Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

The Public Sem 2 > The Public Semester 2 > Flashcards

The Public Semester 2 Flashcards

1
Q

What is cystic fibrosis?

A
  • Chronic disease affecting 1 in 25 which results in a build up of mucous which is too viscous therefore stays in the throat therefore infection lingers.
  • Life expectancy –> 45
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes cystic fibrosis?

A
  • Single faulty gene CTFR
  • Chest infections
  • Fatty diarrhoea as fat isn’t properly absorbed from diet
  • Poor weight gain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where is S.aureus found?

A

Skin - causes infection when in chest and airways.

- If get it <2 years old = increased mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the median age of acquisition of pseudonomas infection in CF?

A

3 years of age (isolation has no impact)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is pseudonomal colonisation associated with?

A
  • Mortality 2.6 more likely to die with 8 years

- Delayed growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Characteristics of psuedonomas?

A
  • Hospital acquired
  • Opportunistic
  • Gram neg rod
  • Single polar flagellum for motility
  • Doesn’t require many nutrients to live
  • 0.5-3um in size
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Psuedonomas source?

A
  • Water
  • Soil
  • Plant
  • Human
  • Animal surfaces
  • Part of normal human flora in some populations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Psuedonomas virulence factors:

A
  • Invasive
  • Toxigenic
  • Minimal nutrition
  • Produces extracellular proteases to assist bacterial adhesion and invasion
  • Produce alginates to aid in biofilm formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is pseudonomas transmitted?

A

Biofilm–> environmental sources i.e. sinks and drains
- invasive medical devices

Human transmission source –> colonisation as part of the normal human flora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pseudonomas diagnosis?

A
  • bacterial culture on agar –> from wound, tissue, blood, sputum, discharge, stool
  • urine analysis
  • FBC = poor blood count
  • corneal scrapings
  • Fluorescence under UV light
  • Sweet fruity odour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are biofilms?

A

organism that grows on surface which can grow extracellular material.

Includes alginates

Matrix encapsulates cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Medical conditions caused by pseudomonas areginosa?

A
  • Respiratory tract infections
  • Sepsis
  • Endocarditis
  • Meningitis or brain abcess
  • Keratitis
  • UTI’s
  • Secondary would infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens to mucus in CF?

A
  • Airways secrete a thick mucus
  • Mucus too thick so cilia mechanism doesn’t work
  • Mucus remains in airways gathering infection.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pathophysiology of pseudonomas?

A
  • Pseudonomas colonises the mucus in the lower respiratory tract and then grows to cover the epithelium:
  • > biofilm proliferation
  • -> scarring and access formation
  • -> Biofilms represent different strains and sensitivites
  • -> Affects antibacterial choices
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How effective is early intervention?

A

Can eradicate pseudonomas for up to 2 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Nebulisation or inhalation of solution (advantages)

A
  • Discrete and portable
  • No loss of efficacy
  • Easy to use covering all ages
  • Dry powder inhalers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Oral antibiotics for psuedomonas:

A

Ciprofloxacin:

  • Fluoroquinolone
  • Well absorbed from GI tract
  • Primary hepatic metabolism which is accelerated in CF patients.

Azithromycin:

  • Interferes with adherence of pseudomonas to epithelium
  • use for anti inflammatory effects
  • Modifies biofilm structure and growth
  • 10mg/kg daily
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Infective exacerbations definition:

A
  • Reduced in FEV1 to <50% of expected
  • Acute changes on Xray
  • Increased breathlessness or decreased exercise intolerance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Actions taken in clinic:

A
  • Sputum sample
  • IV access
  • Admit
  • Empirical antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What empirical antibiotics are used for first pseudonomal infection?

A

Ceftazidimine

  • 3rd gen cephalosporin
  • Particularly active against psuedonomas
  • Reserved in the UK only for this indication

Tobramycin

  • amino glycoside with favourable nephrotoxicity profile
  • good activity against pseudonomas
  • Then onto eradication therapy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are subsequent infections guided by?

A

Sensitivity from last exacerbation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are cephalosporins?

A
  • Most widely prescribed antibiotics
  • Beta lactam AB’s
  • Inhibit cell wall synthesis
  • Broad spectrum
  • Bacteriacidal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is resistance acquired (cephalosporins):

A

I) altered binding site

II) decreased permeability

III) beta lactamases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How many generations of cephalosporins are there?

A

5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Higher generations of cephalosporins generally have expanded spectra against gram negative bacilli. True or false?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Cephalosporin mode of action:

A

Interferes with cross linkage between peptidoglycan chains and structural integrity of cell wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Cephalorsporin resistance:

A

3rd gen are resistant to beta lactamase therefore have broader spectrum of activity G-ve bacteria than pencillins.

