2217 Final Review PDF

2217 final review Abbreviations [] ---------concentration w/o-------without w/i--------within BG--------Blood glucose QoL-------Quality of Life b/c---------because r/t----------related to rxn---------reaction Mobility/functional ability Parkinsons and MS (8 questions) 1) Functional A...

2217 final review Abbreviations [] ---------concentration w/o-------without w/i--------within BG--------Blood glucose QoL-------Quality of Life b/c---------because r/t----------related to rxn---------reaction Mobility/functional ability Parkinsons and MS (8 questions) 1) Functional Ability: a) Definition: Ability to perform the normal daily activities required to meet basic needs; fulfill usually roles in the family, workplace, and community; and maintain health and well-being i) Cognitive, social, physical, and emotional ability to carry on the normal activities of life. b) Scope: linear, full function to disability i) Varies person to person, varies within an individual at different points in time ii) Lifespan consideration (1) Functional ability changes with development (2) Environment, lifestyle, tech changes require some development (3) Infants and young children’s development is marked with milestones (4) Tests determine developmental delays c) Attributes and criteria: i) Functional ability has two dimensions: (1) Attributes: (a) Defining characteristic of functional ability (2) Antecedent: events that must happen before functional ability can exist (a) Capacity to perform specific functional abilities (b) Actual or required performance of functional abilities (c) Ex. - Physiological process: neural, cognitive, endocrine, musculoskeletal, and metabolic - Acquisition of development milestones and skills (d) At any given time, an individual with the capacity to perform a task or self care activity may not because of developmental, social, environmental or cultural factors (3) Also categorised by gradations of capacity or performance (a) Not just what they can or do but with what and how much, and what effort of assistance they do it with, and their effort is. d) Context to Nursing and Health Care i) 3 major dimensions of concern (1) Risk recognition (a) Essential to early identification of factors that affect function (b) Actual deficiency leads to use of resources and support (c) The earlier the ID the better the health outcomes (d) Types f risks:  (i) Developmental abnormalities, physical or psychological trauma or diseases, social and cultural factors (beliefs and perception of health), physical environment. (ii) Comorbidities and socioeconomic factors (iii)Preclinical disability: task modification w/o report of difficulty in performing a specific activity in elderly (iv) Postpartum depression (v) Acute illness or worsening of chronic disease (2) Functional assessment (a) Time-intensive, interprofessional effort using multiple tools (b) Indicated in certain circumstances (c) Ex. Children who are it’d with developmental delays are referred to assessment across domains including adaptive behaviour (functional ability). (d) Best to observe the function of the client (e) Elderly: indicated when there has been a loss of functional ability or a change in mental status, multiple health conditions, or frail living in the community (f) Assessment tools: (i) Self-Report 1. Patients’ perception 2. Potential for inaccurate measurement a. Affected by personal characteristics, preference, and environmental factors, interpretation (ii) Performance based 1. Actual observation of a standardized task 2. SF-36 – physical, social, mental domains of elderly 3. Functional Assessment Screening Tool (FAST-16)- social and behavioural young adults (3) Planning and delivery of individualized care appropriate to level of ability (a) Care Delivery: cross section of help needed and how much help the pt needs to optimize independence ii) Alterations occur as primary or secondary problems (1) Primary problems- ability never developed (2) Secondary problems- loss of ability e) Functional performance is the actual parts of the functional ability a person does in a day 2) ADL a) (Basic) activities of daily living b) Personal care, mobility, eating, hygiene, grooming, bathing, mouth care, dressing, toileting, 3) Instrumental activities of daily living a) More complex skills for living in the community b) Managing money, grocery shopping, cooking, house cleaning, laundry, medicating, telephone, accessing transportation, 4) Independent ADL Parkinsons Pathophysiology - Pathology o Neurological disorder b/c loss of dopamine producing cells in the brain results in motor disability o Degeneration of the dopamine-producing neurons in substantia nigra of the midbrain  o Disrupts normal balance of dopamine and AcH in basal ganglia - Most common in 50+ men - Exact cause unknow - Aggregation of Lewy body proteins in brain - Not considered hereditary but 10% can be linked - Risks: o Well water exposure o Pesticides o Herbicides o Industrial chemicals o Wood pulp mill exposure o Lack of dopamine can cause development o Clinical - Symptoms: Manifestations o Gradual, ongoing o Can start unilaterally o Do not occur until 80% of neurons in substantia nigra are lost o Primary symptoms:  Tremors  First sign  Minimal at first so pt might be the only one who notices it  Affects handwriting  More prominent at rest  Worsened by emotional stress or increased []  Pill rolling  Diaphragm, tongue, lips and jaw  Rarely head shake  Rigidity  Increased resistance to Passive ROM  Jerky (cog-wheel rigidity)  Sustained contraction can cause rigidity and muscle soreness (tired and achy), pain in head, upper body, spine, or legs  Slow movement as a result b/c of alternating contraction and relaxation in opposing muscle groups is inhibited  Akinesia  Absence or loss of control of voluntary muscle movement  Bradykinesia (slowness of movement) is especially prevalent in the loss of automatic movement b/c of physical and chemical changes in the basal ganglia  In unaffected patients, automatic movement is involuntary and subconsciously (blinking, swinging arms, swallowing, saliva, facial and hand movements for expression, and minor movements to adjust posture   In pt with PD does not perform these movements and lack natural activity (stooped posture, masked facial expression, drooling, and shuffling gait  Postural instability  Can’t stop  Pull test- pt will fall o Other symptoms:  Depression, anxiety, apathy, fatigue, pain, urinary retention, constipation, ED, memory changes, sleep disorders o Subtle and mild to more pronounced o Lead to abnormal brain functioning which effects cognition, mood, behaviours o Dopamine is essential for normal function of extrapyramidal motor system (posture, support, voluntary movements) o Early  Mild tremor, slight limp, decreased arm swint o Mid-later  Shuffling gait, near impossible to stop, flexed arm. Loss of postural reflexes, speech difficulties (hypokinetic dysarthria) affect communication and QoL - Secondary Parkinsonism (atypical) o Symptoms can occur post exposure to:  CO  manganese (copper miners)  Medication induced: o Reversable: metoclopramide, methyldopa, lithium, haloperidol, and