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Phase 2a > ICS > Flashcards

ICS Flashcards

1
Q

what is hypertrophy

A

increase in size of tissue due to increase of its constituent parts where cells get bigger

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2
Q

what is hyperplasia

A

increase in size of tissue due to increase in number of constituent cells in cells that can divide

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3
Q

what is atrophy

A

decrease in number of cells or size of cells

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4
Q

what is metaplasia

A

change in differentiation of cells

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5
Q

what is dysplasia

A

morphological changes seen in cells in progression to becoming cancer

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6
Q

what is the difference between resolution and repair

A

resolution - initiating factor removed tissue undamaged or regenerates
repair -initiating factor remains and tissue damaged

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7
Q

describe repair in 2 steps

A
  1. replacement of damaged tissue by fibrous tissue

2. collagen produced by fibroblasts

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8
Q

what is inflammation

A

reaction to injury or infection involving macrophage and neutrophil response

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9
Q

what are the 4 types of inflammation

A

acute
chronic
autoimmune
overreaction

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10
Q

3 reasons for inflammation

A
  1. fight off infection/injury
  2. increase heat to area kill bacteria
  3. make endothelial cells of vessels more permeable so macrophages/lymphocytes can escape to tissue
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11
Q

what cells are present in acute imflammation

A

neutrophil polymorphs

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12
Q

what cells are present in chronic inflammation

A

macrophages

lymphocytes - B for Ab, T for CTL

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13
Q

what is a granuloma

A

collection of macrophages surrounded by lymphocytes

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14
Q

what cell produces collagen

A

fibroblast

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15
Q

which cells dont regenerate

A

myocardial cells

neurones in CNS

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16
Q

5 stages in clotting cascade simplified (aka thrombus formation)

A
  1. endothelial injury = collagen exposed = turbulent flow
  2. collagen activates platelets to stick
  3. platelets release chemicals attract more platelets = aggregation with some RBC stuck inside
  4. clotting factors activated = fibrinogen activated into fibrin
  5. fibrin deposits on aggregation = thrombus
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17
Q

virchows triad

A
  1. change in blood flow
  2. change in vessel wall
  3. change in blood constituents
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18
Q

3 things to treat a thrombus

A
  1. aspirin inhibits platelet aggregation
  2. heparin = anticoagulant
  3. warfarin = anticoagulant
    (compression socks)
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19
Q

what is an embolus

A

mass of material in vascular system that becomes lodges within a vessel

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20
Q

what is a thrombus

A

solid mass of constituents which are formed within the intact vascular system during life

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21
Q

what is ischemia

A

reduction in blood flow to an area where no damage is done

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22
Q

what is infarction

A

reduction in blood flow that results in cell death

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23
Q

what is an atherosclerosis

A

fibrous tissue containing lipids, cholesterol, lymphocytes and SMC found within high pressure systems

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24
Q

what is apoptosis

A

intracellular events leading to death of cell without release of harmful products

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25
Q

4 steps of apoptosis

A
  1. nucleus condenses
  2. cell shrinks
  3. apoptotic bodies form
  4. macrophages remove bodies
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26
Q

give an example of consequences of lack of apoptosis and too much apoptosis

A

lack = cancer

too much = HIV

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27
Q

what is necrosis

A

traumatic cell death of big areas of cells

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28
Q

what is dermal elastosis

A

UBV light causes protein cross links = wrinkles because skin no longer elastic

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29
Q

what is carcinogenesis

A

transformation of normal cells to malignant neoplastic cells through permanent genetic alteration or mutation

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30
Q

what is oncogenesis

A

transformation of normal cells to neoplastic cells through permanent changes not necessarily malignant

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31
Q

what are carcinogens

A

cancer causing agents

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32
Q

what are oncogenes

A

tumour causing agents

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33
Q

what are mutagens

A

factors that alter DNA to cause mutations

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34
Q

5 classes of carcinogens

A 
chemical
viral
radiation
biological factors
miscellaneous
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35
Q

what is a neoplasia

A

lesion resulting from autonomous or relatively autonomous abnormal growth of cells which persists after initiating stimulus has been removed

