bioscience exam Flashcards
1
Q
what is senescence?
A
normal process of changes overtime eventually affecting organ function
2
Q
what are the two main theories of aging?
A
programmed and error theory
3
Q
what ideas does the programmed theory of ageing involve?
A
- programmed longevity
- endocrine theory
- immunological
4
Q
what ideas does the error theory of aging involve?
A
- wear and tear
- cross-linking
- free radicals
- somatic DNA damage
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
6
Q
what is endocrine theory as a programmed theory of aging?
A
where biological clock acts through hormones to control ageing rate
7
Q
what is immunological as a programmed theory of aging?
A
immune system programmed to decline increasing vulnerability
8
Q
what is wear and tear as an error theory of aging?
A
cells and tissues wear out from repeated use
9
Q
what is cross-linking as an error theory of aging?
A
accumulation of cross-linked proteins damages cells/tissues
10
Q
what are free radicals as an error theory of aging?
A
cause damage to macromolecular components
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
12
Q
what is primary ageing?
A
changes that we can expect
13
Q
what are some examples of primary aging?
A
- wrinkles
- brain cell loss
- OA/porosis
- presbyopia
14
Q
what is secondary aging?
A
degenerative diseases which become more common with age
15
Q
what are some examples of secondary aging?
A
- atherosclerosis
- type 2 diabetes
- cancers
- glaucoma
16
Q
when does brain weight begin to decline?
A
in the 20s there is fluid loss and brain remodeling
17
Q
when does neuronal loss begin?
A
30
18
Q
how much of the brain mass can be lost with advancing age?
A
up to one 10th
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
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
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
22
Q
what are the two categories of hearing loss?
A
conductive and sensory neural
23
Q
what is conductive hearing loss?
A
conduction of sound waves through to oval window is impaired
24
Q
what is sensory neural hearing loss?
A
the nervous system of sound is impaired
25
what are some causes of conductive hearing loss?
- obstruction
- less pliable tympanic membrane
- ossification of auditory ossicles
26
what are some causes of sensory neural hearing loss?
- loss of stereocilia
| - loss of neurons in auditory cortex
27
what are some changes that occur in the ear with ageing?
- loss of elasticity of tympanic membrane
- impaired articulation of ossicles
- loss of stereocilia
- noise damage
28
what system maintains balance?
the vestibular system of inner ear
29
what are some age-related changes in the vestibular system?
- loss of hair cells
- degeneration of otoliths
- diminished number of vestibular system nerve cells
30
what occurs to cellular immunity with aging?
- loss of functional capacity of cell-mediated immunity
- lymphocytes have diminished proliferative response
- increase in CD4 and decrease in CD8
31
what is the main function of natural killer cells?
surveillance against diseases
32
what occurs with age in relation to natural killer cells?
decrease in number and effectiveness
33
what is blood pressure the result of?
product of cardiac output and peripheral resistance
34
what is ageing associated with in relation to blood vessels?
breakdown of elastic fibres in arteries and vessels become more rigid
35
what factors is cardiac output dependent on?
- contractility
- end-diastolic volume
- HR
36
how is baroreceptor function affected by age?
becomes less effective, thickening of arterial walls may interfere with ability ti measure degree of stretch
37
what occurs to the respiratory system with age?
- loss of elastic recoil
- thinning/disruption of alveolar walls
- total compliance decreases
- reduction of gaseous exchange
38
what are the most important changes to affect kidney functioning as we age?
vascular degeneration
39
how much can older adults renal flow be reduced by?
from young adults at 600ml/min to as much as half
40
what are changes in the renal system as we age normally related to?
changes in blood vessels
41
what occurs when the glomerular filtration rate is reduced as we age?
- electrolyte imbalance
- acid-base imbalance
- reduced creatinine and other toxic metabolites clearnace
42
what may incontinence be caused by in older age?
- reduce. bladder elasticity and volume
- loss of sphincter tone
- poor bladder control
43
how much does energy requirements decline with age?
for each decade after 50 years caloric requirement declines by 10%
44
what is a primary influence to relieve constipation?
exercise
45
what is reduced in relation to the gastrointestinal system with age?
- taste
- number of fibres innervating olfactory bulb and receptors (reduce smell)
- secretion of pancreatic enzymes
46
what occurs in the gastrointestinal system due to the reduction of pancreatic enzymes?
decreased digestivity ability of small intestine
47
what is sarcopenia?
muscle atrophy and decrease in mass
48
when is maximal muscle mass achieved?
20s and 30s
49
what do changes in muscle tissue include as we age?
- reduced muscle fibre numbers and size
- increased fat
- reduced blood flow
- reduced motor neuron numbers
- decreased efficiency of mitochondria
50
what can contribute to sarcopenia with age?
decreased circulating anabolic hormones such as testosterone
51
when is maximal bone density obtained?
25-30 years
52
what factors contribute to bone loss with age?
reduced. ..
