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(SG) Phase 2A lectures > ICS > Flashcards

ICS Flashcards

1
Q

what are the 2 types of autopsies?

A
  1. hospital
  2. medico-legal (coronial and forensic)
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2
Q

what are the 2 types of medico-legal autopsies?

A
  1. coronial (lawful death)
  2. forensic (non-lawful death)
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3
Q

which type of autopsy is most common?

A

medico-legal: coronial

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4
Q

what does a hospital autopsy require?

A

MCCD (medical certificate of cause of death?)

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5
Q

what are hospital autopsies used for?

A
  • teaching
  • research
  • governance
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6
Q

when are coronial autopsies conducted?

A

when death is lawful

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7
Q

when are forensic autopsies conducted?

A

when there’s a non lawful death

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8
Q

what are the 4 questions of the coroner?

A
  1. who was the deceased?
  2. when did they die?
  3. where did they die?
  4. how did they come about their death?
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9
Q

what does an autopsic pathologist have the same role as?

A

the coroner

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10
Q

what are 3 types of deaths referred to a coroner?

A
  1. presumed natural
  2. presumed iatrogenic
  3. presumed unnatural
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11
Q

what does iatrogenic mean?

A

caused by medical exam/treatment

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12
Q

what is the no. of days where if not seen by a doctor, a presumed natural death is referred to a coroner?

A

14

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13
Q

what is the most common referral reason for autopsy?

A

presumed natural death - not seen doc in last 14d

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14
Q

what are examples of iatrogenic deaths? (4)

A
  1. peri/post-op deaths
  2. anaesthetic deaths
  3. illegal abortion
  4. complications of therapy (even if recognised)
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15
Q

name some examples of presumed unnatural deaths (4)

A
  1. industrial deaths eg asbestos
  2. suicide
  3. unlawful killing
  4. custody deaths
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16
Q

do docs have a statutory duty to refer deaths to coroners?

A

no

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17
Q

who has a statutory duty to refer deaths?

A

registrar of BDM (births, deaths n marriages)

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18
Q

who else can make referrals for autopsy?

A

relatives, police etc

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19
Q

who performs coronial autopsies?

A

forensic pathologists

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20
Q

who performs majority of autopsies (hospital)????

A

histopathologists

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21
Q

what are the 5 steps to an autopsy?

A
  1. history/scene
  2. external examination (formal identifiers etc)
  3. evisceration (removal of external organs)
  4. internal examination
  5. reconstruction
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22
Q

what happened in oct 2016 relating to autopsies?

A

digital - full body CT scan reported by consultant radiologist

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23
Q

define coronial autopsy

A

systematic scientific exam that helps coroner determine who the deceased was, when and where did they die and how they came about their death?

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24
Q

define acute inflammation

A

the initial and often transient series of tissue reactions to injury

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25
Q

how long does acute inflammation often last?

A

few hours to a few days

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26
Q

what is an example of acute inflammation?

A

appendicitis

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27
Q

what is inflammation?

A

(hard to define): local physiological response to tissue injury [often involves cells eg neutrophils n macrophages]

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28
Q

is inflammation a disease?

A

no, but usually a manifestation of disease

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29
Q

what are the benefit(s) of inflammation? (2ish)

A
  • destruction of invading microorganisms and wailing off of an abscess cavity
  • PREVENTING infection spread
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30
Q

what are the negatives of inflammation? (3)

A
  • autoimmunity eg rheumatoid arthiritis
  • when it’s an over-reaction to the stimulus
  • fibrosis resulting from chronic inflammation may distort tissues and alter their function
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31
Q

list 6 causes of inflammation :/

A
  1. microbian infections
  2. hypersensitivity reactions
  3. physical agents
  4. chemicals
  5. acids/alkalis
  6. tissue necrosis
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32
Q

list 4 macroscopic (n essential) appearances of acute inflammation

A
  1. redness [rubor]
  2. heat [calor]
  3. swelling [tumor]
  4. pain [dolor]
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33
Q

what is rubor?

A

redness

1 of the 4 classical signs of acute inflammation

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34
Q

what is calor?

A

heat,

1 of the 4 classical signs of acute inflammation

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35
Q

what is tumor?

A

swelling,

1 of the 4 classical signs of acute inflammation

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36
Q

what is dolor?

A

pain,

1 of the 4 classical signs of acute inflammation

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37
Q

why is there heat/calor in acute inflammation?

A

increased blood flow (AKA hyperaemia) –> vascular dilation

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38
Q

what is hyperaemia?

A

increased blood flow

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39
Q

why is there swelling/tumor in acute inflammation?

A
  • swelling is from oedema/physical mass of inflammatory cells
  • formation of new connective tissue also contributes to swelling
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40
Q

why is there pain/dolor in acute inflammation?

A
  • stretching/tissue distortion due to inflammatory oedema
  • AND pus under pressure in abscess cavity
  • (also some chemical mediators eg bradykinin, prostaglandins are known to induce pain)
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41
Q

what are 3 features of chronic inflammation?

A
  1. slow onset/sequel to acute
  2. long duration
  3. may never resolve
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42
Q

what are 3 features of acute inflammation?

A
  1. sudden onset 2. short duration 3. usually resolves
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43
Q

list 6 cells involved in inflammation

A
  1. neutrophil polymorphs
  2. macrophages
  3. lymphocytes
  4. endothelial cells
  5. fibroblasts
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44
Q

discuss neutrophil polymorphs (5)

A
  • short-lived cells
  • first on scene of acute inflammation
  • cytoplasmic granules full of bacteria-killing enzymes
  • usually die at scene of inflammation
  • release chemicals that attract other inflammatory cells eg macrophages
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45
Q

which wbc is short lived?

A

neutrophils

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46
Q

which cells are first on scene at acute inflammation?

A

neutrophils

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47
Q

do neutrophils die at scene of inflammation?

A

usually

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48
Q

what do neutrophils release?

A

chemicals that attract other inflammatory cells eg macrophages

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49
Q

what is the life span of macrophages?

A

long lived compared to neutrophils - weeks to months

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50
Q

what do macrophages do?

A
  • ingest bacteria n debris
  • may carry debris away
  • may present antigen of lymphocytes
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51
Q

what are kupffer cells an example of?

A

macrophages

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52
Q

what is the lifespan of lymphocytes?

A

years

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53
Q

what do lymphocytes do? (2)

A
  • produce chemicals which attract other inflammatory cells
  • have an immunological memory for past infections and antigens
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54
Q

what do endothelial cells do? (4)

A
  • line capillary blood vessels in areas of inflammation
  • become sticky in areas of inflammation so inflammatory cells adhere to theme
  • become porous to allow inflammatory cells to pass into tissues
  • grow into areas of damage to form new capillary vessels
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55
Q

what do fibroblasts do and what is their lifespan like?

A
  • form collagen in areas of chronic inflammation and repair - they are long-lived cells
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56
Q

where are inflammatory cells?

A

in bone marrow, released into blood

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57
Q

what is the best known chemical mediator in acute inflammation?

