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yr 1 uni work > 131 > Flashcards

131 Flashcards

1
Q

healing as a pathological process

A

stimulated by a pathological stress such as physical injury, collagen deposition in scar tissue

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2
Q

genetic and immune factors as a pathological process

A

affect a cell/organ ability to adapt to environmental stresses leading to different susceptibilities to disease

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3
Q

environmental changes outside the acceptable physiological range gives rise to the cell stress response- give examples

A

osmotic stress
temp stress
oxygen/energy deprivation
injury / infection
homeostasis disruption

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4
Q

what happens when you fast

A

fatty acids are mobilised from adipose tissue this is a normal response from an energy store but long term can lead to atrophy

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5
Q

what occurs when you start lacking calcium

A

calcium is mobilised from bone matrix- leads to calcium deficiency in bones in the long term

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6
Q

physiological definition

A

the normal functions of living organisms

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7
Q

metaplasia

A

from one morphology to another , transformation of one differentiated cell type to another differentiated cell type. The change from one type of cell to another may be part of a normal maturation process

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8
Q

whats a ‘housekeeping’ gene

A

normal structural proteins (non essential proteins)

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9
Q

what happens to housekeeping genes during cell stress

A

they are downregulated so they stop producing non essential proteins

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10
Q

whats a cells stress gene

A

cell-organising/protective functions
eg heat shock proteins (HSPAs), NF-KB, AP-
they have a high degree of evolutionary conservation which promotes essential response to cell survival

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11
Q

what do HSPs do in cell stress

A

act as chaperones, protect proteins, assist refolding, prevent protein aggregation

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12
Q

what does ubiquitin do during cell stress

A

targets protein for destruction by specific proteases(proteasome) - to be recycled/eliminated to prevent them building up and causing disease like lewy body in dementia

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13
Q

what does chronic stress result in

A

visible aggregates of constituents known as inclusion bodies , eg lewt body ( aggregations of a-synuclein) in nerve cells

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14
Q

hyperplasia

A

increase in number of tissue cells due to increased cell division - can be normal eg in breasts for lactation

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15
Q

hypertrophy

A

increase in size of existing cells, matched by increase in functional capacity - eg in muscle cells

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16
Q

is the endometrial lining during menstrual cycle hyperplasia or hypertrophy

A

hyperplasia

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17
Q

are skeletal muscle fibres of athletes hyperplasia or hypertrophy

A

hypertrophy

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18
Q

colonic epithelial hyperplasia

A

normal colon is smooth single layer epithelial cells and short crypts. hyperplasia increases no of cells resulting in deeper crypts

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19
Q

transient colonic epithelial hyperplasia benefit

A

may help expel intestinal pathogens by increasing speed

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20
Q

benign prostatic hyperplasia (BPH)

A

hyperplasia of prostate cells
not a risk factor for carcinoma just normal adaptive response in most cases related to age

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21
Q

apoptosis overview

A

programmed cell death- a way of eliminating itself to protect the surrounding tissue from damage

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22
Q

necrosis overview

A

unable to adapt to stress is when this occurs- it releases contents such as enzymes into surrounding tissues damaging more cells

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23
Q

apoptosis phase 1

A

induction/signalling - anti-apoptotic protiens Bcl-2 deactivated

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24
Q

apoptosis phase 2

A

effector- mitochondrial permeability , looses ionic gradient needed

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25
Q

apoptosis phase 3

A

degradation- proteases- morphology- cells start to shrink and organelles disintigrate

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26
Q

apoptosis pahse 4

A

phagocytic- cell fragments are engulfed and removed - to prevent further damage to surrounding cells

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27
Q

is apoptosis a normal process +example

A

yes- as removal of autoreactive immune cells to prevent autoimmune diseases
intestinal cell turnover
embryogenesis and development

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28
Q

what happens when apoptosis isnt controlled properly

A

leads to caner

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29
Q

necrosis

A

uncontrolled cell death where enzymes and dna are released which will lead to an inflammatory response in surrounding tissues

