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P Intergrated Y2 > EMS lectures 11,12,13,14 > Flashcards

EMS lectures 11,12,13,14 Flashcards

1
Q

define pathogenicity

A

capability of micro-organism to cause an infection

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2
Q

what are the requirements of pathogenicity

A

transmissibility
establishment in host
harmful effects
persistence

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3
Q

what is the chain of infection

A

pathogenic organism –> reservoir (multiplication) –> exit source –> transmission to host –> entry into host –> host infected

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4
Q

Virulence

A

degree to which microorganism can cause disease

enables relative comparison of pathogenic potential

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5
Q

What are virulence factors

A

components of micro-organism that result in harmful effects

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6
Q

what are virulence mechanisms?

A 
Facilitation of adhesion
toxic effects
tissue damage
interference with host defence mechanism
facilitation of invasion
modulation of host cytokine reactions
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7
Q

what are bacterial endotoxins

A

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 =

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8
Q

What are bacterial exotoxins

A

protein produced in living bacteria

- produce specific host effect

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9
Q

Explain Systemic inflammatory response syndrome (SIRS)

A

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

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10
Q

What anaerobe causes Botulism

  • how can you contract botulism
  • what is the presenting complaint with botulism
A

Clostridium botulinum
- contaminated food/dirty wound

PC = diplopia, dysphagia, dysarthria, dry mouth, death

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11
Q

What causes Tetanus

  • what is the toxin
  • what is the action
  • what is the common cause of death
A

Clostridium tetani
- Tetanospasm
- inhibits neurotransmitters in CNS
Death by respiratory paraylisis

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12
Q

Other diseases caused by exotoxins

A 
Cholera
diptheria
whooping cough
c.dif
e.coli
scarlet fever
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13
Q

What are to virulence factors of Streptococcus pyogenes

A
  • 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
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14
Q

How does S pyogenes and S pneumonia inhibit phagocytosis

A

Pyogenes - M protein binds fibrinogen and masks bacterial surface

Pneumoniae - polysaccharide capsule inhibits opsonisation

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15
Q

What are the components of a virus

A

genome (RNA or DNA)
capsid - protein
envelope

unable to exisit without host

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16
Q

Define atherosclerosis

A

degeneration of arterial wall - characterised by fibrosis, lipid deposition and inflammation -limit blood circulation and predisposes to thrombosis

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17
Q

What are the risk factors for artherosclerosis

A

age, male, family history, genetics

hyperlipidaemia, hypertension, smoking, diabetes,

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18
Q

Describe atherosclerotic plaque formation

A

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

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19
Q

What are the differences between a clot and a thrombus

A

Clot
- stagnant blood, enzymatic process, elastic, adopt vessel wall shape

Thrombus
- w/i body during life, platelet dependant, firm

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20
Q

What are platelets

- what do they secrete

A

Fragments of megakaryocytes
bind to collaged exposed by endothelial damage and become activated

secrete alpha granules - fibrinogen, fibronectin
dense granules - chemotactic chemicals

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21
Q

Define Embolus

A

mass of material able to lodge in vessel and block it

can be endo/exogenous

22
Q

What is the commonest emboli

  • risk factors
  • effect of size
A

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

23
Q

What is a systemic emboli

A

arise with in heart and arterial circulation

24
Q

What is an infective emboli

A

usually from infected heart vales

- effects compounded by infective nature - lead to mycotic aneurysm formation

25
Q

What is a tumour embolism

A

parts of tumour break of when penetrating wall - route for dissemination

26
Q

What are the types of gas emboli and when do they occur?

A

Air - vessels opened to air
- obstetric procedures
- chest wall injury
>100ml to cause clinical effects

Nitrogen - decompression sickness - the bends

27
Q

Explain what an amniotic fluid embolism is

  • frequency
  • causes
A

increased uterine pressure causes amniotic fluid into maternal uterine veins
= 1:50,000
- lodge in lungs –> resp distress

28
Q

what is the common cause of a fat embolism

  • % fatality
  • what does it cause
A
  • trauma
  • 15%
  • sudden resp distress
29
Q

How can foreign body emoblism occur

  • common in who?
  • lead to?
A

particles injected IV

  • IVDU
  • granulomatous disease
30
Q

define hypoxia

A

state of reduced tissue oxygen availability

31
Q

Define ischaemia

A

pathological reduction in blood flow to tissue

results in tissue hypoxia

32
Q

How harmful is ischaemia

A

short duration - cell injury reversible

prolonged - cell death by necrosis = irreversible cell damage

33
Q

When will therapeutic reperfusion work?

What happens if ischaemic tissue is reperfused?

A
  • is ischaemia is reversible

- reactive o2 species will call further cell damage = reperfusion injury

34
Q

define infarction

- common causes

A

ischaemic necrosis caused by occlusion

  • thrombosis, embolism
  • vasospasm, atheroma expansion, volvulus, AAA,
  • venous occlusion
35
Q

Morphology of infarction

- how is it classified

A

Classified by colour
Red infarction - hemorrhagic
- dual blood supply/venous infraction

White infarction -anaemic
- single blood supply therefore totally cut off

36
Q

define shock

A

systemic reduction in tissue perfusion
decrease in o2 delivery to tissues
-imbalance o2 delivery and consumption
- leads to cellular hypoxia

37
Q

what are the cellular effects of shock

A 
membrane ion pump dysfunction
intracellular swelling 
leakage of centents 
inadequate regulation of intracellular pH
anerobic respiration - lactic acid
38
Q

What are the SYSTEMIC effects of shock

A

alterations in serum pH
endothelial dysfunction - vascular leakage
stimulation inflammatory and antiinflammatory systems
end - organ damage

39
Q

Explain hypovolaemic shock

  • presentation
  • causes
  • what happens
A

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

40
Q

What is third spacing

A

loss of fluid into internal body cavities

41
Q

explain cardiogenic shock

A

cardiac pump failure

  • low Cardiac Output
  • increased Stroke vol rate
  • myopathic - muscle failure
    -arrythmia related - abnormal beats
  • mechanical
  • extra-cardiac - obstruction
    60-90% mortality
42
Q

explain distributive shock

A

severe vasodilation - low SVR
increase Cardiac Output
- flushed bounding heat

= septic shock, anaphylactic shock, neurogenic shock, toxic shock syndrome

43
Q

explain anaphylactic shock

A

type 1 hypersensitivity reaction

vasodilation

44
Q

neurogenic shock

A

spinal injury, loss of sympathetic vascular tone

vasodilation –> shock

45
Q

toxic shock syndrome

- cause

A

exotoxin - s.aureus, s.pyogenes
nonspecific binfing of class 2 MHC to T cell receptors
massive cytokine activtion - decrease SVR

46
Q

How common is inborn metabolic disease

A

RARE

1-2000 live births

47
Q

What are the clinical effects of hyperammoneaemia toxicity

- what is the cause

A

ammonia accumultion dyr to urea cycle defect

-lethargy, poor feeding, vom, thachypnoea, convulsions, coma, death

48
Q

what accumulates in porphyrais

  • signs acute porphyria
  • signs photosenstive porphyria
A

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

49
Q

when can inborn errors of metaboilism be diagnosed

A

Presymptomatic population screening

Investigation of symptomatic individuals

50
Q

Test for inborn errors of metabolism

A

urine metabolic screening

51
Q

What prenatal screening is available

  • neural tube defect
  • down syndrome
A

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

P Intergrated Y2 (13 decks)

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