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Pathophysiology > Lifespan Development > Flashcards

Lifespan Development Flashcards

1
Q

How many stages of lifespan development are there and what are they ?

A

Infancy ( birth - 2), childhood ( 2-10), adolescence ( 10 - 20), early adulthood ( 20-40), middle aged ( 40-65), old age ( 65+ )

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2
Q

Pre-natal dev: 1st trimester

A

Embryological and foetal development
Major organ systems laid down as ectoderm-mesoderm-endoderm

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3
Q

Prenatal dev:2nd trimester

A

13-27 weeks
Organs and organ systems develop
Foetus looks like human by 6 months

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4
Q

Prenatal dev: 3rd trimester

A

Rapid foetal growth
Major organ systems fully functioning
Deposit adipose tissue

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5
Q

Prenatal organ development
Placenta -
Brain and spinal cord -

A

Placenta - dev from conception in womb
Connected to baby by umbilical cord
Brain and spinal - form at weak 2
Week 3 is heart and foetal circulation
Week 4 is lungs

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6
Q

Discuss foetal critical time periods and risks if exposed to harmful agents

A

Minor/major birth defects and occur.
Exposure during pre-embryonic ( weeks 1-2 ) period may cause spontaneous abortion
During embryonic ( weeks 3-8 ) severe birth defects may occur
Sometimes defects may be reversible.

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7
Q

Discuss foetal circulation before birth

A

Babies blood receives O2 from mother in placenta
Umbilical vein carries O2 blood back to liver and some goes through ductus venosus and enters inferior vena cava ( IVC )
ductus venosus provides “short cut” from umbilical vein to IVC
High O2 blood from placenta mixes with low O2 blood in IVC. high pressure so moves into right atrium.
Right atrium - right ventricle through pulmonary artery to lungs ( fluid sacs as baby in uterus )
High resistance in lungs cause high pressure in pulmonary artery.
Therefore high in right atrium and ventricle so blood enters left atrium from right atrium through foramen ovale.
Then enters left ventricle and squeezed into aorta.
Aorta - umbilical artery, then returns to placenta.

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8
Q

Foetal circulation before birth
Hypoxic pulmonary vasoconstriction -

A

Alveolus in lungs causes arterioles to constrict, therefore high resistance in lungs ( has smooth muscle )
* baby in utero therefore lungs are sacs of fluid which lack O2 due to this fluid

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9
Q

Foetal circulation before birth
Foram ovale -

A

Allows blood to move from right to left atrium.

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10
Q

Foetal circulation before birth
Foram ovale -

A

Allows blood to move from right to left atrium.

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11
Q

Foetal circulation before birth
Ductus arteriosis -

A

Allows blood from pulmonary artery to aorta ( moves from high pressure to low pressure )

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12
Q

Foetal circulation before birth
Ductus arteriosis -

A

Allows blood from pulmonary artery to aorta ( moves from high pressure to low pressure )

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13
Q

Foetal circulation before birth
Why is blood dawn to the placenta ?
Key foetal adaptions:

A

Drawn to placenta bc placenta has low resistance

Umbilical vein
Ductus venosus
Foramen ovale
Ductus arteriosis
Umbilical artery

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14
Q

What changes happen immediately at birth to foetal circulation?

A

Infant first breath - lungs expand and fill with air. Blood will flow to lungs as no longer restricted ( low pressure allowing blood to flow towards )
Blood enters pulmonary system and increases O2 levels, meaning ductus arteriosis constricts
High pressure in left atrium, therefore foramen ovale closes
Cord is clamped
Ductus venosus remains but lack of blood causes it to close hours later

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15
Q

Describe the respiratory system in infancy

A

Soft and cartilaginous rib cage till around 3yrs
Less type 1 muscle fibres - fatigue quickly
Poorly developed intercostal muscles
Small airway diameter -increased airway resistance
Airway prone to collapse due to little cartilage support
Poorly developed cilia so prone to infection
Decreased alveoli at birth ( 150 mil )
Infants - higher resting metabolic rate so require high O2 levels

All means they’re more vulnerable and at higher risk

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16
Q

Describe muskoskeletal system at infancy

A

Born with 300 bones - some will fuse eg. Skull
Bones are soft at birth and will ossify over time
Small and watery muscle fibres - weakness and fatigue is common.