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36
Q

what is a tumour

A

abnormal swelling may be cause by neoplasm or due to inflammation, hypertrophy, hyperplasia

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37
Q

2 components of solid carcinoma

A

neoplastic cells

stroma

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38
Q

features of benign neoplasm

A

localised
non-invasive
slow growth
resemblance to normal tissue

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39
Q

features of malignant neoplasm

A

invasive
can metastasise
rapid growth - many mitotic bodies (tho not necessarily faster than normal tissue)
variable resemblance to normal tissue

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40
Q

what is a papilloma

A

benign neoplasm of non-secretory non-glandular epithelium

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41
Q

what is an adenoma

A

benign neoplasm of secretory or glandular epithelium

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42
Q

what is a carcinoma

A

malignant neoplasm of epithelial cells

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43
Q

what is an adenomcarcinoma

A

malignant neoplasm of glandular secretory epithelium

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44
Q

if a cancer moves, what is it named in the new organ

A

same name as origin

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45
Q

what is a sarcoma

A

malignant neoplasm of connective tissue

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46
Q

what is the main effector cell in acute inflammation

A

neutrophil polymorph

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47
Q

name an example of acute inflammation

A

appendicitis

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48
Q

granulomatous inflammation occurs in what disease

A

Crohns disease

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49
Q

what is the specific name of calcification in disease

A

dystrophic calcification

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50
Q

what cells produce antibodies

A

plasma cells

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51
Q

what disease is chronic inflammation from the start

A

infectious mononucleosis (mono)

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52
Q

how are cancerous neoplasms graded

A

better the tumour resembles the surrounding tissue the lower the grade

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53
Q

what is invasion

A

process of carcinoma cells breaking through basement membrane using enzymes and invading normal tissue structures

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54
Q

what is metastases

A

carcinoma that has spread from original site to form new carcinoma at a different site

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55
Q

what is the name of a carcinoma that has not invaded through the basement membrane

A

carcinoma in situ

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56
Q

3 step process of invasion

A
  1. carcinoma in situ
  2. carcinoma breaks throu bm using enzymes = micro-invasive carcinoma
  3. eat through extracellular matrix = invasive carcinoma
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57
Q

how do carcinomas evade host defence in the blood 3 ways

A
  1. aggregate with platelets to hide
  2. shed surface antigens to confuse lymphocytes
  3. adhere to other carcinoma cells
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58
Q

what types of carcinomas metastasis in the lungs

A

any that invades veins or lymph vessels

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59
Q

what types of carcinomas metastasise in the liver

A

carcinomas of the GI tract because blood drains to liver via portal system

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60
Q

cancers of which organs are most likely to metastasise in bone

A 
BLT KP
breast
lungs
thyroid
kidneys
prostate
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61
Q

3 features of carcinoma

A

spread to lymph nodes
spread to blood to bone
micro-metastases can be present even if tumour is excised

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62
Q

main features of conventional therapy

A

non-selective for tumour cells
hits dividing cells causing bad side effects
good for fast growing tumours

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63
Q

which cancer never metastasises

A

basal cell carcinoma of the skin

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64
Q

what is a lipoma

A

benign neoplasm of adipocytes

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65
Q

what is a chondroma

A

benign neoplasm of cartilage

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66
Q

what is an osteoma

A

benign neoplasm of bone

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67
Q

what is an angioma

A

benign neoplasm of vascular tissues

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68
Q

what is a rhabdomyoma

A

benign neoplasm of striated muscle

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69
Q

what is a leiomyoma

A

benign neoplasm of smooth muscle

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70
Q

what is a neuroma

A

benign neoplasm of nerves

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71
Q

is radon gas a cause of lung cancer

A

yes

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72
Q

out of obesity smoking and drinking which is most likely to cause cancer

A

smoking

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73
Q

where does ovarian cancer commonly spread

A

peritoneum

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74
Q

5 ways to prevent pathogens harming the body

A
  1. skin is physical barrier
  2. pH
  3. mucociliary escalator
  4. phagocytic cells
  5. lysozome in tears
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75
Q

