NURS701 Notes 2021 sem 1 PDF

Title NURS701 Notes 2021 sem 1
Author Soph
Course Integrated Nursing Science
Institution Auckland University of Technology
Pages 105
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Summary

Lecture 2 – PATHOPHYSIOLOGY OF COMPLEX CONDITIONS FOR ADULTSComplexity: ‘Geriatric giants’ awareness and identification Geriatric: >5 years old Normal Aging or underlying pathology: process of slowing down, physically & cognitively Healthy Aging:Adaptation ability to define oneself in relatio...


Description

Lecture 2 – PATHOPHYSIOLOGY OF COMPLEX CONDITIONS FOR ADULTS Complexity: - ‘Geriatric giants’ awareness and identification - Geriatric: >5 years old Normal Aging or underlying pathology: - process of slowing down, physically & cognitively Healthy Aging: Adaptation - ability to define oneself in relation to independence and autonomy Compensation - ability to change one’s lifestyle to accommodate the physical changes Resilience - ability to bounce back, change and adapt Scientific theory of aging: *older adults may present atypically (not usual symptoms) eg. Temp need to be measured against their usual baseline

Case: Mrs Jones , 90-year-old woman who lives alone in her own apartment since her husband died 3yr. Dx: HTN aged 70yrs – taking antihypertensives ; Zopiclon prn Sleep: about 5 hours - naps frequently during the day.

G/U: Usually she wakes 2x during the night to empty her bladder. Physical activity: Reluctant to ‘go for daily walks’ but gets exercise while shopping. M/S: balance is not as good as it used to be. Gets dizzy when she stands. Several tripping incidents. District nurse visiting daily to dress shin & forearm laceration. GI: Says she’s lost her appetite but eats a good meal at the weekly family meal which she hosts. Reports she’s lost a bit of weight Vision: no longer drives at night/ only in daylight. Memory: Is noticing changes eg couldn’t remember where she parked the car when shopping recently but gave detailed account of the event. Doesn’t understand/recall what doctor tells her. Social: stopped participating in group activities. Phone contact with 1 or 2 surviving friends. Enjoys browsing the shops and reading but can’t concentrate / dozes off Family very supportive – live in the same neighbourhood and in frequent contact – running errands, taking her to specialis specialist appointments, dropping in for a cuppa

Cardiovascular changes - Mrs Jones fatigue Physiological changes: Heart ↓cardiac muscle strength Heart valves thickened/more rigid SA node ↓ efficient/pulses slowed Contractions weaker, ↓blood vol & ↓ CO Blood vessels

↓ elasticity Thickened capillary walls Vascular walls more rigid Blood ↓ volume (due to ↓total body H2O) Functional changes: •

Fatigue & ↓ activity tolerance & ↓ intensity is normal in the absence of disease



Older adults usually adjust to cardiac changes but find they need to pace their physical activity



Orthostatic hypotension

Functional ability for everyday life = good Gastro-intestinal system - Is losing appetite and losing weight age-related? Age-related changes: Oral cavity: ↓saliva Oesophagus: ↓gag reflex = ↑aspiration Stomach: Gastric mucosa atrophy / ↓ gastric secretions…. Leads to malabsorption (esp. iron, B12, protein & some meds) Intestines: ↓ peristalsis leads to constipation - Decreased peristalsis also contributes to slower transit time in the large intestine and allows more time for water reabsorption and hardening of the stool. Because of this factor, the nurse should recommend a diet adequate in fiber and fluids.

Functional changes: “fullness” after small amts of food - due to slow peristalsis and loss smooth muscle tone delay gastric emptying - Delayed gastric emptying and reduce gastric sections = indigestion & reduced appetite (Frequent small meals, ). Reduced appetite Indigestion Constipation

*losing appetite is age related, losing weight is a problem in old age Losing weight risk factors: Malnutrition Fatigue and inactivity Frailty

Urinary system – Is nocturnal frequency normal? Renal function: •

↓ Renal blood flow (due to ↓ CO & ↓ GFR



Impaired ability to concentrate urine

Bladder: ↓ muscle tone & incomplete emptying ↓capacity

Functional changes: •

Urinary frequency



Nocturia



Retention of urine (Benign prostatic hyperplasia common (80% males >80yrs)



↑ risk of infection, urgency & incontinence



↓ ability to modify electrolyte imbalance

*Incontinence is not normal in aging. Enlarged prostate: Ø Decreased ability to modify electrolyte imbalance Ø Renal blood flow: half that of young adult Ø Bladder smooth muscle replaced with fibrous CT Ø Benign prostatic hyperplasia common (80% males >80yrs) Nervous System – sleeping less normal for old age? •

