Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Ageing - theories and disease 24/10/22 > Flashcards

Ageing - theories and disease 24/10/22 Flashcards

1
Q

What is aging?

A

A decreasing ability to survive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What negative effects does aging have?

A

-Reduced ability to do work
-Increased susceptibility to major diseases
-Large healthcare commitment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is longevity?

A

A long duration of individual life.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is life expectancy?

A

Mean age of individuals at the time of death. There is a global gradual increase in life expectancy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is life span?

A

Maximum age that can be attained by a species.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the features of aging?

A

-Senescence (a gradual decline in the function of cells, organs, tissues, and body systems)
-Age-related diseases (increased chance of any age-related disease such as diabetes or a heart attack, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How long is a human’s lifespan compared to other animals?

A

Humans live longer than other mammals. An elephant, for example, has a life span of 70 years, while that of a mouse is a mere three years. While the life span of species is inherent, humans are able, to a certain extent, to increase their life expectancy by controlling their environment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the two theories around senescence changes?

A

Senescence changes may cause age-related disease, or they may increase someone’s susceptibility to disease. Both of these could be the cause or only one.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the theories on why we age?

A

-Wear and tear
-Genome theory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the wear and tear theories?

A

-Free radicals
-Glycation
-Waste products
-Error-catastrophe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the genome theories?

A

-Programmed ageing
-Mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is a free radical?

A

Free radical - atom or molecule which contains one or more unpaired electrons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the nature of a free radical?

A

Free radicals are - highly reactive, unstable, have a short half-life, and propagate chain reactions. Free radicals are only stop if two free radicals join with a covalent bond.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the purpose of free radicals in the human body?

A

Free radicals are produced in phagocytic cells in processes aimed at destroying pathogens. They may also be produced during endogenous enzymatic reactions, especially oxidation–reduction reactions associated with hyperglycemia or following exposure to tobacco smoke or ionizing radiation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the different types of free radicals?

A

-Hydroxyl radical (OH*)
-Superoxide radical (O2 )
-Nitric oxide (NO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the sources of free radicals?

A

-Phagocytic cells
-Ionising radiation
-Smoking
-Oxidation-reduction reactions
-Hyperglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do free radicals cause damage and ageing?

A

They damage:
-DNA / RNA (can cause mutations)
-Proteins (can cause them to fragment)
-Enzymes
-Membrane lipids (can cause cells to become leaky)
-Cells (can kill cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is an antioxidant and how can it prevent free radicals?

A

Antioxidant - a substance that will delay or inhibit the oxidation of an oxidizable substrate. Types can be extracellular (vitamin E/C) or intracellular (superoxide dismutase and catalase - which work together to deal with superoxide radicals)

Antioxidants can decrease radical damage which causes aging by using antioxidants that remove free radicals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the equation for superoxide dismutase and catalase?

A

Superoxide dismutase

2H+ + 2O2* –> H2O2 + O2

Catalase

2H2O2 –> 2H2O + O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is protein glycation?

A

This is something that elderly people can be susceptible to because of decreased glucose tolerance and increased incidence of diabetes.

Advanced glycation end products (AGE) are increased in older people and increased in people with diabetes. AGE products accumulate with age, particularly on structural proteins, such as collagen which has a long half-life, and they
can cause increased cross-linking of individual proteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is AGE?

A

They are cross-linked fluorescent structures called advanced glycation end products
(AGEs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the effects of glycation on proteins?

A

-Increased cross-linking (skin wrinkling)
-Increased fluorescence
-Altered activity of enzymes
-Altered immunogenicity (how it is recognised by the immune system)
-Altered half-life
-Altered recognition by receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is accumulation of waste products?

A

During aging, increasing amounts of waste material are accumulated in the cytoplasm of cells. Many of these are waste products of normal cellular metabolism. For example, lipofuscin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is lipofuscin?

A

Lipofuscin is a lipid-rich, yellow-brown pigment produced by the degeneration of cell membranes and organelles and free radical peroxidation. Lipofuscins accumulate with age in many types of cells, particularly nondividing cells such as those of muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the effect of lipofuscin on age?