A

histamine

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58
Q

name an example of chronic inflammation

A

tuberculosis

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59
Q

discuss tuberculosis (5)

A
  1. no initial acute inflammation
  2. mycobacteria ingested by macrophages
  3. macrophages often fail to kill the mycobacteria
  4. lymphocytes and macrophages appear
  5. fibrosis occurs
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60
Q

what are granulomas?

A
  • collection of macrophages - surrounded by lymphocytes?
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61
Q

list 3 medications for inflammation

A
  1. aspirin
  2. ibuprofen
  3. steroids
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62
Q

what is resolution? (2)

A
  • initiating factor removed
  • tissue undamaged or able to regenerate
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63
Q

what is repair? (2)

A
  1. initiating factor still present
  2. tissue damaged and unable to regenerate
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64
Q

which organ is a good example for resolution?

A

liver

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65
Q

what can a paracetamol OD result in?

A

liver failure

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66
Q

how does alcoholism impact regeneration?

A

bc of ongoing damage which results in abnormal architecture (cirrhosis)

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67
Q

can pneumocytes that line the alveoli regenerate?

A

yh

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68
Q

what are the most superficial skin wounds & an example?

A

abrasion eg road rash from cycling

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69
Q

what happens during abrasion?

A

only top cell layer is removed, leaving the bottom layer/follicles/glands for scab to form and for the epidermis to eventually be regenerated

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70
Q

what are the 2 types of skin would healing?

A

healing by 1st n 2nd intention

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71
Q

what is healing by 1st intention?

A
  • edge to edge healing (heals w/ reasonable scar)
  • both ends are sealed together, the slight gap is filled w blood, fibrin etc which holds together a little w stitches
  • epidermis regrows, fibroblasts produce collagen
  • scar line is stronger than surrounding tissue as more blood vessels are grown
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72
Q

do scars along skin creases heal better or worse?

A

better

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73
Q

what does healing by 2nd intention usually involve?

A

traumatic wound where u can’t bring 2 edges together

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74
Q

what forms initially during healing by 2nd intention?

A

granulation –> epithelium slowly grows in from edges (depending on wound size)

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75
Q

define repair

A

replacement of damaged tissue by fibrous tissue

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76
Q

what is damaged tissue replaced by?

A

fibrous tissue

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77
Q

what is collagen prod by?

A

fibroblasts

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78
Q

after a MI, what is there where dead heart tissue was?

A

a fibrous scar

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79
Q

what does MF stand for?

A

myocardial fibrosis

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80
Q

what type of scar does MF (myocardial fibrosis) result in?

A

a dense white fibrous scar (patient may live for a few months but may die after)

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81
Q

which type of healing is preferred?

A

healing by 1st intention

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82
Q

if healing by 2nd intention, we don’t want infection… what may be done to reduce this?

A

artificial skin dressings to keep the skin moist so it doesn’t dry out - sometimes may have growth factors in them

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83
Q

what is fibrosis in the brain called?

A

gliosis

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84
Q

what is gliosis?

A

fibrosis in the brain

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85
Q

is gliosis contagious?

A

not as much as usual fibrosis

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86
Q

how does stroke recovery happen?

A

only the injured (not dead tissue) around the edge of the infarct gets better, with plasticity involved

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87
Q

list some cells that regenerate (5)

A
  1. hepatocytes
  2. pneumocytes
  3. all blood cells
  4. gut and skin epithelium
  5. osteocytes
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88
Q

what are some cells that don’t regenerate?

A
  1. myocardial cells
  2. neurones
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89
Q

what can venous thrombosis potentially cause?

A

pulmonary embolism

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90
Q

what is clotting within an intact vascular system aka

A

thrombosis

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91
Q

what is thrombosis within the arterial system usually due to?

A

damage to the vessel wall (which is often due to the formation of atherosclerotic plaques)

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92
Q

how does platelet aggregation happen?

A

when atherocsclerotic plaques rupture, then connective tissue collagen is exposed to the blood leading to platelets attaching to it

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93
Q

what can platelet aggregation activate?

A

the blood clotting system leading to an occlusion of the vessel

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94
Q

what does occlusion of a coronary artery result in?

A

death of heart muscle due to lack of blood flow (MI)

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95
Q

what does occlusion of a cerebral artery result in?

A

death of brain tissue due to a lack of blood flow (CI)

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96
Q

what is a stroke aka?

A

cerebral infarction (CI)

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97
Q

why does thrombosis in the veins most commonly occur?

A

due to slow blood flow within those veins eg when a patient is lying in bed for long periods of time after a major op

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98
Q

list some preventions of DVT in hosp (3)

A
  1. early mobilisation
  2. use of small doses of anti-coagulants eg heparin
  3. venous stocking to prevent leg veins being full of blood
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99
Q

what is heparin?

A

an anti coagulant

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100
Q

what are the 2 reasons why clots are rare?

A
  1. laminar flow
  2. endothelial cells not sticky when healthy
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101
Q

what is laminar flow? and why is it important?

A

cells travel in the centre of arterial vessels and don’t touch arteries - this is important in reducing risk of blood clots

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102
Q

define thrombosis

A

the formation of a solid mass from blood constituents in an intact vessel in a living person

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103
Q

what is the first stage of thrombosis?

A

platelet aggregation

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104
Q

how do platelets cause other platelets to stick to them? (which also starts clotting cascade off)

A

they release chemicals

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105
Q

why is platelet aggregation and clotting cascade difficult to stop?

A

both pos feedback loops

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106
Q

what is the name of the large protein molecule formed once the clotting cascade has begun?

A

fibrin

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107
Q

what does fibrin do?

A

makes a mesh in which rbc can become entrapped

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108
Q

define embolism

A

the process of a solid mass in the blood being carried through the circulation to a place where it gets stuck and blocks the vessel (most commonly a thrombus)

could also be a bubble of air/fat/foreign etc

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109
Q

what are some less common causes of embolus? (4)

A
  1. air (pressurised systems of IV fluids/blood in infants n kids esp)
  2. tumour
  3. amniotic fluid
  4. fat
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110
Q

if an embolus enters the venous system, where will it lodge?

A

it will travel to the vena cava –> through RHS of heart –> &will lodge in pulmonary arteries

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111
Q

why can’t an embolus in the venous system get through to arterial circulation?

A

bc the blood vessels in the lung split down to capillary size so lung acts as a filter for any venous emboli

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112
Q

what acts as a filter for venous emboli?

A

lungs

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113
Q

what happens if an embolus enters the arterial system?

A

it can travel anywhere downstream of its entry point eg a mural thrombus overlying a myocardial infarct in LV can go anywhere in systemic circulation

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114
Q

define ischaemia

A

a reduction in blood flow to a tissue without any other implications

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115
Q

define infarction

A

reduction in blood flow to a tissue that is so reduced it cannot even support mere maintenance of the cells in that tissue so they die

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116
Q

what is infarction usually caused by?

A

thrombosis of an artery eg thrombosis in LAD coronary artery causing infarction of anterior wall of LV

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117
Q

what is the triad of factors impacting thrombosis?

A

Virchow’s triad

  1. change in vessel wall (endothelial injury)
  2. change in blood flow (stasis of blood flow)
  3. change in blood constituents (hypercoagulability)
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118
Q

what does end arterial supply mean?

