Principles knowledge corrections Flashcards
strict aerobes
pseudomonas - gram -ve
legionella - gram -ve
viruses contain
RNA/DNA
what antibiotics act on bacterial cell wall
penicillins, cephalosporins, glycopeptides
penicilins
safe in preg, exreted via kidney, bactericidal
phenoxymethyl - penicillin
penicilin V
beta lactamase
destroys amoxicillin
co- amoxiclav
tracts everything apart from pseudomonas and MRSA
cephalosporins
bactericidal, sage in preg, excreted via kidneys and urine
gentamicin
aminoglycosides antibiotics, bacteriostatic and bactericidal, not safe in preg , excreted via urine
antibiotics that act on bacterial DNA
metronidazole, trimethoprium +/- sulphanimide, fluroquinolones
sulphanimide- bacteriostatic and makes co-trimoxazole
antibiotics causing C.diff
ciprofloaxan, co- amxoxiclav, clindamycin, cephalosporins/ cefriaxone
acrocentric chromosomes
p arm too short
aneuploidy
abnormal no. of chromosome s
monosomy- 1 missing
trisomy- extra
Robertsonian translocation
chromosome attaches to another chromosome at centromere
13,14,15,21,22
x linked disease
disease on X chromosome
female carriers- 0.5 M and F kids affected
M carriers- F kids carriers
epigenetic variation
changes in the genome that don’t change nucleotide sequence
methylation
inhibits DNA transcription
5 types of leukocytes/ WBC
neutrophils, basophils, mast cells, eosinophils, monocytes, lymphocytes
major opsonins
C3b, collectins, Fc of IgG, CRP
oxidative killing
NADPH oxidase
O2 to free radicals
interferons
limits viral infections
interleukons
tell cells to differentiate
produced by T cells
classical pathway
C1,C4, C2,C3
lectin pathway
manose binding lectin to carbs
no antibodies cause this is like C1 binding
complement inhibitors
C1, factor I and H, C4 binding protein , CD59
IgE activates
mast cells
T cell activation
MHC binding T cell receptor
B7 binding to CD28
IL-4, IL-5, IFNy
activates B cells and increases killing
pro inflammatory cytokines
IL-1, IL-6, TNF
AA groups
non polar hydrophobic, polar uncharged, acidic, basic
central dogma
DNA transcribed to RNA
translated to protein
Pol I, II and III
Pol I and III synthesise stable RNA
Pol II - all RNA
can enzymes change equilibrium position
no
apoenzymes
enzyme without co factor
isoenzymes
catalyse same reactions as enzymes but diff structure
CK
isoenzyme, M form made in skeletal muscle , B form in brain, MB form in heart
Zymogens
inactive precursors of enzymes
comp inhibition
vmax same
km increased
non comp inhibition
vmax lower
km same
T and R
T- enzyme inactive
R- active when there is a substrate
-ve electron transfer protiential
more likely to donate electrons than H2
Vd/ volume distribution
dose/ plasma con
volume where drug is dissoleved
sympathetic pre ganglionic
AcH
cholinergenic
sympathetic post ganglionic
adrenergic
noradrenaline
U1
post ganglionic neurone
Noradrenaline taken up by and broken down by
taken by U2
broken down by COMT
Co/ initial con
D/Vd
t 1/2
0.69 Kel
1rst order kinetic drugs
dose changes Cp but not t 1/2
resting membrane potential/ Vm
-70mV
Na+ channel activation cascade
+ve feedback
refractory period of AP
inactivated Na channels, repolarisation to closed state
supparation
pus, living and dying cells, dead neutrophils, debris, bacteria
granulomatous tissue formation
cappilaries grow into inflammatory exudate with macroohages and fibroblasts
angiogenesis, fibroblast prolycration and collegen synthesis
barretts oesophagus
squamous to glandular epithelium
senescence
deterioation of cell function
modulators of angiogenesis
hypoxia, VEGF, TNF alpha
how to sarcomas metastasise
haematogenous
onogenes
PDGF, ras, src
N1
1-3 lymph nodes
N2
4+ lymph nodes affect
tight junctions
join lateral edges of epithelium cells near apical membranes
Na, K pump
3Na+ out
2K in
2ndary active transport
symport (solute and ion move in the same direction)
antiport- move in opposite directions
baroreceptors
control MAP located in aortic arch and carotid bodies
control centre- meduella oblongata
effectors- heart and blood vessels
CO
volume of blood pumped by each ventricle/ min
SV x HR
SV
volume of blood pumped by each ventricle/ heart beat
in starvation what controls glucose
cortisol and GH
insulin decreases glucose
uptake of glucose by muscle and fat cells
activate liver enzymes
glucose to glucagon
glucagon increases glucose
increase glycogenolysis/ inhibits glycogen synthesis
cortisol increases glucose
stimulate protien catabolism, lypolysis and gluconeogenesis