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EOYS > SSS FunMed > Flashcards

SSS FunMed Flashcards

1
Q

what is the basic structure of gram +ve bacteria? [3]

what does interaction with host cell cause?

A

structure: lipid A, core polysaccharide, O antigen

production of cytokines: results in septic shock, ferver, intravascular coagulation = haemorrage and endotoxin shock

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2
Q

how do CD8 / cytotoxic T cells recognise pathogensi on a cell? [2]

how does apoptosis occur ? [4]

A
  • CD8 T cells have a T cell receptor (TCR) and the CD8 co-receptor
  • they kill pathogen infected cells and tumour cells by:
  • recognises peptide-MHC-I combination that has been presented on the cell (its the same peptide that the dendritic cell initiailly caused clonal expansion to occur by)
  • cell death by apoptosis.
    i) nuclear blebbing
    ii) alteration in cell morophology
    iii) shedding of small membrane vesciles
    iv) apoptotic bodies removed by phagocytosis
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3
Q

how do B cells regonise antigens? [2]

A
  • B-cells have recognition molecules called immunoglobins (Ig): often the eptiope is conformational
  • without help of other cells !!
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4
Q

name a malignant form of cancer that is caused by hyperplasia [1] and what it is caused by? [1]

A

malignant - platelet derived growth factor (PGDR) - leads to glioblastoma

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5
Q

where do drugs with large / small VD distributed to?

A

Large VD: distributed to tissues (fat / bones)

Small VD: distributed to blood

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6
Q

which vertebral levels are:

a) paravertebral ganglia[1]
b) prevertebral ganglia [1]

A

which vertebral levels are:

a) paravertebral ganglia: T1-T4
b) prevertebral ganglia: T5-L2

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7
Q

what colour does ziehl-neelosn stain turn mycobacteria? [1]

A

red

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8
Q

dendritic cells cause the activation of what? [2]

A
  • dendritic cells go around tissue, continually monitoring and assessing environment by processing proteins into peptides.
  • in prescence of pathogen - PAMPS are activated by dendritic cell.
  • dendritic cells go down afferent lympahtics to lymph nodes
  • hold proteins out on MHC Class 1/2 molecules.
  • if recognised by CD4/8 - clonal expansion and cytoxic fun happens
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9
Q

which antibiotics do you use on:

  • gram +ve? [1]
  • gram -ve ? [1]
A

glycopeptide antibiotics: gram postive

polymyxins: gram negative

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10
Q

explain the mechanism of how Burkitt lymphoma occurs

explain the mechanism of how lymphoma (other) occurs

A

explain the mechanism of how Burkitt lymphoma occurs
- c-myc: found on chr 8

  • IgH: chromsome 14. has a very strong promoter
  • translocation of region of chr 8 and 14: myc gets translocated near to promoter of IgH
  • results in strong promoter driving the expression of c-myc: Burkitt lymphoma

explain the mechanism of how lymphoma (other) occurs
- BCl-2 gene is on chromosome 18

  • IgH: chromsome 14. has a very strong promoter
  • switches ON bcl-2 gene (anti-apoptotic protein) in active B-lymphocytes (is normally switched off)
  • cells that harbour mutations do not go into apoptosis
  • causes lymphoma
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11
Q

what are the two pathways initated by growth factor binding to cell, that eventually lead to activation of gene expression and transcription factors occur. [2]

A

MAPK & PI3Kinase

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12
Q

what is the complement cascade?

A

another system of secreted proteins that is good at getting rid of extracellular pathogens, like bacteria.