A

Lipofuscins are chemically inert, strongly cross-linked molecules that are stored in lysosome-like structures. They are not susceptible
to enzymatic digestion by lysosomal enzymes. It has been suggested that a gradual accumulation of substances like lipofuscins within cells interferes with their normal function, however, the actual effect of lipofuscin on age is unknown.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is error-catastrophe theory?

A

Abnormal proteins are produced by random errors of transcription and translation, this accumulation of abnormal proteins impairs cellular function, and can lead to cell death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How may errors in transcription and translation cause aging?

A

When an error in protein synthesis occurs and if the protein in question is an enzyme, such an error may lead to a malfunctioning enzyme and cellular dysfunction, however, it seems that proteins are synthesized appropriately in older cells, and most subsequent changes to their structures occur posttranslationally.

Some studies have indicated that certain enzymes have a changed conformation in older cells. This suggests that enzyme molecules retained inside the cell for long periods are slowly denatured and consequently lose their biological activity. Repair mechanisms that exist to correct changed conformations of molecules may lose their efficacy as the cell ages.

28
Q

What is programmed aging?

A

This theory believes that the number of times a cell undergoes division is fixed and this limit is not affected by the external environment and that cells can memorise how many divisions they have undertaken before the cell dies.

Also thought to be due to telomeres shortening every time the cell divides as a cell can’t divide without telomeres and this limits cell division.

This cell limit was discovered due to embryonic fibroblast cells only dividing 50 times before dying (discovered by Hayflick and called the Hayflick limit). This limit is internal and not affected by the environment.

29
Q

What causes programmed aging?

A

This is thought to be due to telomeres. Telomeric DNA protects the ends of the DNA molecule from damage. When DNA is replicated prior to cell division, telomeric DNA does not replicate. After each cell division, the telomere becomes shorter in length. Once the telomeres shorten to a particular length, the cell can no longer divide and dies. The activity of telomerase can prevent the shortening of telomeres and enable the cell to divide continuously. Most somatic cells contain an inactive form of telomerase although a number of cell types, such as hemopoietic cells
and cancer cells, have permanent telomerase activity. These cells can divide indefinitely and are therefore potentially immortal.

30
Q

Why could the programmed aging be wrong?

A

The number of divisions occurring in vitro may be different from those that occur in vivo. Furthermore, some cells, such as cardiac
muscle cells and neurons, do not divide after birth, so programmed aging may not apply to these cells.

31
Q

What is the gene mutations theory?

A

Errors in the replication of DNA that are not repaired will affect the viability of cells, these repair systems for DNA decrease with age.

32
Q

What is the multifactorial nature of aging?

A

This theory believes that there is no one cause of aging and that most likely ageing is caused by a range of factors such as genetics, lifestyle factors, and the environment. This can determine the rate of ageing, the age-related disease one may get, and therefore, when someone will die.

33
Q

What declines in cellular ageing?

A

-Decline in mitochondrial activity
-Decline in oxidative phosphorylation
-Decline in DNA/RNA synthesis
-Decline in nutrient uptake
-Decline in chromosomal repair
-Accumulation of waste products
-Change in organelle shapes

34
Q

What declines in the immune system?

A

-Decrease in antibody production
-Decline in T cell function
-Atrophy of thymus
-Increase in autoimmune reactions

35
Q

What declines in the skin?

A

-Increased wrinkling caused by changes to collagen, with increased cross-linking and a reduction in elasticity
-Skin pigmentation
-Greying of hair due to a lack of pigment-forming melanocytes
-Loss of hair
-Delayed wound healing

36
Q

What declines in the lungs?

A

-Decrease in lung size
-Decrease in lung elasticity
-Reduced gaseous exchange
-Reduced capacity for strenuous work

37
Q

What declines in the cardiovascular system?

A

-Increased rigidity of blood vessels
-Arterial calcification and hardening
-Increase in blood pressure
-Accumulation of fibrous tissue in heart muscle so it becomes less efficient and the heart enlarges due
-Reduced cardiac output
-Reduced blood supply to tissues

38
Q

What declines in the kidneys?

A

-Decrease in kidney weight/volume by 20-30%
-Loss and replacement of nephrons with scar tissue
-Reduced renal filtration rate and hence the excretory capacity (elimination of waste)
-More at risk of developing renal disease.

39
Q

What declines in the liver?

