Week 1 and 2
Week 3 and 4
Week 5
Week 6
100
what are the two stages of hypersensitivity?


1. sensitisation

2. elicitation

100

list the 5 main causative agents of malaria

  • P flaciparum
  • Pp vivax
  • P ovale
  • P malariae
  • P nowlesi
100

what are the two types of gene expressions in a tissue

1. specific

2. house keeping genes

100

describe the structure and function of platelets

they are a component of blood whose function (along with the coagulation factors) is to react to bleeding from blood vessel injury by clumping, thereby initiating a blood clot.[1] Platelets have no cell nucleus: they are fragments of cytoplasm that are derived from the megakaryocytes

200

What are the immune reactants for the 4 types of hypersensitivities?

1 = IGE

2 = IGG

3 = IGG

4 = TH1 Cells, TH2 Cells, CTL

200

what are the 4 malignant tumour that end with oma

  • Lymphoma
  • Melanoma
  • Mesothelioma
  • Myeloma
200

what is the main diffenrece between leukaemia and lymphoma 

- where they oringinate from 

- leukaemia is maimnly the bone amrrow

lymohoma is mainly the lymph nodes, spleen, thymus etc...

200

what is the hardy Weinberg principle (provide equation)

p2+2pq+q2=1

300

what are the three factors that control ventilation? describe each.


1. airway resistance--> resistance to airflow

2. alveolar surface tension--> this is the pull of the water molecules on the surface of the littlee alveolar sacs

3. lung compliance--> this is the extent to which the lung volume will expand for a given increase in trans pulmonary pressure

300

list 7 side effects of chemotherapy

  • Anaemia
  • Diarhoea
  • Infection
  • Nausea and vomiting
  • Neutropenia
  • Skin reactions
  • Thrombocytopenia
300

blood stem cells come from the bone marrow. what two main stem cells do we get from this

- myeloid stem cell

- lymphoid stem cell

300

provide and explain 2 example of genetic drift

1. founder effect-->-Reduction in genetic variation that results when a small subset of a large population is used to establish a new colony

2. genetic bottleneck-->-Dramatic reduction in population size (& thus its  genetic variation) due to a stochastic event (-e.g. environmental disaster, habitat destruction, hunting to near extinction)


400

name the laryngeal muscles and their nerve supply 

- cricothyroid--> external laryngeal nerve

- thyroarytenoid--> recurrent laryngeal nerve

- posterior cricoarytenoid-->"

- lateral cricoarytenoid-->   "

- transverse and oblique arytenoids--> "

400

list the differences between benign and malignant tumours

  • benign
  •  Local growth
    • Don't spread anywheer
    • Little variation formt he      abnornal to normal cells (little pleomorphisms)
    • Expansile
    • Little necrosis
    • Slow drowth
    • Suffix is usually oma
    • Grow slowly and capsules form aroudn them
  •  
  • Malignant
  •  
    • Has it spread somehere else
    • Infiltrative
    • More pleomorhpic
    • Much necrosis
    • Rapid gorwth
    • Suffix is usually carcinoma      or sarcoma
    • No capsule
400

list and describe the enzymes involved in chromatin remodelling

  • Histon acetyltrasnferase     (HAT)
    • This adds an acetyl group
    • This enhances gene expresion
  • Histone deacetylase (HDAC)
    • This removes acetyl groups
    • This supresses gene      expression
400

what are the 5 factors that can disturb hardy Weinberg equilibrium?


1.Mutation

2.Non-random mating

3.Selection (e.g. natural selection, reproductive fitness)

4.Small population size

5.Migration (gene flow)

500

draw and label waldeyers ring

top = adenoid

lower = tubal

underneath = palatine

bottom = linguinal

500

list and describe the 6 key features to cytotoxic chemotherapy

  • Cell kill
    • Is the drug able to kill      cells
    • Note that we can never kill      the last cancer cell because the sqaure root of 1 is 1
    • Chemotherapy is toxic to      noraml plus malignant cells
  • Kill mechanisms
    • By wha tmechanisms does it      od it
      • Is it a speciifc part of       the cell cycle or is it across a number of parts of the cycle
    • We don’t have gruds that are      particuallrly useful durign the g0 phase
    • In g1 phase (where we      synthesisise the comoponent of DNA
      • The durgs can work at that       biochemcial level, such as anti-metabolites
    • When we go to s and DNA      synthesis, we look at drugs that can stop that syntthetic process
    • When we move into g2      microtoubule inhitors are useful
  • Administer cyclically
    • Are we able to give it in      some sort of cyclcical way?
    • The reason we give it in      cycles is because we are killing fboth cancer cells and normal cells
      • We just hope we kill more       nomral cells than cancer cells
    • So you need a rest period      between those cycles of chemotherpay, aprticaullary toa allow white cells      to regenerate sufficiently so that the patient doesn’t become serously      infected
  • Give as combinaiton
    • Should it eb given in a      combination
    • Using a combinatino can      reduce or mitigate the possibility of resistance by targeting more than      one mechanism 
  • Resistance
    • What likelihood is      resistance
  • Dose instensity/toxicity
500

list and descriube the 2 aspects of epigenetics

  • Histone acetylation and DNA     methylation
    • Histone acetylation
      • You favour gene expression
      • This si an addition of an acetyl group to the tail of the histones
        • This reduces the attraction of the histone s with the DNA
    • DNA methylation
      • You inhibit gene expression
      • After replication, DNA is often modified by addition of methyl groups
      • Occurs most often in the C of CG doublets
      • A lot of CpG islands are methylated
      • As soon as you have cytosine residue methylated it is going to be recognised by MBD (methyl-cpg-Binding domain)
500

demonstrate a haematological examination

GOOD LUCK!