what is innate immunity

A

defence system activated immediately after infection occurs

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76
Q

8 steps in response to trauma

A
  1. coagulation
  2. acute inflammation
  3. kill pathogens and neutralise toxins
  4. clear pathogens
  5. proliferation of cells to repair damage
  6. removal of blood clot
  7. remodel extracellular matrix
  8. reestablish normal tissue function
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77
Q

what cells detect microbes in the blood

A

monocytes

neutrophils

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78
Q

what cells detect microbes in tissue

A

macrophages

dendritic cells

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79
Q

what are PRR

A

pattern recognition receptors

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80
Q

how do cells sense pathogens

A

PRRs recognise PAMPs

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81
Q

what are PAMPs and what do they do

A

pathogen associated molecular patterns

present on microbes and allow identification

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82
Q

what is DAMP

A

damage associated molecular pattern - damage is unique which allows identification

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83
Q

what is adaptive immunity

A

antigen specific immunity which is learned

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84
Q

what is cell mediated immunity

A

interplay between antigen presenting cells and T cells, requires cell to cell contact and MHC

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85
Q

what are T cell receptors TCR

A

similar structure to antibodies and act to recognise foreign antigens as long as antigen present on MHC

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86
Q

3 examples of antigen presenting cells

A

B cells
dendritic cells
macrophages

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87
Q

what is a MHC

A

major histocompatibility complex

displays self and non-self-antigens

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88
Q

describe how the humoural and cell mediated immune response interact together 4 steps

A
  1. T helper with complementary receptor to foreign antigen is selected
  2. T helper interact with MHC2 on B cell with matching receptor
  3. B cell undergoes clonal expansion to produce B memory and plasma cells (mitosis then differentiation)
  4. T cell divide to form T memory cells
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89
Q

what is pattern recognition

A

recognition of microbes and viruses depending on ancient conserved features of them

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90
Q

name 3 different types of PRR and what do they detect

A
  1. toll like receptors TLRs on cell surface membrane recognise range of patterns
  2. nod like receptors NLR detect peptidoglycan and other bacterial cell wall components
  3. rig like receptors RLRs recognise viral RNA/DNA
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91
Q

where does clonal expansion of B cells occur

A

lymph nodes

92
Q

give 2 examples of a microbial peptide secreted in lining fluids and what do they do

A

defensin
cathelicidin
lead to recruitment of immune cells

93
Q

what are lectins and what is their role

A

carbohydrate containing proteins that bind carbs/lipids in microbe walls
= activate complement
= improve phagocytosis

94
Q

what are cell-associated PRRs

A

present on cell membrane or in cytosol of cell and recognise range of molecular patterns

95
Q

what does TLR4 detect

A

lipopolysaccharides of gram -ve bacteria (forms dimer)

96
Q

what does TLR5 detect

A

flagella

97
Q

what does TLR3 detect

A

virus double stranded RNA

98
Q

what do TLR7 and 8 detect

A

single stranded virus RNA

99
Q

what does NOD2 recognise and what is its action

A

recognises muramyl dipeptide MDP

activates inflammatory signalling pathways

100
Q

give a disease for the non-functioning of NOD2 and the hyperfunctioning of NOD2

A 
non-functioning = Crohns disease
hyperfunctioning = Blau syndrome
101
Q

what may TLR4 have a homeostasis effect on

A

blood neutrophil numbers

102
Q

what are damage molecules and what do they indicate

A

molecules produced due to cellular damage and indicate presence of pathogen

103
Q

how does damage recognition occur

A

appearance of host molecules in unfamiliar context = activate TLRs
TLR signalling for inflammation and tissue repair
(may also enhance local antimicrobial signalling)

104
Q

give 3 examples of extracellular damage molecules

A

fibrinogen
hyaluronic acid
tenasin C

105
Q

give 3 examples of intracellular damage molecules

A

mRNA
heat shock molecules
uric acid

106
Q

how are PRRs present in adaptive immunity

A

TLR + other PRR activation = drive cytokine production through APC = increase likelihood of successful T cell activation

