ICS Flashcards
cardinal signs of inflammation
rubor
calor
dolor
tumor
loss of function
main cells in acute and chronic inflammation
acute- neutrophils
chronic- macrophages and lymphocytes
what wbc is raised during viral infection
white blood cell
causes of acute inflammation
microbial infections
hypersensetivity
physical agents, trauma, heat/ cold
chemicals
bacterial toxins
causes of chronic inflammation
autoimmune condition
primary granulomatous disease
transplant rejection
necrotic tissue
stages of inflammation
increase in vessel calibre- vasodilation is mediated by bradykinin, prostacyclin, NO
fluid exudate- vessels get leaky and fluid is forced out
cellular exudate- wbc especially neutrophils leave vessels
neutrophil action in acute inflammatiomm
margination- to edge of bv
adhesion- selectins facilitate binding of neutrophil to endothelium- then roll along bv margin
emigration+ diapedisis- formation of cellular exudate when neut leaves bv, other rbc following it
chemotaxis- cells following cytokines to site of inflammation
@ site of inflam- phagocytosis, phagolysosome + bacteira killing, macrophages clear debris
outcomes of acute inflammation
resolution
supparation- puss
organisation- form granulation tissue or fibrotic tissue- cardiac tissue or neurons never resonve- may become this at best
progression to chronic
define granuloma
aggregate of epitheloid histocytes- baso a bunch of macrophages around central pathogen
granuloma + eosinophil
parasite
granulomas secrete what blood marker
ACE
examples of granulomatous diseases
tb, chrons, leprosy, sarcoidosis
thrombi definition
mass of blood constituents - mainly platelets- forming in vessels during life
stages of throbosis
1- vasospasm
2- primary platelet plug formation- vwf binds to exposedd collagen and then platelet binds to that and get activated. discoid- pseudopoid and platelets bind together
3- coagulaition cascade (intrisic is 12,11,9,8, extrrinsic 3,7,10) to make fibrin mesh
4- plasminogen- plasmin
what influences thrombosis
virchows triad
endotheliam injury - smoking, mi, trauma
hypercoagubility- sepsis, cancer, contraceptives
abnormal bloodflow- af, venous stasis
arterial thrombosis cause, pressure, made from, lead to, treatment
atherogenesis, high pressure
made of platelets
lead to mi or stroke
antiplatelets like aspirin
venous thrombosis cause , pressure, made from, lead to, treatment
venous stasis
low pressure
rbc
dvt/pe
anti-coagulants like warfarin or heparin
eg of an antiplatelet and anticoaguland
antiplatelet- aspirin
anticoagulant- warfarin, heparin
outcomes of thrombi
resolution- plasmin degrades clot
organization- forms scar tissue, cardiac/ neurons at best go back to this
embolism- fragments break off and lodge in distal circulation
ischaemia vs infarction
ischaemia- reduction in blood flow- cardiomyoctes and cerebral neurones most vunerable to this
infatction- reduction in blood flow so severe it leads to cellular deaths
what organs have dual blood supply and therefore r less suseptable to infarctiom
liver
brain
lungs
what can embolism in systemic circulation lead to
atrial fibrilation or ischemic stroke
what can venous embolism lead to
pulmonary embolism if it enters pulmonary artery
apoptosis definition
non inflammatory, programmed cell death- avoids damage to surrounding cells
chromatin ulaltered, cells shrink, organeles retained and cell surface membrane stays intact
what is p53
protein that detects dna damage and triggers apoptosis
apoptosis in cancer and hiv
cancer- dont apoptose when expected to
hiv- t helper cells apoptose
mechanisms of apoptosis
intrinsic- cytochrome c activates caspases
extrinsic- fas ligands or tnf ligands bind to cell surface receptors and activate caspases
cytotoxic– cytotoxic t cells release granzyme b- perforin- caspases
necrosis- def, where does it occur
inflammatory and traumatic cell death where large number of cells die due to external factor- infarction / frostbite
cells burst and organelles splurge out, chromatin mutation is likely
what is the main protein involved in apoptosis
caspases
hypertrophy
tissue increases in size bc cells get bigger- eg muscle cells