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30
Q

necrosis triggers

A

any acute stressor eg metabolic stress, hyposxia, absence of nutrients, trauma

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31
Q

common molecule mechanisms that occur in necrosis

A

-reduction in ATp= cloudy swelling ,reducing biosynthesis
- increase in ca++ activates protein kinases, phospholipases start to break wall
- reduction in ability to scavange ROS causing further damage
- cells swell, lyse and burst

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32
Q

hypoxia

A

reduction or absence of normal o2 supply to an organ - fairly rapid necrosis

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33
Q

specific chemical agents that cause necrosis

A

carbon tetrachloride(CCl4)
paracetamol overuse

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34
Q

infarction definition

A

death of tissue

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35
Q

what does acute ischaemia and reperfusion injury lead to

A

increase in ca++ , phospholipase and lysozymes , cell damage and then necrosis

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36
Q

is apoptosis active or passive

A

active so ATP dependant - does not occur at 4 degrees

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37
Q

is necrosis active or passive

A

passive so occurs at 4 degrees

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38
Q

what happens to cytoplasm in apoptosis

A

shrinks

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39
Q

what happens to cytoplasm in necrosis

A

swelling

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40
Q

apoptosis in gel electrophoresis

A

non- random degradation of dna = ladder pattern on agrose gel as it is a controlled breakdown of dna

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41
Q

necrosis on gel electrophoresis

A

random digestion of dna = smear on agarose gel

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42
Q

dysplasia

A

abnormal growth or development

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43
Q

anaplasia

A

reversion of cell to primitive/undifferentiated state

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44
Q

neoplasia

A

formation of tumour

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45
Q

benign

A

not threatening to health or life

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46
Q

malignant

A

invasion of surrounding tissue/tendancy to metastasize

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47
Q

fixation- light microscope

A

halts biological activity and prevents tissue degradation and renders cells more amenable to staining

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48
Q

e.g. of fixatives for light microscope

A

formaldehyde and glutaraldehyde

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49
Q

embedding in light microscopy

A

supports tissue by embedding in stuff like paraffin wax or freezing or plastic resin
can cause artifacts

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50
Q

artifact

A

distortion in tissue
like fine lines, freeze thaw holes

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51
Q

cryostat

A

tissue frozen (-10-20c)
thickness 10-40um
collected on slides or free-floating

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52
Q

microtome

A

embedded in wax at rtp
thickness 5-40um
collected onto slides

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53
Q

vibratome

A

glued to holder rtp/chilled
thickness 40-400 um
collected on slides or free floating

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54
Q

haematoxylin

A

basic dye- so stains acidic structures purplish blue
nuclei, ribosomes

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55
Q

eosin

A

acidic dye- so stains basic structures red/pink
cytoplasmic proteins

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56
Q

giemsa stain

A

blood cell staining, nucleus dark blue to violet and cytoplasm pale blue

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57
Q

toluidine

A

basic stain
stain acidic components blue/purple

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58
Q

Massons trichrome stain

A

stains connective tissue, nuclei/basophilic structure blue, collagen green or blue, cytoplasm red

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59
Q

periodic acid- Schiff rxn

A

stains complex carbs purple

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60
Q

simple columnar epithelium function

A

absorptive
secretory

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61
Q

stratified epithelia function

A

protective function
e.g. skin

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62
Q

brain tissue function

A

thin axon for rapid-cell communication

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63
Q

smooth muscle tissue

A

elongated cells to maximise contractle properties

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64
Q

human tissue act

A

2004
regulated activities like removal, storage, use and disposal of human tissue.
lawful consent needed
tissue removed and stored for diagnosis not under act

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65
Q

4 cardinal effects of acute inflamation

A

rubor- redness
calor- heat
dolor- pain
tumor- swelling

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66
Q

rubor- redness

A

vessel dilation and increased blood flow to site

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67
Q

calor- heat in inflam

A

vessel dialtion and increased blood flow to site

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68
Q

dolor- pain in inflam

A

pressure on nerve endings/ chemical factors

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69
Q

response to acute inflammation

A

release of chemical mediators that stim production of exudate. this destroys infective agents and damaged tissue is partly liquified and removed from site

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70
Q

exudate (simple)

A

fluid
proteins
blood cells that mobilise local defences

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71
Q

exudate (complicated)

