Shit you just gotta know - Foundation to Resp Flashcards
4 types of heat loss
conduction (touch), convection (carried away), radiation and evaporation
approx how much blood do we have?
5L
a DNA virus cannot be what type of shape?
helical
4 mechanisms of cell injury
mitochondrial damage, membrane damage, protein misfolding/DNA damge or Ca entry
a helical RNA virus always has what?
a lipid envelope
when is coagulative necrosis typical?
infarcts (except cerebral)
2 significant features of apoptosis
cell membrane intact, inflammation usually absent
nerve supply of IV disc? what part of disc
recurrent meningeal nerve - only outer third
significance of posterior longitudinal ligament? where does it run? where does ligamentum flavum run?
branches to cover IV discs while descending. runs in anterior part of vertebral canal.
LF = run horizontally on posterior part of vertebral canal b/w lamina
superficial muscles of back? where do they all attach and act?
trapezius, deltoid, latissimus dorsi, levator scapulae. attach and act on upper limb
describe the types of antagonism (3)
competitive (at binding site), non-competitive (pathway inhibition or functional/physiological antagonism)
3 kinds of allosteric modulation?
- Modulation of orthosteric ligand affinity 2. Modulation of orthosteric ligand efficacy 3. Modulation of receptor activation level
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
5 signs of inflammation
redness, pain, heat, swelling, LOF
2 roles of neutrophil
phagocytosis and enzymes for breakdown of damaged tissue
5 causes of acute inflammation
infection, trauma, burns, infarction, foreign material
causes of pain in acute inflammation
bradykinin and prostaglandins
cause of fever in acute inflammation
IL-1, IL-6, TNF, prostaglandins
causes of vasodilation in acute inflammation
Histamine, prostaglandins, nitric oxide
causes of increased vascular permeability in acute inflammation?
Histamine, serotonin, bradykinin, leukotrienes,
endothelial activation in acute inflammation?
TNF, IL1
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
3 infection that cause granulomatous inflammation other than TB
syphillis, fungal, parasitic
non-infectious cause of granulomatous inflammation. give 2 examples
Deposition of exogenous or endogenous irritant materials e.g. suture, keratin
mechanism of granuloma activation
macrophages present antigen to CD4 T > CD4 T releases Interferon Gamma (activates macrophages) and IL-2 (T ells)
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
describe the structure of gram + and - cell walls
\+ = Peptidoglycan > plasma membrane - = Outer membrane > peptidoglycan > inner membrane
how do bacteria cause tissue damage (3)
toxins (exo and endotoxins), induction of cytokines, induce immunopathology
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
2 types of resistance to beta lactams? MOA
- β-lactamases. destroy penicillins (and cephalosporins) by opening the β-lactam ring.
- 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.
what is coamoxyclav?
amoxycillin (beta-lactam) and clavulinic acid (beta-lactamse inhibitor).
what is vancomycin and when/how is it used?
glycopeptide - used IV only on Gram Positive bacteria in penicillin allergic patients or MRSA
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
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
how can bacteria acquire resistance? (2)
mutation and horizontal gene transfer
explain the 3 types of horizontal gene transfer. why is the 3rd type worrying?
- Transformation - DNA fragments of a lysed cell are taken up by a competent bacteria and incorporated into its genome
- Phage mediated - infection of bacteria by abnormal bacteriophage
- 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
to commence replication what must viruses ultimately produce irrespective of its genome
mRNA
name 4 virus induced changes to a cell
- tumour induction.
- accumulate to cause cell lysis
- chronic infection - slowly release virus while keeping cell alive.
- latent infection - remains inactive in cell until change in circumstances (eg immunosupression)