- oestrogen/testosterone
- growth hormone
- levels of calcium and vitamin d
53
what is a risk factor for osteoarthritis?
increasing age
54
what makes joints more prone to mechanical damage as we age?
decreased chondrocytes
55
why does flexibility decrease with age?
as a result of decreased elasticity of collagen and elastin within ligaments
56
what can assist in delaying changes to the musculoskeletal system as we age?
light exercise and weight-bearing exercise can improve bone density, increase muscle mass and strength
57
why is the epidermis and dermis more likely to separate from simple trauma in old age?
there is reduced contact between them
58
what results in the greying of hair?
reduced melanocytes
59
what does a reduction in subcutaneous fat predispose in the elderly potentially lead to issues with?
pressure sores and hypothermia
60
what are some issues that are associated with aging and metabolism?
- vasoconstriction issues
- heat conservation reduced
- impaired ability to prevent core temp fluctuations
61
what is the cessation of menstrual cycle called in older age?
menopause
62
what is andropause?
for men, and is a collection of changes caused by decline in testosterone
63
when does menopause usually occur?
between 45-55 years
64
with reduced oestrogen what is there a reduction in?
- reduced bone density (osteoporosis risk)
| - reduced vasomotor control (hot flushes)
65
what does andropause result in?
- increased body fat
- reduced muscle/bone mass
- erectile dysfunction and reduced libido
- increased risk of anaemia
66
what will regular exercise improve?
- muscle mass, strength and endurance
- coordination/balance
- joint flexibility
- bone strength
- BP
- body fat
67
what is the role of the innate immune system?
prevent foreign substances entering body
68
what is a self-limiting process?
turns off once invader has been destroyed and healing occurs
69
what is the role of the adaptive immune system?
target and destroy specific substances
70
what cells are involved in humoral immunity?
B cells
71
what cells are involved in cellular immunity?
T cells
72
what are some surface barriers of the innate defenses?
physical and chemical barriers
73
what are some internal defences of the innate immune system?
- phagocytes
- NK cells
- inflammation
- fever
- antimicrobial proteins
74
what is an autoimmune disease?
breakdown in ability of adaptive defences to distinguish self from non-self
75
what are some genetic predispositions as a mechanism of autoimmune disease?
- type of self proteins a person has (HLA proteins)
- 75% women
- ethnicity
76
what is the enviro as a mechanism of autoimmune disease?
chemicals and viral/bacterial infection
77
what is the breakdown of self tolerance as a mechanism of autoimmune disease?
- failure to destroy self-reactive T and B lymphocytes
- failure of regulatory T cells
- antigen mimicry
- release of sequestered antigens
- super antigens
78
what is antigen mimicry in relation to the breakdown of self-tolerance?
foreign antigens resemble self antigens
79
what is the release of sequestered antigens in relation to the breakdown of self-tolerance?
new self antigens revealed
80
what is a superantigen in relation to the breakdown of self-tolerance?
bacterial exotoxins activate indiscriminately
81
what does idiopathic mean?
cause is unknown
82
what are the goals of treating autoimmune diseases?
- relieve symptoms
- replace vital substances
- suppress immune system
- dietary manipulation
83
what type of inflammation is juvenile idiopathic arthritis?
immune-mediated and chronic
84
what is the frequency of juvenile idiopathic arthritis?
effects 1-2 per 1000 children more likely girls
85
what is the mean age of JIA onset?
depends on disease subtype but usually between 1-3yo
86
what is the genetic component of JIA?
- markedly increased risk for close relatives
- females
- most common in caucasian
87
what is immune-mediated chronic inflammation?
normal inflammation/immune response to foreign material. cross reacts with self antigen that is always present but never clears
88
what are infiltration cells?
- activated T cells
- B cells/plasma cells
- macrophages
- neutrophils
89
what are joint cells?
- fibroblasts
- macrophages
- chondrocytes
- osteoclasts
90
what type of joints are fibroblasts in?
synovium
91
what type of joints are macrophages in?
synovium
92
what type of joints are chondrocytes in?
cartilage
93
what type of joints are osteoclasts in?
subchondral bone
94
what are cytokines released by?
activated T cells, macrophages or fibroblasts
95
what causes fever?
endogenous pyrogens
96
what do chemoattractants do?
attract/activate macrophages and other cells, promotes inflammation
97
what do interleukin-1 activate and promote?
activates fibroblasts, chondrocytes and osteoclasts and promotes bone/cartilage destruction
98
what does tumor necrosis factors a (TNFa) stimulate and support?
stimulates blood vessel formation and acute phase response and supports growing pannus
99
what is growing pannus?
synovial fibroblasts grow into joint space
100
what are some symptoms of JIA?
- joint pain/swelling/stiffness
- sleep disturbance, fatigue, irritability
- periods of remission/flare up
101
what are some extra-articular signs depending on JIA category and severity?
- acute phase response
- serositis and vasculitis
- uveitis
- growth factors
102
what do autoantibodies have a role in?
in pathogenesis via immune complex-mediated inflammation
103
what do the autoantibodies cause damage to?
