NURS 209 Midterm Practice Exam

NURS 209 Midterm Practice Exam

What are the trends of the geriatric population

People are living longer and longer

The population of 65+ is getting larger and larger (differentiate between 65+ and 85+)

Women are living longer than men in the geriatric population

The centenarian (100+) group is the fastest growing group

Growing amount of 85+ living in a collective dwelling

What are the trends of elderly people and their personal activites

Lots of people are actively pursuing exercising, socializing, and technology

Tons of elderly engage in passive leisure activities

What is aging in place

Helping adults live independently in their homes, which includes home modifications, consultation, energy conservation, home safety and social interaction

Also includes safe and accessible transportation, and available community support and health services

What are the social determinants of health

50%: Life/Social Environment/Upbringing: Lifestyle, food, education, income, race, housing…

25%: Health Care System; wait times, access, resources

15%: Genetics and Biology

10%: Physical Environment; Air Quality, Civic Infrastructure

What is the dahlgren rainbow model of aging

How SES, culture, environment interact with living/working, social, lifestyle, and genetics

(like a brofenbrenner circles)

What is the active aging model

Social determinants of health, behaviours, medical, environment, lifestyle+culture+gender influence active aging

What are the common issues in gerontology

Aging in place – People need to be able to age where they want (house modifications)

Support caregivers/aging workforce – Older people are staying in the workforce too long, overworked or understaffed

Social engagement – less family support

Elder abuse – overworked elders for example

What are the factors that affect socioeconomic status

Education, income, gender, race/ethnicity, immigration, mortality, health resource utilization

How does education affect socioeconomic status

More educated are able to thrive, are healthier, and have better function

Could be due to being educated on how to navigate a complex health system and understanding the available health services

How does income affect socioeconomic status

Higher income = healthier lifestyles

Low income is linked with higher functional disability

How does gender affect socioeconomic status

Women live longer than men but are less healthy

How does race affect socioeconomic status

Indigenous people are disadvantaged

Other socioeconomic factors are affects (available resources, lower income, social isolation)

How does immigration affect socioeconomic status

Health immigrant effect – Health starts out higher than Canadians but quickly dissolves

Changes in diet, activity, habits, discrimination, lack of navigating the system

How does mortality affect socioeconomic status

More comorbidities

Cancer is the leading cause of death

How does health resource utilization affect socioeconomic status

Geriatric population represents a large majority of inpatient population and ALC use

ALC = elder using health resources ($$) while still awaiting placement

What are the physiological theories of againg

Genetic mutations – mutations that cause abnormalities

Cellular waste accumulation – bodies can’t clean the toxic stuff up

Wear and tear – bodily processes function poorly as we age

What is the telomere shortening aging theory

During cell replication, telomeres at the end of chromosomes get shorter and shorter

Eventually there is DNA loss and a weaker repair and regeneration process

What is the antagonistic pleiotropy aging theory

A single gene causes many effects, both positive and negative

Estrogen which helps fertility but can cause risks for chronic diseases

As we age the negative effect dominates

What is the circadian clock aging theory

We have a typical rhythm which represents out day to day.

A disturbed circadian rhythm causes disruptions in homeostasis which causes the problems associated with aging

What is the reliability aging theory

“A car just will eventually start breaking down”

Ex: thymus gets smaller and smaller which affects it own hormones and affects all other organs that interact with it

What is the effect of our genetic makeup on stressors

Genetic makeup can predispose people to be more resilient to stress

Systems will have to adjust to maintain homeostasis

Stressors will eventually lead to age-related diseases

What is the free-radical formation aging theory

Free radicals which change the expression of genetic material

What is inflammageing

Aging leads to a chronic inflammatory state

Chronic diseases due to inflammation develop (associated with cytokines and interleukines)

What is endothelial dysfunction and how is it inked to aging

A decreased insulin response leads to the problems that are associated with aging

Insulin supports growth and regeneration, lack of = problems

What is the Manslow’s Hierarchy of Needs aging theory

Progressive human motivations

Physiological -> safety -> love/belonging -> esteem/accomplishment -> self-actualization

What is Jung’s Model of lifelong development theory

How do we develop our identity and personality

As we grow older we develop a more authentic identity and more wisdom

What is Erikson’s Theory of psychosocial development

At elderly age, we have ego integrity or despair

We are happy with where we’ve gotten vs. we are unfufilled

What is the elder’s life course theory

5 components that influence how we go through life

Linked lives – social environment (influence of others)
Agency in constraints – experiences are constrained by what’s available
Lives in times and places – how we age depends on the era
Lifelong development – we just constantly develop
Timing in lives – early decisions affect later ones

What is the social clock?

Culturally defined times for social activities to be performed

What is the disengagement theory?

We age, we disengage from prior activities. We become more selective as we can’t invest as much energy in everything

What is the continuity theory?

As we age, we do what we used to do when younger.

Age actively in society.

Is associated with positive perceptions of the aging process

What is the political economy aging theory?

Ageism – society prevents elders from doing specific things

There are power imbalances which prevent people from acting a specific way

What are geriatric syndromes?

Patterns of symptoms and signs with a single underlying cause

Multifactorial and associated with poor outcomes. Have shared risk factors.

Multifactorial health conditions that occur when accumulated impairments in multiple systems occur

Ex: falls, frality, cognitive impairment, urinary incontinence, malnutrition, sleep/sexual dysfunction

What is frality?

Age-related geriatric syndrome with a decline in function/physiological systems

Caused by a hyperinflammable state

Predicts poor outcomes, longer hospital stays, earlier deaths, comorbities

What is the association of life space and clinical frality model?

