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Med 1011 > Week 8 Sem 1 2014 > Flashcards

Week 8 Sem 1 2014 Flashcards

0
Q

Hypertrophy

A

Increase in cell size

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1
Q

Hyperlasia

A

Increase in cell NO.

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2
Q

Atrophy

A

Decrease in cell NO./SIZE

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3
Q

Metaplasia

A

Change in cell TYPE

To better suit the requirement

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4
Q

Neoplasia

A

Abnormal New growth of tissue

Cellular proliferation faster than normal

Partial or complete lack of structural organization + functional coordination wit normal tissue

Can b benign or malignant

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5
Q

Carcinoma

A

Malignant neoplasm of epithelial origin

Be in epithelial regions / r epithelial cells

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6
Q

Benign

A

Non invasive

Abnormal growth that is stable

Encapsulated

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7
Q

Tumour

A

Abnormal growth of tissue

Synonym for neoplasm eg benign tumour, malignant tumour

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8
Q

Ability to regenerate:

Liable tissue

A

Constant turnover (turnover=replacement of old cells with new cells)

Eg skin

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9
Q

Ability to regenerate:

Stable tissue

A

Not ongoing turnover, but can do so (ie regenerate) if need be

Eg kidney

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10
Q

Ability to regenerate:

Permanent tissue

A

Doesnt regenerate

Eg brain & heart

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11
Q

Nerves that release acetylcholine (ACh)

A

= cholinergic nerves

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12
Q

Nerves that release noradrenaline (NA)/ adrenaline

Dopamine

A

= adrenergic nerves

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13
Q

Adrenergic

A

Primarily SNS ( sympathetic nervous system)

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14
Q

Cholinergic

A

(Both SNS + PNS
Sympathetic
Parasympathetic nervous system

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15
Q

Nicotinic receptors

A

Found in muscles n ganglia/brain

Respond to Acetylcholine

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16
Q

Muscarinic receptors

A

Found in all other parts of body xept muscles n ganglia/brain

Respond to acetylcholine

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17
Q

Non-depolarising blockers

A

Competitive( competes/ trying to get to same receptor as neurotransmitters) antagonist (just turn off receptor, no efficacy) at nicotinic (N) receptors

Can overcome this by increasing conc of ACh (clinically, we add anticholinesterase - enzyme that stops ACh from being chopped up)

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18
Q

Tubocurarine

A

Eg of non-depolarising drug

Just simple antagonist-stops ACh from gettin to receptor

Causes paralysis

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19
Q

Depolarising blockers

A

Agonists

Overstimulate Nicotinic receptors so that receptors stays in depolarised state and cant get bak to repolarised state

Initially, get initial contraction cos it acts like ACh but
It stays on receptor much longer than ACh
So get depolarisation blockade - ends up ‘turnin off’ receptor

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20
Q

Suxamethonium

A

Depolarising drug

Made of 2 ACh’s

Once gets into blood, can get chopped off by plasma cholinesterase (problem is, some ppl dont hav this enzyme- so we prefer other drugs to this one)

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21
Q

Botulinum toxin

A

Eg botox!
Bacterial exotoxin

Most toxic subs to man

Normally, vesicles release ACh by dockin at SNAP-25. If we cut up SNAP-25 (which is wat toxin does), cant dock-> no response

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22
Q

Acetyl cholinesterase (AChE)

A

Break down acetyl choline

We need to get rid of ACh (after binding to receptor) asap or else depolarization block would occur
Hence, need AChE!!

