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1
Q

what is paraffin embedding and when is it used?

A

used for preparing a microscope slide. dehydrates the fixed tissue so it can stiffen in order to be cut thinly

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2
Q

what does Haematoxylin bind to and what is there charge?

A

nucleic acids with negative charge

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3
Q

what are the tissue types? what are their origins?

A

connective,epithelia, muscle and neural. Orgin = MAME (meso, all, meso, ecto)

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4
Q

approx how much blood do we have?

A

5L

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5
Q

where are plasma proteins mainly synthesised?

A

liver

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6
Q

what is a Reticulocytes?

A

immature RBC with no nucleus but some organelles

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7
Q

what is platelet? what is its lifespan

A

cell fragment with granules. 8-10days

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8
Q

name the granulocytes

A

neutro, baso and eosinophils

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9
Q

which is the rarest WBC and what is its function

A

basophils - contain histamine

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10
Q

2nd most common WBC and its subtypes?

A

lymphocytes (B, T and NK)

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11
Q

where does haemopoeisis occur? how does this differ in fetus

A

occurs in red bone marrow (axial skeleton and femur). fetus in liver.

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12
Q

what is a fibre? what produces them? what are the main types?

A

protein. fibroblasts. Collagen, Elastin and Reticulin

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13
Q

what and where is ground substance? what are its 3 main components

A

gel-like substance surrounding the cells in connective tissue. made of GAGs (hyaluronic acid), water and glycoproteins.

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14
Q

At rest in a neutral thermal environment the body ____ heat?

A

loses

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15
Q

4 types of heat loss

A

conduction (touch), convection (carried away), radiation and evaporation

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16
Q

At rest in a neutral thermal environment the body loses heat mostly through?

A

conduction (touch), convection (carried away), radiation

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17
Q

Thermoregulation copes better with low or high temps?

A

low

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18
Q

At 45°C, the body cools through? (4)

A

evaporation, cutaneous vasodilation, lethargy and anorexia

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19
Q

a DNA virus cannot be what type of shape?

A

helical

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20
Q

a helical RNA virus always has what?

A

a lipid envelope

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21
Q

why is rotavirus hardy

A

multi-capsid

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22
Q

gold standard for diagnosing infection

A

isolate organism

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23
Q

3 causes of hypoxia to cell

A

reduced blood supply, impaired gas exchange, reduced oxygen carrying capacity of blood

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24
Q

4 mechanisms of cell injury

A

mitochondrial damage, membrane damage, protein misfolding/DNA damge or Ca entry

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25
Q

what is clinically significant about cellular structural changes compared to biochemical ones?

A

Structural cell changes lag behind biochemical ones. (eg MI – myocytes dies after 30 min but no changes in microscope for 12 hours)

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26
Q

when is coagulative necrosis typical?

A

infarcts (except cerebral)

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27
Q

when is liquefactive necrosis typical? what results

A

cerebral infarct -abscess

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28
Q

when is caseous necrosis typical?

A

TB in lungs

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29
Q

what is fibrinoid necrosis?

A

immune-mediated vascular damage

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30
Q

name 5 types of necrosis

A

coag, lique, caseous, fat and fibrionoid

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31
Q

2 significant features of apoptosis

A

cell membrane intact, inflammation usually absent

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32
Q

nerve supply of IV disc? what part of disc

A

recurrent meningeal nerve - only outer third

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33
Q

significance of posterior longitudinal ligament? where does it run

A

branches to cover IV discs while descending. runs in anterior part of vertebral canal

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34
Q

where does ligamentum flavum run?

A

run horizontally on posterior part of vertebral canal b/w lamina

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35
Q

superficial muscles of back? where do they all attach and act?

A

trapezius, deltoid, latissimus dorsi, levator scapulae. attach and act on upper limb

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36
Q

Intermediate muscles of the back? where do they act

A

serratus posterior superior and inferior. act on ribs

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37
Q

deep muscles of back?

A

erector spinae and transversospinalis

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38
Q

parts of erector spinae (medial to lateral)

A

Spinalis, Longissimus & Iliocostalis

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39
Q

what is significant about Lateral border of erector spinae ?

A

corresponds with angle of rib – most common site of rib fracture

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40
Q

nerve supply of back muscles

A

deep get posterior rami. anterior do rest

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41
Q

apart from deep back muscles what else do posterior rami innervate in relation to the spine (2)?

A

facet joints, overlying skin

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42
Q

A molecule that binds to a receptor is a?

A

ligand

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43
Q

why may a partial agonist be better in some cases?

A

partial can be better coz causes less desentitization

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44
Q

why might a partial agonist be less effective in chronic heart failure

A

receptors down-regulate

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45
Q

describe the types of antagonism (3)

A

competitive (at binding site), non-competitive (pathway inhibition or functional/physiological antagonism)

46
Q

3 kinds of allosteric modulation?

