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enabling occupational performance > bioscience exam > Flashcards

bioscience exam Flashcards

1
Q

what is senescence?

A

normal process of changes overtime eventually affecting organ function

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2
Q

what are the two main theories of aging?

A

programmed and error theory

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3
Q

what ideas does the programmed theory of ageing involve?

A
  • programmed longevity
  • endocrine theory
  • immunological
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4
Q

what ideas does the error theory of aging involve?

A
  • wear and tear
  • cross-linking
  • free radicals
  • somatic DNA damage
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5
Q

what is programmed longevity as a programmed theory of aging?

A

ageing is the result of certain genes being switched off/on over time

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6
Q

what is endocrine theory as a programmed theory of aging?

A

where biological clock acts through hormones to control ageing rate

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7
Q

what is immunological as a programmed theory of aging?

A

immune system programmed to decline increasing vulnerability

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8
Q

what is wear and tear as an error theory of aging?

A

cells and tissues wear out from repeated use

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9
Q

what is cross-linking as an error theory of aging?

A

accumulation of cross-linked proteins damages cells/tissues

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10
Q

what are free radicals as an error theory of aging?

A

cause damage to macromolecular components

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11
Q

what is somatic DNA damage as an error theory of aging?

A

DNA damage causes them to age, telomeres shorten with cell division

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12
Q

what is primary ageing?

A

changes that we can expect

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13
Q

what are some examples of primary aging?

A
  • wrinkles
  • brain cell loss
  • OA/porosis
  • presbyopia
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14
Q

what is secondary aging?

A

degenerative diseases which become more common with age

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15
Q

what are some examples of secondary aging?

A
  • atherosclerosis
  • type 2 diabetes
  • cancers
  • glaucoma
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16
Q

when does brain weight begin to decline?

A

in the 20s there is fluid loss and brain remodeling

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17
Q

when does neuronal loss begin?

A

30

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18
Q

how much of the brain mass can be lost with advancing age?

A

up to one 10th

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19
Q

what do most age-associated impairments of the nervous system result from?

A

factors affecting plasticity, cellular connectivity, calcium regulation, and region-specific dendritic morphology

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20
Q

what are some changes within the lens that occurs with age?

A
  • thickening reduces amount of light passing through
  • yellowing
  • impaired night vision
  • cataracts
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21
Q

what are some changes that occur to the pupils with age?

A
  • reduction in pupil size due to atrophy of dilating muscles
  • less responsive to changing light
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22
Q

what are the two categories of hearing loss?

A

conductive and sensory neural

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23
Q

what is conductive hearing loss?

A

conduction of sound waves through to oval window is impaired

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24
Q

what is sensory neural hearing loss?

A

the nervous system of sound is impaired

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25
Q

what are some causes of conductive hearing loss?

A
  • obstruction
  • less pliable tympanic membrane
  • ossification of auditory ossicles
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26
Q

what are some causes of sensory neural hearing loss?

A
  • loss of stereocilia

- loss of neurons in auditory cortex

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27
Q

what are some changes that occur in the ear with ageing?

A
  • loss of elasticity of tympanic membrane
  • impaired articulation of ossicles
  • loss of stereocilia
  • noise damage
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28
Q

what system maintains balance?

A

the vestibular system of inner ear

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29
Q

what are some age-related changes in the vestibular system?

A
  • loss of hair cells
  • degeneration of otoliths
  • diminished number of vestibular system nerve cells
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30
Q

what occurs to cellular immunity with aging?

A
  • loss of functional capacity of cell-mediated immunity
  • lymphocytes have diminished proliferative response
  • increase in CD4 and decrease in CD8
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31
Q

what is the main function of natural killer cells?

A

surveillance against diseases

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32
Q

what occurs with age in relation to natural killer cells?

A

decrease in number and effectiveness

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33
Q

what is blood pressure the result of?

A

product of cardiac output and peripheral resistance

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34
Q

what is ageing associated with in relation to blood vessels?

A

breakdown of elastic fibres in arteries and vessels become more rigid

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35
Q

what factors is cardiac output dependent on?

A
  • contractility
  • end-diastolic volume
  • HR
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36
Q

how is baroreceptor function affected by age?

A

becomes less effective, thickening of arterial walls may interfere with ability ti measure degree of stretch

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37
Q

what occurs to the respiratory system with age?

A
  • loss of elastic recoil
  • thinning/disruption of alveolar walls
  • total compliance decreases
  • reduction of gaseous exchange
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38
Q

what are the most important changes to affect kidney functioning as we age?

A

vascular degeneration

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39
Q

how much can older adults renal flow be reduced by?

A

from young adults at 600ml/min to as much as half

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40
Q

what are changes in the renal system as we age normally related to?

A

changes in blood vessels

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41
Q

what occurs when the glomerular filtration rate is reduced as we age?

A
  • electrolyte imbalance
  • acid-base imbalance
  • reduced creatinine and other toxic metabolites clearnace
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42
Q

what may incontinence be caused by in older age?

A
  • reduce. bladder elasticity and volume
  • loss of sphincter tone
  • poor bladder control
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43
Q

how much does energy requirements decline with age?

A

for each decade after 50 years caloric requirement declines by 10%

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44
Q

what is a primary influence to relieve constipation?

A

exercise

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45
Q

what is reduced in relation to the gastrointestinal system with age?

A
  • taste
  • number of fibres innervating olfactory bulb and receptors (reduce smell)
  • secretion of pancreatic enzymes
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46
Q

what occurs in the gastrointestinal system due to the reduction of pancreatic enzymes?

A

decreased digestivity ability of small intestine

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47
Q

what is sarcopenia?

A

muscle atrophy and decrease in mass

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48
Q

when is maximal muscle mass achieved?

A

20s and 30s

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49
Q

what do changes in muscle tissue include as we age?

A
  • reduced muscle fibre numbers and size
  • increased fat
  • reduced blood flow
  • reduced motor neuron numbers
  • decreased efficiency of mitochondria
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50
Q

what can contribute to sarcopenia with age?

