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NURS 2004 Midterm: N2003 Midterm 2
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Department
Nursing
Course
NURS 2004
Professor
R.Crossman
Semester
Winter

Description
Pain Pain A physiologic response that serves as a warning Pain is whatever the person says it is, existing whenever he/she says it does An unpleasant, emotional, sensory experience with actual or potential damage and described in terms of such damage Nociception The perception of pain Chemicals of Lactic Acid- from anaerobic metabolism- stimulates nociceptors Nociception pGs- from exposed phospholipid of broken cell membranes; stimulates and increase sensitivity Multiple chemicals act as neurotransmitters/ neuromodulators: - Substance P, glutamate, aspartate, calcitonin (excitatory) - Serotonin, GABA, glycine, endogenous opioids (inhibitory) Pain Pathway Sensors: Pain Nociceptors Receptors Free nerve endings Stimulated by multiple chemical mediators, pressure, temperature Stimulation initiates depolarization and impulse transmission * These are not evening distributed Peripheral Nerves A-Delta: myelinated, fast, sharp, localized pain C- unmyelinated, slow, dull/ burning, diffuse pain A-Beta: large, mechanical, non-painful Spinothalamic Carries impulses from dorsal horn to CNS Tract - Sharp, fast (neo) - Dull, slow (paleo) Dorsal Horn Butterfly shaped, in vertebrae “Relay station” between peripheral and CNS Impulse from peripheral nerve crosses synapse in dorsal horn (in the substantia gelatinosa) and activates nerve in spinal cord CNS Integrates signal and interprets messages Thalamus Pain perception center, sends messages to: - Reticular and limbic system (pain awareness, emotion) - HPA (response) - Muscles (motor response) Descending Pathway of Pain 1 Pain impulse travels along ascending pathway via A delta fibres Pain is perceived by CNS Message sent back for motor response and stimulation Large A beta fibres in periphery take over A delta fibres and send non- painful messages to brain e.g. rubbing, squeezing, tapping via ascending pathway and inhibitory Nt are released Closes the pain gate Descending Pathway of Pain 2 Pain message in brain region of midbraina message to PAG (periaqueductal grey) Axons from PAG connect via NRM (nucleus raphe magnus) area into the dorsal horn Stimulation of NRM area causes release of endorphins in dorsal horn and inhibits release of excitatory Nt Endorphins bind to ahorn (Closes the gate)s in post-synaptic neurons in dorsal Post-synaptic transmission of pain impulses from periphery decreases so pain decreases Diffuse Noxious Activates when another area is receviing noxious stimuli at the same Inhibitory Control time as the original painful area (DNIC) E.g. acupuncture, deep massage, applying an ice pack Acute Pain Protection, alert A-delta fibres < 3 months duration Intense, sharp, localized pain Short-term stimulus S&S: wincing, crying, HPA activation Remove the source of pain Examples: surgical incision, overuse of muscle Acute Pain: Stimulation of nociceptor by: Incision or Muscle - pGs (incision) or injury/ overuse - Lactic acid (muscle use) Action potential along A- delta fibres to CNS Responses: - Behavioural (protection, guarding, reducign use) - Sharp, intense localized pain - Wincing, change in facial expression - Increas HR, BP, sweating, pallor (HPA activation) - Distress, fear, anxiety, crying (limbic/ reticular activation) Chronic Pain C-fibres >3-6 months duration Buring, diffuse, dull Repeated stimulus S&S: No HPA, probably depressed mood, difficulty eating/ sleeping, “normalize” pain, adapative behaviours Patient action: adaptation Examples: Cancer, post-herpetic neuralgia Neuropathic Pain Chronic pain caused by damage to/ dysfunction of nerves/ nervous system Described as buring, shooting, shock-like tingling Causes increased sensitivity to painful stimuli Examples: phantom limb, diabetic neuropathy, post-herpetic neuralgia, MS, or Parkinson’s Post- Herpetic (from Shingles) Neuralgia Herpes Zoster virus lives in nerve ganglia for many people after they have chicken pox. When reactivated, causes inflammation of neuron with prolonged impulses Vesicles appear along dermatome Substance P is key mediator Buring, electric intense pain (C fibre) Cancer Pain Tumor presses on nerve or nociceptor, obstruction of an area, tissue destruction Metastases to other areas can also cause cell damage. pGs from tissue damage stimulate activation of A and C fibres Chronic/ acute- severe and intractable Cutaneous Superficial Somatic In skin, joints, muscles, diffuse Visceral Major internal organs, lining body cavities, N/V Referred Different site than point of origin (innervated by same spinal segment) Dermatome Region of body wall supplied by a single pair of dorsal root ganglion Pain Threshold Lowest intensity of stimulus perceived as pain Pain Tolerance Amount of time or intesnsity before pain is perceived as pain Drugs - ASA, NSAIDs, cortisone to stop pG synthesis - Morphine hyperpolarizes neruons, disrupts ion channel - Capsaicin depletes substance P - Anaesthetics disrupt ion channels so affect depolarization - Antidepresants block reuptake of serotonin so prolong activity - Gabapentin- GABA (inhibitory) Neoplasia and Examples of Cancer Carcinomas Cancer of epithelial tissue Adenocarcinomas Cancer of ductal or glandular structures Sarcomas Cancer of connective tissue, muscle, or bone Lymphomas Cancer of lymphatic tissue Leukemias Cancer of the blood Benign Tumor Non-cancerous tumors (do not spread to other parts of the body) Malignant Tumor Cancerous umors that grow rapidly (without stopping) and can metastasize Ductal carcinoma in When cancer cells are localized (i.e. have no penetrated the local situ basement membrane or spread to other tissue) Characteristics of - Rapid growth rates Cancerous Tissue - Undergo frequent mitosis (uncontrolled cell division) - Loss of normal organization (not encapsulated) - Altered shape and size (polymorphism) - Loss of anchorage dependence (fibronectin) - Loss of density inhibition (invade local structures) - Loss of differentiation so loss of function (anaplasia) - Create their own blood supply (angiogenesis) Loss of Fibronectin Fibronectin is what keeps cells to a specific area by creating anchorage dependence (i.e. liver cells remain in the liver and can’t travel) Lost or modified fibronectin results in loss of anchorage dependence, so cancers are able to travel and spread Anchorage Occurs when the fibronectin that holds cells in place is modified or lost. Independence As a result, cancer cells are able to travel and spread to other areas Density Dependent The cells do not stop dividing despite little or no space. Cancer cells Inhibition continue to divide/ multiply and push out normal cells and invade local tissues Mechanisms of Direct Pressure + Lytic enzymes (kill normal cells and create space) Metastasis Rapid Growth Rate Loss of adhesion from altered fibronectin (able to move)= loss of anchorage Angiogenesis (creates own blood supply) How tumors center Because cancer cells lack anchorage dependence and possess density- lymphatic and dependent inhibition, these cells are not restricted in movement. circulatory system Cancer cells have the ability to enter the ECM )normal cells would undergo apoptosis and die)- eventually cancer cells release enzymes that digest this ECM- allowing them to enter the basement membrane, eventually entering the blood and lymphatic systems. These systems circulate the body and thus cancer cells circulate until they become lodged in a specific organ and continue to metastasize Angiogenesis Thea ability of cancer cells to create their own blood supply - Allows for more nutrients- faster growth - Newly formed blood vessels facilitate spread of cancer through blood Dysplasia The change/ alteration of existing cells which can be a precursor for neoplasia Neoplasia New and uncontrolled growth of cells. Can be indicative of cancer but can also be benign Tumor Marker Tumors release proteins in the blood that can be measured. Can indicate a specific type of cancer - Testicular cancer release AFP - Prostate cancer release PSA - Colon/ rectal cancer release CEA Mutations that DNA mutations cause by various carcinogens/ mutations: cause cancer - Free radicals in radiation - Diet - Tobacco/ smoking - Obesity - Chemical exposure - Sexual behaviour - Air pollution - Viruses - Bacteria - Chronic inflammation Genetic predispositions Oncogenes Mutant genes that direct synthesis of proteins that promote cancer (ex. Epidermal growth factor) Tumor Suppressor (anti- oncogenes) Gene Genes that halt the synthesis of proteins that promote cancer (ex. BRCA) Immune Most cancerous cells are destroyed by cell mediated immunity and Surveillance humoral immunity Theory Some altered cell lines have mechanisms to elude the immune response: - Make cancer antigens look normal - Secrete chemicals to block the immune response Or loss of immune response with aging/ disease