Frality is caused by the interactions between self and the environment

When environment support<challenges

Individual support<cahllenges

What is the public health framework for healthy aging?

Capacity decline requires a change in services

Health services – preventative measures, and earlier detection

Long-term care- Support those with declined capacity

Environmental – increase accessibility to prevent loss in function

What is the phenotypic markers theory of frality

Only physical manifestations of frailty can be present

Ex: muscle loss, slowness

What is the cumulative deficit model theory of frality

Frailty has multiple morbidities which accumulate to lead to frailty

Include physical, cognitive, behavioral, and mental

What is the physiological pathway of frailty?

(Phenotypic model)
Disease causes change in physiological markers (inflammation) which leads to frailty syndromes which leads to negative outcomes

(Epigenetic model)
Environment interacts with genetics which leads to cellular damage which leads to frailty

What are some determinants of frality

(Socio-economic) – isolation, poverty, nutrition, caregivers

(Physical) – age, visual loss, limb impairments

(Comorbidities) – polypharmacy, other geriatric syndromes

What is the pathogenesis of frality

Multiple factors

Sarcopenia – loss of lean muscle
Chronic inflammation – IL-6 and CRP is high
Altered hormones
CV – decreased HR and more clotting
Anemia and micronutrient deficiencies

What is the effect of the immune system on frailty

Proinflammatory state

Inflammatory markers lead to a loss of muscle, malnutrition, and anorexia

What is the effect of the endocrine system on frailty

Hormone pathways are affected

Less growth hormones, sex hormones are altered

What is the effect of MSK on frailty

Sarcopenia – loss of muscle that is influenced by inflammation and endocrine system

Sarcopenic obesity – gaining fat while losing muscle mass

What is the clinical frailty scale

Measured from 1 – 8 (very frail) and 9 (terminally ill)

Follows the cumulative deficits model. Helps identify people who may need intervention

Highlights that frailty causes a risk of having a poor response to a stressor

What is the comprehensive geriatric assessment

Multidimensional diagnostics and treatments

Medical – Diseases, medications…
Mental health – cognition, fears
ADL’s – ADL’s, gait, activity
Social circumstances – social support, finances
Environmental – Transport, home facilities

What are geriatric interventions for frailty

Physical activity (most effective)

Nutritional interventions – supplements and appetite stimulants are not recommended (for weight gain)

Hormonal interventions – Vitamin D is recommended, not growth hormone

Other approaches – avoid polypharmacy, increase comprehensive geriatric assessments

What is the chronic care model

Organized care from home to hospital to home

What is polypharmacy

5+ medications daily or the use of potentially inappropriate medications

What is hyperpolypharmacy

10+ medications

What is oligopharmacy

Up to 5 medications/daily

What are some trends of polypharmacy

Expensive for healthcare

Prescription drug use rises with age

Polypharmacy is high in elderly

Inappropriate use of medications is very popular

What are contributing factors to polypharmacy

Increase age leads to increased comorbities

Poor coordination of care from pharmacies

Med hoarding

Taking meds that aren’t appropriate anymore

Inappropriate report of taken meds/symptoms

Prescribing cascade – one med’s side effect is treated with another med

What are healthcare provider risk factors for polypharmacy?

Uncoordinated care
No regular medication reviewing
Prescribing to control symptoms (not treating disease)
Hypothetical evidence that a drug is the best drug for a problem
Automatic medication refills without review
Lack of knowledge of geriatric pharmacology
Giving drugs to to fear of ageism of cultural bias

What are the geriatric effects of absorption

Slower absorption but not less

Causes – Reduced GI motility, reduced gastric acid (affects metabolism of drugs as well), medications that don’t mix well with gastric juices, poor GI blood flow

What are geriatric effects on distribution

Body composition – body is more fat and less water (lipid soluble are stored longer)

Blood protein – less protein which increases unbound drug (acidic)

Alpha-1-acid glycoprotein – binds to basic drugs

Blood-brain permeability – decreased p-glycoprotein which pumps drugs away from the brain

What are the geriatric effects on metabolism

Drugs stay in the body longer and take longer to be converted

Liver – less liver bloodflow (results in less metabolism of drug to be eliminated and more drugs being metabolized to be active)

Cytochrome P-450 enzymes – decreased function (phase 1 metabolism drugs stay active longer)

First pass metabolism – decreased function (less drug metabolized before reaching systemic circulation

What are the geriatric effects on elimination

Takes longer to eliminate drugs

Kidneys have poor function

What is the Cockcroft-Gault equation?

Used to estimate renal function on creatine clearance

(140 – age)(weight) / (serum creatine) * 1.2 (M) or 0.85 (F)

What are the geriatric effects on the pharmacodynamics of the CVS

Baroreceptor sensitivity – Decreased response to lower or raise BP (antihypertensives affect this)

Beta-adrenoreceptors – High doses may be required to affect the decreased sensitivity of them

Arrhythmias – elders are more susceptible to prolonged QT intervals (common side effect)

Hypovolemia and electrolyte disturbances (diuretics)

What are the geriatric effects on the pharmacodynamics of the CNS

Increased effect on the CNS due to altered receptors – benzos, antipsychotics, and antidepressants

Leads to sedation, anticholinergic effects, orthostatic hypotension, and arrhythmias

What are the 7 reasons for med-related problems

New medical condition leads to drug prescription
2. Drug is no longer necessary
3. Wrong drug for condition
4. Right drug, too low dose
5. Right drug, too high dose
6. ADRs
7. Incorrect drug usage