- pericardium, myocardium
- lung pleura
- lacrimal and salivary glands
- blood vessels
- nerve pain
104
what occurs when there is damage by autoantibodies to the pericardium and myocardium?
impaired function and pain
105
what occurs when there is damage by autoantibodies to the lung pleura?
impaired function and pain
106
what occurs when there is damage by autoantibodies to the lacrimal and salivary glands?
dry eyes and mouth
107
what occurs when there is damage by autoantibodies to the blood vessels (vasculitis)?
ischaemia > necrosis in skin, heart, nerves and brain
108
what is uveitis?
inflammation of uvea
109
what can occur with long-term uveitis?
permanent eye damage and blindness
110
how is uveitis treated?
regular ophthalmologic exams and topical corticosteroids
111
what are some different types of growth failures?
- reduced overall rate of growth (small stature)
- uneven limb/joint
- low bone mineral density
112
what causes reduced the overall rate of growth (small stature) as a growth failure?
high level of circulating inflammatory cytokines (IL-6)
113
what are some treatments for the reduced overall rate of growth (small stature)?
corticosteroid treatment and some success using growth hormones
114
what causes uneven limb/joint growth as a growth failure?
increased blood supply to growth plates may cause affected joint/limb to grow faster
115
what is low bone mineral density due to growth failure?
increased osteoclast activity
116
what are the three major types of JIA?
- oligoarticular
- polyarticular
- systemic
117
what are some minor types of JIA?
- enthesitis-associated JIA
- psoriatric
- undifferentiated
118
what joints are affected by enthesitis-associated JIA?
typically knee, ankle, intervertebral joints
119
what joints are affected in psoriatic JIA?
any joint
120
what are some systemic features of enthesitis-associated JIA?
inflammation of tendons at muscle insertion and increased risk of uveitis
121
what are some systemic features of psoriatic JIA?
- psoriasis
- may have dactylitis (inflammation of digit) or oncholysis (nail pitting and loss)
- increased risk of. uveitis
122
what type of joints are affected by oligoarticular JIA?
- medium-large eg. knees, ankles
- asymmetric
- non-destructive
123
what type of joints are affected by polyarticular JIA?
- any joint- usually smaller eg. hands and wrists
- usually symmetric
- destructive arthritis
124
what type of joints are affected by systemic JIA?
- any joint
- usually symmetric
- destructive
125
what are the systemic features of oligoarticular JIA?
-~20% uveitis
126
what are the systemic features of polyarticular JIA?
- < 10% uveitis (usually associated with asymmetrical disease)
- RF+ may have symptoms like systemic JIA
127
what are the systemic features of systemic JIA?
daily fever, rash, enlarged spleen, liver, inflammation of cardiac and pleural membranes
128
what are some long-term issues of oligoarticular JIA?
limb length discrepancy, flexion. contracture
129
what are some long-term issues of polyarticular JIA?
RF + decreases chance of remission
130
what are some long-term issues of systemic JIA?
growth failure, acute phase response
131
what is the pharmacological intervention for autoimmune disease determined by?
disease category and degree of severity
132
what is part of the 1st line pharmacological intervention?
NSAIDs and corticosteroids
133
what is part of the 2nd line pharmacological intervention?
DMARDs (methotrexate)
134
what is part of biologics pharmacological intervention?
immune response modifiers
135
what do NSAIDs do?
anti-inflammatory but does not prevent joint destruction or slow disease progression
136
what are some side effects of NSAIDs?
- generally well tolerated by children
- <1% mild nausea
- bruising more common
137
can corticosteroids prevent joint destruction?
yes
138
what can intra-articular injection of corticosteroids prevent?
local joint deformity, muscle atrophy and thus growth disturbances
139
side effects of corticosteroids?
- immunosuppressant so increased risk of infection
- growth retardation
- decreased bone mineral density
- weight gain, fluid retention
140
what are some preventative measures for increased risk of infection as a side effect of corticosteroids as an immunosuppressant?
- hand hygiene
- avoiding unwell people
- immunisation
141
what are some preventative measures of growth retardation as a side effect of corticosteroids?
short courses of systemic treatment and growth hormone supplements
142
what are some preventative measures of decreased bone mineral density as a side effect of corticosteroids?
physical exercise and calcium/vitamin D supplementation
143
what are some preventative measures of weight gain and fluid retention as a side effect of corticosteroids?
healthy/low salt diet and physical exercise
144
are DMARDs slow or fast acting?
slow (1-2 month for effect)
145
when are biologics used?
when 1st and 2nd line therapy fails to control
146
what is the onset time for biologics?
more rapid (1-2weeks)
147
what do biologics do?
Immunosuppressants suppress immune-mediated inflammation and block production and activity of cytokines/activation of T cells
148
what does biologic use as an immunosuppressant result in?
- impair inflammatory response
- slow disease progression
- increased frequency/severity of infection
149
what are biologics administered by?
subcutaneous injections
150
what are some non-pharmacological treatment options for JIA?
- physical conditioning
- resting anf functional splints
- serial casting
- shoe lifts and inserts to equalise leg lengths
- personal, household and educational aids
151
what are some pain management techniques for JIA?
- breathing and relaxation techniques
- heat, cold. or water therapy
- massage
152
what are some nutrition treatment options for JIA?
- vitamin d and calcium supplements
| - omega-3 fatty acids
153
what are surgery options to treat JIA?