Illicit drugs- amphetamine, methamphetamine o Irreversible: meperidine o Other causes:  Hydrocephalus  Neurodegenerative disorders  Hypoparathyroidism  Infection  Stroke  Tumour  Trauma - Complications: o Often results in severe dementia o Malnutrition and aspiration b/c swallow ability decreases o Weakness o Pneumonia o Uti, skin breakdown o Orthostatic hypotension o Increased fall risk - Dx studies  o Hx and clinical features, TRAP is required and asymmetrical onset o Positive response to Antiparkinsons medication Medical Nursing - Interprofessional care management o Symptom management - Medication therapy o Focus on correcting balance of acetylcholine and dopamine within the CNS o (enhance dopamine and decrease ACh) o Levodopa/carbidopa (precursor to dopamine and prevents breakdown of levodopa in Peripheral tissues) o Pramipexole (Mirapex) can be used alone or with Sinemet o Rotigotine – transdermal patch o Anticholinergics – decrease ACh activity  Trihexyphenidyl o Monoamine oxidase inhibitors type- B  Selgiline and rasagiline  Reduce breakdown of dopamine o COMT  Entacapone blocks catechol-o-methyltransferase which breaks down levodopa in peripheral tissues o Within 3-5 years of treatment for PD pt usually experience episodes of hypomobility towards the end of the dosing interval (end-of-dose wearing off) or at unpredictable times (spontaneous on/off) o Entacapone helps reduce wearing off - Gene Therapy o Experimental o Inject genes into pt to hopefully replace malfunctioning genes - Surgical therapy o Relief of symptoms o Usually for pt unresponsive to medication o Three categories  Ablation (destruction)  Stereotactic destruction of areas in the thalamus (thalamotomy), globus pallidus (pallidotomy), and subthalami nucleus (subthalamic nucleotomy)  Used for 50 years but Hae been replaced with DBS  Deep brain stimulations (DBS)  Placing an electrode in the thalamus, globus pallidus or subthalamic nucleus  Connecting it to a “pacemaker” generator and sending electrical stimuli at specific intervals and currents  Can be adjusted to best relieve symptoms  Reversable  Blocks neural impulses that contribute to motor symptoms   Transplantation  Fetal neural tissue into the basal ganglia to give brain dopamine agonist-producing cells  Abandoned - Nutritional therapy o Malnutrition and constipation b/c poor nutrition and impaired motility o Food needs to be appetizing and easy to chew and swallow o High fiber and fruit o 6 small meals > 3 big meals b/c less exhausting o Protein and vit b6 impure levodopa absorption so only eat in evenings to reduce symptoms o Physical exercise and a well-balanced diet - Occupational therapy o Strategies to increase self care ability like eating and dressing o Upright chairs o Raised toilet seats o Remove rugs o Elevate legs o Slip on shoes and Velcro/ zippers rather than buttons and hooks/clasps - Other: management of sleep disorders Multiple Sclerosis Pathophysiology - Chronic, progressive, degenerative, autoimmune disorder of the CNS - Dissemination of demyelination of nerve fibres of the brain, spinal cord, and optic nerve - 20-50 you women, usually 30 with 1st appearance of symptoms - Usually North US, Europe, Canada - Moving low risk to high-risk pre 15 y/o = risk of new environment - MS risk 2x lower in indigenous peoples, less common in Hispanics, Asians, and African descent. - Reason unknown, could be infection or genetics (multiple genes = hard to pinpoint) - Common thought that MS develops in genetically susceptible person after infection or environmental exposure - Possible precipitating factors: infection, smoking, injury, emotional stress, excessive fatigue, pregnancy, poor health, - Pathogens TBD 3 processes: 1) Chronic inflammation a) Primary condition is an autoimmune disorder driven by T cells in the systemic circulation which travel to the CNS and disrupt the Blood-Brain Barrier, antigen-antibody rxn in the CNS activates inflammatory response 2) Demyelination a) Inflammation leads to axon demyelination in the brain and spinal cord. Myelin sheath is damaged, but nerve fiber is intact for now and nerve impulse is still transmitted.  3) Gliosis in the CNS a) Myelin is replaced by glial scars (hard sclerotic plaques) in multiple regions of the CNS. b) W/o Myelin nerve impulses slow c) When nerve axons get destroyed impulses are totally blocked resulting in permanent loss of function, demyelination continues with progressive loss of nerve function Clinical - Symptoms: Manifestations o Motor:  Weakness or paralysis of limbs, trunk, head  Diplopia: scanning speech (slow, pauses, or tonal changes)  Spasticity o Sensory:  Numbness and tingling  Paresthesia  Patchy blindness (scotomas)  Blurred vision  Vertigo  Tinnitus  Decreased hearing  Chronic neuropathic pain  Radicular (nerve root) pain in low thoracic and abdominal regions  Lhermitte sign transient sensory symptom. Electric shock feeling radiating down the spine or into limbs with flexion of the neck o Cerebellar signs: nystagmus, ataxia, dysrhythmias, dysphagia o Severe fatigue o Bowel and bladder function (constipation- lesion in elimination center of CNS) o spastic/uninhibited bladder (lesion in second sacral nerve) increased Frequency and urgency o Flaccid (hypotonic) bladder (lesions in reflex arc) has urinary retention o Sexual issues Men – erectile dysfunction, decreased sensation o Sexual issues women- decreased desire, difficulty with orgasm, painful intercourse, decreased vaginal lubrication, decreased sensation. Can improve or remiss with pregnancy/ gestational term but greater risk of relapse post birth  No apparent effect on course of pregnancy, labour, delivery, or lactation o ½ people with MS have difficulties with cognitive function. Most have short term memory problems, attention, information process, planning, visual perception and word finding. mild and can be overlooked o General intellect remains unchanged and intact (long-term memory, conversation skills, reading comprehension) - Early: o Onset slow and gradual  o Vague symptoms periodically months or years Do not prompt pt to seek immediate attention so may not be diagnosed for a while o MS can be marked by rapid, progressive deterioration  Some pt have severe long-lasting symptoms early in disease o Other is remission and exacerbation  Overall trend is progressive deterioration in neurological function o Spotty distribution in the CNS = symptoms vary o (when myelin is attacked but nerve fiber is intact) pt will complain of weakness and impaired function, but myelin can repair which can lead to a decrease in symptoms (remission) - permanent loss of function - Average life expectancy is more than 25 years after onset of symptoms - Death from complications of infection r/t immobility (pneumonia) pr because of an unrelated disease Medical Nursing 1) Diagnostic tests management a) Hx b) Manifestations c) MRI of brain and spinal cord can show plaques, inflammation, atrophy and tissue breakdown d) Cerebrospinal fluid analysis can show increased IGg and oligoclonal banding e) Delayed reflexes f) Delayed responses b/c of demyelination from eyes and ears to brain 2) Diagnostic criteria a) 2 demyelinated