What are trends of polypharmacy

Serious ADR’s are a risk
ADR’s are due to prescription
Hospital admissions due to ADR’s
Lack of knowledge regarding usage of drugs

What is the BEERS criteria

Inappropriate drugs for the elderly

Anticholinergics – confusion
Psychotropics – extrapyramidal
NSAID’s
Hypoglycemics – falls
Diuretics
Anticonvulsants
Benzodiazepine receptor agonists

What are the extrapyramidal side effets

ADAPT (antipsychotics)

A- Akathisia (restlessness, agitation)
D- Dystonia (muscle spasms)
A – Akinesia (impaired voluntary movement)
P – Pseudoparkinism (parkinson’s like symptoms – tremors)
T- Tardive dyskinesia (involuntary movements)

What is the pathophysiology of antipsychotics

Antipsychotics – dopamine antagonists (leads to ACh overpowering)

ACh overload leads to muscle contractions

Treated with anticholinergics

What are the anticholinergic side effects

AABBCCDDE

A- Anorexia
A – Anhidrosis (lack of sweating leading to hyperthermia)
B- Blurred vision (pupil dilation and increase intraocular pressure)
B- Bladder urinary retention
C- Constipation
C – Confusion
D- Dry mouth
D- Dry eyes
E – Excessive HR/BP

What are side effects of oral hypoglycemic agents

Increased fall risk due to hypoglycemia

Cardiac ischemia and dementia as less glucose available

Sulfonylureas – hypoglycemia causing (insulin releasing)

Metformin – first line (can’t be used with HF and renal impairment)

What are side effects of PPI’s?

Low vitamin B12 (decreased intrinsic factor to activate B12)

Bone fractures and osteoporosis (interferes with calcium absorption)

Pneumonia (decreased stomach acid immune function – aspiration)

Intestinal infections (decreased stomach acid immune function)

Why are PPI’s still continued nevertheless

Barrett’s Esophagus – esophagus is similar to stomach lining (linked to esophageal cancer)

Severe Esophageal inflammation

Stomach ulcer bleeds

What are the side effects of NSAID’s

Gastropathies – Gastric/duodenal ulcers, bleeds, and peptic ulcer disease

Pro-hypertensive effects (increased RAAS)

Heart failure exacerbation (decreased renal blood flow= increased RAAS)

Antiplatelet activity (decreased Thromboxane A2)

Aspirin-induced asthma

Acute renal failure (renal hypertension) – can lead to drug toxicity

Elevated liver enzymes

What are the side effects of benzos and Z-drugs

Dependence, memory problems, daytime fatigue

Used anyways for neurological problems and alcohol withdrawal

What are the side effects of antipsychotics

ADAPT and anticholinergic (AABBCCDDE)

Bladder infections, urinary retention weight gain, diabetes, heart attacks, strokes, death

What is neuroleptic malignant syndrome (NMS)

ADR of antipsychotics

HIDAD

H – Hyperthermia
I – increased muscle tone (cogwheel and leadpipe)
D- Dysrhythmias
A- Autonomic instability
D- Diaphoresis

What is the treatment of NMS

Stop antipsychotics

Supportive care – rehydration, cooling, antipyretics, benzos

What is the pathogenesis of NMS

Dopamine blockage – Hyperthermia and dysautonomia, pseudoparkinsonism

Disrupted sympathetic activity – increased muscle tone and metabolism, sweat, and BP

What are the manifestations of serotonin syndrome

Diaphoresis, tachycardia, hyperthermia, hypertension, vomiting, tremors, muscle rigidity, myoclonus, hyperreflexia

Positive babinski reflex

What is the clinical presentation of serotonin syndrome

Altered mental status
Autonomic dysfunction
Neuromuscular abnormalities

What are tips for managing polypharmacy

Deprescribing

Frequent follow-up monitoring medication lists

Compliance – Elders tend to not comply with medications

Patient education retention – is medication education good enough

What are practical tips to reduce polypharmacy

Complete a full medication list with herbals and OTC’s

Involve caregivers to promote compliance

Start low, go slow, but go

Use non-pharmacological interventions

What are the layers of the skin

epidermis, dermis, hypodermis

What are the squamous cell layers of the skin

basale, spinosum, granulosum, lucidum, corneum

What is the normal period of skin shedding

14-28 days

What are intrinsic factors of skin aging

Reduced cellular turnover, impaired barrier function, less immune response, less SQ fat, less vascular, impaired thermoregulation

What are extrinsic factors affecting skin aging

UV exposure, environmental pollution, smoking, lifestyle

What are the mechanisms of skin aging

Dermal matrix atrophy (Type 1 and Type 3 collagen deposition)
Decreased lipid processing
Disintegration of elastin
Disorganized material deposition
Dermal-epidermal junction flattening

What are components of the primary and secondary prevention of skin aging

Sun protection, stop smoking, no harsh soaps, prevent skin tears, pressure ulcers, and incontinece, avoid irritants and allergen exposure

What is necessary to describe skin lesions

Size, shape/symmetry, type, colour/pigmentation, surface area, location/distribution

What is a primary lesion

Basic reaction patters of the skin with definite morphology

What is a secondary lesion

Lesion developed in skin disease evolution or made by scratching or infeciton

What are characteristics of flat skin lesions

Flat, circumscribed areas with changes in skin colour
– Macule (<1cm)
– Patch (>1 cm)