Neurons



↓neurons in brain & spinal cord



↓ Synthesis & metabolism of neurotransmitters



Gradual ↓ brain mass



Disturbed sleep patterns



Slowed reaction time

Cognitive Aging: •

Sensory - remembering an image shortly after seeing it – doesn’t change with ageing



short-term - i.e. recall recent events - slowly declines. Any negative effects can be reduced by conversing in a relaxed and non-evaluative style (i.e. the possible threat of failing eg checklist of Q’s will reduce recall or complex information will reduce recall)



long-term – retrieval is slowed depending on recognition of the material, usefulness of information and type of task & motivation. Tend to remember stories

Assessment: MMSE – 30 point questionnaire to measure cognitive impairment (memory, thinking & simple p-

solving) Orientation- year, where are you, prime minister.. Registration – name 3 object placed on the table Attention and calculation – (simple calcs) subtract 7 from 100 Continue 5x: 100, 93, 86, 79, 65 Recall the 3 objects on the table earlier (now removed) - memory Language eg give 3 commands eg “place index finger of right hand on your nose and then on your left ear” etc Copying: provide a picture of a pair of intersecting pentagons & instruct to copy Older people with depression Case: First Admission Mrs Jones, 90yrs, admitted acutely to hospital via ambulance Fell while out shopping. Bystanders report no loss of consciousness, alert and orientated. Recalls events. Pain in L)knee. Diagnosis: # patellar. Surgical repair. Stabilized with leg brace Uneventful recovery. Discharged 7/7 with instructions to attend OP orthopaedics to have brace angle changed 2/52. Referred for NASC assessment. Meanwhile daughter lived in to care for her mother Readmission Readmitted 3wks post op via ambulance following a fall at home and reports of hallucination Findings:

Cognition: orientated to time and place; correct recall of events; some memory loss Neurological: delusional; hypervigilant & not slept for 48hrs. Family report that she was sleeping 20/24hrs for the past week until 2 dys ago when she ‘started seeing things’. Family rostered 24/7 supervision at this time Neuro obs: T 35.6-36.2; RR 16-18; PR 62-88; BP 110/70- 172/90 FBC: nothing significant. Mild dehydration Pain: occasional sharp positional L) knee pain that passes on repositioning Mobility: Mobilizing well with walker Delirium: - transient, reversible syndrome that is acute and fluctuating - Medical emergency: lead to cascade of events ie falls, fractures, functional decline, dementia Subtype ·

Hyperactive

- Confusion, agitation, disruptive behaviours, labile mood, psychotic symptoms ·

Hypoactive

- confusion, apathy, lethargy ·

Mixed

- has both features Geriatric Syndrome - Geriatric syndromes represent common, serious conditions for older persons, leading to dependence - Predictable problems experienced by older adults which are often preventable and lead to poor outcomes

- They are Not particular diseases - Syndrome = syndrome refers to a pattern of symptoms and signs with a single underlying cause that may not yet be known - Therefore pathophysiology is problematic - For a given geriatric syndrome= Multiple risk factors and multiple organ systems are often involved =multicauses **Each geriatric syndrome is distinct but has shared risk factors: eg, Risk factors that increase the falls risk = sedative use, cognitive impairment, lower extremity disability, poor balance and gait, as well as foot problems Prevention = Need strategies to address the many components that lead to falls risk – little point focusing on eg #patella to the exclusion of previous history of falls Examples of such potentially beneficial interventions include hormones, statins, antioxidants, as well as as exercise, improved nutrition. Functional decline is a common complication in hospitalised older patients associated with low mobility and physical inactivity Dementia: - impaired memory - gradual loss of language (aphasia, agnosia) - Impaired executive function ie problem solving, decision making, planning, abstract thinking - impaired mobility - changes in mood and personality Frailty: Chronic diseases - multimorbidity is associated with frailty

Frailty impairment in mobility, balance, muscle strength, cognition, nutrition, endurance, and physical activity At risk •

Hospitalisation;



Hospital-associated complications eg falls & delirium, functional decline & pressure ulcers;