hyperplasia
tissue increases in size bc no. of cells increase via mitosis
atrophy
tissue sizs decreases bc number of cells or size of cell decreases
metaplasia
change from one type of cell to another
dysplasia
change of a differentiated cell type to a poorly differentiated type- usually a precancerous change
carcinogenesis definition
transformation of normal to neoplastic cell through permanent mutation
neoplasm definition
autonomous abnormal persistent new growth of tissue
a neoplasm can only happen to what type of cells
nucleated cells- eg not erythrocytes
what is a tumor
any abnormal swelling
what can tumours be classified by
behaviour or histogenesis
behavioral classification on tumor- benign
no bm invasion
slow growing- low mitotic activity
well circumsized
well differentiated
behavioural tumor classification- malignant
bm invasion
fast growing- high mitotic activity
poorly circumscribed
common ulceration/ necrosis
poorly differentiatedd- little resemblance to normal tissue
reason for adjuvent thrapy with cancer
micrometastases could still be present after tumor completely excised
papilloma
benign neoplasm of epithelial tissue
carcinoma
malignant neoplasm of epithelial tissue
adenoma
benign neoplasm of glandular tissue
adenocarcinoma
malignant neoplasm of glandular tissue
benign and malignant neoplasm of adipocytes
lipoma, liposarcoma
benign and malignant neoplasm of striated muscle
rhabdomyoma, rhabdomyosarcoma
benign and malignant neoplasm of smooth muscle
leiomyoma, leiomyosarcoma
benign and malignant neoplasm of cartilage
chondroma, chondrosarcoma
benign and malignant neoplasm of bone
osteoma, osteosarcoma
is a grade 1 or grade 3 tumor more differentiated
grade 1- well differentiated- most cells resemble parent cell
grade 2- some cells resemble parent
grade 3- poorly differentiated- most cells look nothing like parent
characteristics of neoplastic cells
autocrine growth stimulation- overexpress gh and underexpress growth inhibitors
mutation of tumour supression genes like p53
can evade apoptosis and escape immune surveillance
telomerase is prevented from shortening with each replication
sustained angiogenesis
classes of carcinogens
miscellaneous- asbestos
hormones, parasites, mycotoxins
ionizing+ non ionizing radiation
viruses
chemical
pathway of metastesis
detatchment from first cancer
invades other tissue
invades blood vessel- collagenases + cell motility
evades host defense + adheres bv wall- platelet aggregation, shed surface antigens, adhesion to other tumour cells
extravasation to distant site- adhesion receptors, collagenase, cell motility
how does cancer evade immune system
platelet aggregation- body doesnt see anything but harmful platelets
shedding antigens from cell surface- macrophages engulf this instead of cell
adhesion to other tumour cells- ones in center dont get eaten
angiogenesis promoting and inhibitng factors
vascular endothelial growth factors
basic fibroblast growth factor
angiostatin
endostatin
vasculostatin
method of spread for tumours
haematogenous- via blood- form secondary tumors in organs
lymphatic- secondary formation in lymph nodes
transcolemic- via exudate fluid acculiation (baso effusions)
5 main metastesis to bone
breat, lung, thyroid, kidney, prostate
tumours that spread to liver
pancreas, stomach, colon, carcinoid tumour of intestine
how do sarcomas usuallt spread
mostly haematogenous
how do carcinomas mainly spread
mainly lymphatic
main method to stage tumour
tnm- tumour, node, metastases
what type of prevention is screening
secondary prevention
cancers that are screened for in the uk
cervical- cervical swab
breast- mamogram
colorectal- faecal occult
cells that regenerate
hepatocytes, blood cells, skin epithelium, osteocytes
cells that dont regenerate
myocardial cells
neurones
what is the pluripotent stell cells which blood cells r formed from
haematocytoblast
which precursor are innate cells from
common myeloid progenitor - eosinophil, basophil, neutrophil,macrophage
what precursor are adaptive cells from
common lymphoid progenitor- b, t cells and nk cells
lymphoid organs and what happens in them