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17
Q

Describe neurological system at infancy

A

Brain is 1/4 of total infant weight
Lower centres of brain are most developed - medulla and brain stem

Involuntary functions - ‘flexural tones’ - curled up
Posses primitative reflex eg rooting reflex - to feed and grasping reflex

Neurone and nerves are present, just need to learn what to do.

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18
Q

Physical growth of a infant

A

1/3 of adult height
There are 3 phases of growth
Weight will increase before height
Growth stages:
Bones - muscles - hands - fest - legs - arms

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19
Q

Genetic factors that influence growth and development

A

Sex
Physical status
Race

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20
Q

Environmental factors influencing growth and development

A

Family
Religion
Community
Food availability- poorly nourished child more likely to have infections and not attain full height potential

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21
Q

Explain physical growth stages from infancy to adolescence

A

Double weight by 4-6months and triple it by 1 year
1st 6 months - 2lb weight gain per month, and after that 1lb per month
Factors will influence this
Childhood: slow steady physical growth
Refine motor skills
Adolescence: rapid hormonal changes
Puberty - 10-14 girls
12-16 boys

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22
Q

Explain muscoskeletal system in adolescence

A

Accelerated skeletal growth - closure of epiphyseal plates
Increased strength and endurance of skeletal muscle
Testosterone has a greater effect than oestrogen, therefore leading to significant difference in muscle mass between genders.

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23
Q

Describe the neurological system during adolescence

A

Sex hormones will affect CNS
Leads to increased sex drive and sexual behaviour - triggered by testosterone and oestrogen

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24
Q

Describe the cardiorespiratory system during adolescence

A

Increased testosterone for males increases blood volume and disproportionate growth of the larynx and thickening vocal cords. leading to a deeper voice.

25
Q

Describe what happens to individuals after puberty

A

Sex differences are maintained due to background hormone secretion
Between 18-21 years will grow but at a slower pace
Adolescence to maturity is hazy
Adolescence ends when growth stops ( 21 )

26
Q

What is primary aging?

A

Inevitable process, bodies natural deterioration that takes place during life.

27
Q

What is secondary aging ?

A

Results from disease and poor health practises. Often is preventable to a certain degree.

28
Q

Aging manifestations:
Aging of tissues -

A

Maintenance process slows, therefore slower healing time
Speed and effectiveness of tissue repair decreases
Structure and chemical composition is altered
This means tissues are more fragile

29
Q

Aging manifestations
Appearance -

A

Skin alterations - epidermis thins, decreased vitamin D
Thinning of dermis ( below epidermis ), decreased blood supply and hair production
Skin becomes saggy and discoloured
Hair loss and greying due to less melonin

30
Q

Practical precautions due to manifestations of aging -

A

No jewellery, short nails, hand washing frequently
Be aware of friction against skin when man handling patients
Regular patient position changes to avoid skin breakdown

31
Q

Manifestations of aging:
Immunity -

A

T cells are less responsive, therefore meaning so are B cells
Increased likelihood of cancer
Impact of alterations to skin

32
Q

Manifestations of aging:
Digestion, urinary and reproduction -

A

Decline in olfactory sensitivity - loss of smell and effect on appetite. Will consume smaller portions
Decreased kidney function causing urinary issues
Menopause and andropause

33
Q

Manifestations of aging:
Muscoskeletal system -

A

Muscle: muscle fibres decrease in diameter
Skeletal muscle less elastic
Reduced tolerance to exercise
Reduced ability to recover from injury. Biproducts eg heat become too much

Bones: loss of height
Osteopenia - natural bone loss
Osteoporosis - increase risk of fractures due to maybe dramatic bone density loss
Osteoarthritis - longer you live, the more stress you put on joints.