Examples
– Measles, Rubella, Tinea Versicolour

What are characteristics of raised skin lesions

Elevated, firm, and circumscribed

-Papule (<0.5 cm)
– Nodule (1-2 cm)
– Tumour (>2 cm, solid)
– Cyst (> 2 cm, liquid or semi solid)

Examples
– Acne

What are fluid-filled lesions

Elevated, circumscribed and filled with fluid

– Vesicle (<0.5 cm)
– Bulla (> 0.5 cm)
– Pustule (filled with pus

Examples
– Herpes Zoster

What are characteristics of shingles

Only across one nerve dermatome (vesicles)

Can cause posttherpetic neuralgia, dermatomal rash, blindness, and hearing loss

Vaccines available
– Shingrix is recommended greater than 50

What are characteristics of bullous pemphigold

(autoimmune disease that is deep in skin)

Affects the elderly
Chronic and itchy
Caused by antibodies against hemidemonal protein
Tense, deep, blisters
On areas of flexing
Negative Nikolsky’s sign
Rare mucosal involvement
Good prognosis

What are characteristics of pemphigus vulgaris

Affects the middle aged
Acute, non-itchy
Antibodies against desmoglein
Faccid, superficial blisters
On trunk, flexures, and scalp
Positive Nikolsky’s sign
Common Mucosal involvement
Most die without treatment

What is the Nikolsky’s sign

Rubbing over the blister breaks the blister

What is the Asboe-Hansen sign?

The fluid in the blister is able to be moved around and even in unaffected skin

Present in pemphigus

What are pustules

Pus found in a blister

Pustules can indicate an infection (furnuncle)

What are cysts

Fluid/semi-solid filled dead skin cells

What are wheals

Transitory, compressible papule due to dermal edema/fluid

What are characteristics of discoloured skin lesions

Red-purple, non blanchable discoloration due to RBC extravasation

Petechia (<0.5 cm)
Purpura (>0.5 cm)
Ecchymosis (variable, >0.5 cm)

What are characteristics of plaque

Circumscribed, firm, plateau-like skin elevation with flat-top

>1cm

What are characteristics of psoriasis

Built up skin cells

Due to environmental stress-triggerred

Presentations
– Silvery plaque
– Pitting nails
– Teardrop-shaped bumps
-Pustular psoriasis
– erythrodermic psoriasis

Symptoms
– Psoriatic arthritis
– inflammed joints and eyes
– Skin rashes
– Heel pain

What are types of secondary lesions

Erosion- loss of epidermis, moist, glistening after blister rupture

Ulcer – loss of epidermis and dermis

Scale, crust, fissure, scar, sinus, atrophy, lichenification

What are characteristics of seborrheic keratoses

Brown/black growth like warts

Slightly elevated, in clusters of single growths
Usually benign and genetically wired to develop

Can be cosmetically removed

What are the levels of skin cancers

Squamous cell carcinoma, basal cell carcinoma, melanoma (worst)

What is the tool to recognize melanoma

ABCDE

A- Assymetry
B- Irregular borders
C- Change in colour
D- Diameter (>6cm)
E – Evolution

What are risk factors of melanoma

UV radiation, painful sunburns, family history, CDKN2A gene mutation, immunocompromised, many moles

What is basal cell carcinoma

Smaller, superficial, slow growing, least aggressive

Clinical identification
– Pearly surface
– Arborizing telanglectasia
– Central ulceration
– Rolled edges

What is squamous cell carcinoma

Faster, more aggressive

Firm, red pimple, more nodular, and erythematous

What are characteristics of atropic dermatitis

Eczema

Found around folds, face. Triggers due to stress and triggers

Syndrome
– Itching
– Lichenification (thickened, scaly areas)
– Dennie-morgan folds (lower eyelid wrinkled skin)
– Hand eczema
-immunological (increased IgE)

What is seborrheic dermatitis?

Erythema and yellow greasy scales which affects the sebaceous galnds

Causes
-Possible yeast
– Common with neurological disorders and immnocompromised

What is contact irritant dermatitis

Causes
– Skin injury
– Direct cytotoxics
– Cutaneous inflammation to chemimcal irritnat

Decresencdo phemomenon (rapid onset)

What is incontinence-associated dermatitis

Inflammatory damage to water-protein-lipid skin matrix with extended effluent contact

Urine is alkaline whereas skin should be slightly acidic

Enzymes present
Moist skin
Introduces microbes

Symptoms
– Erythema, edema, blistering, erosion

What are trends of infection in the elderly

Asymptomatic bacertiuria is common

Febrile responses can be blunted due to low immune system (no high WBC count)

Hypothermia may be present with infection

Medications can reduce the febrile response

Vaccines – influenza, pneu- P-23

What are risk factors to infection

Immune system
Malnutrition
Comorbidities
Polypharmacy
SES
Frality
Impaired cognition
Urinary incontinence
Immobility

What are ways of detecting infection in the geriatric population

Functional status decline
Temperature over 38.3
Hypothermia is also a risk of systemic infection

What are the symptoms of sepsis

SEPSIS

S-Shiver
E- Extreme pain
P – Pale or discolored skin
S- Sleepy/confused
I – I feel like I might die
S- Short of breath

Plus Elevated heart rate

What is asymptomatic bacteruria

The presence of bacteria in the urine without symptoms

What is symptomatic infeciton

Quantitative sample

Bacteria must grow to be more than 10 to the power of 5 (bacteruria)

Bacteruria is assumed after 30 days of urinary catheterization (10 to the power of 3)

What are symptoms of pylonephritis

Flank pain
High fever
Malaise
WBC’s and bacteria in urine
Urinary symptoms similar to cystitis