A
  • salt, fibril, neutrophils (first on site of infection, phagocytic cells), macrophages( phagocytes+ produce cytokines,2nd wave response), dendritic cells (present antigen to t-cells), lymphocytes(cytotoxic and helper t-cells) ENTER WHEN BLOOD VESSELS BECOME LEAKY
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72
Q

exudation

A

when flow slows/vessels dilate, endothelial cells swell and partially retract, water salts proteins

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73
Q

transmigration/ diapedesis

A

The tissue macrophages release chemokines and cytokines which the leukocytes are attracted to , this is mediated by selectins on endothelial cells and integrins on leukocytes. Leukocytes then form pseudopodia and produce proteases to help move through the endothelial cells of veins to go into the tissue

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74
Q

how can chronic inflammation develop

A
  • damaging stimuli persist and healing cant occur necrosis, organisation and repair all happening at once. tissues are infiltrated by activated lymphoid cells
  • continued tissue damage- tissue-based immune response where lymphoid cells and macrophage are infiltrated
  • macrophages are the main effector cell and they may form clusters called granulomas= granulomatous inflammation
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75
Q

tuberculosis

A

mycobacterium tuberculosis invades and replicates within macrophages which evades acute inflammation response. granulomas form in the lung surrounded by necrotic tissue

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76
Q

crohns disease

A

chronic intestinal inflammation
cycle of relapse and remission
complications are fibrosis and stricture (prevent food movement in gut)
no defined cause but could be wrong response to commensal microflora

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77
Q

microscopy

A

Subjective interpretation- human error
Cost of human labour
Widely available
Little training
Use antibodies for specific labelling
Difficult to assess multiple types of antigens at same time
Preserve tissue structure
Low throughput

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78
Q

flow cytometry

A

Automated reducing error
Cost of equipment
Less available
Require training
Use antibodies for specific labelling
Multiple cell types can be assessed at the same time
Loss of tissue structure during procedure
High throughput

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79
Q

ultrasound

A

high frequency sound waves
low resolution

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80
Q

CT

A

computerised tomography
uses x-ray to image quickly
less detail than ultrasound and MRI

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81
Q

MRI

A

magnetic resonance imaging
strong magnetic fields and radio waves
more detail but slower than CT

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82
Q

neoplastic transformation

A

loss of differentiation- cells become more like precursor cells

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83
Q

anaplasia

A

poorly differentiated cells
cells look dissimilar to normal tissues where there is also a lack of anchorage-dependant growth and loss of contact inhibition

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84
Q

protozoa

A

single celled animals, infect all tissues/organs. usually in tropic regions, bite transmission/ accidental ingestion
intracellular parasites or as extracellular parasites infection

asexual reproduction

85
Q

how are viruses classified

A

type of nucleic acid, mode of replication, symmetry, presence of envelope

86
Q

bacteria classification

A

practical characteristics such as size, shape, colour, immunologic, respiration. etc.

87
Q

conventional specimen processing

A

details checked against request form
specimen grown on relevant culture media
incubated

88
Q

commensal microorganisms

A

1 organism survives in another without causing harm (debated)

89
Q

opportunistic infection

A

because of weakend immune system

90
Q

why do microbes rarely lead to disease

A

an infection is dependent on mechanisms of both innate and required resistance as it is a conflict between 2 organisms

91
Q

pneumonia

A

most common cause of infection-related deaths in USA and Europe
caused by large range of microorganisms (children usually viral and adults bacterial origin)
indistinguishable symptoms (lab id needed)
infection through inhalation, aspiration of normal flora, via blood

92
Q

pneumonia symptoms

A

cough
chest pain
fever
confusion
shortness of breath

93
Q

epidemiology definition

A

study of factors, implicated in disease progression that determines its frequency, distribution and severity in cohorts of individuals

94
Q

endemic definition

A

diseases that occur at a constant rate within a given population

95
Q

epidemic

A

incidence of disease above the endemic rate

96
Q

pandemic definition

A

worldwide epidemic- new strains little immunity

97
Q

influenza

A

influenza A undergoes major genetic changes rapidly so immunity becomes redundant
2009 pandemic was a re-assortment of genes between human, avian and pig flu strains