A

decreased circulating anabolic hormones such as testosterone

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51
Q

when is maximal bone density obtained?

A

25-30 years

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52
Q

what factors contribute to bone loss with age?

A

reduced. ..
- oestrogen/testosterone
- growth hormone
- levels of calcium and vitamin d

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53
Q

what is a risk factor for osteoarthritis?

A

increasing age

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54
Q

what makes joints more prone to mechanical damage as we age?

A

decreased chondrocytes

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55
Q

why does flexibility decrease with age?

A

as a result of decreased elasticity of collagen and elastin within ligaments

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56
Q

what can assist in delaying changes to the musculoskeletal system as we age?

A

light exercise and weight-bearing exercise can improve bone density, increase muscle mass and strength

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57
Q

why is the epidermis and dermis more likely to separate from simple trauma in old age?

A

there is reduced contact between them

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58
Q

what results in the greying of hair?

A

reduced melanocytes

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59
Q

what does a reduction in subcutaneous fat predispose in the elderly potentially lead to issues with?

A

pressure sores and hypothermia

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60
Q

what are some issues that are associated with aging and metabolism?

A
  • vasoconstriction issues
  • heat conservation reduced
  • impaired ability to prevent core temp fluctuations
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61
Q

what is the cessation of menstrual cycle called in older age?

A

menopause

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62
Q

what is andropause?

A

for men, and is a collection of changes caused by decline in testosterone

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63
Q

when does menopause usually occur?

A

between 45-55 years

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64
Q

with reduced oestrogen what is there a reduction in?

A
  • reduced bone density (osteoporosis risk)

- reduced vasomotor control (hot flushes)

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65
Q

what does andropause result in?

A
  • increased body fat
  • reduced muscle/bone mass
  • erectile dysfunction and reduced libido
  • increased risk of anaemia
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66
Q

what will regular exercise improve?

A
  • muscle mass, strength and endurance
  • coordination/balance
  • joint flexibility
  • bone strength
  • BP
  • body fat
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67
Q

what is the role of the innate immune system?

A

prevent foreign substances entering body

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68
Q

what is a self-limiting process?

A

turns off once invader has been destroyed and healing occurs

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69
Q

what is the role of the adaptive immune system?

A

target and destroy specific substances

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70
Q

what cells are involved in humoral immunity?

A

B cells

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71
Q

what cells are involved in cellular immunity?

A

T cells

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72
Q

what are some surface barriers of the innate defenses?

A

physical and chemical barriers

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73
Q

what are some internal defences of the innate immune system?

A
  • phagocytes
  • NK cells
  • inflammation
  • fever
  • antimicrobial proteins
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74
Q

what is an autoimmune disease?

A

breakdown in ability of adaptive defences to distinguish self from non-self

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75
Q

what are some genetic predispositions as a mechanism of autoimmune disease?

A
  • type of self proteins a person has (HLA proteins)
  • 75% women
  • ethnicity
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76
Q

what is the enviro as a mechanism of autoimmune disease?

A

chemicals and viral/bacterial infection

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77
Q

what is the breakdown of self tolerance as a mechanism of autoimmune disease?

A
  • failure to destroy self-reactive T and B lymphocytes
  • failure of regulatory T cells
  • antigen mimicry
  • release of sequestered antigens
  • super antigens
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78
Q

what is antigen mimicry in relation to the breakdown of self-tolerance?

A

foreign antigens resemble self antigens

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79
Q

what is the release of sequestered antigens in relation to the breakdown of self-tolerance?

A

new self antigens revealed

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80
Q

what is a superantigen in relation to the breakdown of self-tolerance?

A

bacterial exotoxins activate indiscriminately

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81
Q

what does idiopathic mean?

A

cause is unknown

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82
Q

what are the goals of treating autoimmune diseases?

A
  • relieve symptoms
  • replace vital substances
  • suppress immune system
  • dietary manipulation
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83
Q

what type of inflammation is juvenile idiopathic arthritis?

A

immune-mediated and chronic

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84
Q

what is the frequency of juvenile idiopathic arthritis?

A

effects 1-2 per 1000 children more likely girls

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85
Q

what is the mean age of JIA onset?

A

depends on disease subtype but usually between 1-3yo

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86
Q

what is the genetic component of JIA?

A
  • markedly increased risk for close relatives
  • females
  • most common in caucasian
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87
Q

what is immune-mediated chronic inflammation?

A

normal inflammation/immune response to foreign material. cross reacts with self antigen that is always present but never clears

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88
Q

what are infiltration cells?

A
  • activated T cells
  • B cells/plasma cells
  • macrophages
  • neutrophils
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89
Q

what are joint cells?

A
  • fibroblasts
  • macrophages
  • chondrocytes
  • osteoclasts
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90
Q

what type of joints are fibroblasts in?

A

synovium

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91
Q

what type of joints are macrophages in?

A

synovium

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92
Q

what type of joints are chondrocytes in?

A

cartilage

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93
Q

what type of joints are osteoclasts in?

A

subchondral bone

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94
Q

what are cytokines released by?

A

activated T cells, macrophages or fibroblasts

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95
Q

what causes fever?

A

endogenous pyrogens

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96
Q

what do chemoattractants do?

A

attract/activate macrophages and other cells, promotes inflammation

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97
Q

what do interleukin-1 activate and promote?

A

activates fibroblasts, chondrocytes and osteoclasts and promotes bone/cartilage destruction

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98
Q

what does tumor necrosis factors a (TNFa) stimulate and support?

A

stimulates blood vessel formation and acute phase response and supports growing pannus

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99
Q

what is growing pannus?

A

synovial fibroblasts grow into joint space

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100
Q

what are some symptoms of JIA?

A
  • joint pain/swelling/stiffness
  • sleep disturbance, fatigue, irritability
  • periods of remission/flare up
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101
Q

what are some extra-articular signs depending on JIA category and severity?

A
  • acute phase response
  • serositis and vasculitis
  • uveitis
  • growth factors
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102
Q

what do autoantibodies have a role in?

A

in pathogenesis via immune complex-mediated inflammation

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103
Q

what do the autoantibodies cause damage to?

A
  • pericardium, myocardium
  • lung pleura
  • lacrimal and salivary glands
  • blood vessels
  • nerve pain
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104
Q

what occurs when there is damage by autoantibodies to the pericardium and myocardium?

A

impaired function and pain

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105
Q

what occurs when there is damage by autoantibodies to the lung pleura?

A

impaired function and pain

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106
Q

what occurs when there is damage by autoantibodies to the lacrimal and salivary glands?

A

dry eyes and mouth

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107
Q

what occurs when there is damage by autoantibodies to the blood vessels (vasculitis)?

A

ischaemia > necrosis in skin, heart, nerves and brain

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108
Q

what is uveitis?

A

inflammation of uvea

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109
Q

what can occur with long-term uveitis?

A

permanent eye damage and blindness

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110
Q

how is uveitis treated?

A

regular ophthalmologic exams and topical corticosteroids

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111
Q

what are some different types of growth failures?

A
  • reduced overall rate of growth (small stature)
  • uneven limb/joint
  • low bone mineral density
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112
Q

what causes reduced the overall rate of growth (small stature) as a growth failure?

A

high level of circulating inflammatory cytokines (IL-6)

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113
Q

what are some treatments for the reduced overall rate of growth (small stature)?

A

corticosteroid treatment and some success using growth hormones

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114
Q

what causes uneven limb/joint growth as a growth failure?

A

increased blood supply to growth plates may cause affected joint/limb to grow faster

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115
Q

what is low bone mineral density due to growth failure?

A

increased osteoclast activity

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116
Q

what are the three major types of JIA?

A
  • oligoarticular
  • polyarticular
  • systemic
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117
Q

what are some minor types of JIA?

A
  • enthesitis-associated JIA
  • psoriatric
  • undifferentiated
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118
Q

what joints are affected by enthesitis-associated JIA?

A

typically knee, ankle, intervertebral joints

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119
Q

what joints are affected in psoriatic JIA?

A

any joint

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120
Q

what are some systemic features of enthesitis-associated JIA?

A

inflammation of tendons at muscle insertion and increased risk of uveitis

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121
Q

what are some systemic features of psoriatic JIA?

A
  • psoriasis
  • may have dactylitis (inflammation of digit) or oncholysis (nail pitting and loss)
  • increased risk of. uveitis
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122
Q

what type of joints are affected by oligoarticular JIA?

A
  • medium-large eg. knees, ankles
  • asymmetric
  • non-destructive
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123
Q

what type of joints are affected by polyarticular JIA?

A
  • any joint- usually smaller eg. hands and wrists
  • usually symmetric
  • destructive arthritis
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124
Q

what type of joints are affected by systemic JIA?

A
  • any joint
  • usually symmetric
  • destructive
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125
Q

what are the systemic features of oligoarticular JIA?

A

-~20% uveitis

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126
Q

what are the systemic features of polyarticular JIA?

A
  • < 10% uveitis (usually associated with asymmetrical disease)
  • RF+ may have symptoms like systemic JIA
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127
Q

what are the systemic features of systemic JIA?

A

daily fever, rash, enlarged spleen, liver, inflammation of cardiac and pleural membranes

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128
Q

what are some long-term issues of oligoarticular JIA?

A

limb length discrepancy, flexion. contracture

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129
Q

what are some long-term issues of polyarticular JIA?

A

RF + decreases chance of remission

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130
Q

what are some long-term issues of systemic JIA?

A

growth failure, acute phase response

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131
Q

what is the pharmacological intervention for autoimmune disease determined by?

A

disease category and degree of severity

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132
Q

what is part of the 1st line pharmacological intervention?

A

NSAIDs and corticosteroids

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133
Q

what is part of the 2nd line pharmacological intervention?

A

DMARDs (methotrexate)

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134
Q

what is part of biologics pharmacological intervention?

A

immune response modifiers

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135
Q

what do NSAIDs do?

A

anti-inflammatory but does not prevent joint destruction or slow disease progression

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136
Q

what are some side effects of NSAIDs?

A
  • generally well tolerated by children
  • <1% mild nausea
  • bruising more common
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137
Q

can corticosteroids prevent joint destruction?

A

yes

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138
Q

what can intra-articular injection of corticosteroids prevent?

A

local joint deformity, muscle atrophy and thus growth disturbances

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139
Q

side effects of corticosteroids?

A
  • immunosuppressant so increased risk of infection
  • growth retardation
  • decreased bone mineral density
  • weight gain, fluid retention
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140
Q

what are some preventative measures for increased risk of infection as a side effect of corticosteroids as an immunosuppressant?

A
  • hand hygiene
  • avoiding unwell people
  • immunisation
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141
Q

what are some preventative measures of growth retardation as a side effect of corticosteroids?

A

short courses of systemic treatment and growth hormone supplements

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142
Q

what are some preventative measures of decreased bone mineral density as a side effect of corticosteroids?

A

physical exercise and calcium/vitamin D supplementation

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143
Q

what are some preventative measures of weight gain and fluid retention as a side effect of corticosteroids?

A

healthy/low salt diet and physical exercise

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144
Q

are DMARDs slow or fast acting?

A

slow (1-2 month for effect)

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145
Q

when are biologics used?

A

when 1st and 2nd line therapy fails to control

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146
Q

what is the onset time for biologics?

A

more rapid (1-2weeks)

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147
Q

what do biologics do?

A

Immunosuppressants suppress immune-mediated inflammation and block production and activity of cytokines/activation of T cells

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148
Q

what does biologic use as an immunosuppressant result in?

A
  • impair inflammatory response
  • slow disease progression
  • increased frequency/severity of infection
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149
Q

what are biologics administered by?

A

subcutaneous injections

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150
Q

what are some non-pharmacological treatment options for JIA?

A
  • physical conditioning
  • resting anf functional splints
  • serial casting
  • shoe lifts and inserts to equalise leg lengths
  • personal, household and educational aids
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151
Q

what are some pain management techniques for JIA?