Overuse has created new resistance mechanisms:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are ESBL’s?

A

Extended spectrum beta lactamases - no less dangerous than MRSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How are ESBL genes transmitted between cells?

A
  • Plasmid DNA using pili
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Treatment of ESBL?

A

Aminoglycosides:

  • Conc dependent action
  • Nephrotoxic
  • Opotoxic
  • Trough levels 22mg/L
  • Hypermetabolised by CF patients.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Chronic treatment?

A

Frequent exacerbations lead some patients to have regular iv AB therapy:

  • 3 monthly cycles of 2weeks
  • Antimicrobial choices led by previous sensitivities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What HCP’s prescribe the most antibiotics?

A 
GP's = 74%
Inpatients = 11%
Outpatients = 7%
Dentists = 3%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is MRSA?

A
  • Methicillin resistant staphylococcus aureus

- Gram positive cocci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How is is MRSA detected?

A

By displacing resistance to methicillin (but is also resistant to all beta lactams available (penicillins, cephalosporins, carbapenems)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Can people be carriers of MRSA?

A

Yes - they can carry MRSA and have no symptoms however they are at risk developing it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the MRSA sites of colonisation?

A

Nose and skin, axilla (armpit) and groin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How to reduce MRSA infection?

A
  • screen at risk patients
  • isolate patients
  • decontamination therapy
  • hand washing
  • aseptic non touch treatments for care
  • antibiotic prophylaxis
  • antibiotic stewardship
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How is MRSA treated?

A

For serious systemic infections:
1st line- glycoproteins e.g. IV vancomycin or teicoplanin

2nd line - linezolid, daptomycin, tigelycin = expensive and require intensive monitoring.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are multi resistant coliforms?

A
  • biggest threat in terms of antibiotic resistance

- coliforms = gram negative bacilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the reserve antibiotics?

A

Carbapenems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How can UTI’s progress to septicaemia?

A

When caused by ESBL producing e coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is glycopeptide resistant enterococci (GRE)?

A

Enterococci is a gram positive organism in the gut

  • Glycopeptide can become colonised in their bowel with GRE.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

When are infections with GRF most frequently seen?

A

In patients with frequent antibiotic exposure.

often IV line associated infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is misuse of antibiotics?

A
  • When AB’s prescribed unnecessarily
  • When AB admin is delayed
  • When broad spec AB’s are used too generously or when narrow spec AB’s are used incorrectly
  • When dose = too high or too low
  • When duration = too short or too long
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is clostridium difficile?

A
  • Antibiotics = major risk factor for developing CD

- Gram positive anaerobic organism that can cause an infection of the intestines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Whom is CD most common in?

A

Elderly with underlying disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What % of adult population have CD present in the gut?

A

<5% - but most patients acquire CDI by cross infection or toxigenic strain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Symptoms of CD?

A

Range from mild diarrhoea to severe illness with ulceration and bleeding from colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What causes the symptoms acquired by CD?

A

Toxins produced by the organism.

When there is a disturbance in normal flora of colon (CD can grow and multiply)

CD produces spores that can survive for a long time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

CD treatment?

A
  • Assess severity including WCC, abdomen pain, temp
  • Stop prescribing AB’s if possible
  • Stop laxatives
  • Assess fluid balance and ensure adequate hydration
  • Assess nutritional status
MILD = oral metronidazole 
SEVERE = orla vancomycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Prevention of CD:

A
  • Prudent use of AB’s
  • Minimum exposure:
  • -> Fluoroquinolones
  • -> cephalosporins
  • -> clindamycin
  • avoid prolonged courses duration
  • avoid exposure to multiple AB’s
  • infection control = isolation of infected patients with own toilet
  • enforce hand washing to prevent spread and reinfection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is sepsis?

A

Presence of infection together with systemic manifestations of infection:

  • pyrexia
  • tachycardia
  • raised infection markers in blood WCC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Definition of severe sepsis?

A

Sepsis plus sepsis induced organ dysfunction or tissue hypoperfusion–>
- Low urine output 0.5ml/kg/hr

  • Low arterial oxygen concentration
  • Changes in blood clotting
  • Raised in bilirubin (>79 micromol/L)
  • Raised lactate >1mmol/L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is septic shock?

A

Sepsis induced hypotension persisting despite fluid resuscitation.

Systolic BP <90mmHg (normal = 100-120)

MABP = 70mmHg (normal = 75)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Causes of sepsis?

