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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
Q

Anticholinesterase

A

Blocks acetyl cholinesterase from choppin up ACh

Can b reversible/short acting
Or irreversible/long lasting

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25
Q

Myasthenia gravis

A

Autoimmune disease affectin neuromuscular (NM) transmission- stops ability of ACh from binding to receptor cos antibodies r binding to N receptors

26
Q

Myasthenia gravis treatment

A
  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
Q

Ptosis

A

Droopin of eyelids

One of first signs of envenomin

28
Q

LD50

A

Dose of venom that kills 50% of mice over a 24/48 h period

29
Q

Venomous

A

Toxin + animal must hav some venom apparatus ( eg fang sting etc

30
Q

Poisonous

A

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
Q

Signs symptoms of snake bites

A 
Paralysis 
Ptosis
Loss of facial expression
Dysarthria (difficulty speaking) 
Etc

Early sign of envenomin of snake:
Uncoagulatable boold

32
Q

Snake neurotoxins

A 
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
Q

Treatin snake bites

A

First aid.n pressure immobilisation (to stop lymph flow not blodd flow)
N stoppin movement of patient

34
Q

Antivenom

A

= 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
Q

Irukandji syndrome

A

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
Q

Myotoxins

A

Cause skeletal muscle necrosis

37
Q

Redback envenomin

A

Only female dangerous

Venom act presynaptically: stimulate increased telease of ACh n NA- lead to depolarisin block

Sympoms: tachycardia, hypertension,pain

38
Q

Funnel web envenoming

A

Neurotoxins act presynaptically

Causing ‘autonomic storm’ then cardio respiratory arrest

39
Q

Carcinogen

A

Any agent that directly causes cancer

Eg UV light, tobacco smoke, meat preservatives, ionizing radiation

40
Q

Penetrance

A

% 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
Q

% of all cancers that were due to INHERITeD genes

A

10%

42
Q

Viruses can cause up to…

A

15% of cancer cases

43
Q

Breast cancer

A

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
Q

Proto-oncogenes

A

Normal genes that regulate cell growth n division

45
Q

Oncogenes

A

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
Q

STI-571

Aka Gleevec/imatinib (trade name of drug)

A

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
Q

CML

A

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
Q

Abl tyrosine kinase

A

Type of tyrosine kinase playin major role in CML

49
Q

Tyrosine kinase

A

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
Q

Drugs that inhibit tyrosine kinase

A

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
Q

p53

A

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
Q

Mismatch repair genes (MMR genes)

A

Repair DNA if error occurs during DNA replication

Follows 2 hit hypothesis

8 types

53
Q

2 hit hypothesis

A

Both genes must b knocked out/mutated to confer loss of function- n hence get cancer

54
Q

Tumour suppressor genes (TSGS)

Eg P53 gene n RB gene

A

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
Q

Rb gene

A

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
Q

Retinoblastoma

A

Childhood tumour or retina

57
Q

Key concept of cancer

A

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
Q

Stress: 3 approaches

A
  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
Q

Primary appraisal (stress approach 2)

A

How the person initially views the stressful event

60
Q

Secondary appraisal (stress approach 2)

A

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
Q

Autonomic nervous system (ANS)

A

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
Q

Stress as an Internal Physiological Reaction (stress approach 3)

A

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
Q

Chronic stress

A

Leads to burnout

Med 1011 (12 decks)

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