What are the symptoms of cystitis

Increased urinary frequency
Urgency
Dysuria (painful urination)
Pain above the pubic region
WBC’s and bacteria in urine
More common in women

What is the SHEA criteria

Classifying symptoms of UTI in men

Swelling or tenderness of testes, epididymis, or prostate

Fever or high WBC (1 only, 2 if not)
– Acute costovertebral angle pain or tenderness
– Suprapubic pain
– Gross hematuria
– New or marked increase in incontinence
– New or marked increase in urgency or frequency

With catheter (1 only)
Fever, hypotension, functional decline, leukocytosis, suprapubic pain or costovertebral angle pain, purulent discharge, or swelling of the organs

What are ways of evaluating UTI’s

Urinalysis (asymptomatic bacteruiria complicates this)
Lab diagnostics
Elevated WBC count
Proper symptom presentation

What are tips to prevent CAUTI’s

Increase the acidity of the urine so that encrustation cannot occur

Prevent blockages of the catheter
– Proper fluid intake (1500-2000)

Catheter care
– Sterile water for inflation
– Proper perianal cleaning
– Proper stabilization
– Emptying bags
– Use larger catheter lumens

Intermittent catheterization over indwelling catheters

Aseptic insertion

Train for catheter care

When are times of appropriate indwelling catheterization

Postoperative urinary retention
Healing of sacral ulcer
End of life care

What is the pathogenesis of UTI’s

Colonization (urethra) -> uroepithelium penetration (bladder) -> ascension (ureters) -> pyenophritis and acute kidney injury (kidneys)

What are the percentage of renal problems

Pre-renal is the most (CHF)

Intra-renal (damage to the kidneys (renal hypertension)

Post-renal (kidney stones)

What are laboratory assessments of renal functions

Blood urea nitrogen
(Diet high in protein, dehydration)

Serum creatine (muscle mass, meat consumption)

What are the values of pre-renal lab assessments

BUN/Cr 20:1 (higher urea)

Urine osmality (>500)

Urine sodium (<20)

Urine microscopy (normal)

What are the values of intra-renal lab assessments

BUN/Cr (10:1)

Urine osmolality (<350)

Urine sodium (>30-40)

Urine microscopy (granular cysts)

What are risk factors of pneumonia

Slower, less efficient mucocilliary elevator
Reduced cough and gag reflex
Decreased chest wall mobility and compliance
Oropharyngeal dysphagia (aspiration)
Malnutrition
Bedridden
Comorbidities

What are clinical presentations of pneumonia

Afebrile
Confusion
Functional decline
Leukocytosis
Neutrophils

What is the CURB-65

Confusion
Urea >20
RR >30
BP low <90 systolic or <60 diastolic
65 years or older

More indicators, higher mortality risk

What are management options of pneumonia

Antibiotics
Oral hygiene
Physical activity
Immunization

What are risk factors of GI infecitons

Pharmacotherapy (antibiotics and PPI’s)
Healthcare exposure
Weakened immunity
Old age

What are management options of GI infections

Supportive care
Discontinue antimicrobials if appropriate
Anti-C.diff therapy
(fecal transplant, probiotics)

What are types of Skin and soft tissue infections

Cellulitis, Necrotizing fascitis, furnucles, carbuncles, pressure injuries, surgical site infections

What is the Levine technique

Technique to acquire cultures

Cleanse with N/S and rotate swab over fluid tissue area over 1cm squared

What are upper SSTI’s

UPPER

U- Unhealthy tissue
P- Poor healing
P- Pain
E- Exudate
R- Reek

What are lower SSTI’s

LOWER

L- Larger
O – osseous (bone visible)
W – Warmth
E – Edema
R- Redness

What is trabecular outflow

Pressure dependent outflow of aqueous humor through the trabecular meshwork and Schlemm’s canal

What is uveoscleral outflow

Secondary non-pressure dependent outflow system of aqueous humor

What are age related changes to vision

Higher dark adaptation threshold (more light needed in the dark)
Decreased contrast (colours and corners are blurred)
Light sensitivity
Diminished depth perception
Presbyopia (farsightedness)
Fewer cones
Dry eyes
Corneal toricity changes
Arcus senilis (blue/white/grey opaque ring

What are cataracts

#1 preventable cause of blindness

Lens clouding or occlusion

What are risks factors of cataracts

UV light exposure
Smoking
Ocular diseases, trauma, surgery
Steroid use
Diabetes
Genetics

What are the types of cataracts

Nuclear (age related – yellowing/hardening of the lens)
Subcapsular (diabetic/steroid related – granular deposits at back of lens)
Cortical (occurs on outer edges due to water changes)

What is the treatment of cataracts

Surgical intervention

Removal of cataract and implantation of lens

What is macular degeneration

Loss of central vision as macula is concentrated with photoreceptors

What are the types of macular degeneration

Dry – non-neovascular (protein accumulation)

Wet – neovascular (leaking and bleeding new blood vessels)

What are risk factors of macular degeneration

Sunlgiht
Smoking
Age
Family history
Genetics
Female
White
Being farsighted

What is the treatment of macular degeneration

Medical lasers to inhibit neovascularization

Anti-VEGF prevents new vascularization and will not restore lost vision

What are recommendations for macular degeneration

No smoking
AREDS multivitamins
Green, leafy vegetables and fruits
Amsler chart monitoring

What is glaucoma

increased intraocular pressure

What are the types of glaucoma

Open angle – fluid drains still

Close angle – fluid is blocked due to iris

What are symptoms of glaucoma

Optic nerve compression (blurred vision)
Eye redness
Tears
Head/eye pain
Tunnel vision