A

most organs only have a single artery supplying them so they are very susceptible to infarction if this supply is interrupted

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119
Q

name some organs which don’t have end arterial supply (3)

A
  • liver: portal venous and hepatic artery supplies
  • lung: pulmonary venous and bronchial artery supplies
  • brain: around COW w multiple arterial supplies
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120
Q

what do endothelial cells act as?

A

a teflon coating

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121
Q

what can injury lead to exposure of?

A

collagen

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122
Q

what does fibrinogen get activated by?

A

chemicals the platelets release

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123
Q

an LAD CA thrombus can led to an MI. how will this present on ecg?

A

ST elevation on chest leads

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124
Q

how does cigarette smoke change vessel walls?

A

kills endothhelial cells

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125
Q

why does CO inhalation result in an increased risk of thrombosis?

A
  • inhaling lots of CO
  • –> more rbc production
  • –> more cells
  • = blood more turgid
  • –> can thrombus more easily
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126
Q

how does atherosclerosis disrupt laminar flow?

A

makes artery walls sticky

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127
Q

what is aspirin in low doses daily good for?

A

inhibits platelet aggregation

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128
Q

what is the most common cause of an embolus?

A

broken off thrombus travelling in blood stream

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129
Q

what is significant about IV drug abusers?

A
  • street heroin is often cut with talcum powder which isn’t v soluble
  • –> injected emboli into veins
  • –> usually filtered in lungs, sometimes liver
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130
Q

above what ml of air can cause an embolus?

A

150

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131
Q

what is infarction a subset of?

A

ischaemia

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132
Q

what is the diff btwn ischaemia and infarction?

A
  • ischaemia = any red in blood flow
  • infarction = death of cells due to lack of blood cells(?)
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133
Q

what causes atherosclerosis?

A

atheromas

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134
Q

define atheroma

A

pathology of arteries in which there is deposition of lipids in the arterial wall with surrounding fibrosis and chronic inflammation

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135
Q

what is the predominant cause of M/CI?

A

atherosclerotic plaques

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136
Q

list 3 risk factors for atheromas

A
  1. raised serum lipids
  2. hypertension
  3. diabetes mellitus
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137
Q

what is the linkage between high serum lipids and atherosclerosis?

A

lipids cause endothelial damage

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138
Q

what is the major process after endothelial damage (and with which cells)?

A

chronic inflammation - with macrophages/fibroblasts

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139
Q

name 3 factors that can reduce endothelial damage

A
  1. reduced lipids
  2. lowered BP
  3. stopping smoking
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140
Q

which drug can reduce the amount of platelet aggregation at the site of endothelial damage?

A

taking low dose aspirin

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141
Q

define atherosclerosis

A

narrowing of arteries due to plaque formation

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142
Q

what is the diff btwn atherosclerosis and arteriosclerosis?

A
  • athero = narrowing of arteries due to plaque formation
  • arterio = hardening of arteries
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143
Q

define arteriosclerosis

A

hardening of the arteries

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144
Q

can u have a genetic predisposition to atherosclerosis?

A

yes

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145
Q

when is complicated atherosclerosis usually seen?

A

later in life

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146
Q

what is significant about atherosclerosis?

A

it is mostly based on incremental episodes of endothelial cell damage over a LONG period of time eg decades

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147
Q

what is in a plaque? (3)

A
  1. quite a lot of fibrous tissue
  2. lipids
  3. lymphocytes (maybe also inflammation)
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148
Q

name 4 risk factors for atherosclerosis

A
  1. smoking
  2. hypertension
  3. diabetes
  4. increased deprivation :(
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149
Q

why does vaping have adv over smoking?

A

free radicals in cig smoke/CO/nicotine kills endothelial cells, vaping has fewer free rads and no CO

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150
Q

list the journey from smoking –> chest pain

A
  • smoking
  • endothelial cell damage
  • thrombus
  • heals bc endothelial cell layer grows over
  • small bump
  • not much impact
  • repeated endothelial damage
  • cycle continues w/o symptoms
  • symptoms may finally begin after years eg slight chest pain OR still asymptomatic
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151
Q

what are the symptoms of atherosclerosis in coronary arteries?

A
  • vomiting
  • anxiety
  • angina
  • coughing
  • feeling faint
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152
Q

what can atherosclerosis in coronary arteries result in?

A

ischaemia of cardiac muscle cells

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153
Q

list some symptoms of atherosclerosis in carotid arteries

A
  • weakness
  • dyspnea
  • facial numbness
  • paralysis
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154
Q

what is dyspnea?

A

shortness of breath

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155
Q

wich disease can atherosclerotic plaque also cause?

A

peripheral vascular disease

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156
Q

what are some symptoms of peripheral vascular disease?

A
  • hair loss
  • erectile dysfunction
  • weakening of area
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157
Q

what are some symptoms of atherosclerosis in renal arteries?

A
  • reduced appetite
  • hand swelling
  • renin release can be increased –> BP may be sig increased
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158
Q

high or low amounts of circulating LDL can lead to endothelial dysfunction?

A

high

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159
Q

plaque formation steps?

A

?

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160
Q

define apoptosis

A

programmed cell death of a single cell

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161
Q

define necrosis

A

unprogrammed death of a large number of cells due to an adverse event

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162
Q

list some examples of adverse events that could result in necrosis?

A
  • infarction
  • burns
  • frostbite
  • etc
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163
Q

which type of cell death is important in the normal function of the human body?

A

apoptosis?

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164
Q

why is apoptosis important in embryogenesis?

A

apoptosis removes cells that are no longer needed as organs develop eg tissue btwn fingers/toes so we dot s so that we dont end up w webbed feet n hands

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165
Q

what 2 things is apoptosis implemented by?

A

caspases and BCl2 protein

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166
Q

what can an aging or ill cell do besides apoptose?

A
  • autophagy
  • closing down protein synthesis
  • cell cycle arrest
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167
Q

when can abomal apoptosis occur?

A

in a variety of situations inc:

  • drugs
  • graft vs host disease after bone marrow transplantation
  • neurodegeneration
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168
Q

thermal injury of a burn that physically causes the death of many cells is by what?

A

necrosis

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169
Q

what are condensed bodies in apoptosis aka

A

apoptic bodies

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170
Q

is apoptosis a well-coordinated process?

A

yes

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171
Q

are there any accompanying inflammatory reactions with apoptosis?

A

no

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172
Q

what does p53 protein detect?

A

dna damage in dividing cells

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173
Q

why do cancers get bigger?

A

bc apoptosis is lacking (often bc of a mutation in p53 gene so dna damage is not recognised)

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174
Q

why is apoptosis switched off in HIV?

A

as p53 is switched on to kill myphocytes?

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175
Q

what happens to the contents of cells in necrosis?

A

swelling and disintegration of small bodies of cell

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176
Q

list some examples of necrosis

A
  1. frostbite
  2. CI
  3. avascular necrosis of bone
  4. pancreatitis
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177
Q

where do congenital and acquired diseases tend to predominate?

A

congenital = paeds acquired = geriatric

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178
Q

where do autosomal diseases occur?

