SSS FunMed Flashcards
(52 cards)
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
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
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 !!
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
5
Q
where do drugs with large / small VD distributed to?
A
Large VD: distributed to tissues (fat / bones)
Small VD: distributed to blood
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
7
Q
what colour does ziehl-neelosn stain turn mycobacteria? [1]
A
red
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
9
Q
which antibiotics do you use on:
- gram +ve? [1]
- gram -ve ? [1]
A
glycopeptide antibiotics: gram postive
polymyxins: gram negative
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
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
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 !
13
Q
how can some bacteria destroy IgA? [1]
A
using IgA proteases
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
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.
16
Q
which molecule causes receptor modulation? [1]
A
B arrestin
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]
18
Q
A
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)
20
Q
A
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
state the 3 mechanisms of spontaneous mutations [3]
**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
how can some pathogens resist toxic oxygen derived substances from host? [2]
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
what happens to drugs if reabsorbed back into bile?
phase 1 drug? [1]
phase 2 drug? [1]
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
# define drug
a) tachyphylaxis [1]
b) tolerance [1]
# 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
## Footnote
explain how 1) smoking and 2) uv can cauese cancer
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
what are the properties of MHC that ensure the maximum number of peptides can be presented?
* *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
what is the baltimore classifcation for:
- coronavirus
- influenza
- HIV
- coronavirus: (+)ssRNA viruses
- influenza :(-)ssRNA viruses
- HIV: ssRNA-RT viruses
32
what are the DNA and RNA start and stop codons?
**RNA**: start - AUG. (methionine) stop - UAA, UGA, UAG
**DNA**: start - ATG. stop - TAA, TGA, TAG
-
33
what is clearance?
how calculate?
clearance: rate of elimination in relation to the drug concentration
## Footnote
**clearance = rate of elimination (through urine) / concentration remaining (in blood plasma)**
34
how does muscarininc acetylcholine receptor work?
- acteylcholine binds to acteylcholine receptor
- trimeric G-protein activated
- alpha subunit of trimeric G-protein binds to activated ion channel
35
whats the equation for chemical buffer system of HCO3?
1. chemical buffer system in blood and ICF (HCO3-): immediate action.
* *H20 + CO2 ⇌ H2CO3 + HCO3- + H+**
36
how do you test to determine if patient has metabolic acidosis? [1]
check anion gap: **values greater than 12 = metabolic acidosis**
37
what is general difference between response for extracelluar vs intracellular pathogens?
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
give 4 examples of molecules that undergo intracellular communication [4]
**steroid H
thyroid H
vitamin D
retinoids**
39
explain how C-myc proto oncogenes cause cancer
- 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
what are the two types of MHC cells? which cells express each type?
* *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
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?
**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
what are the lytic granules CD8 toxic cells contain? [2]
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
how does the kidney produce bicarbonate?
- Glutamine -\> glucose, HCO3-, NH4+
44
name 4 methods that are acquired antiobiotic resitance mechanisms [4]
* *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
what is RNA cap made from? which end?
5' end: 7-methly guanoside and triphosphate linkage
46
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?
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
what are glycoproteins?[1]
where do you find glycoproteins? [1]
what are proteoglycans?[1]
where do you find proteoglycans? [1]
▪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
what is the warburg effect?
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
what are the two mechanisms for cartilage production? [2]1
a) **Interstitial growth**: chondrocytes grow and divide and lay down more matrix inside the existing cartilage f
**b) appositional growt**h: undiff. cells at the surface of the cartilage (perichondrium)
50
which pathways does Ras pathway swtich on
AKT & ERK pathways
51
what are the receptors found on lymphocytes? - explain basic overview of adaptive immune system
what receptors found in innate immune system? on which cells/
52
how is the great number of receptor diversity generated on antibodies?
- 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
