Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

LIFE > Case studies > Flashcards

Case studies Flashcards

1
Q

4 tactile? tests to test for Alzheimers (AD)

A

Blood tests, electroencephalography (EEG), MRI

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

What is electroencephalography (EEG)

A

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

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

What does MRI measure

A

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

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

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

4 examples of dementia

A

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

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

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

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

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

Info on Vascular dementia

A

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

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

4 stages of AD

A

Mild, moderate, late, advanced

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

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

Aetiology meaning

A

Cause of a disease or condition

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

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

Challenges of treading mild AD

A

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

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

What is donepezil

A

A colinesterase inhibitor

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

3 medicines used for mild AD

A

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

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

Why is colinesterase inhibitor used for AD

A

Lower concs of acetylcholine in AD. “Cholinergic hypothesis”

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

Memantine use + action in body

A

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

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

What is excitotoxicity relating to glutamate

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
2 types of tumours
Benign, Malignant
26
Info about benign tumours
Do not metastasise, usually encapsulated, in any tissue - resembels original tissue, well differentiated (slow growing), often relatively harmless
27
Metastasise meaning
(of a cancer) spread to other sites in the body
28
Info about malignant tumours
Intravasation then metastasis, poorly differentiated - frequent cell devisions = fast growing
29
What is intravasation
When tumour enters circulation (into vessel especially blood)
30
What can cause mutagenic initiation
Chemicals, radiation, viruses, spontaneous change, genome instability
31
What mutations can be caused in dna
Nonsense, silent mutations or chromosomal alterations: deletions, insertions, translocation
32
Epigenetic (genes) alterations
Acetylations, methylation
33
Steps of metastasis cascade
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
6 original hallmarks of cancer
Resisting cell death, sustaining proliferative (growing) signalling, evading growth supressors, activating invasion and metastasis, enabling replicative immortality, inducing angiogenesis
35
4 new emerging + enabling hallmarks of cancer
Deregulating cellular energetics (put energy into what tumour needs), avoiding immune destruction, genome instability and mutation, tumour-promoting inflammation
36
Where is angeiogenesis used in normal processes in body
Development, menstrual cycle, wound healing
36
How does a normal cell transform into a cancer cell (short answer)
Accrual (accumulation) of multiple genetic mutations over time
37
What does leaky vessels mean and what does it casue
Fluid leaks from blood vessels into surrounding tissue. Causes drop in blood pressure
38
Differences between normal vs tumour angiogenesis
Normal: Controlled, regulated, organised, mature and low interstitial (outside vessels) pressure. Pathological (tumour) is the opposite
39
Negative effect of higher interstitial pressure
Medication can't leave bc can't go down pressure gradient as it is lower in tumour vascular
40
4 modes of vessel formation
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
What happens in sprouting engiogenesis (vessel brancing)
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
3 treatments for cancer
Surgery, chemotherapy and radiotherapy
43
Info about surgery for cancer
Invasive, facilitates further treatment (better access for chemo), prevention (removal of moles), debulking (remove bulk of tumour before chemo)
44
Info + types of chemotherapy
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
What are some issued with chemotherapy
Bone marrow, GI tract, hair follicles are normal cells that are rapidly dividing, nausea, myelosupression (decrease blood cells), diarrhoea, cardiovascular toxicity
46
Info on radiotherapy
External beam target tissue. Can otherwise implant "seeds" in body. Can causes rash/burns to skin. Causes damage to normal tissue too.
47
Other ways to target cancer treatment
Target growth and death (tumour supressors etc), anti-oestrogen or androgen signalling, target cell signalling (angiogenesis inhibitor)
48
What is VEGF-A
Vascular endothelial growth factor. Protein, affects proliferation, cell survival... Regulated blood flow and vascular tone - more VEGF = more vasodilated
49
How does VEGF bind to receptor etc
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
4 types of VEGF inhibition
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
What does it mean if medicine ends in mab
Monoclonal antibody!
52
Name of medicine that inhibits VEGFA
Bevacizumab (or avastin)
53
Info and problems of inhibition of VEGFR2
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
Consequences of VEGF inhibition
Hypertension, bad wound healing, cardiac dysfunction (hypertension), renal toxic effects, haemorrhage, blood clots
55

LIFE (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions