What determines rate of ageing? Which species have short life spans? Which species have long life spans?
- Mating strategy and production of gametes determines rate of ageing.
- species producing large numbers of gametes in a single mating season, or having multiple mating seasons in a single year have short life spans
- species having typically single offspring in which extensive parental care is invested have long life spans
- species producing large numbers of gametes in a single mating season, or having multiple mating seasons in a single year have short life spans
- species having typically single offspring in which extensive parental care is invested have long life spans
What is the effect of aging on renal function? What implications does this have on the prescription of elderly?
Glomeruler Filtration rate (GFR) decreases from the age of 20, by 75 it has decreased by 50%.
N.B creatinine is not a good indicator, because of reduced muscle mass.
The effect on drug choice in the elderly:
- avoid drugs which are nephrotoxic or unsafe in renal impairment
- reduce dose of other renally excreted drugs
N.B creatinine is not a good indicator, because of reduced muscle mass.
The effect on drug choice in the elderly:
- avoid drugs which are nephrotoxic or unsafe in renal impairment
- reduce dose of other renally excreted drugs
What affects digoxin concentration?
- reduced GFR
(increased concentration due to reduced excretion)
- reduced lean body mass (Vd decreases)
increased concdntration due to reduced Vd
- reduced body water
increased concentration due to reduced Vd
- decreased albumin
increased free(active) concentration
(increased concentration due to reduced excretion)
- reduced lean body mass (Vd decreases)
increased concdntration due to reduced Vd
- reduced body water
increased concentration due to reduced Vd
- decreased albumin
increased free(active) concentration
Why don't we prescribe sleeping tablets in elderly?
Benzodiazepines accumulate due to
- reduced hepatic metabolism
- increased Vd
- reduced albumin bindings
ADRs
- hypothermia, increased dependence, increased sedation, hangover effects, confusion, ataxia, memory problems, unsteady gait and balance problems
- reduced hepatic metabolism
- increased Vd
- reduced albumin bindings
ADRs
- hypothermia, increased dependence, increased sedation, hangover effects, confusion, ataxia, memory problems, unsteady gait and balance problems
Would you prescribe amitriptyline or sertraline to an elderly?
- setraline - SSRI- safer
- amitrityline -- tricyclic
anti- muscarinic SEs: Constipation, urinary retention, dry mouth, glaucoma, drowsiness, dizziness, syncope, confusion, postural hypotension, hyponatraemia, hypothermia and cardiac arrhythmias.
- low dose with caution
interactions may also be problematic (e.g. with antiarrhythmics and antiepilectics)
- amitrityline -- tricyclic
anti- muscarinic SEs: Constipation, urinary retention, dry mouth, glaucoma, drowsiness, dizziness, syncope, confusion, postural hypotension, hyponatraemia, hypothermia and cardiac arrhythmias.
- low dose with caution
interactions may also be problematic (e.g. with antiarrhythmics and antiepilectics)
What fibres do the superior, middle and inferior peduncles of the cerebellum carry?
- superiro peduncle mainly carries fibres from the dentate nucleus to the contralateral red nucleus
- the middle carries fibres from teh contralateral pointine culcei to the cortex,
- the inferior peduncle carries mainly fibres from the spino-cerebellar tracts and from the olivary nuclei to the cortex
- the middle carries fibres from teh contralateral pointine culcei to the cortex,
- the inferior peduncle carries mainly fibres from the spino-cerebellar tracts and from the olivary nuclei to the cortex
Which cells provide the only output of the cortex?
Which cells provide the input to the cortex?
Which cells provide the input to the cortex?
- purkinje cells > output of cortex
input
- climbing fibres > from the olivary nuclei, for multiple synaptic contacts on a single purkinje cells
- mossy fibres--> form synaptic contact with granule cell; originate from pons and spinal cord
input
- climbing fibres > from the olivary nuclei, for multiple synaptic contacts on a single purkinje cells
- mossy fibres--> form synaptic contact with granule cell; originate from pons and spinal cord
What do fibres of the dorsal spinocerebellar tract carry? How do they enter the cerebellum? Do they provide ipsilateral or contralateral branches?
