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Case studies Flashcards

1
Q

4 tactile? tests to test for Alzheimers (AD)

A

Blood tests, electroencephalography (EEG), MRI

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2
Q

What is electroencephalography (EEG)

A

measures cortical activity = sum of each neuron firing. Measures sleep disorders, epilepsy, coma, brian death

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3
Q

What does MRI measure

A

Cerebrovascular damage = blood flow and the blood vessels in the brain

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4
Q

Structure of Mini-cog test for DA

A

3 word registration (repeat 3 words), clock drawing + draw hands at time, word recall of 3 word registration. Gives a score of likelihood of cognitive impairment

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5
Q

4 examples of dementia

A

Alzheimers dis, Vascular dem, frontotemporal dem, dem with Lewy bodies

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6
Q

Info on frontotemporal dementia

A

Global cognitive impairment + motor deficits - fatal after aorund 8 years. Early onset dementia (<65 yrs). Deterioration of behaviour, loss of empathy, OCD, dietary changes

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7
Q

What is the frontal love and temporal lobe associated with in the brain

A

Frontal: Movement, decision making, emotional behaviour. Temporal: Auditory processing

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8
Q

Info on demential with Lewy Bodies (DWL)

A

In Alzheimers + Parkinsons. Formation of Lewy bodies containing α-synuclein originating from brain stem -> progressing to limbic system (emotions) and cerebral cortex. Changes in cognition, hallucinations, rapid eye movement

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9
Q

Info on Vascular dementia

A

Variable cognitive impairment - cause not determined. Associated with demographic, genetic, stroke related risk factors.

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10
Q

4 stages of AD

A

Mild, moderate, late, advanced

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11
Q

What happens on macroscopic level to brain in Alzheimers

A

Widening of sulcal spaces + narrowing of gyri. Cortical atrophy. Enlarged frontal + temporal horns of lateral ventricles (some holes in middle of brain)

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12
Q

What happens on microscopic level to brain in Alzheimers

A
  1. Amyloid plaques formed from Aβ40 and Aβ42 (mainly).
  2. Neurofibrillary tangles: Composed of filamentous tau protein. In AD: they become hyperphosphorylated + abnormally folded -> loss in tau function. (death of neurons - tau stabilises neuron skeleton)
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13
Q

Aetiology meaning

A

Cause of a disease or condition

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14
Q

Aetiology of AD (1 genetic reason)

A

Apolipoprotein E (APOE) transports cholesterol to neurons to support their normal function. ε2, ε3, ε4 alleles. Heterozygous and homozygous ε4 (APOE4) leads to increased risk of AD

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15
Q

Challenges of treading mild AD

A

Delay in efficacy, improves but doesn’t treat, side-effect of medicine is confusion

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16
Q

How does acetyl choline NT work w cholinesterase in neurone

A
  1. Synthesis of Acetyl chlone by Acetyl CoA + Choline by emzyme. 2. Storage in synaptic vesicles. 3. They move to pre-synaptic nerve terminal. Fuse with pre-synap terminal. 4. Release of NT (acetyl choline) to synpatic cleft. 5. Some acetyl choline bind to its receptors on post-synap (muscarinic or nicotinic). Some broken down by acetylcholineesterase -> acetate + choline. 6. Choline reused as precursor of acetyl choline. Acetate removed.
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17
Q

What is donepezil

A

A colinesterase inhibitor

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18
Q

3 medicines used for mild AD

A

Donepezil (tablet), Rivastigmine (patch), Galantamine (extended release formulation)

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19
Q

Why is colinesterase inhibitor used for AD

A

Lower concs of acetylcholine in AD. “Cholinergic hypothesis”

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20
Q

Memantine use + action in body

A

NMDA receptor antagonist for moderate/severed AD. Protects against excessive glutamate realeased from excitotoxicity.

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21
Q

What is excitotoxicity relating to glutamate

A

Occurs following excessive exposure to glutamate/overstimulation of glutamate receptors -> neuronal death

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22
Q

Theories for why memantine works for AD

A
  1. β-amyloid peptide -> glutamate excitotoxicity through interaction with NMDA receptors.
  2. Tau protein + glutamade excitotox link - glutamate-induced neurodegeneration
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23
Q

Mechanism + non-mechanism based approaches for future research of AD

A

Mech: Targer amyloid, tau, APOE, neuroprotective therapies. Non-mech: cognitive enhancers, prevention

24
Q

Angiogenesis meaning

A

Formation of new blood vessels from pre-existing vascular into avascular (due to VEGF-stimulus)

25
Q

2 types of tumours

A

Benign, Malignant

26
Q

Info about benign tumours

A

Do not metastasise, usually encapsulated, in any tissue - resembels original tissue, well differentiated (slow growing), often relatively harmless

27
Q

Metastasise meaning

A

(of a cancer) spread to other sites in the body

28
Q

Info about malignant tumours

A

Intravasation then metastasis, poorly differentiated - frequent cell devisions = fast growing

29
Q

What is intravasation

A

When tumour enters circulation (into vessel especially blood)

30
Q

What can cause mutagenic initiation

A

Chemicals, radiation, viruses, spontaneous change, genome instability

31
Q

What mutations can be caused in dna

A

Nonsense, silent mutations or chromosomal alterations: deletions, insertions, translocation

