |
| wernicke's area | comprehend language; receptive aphasia |
| frontal lobe | reasoning (judgement), behavior (emotions), thinking initiation, movement, speaking, memory |
| parietal lobe | understanding spatial relationships, knowing right from left, sensation, reading |
| temporal lobe | understanding language, behavior, memory, hearing |
| occipital lobe | vision, color blindness |
| brainstem | breathing, blood pressure, heartbeat, alertness/sleep |
| cerebellum | balance, coordination, fine muscle control |
| brainstem | cranial nerves originate |
| midbrain | vision, hearing, movement |
| pons | consciousness and sleep |
| medulla oblongata | vital body functions |
| cerebellum | coordinated movement and equilibrium |
| ataxic gait | uncoordinated walking |
| internal carotid | serves brain's anterior and middle cerebral arteries |
| anterior cerebral artery | frontal lobe |
| middle cerebral artery | lateral cortex, 80% of brain's tissue; most strokes involve branch of this artery |
| R/L vertebral arteries | feed posterior brain |
| circle of willis | base of brain, provides collateral circulation, formed by posterior cerebral artery and internal carotid; common site for aneurysms (weakness in arterial wall) |
| cranial nerves | 12 pairs, 1-12; either motor, sensory or both; brain injury, tumor, or stroke can disrupt cranial nerve functioning; cranial nerve abnormalities may be a sign of inc intracranial pressure |
| brain | most energy-consuming organism, 20% of oxygen, brain cells not capable of anaerobic metabolism, brain cells die 5-6 mins, irreversible damage may occur |
| there must be a continuous supply of oxygen and glucose | for cell metabolism |
| hypoglycemia and hypoxia affect | brain functioning |
| 2 types of stroke | ischemic or hemorrhagic |
| ischemic stroke (85%) | thrombus or embolus, leads to cerebral artery; most common in internal carotid and middle cerebral artery |
| hemorrhagic stroke (15%) | rupture of cerebral artery; caused by htn, aneurysm rupture (most common in circle of willis), subarachnoid hemorrhage (arterial branch in subarachnoid space ruptures) |
| transient ischemic attack (tia) | ischemic injury "mini stroke"; disruption of cerebral circulation lasting less than 24 hrs; no permanent injury but can warn of future attacks |
| causes of ischemic stroke | cerebral arteriosclerosis, carotid stenosis, atrial fibrillation |
| atrial fibrillation | stasis of blood leads to clot formation |
| cerebral ischemia develops gradually | if completely occluded: neurons in core area of ischemia suffer irreversible infarction within minutes |
| ischemic penumbra | perimeter of ischemic zone; less perfusion but not irreversible damage; rapid reperfusion is critical to recover cells |
| cerebral edema | may develop in area causing further damage |
| glutamate toxicity | excritatory neurotransmitter; occurs from failure of cellular ion pumps; inc in glutamate extracellularly, Ca influx intracellularly (cell death) |
| transient ischemic attacks are temporary and resolve | 20-25% of tias progress to stroke; neurological changes may go unnoticed by patient (observable by bystanders, resolved by time medical staff comes, interview and observation key) |
| lacunar infarct | small infarcts in brain due to occlusion of tiny blood vessels |
| tia cause needs to be identified and corrected | usually blocked carotid arteries and cerebral artieries from atherosclerotic plaques |
| hemorrhagic stroke pathophysiology | blood flows into brain, compresses and displaces brain tissue, blood causes vasospasm of adjacent blood vessels, blood released is toxic to surrounding cells, anoxic encephalopathy, cerebral edema, cushing's triad, hematoma and clot form |
| anoxic encephalopathy | lack of oxygen delivery causes decreased level of consciousness |
| cerebral edema may occur w hemorrhagic stroke, putting pressure on brain tissues | pressure on brainstem causes alteration in HR, breathing, pupil dilation |
| cushing's triad: pressure on brainstem | bradypnea (irregular respirations), bradycardia, hypertension |