primary-
- bone marrow- b and t cells made and b cells mature
-thymus- t cell maturation
secondary
- lymph nodes- apc+ b and t cell interaction
-spleen- rbc recylcing
tertiary
- germinal center of rapidly proliferating lymphocytes- pathological
physical and chemical barriers of innate immunity
physical- skin, mucus, cilia
chemical- lysosyme in tears, stomach acid
polymorphonuclear leukocytes + mononuclear leukocytes
neutrophil, basophil, eosinophil (granulocytes)
mono= monocytes, lymphocytes (agranulocytes)
what cell is most commonly seen in parasitic infections
eosinophils
difference between basophils and mast cells
basophils circulate around the body
mast cells are fixed in tissues
phagocytic cells
macrophage
neutrophil
dendritic cell
what are compliments + what immune system is it part of
proteins that are secreted in the liver and need to be activated to be functional- part of innate response
modes of action for compliment system
classical- ab antigen complex binds to microbe
alternative- compliment binds to microbe
lectin- lectin binds to microbe
outcomes of compliment (how it kills)
direct lysis- membrane attack complex
chemotacix- c3a and c5a- recruit leukocytes to site of infection
opsonisation-c3b
what is tnf-a secreted by and involved in
prod by macrophages and activates macrophages- involved in inflammation
cytokines: inteferons
limits spread of viral infection
cytokines: colony stimulating factor
controls division and differentiation of bone marrow stem cells
what do chemokines do
direct movement of wbc from blood to tissue/ lymph organs
what is il4 involved in
allergies
what are tlrs and nlr
innate immune sensors that respond to pathogen or damage associated molecular patterns
tlr2
2- peptidoglycan on gram positive bacteria
tlr4
pamp= lipopolysacharide / endotoxin- gram negative bacteria
tlr 5
pamp= flagellin- on flagellated bacteria
tlr 9
- pamp- dsDNA on viruses
tlr 3,7,8,9 present on
viruses
membrane bound prr example
toll like receptor
cytoplasmic prr example
nod like receptor
examples of prr (these r outside of a cell)
scavenger receptor- lipids
c type lectin receptors
toll like receptors
what r rig like receptors for
sense cytoplasmic viral rna and produce inteferons
what are nod like receptors for
sense cytoplasmc bacterial pathogens and DAMPs
why dont we recognise our own dna and rna in innate response
dna and rna are where prrs cant acess it
is damp on your own cell or another
on ur own- eg dna damage
types of apc + professional ones
dendritic cells, b cells, macrophages
what do apcs do
stimulate further t helper cell proliferation
stimulate b cell production and proliferaiton
cell mediated vs humoral response
cell mediated= intraceullar microbes- t cell
humoural- extracellular microbes- b cells
whats a naive t cell
never encountered an antigen- not matured in thymus yet
th1 vs th2
cause apc to phagocytose
th2- ab production
what happens to t cells that recognize self
killed in foetal thymus
il4 and il5 released by th2
4- clonal expansion
5- differention
high levels of il12 do what
th1- t cell mediated
absence of this causes b cell
how are t helper cells activated
apc binding and mhc interaction
intrisic antigen triggers what mhc and what t cell
intrisic antigen binds to mhc 1- activates cd8 cell- kill infected cell
extrinsic antigen- mhc and t cell
extrinsic- mhc class 2- cd4 cell- helo b cell make ab
ch4 cells will interact with what mch
2
cd4 cells will interact with what mhc
mhc1
mhc 1 and 2 are found on what cell
1- on all nucleated cells
2- on apcs
what do ab do
neutralise toxin by binding to it
increase opsonisation for phagocytosis
activate compliment
what are ab usually secreted as
ig m- later class switch to igg but hve specificity to same antigen
what is somatic hypermutation
point mutation of evolutionary measure- eg igs will mutate if u have a slightly different strain of covid
what is the fc and fab region of anitbodies
fc- constant- self and binds to surface of wbc (big stick)
fab- antobody binding region- binds to epitope of antigen
igg-
most abundant in blood
important in secondary immune response