A
  • breathing and relaxation techniques
  • heat, cold. or water therapy
  • massage
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152
Q

what are some nutrition treatment options for JIA?

A
  • vitamin d and calcium supplements

- omega-3 fatty acids

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153
Q

what are surgery options to treat JIA?

A
  • osteotomy
  • epiphysiodesis
  • joint replacement
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154
Q

what is osteotomy?

A

removing or inserting wedge of bone to allow more normal joint alignment

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155
Q

what is epiphysiodesis?

A

removal/impairment of growth plate to stop growth

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156
Q

what is poor prognosis of JIA associated with?

A
  • early hip/wrist involvement
  • symmetrical disease and rheumatoid factor
  • persistent inflammation
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157
Q

what is the structure of smooth muscle?

A

spindle shaped, non-striated fibres and one central nucleus

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158
Q

what is the structure of cardiac muscle?

A

branched, striated fibres, usually one central nucleus

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159
Q

what is the structure of skeletal muscle?

A

long cylindrical striated fibres and numerous peripheral nuclei

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160
Q

what is a fascicles?

A

bundle of muscle fibres

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161
Q

what are the three layers of skeletal muscle?

A
  • endomysium
  • perimysium
  • epimysium
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162
Q

what are sarcomeres?

A

contractile units

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163
Q

what do sarcomeres contain?

A

myofilaments

164
Q

what is a nerve?

A

bundle of axons held together with connective tissue

165
Q

what is the purpose of myelin sheath?

A

for insulation and protection

166
Q

where are somatic motor impulses generated?

A

PMC

167
Q

how are somatic motor impulses carried to skeletal muscles?

A

via upper and lower motor via corticospinal pathways

168
Q

what ensures coordination of movement?

A

basal nuclei and cerebellum

169
Q

what is hypertrophy response to?

A

regular forceful use

170
Q

what does hypertrophy result in an increase in?

A
  • no.of and diameter of contractile proteins

- increase in diameter of individual fibres not increase in no.of muscle fibres

171
Q

what is atrophy a response to?

A

disuse

172
Q

what occurs with atrophy?

A

initially fibres shrink as contractile proteins are broken down and muscle fibres may later decrease and be replaced by fibrous tissue

173
Q

what will the most damaged area of muscle tissue be patched with when repairing?

A

fibrous scar tissue that is non-contractile

174
Q

what can neuromuscular disease be directly due to?

A

muscle pathology

175
Q

what can neuromuscular disease be indirectly due to?

A

nervous system pathology

176
Q

what may neuromuscular disease be caused by?

A
  • myopathy
  • neuropathy
  • junctionopathy
177
Q

what may symptoms of the neuromuscular disease include?

A
  • muscle weakness/paralysis
  • muscle wastage
  • continuous muscle spasm
  • muscle twitching
  • muscle pain
  • breathing and swallowing difficulty
178
Q

what is myotonia?

A

continuous muscle spasm

179
Q

what is fasciculation?

A

muscle twitching

180
Q

what is myalgia?

A

muscle pain

181
Q

what are some causes of neuromuscular disease?

A
  • genetic mutation
  • viral infection
  • autoimmune/hormonal/metabolic disorder
  • dietary deficiency
  • certain drugs/poison
  • unknown factors
182
Q

what are types of inherited myopathies?

A

-muscular dystrophy

congenital/metabolic/mitochondrial myopathy

183
Q

what are types of acquired myopathies?

A
  • infection
  • inflammatory myopathy
  • toxic myopathy
  • associated with systemic disease
184
Q

what is junctionopathy related to neuromuscular disease?

A

diseases originating in neuromuscular junction

185
Q

what are types of upper motor neuron diseases?

A
  • stroke
  • CP
  • ALS/MND
  • spinal cord trauma
186
Q

what are types of lower motor neuron diseases?

A
  • peripheral neuropathies
  • spinal (anterior horn) nerve
  • poliomyelitis
187
Q

what are some brain-origin diseases?

A
  • parkinson’s

- alcohol related brain damage

188
Q

what is muscular dystrophy a breakdown in?

A

dystrophin-glycoprotein complex which is a network of fibrous proteins

189
Q

what does dystrophin-glycoprotein complex do?

A

stabilises sarcolemma during contraction and relaxation

190
Q

where is the mutation in Duchenne muscular dystrophy?

A

in dystrophin gene on X chromosome

191
Q

what symptoms appear in Duchenne muscular dystrophy at between 1-5 years?

A
  • late walking
  • toe walking, enlarged calf muscles
  • difficulty standing
192
Q

what are the three main types of chronic inflammatory myopathy?

A
  • polymyositis
  • dermatomyositis
  • inclusion body myositis
193
Q

what are some symptoms of toxic myopathy?

A
  • muscle weakness
  • myalgia
  • myoglobinuria
  • elevated creatine kinase
194
Q

what can cause toxic myopathies?

A

alcohol and certain snake venoms

195
Q

what is the most common type of drug-induced myopathy?

A

glucocorticoid-induced myopathy

196
Q

what is glucocorticoid-induced myopathy a side affect of?

A

corticosteroid therapy

197
Q

what does glucocorticoids do?

A

catabolic effect on skeletal muscle

198
Q

what causes Cushing’s disease?

A

adrenal glands produce high levels of cortisol

199
Q

what is junctionopathy due to?

A

defect in transmission at neuromuscular junction

200
Q

who does myasthenia gravis affect?

A

young women and older men

201
Q

what are some symptoms of myasthenia gravis?

A
  • muscle weakness
  • fatigue
  • visual disturbances
  • ptosis- droopy eyelids
  • swallowing/breathing difficulty
202
Q

what is the treatment for myasthenia gravis?

A
  • acetylcholinesterase inhibitors
  • immunosuppressants
  • thymectomy
203
Q

what does botulism prevent release of at axon terminals

A

ACh

204
Q

how does organophosphate get into the body and cause poisoning?

A

inhaled, ingested or absorbed via skin

205
Q

what are some symptoms of organophosphate?