| if hemorrhage is large, hematoma and clot form; may expand in 24 hrs w worsening symptoms | immune response and scar tissue form |
| risks for stroke | htn, hyperlipidemia, diabetes, smoking, obesity, lack of exercise, atrial fibrillation, oral contraceptives, excess alcohol, fam history, age 65+, male, afr amer, sickle cell disease, tia, avm |
| signs of stroke | middle cerebral artery most common stroke location: speech, motor, sensory deficits; neurological deficits on one side of body: slurred speech, loss of gag reflex, facial droop, hempiaresis, hemiplegia, loss of sensation/vision, disorientation, confusion |
| FAST | facial droop, arm weakness, speech difficulty, time to call 911 |
| subarachnoid hemorrhage (SAH) | presents differently than most hemorrhagic strokes; sudden onset (worst headache ever), vomiting, photophobia, seizures, dec LOC, neuro deficits, poor prognosis |
| vertebrobasilar insufficiency (vbi) | ischemia of vertebrobasilar circulation from compression of vertebral or basilar arteries (space bw C1 and occiput); dizziness, vertigo, headache; cracking neck |
| any sudden changes in neurological function should be assessed | no reliable clinical presentation to distinguish bw ischemic or hemorrhagic stroke |
| 1 sided symptoms and signs | slurring speech, facial droop, hemiparalysis |
| diagnosis of strokes | ct scans w/o contrast for acute phase (identify or exclude hemorrhagic stroke); ct scan w dye may allow better visualization for ischemia; magnetic resonance angiography (mra); transcranial doppler; national institutes of health stroke scale (nihss) |
| magnetic resonance angiography | can distinguish bw ischemic and hemorrhagic stroke |
| national institutes of health stroke scale (nihss) | neurological exam w 11 categories, quantity deficits attributed to stroke (>25 severe impairment), monitor progress |
| treatment for ischemic strokes | iv thrombolyis, Rt-PA: recomibinant tissue-type plasminogen activator (clot buster); surgical thrombectomy for eligible candidates, rehabilitation (1st 4 weeks post-stroke especially important to regain function) |
| treatment of hemorrhagic strokes | hemodynamic stabilization, intubation and bp reduction, manage cerebral edema, surgical treatment |
| peripheral nervous system nerves | somatic nerves (motor/sensory) & autonomic nervous system |
| neurons | conduct electrical signals |
| glial cells | support cells |
| neurotransmitters | released into synapses of nerves causing next neuron to fire or be stimulated; can activate or inhibit functions |
| examples of neurotransmitters | GABA, epinephrine, norepinephrine, acetylcholine, dopamine, endorphins, serotonin |
| nerve conduction | movement of ions |
| depolarization | sodium influx-generates action potential |
| repolarization | potassium efflux-return to rest phase |
| resting membrane potential | polarization of cell |
| refractory period | rest period where cell cannot repeat action potential |
| myelin | productive sheath around axon of some neruons |
| insulator | myelin sheath contains lipids, "white matter", helps conduct electrical signal more quickly |
| some disorders cause degeneration of myelin | multiple sclerosis, amyotrophic lateral sclerosis |
| myelin regrowth | may be possible for some time |
| assessment of neurological system | may be difficult to diagnose initially, degenerative disorders progress and be apparent later; speech, demeanor, emotional state; cognitive function; head trauma; upper/lower motor strength; reflexes, sensation, examine gait, cranial nerve assessment |
| reflexes | babinski-negative-toes flex inward; positive toes flare out (upper motor neuron disorder) |
| hemiparesis | half of body is weak/partial paralysis |
| hemiplegia | half body paralyzed |
| upper motor neuron (UMN) | problem in brain's area of motor control, responsible for voluntary movement and modulating involuntary movement, damage causes spasticity |
| lower motor neuron (LMN) | problem at the region where motor nerves exit the spinal cord, prevent excessive muscle movement, damage causes flaccidity |
| epilepsy | chronic neurological disorder with recurrent seizures; manifestations depend on area affected |