98
Q

factors that influence disease distribution

A

person- age, gender, ethnic background, education, occupation
location- geographic, social
occurrence- episodic, cyclical, secular

99
Q

epidemiology of cancer

A
  • leading cause of death worldwide for 7.6 million deaths in 2008
  • tobacco use is major risk factor, also alcohol, diet and inactivity
  • more than 30% of cancer deaths can be prevented
100
Q

examples of sample media

A

urine, faeces, cerebral fluid, sweat, saliva, arterial blood

101
Q

internal quality assurance

A

daily/ every time a test is used, test results compared to monitor performance

102
Q

external quality assurance

A

identical samples distributed to several labs and comparison of the labs to maintain high standards

103
Q

precision

A

reproducibility- how many times do you get same results

104
Q

accuracy

A

how close the measured value is to the actual value

105
Q

sensitivity

A

how little of the analyte can be detected by the assay

106
Q

specificity

A

how good is the assay at discriminating between the requested analyte and other interfering substances

107
Q

common errors in collection of biochemical specimens

A

gender, diet, stress/anxiety/ menstrual cycle, strenuous exercise, time of day

108
Q

Us and Es test

A

urea and creatinine and electrolytes

109
Q

LFT test

A

alkanine phosphatase; alanine amino transferase, bilirubin, albumin

110
Q

kidney function

A
  • regulates extracellular fluid vol and electrolyte balance
  • selective reabsorption of ions
  • secondary endocrine function- hormones like renin
111
Q

urea

A

breakdown product of protein in liver

112
Q

creatinine produced?

A

muscles

113
Q

normal GFR

A

100-120

114
Q

whats GFR

A

glomerular filtration rate

115
Q

what happens when GFR is reduced

A

serum urea and creatinine increase when GFR in kidneys is reduced (so less excreted)

116
Q

ADH

A

from pituitary gland
causes reabsorption of water in collecting ducts, released after hypothalamus detects low water in blood

117
Q

aldosterone

A

from adrenal gland
causes reabsorption of Na+ in nephron and water releases from renal via the renin-angiotensin-aldosterone system (RAAS)

118
Q

distal

A

tubule far away from glomerulus

119
Q

normal na levels

A

135-145 mmol/l

120
Q

hyponatraemia oedematous symptoms

A

oedematous(swelling)
heart failure?
decrease in effective blood volume(water moved to brain)
aldosterone and ADH secreted
salt and water retained

121
Q

hyponatraemia non-oedematous symptoms

A

too much water in collecting ducts of kidney
ADH released

122
Q

hyponatraemia oedematous treatment

A

diuretic and restrict fluid + treat condition

123
Q

hyponatraemia non-oedematous treatment

A

restrict fluid

124
Q

hyponatraemia na levels

A

na> 135 mmol/l

125
Q

hypernatraemia na levels

A

na>145 mmol/l

126
Q

hypernatraemia causes

A

water depletion
excessive na intake
renal failure

127
Q

hypernatraemia clinical signs

A

decreased blood pressure (increased if salt gain)
low urine output
dry mucous membranes

128
Q

hypernatraemia treatment

A

oral water
IV 5% dextrose

129
Q

hyperkalaemia K+ levels

A

K+ > 4.9 mmol/l

130
Q

hyperkalaemia causes

A

renal failure
adrenal failure
renal failure
k+ release from damaged cells

131
Q

hyperkalaemia treatment

A

calcium gluconate , insulin + glucose, dialysis

132
Q

hypokalaemia k levels

A

K+ < 3.4 mmol/l

133
Q

hypokalaemia causes

A

vomiting
diarrhoea
diruetics

134
Q

hypokalaemia symptoms

A

weak cardiac arrhythmias
vomiting/ diarrohea

135
Q

hypokalaemia treatments

A

oral or IV K (slowly with ECG monitoring)

136
Q

anuric

A

no urine

137
Q

oliguric

A

<400ml/day

138
Q

acute renal failure (ARF) sympotoms

A

concentrated urine
serum urea and creatine increase
hyperkalaemia- nephron cant excrete K when GFR decrease