crosses placenta
iga
most abundant in body
in mucisal lining- colustrum and breastmilk
igm
first released in adaptive response
ige
activates mast cells and basophils
type 1 hypersensetivity
anaphylaxis- ige mediated
ige binds to basophil or mast cell- degranulation- histamine (vasodilation and increased vessel permeability, bronchoconstriction, facial flush, swollen tongue and face)
type 2 hypersensetivity
antigen-antibody complex- igg/igm binds to antigen and activates compliment at the site of a-a binding
eg- goodpastures, pernicious anemia, rheumatic fever
type 3 hypersensitivity
immune complex deposition
igg/iga binds to antigen and activates compliment at the site of a-a deposition
eg- sle, post strep glomerulonephritis or iga glumerulonepohritis (affects kidney hard)
type 4 hypersenstivity
t cell mediated, delayed response
eg dmt1, tb, ms, guillain barre
what is immune tolerance, central tolerance and peripheral tolerance
immune tolerance is physiological to prevent faulty t/b cells self response
central tolerance is thymic tolerance where immature t cells are maturing and dealt with positively or negatively
peripheral tolerance occurs in secondary lymphoid organs and occur if faulty t/b cells evade thymic tolerancew
when you get a vaccine what ab is initially made and what ig wwill be there when pathogen is encountered again
initially- igm
reencounter- igg
natural active immunity
body encouonters pathogen and produces memory cells after infection
artificial active immunity
vaccine mimics encountering a pathogen and stimulates ig production
natural passive immunity
maternal igs passed onto feeding baby in breastmilk/ colostrum- no memory cells
artificial passive immunity
antivenom (injection of ig from another organism)
covid 19 vaccines are called what and what are they made of
pfizer and biotech moderna- made of mRNA
define passive immunity and give advantages and disadvantages
short term results from introduction of antibodies from another person or animal
adv- immeadiate protection and effective in immunocompromised patients
disadv- short lived and no memory cells and possible transfer of pathogen
define active immunity
antigenic substance prepared from acausative agent of disease- introduces pathogenic foriegn pathogens to trigger t lymphocytes, acp then b memory cell
vaccines can be…
non living- whole killed, toxoids
living- live attenuated
eg of whole killed vaccines- describe them and give advantage and disadvantage
influenza, rabies, sars-co-v2
doesnt cause infection byt contains antigen which produces immune response
adv- good for immunoconpromise and doest need to be refrigerated so can be transported
disadv0 need at least 2 shots, weaker response and lack of t cell response
what are toxoids in vaccines
inactivated toxins
what are live attenuated vaccines, examples and adv and disadv
organism is cultured in a way which it doesnt cause disease when innoculated; loss pathogenicity but kept antigenicity
eg bcg and mmr
adv- lower dose and less dose needed, immune response mimics that of real infection
disadv- transmissiability, vaccines need to be refreigerated so less transport
what are old people vaccinated for
pneumococcal
influenza
covid-19
what are routes of administration for drugs for systemic and local effects
sysmtemic:
- enteral (gi tract involved- per oral/ per rectal)
-parenteral (non gi tract- im, iv, subcutaneous)
local:
- inhaled
- topical (cream)
eg of drug targets
mostly receptors- also enzymes (ace i), ion channels, membrane transporters
what is a ligand- exogenous and endogenous
anything that binds to a receptor
- exogenous is drugs, endogenous is hormones
what is an agonist and antagonist
agonist- full affinity (binds) and full efficiacy (activates receptor to reach a response)
antagonist- full affinity but no efficiacy- binds but doesnt activates
a full agonist and inverse agonist and antagonist will produce what response
full agonist-100% response
inverse agonist- priduce effect opposite to agonist
antagonist- no effect of its own, just blocks effect s of agonist
what do u call the strength of a drug
potency