  • surface of bacteria can bind to complement proteins
  • forms a pore on bacteria
  • pops them !
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13
Q

how can some bacteria destroy IgA? [1]

A

using IgA proteases

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14
Q

name 2 complement blood proteins used in innate immunity [2]

A

Uses complement blood proteins that

•opsonise (act as markers for phagocytes)

•cytolyse (directly attack via membrane attack complex (MAC))

•enhance inflammation

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15
Q

describe structure of proteoglycan [2]

what gives proteoglycans their negative charge? [1]

A
  • Proteoglycans form large aggregates within tissues made up of lots of side chains of negatively charged GAGs
  • **peptide chain with covalently bound sugars. - mainly made of GAGs (glycosaminoglycans)
  • 95% carb, 5% protein**
  • GAG side chains have sulphate group - gives a negative charge. this attracts water and so water moves into ECM
  • gel forming components of ECM.
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16
Q

which molecule causes receptor modulation? [1]

A

B arrestin

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17
Q

what is EC50?

A

Half maximal effective concentration (EC50) refers to the concentration of a drug, antibody or toxicant which induces a response halfway between the baseline and maximum after a specified exposure time.[1]

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18
Q
A
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19
Q

when is each cyclin actived?

A

- G1 checkpoint passed: activates cyclin D (regulates early G1 phase) and cyclin E (regulates early G1 phase and triggers S phase)

  • S checkpoint passed: activates cyclin A (cyclin A acitvates DNA replication in S phase and movement into G2 phase)

- G2 / M checkpoint passed: activates cyclin B (takes cells into mitosis)

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20
Q
A
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21
Q

what are the properties of MHC that ensure the maximum number of peptides can be presented?

A
  • *1. MHC genes are polygenic**: more than one type of MHC class I and MHC class II molecule - can present slightly different range of peptides
  • *2. MHS genes are highly polymorphic**: multple alleles in the population mean that most people are heterozygous for MHC genes. (as a result - mother and father MHC genes are likely to be different - its this what is a barrier to organ transplant)

polygenic and polymorphic of MHC genes ensures mutlple different MHC molecules expressed, increasing the reportoire of peptides that can be presented

22
Q

what is role of integrase (viral protein)?

A

Integrase – integrates viral DNA with host genome

23
Q

how do u work out 1/2 life of a drug?

A
24
Q

what is the mechanism for cytotoxic / CD8 cells knowing which exact target cells to bind to?

A
  • CD8 cell comes close to potential target cell
  • creates a non-specific adhesion with the target cell
  • then, the TCR binds with MHC-I (which holds pathogen peptide)
  • once activated by TCR, get reorganisation of the microtubule organising centre, and GA, lytic granules in the CD8 cell, to line up close to TCR-MHC-I
  • lytic granule release occurs
  • apoptosis
25
Q

state the 3 mechanisms of spontaneous mutations [3]

A

1. tautomeric shift (base substitution)

2. depurination
- loss of a purine base (A or G)
- leads to deletion mutation
(can occur in double DNA helix)

  • *3. deamination**
  • removal of the amino (-NH3) group through hydrolysis water
  • leads to substitution reaction

2 & 3 corrected by: polymerase enzymes

26
Q

how can some pathogens resist toxic oxygen derived substances from host? [2]

A

detoxifcation of oxygen derived harmful substances from the host:

e.g. some microbes have:

  • superoxide dismutase (SOD): neutralises free radicals such as O2
  • *- catalase (breaks down H2O2):** e.g. Staph. aureas
27
Q

what happens to drugs if reabsorbed back into bile?

phase 1 drug? [1]
phase 2 drug? [1]

A

what happens to drugs if reabsorbed back into bile?

  • *i) phase 1 drug:** reabsorbed from GI system and goes back to liver 4 further met.
  • *ii) phase 2 drug**: exits via defecation
28
Q

define drug

a) tachyphylaxis [1]
b) tolerance [1]

A

define drug

a) tachyphylaxis [1] acute tolerance from rapid and repeated admin of drugs in short intervals
b) tolerance [1] chronic longer term admin can reduce drug effect (e.g. alchohol)

29
Q

explain how 1) smoking and 2) uv can cauese cancer

A

smoking
- (benzopryene (BP) from smoke is oxidised (x2))- results in BPDE (ultimate carcinogen)

  • BPDE forms adduct with guanosine residues in lung epithelial cells
  • occurs often in tumour suppressor genes, such as p53

UV:
- damage in basal cells of melansomes (particularly keratinocytes)

  • p53 implicated
  • formation of cylobutane pyrmindine dimers (CPD) covalent bonds form between 2 adjacent pyrimidines in same DNA strand. VERY STRONG BOND
30
Q

what are the properties of MHC that ensure the maximum number of peptides can be presented?