lesions in 2 different locations of CNS b) Damage or an attack occurring at two different times (> or = 1 month apart) c) All other DX ruled out If only one lesion or one clinical attack the interprofessional team will monitor 3) Interprofessional care a) Aim is to decrease progression b/c no cure b) Med therapy: decrease progression of the disease and control symptoms i) Acute exacerbation (reduce edema and inflammation at site of demyelination) (For all types of MS) (1) Adrenocorticotrophic hormone (2) Methylprednisolone (3) Prednisone ii) Other complications (Progressive-Relapsing, Secondary-Progressive, Primary-Progressive) (1) Immunosuppressive medication (2) Azathioprine (3) Methotrexate (4) Cyclophosphamide iii) Modify Disease Process  (1) Immunomodulator medications (antivirals) (a) Interferon beta-1b (relapsing-remitting and ambulatory) (b) Interferon beta-1a (i) Like above and used in similar groups of people with MS (2) Immunomodulator medications (a) Teriflunomide (relapsing-remitting) (i) Decrease number of MS relapses and reduces progression (b) Mitoxantrone (PP and PR MS) (i) antineoplastic agent (ii) reduces T and B WBC (iii)impairs antigen presentation (iv) lifetime dose limit b/c cardiac toxicity, cannot be used for more than 2 or 3 years iv) Symptom management (1) Fatigue (a) Amantadine (b) Fluoxetine (2) Bladder changes (a) Anticholinergics (3) Pain (a) Tricyclic antidepressants (b) Antiseizure medications c) Alternative therapies i) Surgical (1) Neurectomy (2) Rhizotomy (3) Cordotomy (4) Dorsal-column electrical stimulation (5) Intrathecal baclofen pump- spasticity (6) Thalamotomy or deep brain stimulation ii) Physiotherapy iii) Speech therapy iv) Exercise improves Daily functioning when not experiencing exacerbation (1) Decreases spasticity (2) Increases coordination (3) Muscle strength (4) Improves mobilization, gait, fatigue, QoL (5) Avoid exercising to the pint of exhaustion and exercise with rests v) Heat therapy vi) Massage vii) Acupuncture viii) Bee sting ix) Aromatherapy x) Stem cell therapy (studies show mesenchymal stem cells reduce brain inflammation) xi) Nutritional therapy  (1) Mega vitamins (cobalamin (vit B12), vit c, vit d) (2) Low fat, gluten free, raw veggies (3) Well balanced (4) High protein (5) High roughage (6) Adapt based on aspiration risk - Use the nursing process as a framework for care of patients with Parkinson’s disease and multiple sclerosis in relation to functional ability Clinical Judgment, Communication, Cognition (5 questions) - Discuss the nurse’s responsibility in problem solving and decision making. - Gain beginning practice in problem solving and decision making using the nursing process within the context of a case scenario. - Explore the use of nursing models for nursing practice. - Describe the purpose and content of a change-of-shift report. - Demonstrate use of standardized tools for clear communication affecting patient care. - Analyze and practice using standardized tools to assess for signs of delirium, depression, and dementia. E.g. Geriatric Depression Scale (GDS), SLUMS, Confusion Assessment Model (CAM). - Explore nursing interventions to support persons experiencing cognitive changes. - Interpret the nursing process as it relates to the concept of cognition. Ethics; topics goals of care, advanced directives, professional boundaries, client rights - Discuss CNA ethical values in relation to goals of care, advanced directives, professional boundaries and client rights. - Describe the following advanced directives: living will, medical directives and power of attorney for personal care. - Describe nursing responsibilities regarding advance directives and decisions about care. - Define professional boundaries for the nurse. - Identify the actions to take when a colleague is exhibiting signs of a boundary violation. - Discuss client rights as it relates to obtaining health care services. Concept: Glucose regulation; topics Type 1 & Type 2 diabetes (7 questions) - Definition: o The process of maintaining proper blood glucose balance/ optimal levels o Balance between nutritional intake, hormone signalling, and glucose uptake by the cell  Glucose enters the cell, and it is oxidized through cellular respiration into ATP for energy  Efficiency of glucose metabolism is signified by the blood glucose levels - Scope: o Hypoglycemia  < 70 mg/dL  o Euglycemia  Fasting euglycemia= 70-99 mg/dL  2hr-postprandial state= 100 -140 mg/dL o Hyperglycemia  > 100 mg/dL fasting  > 140 mg/dL 2hr-postprandial - Normal Physiology o Insulin is produced by the beta cells of the islet of Langerhans in the pancreas to lower the blood glucose by allowing the cells to be more permeable to glucose (increases uptake)  After eating, insulin will be released b/c of increased glucose  Binds to the cell walls and signals glucose transporter molecules to help glucose enter the cell  Insulin supresses the secretion of glucagon and facilitates glycogen storage o Counterregulatory hormones are produced to increase BG if increased demand  Result in utilizing glycogen stores  Increase with stress related conditions (physical and emotional)  Glucagon is released when there is low cellular glucose  Suppresses insulin and stimulates hepatic glucose production from glycogen  Cortisol  Growth hormone  Epinephrine/norepinephrine  Steroid medications and stress also cause gluconeogenesis (creation of glucose when stores are low)  Increase risk of muscle mass loss - Risk factors: o Populations at risk:  Pregnant women  Pregnancy and the associated hormone changes  State of insulin resistance  Higher hyperglycemia risk (especially postprandial hyperglycemia)  Infants:  (larger infants’ higher risk?)  Older adults:  Greater risk b/c of increased visceral fat and decreased lean muscle  Often also age-related insulin reduction  Reduced capacity to regulate and metabolize glucose []  Racial/ ethnic groups  Greater genetic predisposition to insulin resistance = increased risk for T2D  Nativ/ Aboriginal “American Indian/Alaskan natives” in Giddens  African Americans  Hispanics/ Latinos o Puerto Ricans and Mexican Americans having the highest of subclass  Asian Americans  More prominent in communities with less infectious diseases but have a sudden increase of noncommunicable diseases and urbanization that results in more sedentary lifestyles  Europe have a genetic tendency for the autoimmune form of diabetes o Individuals at risk  Genetic factors  HLA genes for T2D  Fam Hx of T2D, Obesity, or other metabolic syndrome factors   Lifestyle risk factors  Promote and worsen insulin resistance o Poor diet, (high trans and saturated fats) o Excess calorie intake leading to obesity o Low fiber high carbs o Lack of physical activity  Medications o Most common:  Insulin and oral antihyperglycemic agents (sulfonylurea)  Corticosteroids  Estrogen  ACE Inhibitors  Beta-blockers  Potassium-depleting diuretics  Bronchodilators  Antipsychotics  Antibiotics - Hypoglycemia o Low BG because of insufficient nutrients intake, medications, excessive exercise, or other dx. o Combo of factors  Insufficient nutrient intake  Malnutrition depletes glycogen stores in liver and adipose