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Fundamental Biology 2X > Ageing and Disease > Flashcards

Ageing and Disease Flashcards

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1
Q

What does aging describe in biology

A

he result of a build-up of cellular and molecular damage over time that leads to a gradual decline in physical and mental abilities

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2
Q

Give some examples of diseases which are more predominant in aging populations

A

Cancer/ coronary heart disease/ dementia (Alzheimer’s is a type of dementia)

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3
Q

What is progeroid syndrome ?

A

A genetic disorder which is characterised through features mimicking physiological aging.

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4
Q

What is apoptosis?

A

programmed cell death - required to prevent cancer

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5
Q

What is longevity?

A

How long an organism lives for

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6
Q

What is senescene?

A

time-related deterioration

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7
Q

What is semelparity?

A

Group of organism which live up until they reproduce

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8
Q

Give some hallmarks of ageing.

A

Cellular senescence /mitochondrial dysfunction/ epigenetic alterations/ genomic instability / stem cell exhaustion …

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9
Q

What is genome integrity?

A

The ability to maintain the genome or all its DNA in a cell during cell division

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10
Q

What are some mechanisms used by cells to prevent DNA damage?

A

DNA REPAIR - // SCANNING FOR DNA DAMAGE-

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11
Q

What is the relationship between insulin signalling and longevity ?

A

calorific restriction promotes longevity (and increases insulin sensitibity)// mutants which partially block insulin signalling promote longevity

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12
Q

What is the role of animal models in investigating age?

A

Using a worm as a model the A.C. elegan mutation was found to double life expectancy

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13
Q

What is the role of the P53(“guardian of the genome”)?

A

A tumour repressing gene which activates apoptosis / senesce and DNA repair in response to DNA damage/ telomere dysfunction/ oncogene activation

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14
Q

What is the role of telomerase?

A

A reverse transcriptase which grows telomers (end units of a gene which are not often replicated and are therefore lost)

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15
Q

What is cellular senescene?

A

a tumour repressor which prevents the accumulation of excess cells by stopping cell division

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16
Q

What is the biological function of amyloid precursor protein(APP)?

A

To bind other proteins on the surface of cells or help other cells attach to one another//

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17
Q

What is proteolytic processing?

A

the cleavage of specific peptide bonds within a protein precursor changing the conformation of the protein

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18
Q

What proteolytic processes amyloid precursor protein?

A

APP is cleaved by Beta and gamma secretase, with beta gamma secretase being harmful as it cleaves the peptide at length 40-42, this creates aggregation and therefore cell death and dementia

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19
Q

What is the association between Amyloid precursor protein gene variants and familial forms of Alzheimer’s disease?

A

Different enzymes cleave the APP at different lengths, gamma secretase cleaves the peptide at length 40-42 amino acids, this is harmful, creating aggregation, cell death and therefore dementia

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20
Q

What is proteostasis?

A

The process by which cells maintain the balance of functional proteins (protein homeostasis )

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21
Q

Give examples of diseases which are associated with protein folding issues?

A

ALZHEIMER’S -> formation of amyloid plaques and neurofibrillary tangles // PARKINSONS-> lewy bodies are formed from x -synuclein

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22
Q

What are the 3 main types of proliferation of cells ?

A

Mitotic cells (continuously dividing~)// post-mitotic or quiescent (low or no division can e stimulate) // fixed post mitotic (no division under a stimulus)

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23
Q

What are the two types of late onset alzhiers disease?

A
  1. FAMILIAL - autosomal dominant, involves the APP and PSEN1 // 2. SPORADIC -> general population
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24
Q

What is the role of proto-oncogenes?

A

cell proliferation

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25
Q

What is the role of tumour repressor gene?

A

prevents cell proliferation, controlling cell growth

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26
Q

What is the difference between a mutagen and a carcinogen?

A

Mutagen binds to DNA and creates changes but carcinogens do not bind to DNA but are associated with cancer

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27
Q

What are the 3 basic stages of cancer development?

A
  1. INITATION- first mutation // 2. PROMOTION creation of the correct environment around the tumour // 3.PROGRESSION - cells proliferate
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28
Q

What is the difference between germline and somatic mutations ?

A

germline are heritable but germline are not

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29
Q

What processes can convert proto-oncogenes into oncogenes ?

A
  1. POINT MUTATION- deletion or point mutation in the coding sequence forming hyperactive protein // 2. GENE AMPLIFICATION- normal protein is produced just in large quantities // 3. CHROMSOMAL REARRANGMENT - the breaking and re-joining of protein’s forming overproducing proteins
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30
Q

What are some category’s of oncogenes?

A

GROWTH FACTOR -induces cell proliferation// RECEPTOR TYROSINE KINASES- transduce signalling for cell proliferation // SIGNAL-TRANSDUCTING PROTEINS- involved in signalling // TRANSCRIPTION FACTORS- regulates transcription of genes which induce proliferation

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31
Q

What are the two main categories of cancer and what is there characteristics in the context of breast cancer ?