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23
Q

Non specific ‘pseudo’cholinesterase

A

Break down other stuff that is similar to ACh

Eg suxamethonium

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24
Anticholinesterase
Blocks acetyl cholinesterase from choppin up ACh Can b reversible/short acting Or irreversible/long lasting
25
Myasthenia gravis
Autoimmune disease affectin neuromuscular (NM) transmission- stops ability of ACh from binding to receptor cos antibodies r binding to N receptors
26
Myasthenia gravis treatment
1. Anticholinesterase (increase [ACh] 2. Add atropine (cos ACh goes everywhere, not just skeletal muscles. Use atropine to stop unwanted M(muscarinic) effects) 3. Immunosuppressants (suppress anitbody formation)
27
Ptosis
Droopin of eyelids One of first signs of envenomin
28
LD50
Dose of venom that kills 50% of mice over a 24/48 h period
29
Venomous
Toxin + animal must hav some venom apparatus ( eg fang sting etc
30
Poisonous
Toxin We hav to eg ingest it to get poisoned No special delivery mechanism Eg frog How it delivers determinew whether animal is venomous or poisonous
31
Signs symptoms of snake bites
``` Paralysis Ptosis Loss of facial expression Dysarthria (difficulty speaking) Etc ``` Early sign of envenomin of snake: Uncoagulatable boold
32
Snake neurotoxins
``` Beta neurotoxins Presynaptic Stop recylcin of vesicles Rapid onset Reversible Respnd to anticholinesterase n antivenom ``` ``` Alpha neurotoxins Postsynaptic Stop binding of ACh to receptors Slow onset Irreversible Only respnd to antivenom of given early ```
33
Treatin snake bites
First aid.n pressure immobilisation (to stop lymph flow not blodd flow) N stoppin movement of patient
34
Antivenom
= antibodies produced wen animal (eg horse) injected wit snake venom. Giv horse antibody to patient Monovalent antivenom- get one type of antibody cos venom given to horse was from 1 species Polyvalent antivenom- get many types of antibody cos venom given to horse was from 2+ species
35
Irukandji syndrome
Envenomin by carybdeid jellyfish Get severe hypertension, nausea vomittin etc Treatent for jelly fish envenoming- add VINEGAR (not alcohol), antivenom Dont do pressure/immobilisation
36
Myotoxins
Cause skeletal muscle necrosis
37
Redback envenomin
Only female dangerous Venom act presynaptically: stimulate increased telease of ACh n NA- lead to depolarisin block Sympoms: tachycardia, hypertension,pain
38
Funnel web envenoming
Neurotoxins act presynaptically | Causing 'autonomic storm' then cardio respiratory arrest
39
Carcinogen
Any agent that directly causes cancer Eg UV light, tobacco smoke, meat preservatives, ionizing radiation
40
Penetrance
% of ppl wit a genetic predisposition who will develop cancer Eg colon= 100% penetrance ie if u inherited this gene- irrespective of any other factor- u WILL get colon cancer Breast cancer= 40-70% penetrance
41
% of all cancers that were due to INHERITeD genes
10%
42
Viruses can cause up to...
15% of cancer cases
43
Breast cancer
Hereditary genes causin it: BRCA 17q BRCA 13q Up to 10% breast cancer is due to genetic predisposition Life time risk of breast cancer- BRCA1 and BRCA2 83- 88% by age of 70
44
Proto-oncogenes
Normal genes that regulate cell growth n division
45
Oncogenes
Promote cancer Wen proto-oncogenes get damage they become Oncogenes. This may be bc: 1) gain of f(x) mutation eg pnt mutation 2) gene amplification (leadin 2 over expressed proteins) 3) chromosomal translocation
46
STI-571 | Aka Gleevec/imatinib (trade name of drug)
Blocks binding of ATP to BCR-ABL tyrosine kinase So that receptor cant phosphorylate its substrates Hence slowing growth of cancer cells Used to treat CML and GISTs (gastrointestinal stromal tumours)
47
CML
Chronic myelogenous leukemia Increased n unregulated growth of myeloid cells in bone marrow n accumulation of these cells in blood Only leukemic cells of this cancer has 9:22 translocation
48
Abl tyrosine kinase
Type of tyrosine kinase playin major role in CML
49
Tyrosine kinase
Genes coding for this= Largest group of oncogenes Gp of protein receptors Activate by binding to growth factors/cytokines Wen stimulated results in cell proliferation/survival etc
50
Drugs that inhibit tyrosine kinase
ATP-competitve inhibitors eg imatinib Antibodies against tyrosine kinase receptor or their ligands (block binding of ligand to tyrosine kinase receptor) eg in breast cancer Anti-angiogenics
51
p53
A protein expressed by TP53 gene that induces cell cycle arrest, differentiation, DNA repair, APOPTOSIS basically it is a tumour suppressor. (TP53 is a tumour suppressor gene) Cancer cells wit defective p53: Escape apoptosis, has damaged DNA cos dont halt proliferation to repair DNA 50% of tumours show mutation/loss of p53 Just lost of one good copy can still contribute to cancer (ie 'growth advantage' due to reduced apoptosis) Eg in skin cancer (squamous cell carcinoma)
52
Mismatch repair genes (MMR genes)
Repair DNA if error occurs during DNA replication Follows 2 hit hypothesis 8 types
53
2 hit hypothesis
Both genes must b knocked out/mutated to confer loss of function- n hence get cancer
54
Tumour suppressor genes (TSGS) Eg P53 gene n RB gene
Genes that act to prevent cancer Control check pnts in cell cycle, Induce transcription of regulatory inhibitory genes, Prevent cells from goin through cell cycle= rapid cell cyclin/division:allow for DNA repair Follows 2 hit hypothesis Normal genes present in all cells
55
Rb gene
Retinoblastoma gene Prevents transcriptional activation of other genes needed for onset of S phase Plays a role in differentiation, dNA replication n apoptosis 2 copies must be lost to get cancer (retinoblastoma etc
56
Retinoblastoma
Childhood tumour or retina
57
Key concept of cancer
MULTIPLE GENES R AFFECTED (activation of oncogenes Loss of tumour suppressor genes Loss of mismatch repair genes) Cancer is due to GENETIC MUTATIONS + ENVIRONMENTAL FACTORS
58
Stress: 3 approaches
1. stress as an external stimulus (how outside affects us) 2. Stress as a transaction bw external envrio n individuals reaction (nature of outside stuff + how we react to outside stuff) 3. Stress as a internal physiological reaction (bio stuff)
59
Primary appraisal (stress approach 2)
How the person initially views the stressful event
60
Secondary appraisal (stress approach 2)
How the person sees their own resources n their ability to cope Later, also how the person's emotional repsonse influeneces how they see everythin
61
Autonomic nervous system (ANS)
Part or peripheral nervous system Control many unconscious bodily f(x)s eg heart rate, digestion, respiration rate, sexual arousal Divided into 2 subsystems: SNS:sympathetic nervous system ('accelerator' fight or flight) PNS: parasympathetic nervous system ('Brake' rest and digest)
62
Stress as an Internal Physiological Reaction (stress approach 3)
involves ANS: SNS- acute response to stress via fight or flight response PNS- gets body bak to normal Neuro-endocrine system: Triggers hypothalamic-pituitary-adrenal axis. Results in release of hormones that prepare body for the stressful situation
63
Chronic stress
Leads to burnout

Med 1011 (12 decks)

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