A
  1. Modulation of orthosteric ligand affinity 2. Modulation of orthosteric ligand efficacy 3. Modulation of receptor activation level
47
Q

explain surmountable antagonism (competitive antagonism)

A

antagonist will compete with available agonist for receptor binding. Sufficient antagonist will displace the agonist from the binding sites, resulting in a lower frequency of receptor activation. Conversely increased agonist will displace the antagonist

48
Q

explain the outcome of non-competitive antagonists (insurmountable). name one way this is achieved?

A

non-competitive antagonists reduce the magnitude of the maximum response that can be attained by any amount of agonist.
Allosteric modulation.

49
Q

components of an exudate

A

neutrophils, fluid and fibrin

50
Q

5 signs of inflammation

A

redness, pain, heat, swelling, LOF

51
Q

2 roles of neutrophil

A

phagocytosis and enzymes for breakdown of damaged tissue

52
Q

5 causes of acute inflammation

A

infection, trauma, burns, infarction, foreign material

53
Q

causes of pain in acute inflammation

A

bradykinin and prostaglandins

54
Q

cause of fever in acute inflammation

A

IL-1, IL-6, TNF, prostaglandins

55
Q

causes of vasodilation in acute inflammation

A

Histamine, prostaglandins, nitric oxide

56
Q

causes of increased vascular permeability in acute inflammation?

A

Histamine, serotonin, bradykinin, leukotrienes,

57
Q

endothelial activation in acute inflammation?

A

TNF, IL1

58
Q

outcomes of acute inflammation? what leads into each outcome?

A

resolution, healing by repair or chronic inflammation.
minimal tissue damage > resolution.
some tissue damage > organization through phagocytosis and granulomatous tissue formation.
persistent tissue damage > chronic

59
Q

progress of granulation tissue (3)

A

nitially very cellular and vascular, later fibrous, eventually mature scar forms.

60
Q

what is a keloid

A

an overgrowth of granulation tissue at the site of a healed skin injury

61
Q

3 infection that cause granulomatous inflammation other than TB

A

syphillis, fungal, parasitic

62
Q

non-infectious cause of granulomatous inflammation. give 2 examples

A

Deposition of exogenous or endogenous irritant materials e.g. suture, keratin

63
Q

Characteristics of granulomatous inflammation

A

epithelioid macrophages and frequently multinucleate giant cells +/- necrosis

64
Q

mechanism of granuloma activation

A

macrophages present antigen to CD4 T > CD4 T releases Interferon Gamma (activates macrophages) and IL-2 (T ells)

65
Q

what actually occurs in chronic inflammation?

A
  • Ongoing inflammation and tissue damage proceed at the same time as attempts at healing
  • Will persist until the damaging stimulus is eradicated
66
Q

what does bacteria’s cytoplasmic membrane allow it to do?

A

selective interaction with environment: entry of nutrients and elimination of waste

67
Q

describe the difference b/w “core, accessory and pan” genome using E. Coli as an example

A

core is essential for survival (all e coli’s will have this). Accessory is the additional that this specific E. Coli strain will have. Pan is the every gene of all strains of E. Coli

68
Q

describe the structure of gram + and - cell walls

A 
\+ = Peptidoglycan > plasma membrane
- = Outer membrane > peptidoglycan > inner membrane
69
Q

which type of bacteria have a acid-fast wall. why is this significant

A

mycobacteria, cant gram stain

70
Q

which type of gram wall is more porous?

A

positive

71
Q

which type of gram wall has a thin peptidoglycan

A

negative

72
Q

which type of gram stains wall blue

A

positive

73
Q

function of fimbrae? Most of which gram type have these?

A

adhesion to other cells or each other. Negative

74
Q

purpose of flagella?

A

motility

75
Q

function of a capsule (3)? give example of 1 bacteria with a capsule

A

prevent dehyrdation and phagocytosis. Enhance virulence.

Klebsiella

76
Q

what is an endospore? give a bacteria

A

a dormant, tough, and non-reproductive structure produced by certain bacteria eg. Clostridium

77
Q

how do bacteria often penetrate the epithelium? what initiates this

A

pathogen-mediated endocytosis. Initiated by bacterial surface proteins

78
Q

how might a bacteria resist phagocytosis (2)?

A

directly effect phagocyte. interfere with opsonins (compliment or antibodies)

79
Q

how might a bacteria directly effect a phagocyte(2)?

A

kill it (leukocidins), repel it (anti-inflam toxins)

80
Q

name one way a capsule enhance virulence

A

electrostatic repulsion (both neg charged)

81
Q

how do bacteria cause tissue damage (3)

A

toxins (exo and endotoxins), induction of cytokines, induce immunopathology

82
Q

outline process of bacterial pathogenesis

A

colonization > penetration > multiplication > tissue damage

83
Q 
overall function of a Beta LActam? one example. MOA.
What other drug class have same function - give example
A

inhibit cell wall synthesis. Penicillin
Bind cell wall at the d-ala, d-ala terminal >inhibit cell wall synthesis.> abnormal synthesis induces autolytic enzymes > weakens the cell wall > allows water in >bacteria will rupture.