eg of ligand gated receptor, nuclear receptor, kinase linked receptor
ligand gated- ach receptor
nuclear- steroid receptor
kinase linked- growth factor (catalyse transfer of phosphate between proteins)
what happens when a ligand binds to a g protein receptor
gdp turns into gtp
draw a graph of agonist and competetive and non competetive antagonists
on notes
what does it mean if a beta blocker is non selective
itll bind to both b1 and b2 receptors
how do nsaids work
inhibit cox-1- reduction in prostaglandins which are important for maintaining healthy gi mucosa
what does cox 1 inhibition do
decrease gastric mucosal protection so decreases stomach ph and have a risk of gastropathy
what does cox-2 inhibition do
anti-inflammatory (cox-2 is involved in inflammation)
what does aspirin irreversibly inhibit
cox-1 - its an nsaid
eg of a ppi and what it does
omeprazole
irreversibly inhibits h-k atpase pumps- increases gastric ph to make it less acidic
what is pharamacokinetics
what happens to the drug inside the body
ADME
breifly describe pharmacokinetics
administration- route and entry into body- iv, im… bioavailability is important here
distribution- how well a drug is distributed from plasma into intersitial fluid and intracellular fluid and fat. volume of distribution is important here and consider if it can cross bbb.
metabolism- by kudney and liver, classified by rate and phase
phase 1- microsomal enzymes ad an oh group and theres a slight increase in hydrophulicty
phase 2- conjugation- major increase
excretion- urine and faeces
what si bioavailability and what has 100% bioavailability and why
how fast and to what extent a drug recaches systemic circulation
gold standard is iv as it avoids first pass metabolism (metabolised by kiver or gut first before site of action)
pharmacokinetics- what affects how well a drug will be absorbed
lipid solubility- if more soluble, more will be absorbed
drug ionisation- if ionised, less will be absorbed
pharmacokinetics- what is a high volume of distribution and a low one
if well distributed- high vd
if poorly distributed- low vd
when can drugs cross the bbb
if bery lipid soluble, intrathecal administration, if inflammation is present making barrier leakyq
pharmacokinetics- what things affect drug distribution
hydrophilipity- if its hydrophillic itll be poorer distributed
lipophillicity- if lipophilic better distributed
smaller molec- more distributed
protein bound- less distribution cuz its stuck to one protein
pharmacokinetics- metabolism. what does the liver and kidney metabolise
kidney- smaller, water soluble molecules- pee
liver- larger hydrophobic molec- poo
pharmacokinetics- metabolism- phase 1 and 2
1- slight increase in hydrophilicity via microsomal enzymes - CYP450
2- major increase in hydrophilicty by conjugation
pharmacokinetics- what affects metabolism
cyp450 inducer and inhibitor drugs
inducer will increase metabolism- may result in sub theraputic dose
inhibition will decrease metabolism- may result in toxicity
what is pharmacodynamics
effect a drug has on the body
what is a drugs half life dependant on
clearance and vd (small vd is poorly distributed and cleared quicker)
when is a drug considered to be cleared
5x half life
what is steady state
rate of drug input= rate of drug elimination- between maximum safe concentration and minimim effective concentration
what do you give if time taken to reach steady state is too long
give a loading dose
nt and receptors for autonomic sympathetic nervous system
ach- nicotinic receot–noradrenalin to adrenerigic receptor
nt and receptors for autonomic parasympathetic nervous system
ach- nicotinic receptor—ach to musacrinic ach receptor
what are the ach receptors and where are the m ones found
cholinergic receptors which are muscarinic or nicotinic
m1- brain- cognitive processes
m2- decrease rate and force of heart
m3- smooth muscle contraction- mainly bladder
what does botulinum toxin do
inhibits ach release- paralysis- used in cosmetics
results of overstumulation of ach at nmj junction
cholinergic crisis- SLUDGE
salivation
lacrimation
urination
defication
gi distress
emesis- vomiting