tissues  This prevents the hepatic mechanisms from maintaining normal BG levels  Free fatty acids are mobilized as substrates for glucose production and produces ketones  Eventually life-threatening  Adverse rxn to meds  Inappropriate dosing of exogenous insulin or sulfonylurea which increases endogenous insulin create a regimen with a client who needs insulin to ensure you avoid hypoglycemic episodes  Excessive exercise  During exercise, energy in muscle cells is used up first then glucose form hepatic and circulatory systems are used which lowers BG  After an exercise the body replenishes the cells glucose levels to restore the ATP which also further lowers BG, called a lag effect. o Consequences  Mild nervousness, irritability, diaphoresis, anxiety, palpations  Neurological changes, seizures, LOC, Death  Recurring hypoglycemia makes the counterregulatory hormones more sensitive  Symptoms of hypoglycemia don’t occur until the BG is dangerously low  Risk of fatality is 4-10%  Hypoglycemia unawareness - Hyperglycemia: o High BG b/c:  Insufficient insulin production/secretion  b/c glucose can’t enter the cells  damage to the b cells is usually caused by an autoimmune response with genetic disposition or can be secondary from pancreatitis or pancreatic cancer  Excessive counterregulatory hormone production   Increased cortisol can be caused by stress, pain, sleep disturbances, acute injury or illness o Also, can occur with medication(corticosteroids) o Cushing’s disease o Exacerbate insulin resistance o Increase insulin dose  Or deficient hormone signalling  Body cells respond abnormally to the signalling action of insulin and do not allow glucose into the cells  Receptors or transporter molecules are limited o Consequences:  Proinflammatory (contributes to atherogenesis and plaque formation)  Increases cancer risk  Hypertension  50% of pt w T1D  80% of pt w T2D o High oxidative stress and inflammation o Reduced elasticity of the blood vessels  Angiopathy  b/c of Longstanding uncontrolled high glucose levels  damage to blood vessels o theories:  byproduct of glucose metabolism (sorbitol)  formation of abnormal glucose molecules in basement membrane of small blood vessels (like in eye or kidneys)  oxidative stress in RBC leads to decreased oxygenation  Microvascular: damage basement membranes of small blood vessels in lower extremities o b/c thickening of blood vessels membrans in capillaries and arterioles  can happen in T2D o specific to DM o Impaired adequate oxygenation of tissues o loss of protective sensation o microangiopathy:  Diabetic neuropathy  Most common complication (50% of pt)  Difficulty managing pain and a leading cause of nontraumatic amputation which reduce QoL  Loss of protective sensations in feet  Balance troubles (fall and fractures)  Risk factors: o Long standing poor glycemic control o Smoking o Alcohol o Metabolic abnormalities (hyperlipidemia and hypertension)  Neuropathy: chronic kidney disease that can lead to end stage liver dx o Risk factors: smoking, hyprertension, genetic predisposition, chronic hyperglycemia  o Kidney disease can be reduced w Norm ranges of glucose control o Haggressive BP management for all DM Pt  Ace inhibitors  Angiotensin 2 receptors  Given for Pt wto prevent  Yearly screening  Types o Peripheral neuropathy  High BG is toxic to nerves so it causes numbness and tingling and burning when the nerves get damaged  Increases risk of foot ulcers because protective sensations are gone  Can be seen with prediabetes and be the presenting symptom of impaired glucose utilization o Sensory neuropathy  Onset: Symmetrical, distal, sensory neuropathy  Damage to small nerve fibers results in loss of dermal sensation  Large nerve fibers loss of touch and vibrational sensation  Sensory fibers = paresthesia and pai  Prevention/ Nursing action  Visually inspect feet at each visit and assess loss of protective sensation, well fitting shoes, ulcers  Test:  10g monofilament test (10g of force to make the filament buckle inn 4 areas of planter surfaces of foot)  Assess vibratory sense 128Hz tuning fork on tip of big toes (if pt unable to feel while you can it is abnormal)  Intact peripheral pulses  Tx.  Refer to podiatrist for decreased risk of ulceration in future, symptom management, not reversible o Autonomic neuropathies  Hard to dx, Affects multiple systems  Most concerning is hypoglycemia unawareness  Leads to decreased LOC, seizures, etc.  can’t feel low BG changes in systemic system  Cardio- Resting tachycardia  Postural dizziness  GI- gastroparesis, diarrhea or constipation   Erectile dysfunction  Hyperhidrosis on upper body and hypohidrosis on lower o TX.  Symptom management  Hypoglycemia unawareness- glucose monitor/sensor and higher glucose targets  Orthostatic hypotension- compression socks and increase salt or fluticordison  Gastroparesis- more small meals, meds (metoclopramide stim gastric motility) ED- PDE5 inhibitors  retinopathy  After 15 years, nearly all T1D pt, and 80% of T2D pt will have retinal disorder  Most common cause of new blindness in working age pt  Nonproliferative o Most common o Partial occlusion of the small blood vessels in retina o Microaneurysms in capillary walls makes capillary fluid leak out o Vision may be affected if macula is involved  Proliferative o Most serious o Retina and vitreous o Occlusion of retinal vessels o Light cant reach retina o Vessels tear and bleed o Pt sees black and red spots o Partial or complete retinal detachment o If macula is involved vision is lost o w/o tx, more than half of the pt will be blind  Tx. Laser coagulation therapy, vitrectomy,  Macrovascular: Damages medium and large vessels o Earlier and more frequent o Atherosclerotic plaques r/t altered lipid metabolism o Leads to hypertension, PVD and CVD o MI and Stroke risk is 2-4x higher o Increased risk of foot ulcers and wound infection  Fluid, electrolyte, and acid-base imbalances  Dehydration b/c water deficit r/t osmotic diuresis Hyperosmolar Hyperglycemic state (>600mgd/L, dehydration, and impaired cognitive function)- more common in elderly pt with dementia and children (both type 2)  Diabetic Ketoacidosis (DKA) o Acute metabolic complication o T1D (most common)  o , Hyperglycemia, absolutely no insulin/ insulin is not working at all, use of free fatty acids, excess ketones, metabolic acidosis and dehydration o S&S  Polyphagia  Increased hunger b/c cells aren’t receiving glucose  Polydipsia  To dilute BG  polyuria  b/c of increased thirst and intake and osmotic diuresis when BG > 180mg/dL - Assessments: o Ask/Assess:  Hx  Obesity, meds, social history, fam hx (obesity and diabetes), review of symptoms  Polyphagia, polydipsia, polyurea  Retinopathy- reduced vision  Peripheral neuropathy- decreased sensory perception (pins and needles)  Indicative of poor perfusion:  Non-healing wounds  Lower extremity pain  T2D specific  Sleep apnea  Fatigue (chronic)  Worsening hypertension o Examination  Vitals  BMI  Waist to hip ratio  Hypertension to determine overweight or obesity  Acanthosis nigricans  Velvety darkening of the skin (usually on posterior neck, axillae, skin folds of the groin)  Red flag for Diabetes  