- osteotomy
- epiphysiodesis
- joint replacement
154
what is osteotomy?
removing or inserting wedge of bone to allow more normal joint alignment
155
what is epiphysiodesis?
removal/impairment of growth plate to stop growth
156
what is poor prognosis of JIA associated with?
- early hip/wrist involvement
- symmetrical disease and rheumatoid factor
- persistent inflammation
157
what is the structure of smooth muscle?
spindle shaped, non-striated fibres and one central nucleus
158
what is the structure of cardiac muscle?
branched, striated fibres, usually one central nucleus
159
what is the structure of skeletal muscle?
long cylindrical striated fibres and numerous peripheral nuclei
160
what is a fascicles?
bundle of muscle fibres
161
what are the three layers of skeletal muscle?
- endomysium
- perimysium
- epimysium
162
what are sarcomeres?
contractile units
163
what do sarcomeres contain?
myofilaments
164
what is a nerve?
bundle of axons held together with connective tissue
165
what is the purpose of myelin sheath?
for insulation and protection
166
where are somatic motor impulses generated?
PMC
167
how are somatic motor impulses carried to skeletal muscles?
via upper and lower motor via corticospinal pathways
168
what ensures coordination of movement?
basal nuclei and cerebellum
169
what is hypertrophy response to?
regular forceful use
170
what does hypertrophy result in an increase in?
- no.of and diameter of contractile proteins
| - increase in diameter of individual fibres not increase in no.of muscle fibres
171
what is atrophy a response to?
disuse
172
what occurs with atrophy?
initially fibres shrink as contractile proteins are broken down and muscle fibres may later decrease and be replaced by fibrous tissue
173
what will the most damaged area of muscle tissue be patched with when repairing?
fibrous scar tissue that is non-contractile
174
what can neuromuscular disease be directly due to?
muscle pathology
175
what can neuromuscular disease be indirectly due to?
nervous system pathology
176
what may neuromuscular disease be caused by?
- myopathy
- neuropathy
- junctionopathy
177
what may symptoms of the neuromuscular disease include?
- muscle weakness/paralysis
- muscle wastage
- continuous muscle spasm
- muscle twitching
- muscle pain
- breathing and swallowing difficulty
178
what is myotonia?
continuous muscle spasm
179
what is fasciculation?
muscle twitching
180
what is myalgia?
muscle pain
181
what are some causes of neuromuscular disease?
- genetic mutation
- viral infection
- autoimmune/hormonal/metabolic disorder
- dietary deficiency
- certain drugs/poison
- unknown factors
182
what are types of inherited myopathies?
-muscular dystrophy
| congenital/metabolic/mitochondrial myopathy
183
what are types of acquired myopathies?
- infection
- inflammatory myopathy
- toxic myopathy
- associated with systemic disease
184
what is junctionopathy related to neuromuscular disease?
diseases originating in neuromuscular junction
185
what are types of upper motor neuron diseases?
- stroke
- CP
- ALS/MND
- spinal cord trauma
186
what are types of lower motor neuron diseases?
- peripheral neuropathies
- spinal (anterior horn) nerve
- poliomyelitis
187
what are some brain-origin diseases?
- parkinson's
| - alcohol related brain damage
188
what is muscular dystrophy a breakdown in?
dystrophin-glycoprotein complex which is a network of fibrous proteins
189
what does dystrophin-glycoprotein complex do?
stabilises sarcolemma during contraction and relaxation
190
where is the mutation in Duchenne muscular dystrophy?
in dystrophin gene on X chromosome
191
what symptoms appear in Duchenne muscular dystrophy at between 1-5 years?
- late walking
- toe walking, enlarged calf muscles
- difficulty standing
192
what are the three main types of chronic inflammatory myopathy?
- polymyositis
- dermatomyositis
- inclusion body myositis
193
what are some symptoms of toxic myopathy?
- muscle weakness
- myalgia
- myoglobinuria
- elevated creatine kinase
194
what can cause toxic myopathies?
alcohol and certain snake venoms
195
what is the most common type of drug-induced myopathy?
glucocorticoid-induced myopathy
196
what is glucocorticoid-induced myopathy a side affect of?
corticosteroid therapy
197
what does glucocorticoids do?
catabolic effect on skeletal muscle
198
what causes Cushing's disease?
adrenal glands produce high levels of cortisol
199
what is junctionopathy due to?
defect in transmission at neuromuscular junction
200
who does myasthenia gravis affect?
young women and older men
201
what are some symptoms of myasthenia gravis?
- muscle weakness
- fatigue
- visual disturbances
- ptosis- droopy eyelids
- swallowing/breathing difficulty
202
what is the treatment for myasthenia gravis?
- acetylcholinesterase inhibitors
- immunosuppressants
- thymectomy
203
what does botulism prevent release of at axon terminals
ACh
204
how does organophosphate get into the body and cause poisoning?
inhaled, ingested or absorbed via skin
205
what are some symptoms of organophosphate?
- copious respiratory and oral secretions
- diarrhoea and vomiting
- sweating
- altered mental status
- autonomic instability
- muscle weakness/paralysis and respiratory arrest
206
what is acetylcholinesterase?
enzyme that dggrades ACh
207
what do organophosphates inhibit and what occurs as a result?
acetylcholinesterase and results in an accumulation of ACh at NMJ and continuous cholinergic stimulation
208
what is the treatment for organophosphate poisoning?