A
  • copious respiratory and oral secretions
  • diarrhoea and vomiting
  • sweating
  • altered mental status
  • autonomic instability
  • muscle weakness/paralysis and respiratory arrest
206
Q

what is acetylcholinesterase?

A

enzyme that dggrades ACh

207
Q

what do organophosphates inhibit and what occurs as a result?

A

acetylcholinesterase and results in an accumulation of ACh at NMJ and continuous cholinergic stimulation

208
Q

what is the treatment for organophosphate poisoning?

A

ACh competitors reduce stimulation

209
Q

what does neuropathy diseases originate from?

A

originates in somatic motor neuron

210
Q

what occurs peripheral neuropathies caused by and result in?

A

damage to peripheral nerves can occur from diabetes and Guillian-Barre syndrome, leading to weakness, numbness., pain/tingling

211
Q

what do anterior horn (spinal nerve) diseases result from?

A

diseases such as poliomyelitis can destroy cells of anterior horns

212
Q

what does chronic high blood glucose levels from diabetic peripheral neuropathy incite?

A

nerve and capillary damage

213
Q

what are the symptoms of diabetic peripheral neuropathy?

A

-numbness, reduced detection if sensations
-tingling/burning
-sharp pains
-increased sensitivity to touch
ulcers/infections
-muscle weakness

214
Q

what is Guillian-Barre syndrome triggered by?

A

acute viral/bacterial infection

215
Q

what are the symptoms of Guilian-Barre syndrome?

A
  • myalgia
  • muscle weakness
  • jerky/uncoordinated movement
  • paralysis
216
Q

what type of disease is poliomyelitis?

A

anterior horn

217
Q

who does poliomyelitis mainly affect?

A

children under 5

218
Q

what are the initial symptoms of poliomyelitis?

A
  • fever
  • fatigue
  • headache
  • vomiting
  • neck stiffness
  • pain in limbs
219
Q

what are some upper motor neuron diseases?

A
  • motor neuron disease/Lou Gehrig’s disease/ALS
  • CP
  • multiple sclerosis
220
Q

what are the early symptoms of amyotrophic lateral sclerosis?

A
  • fasciculations

- muscle cramps/spasticity/weakness

221
Q

what are the late symptoms of amyotrophic lateral sclerosis?

A
  • breathing difficulty

- fatigue

222
Q

what may cause the development of CP?

A
  • interruption of oxygen supply
  • maternal infection
  • meningitis
  • head injury after birth
223
Q

when is CP usually diagnosed?

A

between 3-5 years when milestones arent met

224
Q

what disturbances may accompany CP?

A
  • sensation
  • cognition
  • communication
  • perception
  • behaviour
  • seizures
225
Q

what percentage of CP is spastic?

A

75-85%

226
Q

what is the effect of spastic CP on upper limbs?

A

flexion at elbow/wrist/fingers (fist)

227
Q

what is the effect of spastic CP on lower limbs?

A
  • flexion at hip/knee
  • adduction of thigh
  • equinovarus foot position from tight calves
  • hyperextension of big toes
228
Q

what does spastic CP affect?

A
  • stand/sit upright
  • transfer
  • walk and run
229
Q

what are the effects of spasticity over time?

A

-stiffness, atrophy and fibrosis
-muscle contracture
-bone deformity
pain

230
Q

when does stroke occur?

A

when blood flow to part of brain or whole brain is interrupted

231
Q

what may stroke be due to?

A
  • blockage (occlusive)

- bleeding (haemorrhagic)

232
Q

what is CVA?

A

tissue which has died because of failed blood supply is infarcted

233
Q

what occurs where brain tissue dies?

A

undergoes liquefactive necrosis

234
Q

what are some risk factors for stroke?

A
  • increasing age
  • hypertension
  • heart disease
  • atherosclerosis
  • diabetes mellitus
  • smoking
  • cocaine
235
Q

what large vessels may thrombi form in during ischaemic stroke?

A
  • carotid arteries
  • vertebral arteries
  • circle of willis
236
Q

what smaller vessels may thrombi form within in ischaemic stroke?

A

smaller arteries within brain

237
Q

what is a major cause of thrombus formation?

A

atheroclerosis

238
Q

what is the most common sites of thrombotic occlusion?

A

arterial branch points

239
Q

where do emboli commonly arise from?

A

heart especially in atrial fibrillation

240
Q

what is lipohyalinosis?

A

build up of fatty hyaline matter in blood vessel from high bp and ageing

241
Q

what may arterial anastomoses allow?

A

some areas to receive blood even though their main supplying artery is blocked

242
Q

where may blood clots occur in brain to occlude blood supply?

A

may occur in cortex but not in internal structures of brain which are supplied by small, non-anastomosing arterial branches

243
Q

within the ischaemic area what are the two major zones of injury?

A

ischaemic penumbra and core ischaemic

244
Q

what are some presentations in acute stroke?

A
  • altered consciousness
  • headaches
  • aphasia
  • incoordination, weakness, paralysis or sensory loss in limbs
  • facial weakness/asymmetry
245
Q

what are some alterations in consciousness in acute stroke?

A
  • stupor or coma
  • confusion or agitation/memory loss
  • seizures
  • delirium
246
Q

what is aphasia?

A

incoherent speech or difficulty understanding speech

247
Q

what is ataxia as a symptom of stroke?

A

poor balance, clumsiness, difficulty walking

248
Q

what areas of the brain are responsible for hearing?

A

primary auditory cortex and auditory association area

249
Q

what areas of the brain are responsible for visual?

A

primary visual cortex and visual association area and occipital lobe

250
Q

what are some common patterns in left hemisphere stroke?

A
  • aphasia
  • R hemiparesis
  • R-sided sensory loss
  • R-field defect
  • poor R conjugate gaze
  • dysarthria
  • difficulty reading, writing and calculating
251
Q

what are some common patterns with right hemisphere stroke?