A

Infection ANYWHERE in the body can cause sepsis

Most common = respiratory, abdomen, UTI, soft tissue

Sever sepsis occurs when signs and symptoms of infection come together.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Risk factors of sepsis:

A
  • Immunocompromised
    • -> HIV
    • -> Cancer chemo
  • Neonates and infants
  • Chronic disease
  • Recent surgery
  • Invasive procedures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Mortality of sepsis?

A

Sepsis: 15% (systemic inflammation syndrome)

Severe sepsis = 20% (sepsis plus organ failure)

Septic shock = 45% (sever sepsis plus refractory hypotension)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Pathophysiology of sepsis:

A
  • Septic shock = deregulated inflammatory response - bacterial proteins activate cellular defence mechanisms
  • Release of inflammatory cytokines (TNF, interleukin 1+6)
  • Nitric oxide release - triggers vasodilation
  • Endothelial activation - allows immune cells to stick and stay where they’re needed. Cause capillaries to become porous.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Vasodilation causes a ____ in systemic vascular resistance.

A

REDUCTION

Body becomes relatively fluid depleted - hypovolaemia
Tissue ischaemia.

12 HOURS = DEATH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the Sepsis Six?

A

1) Admin oxygen
2) Take blood cultures
3) Give broad spec antibiotics
4) Give fluid resuscitation
5) Measure lactate and Hb.
6) Measure urine output.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Why administer oxygen for sepsis?

A

Increase oxygen delivery to organs

Indications = lactase, venous O2 saturation

Treatment = 100%, oxygen through face mask

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Why is taking blood cultures part of the sepsis six?

A
  • Start smart then focus
  • Most patients will be culture neg. after a single dose of AB
  • DO NOT DELAY antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Why give broad spec antibiotics (sepsis)?

A

Goal is to treat infection

Indicators = inflammatory markers

Treatment = depends on what you’re treating
= empirical therapy for first 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Infection treatment regime for sepsis?

A

Start smart then focus

  • G+ and G- cover at first (3rd gen cephalosporin)
  • Macrolide of penicillin allergic

If neutropenia (Low WCC):

  • Use broad spec penicillin
  • Add in aminoglycoside

Then focus - depends on bacteria–>

  • Staphylcocci
  • Coliforms
  • Pseudomonas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

AB’s used for staphylococci infection:

A

flucloxacillin, rifampicin, vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

AB’s used for coliform infection:

A

co amoxiclav, carbapenem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

AB’s used for pseudomonas:

A

ceftazidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Why is fluid resuscitation part of the Sepsis Six?

A

Restores circulating fluid volume and improves tissue perfusion to restore lactate, venous O2 stat, urine output and BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Fluid resuscitation dose used?

A

0.9% NaCl diffusion given as fast as possible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Why is measuring lactate part of the sepsis six?

A
  • Markers of anaerobic respiration
  • By product of glucose metabolism
  • Alerts us to tissue hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Sepsis six outcomes:

A
  • Reduce overall morality by 50%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Two most impactful interventions:

A
  • Blood cultures

- Antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is staphylococcus aureus?

A
  • Gram positive
  • Spherical and non motile
  • Size = 1 micrometer in diameter
  • Yellow/golden colour
  • Colonises skin, nasal passages and GI tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Transmission of staphylococcus aureus:

A

Air borne, human contact, infected surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Growth of staphylococcus aureus:

A
  • Aerobic respiration or facultative anaerobe
  • Binary cell division reproduction
  • Staphylococcus = “bunch of grapes” in greek
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Staphylococcus A strains?

A
  • Methicillin sensitive staph A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What does staphylococcus use as a marker?

A

Coagulase - also is a virulence factor which confers resistance to phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Patient groups affected by hospital acquried MRSA:

A
  • Patients over 60
  • Admission and procedures
  • Immunocompromised, dialysis patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is community acquired MRSA?

A

Younger otherwise healthy patients affected

- Transmission = patients are already colonised and trauma and cuts (soft tissue and skin infections)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Medical conditions caused by S.aureus infection:

A

SKIN

  • Mucosal membrane infections
  • Pimples
  • Boils
  • Leg ulcers
  • Cellulitis

INVASIVE

  • Surgical wound infections
  • UTI’s
  • Septicaemia
  • pneumonia
  • Arthiritis
  • Meningitis

OTHER
- Food poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is conjunctivitis?

A

Infection caused by staphylococcus aureus
(also streptococci, gonorrhoea, chlamydia, viruses)

Affects young, old, diabetes and immunocompromised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Signs and symptoms of conjunctivitis:

A

Grittiness, itching, discharge, pink eye

Complications–> scarring, secondary systemic infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Treatments of conjunctivitis:

A
  • Self limiting (1-2 weeks)
  • Chloramphenicol 2 hourly QDS
  • Fusidic acid gel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Can chloramphenicol hourly and fusidic acid gel be given via PGD?