A
  • *1. MHC genes are polygenic**: more than one type of MHC class I and MHC class II molecule - can present slightly different range of peptides
  • *2. MHS genes are highly polymorphic**: multple alleles in the population mean that most people are heterozygous for MHC genes. (as a result - mother and father MHC genes are likely to be different - its this what is a barrier to organ transplant)

polygenic and polymorphic of MHC genes ensures mutlple different MHC molecules expressed, increasing the reportoire of peptides that can be presented

31
Q

what is the baltimore classifcation for:

  • coronavirus
  • influenza
  • HIV
A
  • coronavirus: (+)ssRNA viruses
  • influenza :(-)ssRNA viruses
  • HIV: ssRNA-RT viruses
32
Q

what are the DNA and RNA start and stop codons?

A

RNA: start - AUG. (methionine) stop - UAA, UGA, UAG

DNA: start - ATG. stop - TAA, TGA, TAG

-

33
Q

what is clearance?

how calculate?

A

clearance: rate of elimination in relation to the drug concentration

clearance = rate of elimination (through urine) / concentration remaining (in blood plasma)

34
Q

how does muscarininc acetylcholine receptor work?

A
  • acteylcholine binds to acteylcholine receptor
  • trimeric G-protein activated
  • alpha subunit of trimeric G-protein binds to activated ion channel
35
Q

whats the equation for chemical buffer system of HCO3?

A
  1. chemical buffer system in blood and ICF (HCO3-): immediate action.
    * *H20 + CO2 ⇌ H2CO3 + HCO3- + H+**
36
Q

how do you test to determine if patient has metabolic acidosis? [1]

A

check anion gap: values greater than 12 = metabolic acidosis

37
Q

what is general difference between response for extracelluar vs intracellular pathogens?

A

extracellular: humoral immune response. secretion of:
- antibodies
- complement proteins
- antimicrobrial peptides

intracellular: can’t secrete cuz pathogen is inside cell
- cytotoxic t cells
- NK cells
- T cell-dependent macrophage activation

38
Q

give 4 examples of molecules that undergo intracellular communication [4]

A

steroid H
thyroid H
vitamin D
retinoids

39
Q

explain how C-myc proto oncogenes cause cancer

A
  • proto-oncogene: c-MYK (~50% of cancers)

- promotion of transcription of cyclin genes (promotes cell cycle progression)

  • c-MYK is correlated with agressive tumour pattern and poor clinical outcome

( - causes increased growth, metabolism, cell adhesion, differentiation and metastasis)

  • seen in: Burkitt lymphoma, breast cancer
40
Q

what are the two types of MHC cells? which cells express each type?

A
  • *MHC Class 1**: expresed by all cells. made from:
  • alpha chain with 3 domains
  • peptide-binding cleft between a1 and 2 (see slide)
  • alpha chain is encoded by MHC.
  • alpha chain associates with B2 microglobulin
  • *MHC Class 2:** expressed by APC cells only
  • alpha and beta chains (both formed by cell)
  • peptide-binding cleft: formed from B1 and alpha1

Both have peptide-binding cleft: but the fit between the amino acid side chains inthe peptide and the grove of MHC molecule determine binding

41
Q

Q

define anion gap

what is the equation to work out anion gap?

what is normal anion gap?

what does it indicate if you have greater than normal anion gap?