What is the management of acute glaucoma

Avoid antihistamines and decongestants, and anticholinergics

What are treatments of glaucoma

Special antiglaucoma glasses
Eye drops which reduce intraocular fluid (beta blockers, alpha agonists, carbonic anhydrase)
Avoid blue light for too long

What are risk factors of glaucoma

Age
Family history
Race
Eye problems
Blood comorbidities

What evaluation of glaucoma

Inspect the optic nerve (disc and cup ratio greater than 0.8 is glaucoma)

What are causes of diabetic neuropathy

HTN, glycosylation, retinal damage
VEGF secretion by ischemic retina which allows for fluid and angiogenesis
Hard exudates
Aneurysm
Cotton wool spots (layers of infarct nerve fibers)

what is the progression of diabetic neuropathy

Bulges, cholesterol deposits, blood leakage, vein beading, angiogenesis, blocking, clouding

Can lead to complete vision loss

What is the treatment of diabetic neuropathy

Symptom reporting
Glucose and BP control
Annual exam
Laser and anti-VEGF injections

What are other conditions that affect geriatric vision

Hypertensive retinopathy

Temoral arteritis (autoimmune disease of the temporal artery)

Detached retina

What are types of hearing loss

Conductive – outer and middle ear

Sensorineural – inner ear and auditory nerve

Mixed – both conductive and sensorineural

What are related conditions with hearing loss

Falls (vestibular system impairment)
Depression/QoL
Increased alzheimer’s and dementia
CVD/CKD risk
Mortality, diabetes, hospitalization

What is presbycusis

Age-related sensorineural hearing loss

What is the progression of presbycusis

Higher frequencies are lost (inner hair cell atrophy)
Inner ear angioclerosis
Inner ear membrane calcification
Bioelectric/mechanical imbalances in the inner ear
Neural – Loss of hearing sensory components in the nerves and CNS

What is secondary sensorneural impairment

Hearing impairment that is not due to normal aging

What are causes of secondary sensorineural impairment

Trauma
Infection
Autoimmune
Vascular
Ototoxic meds
Meniere’s disease

What is the Ramsay Hunt syndrome

Herpes Zoster infection that affects the trigeminal nerve which leads to facial weakness and paralysis

What are causes of conductive hearing loss

Cerumen accumulation
Hematoma/foreign body in outer ear
Ossicle or tympanic membrane damage

What is the Weber test

Tests localization and lateralization of sound

Tuning fork that is rung at the forehead.
– Lateralization to the good side (sensorineural)
– Lateralization to the bad side (conductive – solids conduct sound)

What is the Rinne test

Vibrating tuning fork held from ear and then placed on mastoid. In conduction hearing loss they have bone conduction but not air conduction.

What are interventions to hearing loss

Speaking directly at the person and in a deep pitch
Environmental modifications
Assistant listening devices
Hearing aids
Cerumen removal

What are trends regarding falls

Leads to fatal injury if not found in a short time

Leads to a transition to long term care as rehab is necessary

What are causes of falls

ADL’s are the most common

Environmental – trips, slips, misplaced steps

What are the extrinsic factors of falls

Home safety

Floors/walkway/entrances
Lighting
Stairs/steps/ladders
Bathroom
Bedroom, phone, pets, footwear

What are intrinsic factors of falls

Polypharmacy
Fear of falling
Age
Fall history
Chronic illness
Cognitive impairment
Visual impairment, hearing impairment, somatosensory imapirment
Lowe extremity disabilities
Balance/gait abnormalities
Incontinence

What is fear of falling

Individuals avoid activities that they are capable of doing as they are fearful of falling

What is part of the subjective assessment of falls

History of falls
Fear of falls

What is part of the physical assessment of falls

Timed up and go
– Measure the time it takes to stand up, walk 3m, turn around, walk back and sit in cahir

>13.5 seconds is high risk for falls

Balance tests
– Gait tests
– 4 stage balance test (standing, semi-tandem, tandem, single-leg stance)

Lower extremity exams – ROM, strength, tone

Other assessments – Home envrionment, vision/hearing, bone mineral (DEXA), exercise and vitamin D

What is the BEEEACH model

B- Behavioural change (commit)
E – Education
E – Equipment
E- Environment safety and risk factors
A – Activity
C – Clothing
H – Health management (medications, bone, vision, nutrition, disease management)

What are interventions for falls

Exercise!
Multifactorial intervention (BEEACH)
Residential care
Minimizing injuries
– Alarms
– Hip protectors
– Hip airbags

Fall prevention clinical practice decision-making models

What is a fall

A sudden, uncontrolled, unitended loss of upright position causing a downward displace of an individual to a lower level, object, or ground

What are risk factors for falls

Environmental
Behavioural
Biological
Socioeconomic (fear of falling)

What is a transient loss of consciousness

Global cerebral hypoperfusion. Rapid onset, brief duration which leads to a spontaneous recovery

Non-traumatic – syncope, seizures, metabolic disorders, psychogenic causes

Head trauma – Caused from getting hit in the head

What is syncope

A transient loss of consciousness as brain doesn’t get oxygen

What are the types of syncope

Neurally-mediated reflex – baroreceptor failure
Orthostatic hypotension
Cardiac arrhythmia
Structural cardiopulmonary (structure defecits)
Non-syncopal (hypoglycemia)
Unknown

What causes a neurally-mediated reflex

Baroreceptors help regulate blood pressure as it detects changes

Vasconstriction (CN9 for low pressure)