ACh competitors reduce stimulation
209
what does neuropathy diseases originate from?
originates in somatic motor neuron
210
what occurs peripheral neuropathies caused by and result in?
damage to peripheral nerves can occur from diabetes and Guillian-Barre syndrome, leading to weakness, numbness., pain/tingling
211
what do anterior horn (spinal nerve) diseases result from?
diseases such as poliomyelitis can destroy cells of anterior horns
212
what does chronic high blood glucose levels from diabetic peripheral neuropathy incite?
nerve and capillary damage
213
what are the symptoms of diabetic peripheral neuropathy?
-numbness, reduced detection if sensations
-tingling/burning
-sharp pains
-increased sensitivity to touch
ulcers/infections
-muscle weakness
214
what is Guillian-Barre syndrome triggered by?
acute viral/bacterial infection
215
what are the symptoms of Guilian-Barre syndrome?
- myalgia
- muscle weakness
- jerky/uncoordinated movement
- paralysis
216
what type of disease is poliomyelitis?
anterior horn
217
who does poliomyelitis mainly affect?
children under 5
218
what are the initial symptoms of poliomyelitis?
- fever
- fatigue
- headache
- vomiting
- neck stiffness
- pain in limbs
219
what are some upper motor neuron diseases?
- motor neuron disease/Lou Gehrig's disease/ALS
- CP
- multiple sclerosis
220
what are the early symptoms of amyotrophic lateral sclerosis?
- fasciculations
| - muscle cramps/spasticity/weakness
221
what are the late symptoms of amyotrophic lateral sclerosis?
- breathing difficulty
| - fatigue
222
what may cause the development of CP?
- interruption of oxygen supply
- maternal infection
- meningitis
- head injury after birth
223
when is CP usually diagnosed?
between 3-5 years when milestones arent met
224
what disturbances may accompany CP?
- sensation
- cognition
- communication
- perception
- behaviour
- seizures
225
what percentage of CP is spastic?
75-85%
226
what is the effect of spastic CP on upper limbs?
flexion at elbow/wrist/fingers (fist)
227
what is the effect of spastic CP on lower limbs?
- flexion at hip/knee
- adduction of thigh
- equinovarus foot position from tight calves
- hyperextension of big toes
228
what does spastic CP affect?
- stand/sit upright
- transfer
- walk and run
229
what are the effects of spasticity over time?
-stiffness, atrophy and fibrosis
-muscle contracture
-bone deformity
pain
230
when does stroke occur?
when blood flow to part of brain or whole brain is interrupted
231
what may stroke be due to?
- blockage (occlusive)
| - bleeding (haemorrhagic)
232
what is CVA?
tissue which has died because of failed blood supply is infarcted
233
what occurs where brain tissue dies?
undergoes liquefactive necrosis
234
what are some risk factors for stroke?
- increasing age
- hypertension
- heart disease
- atherosclerosis
- diabetes mellitus
- smoking
- cocaine
235
what large vessels may thrombi form in during ischaemic stroke?
- carotid arteries
- vertebral arteries
- circle of willis
236
what smaller vessels may thrombi form within in ischaemic stroke?
smaller arteries within brain
237
what is a major cause of thrombus formation?
atheroclerosis
238
what is the most common sites of thrombotic occlusion?
arterial branch points
239
where do emboli commonly arise from?
heart especially in atrial fibrillation
240
what is lipohyalinosis?
build up of fatty hyaline matter in blood vessel from high bp and ageing
241
what may arterial anastomoses allow?
some areas to receive blood even though their main supplying artery is blocked
242
where may blood clots occur in brain to occlude blood supply?
may occur in cortex but not in internal structures of brain which are supplied by small, non-anastomosing arterial branches
243
within the ischaemic area what are the two major zones of injury?
ischaemic penumbra and core ischaemic
244
what are some presentations in acute stroke?
- altered consciousness
- headaches
- aphasia
- incoordination, weakness, paralysis or sensory loss in limbs
- facial weakness/asymmetry
245
what are some alterations in consciousness in acute stroke?
- stupor or coma
- confusion or agitation/memory loss
- seizures
- delirium
246
what is aphasia?
incoherent speech or difficulty understanding speech
247
what is ataxia as a symptom of stroke?
poor balance, clumsiness, difficulty walking
248
what areas of the brain are responsible for hearing?
primary auditory cortex and auditory association area
249
what areas of the brain are responsible for visual?
primary visual cortex and visual association area and occipital lobe
250
what are some common patterns in left hemisphere stroke?
- aphasia
- R hemiparesis
- R-sided sensory loss
- R-field defect
- poor R conjugate gaze
- dysarthria
- difficulty reading, writing and calculating
251
what are some common patterns with right hemisphere stroke?
- aphasia
- L hemiparesis
- L-sided sensory loss
- L-field defect
- poor L conjugate gaze
- dysarthria
- spatial disorientation
252
what occurs as a common pattern in the brainstem/cerebellum/posterior hemisphere stroke?