107
Q

how can TLR therapy help in disease

A

can enhance or inhibit TLR signalling

108
Q

what is the immunological theory

A

infection with an organism leads to generation of antibodies in serum = protection persists due to immunological memory = can be passed on in passive immunity

109
Q

how does vaccination work in 5 steps

A
  1. exposure to antigen
  2. antigen presentation to T cells
  3. IgM produced = causes establishment of highly specific IgG through clonal expansion of B cells
  4. takes weeks to occur
  5. IgGs produced = memory cells are formed
110
Q

what is passive immunity

A

transfer of preformed antibodies to an individual but immunological memory is not activated so not long term

111
Q

name the 2 types of passive immunity and give examples for each

A
  1. natural = maternal antibodies across placenta

2. artificial = treatment with pooled human IgG or antitoxins

112
Q

definition of inoculation

A

introduction of viable microorganism into a subject

113
Q

definition of vaccination

A

generation of immunity through manipulation of the immune system

114
Q

5 requirements of a good vaccine

A
  1. safe
  2. B and T cell response
  3. induce suitable immune response
  4. stable and easy to transport
  5. not require boosters
115
Q

what is an adjuvant in vaccination

A

any substance added to a vaccine to stimulate an increased immune response e.g. TLR agonist

116
Q

what are capsular polysaccharides

A

cell surface polymers provide protective immunity to encapsulated bacteria by preventing opsonisation by antibodies and complement

117
Q

pharmacodynamics definition

A

effect drug has on the body

118
Q

pharmacokinetic definition

A

effect body has on drug

119
Q

what is a summative effect of combined drug use

A

effect of 2 drugs is added together = greater effect equal to expected

120
Q

what is a syngeristic effect of combined drug use

A

2 drugs added together = effect is greater than expected

121
Q

what is an antagonistic effect of combined drug use

A

where 2 drugs work against eachother = no/less overall effect

122
Q

what is a potentiation effect of combined drug use

A

2 drugs added together = one has greater effect on body than expected

123
Q

what is bioavailability (F) and give the equation

A

fraction of administered drug that reaches systemic circulation unaltered

AUC oral/ AUC IV x 100

124
Q

what is the effect of gut motility on the absorption of a drug

A

greater motility = faster absorption
sympathetic NS = slow down motility because fight or flight
parasympathetic NS = speed up motility as rest and digest

125
Q

how does the acidity of a drug affect its absorption

A

unionised = can cross phospholipid bilayer

changing acidity = changes portions of ionised and unionised

126
Q

what is the significance of a high volume distribution of a drug

A

most of drug is found in tissue and not circulating in plasma

127
Q

what is the significance of low volume distribution of a drug

A

drug found circulating in plasma

128
Q

how does warfarin work

A

protein bound drug = inhibits vitamin K coagulation factors

129
Q

why should we be careful with warfarin and other drugs

A

other protein binding drugs can inhibit or increase effect of warfarin

130
Q

name 4 drug causes of AKI

A

NSAID usage
ACE inhibitors
furosemide
gentamicin

131
Q

what is druggability

A

ability of a protein target to bind to small molecules with high affinity

132
Q

what is a receptor

A

component of a cell that interacts with a specific ligand and acts to initiate a change in biochemical events leading to the ligands observed effect

133
Q

name 3 things receptors communicate with

A

neurotransmitters
autacoids e.g. histamines
hormones

134
Q

what are the 4 types of receptor

A
  1. ligand-gated
  2. G protein coupled
  3. kinase-linked
  4. nuclear receptors
135
Q

give 2 diseases associated with imbalance of drug receptors

A
  1. myasthenia gravis = loss of ACh receptor

2. mastocytosis = increased c-kit receptor

136
Q

name the 4 types of receptor ligands

A
  1. agonist
  2. antagonist
  3. partial antagonist
  4. inverse antagonist
137
Q

what is EC50

A

effective concentration needed to elicit a 50% response

138
Q

what is efficacy

A

maximum response achievable from a dose of a drug = describes how well a ligand activates a receptor

139
Q

what is affinity

A

how well ligand has capacity to bind to a receptor

140
Q

what is intrinsic activity

A

ability of a drug receptor complex to produce a maximum functional response = level to which a receptor can cause a response