A
  • aphasia
  • L hemiparesis
  • L-sided sensory loss
  • L-field defect
  • poor L conjugate gaze
  • dysarthria
  • spatial disorientation
252
Q

what occurs as a common pattern in the brainstem/cerebellum/posterior hemisphere stroke?

A
  • motor/sensory loss in all limbs
  • crossed signs
  • limb or gait ataxia
  • dysarthria
  • amnesia
  • dysconjugate gaze
  • nystagmus
  • bilateral visual field defects
253
Q

what are common patterns within the small subcortical hemisphere or brain stem in a pure motor stroke?

A

weakness of face/limbs on one side without abnormal higher brain functions/sensation/vision

254
Q

what are common patterns within the small subcortical hemisphere or brain stem in a pure motor stroke?

A

decreased sensation of face/limbs on one side and no abnormal higher brain function/motor/vision

255
Q

what does the effect on function depend on following stroke?

A

region of brain infarcted and extent of infarct (size of vessels compromised)

256
Q

what is apraxia of speech?

A

reduced ability to produce spoken words

257
Q

why do we amputate?

A
  • control pain or disease
  • punishment
  • when re-vascularisation is not possible
258
Q

what causes PVD?

A
  • diabetes
  • hypertension
  • hyperlipidaemia
  • smoking
259
Q

what is PVD?

A

narrowing of blood vessels outside brain and heart

260
Q

what is PVD most commonly due to?

A

atherosclerosis

261
Q

what areas are assessed in the skin for PVD?

A
  • touch
  • hair growth
  • appearance
  • nails
  • pulse
262
Q

what areas are assessed for ulcers in PVD?

A
  • pain
  • colour
  • edges
  • location
263
Q

what are treatment options for PVD?

A
  • lifestyle change
  • treatment of exisiting conditions
  • medication
  • angioplasty
  • vascular surgery
  • amputation if re-vascularisation is not possible
264
Q

what are the levels of lower extremity amputation from the toes to ankle?

A
  • amputation of digits
  • partial foot
  • ankle (syme) disarticulation
265
Q

what are the levels of lower extremity amputation from the below the knee to below hip?

A
  • below-knee (transtibial)
  • above-knee (transfemoral)
  • vas-ness rotation/rotationplasty
266
Q

what are the levels of lower extremity amputation from hip to waist?

A
  • hip disarticulation
  • hemipelvectomy/hindquarter
  • hemicorporectomy (at waist)
267
Q

wha does the surgeon need to take into account when deciding the level of amputation?

A
  • adequate vascularisation

- ability to create adequate stump to take prosthetic

268
Q

what are causes of upper extremity amputation?

A
  • severe trauma
  • PVD
  • thermal burns and frost bite
269
Q

what is the pathophysiology of upper extremity amputation?

A
  • severe blood loss, nerve damage and shock
  • impaired circulation
  • tissue necrosis
270
Q

what are the levels of amputation from the fingers to the wrist?

A
  • amputation of digits
  • metacarpal
  • wrist disarticulation
271
Q

what are the levels of amputation from the forearm to elbow?

A
  • forearm

- elbow disarticulation

272
Q

what are the levels of amputation from above the elbow to above arm?

A
  • above-elbow (transhumeral)
  • shoulder disarticulation
  • forequarter
273
Q

what is glycoylsis?

A

glucose used by cell to make ATP

274
Q

how is glucose transported from blood to cells?

A

insulin

275
Q

what is insulin?

A

hormone that allows transport of glucose into cells lowering the blood glucose levels

276
Q

how is insulin synthesised?

A

B cells of islets of Langerhans in pancreas

277
Q

how is insulin stored and released?

A
  • packaged into granules within B cells
  • release triggered by increased BGLs
  • biphasic release > 1st and 2nd phase
278
Q

what do B cells synthesise and secrete and what does this result in?

A

insulin to lower BGL

279
Q

what do a cells synthesise and secrete and what does this result in?

A

glucagon that increases BGL

280
Q

when is the first phase of glucose uptake?

A

within 2 mins of eating lasting 10-15mins

281
Q

when is the second phase of glucose uptake?

A

lasts until BGLs return to normal

282
Q

what type of GLUT is allows glucose transport from cell membrane into liver cells?

A

2

283
Q

what type of GLUT is allows glucose transport from cell membrane into muscle cells?

A

4

284
Q

what type of GLUT is allows glucose transport from cell membrane into fat cells?

A

4

285
Q

do neural cells require insulin?

A

no

286
Q

what goes GLUTs stand for?

A

glucose transport units

287
Q

does insulin lower or increase blood glucose levels?

A

lower

288
Q

does glucagon lower or increase blood glucose levels?

A

increases

289
Q

what occurs in glycogenesis?

A

excess. glucose is converted into glycogen

290
Q

what is glucoeogenesis?

A

production of glucose by liver inhibited

291
Q

what occurs during the absorptive (fasting) state?

A

pancreas releases glucagon from a cells and stored glycogen broken down to glucose

292
Q

what is hyperglycaemia?

A

consistent high blood glucose levels

293
Q

what percentage of diabetes is type 1?

A

15%

294
Q

what percentage of diabetes is type 2?

A

855

295
Q

what causes type 1 diabetes?

A

autoimmune, lack of insulin

296
Q

what causes type 2 diabetes?

A

lifestyle and enviro resulting in deficient/defective insulin

297
Q

what is gestational diabetes?

A

glucose intolerance first appears during pregnancy and usually resolves after birth

298
Q

what causes gestational diabetes?

A

hormones and weight gain with pregnancy

299
Q

what occurs in the liver in type 1 diabetes?

A

increased breakdown of stored glucose and production of glucose from non-carb sources

300
Q

what occurs in the muscles in type 1 diabetes?

A

decreased glucose uptake due to absence pf insulin and glycogenesis

301
Q

what occurs in the adipose tissue in type 1 diabetes?

A

increased breakdown of aft and production of free fatty acids

302
Q

what occurs with protein in type 1 diabetes?

A

decreased acid production and protein synthesis and increased protein breakdown

303
Q

what does obesity inhibit signalling in type 2 diabetes?