A

non-sex chromosomes

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179
Q

what is a congenital disease?

A

a disease that someone is born with (mostly genetic but can be acquired)

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180
Q

what is an acquired disease?

A

one that occurs after birth (often due to env, can be genetic)

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181
Q

name 2 prenatal factors, other than genetic abnormalities that can contribute to disease risk?

A
  • transplacental transmission of env agents eg FA
  • nutritional deprivation
182
Q

what is a genetic disease?

A

1 that occurs primarily from a genetic abnormality

183
Q

what is caused by a point mutation in the beta-globin chain of Hb?

A

sickle cell anaemia

184
Q

in sickle cell anaemia, when do the RBC deform/sickle?

A

when oxygen sat is low

185
Q

single gene disorders are typically classified into what?

A

dominant or recessive

186
Q

an single gene disorders be further classified?

A

autosomal (non-sex chromosomes)

sex-linked (parts of x chromosome that dont have a corresponding region on y chromosome)

187
Q

what type of disorder is breast cancer an example of?

A

polygenic disorders (bc BRCA1/BRCA2 do have a large individual efffect but mostly risk is composed of incremental rises in risks by 100s of unrelated genes)

188
Q

what is the E4 apoprotein associated with?

A

high risk of ischaemic heart disease due to atheroma

3x higher in pop of papa new guinea than caucasians

189
Q

what is spina bifida occulta?

A

malformation of 1+ vertebrae

190
Q

GH excess is usually due to what?

A

pituitary tumour - adenoma

191
Q

define adenoma

A

benign tumour formed from glandular structures in epithelial tissue

192
Q

what does hungtington’s disease result in?

A

death of brain cells

early symptoms - subtle with mood/mental abilities

general lack of coordination and unsteady gait often follow

193
Q

what type of disorder is huntingtons?

A

inherited - autosomal dominant - gene called huntingtin (HTT) on chromosome 4… ≥36

194
Q

increased cell growth is caused by which 2 processes?

A

hypertrophy and hyperplasia

195
Q

define hypertrophy

A

when the SIZE of an individual cell/tissue/organ is increased by an increase in the SIZE OF THE CELLS without the increase number of cells

196
Q

define hyperplasia

A

increased growth of cell/tissue/organ because of an INCREASE IN NUMBER OF CELLS. often accompanied by increase in cell size

197
Q

bodybuilders prefer what? hypertrophy or hyperplasia

A

hypertrophy - increase in size of cells (appearance)

198
Q

athletes prefer what? hypertrophy or hyperplasia?

A

hyperplasia - increased number of cells (or myofibrils in each cell, strength)

199
Q

which 2 factors contribute to hypertrophy?

A

sarcoplasmic hypertrophy - focuses more on increased muscle glycogen storage

myofibrillar hypertrophy - focuses more on increased myofibril size

200
Q

how does hypertrophy/hyperplasia present in pregnancy?

A

hyperplasia - breast epithelial cells respond to increased demands

uterus - both hypertrophy and hyperplasia

201
Q

define atrophy

A

decrease in the size of cells caused by a decrease in NUMBER of cells OR decrease in SIZE

202
Q

why might pathological atrophy happen?

A

bc of loss of blood supply, loss of innervation, pressure, lack of nutrition, lack of hormonal stimulation or bc of hormonal stimulation

203
Q

define metaplasia

A

reversible transofrmation of 1 mature cell type in another fully differentiated cell type

204
Q

what is an example of metaplasia in smokers?

A

transofmration of normal pseudostratified columnar ciliated epithelium of bronchi into squamous epithelium after repeated exposure to cig smoke

205
Q

what is dysplasia?

A

an imprecise term forthe morphological changes seen in cells in the progression to becoming cancer

it’s a premalignant condition characterised by increased growth, cellular atypia and decreased differentiation

206
Q

why does hearing loss occur in older age?

A

hair cells in the cochlear don’t regenerate

207
Q

list some examples of illnesses associated w/ ageing

A

osteoporosis

cataracts

dementia

sarcopaenia (lack of muscle)

deafness

208
Q

what is the generic term for a malignant tumour?

A

cancer

209
Q

how does basal cell carcinoma of the skin act?

A

only invades localy - can be locally excised and cured !

210
Q

most carcinomas spread to where?

A

lymph nodes that drain the site of the carcinoma

211
Q

what are 5 common tumours that spread to bone?

A

breast

prostate

lung

thyroid

kidney

212
Q

what is the easiest way to confirm breast cancer?

A

small needle biopsy

213
Q

what is a lumpectomy?

A

breast conserving surgery / partial masectomy / wide excision

214
Q

what is the most widely used cancer staging system and what does it mean?

A

TMN system

T = extent of tumoour

M = presence of metastases

N = spread to lymph nodes

215
Q

what is the TNM staging converted to?

A

0 = carcinoma in situ

1-3 = size of cancer/nearby spread

4 = metastatic disease

216
Q

define carcinogenesis

A

process which results in the transformation of normal cells to neopalstic cells due to permanent genetic alterations (mutations)

217
Q

what does carcinogenesis only strictly apply to?

A

malignant tumours

218
Q

what are carcinogens?

A

agents known/suspected to participate in the causation of tumours

219
Q

how may env carcinogens be identified?

A

from epidemiological studies

assessment of occupational risks

direct accidental exposure

experiemntal observations

220
Q

what type of process is carcinogenesis? and why?

A

multistep - may require initiating and promoting agents - often resulting in a latent period btwn exposure to carcinogen and clinical recognition of a tumour

221
Q

what is the diff btwn carcinogenic and ongogenic?

A

carcinogenic = cancer causing

oncogenic = tumour causing

222
Q

list some classes of carcinogens

A
  1. chemical
  2. viral
  3. ionising and non-ionising radiation
  4. hormones, parasites and mycotoxins
  5. miscellaneous
223
Q

what are some host factors for carcinogens?

A

race

diet

constitutional factors eg age/gender

premalignant lesions

transplacental exposure

224
Q

what is a neoplasm?

A

a lesion resulting from the autonomous growth of cells which persists after the initiating stimulus has been removed

225
Q

what are benign neoplasms like ?

A

generally slow growign

closely resemble parent tissue

remain localised

226
Q

what are malignant neoplasms like?

A

have the capacity to invade surrounding tissues

grow more rapidly

show variable resemblance to parent tissue

227
Q

all neoplasma are designated by which suffix?

A

“-oma”

228
Q

benign connective tissue neoplasms have a prefix denoting what?

A

cell of orgin

eg lipoma - benign neoplasm arising from adipocyte

229
Q

malignant epithelial tumours = carcinomas

malignant connective tissue neoplasms = ?

A

sarcomas

230
Q

what are neoplasms made up of?

A

neoplastic cells and stroma

231
Q

what is a stroma?

A

supporting networking cells

232
Q

define angiogenesis

A

recruiting blood vessels to help and grow

233
Q

how can neoplasms be classified behaviourally?

A

benign, borderline, malignant

234
Q

why should we worry about “benign” neoplasms?

A

they cause morbidity and mortality through:

  • pressure on adjacent structures
  • obstruct flow
  • produce hormones
  • transform to malignant neoplasms
  • anxiety
235
Q

how can neoplasms be classified histogenetically?