A

YES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is impetigo?

A

Infection caused by staph aureus, streptococcus pneumonid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the two types of impetigo?

A

Primary - infective cut/bite or graze

Secondary- where an underlying skin condition exists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Epidemiology of impetigo:

A
  • Summer months

- Children, teens, young adults, diabetics, immunocompromised, school, nurseries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Signs and symptoms of impetigo:

A

Bullous = affects trunk, arms and legs with large blisters

Non bullous = accounts for 70% of infections - itchy crusts, yellow/brown around nose and mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Complications of impetigo:

A
  • lymphangitis
  • Cellulitis
  • Guttate psoriasis
  • Scarlet fever
  • Septicaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Impetigo treatment:

A

Fusidic cream - TDS/QDS
Mupirocin ointment TDS
Oral flucloxacillin QDS
Oral erythromycin QDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Cause of device related infection:

A

S aureus introduced into the body through surgical opening.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Epidemiology of device related infections:

A
  • Surgical patients
  • Hospitalised patients with IV lines
  • Urinary catheters
  • Tracheostomies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Signs and symptoms of device related infections:

A
  • Redness, warmth, inflammation, pain at site,
  • Fever
  • Malaise
  • Tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Complications of device related infections:

A
  • Endocarditis

- Septicaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Device related infection treatment:

A
  • Removal of temporary device
  • Surgical removal of infected tissue
  • Antibiotics iv = flucloxacillin, calrithromycin, clindamycin (7-10 day course)
  • Biofilms very difficult to treat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is a SSI?

A

Surgical site infection caused when microorganisms get into the part of the body that has been operated on.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Surgical site definiton:

A

incision or cut in the skin made by a surgeon to carry out a surgical procedure and the tissue handled or manipulated during the procedure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

SSI epidemiology:

A
  • Incidence = 2.6% of all operations

- 3rd most common hospital acquired infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Classification of SSI’s:

A

Superficial incisional SSI - skin and subcutaneous

Deep incisional SSI - deep, soft tissue

Organ space - organ space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Classification of operative procedures:

A
  • Clean
  • Clean contaminated
  • Contaminated
  • Dirty
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Most common pathogens in SSI’s:

A
  • S aureus = predominant in orthapeadic categories
  • Coagulase negative staphylococci
  • Enterococcus species
  • E coli
  • Pseduonomas aeruginosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Structure of S aureus:

A
  • Cytoplasmic membrane and cell wall
  • Coagulase - protects it from immune system
  • alpha toxin - damages cells
  • Proteins that allow bacteria to stick i.e. elastin binding, collagen binding
  • Clumping factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

How to reduce incidence of SSI:

A
  • surveillance
  • prophylactic antibiotics
  • asepsis
  • Preparation of incision site
  • warming
  • Oxygenation
  • Glucose control
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Antibiotics for SSI:

A

Given to patients prior to:

  • clean surgery involving prothesis or implant
  • clean contaminated surgery
  • contaminated surgery
  • but not for clean, non prosthetic uncomplicated surgery.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What determines antibiotics for SSI:

A
  • normally based on local formulary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Why is hair removal required for surgery:

A
  • Improved view and access
  • Perceived reduction infection

HOWEVER, use trimmers not razor as it can potentially increase SSI rate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What antiseptics are used for surgical sites:

A

2% chlorhexidine or 10% povidone iodine

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is spreptococcus pyogenes:

A
  • Gram pos cocci
  • arranged in chains
  • group A streptococcus
    • –> lancefield group A
    • -> beta haemolyte
  • Facultative anaerobe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Virulence factors of spreptococcus pyogenes:

A
  • Bacterial capsule
  • Exotoxin production
  • immune evasion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Common spreptococcus pyogenes infections:

A
  • Sore throat
  • impetigo
  • Cellulitis
  • Scarlet fever
  • Meningitis
  • Pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Strep throat transmission:

A

Droplets of air/direct contamination of wound.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Strep throat signs and symptoms:

A
  • swollen tonsils
  • painful tender
  • Discomfort when swallowing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Differential diagnosis of strep throat.