PVD  Lower extremities for poor perfusion and non-healing wounds  Feet  Lesions, ulcers, blisters, nail abnormalities, excessive callouses  Sensation and motor strength (neuropathy)  Visual acuity, intraocular structures, dilated eye exam o Dx testing  Blood glucose testing  Prediabetes= fasting BG 100-126 mg/dL  > or =126 mg/dL on 2 separate tests = diabetes . or = 200 mg/dL is conclusive  Glucose tolerance test (GTT)  Most sensitive and can only be used in early diabetes  A1c  (glycosylated haemoglobin) 3-month range   Diagnostic screening and monitoring of disease management  > or = 6.5% indicates diabetes  An A1c < or = 7% has been associated with reduced risks for complication from diabetes and is the recommended goal for control  Don’t need to fast  Not as sensitive as GTT  Significant variability r/t ethnicity and conditions that alter turnover of the RBC (end stage renal dx, severe thalassemia, heredity spherocytosis, splenomegaly, autoimmune hemolytic anemia, and some hemoglobin variants)  Antibody testing  Used to confirm T1D  Glutamic acid decarboxylase antibody is tested  C-peptide test is indirect insulin measurement  And fasting insulin levels may be measured to determine the quantity of residual insulin production  Lipid analysis  Measure: o Total cholesterol o HDL cholesterol  Severity of resistance  Low = insulin resistant o Triglycerides  General reflection of glycemic control  High glucose= high triglycerides  LDL is calculated from these measurements “calculated LDL”  Renal function test  Early indicator od renal disease associated with diabetes is microscopic protein in urine (albumin- microalbuminuria) o > 300 mcg/dL = renal damage and increases risk of end stage renal disease  Blood urea nitrogen  Creatinine  C-reactive protein  Made by body during stress or infection  Elevated w Diabetes  Assoc. w inflammatory process of insulin resistance and CVD risks  Also elevated in RA and infection - Nursing Considerations/ management: o Assessment above o Nursing Diagnosis:  Inadequate health management r/t insufficient sources  Potential for unstable blood glucose r/t insufficient management  Potential for: peripheral neurovascular dysfunction, injury o Planning  Goals:  Pt is an active participant  Experience few or no episodes of hypoglycemia or acute hyperglycemia emergencies  Maintain BG at normal or near normal levels   To prevent and minimize or delay complications  Adjust lifestyle to accommodate regimen o Implementation/ clinical management  Primary prevention:  Emphasize healthy lifestyle procedures  Metformin can reduce progressing diabetes by 31% o Recommended for pt, under 60, w prediabetes and BMI > or = 35kg/m2 and women with gestational diabetes  Maintain optimal body weight o Obesity is directly linked  Exercise o Improves insulin resistance and cellular metabolism by increasing GLUC4 transporters w/I muscle cells o Moderate aerobic exercise for 150 minutes minimum/week and moderate resistance training 2-3x/week (pt w diabetes and for prevention)  Diet: o Avoid excess calories, sweet drinks o Foods for optimal cellular metabolism (vitamins, fiber, macronutrients):  High in whole grains, fruits, vegetables, (deep orange and leafy green) and legumes/beans  Low-fat milk and lean protein  Low sodium  Maintain good personal hygiene to decrease risk of infection o Emphasis on foot care  Medical identification bracelets and travel  Secondary Prevention (screening)  Screening for susceptible adults  All pregnant women at 24 weeks  For pt with diabetes: A1c 2x/year or Q3Months if not meeting targets  1x/year o Renal and lipid test o Dental, foot and dilated eye exams  T1D o Thyroid function b/c increased risk of autoimmune processes  Collaborative Interventions  Goal: glycemic control  Pt Education o Self-care behaviours (diet, exercise, rest etc.) and injections/medication management, monitoring  Monitoring and Managing Blood Glucose o Two approaches:  Self Monitoring:  Standard meter like a finger prick or a continuos monitor like a Libre 2  Assists with decisions r/t carb intake and insulin/medication dosages  Most effective when pt records readings, levels and related information   Most can share info with provider or medical office  Monitoring A1c  (glycosylated hemoglobin)  Prediabetes or diabetes progression monitoring  Goal: 7% or less o 8% may be target for pt who are at risk for hypoglycemia (less stringent goals) o young children o elderly pt w impaired renal function o pt taking beta blockers o Correcting hypoglycemia  15/15  15 grams of carbs (quick acting) will raise BG by 50mg/dL  Recheck BG after 15 minutes  Repeat until euglycemia  Exceptions written in Giddens: o Severe hypoglycemia is 30g if conscious o Unconscious pt: IV dextrose or glucagon o If given glucagon, roll pt on side to reduce aspiration r/t nausea and vomiting associated with glucagon in high doses  Nutritional therapy  Patient and caregiver teaching o Teach meal planning techniques. o cold symptoms/ Illness  herbal supplements can impair glucose function  hypoglycemic inducing: o aloe, fish oils, a-lipoic acid  Hyperglycemic inducing: o melatonin, st. johns wort, celery seed, rosemary o People with diabetes are at risk of developing depression b/c of “Diabetes Distress” – constant worry and inability to cope or handle dx Concept: Pain; topics chronic pain, non-pharmacological pain management 5 - Perception of Pain: o Cultural  Indigenous populations:  High reports of chronic pain  Face many challenges in accessing HC (culturally sensitive) o Social / Psychological  What patient believes  Ex. A woman in labour who doesn’t want medication o Also: what pt has tried for pain, and affect on ADL - Management: - nociceptive pain o Definition: damage to somatic or visceral tissues o Pathophysiology:  Somatic: aching or throbbing, localized, from bone or joint, muscle or skin, or connective tissues   Visceral pain: from stimuli such as a tumour or obstruction in the internal organs o Nursing process: - Neuropathic pain o Patho:  Damage to nerve vessels or changes in the cns  Burning, shooting, stabbing, or electrical pain  Can be sudden, intense, short-lived, or lingering o Types  Central:  Peripheral: o Causes:  Trauma  Inflammation  Metabolic diseases  Alcoholism  Nervous system pain o Examples:  Trigeminal neuralgia  Diabetic neuropathy  Phantom pain o Tx.  Not well controlled by opioids  Multimodal tx. Adjuvants (antiseizure, tricyclic antidepressants, SNRI’a, antiseizure, transdermal lidocaine, alpha2-adrenergic agonists, - Acute pain o < 3 months o Causes:  Post op, labour pain, trauma  Angina o Tx.  