- motor/sensory loss in all limbs
- crossed signs
- limb or gait ataxia
- dysarthria
- amnesia
- dysconjugate gaze
- nystagmus
- bilateral visual field defects
253
what are common patterns within the small subcortical hemisphere or brain stem in a pure motor stroke?
weakness of face/limbs on one side without abnormal higher brain functions/sensation/vision
254
what are common patterns within the small subcortical hemisphere or brain stem in a pure motor stroke?
decreased sensation of face/limbs on one side and no abnormal higher brain function/motor/vision
255
what does the effect on function depend on following stroke?
region of brain infarcted and extent of infarct (size of vessels compromised)
256
what is apraxia of speech?
reduced ability to produce spoken words
257
why do we amputate?
- control pain or disease
- punishment
- when re-vascularisation is not possible
258
what causes PVD?
- diabetes
- hypertension
- hyperlipidaemia
- smoking
259
what is PVD?
narrowing of blood vessels outside brain and heart
260
what is PVD most commonly due to?
atherosclerosis
261
what areas are assessed in the skin for PVD?
- touch
- hair growth
- appearance
- nails
- pulse
262
what areas are assessed for ulcers in PVD?
- pain
- colour
- edges
- location
263
what are treatment options for PVD?
- lifestyle change
- treatment of exisiting conditions
- medication
- angioplasty
- vascular surgery
- amputation if re-vascularisation is not possible
264
what are the levels of lower extremity amputation from the toes to ankle?
- amputation of digits
- partial foot
- ankle (syme) disarticulation
265
what are the levels of lower extremity amputation from the below the knee to below hip?
- below-knee (transtibial)
- above-knee (transfemoral)
- vas-ness rotation/rotationplasty
266
what are the levels of lower extremity amputation from hip to waist?
- hip disarticulation
- hemipelvectomy/hindquarter
- hemicorporectomy (at waist)
267
wha does the surgeon need to take into account when deciding the level of amputation?
- adequate vascularisation
| - ability to create adequate stump to take prosthetic
268
what are causes of upper extremity amputation?
- severe trauma
- PVD
- thermal burns and frost bite
269
what is the pathophysiology of upper extremity amputation?
- severe blood loss, nerve damage and shock
- impaired circulation
- tissue necrosis
270
what are the levels of amputation from the fingers to the wrist?
- amputation of digits
- metacarpal
- wrist disarticulation
271
what are the levels of amputation from the forearm to elbow?
- forearm
| - elbow disarticulation
272
what are the levels of amputation from above the elbow to above arm?
- above-elbow (transhumeral)
- shoulder disarticulation
- forequarter
273
what is glycoylsis?
glucose used by cell to make ATP
274
how is glucose transported from blood to cells?
insulin
275
what is insulin?
hormone that allows transport of glucose into cells lowering the blood glucose levels
276
how is insulin synthesised?
B cells of islets of Langerhans in pancreas
277
how is insulin stored and released?
- packaged into granules within B cells
- release triggered by increased BGLs
- biphasic release > 1st and 2nd phase
278
what do B cells synthesise and secrete and what does this result in?
insulin to lower BGL
279
what do a cells synthesise and secrete and what does this result in?
glucagon that increases BGL
280
when is the first phase of glucose uptake?
within 2 mins of eating lasting 10-15mins
281
when is the second phase of glucose uptake?
lasts until BGLs return to normal
282
what type of GLUT is allows glucose transport from cell membrane into liver cells?
2
283
what type of GLUT is allows glucose transport from cell membrane into muscle cells?
4
284
what type of GLUT is allows glucose transport from cell membrane into fat cells?
4
285
do neural cells require insulin?
no
286
what goes GLUTs stand for?
glucose transport units
287
does insulin lower or increase blood glucose levels?
lower
288
does glucagon lower or increase blood glucose levels?
increases
289
what occurs in glycogenesis?
excess. glucose is converted into glycogen
290
what is glucoeogenesis?
production of glucose by liver inhibited
291
what occurs during the absorptive (fasting) state?
pancreas releases glucagon from a cells and stored glycogen broken down to glucose
292
what is hyperglycaemia?
consistent high blood glucose levels
293
what percentage of diabetes is type 1?
15%
294
what percentage of diabetes is type 2?
855
295
what causes type 1 diabetes?
autoimmune, lack of insulin
296
what causes type 2 diabetes?
lifestyle and enviro resulting in deficient/defective insulin
297
what is gestational diabetes?
glucose intolerance first appears during pregnancy and usually resolves after birth
298
what causes gestational diabetes?
hormones and weight gain with pregnancy
299
what occurs in the liver in type 1 diabetes?
increased breakdown of stored glucose and production of glucose from non-carb sources
300
what occurs in the muscles in type 1 diabetes?
decreased glucose uptake due to absence pf insulin and glycogenesis
301
what occurs in the adipose tissue in type 1 diabetes?
increased breakdown of aft and production of free fatty acids
302
what occurs with protein in type 1 diabetes?
decreased acid production and protein synthesis and increased protein breakdown
303
what does obesity inhibit signalling in type 2 diabetes?
free fatty acids and cytokines from fat cells
304
why is insulin not secreted from the pancreas due to in type 1 diabetes?
destruction of B cells
305
why is insulin not secreted from the pancreas due to in type 2 diabetes?