A
  1. SPORADIC - no family history / older individuals / one tumour present / one breast (unilateral)// 2. FAMILAL - involves a gene - BRAC1/ younger individuals / multiple tumours present/ both breasts (bilateral)
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32
Q

What is the role of Rb?

A

Within G1 Rb becomes phosphorylates, realising E2F ( a transcription factor which stimulates the production of genes and proteins

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33
Q

Briefly outline the pathway of a normal cell cycle in response to DNA damage

A
  1. DNA damage is identified// 2. Protein kinase is released/ 3. P53 is activated via phosphorylation // 4. transcription produces a protein which inhibits the cell cycle therefore DNA damage is not replicated
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34
Q

Briefly outline the cell cycle in response to DNA damage in the absence of P53.

A
  1. DNA damage is identified// 2. Protein kinase is released/ 3. P53 is not activated due to mutation// 4. protein inhibiting cell cycle is not transcribed therefore not present therefore there is cell division of cell containing DNA damage
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35
Q

Outline some hallmarks of cancer.

A

Sustaining proliferative signalling / resisting cell death/ inducing angiogenesis/ enable replicative immortality / evade growth suppressor / activate invasion and metastis

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36
Q

How can breast cancer be treated?

A

surgery - biopsy// radiation therapy// chemotherapy// gene therapy

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37
Q

How do cancer cells cope with the increased demand of ATP?

A

amplify the number of glucose transporters , increasing glucose in cell used for ATP production via glycolysis // uses anaerobic glycolysis, faster than aerobic making more ATP

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38
Q

What occurs if the tumour repressor is inactive within cancer cells ?

A

cellular proliferation is unchecked and cellular defence mechanisms (apoptosis) no longer function meaning cells containing DNA damage are proliferated

39
Q

What is the role of telomerase? Why is this beneficial to cancer cells?

A

maintain telomere length (during cell divisions telomeres can be lost, overtime this creates cell senesce and the cell stops dividing.)// cancer cells reactive telomerase to ensure division constantly occurs

40
Q

Briefly outline the process of anagenesis .

A
  1. Primary tumour releases angiogenic signals // 2. Enzymes break down extracellular matrix of endothelial cells of blood vessel// 3. cell migrate into blood and proliferate // 4. enzymes break down intracellular endothelial cells, cancer cells migrate out of the blood and form a secondary tumour in a different location of the body
41
Q

What is the theory behind tamoxifen being used to treat cancer?

A

Tamoxifen competes with oestrogen to bind to the receptor, when tamoxifen binds to the receptor there is no shape change of the receptor therefore the receptor cannot bind to co-activators and crate a response of cell proliferation

42
Q

How can herceptin be used as a breast cancer treatment?

A

Herceptin attaches to HER2 receptor, stopping HER2 receptors from signalling to the cell to grow

43
Q

What does anastrozole do?

A

Now used as a treatment for breast cancer/ blocks oestrogen production, as oestrogen is associated with cell proliferation it help control cell growth

44
Q

What is oesteoprosis and oesteopenia?

A

Loss of bone density// oesteoprosis = 1-2.5SD below mean peak bone mass // oesteopenia = bone mass reduces 2.5 SD below mean

45
Q

What are the two main cells involved in the remodelling of bones?

A

osteoblasts = building up bone// osteoclasts = breaking down

46
Q

What is wolff’s law?

A

Physical activity stimulates bone remodelling, with bones being built in response to pressures

47
Q

How does calcium and vitamin D affect bone density?

A

vitamin D is involved in the absorption of calcium, calcium is a key component in the inorganic portion of the matrix, providing flexibility

48
Q

What are some hormones associated with osteoporosis?

A

PTH (parathroid hormone) / Calcitonin= regulate calcium // Glucocorticoids - increases bone reabsorption

49
Q

What is osteoarthritis ?

A

a problem with bones at a joint // catlidge thins and losses water reducing flexibility and free movement of bones

50
Q

What is sarcopenia?

A

loss of skeletal muscle mass, reducing the number and size of muscle fibres

51
Q

What are some prevention methods for sarcopenia/ osteoarthritis/ osteopenia/ osteoporosis?

A

exercise (high magnitude targets bones mass)// nutrient intake (specifically focusing on calcium, vit D and lean protein.)

52
Q

What is an emerging disease?

A

A disease which is increasing in the number of individuals infected within an area

53
Q

What the main categories of emerging disease?

A

NEWLY EMERGING// RE-ERMERGING // DELIBERATLY (bioterrorism~) // ACCIDENTAL

54
Q

What are some risk factors of emerging diseases?