Glycopeptides - vancomycin

84
Q

2 types of resistance to beta lactams? MOA

A
  1. β-lactamases. destroy penicillins (and cephalosporins) by opening the β-lactam ring.
  2. Altered Penicillin Binding protein (PBP). Some bacteria have altered the protein to which penicillin binds. As such the Beta lactams cannot bind as well and the disruption of cell wall synthesis is less effective.
85
Q

where are beta lactamases encoded.

A

bacterial chromosome or by plasmids, some of which can transfer between bacteria, thus spreading resistance

86
Q

what is coamoxyclav?

A

amoxycillin (beta-lactam) and clavulinic acid (beta-lactamse inhibitor).

87
Q

what is vancomycin and when/how is it used?

A

glycopeptide - used IV only on Gram Positive bacteria in penicillin allergic patients or MRSA

88
Q

function MOA of aminoglycosides

A

cause the bacteria to misread the genetic code.
binds to the 30S subunit of bacterial ribosomes > cause distortion of the region where mRNA is translated > incorporation of incorrect amino acids or the premature termination of protein synthesis

89
Q

3 resistance methods to aminoglycosides

A

modified outer membrane leading to reduced entry, enzymatic modification in cytoplasm leading to reduced entry, ribosomal mutation leading to reduced binding and efflux

90
Q

give 2 examples of intrinsic bacterial resistnace

A
  1. All Gram Neg’s resistant to Vancomysin (cant get through cell wall)
  2. Pseudomonas aeruginosa resist to amoxycillin coz of chormosomal encoded genes
91
Q

how can bacteria acquire resistance? (2)

A

mutation and horizontal gene transfer

92
Q

explain the 3 types of horizontal gene transfer. why is the 3rd type worrying?

A
  1. Transformation - DNA fragments of a lysed cell are taken up by a competent bacteria and incorporated into its genome
  2. Phage mediated - infection of bacteria by abnormal bacteriophage
  3. Plasmid mediated - 2 bacteria form cytoplasmic bridge>
    plasmid DNA replicates> is taken up by new bacteria> cells seperate.
    Worrying because bacteria don’t need to be related to receive plasmids
93
Q

what is a bacteriophage?

A

virus that infects bacteria

94
Q

to commence replication what must viruses ultimately produce irrespective of its genome

A

mRNA

95
Q

3 stage viral replication (include sub stages

A
  1. Entry (fusion with membrane via virus receptor > endocytosis).
  2. Replication (uncoating > genome replication >mRNA synthesis > protein synthesis.
  3. release (non enveloped accumulate til cell lysis, enveloped bud out (some secreted out)).
96
Q

name 4 virus induced changes to a cell

A
  1. tumour induction.
  2. accumulate to cause cell lysis
  3. chronic infection - slowly release virus while keeping cell alive.
  4. latent infection - remains inactive in cell until change in circumstances (eg immunosupression)
97
Q

how do viral genomes evolve. give examples of each (3)?

A

mutation - esp. RNA virus
If 2 viruses infect same cell can either:
Recombination - exchange stretches of nucleic acid (esp. DNA virus).
Reassortment - swapping segments of genome (influenza).

98
Q

typical course of viremia?

A

virus infects epithelial cells and multiples > regional lymph node(more replication) > enters blood stream (primary viraemia)> spleen and liver (multiplcation) > enter blood again (2ndary viremia) > focal infection

99
Q

apart from the plasma how else may virus spread. give example

A

cell-mediated - HIV through T cells

100
Q

T/F if false why? An essential step in the replication of all viruses is production of minus sense RNA

A

F - positive strand

101
Q

T/F if false why? Often a conformational change is required to reveal the hydrophobic fusion region of a viral protein.

A

True

102
Q

T/F if false why? Some viruses avoid cytotoxic T cell killing of the infected cell by blocking steps leading up to the loading of peptide onto MHC class I.

A

True

103
Q

T/F Cleavage of the viral haemagglutinin is necessary for viral release from the cell.

A

False - neuraminidase

104
Q

with regard to seasonal influenza Cleavage of the viral haemagglutinin is necessary for what?

A

escape the endosome

105
Q

how often do major flu epidmics occur?

A

2-3 years

106
Q

which types of influenza infect Humans? can either of these infect other species?

A

A and B. A can infect other species

107
Q

why is influenza limited to resp tract?

A

cleavage of the haemagglutinin can only be done by enzymes secreted by Clara cells

108
Q

explain the nomenclature of Influenza type A subtyping

A

different haemagglutinins and neuraminidases. Expressed as HA(H1-H16) and NA(N1-N9) eg. H5N1

109
Q

ancestral host of influenza type A

A

aquatic birds

110
Q

name the 3 subtypes of flu that have infected man in recent decades. which 2 arecurrent?

A

H1N1, H2N2, H3N2 (go in order except last number). H1N1 and H3N2 current

111
Q

one part of influenza is extremely antigenic, which part and brief description

A

epitopes of HA have 5 antigenic sites

112
Q

targets of flu vaccine (2)?

A

antibody to HA blocks attachment. antiobdy to NA blocks release

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