Vasodilation (CN10 for high pressure)

How does the RAAS system cause syndcope

Old people have poor baroreceptors and RAAS system

How does orthostasis result in syncope

Less cardiac output due to blood being forced towards lower extremeties

Poor baroreceptors mean there is less compensatory reactions

What are age-related changes to the CVS

Baroreceptor impairment
Decreased vascular resistance
Sinus rhythm/pacemakers
Kidneys (decreased RAAS – fluid loss)

What are risk factors for reflex syncope

Recurrent syncope history
Vasovagal syncope (due to shock or unpleasantness)
Prolong standing
Postprandial (blood diverted to GI)
Crowded or heat
Head rotation
Pressure on carotid sinus

What are symptoms of vasovagal syncope

Syncope precipitated by pain, fear, or standing

Symptoms
– Dizziness
– Lightheadedness
– Seeing stars
– Hearing ringing
– Blurred vision

What are symptoms of carotid sinus syndrome

Carotid massage or stimulation

Parasympathetic system stimulation

What is orthostatic hypotension

Drop by 20 systolic or 10 diastolic during 3 minutes of active standing

Caused by an autonomic reflex failure

How do cardiac arrhythmias cause cardiac syncope

brachycardia, tachycardia, prolonged QT interval which cause poor cardiac output

How do structural cardiopulmonary defects cause cardiac syncope

Stenosis and valve dysfunction

Example – a blocked subclavian which prevents blood from reaching the brain

What is the evaluation of syncope

Physical exam
Discovery of orthostatic hypotension
ECG to rule out arrythmias
Echocardiography to discover structural problems of the heart

What are syncope managments

Pharmacological
– Fludrocortisone (aldosterone mimic)
– Midodrine (vasopressor)

Non-pharmacological
– Increase water and sodium (not in HF)
– Avoid predisposing situations
– Reduce diuretics (caffeine and alcohol)
– Compression stockings
– Elevated HoB
– Smaller amounts of meals more frequently
– Avoid constipation

What is Parkinson’s disease

Chronic, progressive, neurogenerative movement disorder with nonmotor symptoms

Caused primarily by a dopamine deficiency

What is the pathology of Parkinson’s

Lack of substantia nigra (area of dopamine receptors)

Lewy body inclusions – proteins that interfere with the brain

Neuronal loss – loss of brain structures which support movement

What are the key symptoms of Parkinson’s

TARP

T-Tremors (pill-rolling)
R- Rigidity (cogwheel)
A- Alkinesia (slow, uncoordinated movements, drool, hindered speech)
P – Postural instability

What are presentations of Parkinson’s

Gait changes – shuffling, stooping, less arm involvement,

A festinating gait (short shuffle then stop)

Speech (monotone, slurred, soft)

What are other non observable symptoms of Parkinson’s

Depression, forced eyelid closure, cognitive impairment

Autonomic – Sleep disorders, orthostatic hypotension, sweating

GI/GU – Constipation, sexual

What are the pharmacological managments of parkinsons’

Levodopa

Dopa Decarboxylase (DDC) inhibitor/carbidopa

MAO-B inhibitor

COMT – inhibitor

What are characteristics of levodopa

Levodopa (pro drug that becomes dopamine)

Side effects
– N/V
– Confusion
– Hallucinations
– Delusions
– Orthostatic hypotension

Becomes ineffective in the long term

What are characteristics of DOPA decarboxylase inhibitor (carbidopa)

Inhibits peripheral metabolism of levodopa meaning more is available for the brain

What are characteristics of MAO-B inhibitor

Preserves the existing dopamine in the brain

What are characteristics of COMT inhibitor

Reduces the breakdown of dopamine centrally and peripherally

What is deep brain stimulation

Surgically implanted electrodes to provide electrical impulses, help with tremor, rigidity and slowness of movement and balance

Last resort management

What is osteoporosis

Decrease in bone density or an increase in bone porosity

How do osteoblasts and osteoclasts function in osteoporosis

Decreased osteoblast (deposits new bone) activity
– secrete RANKL which activates osteoclasts

Increased osteoclast (dissolves new bone) activity
– increased RANKL will also support osteoporosis

What are the risk factors for osteoporosis?

female sex, increasing age, family history of osteoporosis, white or Asian race, small stature, weight loss, alcohol, caffeine, sedentary lifestyle, low calcium

Low estrogen
Immobility
Malnutrition
Hyperthyroidism
Hyperparathyroidism
Medications that interfere with calcium absorption

What is the DEXA scan

Dual Energy Xray Absorption
– bone mineral density test (osteopenia vs osteoporosis)

What are clinical assessments of osteoporosis

Weight loss
Height changes
Kyphosis
TUG test – fall risk
Falls history

What are pharmacologic interventions for osteoporosis

Denosumab (RANKL inhibitor – interferes osteoclast activation)

Calcitonin – inhibit osteclasts

Raloxifene – Hormone therapy

Siphosphonates – inhibits osteoclasts

What are interventions of osteoporosis

Calcium supplementation – 1200 mg daily
– Requires acidic environment
– Risk of toxicity

Calcitonin

Vitamin D – necessary to absorb calcium
– 10-25 mcg , < 50 and no osteoporosis
– 20-50 mcg, > 50 and high osteoporosis risk

Exercise

Hip-protectors (generally avoid falls)

What is a post fall assessment

Neuro
-PERRLA, strength, LOC

Peripheral
– Vasculature
– Pulses

Antalgic gait
– walking to avoid pain

Other injuries
– Wounds, scrapes

Rhabdomyolysis

Electrolytes

What is rhabdomyolysis?

