SBA

Question 1

what is the antagonistic pleiotropy theory of ageing?

Answer 1

alleles which increase early life fitness are selected for in detriment if later life fitness

Question 2

what is the disposable soma theory of ageing?

Answer 2

somatic cells accumulate damage overtime and repair is possible but at high energy cost- better off investing in reproduction than repair

Question 3

what is the programmed and stochastic theory of ageing?

Answer 3

programmed- ageing and length of life are genetically determined
stochastic- accumulation of damage overtime- wear and tear

Question 4

what is the the genomic instability mechanism of ageing?

Answer 4

accumulation of genetic mutations over time leads to genomic instability and can cause cells to undergo apoptosis

Question 5

what is telomere attrition?

Answer 5

telomeres limit the number of times a cell can divide- heyflick limit, so as they shorten fewer cell divisions occur and tissue regeneration occurs less often

Question 6

how do epigenetic alterations contribute to ageing?

Answer 6

epigenetic modification of DNA can affect DNA repair mechanisms and cause chromosomal instability thus contributing to ageing

Question 7

how does loss of proteostasis contribute to ageing?

Answer 7

proteostasis ensures that misfolded/damaged proteins are degraded by the proteasome. with ageing there is a loss of proteostasis which can lead to accumulation of misfolded proteins which contributes to ageing

Question 8

how does deregulated nutrient sensing contribute to ageing?

Answer 8

changes in signalling pathways such as glucose sensing (insulin, IGF-1) and low energy sensing (sirtuins, AMP levels) which feed into mTOR, which has an effect on ageing

Question 9

how does mitochondrial dysfunction contribute to ageing?

Answer 9

respiration produces free radicals which are normally dealt with by compensatory mechanisms but as we age the compensatory mechanisms cannot control them and the free radicals damage proteins and DNA leading to proteostasis and genomic instability

Question 10

how does cellular senescence contribute to ageing?

Answer 10

in ageing there is increased cellular senescence (arrest of the cell cycle) but the damaged cells cannot be properly cleared leading to reduced function of tissues, increased inflammation and stem cell exhaustion which all contribute to ageing

Question 11

how does altered cellular communication?

Answer 11

the increased inflammatory environment caused by ageing mechanisms causes disruption to endocrine, neuroendocrine and neuronal signalling and this can contribute to ageing

Question 12

what changes in the GI tract occur with ageing?

Answer 12

mouth- dry, reduced taste and smell, reduced power of chewing muscles, changes to swallowing, teeth loss
stomach- reduced gastric acid production, delayed gastric emptying
small intestine- reduced nutrient absorption, changes to microbiata
large intestine- slowed motility leading to constipation
rectum- reduced elasticing
anus- reduced sphincter pressure

Question 13

what are the metabolic changes in the GI tract with ageing?

Answer 13

pancreas- decreased volume, fibrosis/atrophy causing impaired exocrine function leading to maldigestion and malnutrition
glucose intolerance- slower glucose absorption, decreased insulin production, and reduced lean body mass contribute to glucose intolerance
skeletal muscle- decrease in skeletal muscle causing disruption to the normal rate of glucose uptake

Question 14

what are the risk factors for malnutrition in ageing?

Answer 14

social, biological and cognitive issues
age related disease 
nutritional frailty- sudden significant weight loss
disability and loss of independence 
difficulty swallowing 
poor appetite 
ability to shop/cook

Question 15

what is the function of osteoblasts?

Answer 15

synthesise and mineralise collagen to form osteoid they then become inactive osteocytes and become trapped within the bone matrix

Question 16

what is the function of osteoclasts?

Answer 16

they control the resorption of bone in remodelling

Question 17

how do osteoclasts control the resorption of bone?

Answer 17

osteoclasts secrete H+ and Cl- ions to create an acidic environment which solubilises the bone matrix. they also secrete cathepsin K protease into the subosteoclatic compartment to degrade collagen and proteins.

Question 18

which hormone stimulates osteoclast activity?

Answer 18

parathyroid hormone

Question 19

how is calcium absorbed in the intestine?

Answer 19

in the ileum it moves passively into the blood.
in the duodenum Ca2+ can move into the epithelial cells by diffusion as calbindin mops up Ca2+ within the cell maintaining the concentration gradient. from the cell Ca2+ moves into the blood by active transport via the Ca2+/Na+ cotransporter or the Ca2+ ATP pump

Question 20

how is calcium concentration controlled in the kidney?

Answer 20

60% of total plasma calcium is filtered into the urine at the glomerulus. of this 60% is reabsorbed by active transport in the proximal tubule, 30%is reabsorbed by passive diffusion in the loop of henle, 9% is reabsorbed by active transport in the distal tubule and 1% is excreted in urine

Question 21

how does parathyroid hormone regulate calcium levels?

Answer 21

acts on:
bone- increases osteoclast number and activity to promote bone resorption and Ca2+ release. also acts to inhibit bone formation by osteoblasts
kidney- stimulates Ca2+ reabsorption in the distal tubule. also stimulates the activity of 1-alpha hydroxylase which catalyses the formation of 1,25-DHCC from vitamin D
intestine- has no direct effect but 1,25-DHCC stimulates calcium absorption

Question 22

how does 1,25-DHCC regulate calcium levels?

Answer 22

intestine- increases the action of calbindin to stimulate Ca2+ absorption
kidney- increases tubular reabsorption of Ca2+
bone- promotes actions of PTH

Question 23

what is the action of calcitonin?

Answer 23

inhibits osteoclast activity and therefore inhibits bone resorption
also decreases tubular reabsorption of Ca2+
however it has a minor effect on overall calcium homeostasis.

Question 24

how are hip fractures classified?

Answer 24

NOF classification- intracapsular (blood vessels can be disrupted, exposed to synovial fluid- haematoma does not form) or extra capsular
gardens classification- 1-incomplete, nondisplaced, 2- complete non-displaced, 3- complete partially displaced, 4- complete, fully displaced
Pauwels classification- classified by angle of fracture line
anatomical classification- sub capital, transcervical, base of neck, intertrochanteric, subtrochanteric

Question 25

what are the options for repair of neck of femur fracture?

Answer 25

fixation devices- screws and nails

arthroplasty- hip replacement- hemi-arthroplasty or total arthroplasty

Question 26

what is the process of direct fracture healing?

Answer 26

fragments fixed together by compression (fixation), no callus formation the bony ends are joined by direct remodelling of lamellar bone Haversian canals and blood vessels
aim of open reduction and internal fixation

Question 27

what is the process of indirect fracture healing?

Answer 27

relative stability, small amount of motion. steps:
haematoma formation
fibrocartilagenous callus formation 
bony calus formation 
bone remodelling 
process involves endochondral healing

Question 28

what are the stages of the locomotor cycle?

Answer 28

heel strike- heel strikes floor with knee extended and ankle dorsiflexed
support- the rest of the leading foot hits the floor and muscles work to cope with the force passing through the leg- knee extended
toe-off- foot leaves the ground heel first, thigh extends at hip, knee extended, ankle plantarflexed
leg lift- once the foot has left the ground the knee flexes and ankle dorsiflexes
swing- raised leg is propelled forward, thigh flexes at hip, leg extends at knee, ankle dorsiflexed in preparation for heel strike