A

-Reduction in liver size and hepatocytes due to cell loss
-Decline in some liver functions e.g., drug detoxification

40
Q

What declines in the muscle?

A

-Muscles undergo atrophy due to a reduction in the size of muscle groups and the loss of individual muscle fibers
-Decreased capacity for work
-Disease (arthritis) can reduce movement which can cause more atrophy

41
Q

What declines in the endocrine system?

A

-Decline in hormone production
-Decline in hormone receptors

42
Q

What declines in the brain?

A

-Loss in weight
-Loss of nerve cells
-Increase in amyloid deposition
-Accumulation of lipofuscin
-Enlargement of the ventricles and a widening
of the surface channels
-Results in a lengthening in reaction times, a decline in problem-solving and learning
abilities and impairment of memory

43
Q

What declines in the eye?

A

-The decreased ability of the lens to change shape so glasses are needed
-Changes also occur in the lens proteins (crystallins) which increases cross-linking and browning in colour of lens proteins
-This results in more scattering and absorption of light with less light reaching the retina

44
Q

What declines with the body composition?

A

-Decrease in muscle mass
-Increase in total body fat

45
Q

What is progeria and its symptoms?

A

Hutchinson-Gilford progeria syndrome is a genetic condition characterized by the dramatic, rapid appearance of aging beginning in childhood. Affected children typically look normal at birth and in early infancy and then symptoms begin.

Symptoms are a characteristic facial appearance including prominent eyes, a thin nose with a beaked tip, thin lips, a small chin, and protruding ears, thin/wrinkling skin, squeaky voice, short stature, hair loss (alopecia), aged-looking skin, joint abnormalities (arthritis/osteoporosis), and a loss of fat under the skin (subcutaneous fat), severe hardening of the arteries (arteriosclerosis) beginning in childhood, normal intelligence, delayed development of teeth and sexual maturity.

46
Q

How common is progeria?

A

Very rare 1 in 10 million, around 30 cases worldwide and 100 cases in history.

47
Q

What causes progeria?

A

It’s believed to be caused by a sporadic dominant mutation, a reduced lifespan of cells, and a reduced repair of damaged DNA.

48
Q

What is the lifespan of someone with progeria?

A

Around 13 years.

49
Q

What is the life expectancy of someone with progeria?

A

7-27 years.

50
Q

What is the most common death of those with progeria?

A

Coronary heart disease, stroke, heart attack
or cerebrovascular disease.

51
Q

What laboratory tests can diagnose progeria?

A

There is raised urinary hyaluronic acid, but no other diagnostics is known because it’s so rare.

52
Q

What is the management of progeria?

A

-No cure for progeria
-Education / psychological support
-Drugs to relieve symptoms (low-dose aspirin therapies to delay symptoms of atherosclerosis)

53
Q

What is a way of increasing lifespan?

A

Calorie restriction. This extends lifespan and delays age-related diseases. This is because it reduces age-associated mutations, reduces free radical damage, reduces advanced glycation end products.

54
Q

How does the mechanism of calorie restriction increase lifespan?

A

A high-calorie diet may increase free radical-mediated damage as the increased availability of nutrients to mitochondria increases the production of the superoxide radical. Thus, a calorie-restricted diet appears to reduce
free radical damage to lipids, protein, and DNA and improves the antioxidant status. Calorie restriction in animals has also been shown to reduce levels of tissue AGEs.

55
Q

What companies are researching antiageing therapies?

A

-Centagenetix
-Elixir
-Eukarion
-Alteon
-Geron Corporation

56
Q

What does Centagenetix do?

A

They’re seeking genes responsible for longevity by collecting DNA from people with long lifespans (over 100 years). Gene identified on chromosome 4 helps carriers have long lifespan. Pharmacological compound to mimic activity of proteins coded by gene.

57
Q

What does Elixir do?

A

Nematode worms with more than one copy of gene SIR2 live 50% longer, during calorie restriction, SIR2 reduces cellular activity promoting lifespan. Identifying such genes so can develop anti-ageing drugs against them.

58
Q

What does eurkarion do?

A

Produced genetically engineered mice that can’t make superoxide dismutase, such mice die within a week due to damage to liver, brain and heart. Injection with compounds possessing superoxide dismutase and catalase activity promotes lifespan antioxidant drugs could promote lifespan.

