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Med 1011 > Week 9 Sem 1 2014 > Flashcards

Week 9 Sem 1 2014 Flashcards

0
Q

Colliquative (liquefactive) necrosis

A

Tissue liquefies

Occurs in brain (cos brain doesnt have supportin stroma)

Cavity forms

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1
Q

Coagulative necrosis

A

Devitalised tissue retains its architecture

Eventually coagulates (=form solid/semi solid) n forms scar

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2
Q

Caseous necrosis

A

Cheese like texture

Amorphous (ie has no clear structure)

Typically due to tuberculosis infection

Has Langhan’s giant cells (wich r arranged in horse shoe arrangement)

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3
Q

Gangrene

A

Wen tissue has necrosis n then a secondary bacterial infection appears there

Not a type of necrosis

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4
Q

Fibrinoid necrosis

A

Occurs in vasculitis

Ab-Ag complexes deposit in vessel wall -> lead to inflammation + necrosis of vessel wall

Fibrin leaks out of vessels

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5
Q

Fat necrosis

A

Cells release/leak fats, causing inflammatory response n eventually fibrosis

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6
Q

Key concepts in immunity

A

Recognition (ie recognise self from non self)
Effector f(x)s (immune cells destroy stuff)
Regulation (n also down regulation..cos we dont want immune system going all the time)
Memory

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7
Q

Pathogen Associated Molecular Patterns (PAMPS)

A

Receptors on microbes that r not specific to a particular eg bacteria

‘Conserved patterns’ found on bacteria
Viruses, pathogens

Involved in the ‘innate’ immune response

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8
Q

Pattern Recognition Receptor (PRR)

A

Receptors on our immune cells that recognise PAMPS

Part of innate response

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9
Q

Tolerance

A

Lack of response of immune system to self

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10
Q

Commensal

A

Something living in another organism, without affecting its host

Eg bacteria in GIT as part of innate non-specific immunity

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11
Q

B lymphocytes

A

Differentiate into plasma cells(wich r WBC) wich secrete antibodies

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12
Q

Antibodies

A

Y shaped protein

Can recognise foreign stuff eg bacteria n viruses by binding to foreign stuff’s antigen. Then can either

1) tag the microbe (so that it gets attacker by other parts of immune system or
2) neutralise microbe directly (eg by blockin microbe’s part that is essential for invasion n survival)

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13
Q

T lymphocyte (lymphocyte= WBC btw)

A

Distinguished from other lymphocytes by presence of T-cell receptor

Mature in thymus (hence the ‘T’)

Basically fight infection in many ways

Types of T cells : ?

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14
Q

Dendritic cells

A

Antigen presenting cells

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15
Q

Phagocytes

A

Eat harmful foreign particles, bacteria, dead or dying cells

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16
Q

Natural killer cells (NK cells)

A

Kills virus-infected cells or cancerous cells

Can kill target cells even in absence of antibody or antigenic stimulation

Have no memory

Have wide range of targets

Minimal specificity

Part of innate immunity

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17
Q

Infarction

A 
Tissue death (necrosis) due to 
Local lack of oxy due to
Obstruction of tissue's blood supply
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18
Q

Anoxia

A

Total Depletion of oxygen

Worse form of hypoxia= low/ inadequate oxygen

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19
Q

Barretts metaplasia

A

Metaplasia in oesophagus where
Squamous mucosa changes to
Intestinal glandular mucosa

20
Q

Myocardium

A

Muscular Tissue of heart

Made of cardiac muscle

21
Q

Pericardium

A

Connective tissue layer around the heart

22
Q

Cultural awareness

A

Observin n being conscious of similarities n differences bw cultural groups

Everyone has their own cultural influences (eg stereotypes)

23
Q

Cultural sensitivity

A

Being aware n understanding our own values of our culture and how it can shape our approach to patients from dif cultures

Eg views on abortion

24
Q

Cultural competence

A

Attitudes knowledge n skills of doctors to become effective health care providers for patients from dif cultures

  • Acknowledgin culture
  • Respect cultural differences
  • Minimisation of any neg consequences of cultural differencws
25
Q

Cultural safety

A

We hav culturally safe encounter wen Patient feels comfortable in doc-patient relationship

Doc reflects on their own identity/values n dif bw cultures

Culturally safe practice = keep these differin perspectives in mind whilst treating patients wit RESPECT as a person in their own right

26
Q

Alkylating agents

Anticancer drug

A 
Insert alkyl group into DNA structure
This forms strong covalent bonds/cross links with particular bases (esp G bases) n proteins ie formin chemcial chains across DNA
DNa cant replicate 
If tries, it will break
Hopefully cell will die

Cycle non-specific

27
Q

Cytotoxic antibiotics

Anti cancer drugs

A

Was too toxic to use for infections, but for cancer, benefit out weighs cost so haha

Inhibit transcription translation
(So protein synthesis affected
So proteins necessary for growth affected
So cell doesnt proliferate

Work in some stages of cell cycle better than others

28
Q

Antimetabolites

Anticancer drug

A

Substitute themselves into DNA pathway= block DNA synthesis/makes DNA non functional

Or can affect pathway involving folate/specific bases eg adenine synthesis

Cycle specific: S phase inhibitors

29
Q

Mitotic poisons

Anticancer drugs

A

Comes from plants

Those that inhibit microtubule formation (which is needed in mitosis) =M phase inhibitors

Those that inhibit topoisomerase (needed in DNA replication) =S phase inhibitors

Vinca alkaloids (derived from periwinkle plant)
Taxanes ( derived from euro yew tree)
Etiposide ( from mandrake)

30
Q

Hormone and hormone antagonists:
SERM
(Anticancer drug)

A

Act as antagonist in some parts of body n agonist in other parts

In breast cancer cells, act as antagonist on eostrogen receptors- competitively inhibiting eostrogen (wich is a growth factor for breast tumour cells)

Hence reduce rate of growth of cells

31
Q

Hormone and hormone antagonist:
Antiandrogens
(Anticancer drug)

A

Used in prostate cancer

Antagonists that sit on receptors on prostate cells, inhibiting growth factors (androgens) from binding

So switch off growth of testes

32
Q

Androgen

A

Hormone that Stimulate male organ growth eg prostate

33
Q

Gonadotrophin

A

Hormones that stimulate sexual development/gonads growin into ovaries/testes etc

34
Q

Hormone and hormone antagonists:
Gonadotrophin-RH analogues
(Anticancer drug)

A

Drug Used in prostate cancer

Act like GONADOTROPHIN RELEASING HORMONES (wich r homones that stimulate pituitary to release gonadotrophins + in the testes, that causes a rise in circulating androgen levels

Initially in 1 dose= growth like normal
After many doses= through negative feedbakc:
Switch off production of gonadotrophins (levels decrease)
Androgen levels drop
Switch off growth of tissue

35
Q

Prostate cancer

A

WE WANT DECREASE IN ANDROGEN LEVELS IN PROSTATE CANCER!

36
Q

Hormone and hormone antagonists:
Glucocorticoids
(Anticancer drug)

A

Hormones useful in blood-borne cancers (leukaemia, lymphoma)

Cause cells to leave circulation n enter lymph nodes/spleen, where they r more likely to encounter immune cells

High doses also leads to lysis of cancer cells in blood stream

Danger: high levels of cortisol can lead to cushioning syndrome

37
Q

Common adverse effects of anticancer drugs

A

Heart-get arrithymia
Kidney- get renal failure
Nervous system- affect microtubule formation= affect neuro f(x), paresthesia
Urinary- haemorrhage

38
Q

Paresthesia

A

Abnormal sensations eg tingling, numbin, burnin due to nerve damage

39
Q

Antiemetic drugs

A

Drug effective against vomittin n nausea

Inhibit medullary centre of brain

Eg dopamine/serotonin/neurokinin receptor antagonists
Glucocorticoids eg dexamethasone -counter side effects of chemotherapy

40
Q

Colony stimulating factors (CSFs)

A

Bind to receptors on haematopoietic stem cells to stimulate blood cell production

Eg filigrastim - stimulate WBC production - so not as suscep to infection

Erythropoietin- boost RBC count -so not anemic during therapy

41
Q

Mesna

A

Drug deals wit organ toxicity due to anticancer drugs

Acts on toxic metabolites (from metabolites of other drugs (alkylating agents like cyclophosphamide n ifosfamide) to prevent urinary bladder damage

Doesnt stop anticancer drug

Its an adjuvent ( modifies effect of another drug)

42
Q

Novel agents for cancer treatment (higher selective toxicity)

A 
Monoclonal antibodies
Biological response modifiers
Cytokine treatment of sampled immune cells
Tyrosine-kinase inhibitors
Sensitising agent
43
Q

Monoclonal antibodies

For cancer

A

Eg rutiximab- triggers cancered B cell lysis

Eg trastuzumab-
Binds to HER2 (human growth factor 2)

Or we can attach cytotoxic agent to monoclonal antibodies

44
Q

Biological response modifiers

A

Make cancer cell more ‘tasty’ to immune system by
Altering antigen expression in tumour cells n immune cells

Also augment cytotoxicity of Immune cells, High doses inhibit cell proliferation

Through use of eg interferon

45
Q

Interleukin-2 (IL-2)

Biological response modifier

A

Stimulate lymphocyte proliferation n cellular immunity, sensitises immune system against tumour cells

Need to take patient’s lymphocytes out, expose them to IL-2 + cancer cell antigen
Then put lymphocytes bak

46
Q

Inhibitors of intracellular signalling molecules

A 
'Small molecule' drug binds to protein kinases (eg tyrosine kinase, serine-threonine kinase) whihc
Inhibit enzyme
Inactivate enzyme
Disrupt intracellular signallin
Stop cell proliferation

Some protein kinases inhibitors r also angiogenesis inhibitors

Kinase inhibitors end in ‘inib’

47
Q

Sensitising agents

A

Make cells more immunoreactive-
Spray this on a tumour, so tumour has marker saying that its differnt to normal cells, so now immune system can recognise n act on them

48
Q

Cancer treatment complications

A
  1. Drug resistance- so use a combo of drugs, take a ‘drug holiday’
  2. Tumour cell sanctuaries- ie cell grows in compartments that r unaccessible to drugs - so use combo therapy (ie drugs + surgery etc)
  3. Dose exhaustion- ie if we keep pushin the dose, can become too toxic/ immune cells wont be able to combat cancer cells- so use combo therapy

Med 1011 (12 decks)

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