- they are composed of axons of neurons in the nucleus dorsalis and in the accessoory cuneate nucleus.
- enter cerebellum ipsilaterally via the inferior cerebellar peduncle
- input is provided by collateral branches of a variety primary afferent neurons, including those from muscle spindles, tendon organs, joint and cutenous mechanoreceptors.
- enter cerebellum ipsilaterally via the inferior cerebellar peduncle
- input is provided by collateral branches of a variety primary afferent neurons, including those from muscle spindles, tendon organs, joint and cutenous mechanoreceptors.
What is the vetnral spinocerebellar tract composed of?
Do they enter contralaterally or ipsilaterally? What inpt does it get?
Do they enter contralaterally or ipsilaterally? What inpt does it get?
- composed of axons of large neurons located between the dorsal and ventral grey columns of the spinal cord.
- the axons cross the midline in their segment of orgion, ascend thorugh the inferior peduncle, before entering the cerebellum via the contalateral superior pedunce.
they therefore cross the midline twice and so return ipsilateral to their side of origin on entering the cerebellum.
- get sensory input from various types of large receptive field afferents, including those of flexor reflex system,
- also receive input from all desceding tracts (corticospinal, reticulospinal and vestibulospinal)
- the axons cross the midline in their segment of orgion, ascend thorugh the inferior peduncle, before entering the cerebellum via the contalateral superior pedunce.
they therefore cross the midline twice and so return ipsilateral to their side of origin on entering the cerebellum.
- get sensory input from various types of large receptive field afferents, including those of flexor reflex system,
- also receive input from all desceding tracts (corticospinal, reticulospinal and vestibulospinal)
What happens to body composition in the elderly and how can this affect drug handling?
1. body water
2. body fat
3. lean body mass
1. body water
2. body fat
3. lean body mass
1. Body water
- decreases by up to 15%
- Vd of polar (water soluble drugs decreases
- plasma concentratoin goes up (digoxin, cimetidine)
N.B diuretics exacerbate this
2. Body fat
- increases as a proportion of body mass
- Vd of fat soluble drugs increases
- accumulation of drugs ( e.g benzodiazepines)
3. Lean body mass
- decreases
- Vd of highly protein bound drugs decreases
- increased plasma concentration (e.g. digoxin)
- use lean body weight for doese calculations
- decreases by up to 15%
- Vd of polar (water soluble drugs decreases
- plasma concentratoin goes up (digoxin, cimetidine)
N.B diuretics exacerbate this
2. Body fat
- increases as a proportion of body mass
- Vd of fat soluble drugs increases
- accumulation of drugs ( e.g benzodiazepines)
3. Lean body mass
- decreases
- Vd of highly protein bound drugs decreases
- increased plasma concentration (e.g. digoxin)
- use lean body weight for doese calculations
Metabolism in the liver is mediated through two pathways. Which is most affected in the elderly? Name 3 drugs metabolised by this pathway which should therefore be used with caution in the elderly.
- phase 1 is most affected
- microsomal mixed function oxidase
- metabolising capacity decreases by up to 60%
Drugs metabolised by phase 1 are:
- diazepam, warfarin, phenytoin, analgesics, theophylline.
- microsomal mixed function oxidase
- metabolising capacity decreases by up to 60%
Drugs metabolised by phase 1 are:
- diazepam, warfarin, phenytoin, analgesics, theophylline.
What is the difference between mild cognitive impairment and dementia?
features are
- memory complaint
- normal activities of daily living
- normal general cognitive function
- abnormal memory for age
mild cognitive impairment is often considered the middles tage between ageing and dementia. People with MCI can however function normally.
- memory complaint
- normal activities of daily living
- normal general cognitive function
- abnormal memory for age
mild cognitive impairment is often considered the middles tage between ageing and dementia. People with MCI can however function normally.
What is the commonest form of dementia?
What is the second commonest?
Who is more affected?
What is the second commonest?
Who is more affected?