59
Q

What does Alteon do?

A

Anti-glycation drugs reduce AGEs, conducted unsuccessful trial with aminoguanidine and are developing drugs capable of breaking AGE-crosslinks.

60
Q

What does Geron do?

A

Telomerase protects telomeres at the ends of chromosome, drugs that switch off telomerase in cancer cells stops them dividing and drugs that switch on telomerase could protect telomeres and extend lifespan.

61
Q

What is the involvement of cancer with aging?

A

Cancer increases with age.

Two reasons can be an age-related accumulation of carcinogenic substances which may increase the incidence of cancers in the elderly.

The second hypothesis proposes that age-related changes may make cells more vulnerable to becoming cancerous. Changes in immune, nutritional, metabolic, and endocrine status occur with age and may create a more favorable environment for the induction of cancer. Such physiological changes
may affect a number of cellular processes such as the detoxification of mutagenic agents and the repair of damaged DNA.

62
Q

What is the involvement of cardiovascular disease with aging?

A

Many of the changes in the cardiovascular system may be caused by disease rather than old age. The concentration of cholesterol in the plasma increases with age. Elevated levels over the years are thought to contribute to the high incidence of mortality from coronary heart disease especially if other risk factors are present. This risk may be decreased by changes to lifestyle, since eating an inappropriate diet, smoking, and lack of exercise are known to be associated with atherosclerosis.

63
Q

What is the involvement of senile cataract with aging?

A

A cataract is a partial or complete opacity of the lens of the eye that causes blurred vision. This affects the passage of light through the lens causing blindness. There are many different types of cataracts but one of the most common is senile cataracts. Another risk factor for cataracts is diabetes. Cataracts are treated by the removal of the opaque lens and its replacement with a plastic lens.

64
Q

What is the involvement of diabetes 2 with aging?

A

Many older people have some degree of impaired glucose tolerance that can be severe enough to be classified as type 2 diabetes mellitus. The main reason for high concentrations of blood sugar in the elderly is increased resistance to the effects of insulin in peripheral tissues which are associated with increased insulin levels after a meal. Diabetes in older people is strongly influenced by diet and exercise.

65
Q

What is the involvement of arthritis with aging?

A

Arthritis is inflammation of the joints producing swelling, pain, and restricted movement. Osteoarthritis affects the joint cartilage and underlying bone. It is particularly associated with increasing age, although it can occur in younger individuals who excessively use their joints in work or athletic activities.

Osteoarthritis affects fingers, hip joints, and knees but, unlike rheumatoid arthritis, does not always cause pain and inflammation. X-raying
of joints usually shows some degree of osteoarthritis in nearly all elderly patients although few present with any symptoms. In severe cases, the joints of the fingers often show overgrowth referred to as Heberden’s nodes although these tend not to be painful. Osteoarthritis cannot be cured although mild exercise can improve joint mobility.

Rheumatoid arthritis is characterized by chronic inflammation of the joints that usually arises from an autoimmune reaction. It is also more
common in the elderly, although its onset can occur in any age group. This result in severe pain and disability. What initiates rheumatoid arthritis is not clear although a variety of bacteria, especially mycobacteria, have been
implicated. The treatment of rheumatoid arthritis involves using nonsteroidal anti-inflammatory drugs. The surgical replacement of hip or knee joints may also be required in patients who become severely disabled.

66
Q

What is the neurodegenerative disease with aging?

A

Parkinson’s disease affects between 1 and 2% of individuals over the age of 70. The major defect in Parkinson’s disease is the degeneration of dopamine-secreting nerve cells although other neurons and neurotransmitters may also be affected. Patients have severe attacks of tremors that affect one hand and then spread to the leg on the same side and then to other limbs. The average survival time is eight to 10 years after diagnosis.

Parkinson’s is distinct from Alzheimer’s disease in that different nerve cells are affected and there is a loss of motor function, which is usually unaffected in Alzheimer’s disease. A further feature of Parkinson’s disease is the presence
of cytoplasmic inclusions called Lewy bodies in some of the surviving neurons. Some researchers believe that an excess of free radicals causes the degeneration of these neurons.

Pathology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions