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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
Cultural competence
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
Cultural safety
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
Alkylating agents | Anticancer drug
``` 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
Cytotoxic antibiotics | Anti cancer drugs
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
Antimetabolites | Anticancer drug
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
Mitotic poisons | Anticancer drugs
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
Hormone and hormone antagonists: SERM (Anticancer drug)
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
Hormone and hormone antagonist: Antiandrogens (Anticancer drug)
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
Androgen
Hormone that Stimulate male organ growth eg prostate
33
Gonadotrophin
Hormones that stimulate sexual development/gonads growin into ovaries/testes etc
34
Hormone and hormone antagonists: Gonadotrophin-RH analogues (Anticancer drug)
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
Prostate cancer
WE WANT DECREASE IN ANDROGEN LEVELS IN PROSTATE CANCER!
36
Hormone and hormone antagonists: Glucocorticoids (Anticancer drug)
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
Common adverse effects of anticancer drugs
Heart-get arrithymia Kidney- get renal failure Nervous system- affect microtubule formation= affect neuro f(x), paresthesia Urinary- haemorrhage
38
Paresthesia
Abnormal sensations eg tingling, numbin, burnin due to nerve damage
39
Antiemetic drugs
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
Colony stimulating factors (CSFs)
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
Mesna
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
Novel agents for cancer treatment (higher selective toxicity)
``` Monoclonal antibodies Biological response modifiers Cytokine treatment of sampled immune cells Tyrosine-kinase inhibitors Sensitising agent ```
43
Monoclonal antibodies | For cancer
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
Biological response modifiers
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
Interleukin-2 (IL-2) | Biological response modifier
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
Inhibitors of intracellular signalling molecules
``` '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
Sensitising agents
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
Cancer treatment complications
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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