32
Q

Epigenetic (genes) alterations

A

Acetylations, methylation

33
Q

Steps of metastasis cascade

A
  1. Primary tumour formation.
  2. Localised invasion (towards blood vessel)
  3. Intravasation - into blood stream
  4. Transport through circulation
  5. Arrest in microvessels of organs eg Lungs, bone, brain (cells get stuck in tiny vessels)
  6. Extravasation - into tissue
  7. Formation of micrometastasis - too small for scan
  8. Colonisation: Formation of macrometastasis
34
Q

6 original hallmarks of cancer

A

Resisting cell death, sustaining proliferative (growing) signalling, evading growth supressors, activating invasion and metastasis, enabling replicative immortality, inducing angiogenesis

35
Q

4 new emerging + enabling hallmarks of cancer

A

Deregulating cellular energetics (put energy into what tumour needs), avoiding immune destruction, genome instability and mutation, tumour-promoting inflammation

36
Q

Where is angeiogenesis used in normal processes in body

A

Development, menstrual cycle, wound healing

36
Q

How does a normal cell transform into a cancer cell (short answer)

A

Accrual (accumulation) of multiple genetic mutations over time

37
Q

What does leaky vessels mean and what does it casue

A

Fluid leaks from blood vessels into surrounding tissue. Causes drop in blood pressure

38
Q

Differences between normal vs tumour angiogenesis

A

Normal: Controlled, regulated, organised, mature and low interstitial (outside vessels) pressure. Pathological (tumour) is the opposite

39
Q

Negative effect of higher interstitial pressure

A

Medication can’t leave bc can’t go down pressure gradient as it is lower in tumour vascular

40
Q

4 modes of vessel formation

A

Sprouting angiogenesis (2 vessels get connected), vasculogenesis (bone marrow differentiates - brand new vessel), intussuseption (hole in vessel expands to become 2), vessel co-option (tumour cells co-opt pre-existing vessels, sit by it)

41
Q

What happens in sprouting engiogenesis (vessel brancing)

A

Angiogenic factors = stimulus to quiescent (normal) vessel (eg VEGF) - tells cell in vessel to change phenotype = tip-cell formation. Has little hairs that are sensors. Tip-cell signals to cells besides to follow tip-cell to stimulus and change phenotype = stalk cells + stalk elongation. Same happens in adjacent vessel. Blood flow starts coming behind it as moves out. Eventually blood vessels connect = quiescent phalanx resolution. Pericyte cells give protection + stability to growing + maturing blood vessel.

42
Q

3 treatments for cancer

A

Surgery, chemotherapy and radiotherapy

43
Q

Info about surgery for cancer

A

Invasive, facilitates further treatment (better access for chemo), prevention (removal of moles), debulking (remove bulk of tumour before chemo)

44
Q

Info + types of chemotherapy

A

Alkylating-like agents, anti-metabolites, topoisomerase inhibitors, microtubule inhibitors. All interfere with cell cycle (s-phase) + attack rapidly proliferating cells EXCEPT microtubule - changes where chromosomes line up - don’t complete M phase of cell cycle.

45
Q

What are some issued with chemotherapy

A

Bone marrow, GI tract, hair follicles are normal cells that are rapidly dividing, nausea, myelosupression (decrease blood cells), diarrhoea, cardiovascular toxicity

46
Q

Info on radiotherapy

A

External beam target tissue. Can otherwise implant “seeds” in body. Can causes rash/burns to skin. Causes damage to normal tissue too.

47
Q

Other ways to target cancer treatment

A

Target growth and death (tumour supressors etc), anti-oestrogen or androgen signalling, target cell signalling (angiogenesis inhibitor)

48
Q

What is VEGF-A

A

Vascular endothelial growth factor. Protein, affects proliferation, cell survival… Regulated blood flow and vascular tone - more VEGF = more vasodilated

49
Q

How does VEGF bind to receptor etc

A

Released by tumour (or something else). Dimerises then binds to receptor - VEGFR2 (3 diff types but focus on R2). Receptor dimersises: tyrosine kinase domain comes together. RTK become autophosphorylated. Then signalling starts

50
Q

4 types of VEGF inhibition

A
  1. Inhib of VEGFA ligand (by an antibody that captures it). 2. VEGFR2 (receptor) - small molec inhibitor by crossing cell membrane and stopping phosporylation of RTK, 3. VEGFR2 downstream signalling. 4. anti-VEGFR1 or R2 antibodies
51
Q

What does it mean if medicine ends in mab

A

Monoclonal antibody!

52
Q

Name of medicine that inhibits VEGFA

A

Bevacizumab (or avastin)

53
Q

Info and problems of inhibition of VEGFR2

A

Sunitinib, sorafenib. RTK inhibitors used. Competitive OR allosteric inhib. Multi-targeted - many side effects. Leads to resistance and toxicities. Left ventricle dysfunction-> onset of heart faliure

54
Q

Consequences of VEGF inhibition

A

Hypertension, bad wound healing, cardiac dysfunction (hypertension), renal toxic effects, haemorrhage, blood clots

55
Q
A

LIFE (4 decks)

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