141
Q

what is signal transduction

A

process that occurs between a ligand bonding to a receptor and a response occuring

142
Q

what is signal amplification

A

process of a receptor increasing signal size

143
Q

what is selective agonism

A

potency of a range of agonists

144
Q

what factors govern drug action

A
  1. receptors = affinity/efficacy

2. tissue related = no. of receptors, signal amplification

145
Q

what is receptor reserve

A

condition in tissue where agonist need to activate only a small fraction of receptors to produce a maximal response
reserve can be large or small depending on tissue

146
Q

what is tolerance

A

reduction in agonist effect over time

down regulation of receptors with prolonged use which requires higher doses to be used for an effect

147
Q

what is desensitisation

A

receptor decreases response to agonist at high concentration =
after prolonged agonist exposure receptor is uncoupled from signalling cascade

148
Q

what are the 2 types of enzyme interaction

A

irreversible and reversible

149
Q

give 2 examples of enzyme inhibiting drugs

A
  1. statins

2. ACE inhibitors

150
Q

what is a uniporter

A

uses ATP to pull molecules in

151
Q

what is a symporter

A

use movement of 1 molecule to pull in another molecule against the concentration gradient

152
Q

what is an antiporter

A

1 substance moves across a gradient using energy from another substance moving down a gradient

153
Q

describe 3 ways drugs are used in parkinsons

A
  1. target enzyme that breaks down dopamine
  2. block conversion of dopamine to 3MT in the brain
  3. central dopamine receptor agonists act on dopamine receptors = mimick dopamine
154
Q

give examples of 3 drugs that work on voltage gated ion channels

A
  1. amlodipine (Ca)
  2. lidocaine (Na)
  3. repaglinide (K)
155
Q

what is dependency

A

individual has psychological need for drug and will suffer withdrawal without it

156
Q

what is potency

A

whether drug is strong or weak = relates to how well drug binds to receptors based on receptor binding affinity

157
Q

name 3 side effects of opioid addiction

A
  1. respiratory depression
  2. sedation
  3. nausea and vomiting
158
Q

what is the opioid antagonist

A

naloxone

159
Q

what must you be aware of when admininstering naloxone

A

has short half life could wear off fast

160
Q

definition of drug absorption

A

process of drug transfer from site of administration into general or systemic circulation

161
Q

definition of drug distribution

A

process by which drug is transferred reversibly from general circulation to tissues as blood concentration increases then returns from tissues to blood when blood conc falls

162
Q

what is the volume of distribution (Vd)

A

represents the degree to which a drug is distributed in body tissue rather than the plasma
higher Vd = indicates greater amount of tissue distribution
Vd = amount of drug in tissues/concentration of drug in plasma

163
Q

drug metabolism definition

A

production of a new compound from a parent drug = ususally more hydrophilic so product can be removed in urine

164
Q

what is first pass metabolism

A

drug metabolism occurs before target organ is reached, occurs in intestines liver and lungs

165
Q

how to calculate total urine excretion

A

glomerular filtrate + tubular secretion - reabsorption

166
Q

what is clearance CL

A

volume of blood or plasma cleared of drug per unit time

167
Q

what is steady state (Css)

A

balance between drug input and drug elimination

168
Q

what is a loading dose

A

if drug has long half life then will take long time to achieve steady state = high initial dose will shorten this time
e.g. giving IV bolus + IV infusion

169
Q

what is the equation of loading dose

A

loading does = steady state x volume of distribution

170
Q

what is the equation for steady state for iv doses (??)

A

Css = rate of infusion / CL

171
Q

what is the equation for steady state for oral doses (??)

