All Flashcards
(112 cards)
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
2
Q
what does Haematoxylin bind to and what is there charge?
A
nucleic acids with negative charge
3
Q
what are the tissue types? what are their origins?
A
connective,epithelia, muscle and neural. Orgin = MAME (meso, all, meso, ecto)
4
Q
approx how much blood do we have?
A
5L
5
Q
where are plasma proteins mainly synthesised?
A
liver
6
Q
what is a Reticulocytes?
A
immature RBC with no nucleus but some organelles
7
Q
what is platelet? what is its lifespan
A
cell fragment with granules. 8-10days
8
Q
name the granulocytes
A
neutro, baso and eosinophils
9
Q
which is the rarest WBC and what is its function
A
basophils - contain histamine
10
Q
2nd most common WBC and its subtypes?
A
lymphocytes (B, T and NK)
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.
12
Q
what is a fibre? what produces them? what are the main types?
A
protein. fibroblasts. Collagen, Elastin and Reticulin
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.
14
Q
At rest in a neutral thermal environment the body ____ heat?
A
loses
15
Q
4 types of heat loss
A
conduction (touch), convection (carried away), radiation and evaporation
16
Q
At rest in a neutral thermal environment the body loses heat mostly through?
A
conduction (touch), convection (carried away), radiation
17
Q
Thermoregulation copes better with low or high temps?
A
low
18
Q
At 45°C, the body cools through? (4)
A
evaporation, cutaneous vasodilation, lethargy and anorexia
19
Q
a DNA virus cannot be what type of shape?
A
helical
20
Q
a helical RNA virus always has what?
A
a lipid envelope
21
Q
why is rotavirus hardy
A
multi-capsid
22
Q
gold standard for diagnosing infection
A
isolate organism
23
Q
3 causes of hypoxia to cell
A
reduced blood supply, impaired gas exchange, reduced oxygen carrying capacity of blood
24
Q
4 mechanisms of cell injury
A
mitochondrial damage, membrane damage, protein misfolding/DNA damge or Ca entry
25
what is clinically significant about cellular structural changes compared to biochemical ones?
Structural cell changes lag behind biochemical ones. (eg MI – myocytes dies after 30 min but no changes in microscope for 12 hours)
26
when is coagulative necrosis typical?
infarcts (except cerebral)
27
when is liquefactive necrosis typical? what results
cerebral infarct -abscess
28
when is caseous necrosis typical?
TB in lungs
29
what is fibrinoid necrosis?
immune-mediated vascular damage
30
name 5 types of necrosis
coag, lique, caseous, fat and fibrionoid
31
2 significant features of apoptosis
cell membrane intact, inflammation usually absent
32
nerve supply of IV disc? what part of disc
recurrent meningeal nerve - only outer third
33
significance of posterior longitudinal ligament? where does it run
branches to cover IV discs while descending. runs in anterior part of vertebral canal
34
where does ligamentum flavum run?
run horizontally on posterior part of vertebral canal b/w lamina
35
superficial muscles of back? where do they all attach and act?
trapezius, deltoid, latissimus dorsi, levator scapulae. attach and act on upper limb
36
Intermediate muscles of the back? where do they act
serratus posterior superior and inferior. act on ribs
37
deep muscles of back?
erector spinae and transversospinalis
38
parts of erector spinae (medial to lateral)
Spinalis, Longissimus & Iliocostalis
39
what is significant about Lateral border of erector spinae ?
corresponds with angle of rib – most common site of rib fracture
40
nerve supply of back muscles
deep get posterior rami. anterior do rest
41
apart from deep back muscles what else do posterior rami innervate in relation to the spine (2)?
facet joints, overlying skin
42
A molecule that binds to a receptor is a?
ligand
43
why may a partial agonist be better in some cases?
partial can be better coz causes less desentitization
44
why might a partial agonist be less effective in chronic heart failure
receptors down-regulate
45
describe the types of antagonism (3)
competitive (at binding site), non-competitive (pathway inhibition or functional/physiological antagonism)
46
3 kinds of allosteric modulation?
1. Modulation of orthosteric ligand affinity 2. Modulation of orthosteric ligand efficacy 3. Modulation of receptor activation level
47
explain surmountable antagonism (competitive antagonism)
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
explain the outcome of non-competitive antagonists (insurmountable). name one way this is achieved?
non-competitive antagonists reduce the magnitude of the maximum response that can be attained by any amount of agonist.
Allosteric modulation.
49
components of an exudate
neutrophils, fluid and fibrin
50
5 signs of inflammation
redness, pain, heat, swelling, LOF
51
2 roles of neutrophil
phagocytosis and enzymes for breakdown of damaged tissue
52
5 causes of acute inflammation
infection, trauma, burns, infarction, foreign material
53
causes of pain in acute inflammation
bradykinin and prostaglandins
54
cause of fever in acute inflammation
IL-1, IL-6, TNF, prostaglandins
55
causes of vasodilation in acute inflammation
Histamine, prostaglandins, nitric oxide
56
causes of increased vascular permeability in acute inflammation?
Histamine, serotonin, bradykinin, leukotrienes,
57
endothelial activation in acute inflammation?
TNF, IL1
58
outcomes of acute inflammation? what leads into each outcome?