Alzheimer's disease is commonest with 50 % of all dementia patients having it. It is more common in women
Vascular dementia is second commonest with 25 %; more men than women have it
Dementia with lewy bodies may be 10 %
Vascular dementia is second commonest with 25 %; more men than women have it
Dementia with lewy bodies may be 10 %
give general features of dementia:
1. Behavior
- inability to make decisions
- loss of interest and initative
- social withdrawal
2. Thinking
- reduced concentration
- preservation ( getting fixed on one object or topic)
- less flexible
- confabulation (fill in gabs in ones memory with fabricatiosn that one beleives to be facts
3. Speech
- difficulty with names
- less complex
- more disorganised
4. Memory
- difficulty with new learning
- recent > remote (but both affected)
- disruption of temporal sequences
5. Insigt
- may be present early on, later generally lost
- inability to make decisions
- loss of interest and initative
- social withdrawal
2. Thinking
- reduced concentration
- preservation ( getting fixed on one object or topic)
- less flexible
- confabulation (fill in gabs in ones memory with fabricatiosn that one beleives to be facts
3. Speech
- difficulty with names
- less complex
- more disorganised
4. Memory
- difficulty with new learning
- recent > remote (but both affected)
- disruption of temporal sequences
5. Insigt
- may be present early on, later generally lost
What is progeria? What are its characteristics at genetic level?
What are the two types?
What are the two types?
- rare genetic disease in which individuals display accelerated ageing
- genes mutated in progeria are likely to be required for maintaining or repairing cells/tissue
1. unimodal progeroid syndrome - only a single tissue is affected e.g alzheimers disease
2. Segmental progeroid syndromes - multiple tissues affected but some features of ageing not observed
- genes mutated in progeria are likely to be required for maintaining or repairing cells/tissue
1. unimodal progeroid syndrome - only a single tissue is affected e.g alzheimers disease
2. Segmental progeroid syndromes - multiple tissues affected but some features of ageing not observed
What are features of Werner's syndrome?
- short stature
- graying and/or loss of hair
- osteoporosis
- skin ageing
- cataract
- diabetes
-mental retardation
- predisposition to cancer
defective RecQ helicase (also mutated in Bloom's syndrome)
result in failure of DNA excision repair mechanisms, genome Instability and replicative senescence
- graying and/or loss of hair
- osteoporosis
- skin ageing
- cataract
- diabetes
-mental retardation
- predisposition to cancer
defective RecQ helicase (also mutated in Bloom's syndrome)
result in failure of DNA excision repair mechanisms, genome Instability and replicative senescence
Give examples of Childhood progeroid syndromes:
What are the clinical features?
What are the defective genes?
prognosis?
What are the clinical features?
What are the defective genes?
prognosis?
Hutchinson- Gilford syndrome -
LMNA defect ( a a member of the intermediate filament super gene family and forms part of the nuclear lamina/nucleoskeleton. The lamia protects the nucleus fromphysical damage, acts as a sensor foroxidative stress and controls the differentiation of adult stem cells)
clincial features for HGPS are: short stature, atrophy of sub cutaneous fat, alopecia, musculoskeletal abnormalities, osteolysis, premature atherosclerosis,
Widermann- Rautenstrauch syndrome - genes unkown
mutations of genes lead to replicative senescence and genome instability including telomere shortening and aneuploidy
clincal features general:
failure to thrive-
short stature
alopecia,
manibular dysplasia
hyperlipidemia,
type 2 diabets,
atherosclerosis
osteolysis
death before second decade from coronary artery disease or stroke
LMNA defect ( a a member of the intermediate filament super gene family and forms part of the nuclear lamina/nucleoskeleton. The lamia protects the nucleus fromphysical damage, acts as a sensor foroxidative stress and controls the differentiation of adult stem cells)
clincial features for HGPS are: short stature, atrophy of sub cutaneous fat, alopecia, musculoskeletal abnormalities, osteolysis, premature atherosclerosis,
Widermann- Rautenstrauch syndrome - genes unkown
mutations of genes lead to replicative senescence and genome instability including telomere shortening and aneuploidy
clincal features general:
failure to thrive-
short stature
alopecia,
manibular dysplasia
hyperlipidemia,
type 2 diabets,
atherosclerosis
osteolysis
death before second decade from coronary artery disease or stroke
Flashcard set info:
Author: bonzei69
Main topic: Medicine
Topic: Life cycle
Published: 28.02.2010
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