34
Q

Manifestations of aging:
Cardio system - heart:

A

Decreased max cardio output meaning tissues receive less O2 and less nutrients
Decreased efficiency of removing waste
Decreased elasticity of cardiac muscle

35
Q

Manifestations of aging
Cardio system - vascular:

A

Less RBC’s therefore increase anaemia risk
Artherscelerosis- build up of plac in arteries
Increased aneurysm risk due to weak/thin vessel walls
Decreased function of valves in veins

36
Q

Manifestations of aging
Cardio system: respiratory -

A

Decreased vital capacity
Increased residual vol ( air left in lungs ) - can cause gas trapping which means it will be harder to move air in and out
Stiffening of rib cage

37
Q

Manifestations of aging
Neurological systems - brain -
Nervous system -

A

Decreased in size and weight
Loss of neurones and neurotransmitters
Decreased bloodlfow
Gradual decline in function
Degenerative changes - memory loss, dementia, Alzheimer’s

Nervous system - slower motor skills
Reduced reaction times
Increased pain threshold
Decreased REM phase so often will wake up

38
Q

Consequences of manifestions of aging:

A

Reduced mobility and higher fall risks
Increased likelihood of more severe impact from fall due to reduced speed and effectiveness of recovery
Lower exercise tolerance and increased sedentary lifestyle.

39
Q

Manifestations of aging
Kidney -
Gastrointestinal -

A

Kidney - decreased renal bloodlfow - tendency to uraemia and decreased exertion of drugs and metabolics

Gastrointestinal - decreased colonic mortility therefore constipation
Decreased secretory mechanisms
Loss of muscular strength and tone

40
Q

Manifestations of aging
Teeth -
Liver -

A

Teeth - reduction of saliva
Atrophy of bone and gum tissues
Teeth fall out

Liver- altered hepatic bloodlfow and enzyme activity
Therefore effects drug metabolism and clearance ( its slower )

41
Q

Osteoarthritis
Aetiology -
Predisposing factors -

A

Aetiology - deterioration of cartilage at a joint meaning bones may rub together. Leads to bone and connective tissue deterioration

Predisposing factors - old age, sex, obesity, genetics, joint injuries.

42
Q

Osteoarthritis
Pathological changes -
Course of disease -

A

Pathological changes - gradual decrease in articular cartilage
Inflammation and subchondral bone thickening
Ligament deterioration

Course - varies between patients
Level 1 ( early arthritis ) level 2 ( moderate ) level 3 ( advanced ) level 4 ( surgical stage )
Some remain stable for decades, others experience rapid decline.

43
Q

Osteoarthritis
Signs and symptoms -
Therapeutic interventions -

A

Signs and symptoms - painful joints and joint stiffness
Joint tenderness
Loss of flexibility and no full ROM
Grating sensation when moving
Swelling

Therapeutic - integrated exercise program
Enhance muscle strength
Steroid injections
Optimal body weight

44
Q

Arteriosclerosis
Aetiology -
Predisposing factors -

A

Aetiology - inner inning artery damage triggers inflammatory response, attracting cholesterol and other substances to accumulate. From plaques which harden and narrow arteries and restrict blood flow

Predisposing - high BP - damages inner layer
Smoking as increases cholesterol levels
Diabetes increases blood sugar and damages arteries
Obesity
Physical activity as can increase cholesterol

45
Q

Artherosclerosis
Course of disease -
Pathological changes -

A

Course - gradual plaque build up. Endothelial damage allows LDL cholesterol to accumulate. Bloodlfow reduced. If plaque ruptures, blood clots may occur leading to blocked arteries. Therefore risk of heart attack/stroke.

Pathological - reduced blood flow due to fatty deposit build up
Arteries narrowed causing inflammation and high BP

46
Q

Artherosclerosis
Signs and symptoms -
Therapeutic interventions -

A

Signs - chest pain, pain in limbs, fatigue, reduced blood flow to brain resulting in confusion, weak muscles

Therapeutic - choose healthy foods, physical activity, quit smoking, beta blockers and weight loss

47
Q

Heart failure
Aetiology -
Predisposing factors -

A

Aetiology - cardiac muscle stiffens/weakens therefore reducing blood flow
Coronary artery disease is a common cause
Hypertension - narrowing arteries therefore become tighter and less elastic
Behaviours like excessive eating and drinking can further contribute

Predisposing - heart conditions like coronary heart disease
High BP and heart rhythm issues
Genetics - inherited heart conditions
Again, higher risk 65 years and above
Lifestyle ie unhealthy diet