| seizure | sudden, abnormal, disorderly discharge of neurons within the brain |
| diagnosis of epilepsy | 2 unprovoked seizures at least 24 hrs apart |
| epileptogenesis | transformation of normal neuronal region into hyperexcitable area |
| focal seizures | localized within 1 cerebral hemisphere |
| initiation phase of seizure | high frequency action potentials and hyper synchronization (spike on eeg) |
| generalized seizure | involve both cerebral hemispheres |
| 3 types of seizures | focal, generalized, unknown |
| seizures cause | motor, nonmotor, or both symptoms |
| clonic | sustained rhythmical jerking |
| atonic | weak or limp muscles |
| tonic | rigid or tense muscles |
| myoclonus | muscle twitching |
| epileptic spasms | repeated flexion and extension of the whole body |
| nonmotor symptom | absence seizures, staring spells w no movement |
| aura | sensation before a seizure |
| ictal period | time of seizure |
| postictal | after seizure complete, person may be tired, confused, nauseated, may have amnesia |
| interictal | if multiple seizures occur in short time, the time bw seizures |
| seizure etiology | head trauma (most common), stroke (elderly), brain neoplasmss, congenital malformation, degenerative brain disorders (alzheimers), environmental stimuli (blinking lights), genetic predisposition, infections, hypoglycemia, hyponatremia, respiratoryalkalosi |
| seizure etiology 2 | perinatal injury (hypoxia), withdrawal from alcohol or sedative-hypnotic drugs |
| diagnosis of seizures | cbc, serum chemistry, brain imaging studies (mri, ct), and eeg (sleep deprivation inc sensitivity) |
| emergency seizure care | during-protect patient from injury, move objects out of way, do not physically restrain, do not put anything in his/her mouth; after-place patient on left side and turn head, any emesis or oral secretions will drain out of mouth and will not be inhaled |
| primary headaches | arise independently of any other medical illness or traumatic cause, tension-type, migraine, and tri-geminal autonomic cephalgia |
| secondary headaches | caused by another primary condition, head injury, vascular problems, medication side effects, sinus disease, and tumors |
| tension type headache (tth) | most common primary headache (infrequent, frequent, chronic), bilateral pain with mild to moderate pressure, doesnt worsen w physical activity, no vomiting/nausea, iinc cervical and pericranial muscle activity; diagnosis: clinical finding |
| migraine headache | periodic, throbbing headaches, altered perceptions, nausea, severe pain, photophobia, phonophobia, worsens w movements, aura may precede headache, 75% migraine sufferers are women |
| migraine headache phases | prodrome (neural hyperexcitability), aura (cortical spreading depression occurs), pain (trigeminovascular complex activation), postdrome (sensitization of trigeminovascular complex persists) |
| migraine pathophysiology | serotonin dec and calcitonin gene-related peptide (crgp) inc thought to play a role (crgp=vasodilator) |
| migraine triggers | stress, hormone shifts, excessive exercise, lack of sleep, fatigue, hypoglycemia, certain foods |
| sinus headache | caused by sinus infection, fever and rhinorrhea present, pain worsens when patient leans over (facial areas over frontal and maxillary sinuses may be tender), transilumination of sinuses may show nontransparency, treatment-antibiotics/nasal decongestants |
| brain tumor headaches | 50% of those w brain tumor will experience headache |
| headache is dull and constant, may throb | usually bifrontal, with worse pain on same side as tumor, generalized head pain may occur w inc intracranial pressure |
| papilledema and cranial nerve may be present | in brain tumor headache |
| worsening of headache with change in body position | any maneuver that raises intrathoracic pressure or intracranial pressure |
| parkinsons disease | men and women equally affected, progressive loss of dopamine-producing cells in substantia nigra; movements such as posure, standing, walking and writing affected |