A
  • Glandular fever = viral
  • Cancer = persistant sore throat
  • Quinsy= painful collection of pus

Epiglottis = inflammation of epiglottis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Danger eliminations of strep throat:

A
  • Persistent high temp above 38 degrees
  • Frequent action
  • Symptoms of longer than 4-5 days which don’t respond to medication
  • Difficult swallowing/breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Strep throat diagnosis:

A
  • Physical examination
  • Throat swabs of affected tissue or saliva
  • Blood test- Antibodies
  • Invasive infection – Blood cultures for bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Strep throat treatment:

A
  • Often no treatment required
  • OTC- analgesics / anaesthetic & antibacterial lozenges /sprays/ mouthwashes
  • Antibiotics
  • Invasive infection- medical emergency -> Hospitalisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Complications of Group A Strep infections:

A

Acute rheumatic fever

Rheumatic heart disease

Post streptococcal glomerulonephritis

Bacteraemia / septicaemia

Necrotising Fasciitis

Streptococcal toxic shock syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What is cellulitis?

A

1) Skin surface damage
2) Bacterial entry
3) Bacteria attack skin and tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Aetiology of cellulitis:

A

Obese

Weakened immune system

Poorly controlled diabetes / circulation problems

Chickenpox or shingles

Lymphoedema

IV drug use

Previous episodes of cellulitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Bacterial source.

Endogenous carriers of Gp A streptococci:

A
  • Interdigital toe spaces
  • Vagina
  • Anus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Cellulitis - Signs and symptoms:

A
  • Skin becomes red, hot, swollen, tender, painful
  • Commonly affects legs
  • Blisters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Cellulitis - Differential diagnosis->

A
  • Eczema
    In particular varicose eczema
  • Lymphoedema
  • Allergic Reaction
123
Q

Cellulitis Diagnosis:

A
  • Physical examination
  • Skin swab- open wound
  • Blood tests
124
Q

Cellulitis Treatment:

A

Mild/moderate infection

  • 7-14 day oral antibiotic course at home
  • Phenoxymethylpenicillin (clarithromycin/clindamycin)

Advanced infection
Hospital admission – IV Benzylpenicillin (Vancomycin)

125
Q

Complications of Cellulitis:

A

Bacteraemia / septicaemia (blood poisoning)

  • Bacteria enters bloodstream
  • High temperature
  • Rapid heart beat/breathing
  • Confusion/disorientation

Necrotising fasciitis
- Severe infection causing tissue death

Abscess
- Abscess at site of infection

Facial cellulitis & meningitis

  • Uncommon
  • Potentially spread to outer brain
126
Q

What is cancer:

A
  • Cancer is a collection of diseases with the common feature of uncontrolled growth
  • Several cellular changes are required to generate cancer.
127
Q

What is it called when cancer spreads:

A

METASTASIS

128
Q

What makes a cell cancerous?

A

Hallmarks of cancer

1) Inflammatory microenvironment
2) Insenstivity to growth inhibitors
3) Self sufficiency in growth signals
4) Limitless replicative potential
5) Sustained angiogenesis
6) Evasion of apoptosis
7) Tissue invasion and metastasis

129
Q

What is chemotherapy?

A
  • Chemotherapy prevents cell growth

- It also targets rapidly multiplying non cancerous cells such as hair follicles, intestinal cells, immune system.

130
Q

Two main modes of action of chemo:

A

1) Direct interaction with DNA

2) Prevention of nucleic acid synthesis by inhibiting one or more of the enzymes involved in DNA/RNA synthesis

131
Q

Three types of drugs that have direct action with DNA:

A
  • Alkylating agents
  • Metal complexes that bind to DNA
  • Intercalating agents
132
Q

What are alkylating agents?

A

“mustards”
e.g. nitrogen mustard and sulphur mustard

  • Nitrogen mustard – first drug used in cancer therapy, related to the war gas sulphur mustard and found to have antitumour activity
  • Sulphur mustard too toxic and reactive but isosteric nitrogen mustard less toxic but still very reactive with toxic side-effects
133
Q

Mode of action of alkylating agents?

A
  • Alkylating agents attach and alkyl group to DNA

- This causes linkages between strands of DNA that inhibits DNA synthesis - cytotoxic

134
Q

Problems with alkylating agents:

A
  • Alkylating agents will also target normal cells that divide frequently (GI tract, bone marrow, testicles and ovaries – infertility)
  • Alkylating agents are carcinogenic in their own right – long term side effects
135
Q

3 ways to reduce toxicity of mustards:

A
  1. ) Only form the electrophile slowly in the tumour:
    - Nitrogen lone pair delocalised onto aromatic ring, making electrophile formation more difficult.
    - One of the least toxic nitrogen mustards

e.g. CHLORAMBUCIL

  1. ) Attach alkylating agent to an “amino acid”:
    - Tumours require a large quantity of amino acids for protein synthesis
    - Drug enters tumour cell by the phenylalanine amino acid transporter

e. g. MELPHALAN
3. ) Pro-drug – requiring reductive activation
e. g. MITOMYCIN C

136
Q

What are Metal complexes that bind to DNA?