139
Q

acute renal failure causes

A

pre-renal= blood supply to kidney failure
renal= damage to kidney tissue
post renal= obstruction blocks urinary drainage

140
Q

acute renal failure treatment

A

treat underlying disease
dialysis if severe

141
Q

chronic renal failure (CRF)

A

hyperkalaemia- nephron cant excrete k when GFR decreases
serum urea and creatinine high

142
Q

management of CRF

A

sodium restriction
diuretics
dietary restriction of protein
oral ion exchange resin (k removal)
longer-term plans for dialysis or transplant

143
Q

myocardial

A

heat muscle

144
Q

infarction

A

death of tissue after lack of blood supply

145
Q

morbidity

A

the condition of suffering from a disease/medical condition

146
Q

left coronary artery

A

circumflex artery -left ventricle and atrium,

147
Q

anterior interventricular branch

A

both ventricles

148
Q

post interventricular branch

A

right coronary artery
both ventricles

149
Q

marginal branch

A

right coronary artery
right ventricle after entering capillaries, blood drains into coronary veins then coronary sinus and empties into right atrium

150
Q

tunica intima

A

endothelium
basement membrane
internal elastic lamina

151
Q

tunica media

A

smooth muscle
external elastic lamina

152
Q

tunica externa

A

elastic and collagen

153
Q

usual reason for MI

A

atheromatous plaque residue with overlying thrombosis

154
Q

cause of MI steps

A
  • Initial damage to endothelium in arteries (>2mm diameter).
  • Cholesterol-rich low density lipoproteins enter the intima and taken up by macrophages
  • Fat-laden macrophages (FOAM CELLS) underneath endothelial cells = FATTY STREAK
  • Macrophages release lipid (and chemical signals) into intima.
  • Cells of intima release collagen in response to signals.
  • Formation of a raised yellow smooth area = LIPID PLAQUE
  • Fibrolipid cap forms
  • Endothelium fragile and often ulcerates
  • Platelets aggregate on plaque which stimulates thrombus formation
155
Q

consequences of atheroma

A
  • artery narrowing- ischaemia, hypoxia, angina pectoris, pain
  • thrombus formation on plaque- Mi
  • bleeding into the plague- can occur in coronary arteries
  • aneurysm
156
Q

arteriosclerosis

A

thickening/hardening o arery wall

157
Q

atherosclerosis

A

thickening/hardening of high pressure artery wall caused by atheroma

158
Q

atheroma

A

lipid-rich accumulation in arteries

159
Q

acute MI

A

altered level of cardiac muscle biomarker, crushing chest pain, ECG changes, imaging evidence

160
Q

how long does an MI ECG take to develop- impact

A

24hours
so may be difficult to interpret but show an elevated ST region

161
Q

cardiac biomarkers

A

enzymes- creatine kinase, lactate dehydrogenase and aspartate amino transferase (not used since 2000)
muscle proteins- myoglobin (detectable 2/3 hours after Mi), troponin I and T

162
Q

troponins

A

a complex with actin and myosin and regulates the concentration of striatedd muscles
3 forms= C, I, T

163
Q

troponin c

A

binds calcium- regulates the action of the filaments during contraction

164
Q

troponin I

A

inhibitory subunit- prevents contraction in the absence of calcium and troponin C

165
Q

troponin T

A

binds the complex to tropomyosin

166
Q

how to diagnose MI

A

cardiac damage causes release of cell components into bloodstream and you can measure the cTnT or cTnI to diagnose infarction

167
Q

treatments for MI

A

thrombolytic agents - streptokinase
anticoagulant-heparin
coronary angioplasty
coronary bypass

168
Q

coronary angioplasty

A
  • catheter inflated in obstructed vessel to remove obstruction and enable blood flow
169
Q

coronary bypass

A

graft of artery or vein to coronary artery which enables blood to glow around the obstruction

170
Q

hyperglycaemia

A

diabetes, insulin released and the glucose enters cells

171
Q

hypoglycaemia

A

hyperinsulinism, glycogen storage disease. Low blood glucose, glucagon release and the liver cells release glucose