| acetylcholine stimulates muscle movement, while dopamine has an inhibitory effect | dopamine depletion imbalance causes unopposed acetylcholine (tremors, uncoordinated movements) |
| accumulation of alpha-synucle | abnormal protein found in structures called lewy bodies in brainstem, spinal cord, and regions of cortex |
| parkinsons can affect ans | causing nonmotor symptoms |
| symptoms of parkinsons | begin unilaterally, progressively to both sides, classic triad, postural instability, nonmotor, neuropsychiatric |
| classic triad of parkinsons | bradykinesia (slow movement), resting tremor (pill-rolling), muscle rigidity (cogwheel, ratchet movement) |
| diagnosis of parkinsons | TRAP (tremor at rest, rigidity, akinesia (bradykinesia), postural/gait instability) |
| amyotrophic lateral sclerosis (als) | lou gehrigs disease, progressive loss umn and lmn: painless muscle weakness and atrophy, sensory neurons and cognitive function, eventually respiratory failure (mechanical ventilation needed) |
| als signs/symptoms | muscle weakness, speech changes, dysphagia, muscle spasticity, positive babinski reflex, diaphragm affected |
| multiple sclerosis | chronic demyelinating disorder, affects brain, spinal cord, and optic nerves; remissions and exacerbations (damage heals during remission) |
| multiple sclerosis risks | genetic predisposition, viral process, trauma, female, northern european descent, living in cooler climates |
| both sensory and motor neurons affected | t cell mediated attack of myelin |
| relapse and remission in most forms | multiple sclerosis |
| symptoms of multiple sclerosis | weakness, numbness, balance problems, blurred vision; dysphagia, hemiparesis, paraparesis |
| cognitive functioning | recent memory, abstract reasoning, attention can be affected |
| multiple sclerosis affective symptoms | depression |
| multiple sclerosis diagnosis | lesions of demyelination, mcdonald criteria (mri evidence and patient symptoms), blood work to rule out other conditions w neurological presentation (lyme disease, syphilis), csf analysis |
| guillain-barré syndrome (gbs) | postinfections disease, acute inflammatory demyelination, weakness varies from mild weakness to complete paralysis, including respiratory muscles (recovery is steady over weeks and months) |
| myasthenia gravis (mg) | autoimmune disease (attack of ach receptors), diagnosis (ach receptor antibodies), muscle weakness and fatigue, extraocular muscles often affected first ptosis; b and t cell mediated, thymus involved, 70% of patients with mg have thymus gland hyperplasia |
| myasthenia gravis presents in 2 ways | ocular form: often patients first present with ocular changes; vs general form |
| flunctuating skeletal muscle weakness is cardinal feature | true muscle fatigue, not a sense of tiredness, dec contractile force w repetitive motions, blinking, walking, talking, chewing, swallowing and respiratory function may be affected |
| myasthenia gravis extras | rest improves muscle function, weakness severe enough to cause respiratory failure leading to mechanical ventilation, aspiration and respiratory failure cause death in severe mg |
| diagnosis of myasthenia gravis | edrophonium testing (acetylcholinesterone inhibitor), allows more ach to remain in the synapses for a longer period of time, 30-45 secs after administration, improved muscle contraction |
| traumatic brain injury (tbi) | sudden, physical damage to brain, closed or penetrating injury, concussion (ex), falls most common cause, males affected more than females |
| spinal cord injury (sci) | damage results in loss of mobility or sensation, even if cord remains intact there is a loss of nerve injury below the injury |
| intracranial pressure (icp) | pressure inside the skull, brain tissue and csf; normal (5-15 mm Hg (supine), icp inc w changes in volume to any one of the components; compensation (dec vol of other components, monroe-kellie hypothesis), inc icp after tbi related to inc mortality |
| supine | laying down |