A

Human (population growth// human travel// hunting…)// Ecological (climate events / El Nino South osscilation)

55
Q

What are some factors which allowed West Nile Virus to get more established?

A

NEW YORK 1999
- dry spring
- reduction in predators
mosquito to bird transmission allowed birds to act as a revivor
- human travel transported the infected mosquito (the vector) to new York via aircraft
- climate change, warmer climate allowed virus to survive and thrive

56
Q

Why do some CV diseases lead to other diseases?

A

Directly effects all somatic cells and organs through changing blood flow therefore altering oxygen and nutrient avalibility

57
Q

What are some theories associated with aging and diseases?

A

WEAR AND TEAR// CELLUALR - stem cell exhaustion// GENETIC MUTATION - increases with age// AUTOIMMUNE THEORY - aging is involved in the decline of the body’s immune system

58
Q

What causes the skin to wrinkle?

A

Dermal layer thins/ less collagen is produced/ elastin fibres providing elasticity wear out // reduction in function of sweat glands forming dry skin

59
Q

What is sinus arrhythmias and sinus bradycardia?

A

both describe an irregular heart rate // Arrhythmias = 10% faster // Bradycardia = slower than 60bpm

60
Q

What are some treatments applied to heart failure?

A

NITRATES - dilate blood vessels// POSITIVE INOTROPIC- reduces heart rate but increases force of contractions// ACE INHIBITORS - reduces blood pressure through reducing water retention in kidneys

61
Q

What are some treatments used for reducing blood pressure?

A

Beta blockers/ calcium channel blockers / lifestyle changes (diet and exercise)

62
Q

What is calcification?

A

reduction in elastin and an increase in collagen(reducing flexibility and ability to adapt to blood pressure)

63
Q

How does aging impact coronary arteries?

A

reduces blood flow, reducing O2 delivery to cardiac muscle altering power and rate of contractions resulting in angina (a pain)

64
Q

What is metformin? Why is it used for in industry?

A

A hormone which regulates cardiac rhythm// can now be used as a treatment for Alzheimer’s/ ischaemia stroke and cancer

65
Q

What factors increase Type II diabetes likelihood with age?

A

reduced exercise levels / obesity/ reduction in insulin sensitivity/ reduction in muscle mass/ weight gain/ insulin secretion level reduces

66
Q

What is a hormone and how does it travel around the body?

A

A chemical signalling molecule, produced by organs, cells or glands which travel through the blood.

67
Q

What are some differences with water soluble and lipid soluble hormones?

A

LIPID SOLUBLE(steroid ) - Hydrophobic //Circulate primary bound to plasma proteins//Intracellular receptors // Promotes or supress gene transcription//// WATER

SOLUBLE (hormones)- Hydrophilic //Circulate primary dissolved in plasma //Cell surface receptors on target cells //Act via secondary messenger system //Modify target proteins (e.g. opens a membrane channel)

68
Q

Give some examples of functions of the endocrine system

A

Homeostasis
Electrolyte, water , nutrient balance in blood
Cellular metabolism
Glucose and mineral homeostasis
Growth and development
Reproduction
Blood pressure control
Response to a stress
Production of immune cells

69
Q

Outline the structure and function of the endocrine system.

A

hypothalamus - regulates pituitary gland// pituitary gland -> 1. posterior = extension of hypothalamus 2. anterior = synthesises and secretes some peptide hormones// thyroid and adrenals - produces hormones, controlling metabolism// pancreases- produces hormones regulating blood sugar levels / testes- produces testosterone // ovaries - produces oestrogen //

70
Q

Outline the organisation of the endocrine system

A

Made up of gland and organs which produce and control hormones.

71
Q

How is hormone secretion regulated?

A

1.Hypothalamus releases either releasing or inhibiting hormones to the anterior pituitary// releasing hormones makes anti pituitary secrete hormones into blood creating a response// inhibiting hormones stops hormone secretion from the anterior pituitary changing the effect on the target tissue

72
Q

Give an example of a negative feedback system in the endocrine system

A

HYPOTHALAMIC-PITUITARY-THYROID-AXIS= 1. thyroid realising hormones (TRH) are released from hypothalamus // 2. stimulating hormonal release from anterior pituitary/ 3. T3 and T4 are released from the thyroid // 4. creates negative feedback on the anterior pititary and hypothalamus
*aim = maintain a hormonal balance

73
Q

Give an example of a positive feedback system within the endocrine system

A

OESTROGEN
1. before ovulation oestrogen levels increase to develop the follicle creating a positive feedback loop// 2. increases LH stimulating granulosa cells (converts androgens to oestrogen// 3. triggers ovulation further increasing oestrogen

*this feedback loop becomes negative when ovulation halts and oestrogen levels drop

74
Q

Describe some endocrine changes of the menopause

A

A lack of oestrogen is produced due to the progressive loss of follicles and therefore granulosa cells , creating a negative feedback loop. To compensate pituitary increases FSH (follicle stimulating hormones)

75
Q

Give some examples of the effect of aging on the endocrine system.