A
  • Neutral inactive molecule acting as a pro-drug
  • Platinum covalently linked to chloro substituents
  • Ammonia molecules act as ligands
  • Activated in cells with low - chloride ion concentration
  • Chloro-substituents replaced with neutral water ligands
  • Produces positively charged species

e.g. cisplatin

137
Q

Cisplatin mode of action:

A
  • Binds to DNA in regions rich in guanine units

- Intra-strand links rather than inter-strand

138
Q

Cisplatin toxic side-effects limited initial clinical application;

A

(i) severe nausea and vomiting
(ii) nephrotoxicity (dose limiting)
(iii) ototoxicity (ears)
(iv) bone marrow suppression

139
Q

How can toxic side effects of cisplatin be overcome:

A

Improved administration and hydration procedures and co-administration of anti-sickness medication e.g.metoclopramide

140
Q

How do intercalating agents work?

A
  • It slides in between the stacked bases bases e.g. Doxorubicin
141
Q

Doxorubicin: mechanism of action?

A
  • DNA intercalating agent
  • Planar tetracyclic chromophore inserted between adjacent pairs
  • Stabilised by electrostatic interactions between DNA phosphate groups and the +vely charged amino group of the sugar moiety
  • As a result in inhibits the action of topoisomerase II
  • Generates oxygen free radicals = DNA damage
142
Q

Side effects of Doxorubicin :

A
  • Nausea and vomiting
  • Myelosuppression
  • Alopecia
  • Cardiotoxicty (develops up to 6 months after the last dose)
  • The cardiotoxicity is reduced by DEXRAZOXANE which has an EDTA-like structure and removes Fe from adriamycin
  • Used to treat breast cancer, bladder cancer, sarcoma and lymphoma
143
Q

What are DNA Topoisoemrases?

A

Topoisomerases modify the topological state of DNA by inducing either transient single strand (topo I) or double strand (Topo II) DNA beaks

Essential for uncoiling DNA for subsequent replication, transcriptional, repair or recombination processes

Topoisomerase inhibitors block the action of topoisomerase and as a consequence elicit a permanent single stranded (topo I) or double strand (topo II) DNA strand breaks

144
Q

What is the action of topoisomerase II?

A
  • Relieves the strain in the DNA helix by temporarily cleaving the DNA chain and crossing an intact strand through the broken strand
  • Tyrosine residues in the enzyme are involved in the chain breaking process
  • The residues form covalent bonds to DNA
  • The enzyme pulls the chains apart to create a gap
  • The intact strand of DNA is passed through the gap
  • The break is resealed
145
Q

Example of a topoisomerase II inhibitors:

A

e. g. ETOPOSIDE
- A semisynthetic derivative of PODOPHYLLOTOXIN poison extracted from the Mandrake plant.
- Forms a ternary complex with DNA and the topisomerase II enzyme
- Prevents DNA re-ligation = double strand breaks
- Causes errors in DNA synthesis = cytotoxic

146
Q

Clinical use of etoposide:

A
  • Has been used for more than a decade

- Effective only in chemo-sensitive tumours such as leukaemias, testicular cancer and small cell lung cancer.

147
Q

Side effects of etoposide:

A
  • Myelosuppression
  • Nausea and vomitting
  • Hair loss
148
Q

Major advantage of etoposide:

A

Lack of any long term irreversible organ specific toxicity (compared to cisplatin or doxorubicin).

149
Q

What are anti-metabolites?

A

Anti-metabolites interfere with the production of nucleic acids:

150
Q

How do anti-metabolites work?

A
  1. ) Inhibit the production of deoxyribonucleoside triphosphates, the precursors of DNA synthesis.
    - Inhibit the formation of normal precursors by competing for metabolic enzymes
    2) Some are similar in structure to normal purine or pyrimidine bases and the drugs are substitute for them in anabolic pathways.

-The drugs get incorporated into RNA and DNA instead of
normal triphosphates

151
Q

Name two chemotherapy drugs that affect mitosis

A

1) Vincristine & Vinblastine = prevents polymerization of microtubules
2) Taxol (Paclitaxel) = binds and stabilizes microtubules

152
Q

What is inflammation?