A

anion gap: quantity difference between cations (positively charged ions) and anions (negatively charged ions) in serum, plasma, or urine. measure of Na+, Cl- & HC03 in blood

[Na+] - ([Cl-] + [HCO3-]) = 8 to 12 mEq/L

what is normal anion gap: 8-12

high anion gap = acidosis,

42
Q

what are the lytic granules CD8 toxic cells contain? [2]

A

have lytic granules (modified lysosomes), containing:

  • perforin: forms pores in cell membrane
  • granzymes: bind to proteins in cell membrane to get into cell and then: proteases start chopping up proteins in cell.

= apoptosis

43
Q

how does the kidney produce bicarbonate?

A
  • Glutamine -> glucose, HCO3-, NH4+
44
Q

name 4 methods that are acquired antiobiotic resitance mechanisms [4]

A
  • *1. drug inactivation
    2. activation of drug pumps (pump out)
    3. modification of target: e**.g. acquire new gene that methylates Rb, so is resistant to drugs that target Rb.
  • *4. alternative metabolic pathways**: e.g. with FA production, get mutations which mean that enzymes change structure so cant be targeted
45
Q

what is RNA cap made from? which end?

A

5’ end: 7-methly guanoside and triphosphate linkage

46
Q

how do activated NK cells know that a cell is infected? concept of missing self H:?

what happens when NK cell recognises cell as self or not self?

when does an NK cell cause apoptosis?

A

use: missing-self hypothesis:

  • recognition of ‘self’ = inhbition of killing by NK cells
  • recongiition of ‘missing-self’ = killing by NK cells (if not from self - could be from transplant, OR if pregnant - also ‘not from self’ from embryo cells)

SO:

- NK cell recognises that the MHC-I molecules is from own body -> inhib. receptor on NK cell switches off the NK cell

or

- NK cell recognises that the MHC-I molecules is from pathogen (not self) -> inhib. receptor on NK cell still switches off the NK cell
therefore - cytotoxic cells come along instead and kill

BUT: some viruses cause MHC-I cells to be trapped inside the pathogen infected - so cant recognise it.
- but because the MHC-I cells arent present on infected cell, the inhibitory receptors on the NK cells dont recognise the cell as self - cause apoptosis.

47
Q

what are glycoproteins?[1]
where do you find glycoproteins? [1]

what are proteoglycans?[1]
where do you find proteoglycans? [1]

A

▪Glycoproteins:
Molecules made up of proteins and carbohydrates e.g., laminin and fibronectin
Found on the surface of the lipid bilayer of cell membranes (cell surface)

▪Proteoglycans:
Molecules made up of a core protein attached to glycosaminoglycans (GAGs)
Found in connective tissues

48
Q

what is the warburg effect?

A

A

Modification of metabolism to support neoplastic proliferation – Warburg effect:

cancer exhibit glucose fermentation even when enough oxygen - allows proliferating cells to convert nutrients such as glucose more efficiently into biomass promoting anabolism.

49
Q

what are the two mechanisms for cartilage production? [2]1

A

a) Interstitial growth: chondrocytes grow and divide and lay down more matrix inside the existing cartilage f

b) appositional growth: undiff. cells at the surface of the cartilage (perichondrium)

50
Q

which pathways does Ras pathway swtich on

A

AKT & ERK pathways

51
Q

what are the receptors found on lymphocytes? - explain basic overview of adaptive immune system

what receptors found in innate immune system? on which cells/

A
52
Q

how is the great number of receptor diversity generated on antibodies?

A
  • each developing B cells expresses a distinct receptor
  • not different genes for millions of different receptors
  • INSTEAD: diversity is generated by mixing and matching gene segements within the heavy and light chain loci:

- Immunglobin heavy chain has:

a) V segments (40); b) D segments (25); c) J segments (6)
- get splicing of each of ^ to make lots of different genes: combinatorial diversity
- also: additional nucleotides can be added at the joints of ^^ to make more variation: junctional diversity

THEN:
any of immunoheavy chain stuff can associate with any of the light chains: more diversity: combinatorial diversity

EOYS (39 decks)

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