Analgesia for symptom management  Tx of underlying problems - Chronic Pain o Changes in Nervous system undetectable with standard testing so objective findings will not be indicative of actual functional and severity of impact o Pathophysiology:  3 months +  no adaptive role  disabeling  often with depression or anxiety o Non-pharmacological interventions  Heat and cold tx  Massage  Exercise  Turning and positioning  Transcutaneous electrical nerve stimulation  Distraction  Relaxation  Self-management (realistic goals, energy conservation, communication skills - Pain assessment (OPQRSTUV) o Also pattern:  Breakthrough pain   Moderate to severdespite tx  Rapid and brief  Common in cancer pain Concept: Technology & Informatics, Adherence; topics home and self-care monitoring devices, annual influenza vaccination, medications, diet 8 - Tech in home settings: o Benefits: o Precautions: - Adherence o Definition: o Levels:  Partial adherence  Non-adherence o Factors that affect adherence  Vaccinations:  Medications:  Diet: o Interrelated concepts: Concept: Perfusion; topics hypertension, ischemic/hemorrhagic stroke, peripheral vascular disease, venous thromboembolism (VTE), pulmonary embolism (PE) 23 1) Normal Physiological of Peripheral Blood Flow a) Physiology: i) Blood is converted to a semi-solid gel from a liquid ii) Fibrin and platelets iii) Hemostasis iv) Complex coagulation process (1) 1st: vasoconstriction to reduce blood flow and blood loss (a) Accumulating blood surrounds vessel to create pressure on vessel nd (2) 2 : triggered by damaged blood vessel (a) Platelet plug forms b/c of von willebrands factor, a protein (b) 3-7 minutes rd (3) 3 : clotting factors are activated either from intrinsic or extrinsic pathways (a) Intrinsic pathway: b/c of collagen in blood vessels exposed to blood (b) Extrinsic: activated by tissues that are damaged when they release tissue factor or tissue thromboplastic (c) Converge at common pathway where thrombin stimulates fibrinogen to form insoluble fibrin v) Pieces: (1) Damaged vessels: (2) Platelets:  (3) Clotting factors: b) Scope: i) Continuum of ineffective clotting to excessive clotting c) How it is impaired i) No clotting factors ii) Clots are made when they shouldn’t be 2) Bleeding a) Physiology b) Risk factors i) Populations at risk (1) Older adults ( increased platelet adhesiveness) (2) Sickle cell anemia (black individuals) (a) Hypoxia, dehydration, low temp, metabolic acidosis changes shape of RBC ii) Individual risk factors (1) Affects all individuals (2) Genetics: hematologic dx, hemophilia (males), von Willebrands dx (men and women) (3) Immobility: slows return of venous blood to heart. Paralysis and decreased LOC, GCS, bed rest, vericose clots (DVT) (4) Smoking c) Management i) Primary prevention: (1) Genetic counsiling before conception (2) Prevent clots (a) Minimize: blood stasis risks, Increased blood viscosity, and vessel injury (i) Leg exercises, walking, wearing compression socks or anticoag therapy as prophylaxis, avoid BC, stop smoking (nicotein- vasoconstriction, damages endothelium, atherosclerosis) ii) Secondary prevention: screening, early diagnosis, prompt tx iii) Collaborative interventions for bleeding disorders (1) Prevention and control: (a) Recognise signs and symptoms of bleeding and notiffe MRHCP (b) Minimize trauma (i) Contact sports (ii) Use a soft bristled tooth brush, electric razor (iii)Avoid hard blowing nose (iv) Avoid tatoos and piercings (v) Count number of pads or tampons used if menstruating (vi) Contact MRHCP before teeth cleanings, manicures/pedicures (vii) Avoid injections or use smallest needle possible (viii) Monitor INR to assess risk (ix) If taking anticoagulants, avoid meds that counteract or contribute to bleeding such as asprin (c) Manage bleeding episodes (i) Direct pressure (ii) Topical agents to slow bleeding within joint space (iii)Meds 1. Replace clotting factors 2. Stmulate clotting factors, replace platelets (iv) Volume replacement (v) Oxygen support 3) Excessive clotting  a) Physiology: i) Blood is converted to a semi-solid gel from a liquid too much ii) Fibrin and platelets iii) Excessive Hemostasis iv) Forms a thrombus, obstructs vessels b) Risk factors c) Management i) Meds: (1) Anticoagulants (warfarin and heparin) (2) Antiplatelets (aspirin and clopidogrel) (3) Direct thrombin inhibitors (bivalirudin) (4) Thrombolytic agents (streptokinase) ii) Procedures (1) Phlebotomy- remove blood volume (a) reduces viscosity and marrow activity Q2-3Months (2) Thrombectomy- remove thrombus (a) Catheter or open surgery (3) Filters (a) Prevention (b) For pt who cant take anticoagulants or have hx of pulmonary emboli (c) Inserted percutaneously through right femoral vein or right internal veins and floated into vena cava iii) Nutritional therapy (1) Warfarin- interferes with vit-k (reduce vitamin K) (a) Green leafy vegetables (spinach, kale, mayo, canola, soybean oil) iv) Positioning (1) Affects blood flow and comfort (2) DVT- elevate legs to facilitate venous return to the heart (3) Arterial thrombus of lower extremities- dependant position so gravity helps improve perfusion to feet (4) Acute phase after a brain attack- Head of bed elevated 30o minimum to help blood flow to the brain to minimize edema (5) All pt on bed rest (a) Repositioning prn to help perfusion in dependant area (b) Wear sequential compression devices to stimulate venous return 4) Venous thromboembolism a) Application to perfusion i) Formation of blood clots or thrombus in a vein ii) 2 main (1) DVT (a) In deep vein (lower leg, thigh, pelvis) (2) Pulmonary Embolism (a) Pathophysiology (i) Blockage of a pulmonary arteries by a thrombus or an embolis or tumour tissue (ii) In lungs or a piece of clot breaks off and travels to lungs (iii)Embolus travels from place of origin to smaller vessels in pulmonary circulation and lodges in alveoli (iv) Mainly in lower lobes b/c increased blood flow (v) causes 1. Most arrive from DVT 2. Fat emboli- broken femur  3. Air emboli- improper iv insertion 4. Bacteria 5. Amniotic fluid 6. Tumours (primary and/or metastatic) (b) Clinical manifestation (i) No leg symptoms at time of dx (ii) Varied and nonspecific (iii)Triad 1. Dyspnea, chest pain, hemoptysis 2. 20% of pt (iv) Slow and sudden (v) Mild to moderate hypoxia w low partial pressure of CO2 in arterioles (vi) Cough (vii) Pleuritic chest pain (viii) Hemoptysis (ix) Crackles (x) Fever (xi) Accentuated plumonic heart sounds (xii) Change in mental status b/c hypoxemia (xiii) Massive emboli 1. Abrupt hypoxia 2. Pallor 3. Severe dyspnea 4. Hypoxemia 5. W or w/o chest pain 6. ECG-tachycardia w R ventricular strain (xiv) Pleural friction rub (c) Risk factors (i) Immobiltiiy or reduced mobility (ii) Surgery w/I 3 months (iii)Hx of dvt (iv) Malignancy, obesity, oral contraceptives, hormone therapy, smoking, air travel, heart failure, pregnancy, clotting dx (d) Application of perfusion (e) Nursing Care/tx (i) If small can be undetected and vague, transient symptoms 1. Unless underlying cardio dx (ii) Removal/TX: 1. Can be removed suddenly/spontaneously 2. Removal of causative device (catheter or pace wires) 3. Mechanical forces a. Sudden changes, Valsalva maneuver (iii)Dx studies 1. Spiral ct w contrast 2. VQ scan a. Ventilation-Perfusion scan b. Perfusion scanning i. Pt who cant have contrast ii. Iv injection of radioisotope iii. Images pulmonary circulation c. Ventilation scanning i. Inhale radioactive gas such as xenon  ii. Shows distribution of gas through the lungs iii. Cooperation of pt is needed (iv) Interprofessional care 1. Prevention: a. Objectives: i. Prevent further growth or multiplication ii. Prevent embolization iii. Provide cardiopulmonary support if needed- Varies according to