A

free fatty acids and cytokines from fat cells

304
Q

why is insulin not secreted from the pancreas due to in type 1 diabetes?

A

destruction of B cells

305
Q

why is insulin not secreted from the pancreas due to in type 2 diabetes?

A

B cell dysfunction/stress

306
Q

what is the treatment options for type 1 diabetes?

A

insulin

307
Q

what is the treatment options for type 2 diabetes?

A
  • diet and exercise

- oral and hypoglycaemic. agents

308
Q

what are some acute consequences of uncontrolled hyperglycaemia for type 1 diabetes?

A

diabetic keto acidosis

309
Q

what are some acute consequences of uncontrolled hyperglycaemia for type 2 diabetes?

A

non-ketotic hyperosmolarcoma

310
Q

what are some chronic consequences of uncontrolled hyperglycaemia for diabetes?

A

vascular complications and neuropathies

311
Q

what are some macrovascular consequences of chronic hyperglycaemia?

A
  • damage to large blood vessels of brain, heart and extremities
  • CVD and stroke
312
Q

what are some microvascular consequences of chronic hyperglycaemia?

A
  • abnormal thickening of basement membrane of capillaries
  • retinopathy
  • nephropathy
313
Q

what does retinopathy as a result of chronic hyperglycaemia?

A

eyes

314
Q

what does nephropathy as a result of chronic hyperglycaemia?

A

kidneys

315
Q

what is peripheral neuropathy?

A

damage to peripheral nerves due to long term hyperglycaemia

316
Q

what are some symptoms of peripheral neuropathy?

A

loss of feelings in hands/feet and reduced pain signalling/awareness

317
Q

what is usually seen with concomitant peripheral vascular disease?

A
  • decreased blood flow
  • poor healing
  • decreased immune response
318
Q

what occurs to a diabetic foot following PVD and diabetic neuropathy?

A
  • loss of sensation
  • impaired wound healing in extremities
  • infection and gangrene
319
Q

what are some causes of diabetic foot ulcers?

A
  • peripheral neuropathy

- deformity, callus, shoes, trauma, pressure

320
Q

what are the four types of primary tissues?

A
  • epithelium
  • connective
  • nervous
  • muscle
321
Q

what is the function of nervous tissue?

A

internal communication

322
Q

what is the function of epithelial tissue?

A

forms boundaries between enviro, protects, secretes, absorbs, and filters

323
Q

what is the function of muscle tissue?

A

contracts to cause movement

324
Q

what is the function of connective tissue?

A

supports, protects, bonds to other tissues

325
Q

where is nervous tissue found?

A

brain, spinal cord, and nerves

326
Q

where is muscle tissue found?

A
  • muscle attached to bone (skeletal)
  • heart (cardiac)
  • muscles of walls of hollow organs (smooth)
327
Q

where is epithelial tissue found?

A
  • skin surface (epidermis)

- lining of GI tract organs and other hollow organs

328
Q

where is connective tissue found?

A
  • bones
  • tendons
  • fat and other soft padding tissue
329
Q

what are the three layers of the skin?

A
  • epidermis
  • dermis
  • hypodermis
330
Q

what layer of the skin is the epidermis?

A

outer epithelial layer

331
Q

what layer of the skin is the dermis?

A

deep supporting layer of dense connective tissue

332
Q

what layer of the skin is the hypodermis?

A

subcutaneous layer composed of loose connective and adipose tissue

333
Q

is the epidermis vascular?

A

no its avascualar

334
Q

what is avascular?

A

lack of blood vessels

335
Q

how often is the epidermis replaced?

A

every 25-45 days

336
Q

what is the epidermis composed of?

A

epithelial cells joined by tight junctions

337
Q

what are the five epidermal layers or strata?

A

stratum. .
- corneum (superficial)
- lucidum
- granulosum
- spinosum
- basal (basal/deepest)

338
Q

how thick is the stratum corneum?

A

20-30 cell layers

339
Q

what is the stratum corneum composed of?

A

dead keratinised flattened cells

340
Q

what is the stratum basale composed of?

A

single layer of dividing stem cells

341
Q

what does the stratum basale also contain?

A

melanocytes which produce pigment

342
Q

what are the five cell types of epidermis?

A
  • keratinocytes
  • epidermal stem cells
  • melanocytes
  • Merkel cells
  • Langerhan/dendritic cells
343
Q

what do keratinocytes produce?

A

keratin

344
Q

what is the purpose of epidermal stem cells?

A

divide

345
Q

what do melanocytes produce?

A

melanin

346
Q

what are Merkel cells?

A

touch receptors

347
Q

what is the purpose of Langerhans and dendritic cells?

A

activates immune responses

348
Q

what type of tissue does the dermis consist of?

A

connective

349
Q

what type of cells are included in the connective tissue of the dermis?

A

fibroblasts and macrophages

350
Q

what do fibroblasts produce?

A

collagen and elastic fibres to provide strength/flexibility

351
Q

what does the dermis contain?

A
  • blood vessels
  • lymphatic vessels
  • nerves and sensory receptors
  • sweat and sebaceous glands
  • hair follicles
352
Q

what areas of body are covered by thick skin?

A

palms, fingertips and soles of feet

353
Q

what areas of body are covered by thin skin?

A

rest of body besides palms, fingertips and soles of feet

354
Q

what are the functions of thick skin?

A
  • very thick epidermis, esp. strata corneum
  • lack of hair/oil glands
  • areas of high use- proteection
355
Q

what are the functions of thin skin?

A
  • thin epidermis which lacks strata lucidum
  • hair, sweat and oil glands present
  • allows suppleness and agility
356
Q

what are appendages of the skin and derivatives of the epidermis?

A
  • sweat glands
  • sebaceous glands
  • hair follicles
  • nails
357
Q

what are the functions of sweat glands?

A

open to surface of epidermis or into hair follicles to regulate temp

358
Q

what are the functions of sebaceous glands?

A

produce oily substance to soften hair/skin and act as water resistance

359
Q

what do blockages of the sebaceous glands cause?