Institutionalisation

Older patients are more likely to be alive and in their own homes at follow-up if they received comprehensive geriatric assessment on admission to hospital (Ellis et al., 2017) – Nurse advocate Case: Mrs. Ram is 86 years old and is in good health. On a recent visit, her daughter noticed that her mother seems confused and has decreased energy and bruising. Possible diagnosis/es: 1. Dementia. 2. A urinary tract infection. 3. Delirium. Medications Prednisone Bronchodilator (reliever) eg Ventolin (Salbutamol) – not a steroid CorticosSteroid (preventer) eg Flixotide, Pulmicort combined preventer/reliever - 2019 NZ study found combined preventer/reliever significantly better managed asthma – Oxygen – at home Beta blockers eg Atenolol or metoprolol work by blocking the effects of the hormone epinephrine, also known as adrenaline HR and with

less force, which lowers blood pressure & helps keep beat regular Diuretics. Eg Frusemide - Diuretics reduce your body's fluid content. CHF can cause your body to retain more fluid than it should. anticoagulants (OA) eg warfarin (known by the brand names Marevan and Coumadin). Since then, new oral anticoagulants -dabigatran & rivaroxaban - have less co-morbidities CHF develops when ventricles can’t pump enough blood volume to the body. Eventually, blood and other fluids can back up inside lungs Self management Nurses need to learn how to support people with long‐term conditions to self‐manage, take more control over their health and improve their health outcomes – to help them adapt and to self‐manage Acute Care: ignore self management – its all about managing the condition and risk factors PHC : don’t really pay much attention to helping patient develop skills for self-mgt – Yet the hcs relies on pt self managing – assume pt will develop skills out of personal interest in keeping well Supporting patient self management requires that nurses •

Understanding patient experience of living with the multiple conditions – deteriorating



Skills for motivating health behaviour changes eg brief interventions



Are aware of patients’ needs and preferences



except

Gawande argues that for those with chronic conditions trust underlies incremental “steady, intimate care” that can help patients. Patients actively engaged with and trusted providers whose actions directly addressed their clinical and non-clinical needs. PHC & GP practice settings are proposed as the ideal environment for supporting selfmanagement

Self-management involves Behavioural change – lack of nurse training in motivational interviewing (a type of behavioural counselling Health literacy Lecture 8 – MUSCULOSKELETAL Skull: - continues to expand to accommodate growing brain tissue - it thickens by adding layers at the surface of the skull and simultaneously there will be reabsorption in inner skull surface Long bones gain length: - via adding at the epiphyseal plate and width through subperiosteal apposition - children are more vulnerable and prone to injuries as this is a weak area Remodelling of the bones as the long bones lengthen: - this is where the bone changes its shape Physiology of how muscles grow is essentially does not grow over the lifespan - growth factors and cellular organelles are important in mitosis in repairing and replacing muscles in adult Muscle growth: - rate of muscle protein synthesis to be greater from the muscle protein breakdown, the rate difference will be equal to muscle growth Factors that affect paediatric musculoskeletal growth: Strength training and inadequate sleep - it can impair the muscular and bone development

Diet - nutritious food can enhance the muscle repair and bone development Environment - hazards can impair muscle and bone development eg lead exposure, muscle fatigue, pesticides exposure Muscle conditions - muscular dystrophy: can hinder the growth of the muscle mass Inherited Traits - ie gender, ethnicity and genes - it detect and determine bone density and muscle mass Paediatric musculoskeletal conditions Scoliosis - cause unknown - early signs: shoulder and/or scapulae asymmetry - waist creases: when spine become curved, there will be a crease in one side of the waist -difference in the way the arms fall beside the body - head not centred - progressively worse relative to the rate of growth: the rapid they grow, the rapid scoliosis progress - born with or develop later in life - seen in between 8 to 18 years old, girls are more affected **When the spinal curves in between 20 degrees to 25 degrees, this need to be reduce in 10

degrees as it is desirable for scoliosis Treatment: - determined by the degree of the spinal curvature - regular imaging to review changes - bracing & physiotherapy: specific to individuals on which it varies on degree and the angle of the spinal curvature. It prevents surgery later of the stage to lessen the spinal angle - exercises Osteomyelitis u Inflammation in a bone u Potential causes Ø Bacterial infection through an open skin wound called haematogenous osteomyelitis – inflammation and infection can be either acute or chronic u Determined through Ø Fever, bone pain Ø History with injuries Ø Blood tests Ø Musculoskeletal assessment Ø Xray Ø Ultrasound, bone scan and/or MRI Ø Needle aspiration Treatment: Ø Dependent on age and severity of infection Ø Gets harder to treat the worse it gets as it became chronic Ø IV antibiotics followed by extended period of oral Abs (common form of treatment) Ø IV ABs only for an extended period Irritable hip - occurs between 3 to 8 yrs old