A breakdown of muscle tissue that releases a damaging substances (calcium and cell components)

Can be precipitated in falls

Damages kidneys as there is more to filter, large proteins can even blcok kidney

Causes hyperphosphatemia, hypo (then hyperkalemia), hypovolemia, compartment syndrome (swelling leading to muscle ischemia)

What are the changes in cognitive function as people age

Brain atrophy – decrease in brain size and brain cells

Cerebral perfusion- reduced blood flow

Neurotransmitter reduction – Dopamine receptors decline

White matter integrity – decreases with age

Cognitive impairment- decreased cognitive function

Reversible cognitive impairment – Metabolic, inflammation, or neurosurgical

What is demtnia

Umbrella term used to describe symptoms that affect memory, behaviours, and thinking

What are the types of dementia

Alzheimer’s Disease
Vascular Dementia
Frontotemporal dementia
Lewy Body Dementia

Rarer ones
– Creutzfeldt-Jakob disesae
-Wernicke-Korsakoff syndrome

What are the symptoms of alzheimer’s dementia

4 A’s

A- Amnesia
A- Aphasia (loss of language skillss)
A – Agnosia (inability to recognize senses)
A – Apraxia (problems with a sequence of actions)

Loss of executive dysfunction
– Affects the frontal lobe (decision making, abstract thinking, emotional regulation)

Alzhemier’s has a gradual prognosis

What are pathological features of alzheimer’s dementia

Amyloid plaques and Tau proteins
– neurotoxic proteins that cause inflammation (indirect cell death)

Wandering behaviour

What are the screening tests for alzheimer’s

Imaging and laboratory tests

MMSE, MOCA, mini-cog

What is MMSE

Mini-mental state exam

Involves orientation, registration, attention, recall, language

What is MOCA

Montreal cognitive assessment (utilizes visuospatial executive function, naming, language, memory, attention, abstract thinking)

Mini-cog – clock drawing

What are risk factors of Alzheimer’s dementia

Age, family history, genetic factor, smoking, antioxidants, Low B vitamins, low omega fatty acids, head trauma, metabolic syndromes

Why is a vitamin B12 deficiency significant

B12 preserves nerve integrity in the CNS and peripheral

Requires intrinsic factor for absorption

Problems with absorption, B12 digestion, intrinsic factor will be bad

What are medical interventions for Alzheimer’s dementia

Cholinesterase inhibitors
– Reduction in ACh is popular and reducing the enzyme will help slow down the progression

NMDA receptor antagonists
– glutamate may be too high which NMDA can help reduce the receptors

Vitamin E
– Antioxident

Ginko biloba
– Antioxident

Estrogen

What are predicting factors of Alzheimer’s dementia

Poor nutrition
Poor education
Smoking

What are strategies and programs to prevent Alzheimer’s dementia

Structure exercises or story-telling groups

Pet, music, or doll therapy

Therapeutic conversations (validation)

Snoezelen multi-sensory environment – restores stimulation to brain cells

What are risk factors of vascular dementia

Vascular disorders

What are characteristics of vascular dementia

Stepwise decline (sudden, sharp declines that occur with each vascular incident)

Stroke association – Stroke like symptoms

Area-specific symptoms (depends on the area of vascular incident)

Emotionally labile (mood swings)

What is the frontotemporal dementia

Frontal – Problems in controlling behaviours and reasoning

Temporal – problems in saying things and understanding things

What are characteristics of frontotemporal dementia

Early onset and poor prognosis

Behavioural frontotemporal dementia
– Disinhibition, poor judgement, loss of social grace, lack of empathy
– Repetitive behaviours (lip smacking)
– Increased cravings

Language frontotemporal dementia
– Progressive aphasia
– Semantic demtnia
– Losing work meaning

What are characteristics of Lewy Body dementia

Vivid hallucinations
Sensitive to antipsychotics
Shared parkinson’s symptoms
Autonomic
Inattention (delirium)

What is delirium

Secondary neurobehavioural syndrome caused by a dysregulated baseline neuronal activity

Results in an altered level of attention and awareness

Acute and rapid onset

What are trends regarding delirium

Longer hospitalization, increased dependence
Development of dementia
Increased mortality
Long-term cognitive impairment

What are the markers of delirium

Attention
Short period of time (acute and fluxuating)
Cognition/perceptual disturbances (hallucinations, disorientation, disorganized thinking)
Physiological cause – Some kind of medical condition is causing it

What are types of delirium

Hyperactive – confused, agitated, hallucinations

Hypoactive – sleepy, withdrawn

What differentiates delirium from demtentia

Delirium
– Acute
– Fluctuates
– Short duration
– Altered LOC
– Impaired attention
– hyper or hypoactive
– Usually reversible

Dementia
– Chronic
– Progressive
– Long duration
– Normal LOC
– Normal attention
– Normal psychomotor
– Irreversible

What are risk factors of delirium

Acute brain dysfunction (stroke, toxins, lack of perfusion, poor BBB)

4M’s
-Medicine
-Microbials
-Medical
-Metabolic

Antipsychotic drug side effects
– weightgain
– extrapyramidal
– Prolonged QT
– Hyperlipidemia

What is the management of delirium

Look for the presence of delirium, then the underlying cause

Non-pharmacological
CHAOS

C- Cause (treat the cause and calm the individual)
H- Hydrate/nourish
A- Ambulate
O – Orientation and observation
S- Safety, security, sensory aid, stimulation, socialization, sleep