172
Q

diabetes mellitus

A
  • Persistent hyperglycaemia
  • Normal blood glucose values 4-6 mmol/l
  • Now information out about diabetes being linked to dementia
  • 9% of children population have diabetes
173
Q

diagnosis of diabetes mellitus

A

urine glucose test
HbA1c
fasting blood glucose
random
oral

174
Q

urine glucose test

A

10 mmol/l glucose overspill- glycosuria

175
Q

HbA1c in diabetes testing

A

as glucose conc rises more HBA becomes glycated and % present as HbA1c increases, shows poorly controlled diabetes, but limitations include the fact other conditions show elevated HbA1c eg opiod abuse, iron deficiency

176
Q

fasting blood glucose

A

> 7 mmol/l

177
Q

random blood glucose

A

> 11 mmol

178
Q

what happens to glucose when blood glucose is too high

A

turned into glycogen as the beta cells release insulin

179
Q

what happens when blood glucose is too low

A

glycogen back into glucose via glucagon which is released via alpha cells

180
Q

beta cells and insulin release

A

Glucose enters b cell- phosphorylated; glycolysis, pyruvate formed,
Atp is produced during this and the k channel closes so k+ rises in cell
The membrane depolarises and calcium channel opens so calcium rises in cell
Insulin granules exocytosis

181
Q

insulin binding to receptors

A

insulin receptor is a tyrosine kinase receptor consisting of 2a and 2b subunits embedded in the plasma membrane.
Binding of insulin to the a-subunits results in phosphorylation of the b-subunits thus activating the kinase activity.
This results in glucose utilisation and further glucose uptake via a range of signal transduction pathways that increase the number of glucose transporters (GLUT 4) in the plasma membrane.

182
Q

type 1 diabetes

A
  • Body does not produce enough insulin
  • 10% adults with diabetes have type 1
  • 95% children with diabetes have type 1
  • Mainly due to autoimmune mediated destruction of pancreatic-b-cells which results in insulin deficiency
  • Weak family trait contracted at ages 9-13
  • Only treated by insulin administration or pancreas transplant
183
Q

type 2 diabetes

A
  • Body produces insulin but cant use it well
    -90% adults with diabetes have type 2
    -2% of children with diabetes have type 2
    -Characterised by insulin resistance on tissues
    -Associated wit over nutrition, obesity, lack of excersize
    -Strong family trait- environmental and genetic
    -Usually seen in over 40s- is now seen in children sometimes
    -Treatment- reduce calories, carbs and exercise, sulphonylureas- b cells secrete more insulin, bariatric surgery for weight loss
184
Q

gestational diabetes

A

temporary during pregnancy

185
Q

long term effects of diabetes

A

microvascular complications
neuropathy
nephropathy- atherosclerosis, arteriosclerosis
heart /brain complications
risk of alzheimers disease
retinopathy

186
Q

neuropathy

A

defective blood supply to neurons, axon degeneration, sensation loss, diabetic trophic ulcers, ischaemia in feet

187
Q

nephropathy

A

Atherosclerosis- aorta and renal arteries nephron ischaemia
Hyaline arteriolsclerosis- thickening of glomerular capillary basement membrane (glycation of proteins)
Expansion of mesangial matrix
Glomerular damage= increased permeability, proteinuria (renal failure), microalbuminuria

188
Q

heart/brain complications in diabetes

A

Type 2 diabetes with blood glucose level of 190mg/dl have a 40% higher risk of dementia
Middle aged type 1 higher risk of brain lesions and slower cognitive function
Experiencing episode of extremely low blood sugar associated with risk of Alzheimer’s disease

189
Q

retinopathy in diabetes

A

Hyaline arteriolosclerosis= membrane thickening in retinal blood vessels (retinal haemorrhage)
Cataracts- glucose attaches to lens proteins and form cloudy vision

190
Q

components of blood

A

55% plasma
45% rbcs
buffy coat- wbc and platelets

191
Q

plasma components

A

90% water
ph 7.4
electrolytes
plasma proteins

192
Q

erythrocytes

A

Biconcave- mean diameter 7.8um and 25um at circumferential border
Larger surface are for oxygen diffusion
No nucleus
120 day lifespan
Oxygen and co2 transport
Each RBC has haemoglobin and enzymes