formation of adrenaline
tyrosine- L dopa- dopamine- noradrenalin- adrenalin
Nad receptors
a1- vasocontriction + bladder contraction
a2- negative feedback
b1- increase heart rate and contractility
b2- bronchodulation
eg of a1 antagonist and whys it important
tamsulosin- effects prostate and bladder- therefore treates benign prostatic hypertrophy - relaxes smooth muscle in prostate and detrusor in bladder
eg of b2 agonist
salbutamon
saba+ laba
give an example of a non selevtive beta blocker antagonist
propanolol
what is a beta 2 antagonist
non selective beta blockers like propanolol
where should adverse drug reactions be reported to
MHRA yellow card scheme
what increases your risk of adverse drug reactions
reduced renal or hepatic clearance
polypharmacy
what are the adverse drug reactions (eg and details in notes)
augmented-common, ecaggerated effect of drugs pharmacology
bizzare- not related to drugs pharmacology- eg allergy of anaphylacitc shock after penecilin
chronic- adr stays after drug is stopped
delayed- adr developed after a while
end of use- developes after drug stoppedd
what is excretion effected by
urine ph- acids cleared fastier in weakly basic urine and vice versa
what are naturally occuring opiods
morphine and codeine
what is the modified version of morphone and how strong is it
diamorphine- heroin. 2x stronger than morphine
oral bioavailibity of morphine
50%
for 10 mg of diamorphine/ heroin how much morphine do you need/
5mg
side effects of opiods like morphine
addiction
gi- constipation, n+v
resp- resp distress/ depression
(receptors found in cns and git and resp centers)
what is the treatment for opioid induced resp depression
naloxone- comp opiod inhibitor.
- it has a short half life so beware of overdose
what is tolerance vs dependance
tolerance- due to overstimulation of opiod receptor so you need more of the dose to acheive the same effect
dependance is psychological state of craving that eurphoria
eg of antiplatlet drug
aspirin
eg of anticoagulants- 2
heparin and warfarin
what is warfarin and if patient is bleeding out on this drug what do you do
anticoag- antivitamin k- i fbleeding out give vit k
dry cough is a common se of which drug
ace inhibitors
diuretics
loop diuretic- furosemide. inhibits nkcc2 channel in ascending loh so more na, water, cl and k is excreted
thiazides- bendroflumethiazide- inhibits nacl cotransptter in dct so more na and cl and water is excreted
spironolactone- inhibts enac channel(aldosterone) - in collecting duct so more na, water excreted. k+ is spared
what are the 3 layers of the normal artery wall and describe them
tunica intima- 1 endothelial layer thick
tunica media- smooth muscle (support and diameter), collagen, elastin (stretch and recoil to accommodate changes in blood pressure)
adventitia- connective tissue, collagen, nerve fibers and vasa vasorium
difference between elastic and muscular arteries
elastic- closer to heart, more elastin in media to withstand higher pressure
muscular- further from heart- more muscle in media to vasoconstrict/ dilate
define arteriole
less than 3 smooth muscle layers in media- site of greatest tpr
what do branches of the rca supply
branches to san + avn
right marginal artery for inferior border of the heart
piv- both ventricles
what do branches of the lca supply
left main stem branches into cx and lad
cx- inferior border, left atrium and ventricle, part of right ventricle
lad- both ventricles
cx branches into left marginal- left ventricle
explain process of atherogenesis
1- endothelial injury- high bp, smoking, inflammation.. damage endothelium making it more permeable to lipids
2- ldl cholesterol penetrates arterial wall and accumulates. becomes oxidised and more toxic, macrophages engulf these and becomes foam cells
foam cells recruit other inflammatory cells like neut+ lymphocytes
3- fatty streak formation- foam cells + smooth muscle
4- fibroblasts produce fibrous cap over plaque
5- non ruptured= stable ruptured= unstable- continuous platelet plug and lumen occlusion
modifiable risk factors for atherosclerosis + why theyre issues
smoking- releases nicotine and co- damages endothelium