A

pimples

360
Q

what do the skin nerve supply located in the dermis control?

A
  • blood flow
  • glandular secretion
  • collect sensory info
361
Q

what allows the control of blood flow to skin by nerves?

A

via pre-capillary sphincters

362
Q

what sensory info is collected by the nerve supply to skin?

A
  • pain
  • temp
  • touch
  • pressure
363
Q

what are the main functions of the skin?

A
  • protection
  • sensation
  • metabolic functions
  • blood reservoir
  • excretion
  • temp regulation
364
Q

what are chemical barriers of the skin?

A
  • low pH secretions precent bacteria multiplying
  • defensins
  • melanin protects DNA from UV
365
Q

what are physical/mechanical barriers of the skin?

A

keratin and oily secretions block most water and water-soluble substances

366
Q

what are some biological barriers of the skin?

A

macrophages engluf organisms that manage to penetrate epidermis

367
Q

what are the three types of receptors providing info to CNS from skin?

A
  • pain (nociceptors)
  • temp (thermoreceptors)
  • touch, pressure, vibration (mechanoreceptors)
368
Q

what are the two processes involved in tissue repair?

A

regeneration and fibrosis

369
Q

what factors does tissue repair success depend on?

A
  • depends on ability of tissue to divide
  • nutrition
  • severity of wound
370
Q

what is regeneration of tissue?

A

replaces destroyed tissue with same kind of tissue

371
Q

when can regeneration repair tissue to normal?

A

damage is minor an epidermis has stem cells to regenerate

372
Q

what is the process of fibrosis?

A

replaces destroyed tissue with scar tissue

373
Q

what is the damage to dermis repaired by in fibrosis?

A

fibroblasts

374
Q

what are the three stages of skin repair?

A
  • inflammation
  • organisation or proliferative
  • maturation or remodelling
375
Q

what occurs in the inflammation stage of skin repair?

A

formation of blood clot

376
Q

what occurs in the organisation/proliferative stage of skin repair?

A

formation of granulation tissue

377
Q

what occurs in the maturation or remodelling stage of skin repair?

A

regeneration and fibrosis

378
Q

what is the function of the inflammation stage of skin repair?

A

prepare wound for repair, eliminate invaders and remove foreign substances

379
Q

how does inflammation stage occur?

A
  • release inflammatory chemicals that make vessels permeable
  • fluid release in area
  • macrophages
  • clotting proteins
  • scab formation
380
Q

what is the function of the organisation or proliferative stage of skin repair?

A

to synthesise extracellular matrix including collagen and restore blood supply

381
Q

what is the blood clot replaced by in the organisation or proliferative stage of skin repair?

A

granulation tissue

382
Q

what is granulation tissue composed of?

A
  • capillaries that grow over wound and bring nutrients /oxygen
  • fibroblasts
  • macrophages
383
Q

what do epithelial stem cells do in organisation or proliferative stage of skin repair?

A

multiply and migrate over granulation tissue

384
Q

what occurs during the maturation or remodelling stage of skin repair?

A

collagen laid down in organisation is remodelled and contracts pull wound edges together

385
Q

if the wound is major and scar tissue is visible what process is mainly responsible for repair?

A

fibrosis

386
Q

what may skin damage due to burns lead to?

A

tissue damage, denatured proteins and cell death

387
Q

what are some immediate threats of burns?

A

dehydration and electrolyte imbalance

388
Q

what does dehydration and electrolyte imbalance from burns lead to?

A

renal shutdown and circulatory shock

389
Q

what is the main threat of burns after initial crisis?

A

infection via bacteria, fungi, and other pathogens

390
Q

what is the severity of a burn dependent on?

A

degree of heat or chemical exposure and depth of penetration

391
Q

how are burns classified by?

A

how much of the skins layers are destroyed

392
Q

what are the levels of burns?

A
  • 1st: superficial
  • 2nd: partial-thickness
  • 3rd: full tickness
  • 4th: subdermal
393
Q

what are some characteristics of 1st degree burns?

A
  • confined to epidermis
  • not significant no barriers altered
  • generally heals itself in less than a week
394
Q

what are some characteristics of 2nd degree superficial partial-thickness burns?

A
  • destruction of entire epidermis and no more than third of dermis
  • leakage of large amounts of plasma
  • blisters
  • healing 1-3 weeks
395
Q

what are some characteristics of 2nd degree deep partial-thickness burns?

A
  • destruction of the epidermis and most of the dermis
  • dead tissue adheres to the underlying viable dermis (no blisters)
  • white and dry
  • blood flow compromised
  • risk of infection
396
Q

what are some characteristics of 3rdd degree full-thickness burns?

A
  • complete destruction of epidermis and dermis
  • significant scarring (skin grafts generally)
  • destroyed blood and nerve supply
397
Q

what are some characteristics of 4th degree burns?

A
  • complete destruction of epidermis and dermis with extension into the underlying tissue
  • appears charred, dry, and brown/white
  • no sensation
  • often requires amputation
398
Q

when is scarring at a low risk to occur?

A

Less severe burns

  • superficial
  • superficial partial thickness
  • heals in less. than 10 days
399
Q

when is scarring at a high risk to occur?

A

severe burns

  • deep partial thickness
  • full thickness
  • burns that require skin grafts
  • over 21 days to heal
400
Q

what is a hypertrophic burn scar?

A

scar with excessive collagen synthesis leading to a raised area obtained within woundmargin

401
Q

what is produced during skin repair in a hypertrophic burn scar?

A

disorganised collagen fibres

402
Q

what colour are hypertrophic burn scars?

A

deep red to purple

403
Q

when are hypertrophic scars more prominent?

A

joints where skin tension and movement are high

404
Q

what are burn scar contractures the pathological result of?

A

long term shrinkage of scar

405
Q

what do burn scar contractures result in?

A

inability to perform full ROM of joint

406
Q

what are treatment options for burn scar contractures?

A
  • stretching
  • splinting
  • massage
  • skin grafting
  • silicon gels

enabling occupational performance (8 decks)

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