severity (supplemental o2, turning, coughing, deep breathing, incentive spirometry) b. Prevent VTE i. Sequential compression ii. Early ambulation iii. Prophylactic anticoagulants iv. Begin Tx as soon as PE suspected c. Medication therapy i. Fibrinolytic meds- (tissue plasminogen activator or Alteplase) dissolve PE amd DVT ii. Heparin prevents clots doesn’t break down d. Surgical therapy i. embolectomy 5) Peripheral Vascular Disease a) Pathophysiology i) Systemic ii) Most symptomatic in aorta or peripheral systems in lower extremities iii) Cause: (1) Atherosclerosis- gradual thickening of intima and media (2) Inflammation and endothelial injury plays a major role b) Clinical manifestation i) When vessels are 60-75% blocked ii) Intermittent claudication: (1) Ischemic muscle ache or leg attack precipitated by exercise, resolves with rest, reproducable (2) Result of anaerobic cellular metabolism byproducts (lactic acid) c) Application to perfusion d) Risk factors i) Smoking ii) Diabetes iii) Hypertension, hyperlipidemia iv) Fam hx, hypertriglyceridemia, age, hyperhomocysteinemia, hyperuricemia, obesity, sedentary lifestyle, stress e) Nursing management 6) Hypertension a) Definition i) Sustained elevation of: (1) systemic arterial BP (> or = 140) (2) diastolic arterial BP (> or = 90) (3) normal 100-130/60-100 ii) Leading call of dr appointments iii) Stage 1  (1) 140-149/90-99 iv) Stage 2 (1) 160 SBP or 100 DBP v) Subtypes: (1) Isolated systolic hypertension (a) Sustained elevated SBP = or > 140 w a DBP 1 x (c) Increases pulse pressure (i) SBP-DBP (ii) Loss of elasticity of larger arteries= widening of pulse pressure (iii)Considered independant risk factors for CVD and end-organ damage (d) 2-4x risk of cardiomegaly, MI, stroke, b) Causes/etiology i) Primary hypertension (1) Majority of all cases (2) No cause identified (genetic and environmental factors probably) (3) Contributing factors: (a) Increased sns activity, overproduction of sodium-retaining hormones, vasoconstrictors, increased sodium intake, > than ideal weight, DM, excessive alcohol ii) Secondary hypertension (1) 5-10% of all cases in adults (2) 80% of all cases in children (3) Signs & symptoms (a) Unprovoked hypokalemia (b) Abdominal bruit (c) Variable pressure w Hx of tachycardia (d) Sweating (e) Tumour (f) Fam hx renal dx (4) Causes: (a) Coarctation or congenital narrowing of aorta (b) Renal dx (stenosis or parenchymal dx) (c) Endocrine disorders (pheochromocytoma, cushings syndrome, hyperaldosteronism (d) Neurological dx (tumours, quadriplegia, head injury) (e) Sleep apnea (f) Medications such as sympathetic stimulants (cocaine) (g) MAOI’s w tyramine-containing foods (h) estrogen replacement therapy (i) oral contraception (j) NSAID’s (k) Pregnancy induced hypertension (5) Tx. Underlying causes c) Pathophysiology i) Two reasons (1) Increased Cardiac Output (a) Early or borderline hypertension (b) Normal later in course (2) SVR (a) Rises later in course (b) Hallmark of Hypertension (persistent increased SVR)  ii) Genes (1) Polygenetic (2) 30-60% variability in BP (3) Familial hereditary is important iii) Sodium and water retention (1) Low sodium shows little to no hypertension iv) Altered Renin-Angiotensin-Aldosterone Mechanism (1) Regulates blood volume and BP (2) High plasma renin activity raises angiotensin 1’s conversion into angiotensinogen v) Stress and increased SNS activity (1) Critical role in BP control (2) Stress response increases (a) Vasoconstriction, increased HR, increased renin release increases aldosterone secretion vi) Insulin resistance and hyperinsulinemia (1) Stimulates SNS and RAAS (2) Impairs NO- mediated vasodilation vii) Endothelial cell dysfunction (1) Source of vasoactive substances like NO and ET viii) Obesity (1) Increases every aspect d) Clinical manifestation i) Lanthanic or silent dx b/c frequently asymptomatic ii) Increased workload of the heart iii) Secondary symptoms (1) Fatigue, reduced activity, tolerance, dizziness, palpations, angina, dyspnea iv) Complications: (1) Most common is target organ dx (a) Hypertensive heart disease (i) CAD 1. Atherosclerosis and plaque formation 2. Avoid heavy meals 3. (ii) L-Ventricular Hypertrophy 1. Increased Cardiac workload 2. Risk 2x w obesity (iii)Heart Failure (b) Cerebrovascular disease (i) Atherosclerosis 1. Common in bifurcation of the common carotid artery 2. Portions of plaque break off and travel to intracerebral vessels= thromboembolism (ii) TIA or stroke 1. Stroke has a 4x higher risk (iii)Hypotensive encephalopathy (c) Peripheral artery disease (i) Speeds up atherosclerosis (d) Nephrosclerosis (i) Marker: microalbuminuria (protein in urine) (ii) Direct result of ischemia b/c of narrow lumen in the blood vessels (iii)Leads to arophy of tubules (e) Retinal damage  (i) Shows how severe and long-standing the hypertendsive process has been e) Application to perfusion f) Nursing management i) Most significant modifiable risk factor for CV DX ii) Expect secondary hypertension in people 2050 y/o iii) Dx. Studied (1) Several elevated readings iv) Prevention (1) Prehypertension needs annual bp assessment v) Interprofessional care (1) Risk assessment (2) Modify lifstyles (a) Diet (i) DASH diet ( for hypertension or risk of hypertension) (ii) Fruits, veggies (iii)Low fat dairy (iv) Low sodium (v) Fibre (vi) Whole grains (vii) Plant proteins (viii) Reduced sat fat (ix) Reduce cholesterol and calories (x) Maintain potassium, calcium, magnesium (b) Limit alcohol (c) Exercise (d) Avoid smoking tobacco (e) Manage stress (f) Lose weight (g) Meds (i) Diuretics (ii) Adrenergic inhibitors (iii)Vasodilators (iv) Angiotensin inhibitors (v) Calcium channel blockers 7) Stroke a) Pathophysiology i) ii) Blood flow to brain: (1) Internal Carotid arteries – anterior circulation (a) Frontal, parietal, temporal lobes, basal ganglia, and diencephalon (2) Vertebral arteries- posterior circulation (a) Some temporal lobe, occipital lobe, cerebellum, brain stem, and diencephalon iii) Types of strokes: (1) Ischemic stroke: (a) Inadequate blood flow to brain (partial or complete occlusion) (b) Men more than women (c) Further divided into causality (i) Thrombotic 1. Blood clot in diseased vessel 2. If increased with plaques  3. Most common 4. 2/3 assoc w hypertension and diabetes mellitus (accelerate atherosclerosis) 5. Most pt usually do not have a decreased LOC in 1st 24hrs (unless brainstem or seizures, increased ICP or Hemorrhage), and may progress in the first 72 hrs as infarction and cerebral edema increases a. Lacunar stroke- occlusion with small artery going to the deep brain tissues i. Hemiplegia, pure sensory stroke, contralateral leg and face weakness, isolated motor and sensory stroke (ii) Embolic 1. Embolus lodges in and occludes a cerebral artery = infarction and edema 2. Second most common cause of stroke 3. Emboli usually og in endocardial tissue of the heart with plaque breaking off 4. Assoc. w valvular heart disease and prosthesis MI, ineffective endocarditis, rheumatic heart disease, intracardiac congenital defects 5. Rapid, severe symptoms, less warning signs 6. Sudden onset 7. Usually remain conscious (iii)Transient Ischemic Stroke 1. Temporary episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia W/O acute infarction of the brain 2. Symptoms lass < 1 hr 3. Cant know weather it will be just a TIA or a stroke will develop 4. Stroke risk greatest immediately after 5. Caused by a microemboli or a plaque that gets temporarily lodged 6. If in carotid system: temp loss of vision in one eye, transiet hemiparesis. Numbness or loss of sensation, sudden inability to speak 7. If in vertebrobasilar system: tinnitus, vertigo, dark or blurry vision, diplopia, ptosis, dysarthria, dysphagia, ataxia, unilateral or bilateral numbness or weakness (2) Hemorrhagic stroke: (a) 15% of strokes (b) Bleeding into: (i) the brain tissue (intracerebral or intraparenchymal hemorrhage) 1. b/c of rupture to a vessel 2. 