| level of consciousness (loc) | self-awareness and reaction to environment, content of consciousness (cognitive function-cerebral cortex), consciousness not located in one region of brain (upper brainstem, reticular activating system, cerebral hemisphere) |
| alertness | highest loc |
| lethargy | individual sleepy but can be aroused easily |
| obtunded or stuporous | difficult to arouse state, with little or no interaction with the environment |
| coma | lowest loc, individual has no interaction with the environment |
| signs of inc intracranial pressure | dec level of consciousness, pupillary dilation, headache, vomiting, papilledema, inc bp; crushing's triad-late signs (htn (widened pulse pressure), bradycardia, abnormal respiratory pattern) |
| tbi mechanisms of injury | blunt trauma, acceleration-deceleration (head stops moving, but brain continues to move forward (stretching and shearing of neurons), coup-ccontrecoup injury (brain strikes one side of skull, rebounds, and strikes other side) |
| penetrating injury | skull is fractured; blast injury |
| cerebral perfusion pressure (cpp) | depends on mean arterial pressure and icp; cpp=map-icp |
| pressure autoregulation | brain maintains normal cerebral blood flow w cpp ranging 50-150 mm Hg; vasodilatory cascade (dec cpp causes vasodilation to maintain flow); if pressure autoregulation disrupted, cerebral blood flow and icp altered;<50 cpp=loss of perfusion to brain tissue |
| mechanisms that inc icp | vasogenic cerebral edema (shearing stress), cytotoxic cerebral edema (reduced oxygen), compression of jugular vein w tracheostomy ties or tight cervical collars may reduce venous flow from brain, inc icp |
| dec icp | external drainage of csf via catheter, lower bp, hypertonic iv, low co2 (vasoconstrict cerebral arteries), removing brain tissue (lobectomy), decompressive craniectomy |
| brain death | irreversible end of brain activity, coma, absence of brainstem reflexes, apnea (vital centers of brainstem disrupted) (brainstem reflexes compromised) |
| brain death may result from inc icp causing brain herniation | transtentorial (uncal) herniation=temporal lobe (uncus) focused thru the tentorial notch compressing brain tissue |
| assessment of tbi | examine for head trauma,neurological exam:loc, mental status, cranial nerve status, motor/sensory status, deep tendon reflex; duration of unconsciousness, post-traumatic amnesia (pta); consciousness/unconsciousness (eye opening to stimulation, not in coma |
| glasgow coma scale (gcs) | assess the severity of brain injury, rating 3 areas (eye opening, verbal response, motor response); lowest gcs 3, highest 15, single gcs score cannot determine severity (use as series of scores, compare over time) |
| coma and posturing | 1/2 rigid positions: decorticate or decerebrate |
| decorticate | flexed arms, clenched fists, rigid legs; corticospinal tract damage |
| decerebrate | arms held straight outward with toes pointed downward; upper brainstem damage |
| tbi diagnosis | severity-mild/minor gcs 13-15, moderate gcs 9-12, severe gcs <9; ct scans-test of choice, demonstrates acute bleeding & pressure on vital structures; ct angiography-uses dye to observe vessels; mri-deeper brain structures: eeg |
| diffuse axonal injury (dai) | common tbi, widespread damage to brain tissue, immediate loss of consciousness, most remain in coma; difficult to detect on imaging studies, mri may be used |
| major cause of unconsciousness and persistent coma after head trauma with dai | w coup-contrecoup injury, diffuse swelling on neuronal axons, hemorrhage, or laceration corpus callosum, Ca entry into damaged axons activates proteases |
| concussion | mild traumatic brain injury (mtbi), traumatic force causes disruption in brain function (may/not involve loss of consciousness); cease sporting activity until evaluation and assessment |
| types of concussion | simple, complex |
| simple concussion | resolve wo complication, may take up to 10 days |
| complex concussion | symptoms may persist for longer, longer loss of consciousness (>1 min) |
| pathology of concussion | direct blow to head, face, neck, or traumatic force transmitted to the head; multiple concussions have cumulative effect; glutamate released from cells, toxic to neurons; overstimulation of neurons and neuronal swelling |