A

little direct effects / hormonal changes occur due to changes in liver and kidney hormonal secretion and metabolism // drugs taken to combat other illnesses associated with ging can reduce hormone levels// most hormone levels reduce // target cells may become less sensitive

76
Q

Why is hormone replacement therapy beneficial for women going through the menopause?

A

contain either oestrogen , progesterone or both// oestrogen - protects the individual from some symptoms// progesterone - protects the individuals from endometrial hyperplasia(thickening of uterus lining) and cancer

77
Q

What are some risks associated with HRT (hormone replacement therapy)?

A

small increase in risk of getting breast and ovarian cancer // increase cardiovascular diseases//

78
Q

What are some alternate treatments for menopause?

A

PHARMACOLOGICAL - anti-depressants / vaginal cream/ anticonvulsants gabapentin(for hot flushes) // NON-PHARMALOGICAL- diet chances, increasing vit D promoting calcium uptake// HORMONE REPLACMENT THERAPHY - alter oestrogen and progesterone levels

79
Q

What is somatopause ?

A

A progressive decline in growth hormone GH secretion with age , often due to reduction in secretion of growth hormone releasing hormone GHRH

80
Q

What are some metabolic changes associated with aging?

A

Increased body fat/ reduced protein synthesis , reducing muscle mass// reduced bone mass// reduced immune functions

81
Q

What two cells develop during each menstrual cycle and what is there effect on oestrogen levels?

A

Theca- cells produce androgen // granulosa- cells convert androgen into oestrogen - both increase oestrogen levels

82
Q

After ovulation what does the ruptured follicle transform into and what is the role of these during fertilisation and no fertilsation?

A

AT FERTILSATIPON 1. Corpus luteum- produces oestrogen and progesterone maintaining early stages of pregnancy after fertilisation 2. placenta take over production of oestrogen later// NO FERTILSATION 1. corpus luteum degenerates and oestrogen and progesterone levels fall

83
Q

Describe neural signalling.

A

Process of communication between neurones the nervous system and other parts of the body. Involving neurotransmitters an synapses as well as chemical and electrical signals// signals travel through axon-> synapse.

84
Q

What are some hallmarks of Alzheimer’s in the moderate stage?

A

MACROSCOPIC
difficulty with daily tasks / inability to remember current and personal events / inability to perceive danger / confused speech / mood changes

MICROPSCOPIC
misfolding and aggregation of proteins creating more neurodegeneration /

85
Q

What are some hallmarks of Alzheimer’s in the late stage?

A

MACROPSCOPIC
inability to recognize family members / inability to do daily activities/ reduced ability to communicate / loss of bladder control / difficulty swallowing

MICROSCOPIC
further misfolding and aggregation of proteins creating more neruodegregation

86
Q

What are the two main microscopic hallmarks of Alzheimer’s ?

A

beta-amyloid plaque formation = dense deposit of beta amyloid plaque outside and around neurons (Extracellular)// neurofibrils tangles = hyperphosphorylated tau creates impaired axon function

87
Q

What is the amyloid cascade hypothesis?

A

theory explaining the primary cause of Alzheimer’s// the accumulation of amyloid-beta peptides in the brain caused by Amyloid precursor protein cleaving amyloid - beta peptide at either AB40 and AB42, When AB42 is produced more aggregation occurs forming plaques

88
Q

What is the issue with diagnosing Alzheimers?

A

brain scans cannot discriminate between brain injury and Alzheimer’s as beta amyloid plaques and tau depositions in neurofibrillary tangles are also associated with brain damage

89
Q

What is the cholinergic hypothesis?

A

A hypothesis explaining a pathological causes of Alzheimer’s// individuals produce less Acytle CoA in the nucleus basil of meynert in basal forebrain therefore the post synaptic cleft is not activated and memory loss occurs

90
Q

What are some biomarkers of cognitive function

A
  1. A-Beta accumulation can be identified through the presence of CP molecules//2. neural degeneration is identified by a lack of glucose
91
Q

What are some molecular pathogenesis of Parkinson disease

A

mitochondrial dysfunction - reduces ATP available to neurones / inflammation / oxidative stress- modifies proteins meaning they can no longer carry out functions/ protein transfer

92
Q

What are some treatments for Parkinson’s disease?

A

REPLACING DOPAMINE LEVELS (MonoAmine Oxydase inhibitors - increases dopamine at synapse// DEEP BRIAN STIMULATION- redues rigidity// TRANSPLANTS USING STEM CELLS

93
Q

What are some hallmarks of Parkinson’s disease?

A

Loss of dopamine neurone in SNpc (substantial nigra pars compacta) therefore delpeting dopamine levels

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