- aka ‘transient synovitis’ preceded by a viral illness/infection. It happened 1 to 2 weeks before the hips starts to be painful and irritable - affects only one hip u Inflammation of a hip joint u Synovial membrane irritation u Preceded by cold or viral infection u Causes hip pain and limping u Affects boys more than girls u Treatment Ø Pain relief Ø Rest Ø Several weeks to recover Musculoskeletal changes in adolescence u Second molars appear around 13 years u Hormones in puberty increase bone mass and strength u Bone development completion late teens/early 20’s u Skeletal growth evident by epiphyseal plate fusing with the diaphysis (bone shaft) u Arms and legs lengthen u Significant increase in muscle mass in boys u Pelvic girdle widens in girls u Development affected by: u Hormone deficiency ie oestrogen & testosterone, growth hormone – these can impair muscle and bone growth u Immunosuppressant drugs (as in cancer) u Arthritis u Prolonged inactivity u Obesity u Malnutrition u High intensity training u Excessive physiological loading - can cause strains that can lead to injuries to the joints, bones and muscle u Excessive exercise that stops menstruation

Tension neck syndrome Causes Ø Poor posture Ø Incorrect sleeping position Ø Repetitive neck movements Ø Teeth grinding Ø Stress Ø Injuries Ø Disc herniation Ø Degenerative diseases Trapezius muscle commonly affected: u Symptoms Ø Neck pain Ø Muscle spasms Ø Sharp intense pain, worsens with movement Ø Stiff neck Ø Headaches Common fractures in adolescents Ø Spiral fracture Ø Open/compound fracture Ø Transverse fracture Ø Oblique fracture (nondisplaced and displaced) Ø Comminuted fracture Ø Avulsion fracture Ø Greenstick fracture Types of bone fractures: Transverse fracture - horizontal line fracture Open/compound

- complete bone fracture and bone will protrude or break to the skin - may or may not visible Oblique - angle pattern - obliques displaced or non-displaced fracture - bone ends are separated apart Avulsed - sharing force of muscle movement, tears a bone fragment from the main compartment Spiral or torsion fracture - when there is a rotating force applied along the axis of the bone Greenstick - bone is bent but not broken through the bone 3 phases of fracture healing: Ø Bleeding and Inflammatory phase - developing bleeding and inflammation - where hematoma forms between the fracture and bone surface - this is because the osteocytes of both ends of the bones die due to hematoma as this obstruct blood flow and deprives osteocytes from oxygen O2 deprived osteocytes = they die and necrosis occurs as this worsen inflammatory response - when the inflammatory response occurs due to necrosis of the osteocytes, there will vasodilation and further oedema - fibroblast and lymphocytes will migrate to the fracture site to: Fibroblast – to form fibrin mesh work and promote granulation tissue and capillary buds which it helps in collagen formation that allows Calcium deposits that contribute to bone growth

*after Ca deposit, callus will begin to form. A material that forms a connecting bridge across the two bone ends to initiate bone growth. Lymphocytes and macrophages – will clean the area to localise and contain the information Ø Reparative phase ‘rebuilding phase’ - second phase in fracture repair - this when the osteoblasts promote the formation of the new bone - osteoclasts will destroy the dead bone and help to synthesise the new bone to make collagen and Calcium deposits to continue build new bon Ø Remodelling phase - excess callus will be removed - new bone will lay down along the fracture line - the fracture site will be calcified and the bones will be attached Fracture complications Ø Compartment syndrome Ø DVT Ø Infection Ø Delayed union Compartment Syndrome Occurs when a facia lined compartment within a limb has a pressure which exceeds the space of the compartment. Thus, reducing circulation to muscles and nerves Decreased perfusion ↓ Capillaries dilate to increase delivery of blood & oxygen ↓ A deficit of blood/oxygen leads to plasma proteins leaking into interstitial space ↓ Oedema increases

↓ Compression of vascular network ↓ Results in risk of sepsis and loss of limb - occurs through fracture or after injury - it happens when a facial line compartment within a limb has a pressure which exceeds the space of the compartment - space where the compartment situated is where the pressure is exceeding - causes swelling and hematoma that puts compartment under stress - ‘on stress’, it reduces circulation to muscles and nerves - it encloses bone, nerves and blood vessels - reduce of circulation, the capillaries will dilate to increase the delivery of blood and O2 - However, deficit of blood and O2, leads to plasma proteins leaking into the interstitial space causing oedema, compression of vascular network on which it result in oedema or loss of limb

u Signs & Symptoms Ø Aching, burning or cramping pain Ø Tight feeling in affected limb Ø Swelling Ø Numbness or tingling Ø Cool & pale observation distal to the affected area Ø Weak pulses distal to the affected area *Musculoskeletal assessment is important u Interventions Ø Neuromuscular - assessment to assess ...


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