A

Css = Dosing rate/CL = dose (D) x bioavailability (F) / CL x dosage interval

172
Q

what is a stereoisomer

A

molecule that has same structural formula and sequence of bonded atoms but differ in 3 dimensional orientations of their atoms in space

173
Q

what is immunotherapy

A

passive transfer of antibodies, they must be species specific

174
Q

what is a sulphonamide nucleus

A

an unreactive and rigid group often found on drugs

175
Q

what is an adverse drug reaction

A

unwanted or harmful reaction following administration of a drug/combination of drugs under normal conditions of use and suspected to be related to drug - has to be unintended and noxious

176
Q

how do side effects differ from ADRs

A

unintended effect of drug but related to pharmacological properties and can include benefits

177
Q

what is a toxic effect

A

effect caused by level of drug beyond therapeutic range

178
Q

what is a hypersensitivity effect

A

effect caused by level of drug far below therapeutic range

179
Q

what is a type A ADR

A 
= augmented
predictable
dose dependent
common
e.g. morphine and constipation
180
Q

what is a type B ADR

A 
= bizarre/idiosyncratic 
unpredictable
not dose dependent
inherited response = enzyme deficiency
abnormal receptor activity = e.g. calcium rise = increase muscle contraction
e.g. penicilin and anaphylaxis
181
Q

what is a type C ADR

A

= chronic
chronic use of a drug causes adverse effects
e.g. steroids and osteoporosis

182
Q

what is a type D ADR

A

= delayed
delayed effect occurs due to drug
e.g. malignancies after immune suppression

183
Q

what is a type E ADR

A

= end of treatment
abruptly stopping drugs can cause bad reaction
e.g. when ending antiseizure medication

184
Q

what is a type F ADR

A

= failure of therapy

drug not working due to other drugs

185
Q

what is DoTS

A

dose relatedness
timing
patient susceptibility

186
Q

when should you suspect an ADR

A
  1. start after new drug started
  2. occur after dosage increase
  3. disappear when drug stopped
  4. reappear when drug restarted
187
Q

name 6 most common ADRs

A 
confusion
nausea
balance problems
diarrhoea
constipation
hypotension
188
Q

what is an allergy

A

abnormal response to harmless foreign material

189
Q

what is atopy

A

tendency to develop allergies

190
Q

what is non immune anaphylaxis

A

reaction identical to allergic anaphylaxis but directly caused by direct mast cell degranulation - some drugs can cause, no previous exposures required

191
Q

how do allergies occur - 2 steps

A
  1. interaction of drug/metabolite with individual = cause antibody formation/immunity
  2. subsequent re-exposure to drug/metabolite = causes a reaction
192
Q

describe a type 1 allergic reaction

A

e.g. anaphylaxis
IgE Ab form after initial exposure
IgE attach to mast cells
re-exposure = mast cell degranulation = histamine release

193
Q

describe a type 2 allergic reaction

A

e.g. autoimmune haemolytic anaemia
allergen combines with protein = body treats as foreign and forms IgG+IgM Ab
Ab-Ag = complement activation
damages cells

194
Q

describe a type 3 allergic reaction

A

e.g. rheumatoid arthritis
Ag-Ab form large immune complex’s
activates complement
cause small vessel damage = leucocytes attracted to site = inflammation

195
Q

describe a type 4 allergic reaction

A

e.g. coeliac disease
delayed hypersensitivity
Ab specific receptors form on T cells at first exposure
2nd exposure = local reaction occur

196
Q

what is zero order kinetics

A

decline of concentration of drug within blood over time decreases at a constant rate often due to enzymes becoming saturated

197
Q

what is second order kinetics

A

decline of conc of drug in blood decreases exponentially as drug is distributed to the tissues

198
Q

what is half life (T1/2)

A

time taken for concentration of drug within blood to half (elimination rate from plasma)

199
Q

what is the equation for half life

A

t1/2 = 0.693 / k (rate constant of elimination)

200
Q

how do you work out clearance CL

A 
CL = dose of drug (IV) / area under blood conc/time curve
CL = dose of drug (oral) x F bioavailability / area under curve
201
Q

what is the rate constant of elimination

A

k = CL/Vd

202
Q

why is Vd important/what does it determine

A

total amount of drug that has to be administered to produce a particular plasma concentration