193
Q

wbc types

A

neutrophils
monocytes
eosinophils
basophils

194
Q

Sickle cell anaemia

A

– abnormal beta chain
-Haemoglobin chains tick when deoxygenated
-Erythrocyte deformed and stuck in capillaries
-Tissues are then starved of oxygen
-GAG to GTG ( glutamic acid to valine)

195
Q

Thalassemias

A

Alpha or beta thalassemia
Reduced rate of synthesis of a or b globin chains
Erythrocytes small and stain weakly with eosin
Abnormal; erythrocytes made then destroyed- anaemia results

196
Q

why do blood transfusions

A

-Needed to replace blood loss e.g. in surgery or trauma
-Needed to correct anaemia e.g. thalassaemias
-Need compatible blood for transfusion

197
Q

complication of blood transfusions

A
  • Wrong blood given to patient resulting in chest and abdomen pain, vomiting
  • Iron overload- repeated transfusions without haemorrhage the iron deposits in organs
  • Infection- new variant Creutzfeldt-Jakob disease, HIV
198
Q

exogenous

A

from another person or the environment

199
Q

endogenous

A

from another site in the patient- But it must be environmentally acquired before hospital admission

200
Q

HAI

A

healthcare associated infection
With earlier discharges to reduce costs fewer are recognised while the patient is still in hospital,
In many hospitals it Is preventable e.g. puerperal fever (uterine tissue infection) came from physicians hands

201
Q

most common HAI

A

-Pneumonia/ respiratory tract infection 22.8%
-UTI 17.2%
-Surgical site infection 15.7%
-Clinical sepsis 10.5%
-Gastrointestinal infections 8.8%
-Bacteraemia- bacteria in blood 7.3%
-Others: pressure sores, hepatits…
-Drug resistant examples include MRSA, VRE, MDRE

202
Q

MRSA

A

methicillin-resistant staphylococcus aureus
Mostly resistance to common antibiotics so very difficult to treat especially when in the blood stream (bacteraemia)
‘search and destroy’- routine MRSA screening of staff and patients
Mandatory reporting of bacteraemia
Government targets to reduce MRSA bacteraemia

203
Q

clostridium difficle

A

Gram positive anaerobic rod
Part of normal gastrointestinal flora
Antibiotics kill other gut flora so the c.difficle increases and produce toxins which cause diarrhoea and pseudomembranous colitis
High morbidity and mortality
c. difficile associated diarrhoea must be recorded.

204
Q

vancomycin-resistant enterococci (VRE)

A

Enterococci are part of normal GI flora
Have resistance to other antimicrobials= multi drug resistance

205
Q

sterilisation

A

is the process of killing or removing all viable microorganisms including the viruses and spores
-Heat 160-180 degrees glassware
-Autoclaves for equipment and dressing
-Irradiation for needles, gloves, vaccines
-Filtration for fluids
-Chemicals e.g. glutaraldehyde for endoscopes

206
Q

disinfection

A

is the process of removing or killing most but not all viable organisms
- Chemical
- Boiling
- Low pressure steam

207
Q

high risk patients include

A

-Very young and elderly
-Lack of vaccines
-Immune defects (HIV, diabetes…etc)
-Immunosuppressive drugs
-Lung, skin or urinary system disease
-Trauma

208
Q

how infection can be eliminated

A

Environmental:
- Cleanliness= sterile equipment, dressings, IV fluid, blood products screened
- Human
Bacterially effective handwashing- alcohol based hand gels
Immunisation and health screening of staff
Bare below the elbows policy

209
Q

how transmission of infection may be reduced

A

The health act 2006: code of practice for the prevention and control of healthcare associated infections in the uk, patients must be cared for in a clean environment
Airborne- check air conditioning, hospital operating theatre ultra clean air, isolation susceptible patients or infected person
Contact- aseptic behaviour, handwashing, alcohol based hand gels
Enhancing hosts ability to resist infection
Infection prevecardiac ntion and control teams to investigate HAI cervi

yr 1 uni work (13 decks)

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