A
  • Inflammation is a critical innate defence in the war between microbial invaders and their hosts.
  • It is a normal process that serves as the body’s primary method of defence against infection and typically ends when injurious agents are killed or removed from the body.
  • Microorganisms trigger inflammation when they are introduced into the body and begin to grow and produce compounds that damage host cells.
153
Q

Acute vs chronic inflammation:

A

CELLS

  • Acute = Neutrophils. Allergy: eosinophils, mast cells
  • Chronic = Macrophages, lymphocytes

CHEMICAL MEDIATORS

  • Acute = Complement, kinins, prostaglandins, leukotrienes, cytokines from various immune cells, interferon-gamma from T cells
  • Chronic = Cytokines from macrophages and T lymphocytes

LESIONS

  • Acute= Rash, pus, abscess
  • Chronic= Rash, fibrosis, granuloma
154
Q

What are cytokines?

A
  • Small non-antibody proteins that regulate the immune response
  • Some diffuse into the vasculature and stimulate endothelial cells to produce selectins thereby recruiting neutrophils in the area of infection
  • Other cytokines act as mediators of intercellular communication
  • They induce cell growth, and direct cellular traffic
155
Q

Three types of cytokines:

A
  • Monokines: secreted by mononuclear phagocytes
  • Lymphokines: secreted by activated T cells, especially helper T cells
  • Interleukins: secreted cytokines mediating signalling between white cells (leukocytes)
156
Q

Inflammatory cytokines and cancer:

A
  • Cytokines secreted by both tumor and immune cells could either induce tumor suppression or promote tumor progression.
  • Acute inflammatory response through IL-2, IL-15, and IL-21 activates immune response by activating NK and CTL cells with antitumor effects.
  • Chronic inflammation on the other side results in tumor cells escaping from immune response through the action of different mediators especially, IL-1, IL-4 and IL-6.
157
Q

What is stress?

A

A specific response by the body to a stimulus that disturbs or interferes with normal physiological equilibrium/homeostasis

158
Q

Examples of stressors:

A

Can be real, imagined, internal or external

  • Physical/environmental
  • Natural disasters
  • Major life changes (good and bad)
  • Day-to-day aggravations
159
Q

How does stress affect the immune system?

A
  • Stress detected in hypothalamus
  • Release of Corticotropin-Releasing Hormone (CRH)
  • Induces the release of adrenocorticotropin hormone (ACTH) from the pituitary
  • ACTH interacts with receptors on adrenocortical cells and cortisol is released from the adrenal glands. Release of cortisol into the circulation has a number of effects, including elevation of blood glucose.
  • The negative feedback of cortisol to the hypothalamus, pituitary and immune system is impaired. This leads to continual activation of the HPA axis and excess cortisol release. Cortisol receptors become desensitized leading to increased activity of the pro-inflammatory immune mediators.
160
Q

How does cortisol impair immune function?

A
  • Changing the cytokines secretion mainly decreasing the levels of the tumour necrosis factor
  • Decreasing IL-2
  • Inducing death of white blood cells
  • Decreasing the inflammatory response
161
Q

Effects of chronic stress:

A
  • Consistently elevated cortisol and catecholamine levels (Stress response chronically
    activated)
- Stressful events predispose to disease (diabetes, insomnia, myocardial infarction, cancer,
autoimmune diseases (Multiple Sclerosis) depression).
162
Q

What is obesity ?

A

In the obese state, there is an increase in the size and number of adipocytes, and in the inflammatory and endothelial compartments of the stromal-vascular fraction.

This change in the composition of the adipose tissue results in the increased secretion of leptin and inflammatory cytokines, and decrease in the secretion of adiponectin. PAI1, plasminogen activator inhibitor 1; TNFα, tumour necrosis factor‑α.

163
Q

Obesity associated adipose inflammation:

A

In the lean (normal) state adipose tissue, immune cells and adipocytes interact to maintain homeostasis and regulation of adipocyte lipid handling and storage.

The main resident immune cells include primarily M2-like macrophages, T regulatory (Treg) cells and eosinophils.

These cells synthesize IL-10, IL-4, and IL-13 and help to maintain an anti-inflammatory environment that contributes to the insulin-sensitive state.

Obesity drives a shift in the number and phenotype of immune cells.

During adipose expansion in obesity monocytes are recruited from the blood into the obese adipose tissue, where they become M1 polarized and produce proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, which contribute to insulin resistance. Other changes include decreased numbers of eosinophils and Tregs, and increased numbers of neutrophils, B cells, mast cells, and interferon γ–producing Th1 and CD8+ T cells.

