EMS lectures 11,12,13,14 Flashcards
define pathogenicity
capability of micro-organism to cause an infection
what are the requirements of pathogenicity
transmissibility
establishment in host
harmful effects
persistence
what is the chain of infection
pathogenic organism –> reservoir (multiplication) –> exit source –> transmission to host –> entry into host –> host infected
Virulence
degree to which microorganism can cause disease
enables relative comparison of pathogenic potential
What are virulence factors
components of micro-organism that result in harmful effects
what are virulence mechanisms?
Facilitation of adhesion toxic effects tissue damage interference with host defence mechanism facilitation of invasion modulation of host cytokine reactions
what are bacterial endotoxins
part of gram negative cell wall,
active component = LPS Lipopolysaccharide
- released from dead/damaged cell walked and bind to host cell receptors
induce uncontrolled cell response =
What are bacterial exotoxins
protein produced in living bacteria
- produce specific host effect
Explain Systemic inflammatory response syndrome (SIRS)
host response to endotoxin
- uncontrolled t lymphocytes
- uncontrolled activation of clotting cascade
- uncontrolled activation of complement
cardiac/renal failure, hypotension, tachycardia, bleeding tendency, collapse, fever
What anaerobe causes Botulism
- how can you contract botulism
- what is the presenting complaint with botulism
Clostridium botulinum
- contaminated food/dirty wound
PC = diplopia, dysphagia, dysarthria, dry mouth, death
What causes Tetanus
- what is the toxin
- what is the action
- what is the common cause of death
Clostridium tetani
- Tetanospasm
- inhibits neurotransmitters in CNS
Death by respiratory paraylisis
Other diseases caused by exotoxins
Cholera diptheria whooping cough c.dif e.coli scarlet fever
What are to virulence factors of Streptococcus pyogenes
- promote connective tissue invasion and breakdown
- Hyaluronidase and streptokinase - break down connective tissue
-C5a peptidase - inactivates complement component C5a - Erythrogenic toxin - causes scarlet fever rash
Toxic shock syndrome toxin -
similar to syndrome of endotoxin release
How does S pyogenes and S pneumonia inhibit phagocytosis
Pyogenes - M protein binds fibrinogen and masks bacterial surface
Pneumoniae - polysaccharide capsule inhibits opsonisation
What are the components of a virus
genome (RNA or DNA)
capsid - protein
envelope
unable to exisit without host
Define atherosclerosis
degeneration of arterial wall - characterised by fibrosis, lipid deposition and inflammation -limit blood circulation and predisposes to thrombosis
What are the risk factors for artherosclerosis
age, male, family history, genetics
hyperlipidaemia, hypertension, smoking, diabetes,
Describe atherosclerotic plaque formation
1) damage to intima of vessel
2) lipid accumulation in intima
3) monocyte migration and ingestion of lipids in intima
4) monocytes become foam cells
5) foam cells secrete cytokines - attrack macrophages, lymphocytes, smooth muscle cells
6) formation of atherosclerotic plaque
7) plaque grows - occludes vessel, weakens vessel wall = aneurysm, erodes vessel
What are the differences between a clot and a thrombus
Clot
- stagnant blood, enzymatic process, elastic, adopt vessel wall shape
Thrombus
- w/i body during life, platelet dependant, firm
What are platelets
- what do they secrete
Fragments of megakaryocytes
bind to collaged exposed by endothelial damage and become activated
secrete alpha granules - fibrinogen, fibronectin
dense granules - chemotactic chemicals
Define Embolus
mass of material able to lodge in vessel and block it
can be endo/exogenous
What is the commonest emboli
- risk factors
- effect of size
Pulmonary emboli
- Factor 5 leiden deficiency, Protien S deficency
- smoking, pregnancy, obesity, heart failure, immobility,
SMALL - pulmonary hypertension
medium - V/Q mismatch, cardiac/ resp failure
Large = death - saddle emboli
What is a systemic emboli
arise with in heart and arterial circulation
What is an infective emboli
usually from infected heart vales
- effects compounded by infective nature - lead to mycotic aneurysm formation
What is a tumour embolism
parts of tumour break of when penetrating wall - route for dissemination
What are the types of gas emboli and when do they occur?