A
  • specific cell of origin of a tumour
  • histopathological exam
  • specifieis tumout type
236
Q

what is a papilloma?

A

benign tumour of non-glandular, non-secretory epithelium

prefix with cell type of origin eg squamous cell papilloma

237
Q

what is an adenoma?

A

benign tumour of glandular/secretory epithelium

prefix with cell type of origin eg thyroid adenoma

238
Q

name 2 benign epithelial neoplasms

A

papilloma

adenoma

239
Q

name 2 malignant epithelial neoplasms

A

carcinoma

adenocarcinoma

240
Q

what is the diff btwn carcinoma and adenocarcinoma?

A

carcinoma - malignant tumour of epithelial cells

adenocarcinoma - carcinomas of glandular epithelum

241
Q

all carcinomas are caused by malignancies of what?

A

epithelium

242
Q

all sarcomas are malignancies of what?

A

connective tissue

243
Q

what is invasion of tumours dependent upon?

A

decreased cellular adehesion

abnormal (increased) cellular motility

prod of enzymes w/ lytic effect on surrounding tissues

244
Q

what is metastasis?

A

process by which a malignant tumour spreads from its primary site to prod secondary tumours at distant sites?

245
Q

metastasis is dependent upon what?

A

a chain of events known as metastatic cascade (detachment, invasion, intravasion, evasion of host defences, arrest, extravasation, vascularisation)

246
Q

what is the diff btwn carcinoma in situ and invasive carcinoma?

A

carcinoma in situ = can’t metastasise, can be locally removed

invasive carcinoma = worry of spreading

247
Q

breast cancer is a malignant tumour arising from what?

A

the epithelial cells lining the ducts and lobules of the breast

248
Q

name a popular anti-oestrogen drug?

A

tamoxifen

249
Q

what are 2 ways of increasing tumour size?

A

cell division

lack of cell death (apoptosis)

250
Q

T cells originate from what and mature where?

A

originate from stem cells in bone marrow

mature in the thymus

travel to blood and lymph

251
Q

does innate immunity depend on lymphocytes?

A

no, adaptive does

252
Q

draw out the graph thing of what a multipotent stem cell differentiates into :)

A
253
Q

polymorphonuclear leucocytes are mainly involved in what?

A

allergic reactions

254
Q

when are neutrophils important and what for?

A

innate immunity

phagocytosis

255
Q

what are eosinophils mainly associated w?

A

parasitic infections and allergic reactions

256
Q

what are basophils similar to? what are they mainly involved in?

A

mast cells

immunity to parasitic infections/allergic reactions

257
Q

when are monocytes important n what for ?

A

innate and adaptive immunity

phagocytosis

258
Q

how are monocytes and macrophages linked?

A

monocytes –> macrophages

once a monocyte leaves blood, it matures into a wandering/fixed macrophage

259
Q

what do T cells expresss

A

CD3 - T cell receptor complex

260
Q

what are complements?

A

group of ≈20 serum proteins that need to be ‘activated’ to be functional

261
Q

what is epitope?

A

part of the antigen that binds to the antibody/receptor binding site

262
Q

what is the most common Ig?

A

IgG

263
Q

what are cytokines?

A

proteins secreted by immune and non-immune cells

264
Q

what are interferons? (IFN)

A

induce a state of antiviral resistance in uninfected cells

limit spread of viral infection

IFNa&b - prod by virus infected cells

265
Q

what are interleukins? (IL)

A

produced by many cells

can be pro-inflammaotry (IL1) or anti-inflammatory (IL-10)

can cause cells to divide, differentiate and secrete factors

266
Q

what are tumour necrosis factors (TNF)

A

mediate inflammation and cytotoxic reactions

potent

267
Q

list examples of cytokines

A

IFN

IL

TNF

268
Q

what 3 things does innate immunity include?

A
  1. physical/chemical barriers
  2. phagocytic cells (neutrophils and macrophages)
  3. serum proteins (complement, acute phase)
269
Q

what is inflammation?

A

a series of reactions that brings cells/molcules of immune system to sites of infection or damage

270
Q

how is bacteria/funghi generally responded to?

A

phagocytosis

killing

271
Q

how are viruses generally handled?

A

cellular shut-down

self-sacrifice

cellular resistance

272
Q

what is pattern recognition

A

recognition of microbes/viruses depends on seeing ancient, conserved features of them

families of receptors exist to detect these in fluids, cell surfaces and compartments and intracellularly

273
Q

what is an adjuvant?

A

a substane which enhances the body’s immune response to an antigen

274
Q

what are the 3 types of drug interaction?

A

synergy

antagonism

other

275
Q

what are some risk factors for drug interaction?

A

patient wise:

  • polypharmacy
  • old age
  • genetics
  • hepatic/renal disease

drug wise:

  • narrow therapeutic index
  • steep dose/response curve
  • saturable metabolism
276
Q

what is the diff btwn pharmacodynamics and pharmacokinetics?

A

pharmacodynamics - what the drug does to the BODY eg falling asleep, slower HR etc

pharmacokinetics - what the body does to the DRUG

277
Q

the pharmacokinetics model of drug interaction looks at which 4 factors?

A

A - absorption

D - distribution

M - metabolism

E - excretion

278
Q

what is the biggest cause of OD in the world?

A

aspirin !

279
Q

name a drug that causes LOTS of drug ineractiosn

A

warfarin !!!!!

280
Q

what are the 3 traditional forms of vaccines?

A

live attenuated

whole killed

toxoids

281
Q

what is passive immunisation?

A

transfer of preformed antibodies

282
Q

define natural immunity

A

transfer of maternal antibodies across placenta to the developing foetus or via breast milk

283
Q

what is artificial immunity?

A

treatment with pooled normal human IgG OR treatment with immunoserum against pathogens/toxins

284
Q

what is inoculation?

A

introduction of viable microorganisms into the subject but basically

inoculation = vaccination = immunisation

285
Q

what are some advantages and disadvantages of whole live attenuated pathogen vaccines?

A

advantages

  • sets up transient infection
  • activation of full natural immune response
  • memory response (t/b cells)

disadvantages

  • immunocompromsied
  • complications
286
Q

what are some adv/disadv of whole killed, inactivated pathogens?

A

advantages

  • no risk of infection
  • storage less critical

disadvantages

  • tend to just acivate humoral response (lack of t cell)
  • immune response may be weak w/o transient infection
  • repeated booster vaccinations required
  • patient compliance can be an issue
287
Q

what are some advantages and disadvantages of subunit vaccines?

A

advantages

  • safe - only parts of pathogen used
  • no risk of infection
  • easy to store n preserve

disadvantages

  • immune response less powerful
  • repeated vaccines
288
Q

what is a drug?

A

chemical substance of known sturcture (other than nutrient/essential vitamin) which, when administered to an organism, produces a biological effect

289
Q

what is the diff btwn pharmacodynamics and pharmacokinetics again?

A

dynamics - effect of drug on body. dynamic effects that a drug may have !

kinetics - effect of body on the drug - kinetically, the drug may behave in many diff ways

290
Q

what is a drug receptor?