203
Q

what is the equation for Vd

A

Vd = total amount of drug in body (dose) / plasma concentration

204
Q

acute inflammation defintion

A

initial and usually transient series of tissue reactions to injury

205
Q

name 5 causes of inflammation

A
  1. microbial infection
  2. hypersensitivity
  3. physical agents
  4. chemicals
  5. tissue necrosis
206
Q

describe the physiological process of inflammation

A
  1. vasodilation = brings neutrophil polymorphs to damaged area
  2. increase vascular permeability = fluid leak into extracellular space = oedema
  3. cellular exudate formation = neutrophils through endothelial cells to extracellular space
207
Q

describe the functions of histamine

A

vasodilation
emigration of neutrophils (chemotaxis)
increased vascular permeability
pain and itching

208
Q

microscopic appearance of chronic inflammation

A

fibrosis
chronic ulcer
abscess cavity
granulatomous inflammation

209
Q

what is a histiocytic giant cell

A

indigestible foreign material cause macrophages to fuse together = become multinuclear giant cells and collect to form granulomas

210
Q

describe the healing process from abrasion

A
  1. epidermis scraped off = scab forms

2. new epidermis grows under scab = normal regeneration

211
Q

describe 1st intention healing (positive)

A
  1. thin incision = fibrinogen exudation
  2. fibrin stitches 2 sides together
  3. collagen production and epidermis regrowth = small scar
212
Q

describe 2nd intention healing (negative)

A
  1. large loss of tissue=granulation tissue formation
  2. wound heals from bottom up = organisation and capillary formation
  3. fibrous tissue formation = large scar
213
Q

what is the consequence of a venous system embolism

A

goes to right side of heart = to pulmonary system = pulmonary embolism

214
Q

what is the consequence of an arterial system embolism

A

goes to left side of heart = into systemic circulation = embolism anywhere

215
Q

describe reperfusion injury

A
  1. reactive hyperaemia = cells overwhelmed with oxygen

2. reactive oxygen species formation = tissue damage and inflammatory response

216
Q

what are watershed areas

A

parts of brain have dual blood supply but ischaemia can occur with low BP

217
Q

what is a transmural MI

A

ischemia in the subendocardium spreads to the epicardium and involves full thickness of the myocardium

218
Q

what is a subendocardial MI

A

also called NSTEMI

involves ischaemia and necrosis of the innermost part of myocardium

219
Q

what is cleft palate

A

cells fail to migrate and join fulcrum of mouth

220
Q

what are some effects of downs syndrome

A

increased beta amyloid production
cause earlier dementia
increased cataracts risk

221
Q

describe 4 features of age related cell damage

A
  1. cross linking of DNA/proteins
  2. loss of Ca influx control = mitochondrial damage
  3. free radical generation and peroxidation of cell membrane
  4. accumulation of toxic byproducts
222
Q

describe the effects of adrenaline following anaphylaxis (4)

A
  1. vasoconstriction = raise BP
  2. stimulate beta 1 adrenergic receptors = postiive ionotropic and chronotropic effects = increase SV and HR
  3. stimulate beta 2 adrenergic receptors = bronchodilation and less oedema
  4. increase intracellular cAMP = reduce inflammatory mediators + prevent histamine release from mast cells/basophils
223
Q

describe the emergency treatment for anaphylaxis

A

ABCDE (disability and exposure)
1. adrenaline 500 micrograms IM
2. establish airway and give O2
3. fluids 500-1000ml bolus
4. steroids = hydrocortisone 200mg IM/slow IV
antihistamines = chlorphenamine 10mg IM/slow IV

224
Q

why might a 2nd dose of adrenaline be required for anaphylaxis

A

adrenaline = 2-3 min half life

may need more to continue effects

225
Q

what blood test is needed to confirm anaphylaxis and when does it need to be taken

A

mast cell tryptase
high tryptase = anaphylaxis or an allergy
negative tryptase = its NOT anaphylaxis
1. asap after Tx
2. 1-2 hrs but no later than 4hrs after symptom onset
3. 24hrs/at follow up

226
Q

describe why a lower does of morphine is given in renal failure

A

morphine -> morphine-6-glucuronide = very potent
M6G excreted very quickly by kindeys
if kidney are not healthy/in failure = M6G build up in kidneys = nephrotoxicity and respiratory depression
= lower dose
= longer dose intervals

Phase 2a (15 decks)

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