| hort-term neurological dysfunction that resolves spontaneously | neuropathological functional changes, but no structural changes, may or may not involve loss of consciousness, grossly normal structural neuroimaging studies |
| during concussion patient may state | seeing stars, dazed, confused, headache, dizzy |
| concussions may have | retrograde and antegrade amnesia, post concussion syndrome (pcs): symptoms longer than 3 weeks may be present |
| concussion diagnosis | rule out cervical spine injury, epidural hematoma, subdural hematoma, subarachnoid hemorrhage; neurological examination; american association of neurology (concussion: grade 1, grade 2, grade 3); signs and symptoms evolve over time, ct scan |
| red flags of concussions | anticoagulation use, alcohol/drug intoxication, neurological deficits, unequal pupils, persistent vomiting, seizure, droway w difficult arousal, headache that worsens, slurred speech, neck pain, weak/numb in legs/arms, change in loc, inc confusion |
| cerebral contusion | bruise of brain tissue, scattered areas of bleeding on brain surface, undersurface frontal and temporal lobes, result from coup-contrecoup injury or penetrating wound; cerebral edema around contusion 48-72 hrs (inc icp/inc risk brain herniation) |
| signs/symptoms cerebral contusion | severe headache, dizziness, vomiting, inc size of one pupil, sudden weakness in arm/leg, agitated/restless, memory loss, medical emergency (dec hr, dec respirations, htn, cannot be awakened) |
| cerebral contusion diagnosis | ct scan, mri (greater sensitivity for cerebral edema), skull xray, delayed enlargement of brain contusion most common cause of clinical deterioration, periodic neurological assessment |
| head trauma/intracranial bleeds | can cause 3 types of intracranial bleeds: epidural hematoma (edh), subdural hematoma (sdh), subarachnoid hemorrhage (sah); present differently, treated differently |
| epidural hematoma | most serious complication of head injury, bleed in space below skull (caused by skull bone fracture lacerating middle meningeal artery; voluminous arterial bleeding); midline shift of brain can be viewed on imaging studies w/in hour of injury |
| epidural hematoma 2 | injury leads to dec loc, followed by lucid period, and rapid deterioration, recognition of edh, presents w severe headache, vomiting, seizure, pupil distortion, cushing's triad; ct scan, skull xray, neurosurgical emergency: surgical evacuation of hematoma |
| subdural hematoma (sdh) | bleeding in space below the dura mater; usually due to tearing of bridging veins in subdural space, most common type of traumatic intracranial hematoma, slow bleeding, but blood can accumulate over time |
| acute sdh | within 72 hrs after head injury |
| subacute sdh | take up to 7 days |
| neurological deficits do not usually occur until substantial bleeding | repeat follow-up neurological exams needed |
| coagulation profiles | anticoagulants, alcohol abuse |
| sdh | ct scan and skull xray, large acute sdh require craniotomy to evacuate blood; small sdh may be slowly reabsorbed by brain |
| traumatic subarachnoid hemorrhage | one of most common head injuries, tearing of cerebral and meningeal vessels w/in subarachnoid space, post-traumatic cerebral vasospasm in response to blood |
| aneurysmal subarachnoid hemorrhage | weakened area of vessel, may rupture; berry aneurysm, in 50% of cases, symptoms precede rupture, thunderclap headache (rapid decline) |
| subarachnoid hemorrhage | rupture of artery causes blood to fill subarachnoid space, blood irritates tissues and puts pressure on brain, sah can cause obstructive hydrocephalus, pressure may cause brain hernation; rule |
| subarachnoid hemorrhage assessment | ottawa subarachnoid hemorrhage |
| subarachnoid hemorrhage diagnosis | ct scan wo contrast |
| skull fracture common sites | temporal bone-most common, orbital fossa, base of skull, foramen magnum |
| 3 types of skull fractures may or may not involve injury to brain | linear: most common, does not affect brain tissues; depressed: often open fracture; basilar: base of skull |