A

biological term for recognition proteins of endogenous mediators

291
Q

a drug which binds to a receptor is termed what?

A

ligand

292
Q

what are the diff types of ligands?

A

agonists - initiate bio response

antagonists - don’t initiate bio response but prevent naturally occuring mediators from binding

293
Q

what does efficacy refer to in drug use?

A

maximum response “drug required to prod 50% of max)

294
Q

what are some types of ligands?

A

exogenous (drugs)

endogenous (hormones, neurotransmitters etc)

295
Q

what are some types of receptors? n what are receptors?

A

principal means by which chemicals communicate

neurotransmitters, autacoids (local) eg cytokines/histamine, hormones

296
Q

what are some types of receptors?

A
  • ligand-gated ion channel
  • g protein coupled receptors
  • kinase-linked receptors
  • cytosolic/nuclear receptors
297
Q

what is an example of a ligand-gated ion channel

A

nicotinic ACh receptor

298
Q

which receptor is beta-adrenoceptors an example of?

A

g protein coupled receptors

299
Q

name a kinase-linked receptor

A

receptors for growth factors

300
Q

name a cytosolic/nuclear receptor

A

steroid receptor

301
Q

what is diff btwn affinity and efficacy?

A

affinity is how well a ligand BINDS to the receptor

efficacy is how well the ligand ACTIVATES the receptor

302
Q

what are some receptor-related factors governing drug action?

A

affinity

efficacy

303
Q

what are some tissue-related factors governing drug action?

A

receptor number

signal amplification

304
Q

what is EC50?

A

conc required for half maximal response

305
Q

sodium channels can be inhibited by afferent nerve fibres by local anaesthetics to what? (3))

A

to prevent pain

in the heart to treat arrhythmia

in the brai to treat epilepsy

306
Q

which channels may be inhibited in vascular smooth muscle to treat hypertension?

A

calcium

307
Q

potassium channels can be inhibited to treat what? (2)

A

arrhythmia

diabetes

308
Q

what are 3 main types of protein ports in cell membranes?

A

uniporters: use energy from ATP to pull molec in

symporters: use movement in of 1 molec to pull in another molec against conc grad

antiporters: 1 substance moves against grad using energy from 2nd substrance moving down its grad)

309
Q

what are xenobioitcs?

A

compounds foreign to an organism’s normal biochem, such as any drug or poison

310
Q

what are the 2 key beliefs influencing patient adherence to med?

A

necessity beliefs: perceptions abt personal need for treatment

concerns abt a range of potential adverse consequences

311
Q

what are the 4 impacts of good doc-patient communication?

A
  1. better health outcomes
  2. higher adherence to therapeutic regimens
  3. higher pt and clinician satisfaction
  4. decrease in malpractice risk
312
Q

what are the key principles of improving patient adherence?

A
  1. improve communication
  2. increase pt involvement
  3. understand pt’s perspective
  4. provide info
  5. assess adherence
  6. review meds
313
Q

what does drug elimination refer to?

A

the removal of a drug from the plasma compartment towards its eventual excretion from the body

314
Q

what is pharmacology?

A

action of drugs in the body inc: absorption, distribution, metabolism, excretion

315
Q

list 10 routes of drug admin

A
  1. oral
  2. IV
  3. IA
  4. IM
  5. SC
  6. inhalational
  7. topical
  8. SL
  9. rectal
  10. intrathecal (injection into spinal canal)
316
Q

what is pinocytosis?

A

aka fluid endocytosis

ingestion of liquid into a cell by the budding of small vesicles from the membrane

317
Q

what is pKA of a drug?

A

pH at which half of substance is ionised n half unionised

318
Q

what is the easiest and most convenient route for many drugs?

A

oral - large SA/high blood flow of S intestine –> rapid.complete absorption

319
Q

drug needs to be _____ soluble to be absorbed from the gut

A

lipid

320
Q

what is 1st pass metabolism?

A

drug taken orally have to pass 4 major metablic barriers to reach circulation:

  1. intestinal wall
  2. intestinal lumen
  3. liver
  4. lungs
321
Q

how do u avoid hepatic 1st pass metabolism

A

by giving drug to region of gut not drained by splanchnic eg mouth or rectum (GTN)

322
Q

what is the fastest route for admin?

A

IV - 20-60 secs

323
Q

what is the slowest route for drug admin?

A

transdermal (topical) - variable, mins to hrs!

324
Q

what is cytochrome p450?

A

fam of membrane bound isoenzymes

present in smooth ER, largely in liver tissue

smoking/alcohol can induce p450 enzymes - more rapid drug metabolism

325
Q

what are some naturally occuring opioids?

A

morphine

codeine (weak)

326
Q

how do opioids work?

A
  • inhibit the release of pain transmitters at SC (sup colliculus? idk)/mid brain
  • modulate pain perception in higher centres
  • euphoria (changes emotional perception of pain)
327
Q

what is potency?

A

whether a drug is strong/weak - relate sto how well the drug binds to receptor

328
Q

what is tolerance?

A

down regulation of receptors with prolonged use

need higher doses to achieve the same effect

329
Q

what is the potential with opioid use?

A

respiratory depression

addiction - esp when used for chronic stuff

330
Q

what are the 2 main neurotransmitters?

A

ACh

NAd

331
Q

where are M1/M2 (muscarinic receptors) mainly found?

A

in the heart

  • their activation slows heart, so we can block these
332
Q

where are M3 muscarinic receptors found

A

glandular and smooth muscle

  • cause bronchoconstriction, sweating,s salivary gland secretion
333
Q

where are M4/5/ muscarinic receptors found?

A

CNS

334
Q

how do u treat bronchoconstriction?

A

block M3 receptor - anti-cholinergics or anti-muscarinics

short-acting: ipratropium bromide

long-acting: LAMAs eg tiotropium

335
Q

ACh is a major transmitter innervating what?

A

skeletal muscle

336
Q

what are some side effects of anti-cholinergics?

A

in the brain - worsen memory, may cause confusion

peripherally - constipation, mouth drying, vision blurring etc

337
Q

what are inotropes?

A

group of drugs that alter contractility of the heart

positive inotropes - incr FORCE OF CONTRACTION of the heart

negative inotropes - weaken it

338
Q

how do chronotropic drugs change the heart rate n rhythm?

A

affecting the electrical conduction system of heart n nerves that influence it eg by changing rhythm prod by SA node

pos chronotropes INCR HEART RATE

neg chronotropes DECR HEART RATE

339
Q

what does alpha 1 activation cause?

A

vasoconstriction particularly in skin and splanchnic (abdo) beds

good for septic shock treatment

340
Q

beta 1 activation will do what to the heart?

A

incr HR

chronotropic effects

may incr risk of arrhythmias

341
Q

when may beta blockers be used?

A

angina

MI prevention

high BP

anxiety

arrhythmias

heart failure

342
Q

what does propranolol do and what group of drugs does it belong to?

A

beta blockers

blocks beta 1 n beta 2

  • will slow HR, reduce tremor, may cause wheeze
343
Q

what does atenolol do n what class of drugs does it belond to?