10% 3. Hypertension is the most important risk factor a. Also: cerebral amyloid angiopathy, vascular malformation, coagulation disorders, anticoagulation and thrombolytic meds, trauma, brain tumours, ruptured aneurysm.  4. Commonly during periods of activity, sudden onset, neurological deficits, headache, nausea, vomiting, decreased LOC, hypertension (50% of pt) (ii) the subarachnoid space or the ventricles (subarachnoid hemorrhage or intraventricular hemorrhage) 1. intracranial bleeding into CSF space between the arachnoid and pia matter 2. commonly b/c ruptured aneurysm 3. other causes: avm, trauma, illicit drugs 4. 35% die b) Risk factors i) Nonmodifiable risk factors: (1) Age, sex, indigenous, African, South American, fam/ med Hx, access to safe food and water, (2) Arteriovenous malformation: tangled veins, increased bleed risk, anywhere in body ii) Modifiable risk factors: (1) Control and prevent other Dx: hypertension, heart disease (AF, MI, cardiomyopathy, valve abnormalities, congenital defects, DM, increased serum cholesterol, carotid stenosis, smoking, alcohol (depends on amount), illicit drugs and older BC pills. c) Causes: i) Atherosclerotic plaques ii) Extent of stroke depends on rapidity of onset, size of the lesion, collateral circulation d) Clinical manifestation i) TIA is a precursor to an ischemic stroke ii) Destroyed neural tissue: neurological dysfunction iii) Change in body functions: (1) Mobility, respiratory function, swallowing and speech, gag reflex, self-care abilities, loss of skilled voluntary movement, impaired integrity of movements. Hyporeflexia then hyperreflexia (a) Post stroke: arms and legs of affected side are weak or paralyzed (i) lesions in cortex- weakness in contralateral lower face only (ii) Facial lesions- ipsilateral upper and lower face (iii)Middle cerebral artery- greater weakness in upper extremities, lower facial drooping 1. Most common iv) Communication (1) L hemisphere is language skills in most people ( not SOME L handed people) (a) Expression and comprehension (2) Aphasia (comprehension and speaking ability when on dominant side of the brain) (3) Dysphasia- impaired communication (interchangeable with aphasia) (a) 4 categories (i) Expressive aphasia- expression speech, writing (ii) Receptive aphasia- difficulty understanding (iii)Anomic or aphasia- least severe form, cant name objects/things/people/events etc. (iv) Global aphasia- loss of all receptive and expressive aphasia (4) Affect (a) Difficulty controlling emotions- exaggerated and unpredictable (b) Depression- common in 1st year (5) Intellectual function (a) Memory and judgement impairment  (i) L: memory w language, cautious with judgement (ii) R: impulsive and quick (6) Spatial-Perceptual Alterations: (a) R: more likely, (b) 4 categories (i) Incorrect perception of self and illness, follows parietal lobe perception- may deny DX or own body parts (ii) Erroneous perception of self in space, may neglect input from affected side, worsened by homonymous hemianopia- blindness occurs in the same half of visual fields of both eyes, tricky spatial orientation ie. Judging distance (iii)Agnosia- cant recognise object with most senses (iv) Apraxia- cant do learned sequential movement on command (7) Elimination (a) Mainly temporary problems e) Nursing management i) Dx studies (1) Goals: (a) Confirm it’s a stroke (b) Id likely cause (2) MRI (a) Extent of injury (3) Non-contrast CT (a) Optimally w/I 25 minutes and read w/I 45 minutes of arrival (b) Indicates size and location (c) Ischemic and hemmorgaic (4) CT angiography (a) Visualize brain vessels (b) Can be done with noncontrast CT ii) Primary prevention: (1) Goals: (a) Control: BP, BG, diet and exercise, reduce smoking, limit alcohol, routine health analysis iii) Meds: (1) To prevent stroke in pt with TIA Hx. (a) Anticoagiulants (i) Asspirin (ii) Clopidogrel (iii)Eapixaban (iv) Dabigatran (v) Rivaroxaban iv) Surgery (1) Transluminal angioplasty- balloon is inserted 8) teaching and learning plan to care for patients with hypertension, stroke and peripheral vascular disease in relation to perfusion. Concept: Healthcare law & interpersonal violence; topics Protection for Persons in Care Act, privacy breach/duty to report, elder abuse 14 a) Health care laws i) Definition: ii) R/t privacy breach iii) Duty to report: iv) Nurses role in managing health info and reporting b) Protection for Persons in Care c) Interpersonal violence: i) Signs and symptoms ii) Risk factors iii) interventions d) Abuse i) Types: (1) Elder abuse (a) Definitions: (i) Harm to older adults from people who thye have a reason to trust (ii) Resident-resident abuse: 1. Between two residents in LTC (b) Risk factors: (i) Socially isolated (ii) Physically impaired (iii)Cognitively impaired (dementia, impaired judgement, lack of insight) (iv) Caregiver factors 1. Life stress 2. Pathologival characteristics 3. Personality 4. Insufficient resources 5. Poor health 6. Cognitive impairment 7. Substance abuse 8. Social isolation 9. Dependence and co-residence 10. Poor interpersonal relations (v) Women (vi) Lives alne or w abuser, depends on abuser for care (vii) Men- more likely to be physical or exploitive abuse (viii) Women- more likely to be neglectful or psychological abusers (ix) Vary by form, several factors/variables, origins in both perpetrator and elder, and relationship (x) Invisabilty to society (xi) vulnerability (c) Types: (i) Neglect 1. Refusal or failure by those responsible to provide food, shelter, health care, or protection fr a vulnerable elder by anyone responsible 2. In nursing homes:  a. Argumentative behaviour, intimidation b. Admin problems, lack of policies, bad staff screening education and training, staff shortages and turnover 3. Mutually neglectful a. Older married couple b. Several psychological risks (both with dementia) 4. Self-neglect a. Behaviour of an elderly person that threatens their own health or safety b. Risks i. Older, chronically ill, limited function, lives alone, socially isolated, low economic resources, dementia, mental illness, substance abuse or hoarding (ii) Abandonment 1. Desertion of a vulnerable elder (iii)Exploitation 1. Illegal taking, misuse, or concealment of funds, property, or assets of a vulnerable elder (iv) Mistreatment (v) Emotional 1. Inflicting mental pain, anguish, or distress on an elder person verbally or nonverbally 2. Most prevalent (vi) Physical