| basilar skull fractures | occur along middle fossa, may involve brain injury; battle's sign: brusing on mastoid process behind the ear on affected side; csf lek from ear (csf ororrhea) or nose (csf rhinorrhea); loss of csf: ha, n/v, and dizziness |
| frontal fossa fractures | can result in periorbital ecchymosis, reffered to as racoon eyes, edema, and csf rhinorrhea |
| diagnosis of skull fractures | x ray of head, ct scan, neurological examination |
| csf skull fracture | rhinorrhea or otorrhea, test for beta-2-transferrin and glucose-diagnostic for csf |
| spinal cord injury (sci) | compression, stretching, or laceration of spinal cord following trauma |
| quadriplegia (tetraplegia) | most common, paralysis of all 4 extremities |
| paraplegia | 2nd most common, paralysis of lower extremities |
| mortality rates highest | first year post sci |
| spinal cord injury | surrounded by meninges and csf; conus medullaris (distal end), cauda equina syndrome (spinal nerves at end of spinal cord); ascending (sensory tracts); descending (motor) tracts |
| primary injury sci | can led to hemorrhage and neuronal cell death |
| secondary injury sci | due to ischemia form primary injury |
| sci worsen | damage over hours to weeks, inflammation and scarring; fluid-filled cysts form |
| sci types of injury | hyperflexion, rotational (unstable), hyperextension, axial loading (vertebral compression) and penetrating injuries |
| diagnosis of sci | xray of spinal column, ct scan, mri, neurological assessment, abcs take precedence, stabilize spine and immobilization |
| areflexia | results from primary injury, flaccid muscles, paralysis, lack of sensation below injury, bowel and bladder dysfunction; loss of anal reflex or bulbocavernosus reflex; autonomic function disrupted |
| spinal shock | cannot assess extent of injury until spinal shock resolves, may take days to weeks (indicated by return of anal reflex and bulbocavernosus relex) |
| bulbocavernosus reflex | contraction of anal sphincter w squeexing of glans penis or tugging on a foley catheter; indicates intact s1, s2, s3 nerves; in spinal shock, reflex absent |
| neurogenic shock | occurs in patients w injuries at t6 and above; abnormal sns signaling; lack of bp, hr, vasoconstriction regulation |
| neurogenic | sci about t6, disrupts sns, different from spinal shock; loss of ability to secrete norepinephrine when needed |
| neurogenic shock is unable to compensate for any decrease in bp | blood pools in extremities from los of venules return and decreased co and bp |
| clinician should be aware that tachycardia may not be present w falling bp | different from hypovolemic shock |
| stabilize pt. hemodynamically and monitor | bp and ecg continuously |
| complete sci | loss of all voluntary motor and sensory function below the level of injury |
| incomplete sci | some motor or sensory function below the injury can remain intact; central cord syndrome, anterior spinal artery syndrome, brown-sequard syndrome, horner's syndrome, cous medullaris syndrome, cauda equina syndrome |
| c1-c3 | unable to breath without respirator, loss of bowel and bladder control, unable to move arms and legs |
| c4-c7 | severe weakness in arms w no motor function or sensation in legs, loss of bowel and bladder control truncal instability |
| thoracic spine | paralysis in legs but arms can still function, truncal instability, loss of bowel and bladder control |
| lumbar sacral | loss of bowel and bladder control, upper body strength and sensation normal, motor weakness or paralysis and sensory loss in hips and legs |
| complication of sci | syringomyelia (fluid-filled cysts), neuropathic joint anthropathy (slow destruction of joints that occur over years), spasticity, cardiovascular and respiratory complications, anatomic dysreflexia, secondary immunodeficiency, bladder/bowel dysfunction |
| complications of sci 2 | pressure injury, neurogenic heterotopic ossification, neuropathic pain (hyperalgesia, allodynnia, paresthesia) |
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