A

beta 1 selective

main efects on heart

beta blocker

344
Q

what is eclampsia?

A

a cond in which 1+ convulsions occur in a pregnant woman suffering from high BP, often followed by coma

345
Q

what is pre-eclampsia?

A

disorder of pregnancy - high BP and either large amts of protein in urine or other organ dysfunction

346
Q

what is an allergic reaction?

A

an inappropriate immune response to an otherwise harmless substance

347
Q

what are some skin clinical indications related to allergy?

A

eczema

itching

reddening

348
Q

what are some airway clinical indications related to allergy?

A

excessive mucus production

bronchoconstriction

349
Q

what are some GI clinical indications related to allergy?

A

abdo bloating

vomiting

diarrhoea

350
Q

what is anaphylaxis?

A

acute allergic reaction to an antigen EG bee sting, to which the body has become hypersensitive

351
Q

what is atopy?

A

tendency to develop allergies

352
Q

what is allergic rhinitis?

A

hayfever

353
Q

how can anaphylaxis be treated?

A

adrenaline !

354
Q

what is an adverse drug reaction?

A

unwanted/harmful reaction following admin of a drug under normal cond of use .. n its suspected to be related to the drug

355
Q

when should an adverse drug reaction be suspected?

A
  • symptoms soon after new drug started
  • symptoms after dosage increase
  • symptoms disappear when drug is stopped
  • symptoms reappear when drug is restarted
356
Q

what are the most common drugs to have adverse reactions?

A

ABs

anti-neoplastics

CV drugs

NSAIDs

357
Q

what are some common ADR’s?

A

confusion

nausea

balance issues

diarrhoea/constipation

358
Q

what are the 4 types of hypersensitivity?

A

t1 - igE mediated drug hypersensitivity

t2 - IgG mediated cytotoxicity

t3 - immune complex deposition

t4 - t cell mediated

359
Q

what happens in anaphylaxis?

A

occurs within mins, lasts 1-2hrs

rash

swelling of lips, face

wheeze/SOB

hypotension

cardiac arrest

vasodilation

incr vascular permeability

bronchoconstriction

angio-oedema

360
Q

what are some common drugs for anaphylaxis?

A

penicillin

aspirin

NSAIDs

361
Q

how does adrenaline affect the heart?

A

vasoconstriction - incr peripheral vascular resistance, incr BP, incr coronary perfusion (alpha1-adrenoceptors)

stimulation of beta1-adrenoceptors - positive inotropic and chronotropic effects

reduces oedema/bronchodilates via beta2adrenoceptors

362
Q

what do u do to a patient with suspected anaphylaxis?

A

immediately: lie flat, raise legs (if breathing not impaired)

when skills/equipment available:

  • establish airway
  • high flow oxygen
  • IV fluid challenge
    monitor: pulse ox, ECG, BP
363
Q

what does helminth mean?

A

parasitic worm

364
Q

what is the pre-patent period in a worm infection?

A

interval btwn infection n appearance of eggs in stool

365
Q

what are the 3 groups of worms (helminths)?

A
  1. roundworms (nematodes)
  2. flatworms, flukes (trematodes)
  3. tapeworms (cestodes)
366
Q

what is ascaris lumbricoides?

A

large roundworms

found worldwide, mainly tropics

children particularly prone

367
Q

what is the only common helminth infestation in the UK

A

pinworm/threadworm

368
Q

what is trichus trichirua?

A

the whipworm

369
Q

what is schistosomiasis?

A

aka bilharzia - an infection caused by a parasitic worm that lives in fresh water in subtropical/tropical regions

370
Q

what is mycobacteria?

A

a bacterium of a group which includes the causative agents of leprosy and tuberculosis

371
Q

what happens in leprosy?

A

causes lots of deformation

damages nerves

loss of sensation: ppl get injured, may lose ends of digits/limbs etc

372
Q

what is acid fast bacilli?

A

mycobacteria!

373
Q

what can mycobacteria cause?

A

tuberculosis, leprosy

374
Q

is mycobacteria easy to culture?

A

no, bc they are slow growing

375
Q

name some viruses that can cause rashes

A

rubella

measles

parovirus

376
Q

list 5 basic properties of viruses

A
  1. grow only inside living cells
  2. possess only 1 type of nucleic acid: RNA or DNA
  3. no cell wall struc but have an outer protein coat
  4. essentially inet outside the host cell
  5. protein receptors on surface allow attachment to susceptible host cells
377
Q

what are the 6 stages of virus replication?

A
  1. attachment
  2. cell entry
  3. interaction w/ host cells
  4. replication
  5. assembly
  6. release
378
Q

list 5 ways in which viruses can cause disease

A
  1. damage by direct destruction of host cells (influenza)
  2. damage by modification of host cell structure/function (HIV)
  3. damage involving over-reactivity of host as a response to infection (hep B/C)
  4. damage through cell proliferation/immortalisation (HPV)
  5. evasion of both EX/IC host defences (measles, Hep B/C etc)
379
Q

what are the medically important pathogens?

A

streptococci

staphylococci

380
Q

what are the 3 structures of bacteria?

A

spherical - COCCUS

rod-shaped - BACILLUS

SPIRAL

381
Q

what are 3 types of microorganism

A

bacteria

viruses

eukaryotic organisms

382
Q

what colour is gram positive?

A

purple

383
Q

what colour is gram negative bacteria?

A

pink / (red)

384
Q

define pathogen

A

organism that is capable of causing disease

385
Q

define comensal

A

organism which colonises the host but causes no disease in normal circumstances

386
Q

what is an opportunist pathogen?

A

microbe that only causes disease if host defence are compromised

387
Q

what is virulence/pathogenicity?

A

the degree to which a given organism is pathogenic

388
Q

what is asymptomatic carriage?

A

when a pathogen is carried harmlessly at a tissue site where it causes no disease

389
Q

what is haemolysis?

A

the ability of bacteria to break down RBC in blood agar

390
Q

what is coagulase?

A

enzyme produced by bacteria that clots blood plasma

391
Q

how can steph aureus be spread?

A

by aerosol (coughs/sneezes) and touch

eg MRSA !

392
Q

what are some infections caused by s.pyogenes?

A

wound infections

tonsilitis/pharyngitis

impetigo

scarlet fever

rheumatic fever

393
Q

what can s.pneumoniae cause?

A

it’s a normal commensal in oro-pharynx that can cause:

pneumonia

sinusitis

meningitis

394
Q

list some important gram-pos bacteria

A

s. aureus
s. epidermidis
s. pyogenes
s. pneumoniaeviridans streptococci
c. diptheriae

395
Q

how can gram positive bacteria be spread?

A

aerosols

surface-to-surface contact

colonisation of prostheses

396
Q

how can gram positive bacteria be managed?

A

antimicrobials

vaccination

397
Q

what is source of bacteraemia often?

A

infection of abdo organ

also wounds, cystitis etc

398
Q

what is the pathogenesis of salmonellosis

A

ingestion of contaminated food/water

invasion of gut epithelium - s intestine

intestinal secretory/inflammatory response

etc

399
Q

list some important gram negative bacteria

A

haemophilus influenzae

h. influenzae

bordetella pertussis (whooping cough)

n. meningitidis (meningococcus)
n. gonorrhoea (gonococcus)

campylobacter (c. jejuni, c. coli)

helicobacter pylori

chlamydiae

400
Q

what is the diff btwn yeast and mould?