Air - vessels opened to air
- obstetric procedures
- chest wall injury
>100ml to cause clinical effects
Nitrogen - decompression sickness - the bends
Explain what an amniotic fluid embolism is
- frequency
- causes
increased uterine pressure causes amniotic fluid into maternal uterine veins
= 1:50,000
- lodge in lungs –> resp distress
what is the common cause of a fat embolism
- % fatality
- what does it cause
- trauma
- 15%
- sudden resp distress
How can foreign body emoblism occur
- common in who?
- lead to?
particles injected IV
- IVDU
- granulomatous disease
define hypoxia
state of reduced tissue oxygen availability
Define ischaemia
pathological reduction in blood flow to tissue
results in tissue hypoxia
How harmful is ischaemia
short duration - cell injury reversible
prolonged - cell death by necrosis = irreversible cell damage
When will therapeutic reperfusion work?
What happens if ischaemic tissue is reperfused?
- is ischaemia is reversible
- reactive o2 species will call further cell damage = reperfusion injury
define infarction
- common causes
ischaemic necrosis caused by occlusion
- thrombosis, embolism
- vasospasm, atheroma expansion, volvulus, AAA,
- venous occlusion
Morphology of infarction
- how is it classified
Classified by colour
Red infarction - hemorrhagic
- dual blood supply/venous infraction
White infarction -anaemic
- single blood supply therefore totally cut off
define shock
systemic reduction in tissue perfusion
decrease in o2 delivery to tissues
-imbalance o2 delivery and consumption
- leads to cellular hypoxia
what are the cellular effects of shock
membrane ion pump dysfunction intracellular swelling leakage of centents inadequate regulation of intracellular pH anerobic respiration - lactic acid
What are the SYSTEMIC effects of shock
alterations in serum pH
endothelial dysfunction - vascular leakage
stimulation inflammatory and antiinflammatory systems
end - organ damage
Explain hypovolaemic shock
- presentation
- causes
- what happens
Intra-vascular fluid loss
lower venous return to heart, lower stroke vol, decreased cardiac output
Increased stroke vol rate (vasocontriction)
present - cool, clammy, shut down
causes - haemorrhage, diarrhoea, vomiting, heatstroke, third spacing
What is third spacing
loss of fluid into internal body cavities
explain cardiogenic shock
cardiac pump failure
- low Cardiac Output
- increased Stroke vol rate
- myopathic - muscle failure
-arrythmia related - abnormal beats - mechanical
- extra-cardiac - obstruction
60-90% mortality
explain distributive shock
severe vasodilation - low SVR
increase Cardiac Output
- flushed bounding heat
= septic shock, anaphylactic shock, neurogenic shock, toxic shock syndrome
explain anaphylactic shock
type 1 hypersensitivity reaction
vasodilation
neurogenic shock
spinal injury, loss of sympathetic vascular tone
vasodilation –> shock
toxic shock syndrome
- cause
exotoxin - s.aureus, s.pyogenes
nonspecific binfing of class 2 MHC to T cell receptors
massive cytokine activtion - decrease SVR
How common is inborn metabolic disease
RARE
1-2000 live births
What are the clinical effects of hyperammoneaemia toxicity
- what is the cause
ammonia accumultion dyr to urea cycle defect
-lethargy, poor feeding, vom, thachypnoea, convulsions, coma, death
what accumulates in porphyrais
- signs acute porphyria
- signs photosenstive porphyria
Porphyrins
Acute
= Abdo pain, vom, insomnia, palpatatoin, HBP, anxiety, seizure,breathing probs, red/brown urine, muscle pain
Photosensitve porphyria
- sensitivity to sun, painful erythema, blisters, itching, fragile skin, inc hair growth, red/brown urine
when can inborn errors of metaboilism be diagnosed
Presymptomatic population screening
Investigation of symptomatic individuals
Test for inborn errors of metabolism
urine metabolic screening
What prenatal screening is available
- neural tube defect
- down syndrome
Neural tube defect
- 16 week ultrasound, maternal serum and Amnoitic fluid AFP
Down syndrome
- 1st trimester - PAPA, HCG, nuchal translucency
- 2nd trimester - maternal serum AFP, HCG, inhibin and estrol