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
progress of granulation tissue (3)
nitially very cellular and vascular, later fibrous, eventually mature scar forms.
60
what is a keloid
an overgrowth of granulation tissue at the site of a healed skin injury
61
3 infection that cause granulomatous inflammation other than TB
syphillis, fungal, parasitic
62
non-infectious cause of granulomatous inflammation. give 2 examples
Deposition of exogenous or endogenous irritant materials e.g. suture, keratin
63
Characteristics of granulomatous inflammation
epithelioid macrophages and frequently multinucleate giant cells +/- necrosis
64
mechanism of granuloma activation
macrophages present antigen to CD4 T > CD4 T releases Interferon Gamma (activates macrophages) and IL-2 (T ells)
65
what actually occurs in chronic inflammation?
* Ongoing inflammation and tissue damage proceed at the same time as attempts at healing
* Will persist until the damaging stimulus is eradicated
66
what does bacteria's cytoplasmic membrane allow it to do?
selective interaction with environment: entry of nutrients and elimination of waste
67
describe the difference b/w "core, accessory and pan" genome using E. Coli as an example
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
describe the structure of gram + and - cell walls
```
+ = Peptidoglycan > plasma membrane
- = Outer membrane > peptidoglycan > inner membrane
```
69
which type of bacteria have a acid-fast wall. why is this significant
mycobacteria, cant gram stain
70
which type of gram wall is more porous?
positive
71
which type of gram wall has a thin peptidoglycan
negative
72
which type of gram stains wall blue
positive
73
function of fimbrae? Most of which gram type have these?
adhesion to other cells or each other. Negative
74
purpose of flagella?
motility
75
function of a capsule (3)? give example of 1 bacteria with a capsule
prevent dehyrdation and phagocytosis. Enhance virulence.
| Klebsiella
76
what is an endospore? give a bacteria
a dormant, tough, and non-reproductive structure produced by certain bacteria eg. Clostridium
77
how do bacteria often penetrate the epithelium? what initiates this
pathogen-mediated endocytosis. Initiated by bacterial surface proteins
78
how might a bacteria resist phagocytosis (2)?
directly effect phagocyte. interfere with opsonins (compliment or antibodies)
79
how might a bacteria directly effect a phagocyte(2)?
kill it (leukocidins), repel it (anti-inflam toxins)
80
name one way a capsule enhance virulence
electrostatic repulsion (both neg charged)
81
how do bacteria cause tissue damage (3)
toxins (exo and endotoxins), induction of cytokines, induce immunopathology
82
outline process of bacterial pathogenesis
colonization > penetration > multiplication > tissue damage
83
```
overall function of a Beta LActam? one example. MOA.
What other drug class have same function - give example
```
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
2 types of resistance to beta lactams? MOA
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
where are beta lactamases encoded.
bacterial chromosome or by plasmids, some of which can transfer between bacteria, thus spreading resistance
86
what is coamoxyclav?
amoxycillin (beta-lactam) and clavulinic acid (beta-lactamse inhibitor).
87
what is vancomycin and when/how is it used?
glycopeptide - used IV only on Gram Positive bacteria in penicillin allergic patients or MRSA
88
function MOA of aminoglycosides
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
3 resistance methods to aminoglycosides
modified outer membrane leading to reduced entry, enzymatic modification in cytoplasm leading to reduced entry, ribosomal mutation leading to reduced binding and efflux
90
give 2 examples of intrinsic bacterial resistnace
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
how can bacteria acquire resistance? (2)
mutation and horizontal gene transfer
92
explain the 3 types of horizontal gene transfer. why is the 3rd type worrying?
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
what is a bacteriophage?
virus that infects bacteria
94
to commence replication what must viruses ultimately produce irrespective of its genome
mRNA
95
3 stage viral replication (include sub stages
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
name 4 virus induced changes to a cell
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
how do viral genomes evolve. give examples of each (3)?
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
typical course of viremia?
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
apart from the plasma how else may virus spread. give example
cell-mediated - HIV through T cells
100
T/F if false why? An essential step in the replication of all viruses is production of minus sense RNA
F - positive strand
101
T/F if false why? Often a conformational change is required to reveal the hydrophobic fusion region of a viral protein.
True
102
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.
True
103
T/F Cleavage of the viral haemagglutinin is necessary for viral release from the cell.
False - neuraminidase
104
with regard to seasonal influenza Cleavage of the viral haemagglutinin is necessary for what?
escape the endosome
105
how often do major flu epidmics occur?
2-3 years
106
which types of influenza infect Humans? can either of these infect other species?
A and B. A can infect other species
107
why is influenza limited to resp tract?
cleavage of the haemagglutinin can only be done by enzymes secreted by Clara cells
108
explain the nomenclature of Influenza type A subtyping
different haemagglutinins and neuraminidases. Expressed as HA(H1-H16) and NA(N1-N9) eg. H5N1
109
ancestral host of influenza type A
aquatic birds
110
name the 3 subtypes of flu that have infected man in recent decades. which 2 arecurrent?
H1N1, H2N2, H3N2 (go in order except last number). H1N1 and H3N2 current
111
one part of influenza is extremely antigenic, which part and brief description
epitopes of HA have 5 antigenic sites
112
targets of flu vaccine (2)?
antibody to HA blocks attachment. antiobdy to NA blocks release