48
Q

Heart failure
Course of disease -
Pathological changes -

A

Course - four stages
1) no symptoms 2) fine when resting but notice small symptoms during activity
3) small basic activities will now trigger symptoms 4) can’t do physical activity without symptoms and will experience discomfort when resting

Pathological - tissues not receiving adequate blood, myocardial damage - infarcts as interruption of myocardial blood flow

49
Q

Heart failure
Signs and symptoms -
Therapeutic interventions -

A

Signs - breathlessness fatigue wheezing light headed appetite loss chest pain persistent cough

Therapeutic - pacemakers
Surgery - heart valves bypass/ heart transplant
Cardiac restoration therapy ( CRT )

50
Q

Dementia
Aetiology -
Predisposing factors -

A

Aetiology - vascular dementia - caused by reduced blood flow to brain so cells are damaged and die
Levy bodies - clumps that damage the way cells work and communicate with eachother casing death of cell.
Frontotemporal - abnormal clumping of proteins in frontal and temporal lobes in brain. Damages nerve cells and causes brain shrinkage

Predisposing - common 65 and above
Lifestyle - smoking drinking physically inactive
Genetics
Nutrient deficits

51
Q

Dementia
Course of disease -
Pathological changes -

A

Course - every dementia type is progressive
Early - 2yrs roughly. Small part of brain is damaged and symptoms will only link to that specific area
Middle - mild symptoms worsen as more cells degenerate. Symptoms - poor memory, poor verbal communication and depression
Late - spreads to other parts of brain. May require help with basic tasks

Pathological - rapid neurone loss - stop functioning and will lose connection to other brain cells and die.

52
Q

Dementia
Signs and symptoms -
Therapeutic interventions -

A

Signs - memory loss, difficulty in conversations, orientation struggles, difficulty completing everyday tasks and frequent and extreme mood changes

Therapeutic - as a physio - exercise programs as positive impact on delaying onset of dementia
Muscle strengthening exercises to aid balance

53
Q

Alzheimer’s
Aetiology -
Pathological changes -

A

Aetiology - abnormal build up of proteins in and around brain cells which disturb the structure.
Eg amyloid which is believed to negatively effect neurotransmitter function

Pathological - accumulation of neurotic and nerurofibrillary tangles in brain causing cognitive decline.
Synaptic dysfunctions
Neuronal loss and inflammation due to plaque build up

54
Q

Alzheimer’s
Course of disease -
Predisposing factors -

A

Course- 1) pre clinical stage - no symptoms
2) mild stage - mild memory changes
3) moderate stage - greater memory loss and changes in behaviour can occur
4) severe stage - massive cognitive decline, loss of communication and ability and surrounding understanding

Predisposing - health conditions - diabetes stroke
Lifestyle habits

55
Q

Alzheimer’s
Signs ands symptoms -
Therapeutic interventions -

A

Signs - (later and more severe stages )
Difficulty eating and swallowing
Difficulty moving around
Gradual speech loss
Urinary and bowel incontinence

56
Q

Osteoporosis
Aetiology -
Predisposing factors -

A

Aetiology - females - reduced oestrogen levels leads to raid decrease in bone density
Reaching menopause before 45 and over exercising all increase chance
Males - reduced testosterone reduces bone health therefore at higher risk

Predisposing - sex - women more risk than men
Age
Family history
Body frame size - smaller frame equals higher risk
Hormone levels and diet

57
Q

Osteoporosis
Course of disease -
Pathological changes -

A

Course - 1) boneloss and bone function are equal - no symptoms
2) osteopenia - loss of bone density within expected range - doesn’t always lead to osteoporosis
3) bone loss higher than bone growth. Doctors can diagnose fractures
4) severe - fractures highly likely and symptoms become obvious

Pathological - decreased bone mass and density
Deterioration of bone tissue
Changes in apoptosis

58
Q

Osteoporosis
Signs and symptoms -
Therapeutic interventions -

A

Signs - undetected until a bone break
Known as the silent disease
Shortness of breath if spinal discs are compressed

Therapeutic interventions - calcium and vitamin D supplements
HRT - hormone replacement therapy
Weight bearing exercises
Flexibility and strength training
Balance training
Bisphosphates - medicine that slows rate bone is broken down.

Pathophysiology (9 decks)

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