B cell dysfunction/stress
306
what is the treatment options for type 1 diabetes?
insulin
307
what is the treatment options for type 2 diabetes?
- diet and exercise
| - oral and hypoglycaemic. agents
308
what are some acute consequences of uncontrolled hyperglycaemia for type 1 diabetes?
diabetic keto acidosis
309
what are some acute consequences of uncontrolled hyperglycaemia for type 2 diabetes?
non-ketotic hyperosmolarcoma
310
what are some chronic consequences of uncontrolled hyperglycaemia for diabetes?
vascular complications and neuropathies
311
what are some macrovascular consequences of chronic hyperglycaemia?
- damage to large blood vessels of brain, heart and extremities
- CVD and stroke
312
what are some microvascular consequences of chronic hyperglycaemia?
- abnormal thickening of basement membrane of capillaries
- retinopathy
- nephropathy
313
what does retinopathy as a result of chronic hyperglycaemia?
eyes
314
what does nephropathy as a result of chronic hyperglycaemia?
kidneys
315
what is peripheral neuropathy?
damage to peripheral nerves due to long term hyperglycaemia
316
what are some symptoms of peripheral neuropathy?
loss of feelings in hands/feet and reduced pain signalling/awareness
317
what is usually seen with concomitant peripheral vascular disease?
- decreased blood flow
- poor healing
- decreased immune response
318
what occurs to a diabetic foot following PVD and diabetic neuropathy?
- loss of sensation
- impaired wound healing in extremities
- infection and gangrene
319
what are some causes of diabetic foot ulcers?
- peripheral neuropathy
| - deformity, callus, shoes, trauma, pressure
320
what are the four types of primary tissues?
- epithelium
- connective
- nervous
- muscle
321
what is the function of nervous tissue?
internal communication
322
what is the function of epithelial tissue?
forms boundaries between enviro, protects, secretes, absorbs, and filters
323
what is the function of muscle tissue?
contracts to cause movement
324
what is the function of connective tissue?
supports, protects, bonds to other tissues
325
where is nervous tissue found?
brain, spinal cord, and nerves
326
where is muscle tissue found?
- muscle attached to bone (skeletal)
- heart (cardiac)
- muscles of walls of hollow organs (smooth)
327
where is epithelial tissue found?
- skin surface (epidermis)
| - lining of GI tract organs and other hollow organs
328
where is connective tissue found?
- bones
- tendons
- fat and other soft padding tissue
329
what are the three layers of the skin?
- epidermis
- dermis
- hypodermis
330
what layer of the skin is the epidermis?
outer epithelial layer
331
what layer of the skin is the dermis?
deep supporting layer of dense connective tissue
332
what layer of the skin is the hypodermis?
subcutaneous layer composed of loose connective and adipose tissue
333
is the epidermis vascular?
no its avascualar
334
what is avascular?
lack of blood vessels
335
how often is the epidermis replaced?
every 25-45 days
336
what is the epidermis composed of?
epithelial cells joined by tight junctions
337
what are the five epidermal layers or strata?
stratum. .
- corneum (superficial)
- lucidum
- granulosum
- spinosum
- basal (basal/deepest)
338
how thick is the stratum corneum?
20-30 cell layers
339
what is the stratum corneum composed of?
dead keratinised flattened cells
340
what is the stratum basale composed of?
single layer of dividing stem cells
341
what does the stratum basale also contain?
melanocytes which produce pigment
342
what are the five cell types of epidermis?
- keratinocytes
- epidermal stem cells
- melanocytes
- Merkel cells
- Langerhan/dendritic cells
343
what do keratinocytes produce?
keratin
344
what is the purpose of epidermal stem cells?
divide
345
what do melanocytes produce?
melanin
346
what are Merkel cells?
touch receptors
347
what is the purpose of Langerhans and dendritic cells?
activates immune responses
348
what type of tissue does the dermis consist of?
connective
349
what type of cells are included in the connective tissue of the dermis?
fibroblasts and macrophages
350
what do fibroblasts produce?
collagen and elastic fibres to provide strength/flexibility
351
what does the dermis contain?
- blood vessels
- lymphatic vessels
- nerves and sensory receptors
- sweat and sebaceous glands
- hair follicles
352
what areas of body are covered by thick skin?
palms, fingertips and soles of feet
353
what areas of body are covered by thin skin?
rest of body besides palms, fingertips and soles of feet
354
what are the functions of thick skin?
- very thick epidermis, esp. strata corneum
- lack of hair/oil glands
- areas of high use- proteection
355
what are the functions of thin skin?
- thin epidermis which lacks strata lucidum
- hair, sweat and oil glands present
- allows suppleness and agility
356
what are appendages of the skin and derivatives of the epidermis?
- sweat glands
- sebaceous glands
- hair follicles
- nails
357
what are the functions of sweat glands?
open to surface of epidermis or into hair follicles to regulate temp
358
what are the functions of sebaceous glands?
produce oily substance to soften hair/skin and act as water resistance
359
what do blockages of the sebaceous glands cause?
pimples
360
what do the skin nerve supply located in the dermis control?