allows for cancer development Not altered enough to be dysfunctional or eliminated by immune response Promoting factors enable/ encourage growth (hormones) So many altered cells, the immune response is overwhelmed Multi Stage Theory 1. Initiation- carcinogen/ mutagen causes mutation 2. Promotion- altered cell line proliferates because of some promoting factor 3. Progression- more mutations and eventual progression to cancer Chemotherapy Drug stops all cell division/ replication. Not very specific- so causes many side effects - Decrease RBC count - Hair loss - Stomatitis - Sore mouth - Sore bladder - Sore stomach - Decrease EBC count - Dry skin Affects rapidly dividing cells most and is more effective on multi- system (wide spread) cancer Radiation Therapy Kills cells at a very focused site but lots of side effects, especially at site Ex. X-ray therapy- causes burns to skin (used for prostate cancer) Immunotherapy Newer therapy geared to enhancing immune system function. Involves monoclonal antibodies directed to antigens on cancer cells (delivers radioactive molecules direct to cancer cells) Complications of - Loss of function Cancer - Obstruction if tumor is large (i.e. can’t swallow) - Metastases (spread)- rate varies by cancer type, often typical pattern from primary site Mechanisms that - Tumor cause pain - Inflammation - Obstruction - Invasion and destruction of tissues - Stimulate nociceptors Bone Marrow (Side effect of chemo) Suppression - Thrombocytopenia- decrease platelets (chronic bleeding) - Leukopenia- decrease WBCs (leads to poor wound healing/ infection control) Anemia (Side effect of chemo) - Chronic bleeding (caused by thrombocytopenia) - Altered iron absorption - Interference with iron recycling - Malnutrition (poor appetite) - Malignancy in bone marrow Factors that Poor skin integrity, poor wound healing, and decreased immune increase risk of response infection Breast Cancer Estrogen Estrogen mediates mammary epithelial cell proliferation thus in breast cancer, estrogen acts as a promoter and increase rate of proliferation in cancer cells Risk Factors for Environmental breast cancer - Radiation development - Chemicals stored in fat that mimic estrogens (plastics, fuels, PBCs) - Diet (increased animal fats) - Overweight (fat secretes estrogen) - Alcohol consumption - Decrease exercise Genetics:st - 1 degree relative increase risk 2-3 times - 2nd degree relative especially before menopause and bilateral - Penetrate dominant genes (5-10%) mutations (BRCA1 females and BRCA 2 males) Hormonal - Early menarche and late menopause (increase estrogen) - Nullpanity (no children/ pregnancy) (breast tissue doesn’t differentiate) - Estrogen/ progesterone combo ** Early removal of ovaries, early 1 pregnancy (especially if breast feeding), removal of pituitary glands protect against breast cancer Clinical - Nipple discharge- tumor obstruction Manifestations of - Local pain/ tenderness- tumor obstruction and inflammation s/t Breast Cancer tumor - Nipple retraction- shortening of mammary ducts - Edema- local inflammation of lymph obstruction - Edema of arm- obstruction of lymphatic drainage in axilla - Chest pain- metastasis Screening - BSE Methods for Breast - Yearly physicals Cancer - Modifiable risk factors - Mammography - Genetic screening - Awareness of role of hormones Age 50+ should get regular mammography If someone in the family has been diagnosed- should start getting mammography up to 10 years earlier than age of woman diagnosed Diagnosis of Breast - Biopsy Cancer - Staging (primary tumor size, presence of lymph nodes, presence of distant metastasis) Treatment of Surgery- can remove the initial tumor, but, is ineffective if the cells have Breast Cancer metastasized - Masectomy- entire breast - Lumpectomy- lump in breast There may also be cancerous cells left behind following surgery which will continue to proliferate- allowing tumor to return Chemo/ radiation- used in conjunction with surgery Hormone therapy- Tamoxifen/ Herception- blocks estrogen receptors on cells- thus estrogen stops acting as a promoter - Can only be used for estrogen positive cancers Colorectal Cancers Risk Factors for - High alcohol consumption Colorectal Cancer - Cigarette smoking - Increase fat and decrease fibre diet - Decrease physical activity - Genetics (familial polyposis) - Inflammatory bowel disease Factors that lead to constipation (diet increase fat/ low in fibre, decrease levels of
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