hypertension- increases pressure damages bv wall
obesity
lack of excersize- helps bp
high cholesterol- more ldl - cuz of processes food
non modifiable risk factors for atherosclerosis
age
sex- m
family history
t1 diabetes (increases glucose and free radicals)
ethnicity
primary, secondary and tertiary prevention for atherosclerosis
primary- (prevent)- excersize more, change diet to less salt and sugar, stop smoking
secondary- statin to lower ldl, antihypertensives like acei, social prescribing like gym voucher
tertiary- surgical intervention- stenting, bypass to make new pathway for blood to flow around blocked artery
what do you treat angina from atherosclerosis with
gtn spray sublingualy
what is anaphylaxis
form of t1 hypersensitivity- acute allergic reaction to an antigen the body hypersensetive too and its severe and life threatening- have to have eithte airway or breathing or circulation propblems associated with skin or mucosal changes
explain pathophysiology of anaphylaxis
1- sensitization- first exposure to antigen- antigen gets picked up by apc- presented to t helper cell- activates b cell- plasma cell- antibodies
il4 will cause b cells to class switch to igE
ige will bind to Fc receptor on mast cells and basophils
2- 2nd exposure- on reexposure of the antigen- antigen will form cross links on igE on mast cells- causes rapid degranulation of mast cells- leukotrines, trypases, histamine- will cause signs and symptoms
presentation of anaphylaxis
occurs within minutes
vasodilation, bronchospasm, utricaria, increased vascular permeability
angioedema
central cyanosis
tachycardia, macroglossa, hypotension (due to vascular permeability, will compensate by raising bp)
wheezing (due to bronchoconstriction due to inflammation and increased vascular permeability)
treatment of anaphylaxis
abcde (remove airways obstruction and traces of allergens like iv, check for bronchospasm like wheezing, colour pulse, responding)
call for help!!!!!!!!!
lay flat and raise legs
ADRENALINE 500 MICROGRAMS IM
give high flow o2 and iv fluid
what does adrenaline do
stimulates beta 1 and 2 adrenoreceptors- positive ionotropic and chronotropic effect and lowers eodema and bronchodilates)
why do you sometimes need to give a second dose of adrenalin
adrenalin has a short half life
factors linked to an increase in allergies
increase in air pollution
change in pollen patterns
increase in caesarian sections- not exposed to microbiomes in vagi
contrasting agents- like x rays
what qualities does a drug need to have to induce anesthesia quickly and why
low protein binding (increases plasma concentration) and high lipid solubility (readily crosses bbb)
do you give iv or volatalile gas anasthesia first and why
iv- because iv drug has high initial plasma concentration - lots to well perfused area like the brain– but then spread to less perfused areas anc conc will decrease
is a competetive and non competetive antagonist reversible or not
competetive is reversible but non competetive is irreversible
most significant risk factor for atherosclerosis
hypercholesterimiea
how does aspirin work (mode of action)
irreversibly inhibits COX to prevent breakdown of arachidonic acid into prostaglandin H2
its non selective for cox 1 and 2
what is clopidogrel
anti- platelet drug
what confirms the diagnosis of tb and what would you see
zeehl neilsen staining- appears as a red rod
what do you do asap if you suspect meningitis
single STAT dose of benzylpenicillin by gp before transfer to hospital
what is legionella pneumonia associated with
travel to spain
exposure to damp
c difficile bacteria is spread through hosptialised pt. what is it usually caused by
c antibiotics- clindamycin, co amoxiclav, cephalosparins
what is the sight campain to prevent spread of c difficile bacteria
suspect
isolate
gloves + apron in pt zone
hand washing b4 and after pt env
test stool for c difficile
cranial and nephrogenic di water deprevation results
cranial- after fluid dep low urine osmolality but high after desmopressin
neph- low for both bc kidney doesnt respond
what is the tumour supression gene
p53