- blood flow
- glandular secretion
- collect sensory info
361
what allows the control of blood flow to skin by nerves?
via pre-capillary sphincters
362
what sensory info is collected by the nerve supply to skin?
- pain
- temp
- touch
- pressure
363
what are the main functions of the skin?
- protection
- sensation
- metabolic functions
- blood reservoir
- excretion
- temp regulation
364
what are chemical barriers of the skin?
- low pH secretions precent bacteria multiplying
- defensins
- melanin protects DNA from UV
365
what are physical/mechanical barriers of the skin?
keratin and oily secretions block most water and water-soluble substances
366
what are some biological barriers of the skin?
macrophages engluf organisms that manage to penetrate epidermis
367
what are the three types of receptors providing info to CNS from skin?
- pain (nociceptors)
- temp (thermoreceptors)
- touch, pressure, vibration (mechanoreceptors)
368
what are the two processes involved in tissue repair?
regeneration and fibrosis
369
what factors does tissue repair success depend on?
- depends on ability of tissue to divide
- nutrition
- severity of wound
370
what is regeneration of tissue?
replaces destroyed tissue with same kind of tissue
371
when can regeneration repair tissue to normal?
damage is minor an epidermis has stem cells to regenerate
372
what is the process of fibrosis?
replaces destroyed tissue with scar tissue
373
what is the damage to dermis repaired by in fibrosis?
fibroblasts
374
what are the three stages of skin repair?
- inflammation
- organisation or proliferative
- maturation or remodelling
375
what occurs in the inflammation stage of skin repair?
formation of blood clot
376
what occurs in the organisation/proliferative stage of skin repair?
formation of granulation tissue
377
what occurs in the maturation or remodelling stage of skin repair?
regeneration and fibrosis
378
what is the function of the inflammation stage of skin repair?
prepare wound for repair, eliminate invaders and remove foreign substances
379
how does inflammation stage occur?
- release inflammatory chemicals that make vessels permeable
- fluid release in area
- macrophages
- clotting proteins
- scab formation
380
what is the function of the organisation or proliferative stage of skin repair?
to synthesise extracellular matrix including collagen and restore blood supply
381
what is the blood clot replaced by in the organisation or proliferative stage of skin repair?
granulation tissue
382
what is granulation tissue composed of?
- capillaries that grow over wound and bring nutrients /oxygen
- fibroblasts
- macrophages
383
what do epithelial stem cells do in organisation or proliferative stage of skin repair?
multiply and migrate over granulation tissue
384
what occurs during the maturation or remodelling stage of skin repair?
collagen laid down in organisation is remodelled and contracts pull wound edges together
385
if the wound is major and scar tissue is visible what process is mainly responsible for repair?
fibrosis
386
what may skin damage due to burns lead to?
tissue damage, denatured proteins and cell death
387
what are some immediate threats of burns?
dehydration and electrolyte imbalance
388
what does dehydration and electrolyte imbalance from burns lead to?
renal shutdown and circulatory shock
389
what is the main threat of burns after initial crisis?
infection via bacteria, fungi, and other pathogens
390
what is the severity of a burn dependent on?
degree of heat or chemical exposure and depth of penetration
391
how are burns classified by?
how much of the skins layers are destroyed
392
what are the levels of burns?
- 1st: superficial
- 2nd: partial-thickness
- 3rd: full tickness
- 4th: subdermal
393
what are some characteristics of 1st degree burns?
- confined to epidermis
- not significant no barriers altered
- generally heals itself in less than a week
394
what are some characteristics of 2nd degree superficial partial-thickness burns?
- destruction of entire epidermis and no more than third of dermis
- leakage of large amounts of plasma
- blisters
- healing 1-3 weeks
395
what are some characteristics of 2nd degree deep partial-thickness burns?
- 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
what are some characteristics of 3rdd degree full-thickness burns?
- complete destruction of epidermis and dermis
- significant scarring (skin grafts generally)
- destroyed blood and nerve supply
397
what are some characteristics of 4th degree burns?
- complete destruction of epidermis and dermis with extension into the underlying tissue
- appears charred, dry, and brown/white
- no sensation
- often requires amputation
398
when is scarring at a low risk to occur?
Less severe burns
- superficial
- superficial partial thickness
- heals in less. than 10 days
399
when is scarring at a high risk to occur?
severe burns
- deep partial thickness
- full thickness
- burns that require skin grafts
- over 21 days to heal
400
what is a hypertrophic burn scar?
scar with excessive collagen synthesis leading to a raised area obtained within woundmargin
401
what is produced during skin repair in a hypertrophic burn scar?
disorganised collagen fibres
402
what colour are hypertrophic burn scars?
deep red to purple
403
when are hypertrophic scars more prominent?
joints where skin tension and movement are high
404
what are burn scar contractures the pathological result of?
long term shrinkage of scar
405
what do burn scar contractures result in?
inability to perform full ROM of joint
406
what are treatment options for burn scar contractures?
- stretching
- splinting
- massage
- skin grafting
- silicon gels