A

yeast - small single celled organisms, divide by budding

moulds - form multicellular hyphae and spores

401
Q

define funghus

A

group of spore-producing organisms feeding on organic matter, inc moulds, yeast, mushrooms

402
Q

what is a spore?

A

unit of sexual/asexual reproduction - may be adapted for dispersal/survival, often for extende dperiods of time, in unfavourable cond

spores form part of life cycles of many plants, algae, fungi and protozoa

403
Q

what is mucosal candidiasis?

A

thrush

404
Q

the prodution of what, by t cells/macrophages, is important in controlling the spread of virus from 1 cell to another?

A

gamma-interferon

405
Q

how are worms in the body killed?

A

eg schistosomes coated with IgG/IgE - recognised by eosinophils - release toxic substances to kill them

406
Q

what are key attributes of pathogens?

A

infectivity

virulence

invasiveness

407
Q

what is antigenic drift n what can it result in?

A

viral spontaneous mutations, occur gradually, giving minor changes - epidemics

408
Q

what is antigenic shift n what can it result in?

A

sudden emergence of new subtype diff to that of preceding virus - pandemics

409
Q

what do adhesins do

A

help bacteria bind to mucosal surfaces

410
Q

what do pattern recognition receptors do (PRR)

A

recognise PAMPs (pathogen associated molecular patterns) but also damage associated molecular patterns from host cells

411
Q

what is a protozoa?

A

single-celled eukaryote that commonly show characteristics usually associated with animals, most notably mobility/heterotrophy

412
Q

what is african trpanosmiasis aka

A

sleeping sickness !

413
Q

what is a chancre?

A

painless genital ulcer

414
Q

what is american trypanosomiasis aka?

A

chagas disease

415
Q

discuss faecal-oral transmission

A

occurs when bacteria/viruses found in stool of 1 child/animal are swallowed by another child

416
Q

what can amoebiasis result in

A

dysentry

colitis

liver and lung abscesses

417
Q

what is myalgia

A

muscle pains

418
Q

what is a fancy word for high temp?

A

pyrexia

419
Q

if there’s fever and recent travel, question WHAT?

A

malarrrrrrrrrIA!

420
Q

how is malaria transmitted?

A

bite of female anopheles mosquito

421
Q

which plasmodium of malaria has the most severe disease?

A

plasmodium falciparum

422
Q

what kind of infection is malaria?

A

protozoan - can have up to 1 yr incubatiionperiod

423
Q

how do u diagnose malaria

A

blood film

424
Q

what are malaria symptoms?

A

FEVER

FEVER

FEVER

also: chills, headache, myalgia, fatigue, D&V, abdo pain

425
Q

what are some signs of malaria?

A

anaemia

jaundice

hepatosplenomegaly (lack water fever)

426
Q

what are some complications of malaria?

A

acute resp distress syndrome

renal failure

bleeding

shock

427
Q

what is hypovolaemic shock?

A

clinical state in which loss of blood/plasma causes inadequate tissue perfusion

428
Q

what is clostrium difficile?

A

bacterium - can infect bowel n cause diarrhoea

429
Q

how might bacteria resist ABs

A

mutations

destroy ABs

antigenic variation

430
Q

what does MRSA stand for

A

methicillin resistant stapylococcus aureus

431
Q

which factors should be considered when determining if ABs are safe for patient use?

A
  • intolerance, allergy and anaphylaxis
  • side effects
  • age
  • renal and liver function
  • pregnancy n breast feeding
  • drug interactions
432
Q

what are beta lactams?

A

cell wall (peptidoglycan) killers

433
Q

name some causative organisms for hosp acquired infectiosn

A

staphyloccocus aureus (inc MRSA)

streptococcus pyogenes (group A streptococcus)

434
Q

what are key components of infection prevention n control?

A

infection prevention n control team

ward teams

microbio/virology labs

etc

435
Q

what is the major means of HIV transmission worldwide?

A

heterosexual intercourse

other risk factors include: homosexual intercourse, IVDU, blood transfusions

436
Q

when is HIV untransmittable?

A

when it’s undetectable

(so if ur HIV+, take treatment, maintain undetectable viral load - can have sex knowing u won’t pass it on)

437
Q

what treatment is there for HIV?

A

HAART - highly active antiretroviral treatment

438
Q

in HIV how do u measure how well the immune system is doing?

A

CD4 count

439
Q

what are some methods of HIV prevention?

A

circumcision

PEP

STI control

vaccines

diagnosis/partner notif

HAART treatment as prevention

screen blood prods/needle exchange

440
Q

maintain a high index of HIV suspicion if what?

A

prolonged episodes of herpes simplex

persistent thrush

oral thrush

recent/worsening skin conditions

unexplained weight loss

441
Q

what is HIV caused by?

A

HIV-1 or HIV-2

442
Q

what happens in HIV?

A

decrease in number of CD4 t-lymphocytes by a number of related mechanisms including cell death by apoptis sand increased trapping of cells in lymphoidal tissue

443
Q

after a HIV infection, there is a variable period of _-_ months before the antibody test is positive

A

3-6

444
Q

what is the approx HIV clinically latent period before ppl start getting unwell?

A

≈ 7 years

445
Q

on presentation of antigen, CD4 cells mature in 2 types of helper cells… waht do these then prod?

A

Th1 - prod specific interleukins (IL4, 5, 10, 13)

Th2 - prod IFN alpha and TNF

446
Q

what are the 9 steps of HIV replication?

A
  1. attachment
  2. entry
  3. uncoating
  4. reverse transcription
  5. genome integration
  6. transcription of viral RNA
  7. splicing of mRNA and translation into proteins
  8. assembly of new virions
  9. budding
447
Q

how does the immune system respond to HIV? (draw the graph LOL)

A
448
Q

what is shingle in HIV patients like?

A

usually more severe

can be multidermatomal

usually occurs in elderly

449
Q

when is a HIV patient said to have AIDS?

A

when CD4 count < 200

or

when “AIDS defining illness” is present

450
Q

what are the 3 stages of a HIV/AIDS epidemic?

A
  1. nascent: HIV prevalence less than 5%
  2. concentrated: prevalence has surpassed 5% in 1+ high risk populations, but prevalence among women attending urban antenatal clinics still less than 5%
  3. generalised: HIV has spread far beyond original subpopulations - prevalence among women attending urban atenatal clinics is 5%+
451
Q

why does circumcision lower the risk of HIV?

A
  1. reduced ability of HIV to penetrate due to keratinisation of inner aspect of remaining foreskin
  2. inner part of foreskin contains langerhan cells: prime targets for hiv. these are removed w/ foreskin
  3. ulcers (characteristics of some STI’s that ca facilitate HIV transmission) often occur on foreskin
  4. foreskin may suffer abrasions/inflammation during sex that could facilitate the passage of HIV
452
Q
A

(SG) Phase 2A lectures (14 decks)

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