164
Q

Antibodies as drugs - What is Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)

A
  • Antibodies bind antigens on the surface of target cells
  • NK cell CD16 Fc receptors recognise cell bound antibodies
  • Cross linking of CD16 triggers degranulation into a lytic synapse
  • Tumour cells die by apoptosis
165
Q

Internal factors affecting immune responses to therapeutic proteins

A
  • Genetic factors modulating the immune response
  • Genetic factors related to a gene defect
  • Age-related factors
  • Disease-related factors
  • Concomitant treatment
  • Treatment-related factors
166
Q

Exernal factors affecting immune responses to therapeutic proteins

A
  • Protein structure
  • Formulation and packaging
  • Aggregation and adduct formation
  • Impurities
167
Q

Ways to reduce immunogenicity?

A
  • Change the amino acid sequence of the product or the glycosylation pattern of the protein
  • Link proteins to polymers such as polyethylene glycol or low molecular weight dextran
  • Use humanized versions of the proteins
  • Reduce the immunogenic response by immunosuppressive treatments
  • Select another route of administration
168
Q

RNA as a target for anti-cancer drugs: Antisense Therapy

Advantages:

A
  • Same effect as an enzyme inhibitor or receptor antagonist
  • Highly specific where the oligonucleotide is 17 nucleotides or more
  • Smaller dose levels required compared to inhibitors or antagonists
  • Potentially less side effects
169
Q

RNA as a target for anti-cancer drugs: Antisense Therapy

Disadvantages:

A
  • ‘Exposed’ sections of mRNA must be targeted
  • Instability and polarity of oligonucleotides (pharmacokinetics)
  • Short lifetime of oligonucleotides and poor absorption across cell membranes
170
Q

What is micro-RNA (miRNA)

A
  • Short segments of double stranded RNA
  • Recognised by enzyme complex RISC to produce single stranded RNA - small interfering or small inhibitory RNA (siRNA)
  • Binds to complementary region of mRNA
  • mRNA is cleaved by enzyme complex – degradation – no gene product synthesised
171
Q

Micro-RNA (miRNA) advantages?

A
  • siRNAs have potential to be used in gene therapy
  • Greater efficiency in silencing mRNA than conventional antisense therapy
  • One siRNA could lead to cleavage of many mRNA molecules
172
Q

Micro-RNA (miRNA) disadvantages?

A
  • siRNAs need to be metabolically stable
  • Difficult to reach target cells
  • Devise a mechanism to ensure entry to target cells
173
Q

What is signal transduction process?

A
  • Receptor proteins bind “signals” i.e. drugs & endogenous ligands with high affinity
  • Conformational changes in the structure of the receptor protein then convert the external signal into one or more intra-cellular signals.
  • This process is known as signal transduction
174
Q

What are tyrosine kinase receptors?

A
  • Receptors with an extra-cellular and intra-cellular domain
  • Intracellular domain capable of phosphorylating tyrosine residues in target proteins.
  • This can initiate a signalling cascade leading to changes in expression of genes that is important for:
    • -> Proliferation
    • -> Evasion of apoptosis
    • ->Induction of angiogenesis
    • ->Generating metastasis
175
Q

Tyrosine kinase receptors: structure:

A

All RTKs have 3 essential components:

1) Ligand binding site (extracellular domain)
2) Transmembrane domain (α helix)
3) Domain with tyrosine kinase activity (cytosolic)

176
Q

How are tyrosine kinase receptors activated?

A
  • Ligand induces association between adjacent RTKs
  • This causes activation of their kinase activity
  • They phosphorylate tyrosine residues
  • Once the kinase receptor is phosphorylated, the phospho-tyrosine groups act as binding sites for signalling proteins
  • Each phosphorylated tyrosine region can bind a signalling protein
  • These molecules may also become phosphorylated and act as further binding sites
  • Phosphorylation cascade (kinases)
  • Reversed by phosphatases – negative feedback loop - often inhibited in cancers
177
Q

The modulation of kinase activity can be

achieved through what strategies?

A

1) Disruption of ligand-receptor interactions

2) nInhibition of kinase (phosphorylation) activity (block ATP binding)

178
Q

Give examples of drugs that disrupt ligand-receptor interactions and its mode of action:

A

e. g. Bevacizumab binds to a growth factor (VEGF) thus preventing its binding to receptors (RTK)
- This interferes with tumour blood vessel development.
- First line treatment for colorectal cancers

e. g. Trastuzumab (Herceptin) targets the HER2 receptor, which is over expressed in (5-20%) of all late stage breast cancers
- Herceptin prevents binding of EGF to the HER2 receptor and thus prevents signal transduction
- However its use is limited to cancers which test as HER2 +, since it only works on tumours in which this protein is over expressed.
- Needs to be used in conjunction with a diagnostic test for HER2 overexpression

179
Q

Give examples of drugs that inhibit kinase activity - block ATP binding.

A

e.g. Imatinib mesylate (2001)
Protein tyrosine kinase inhibitor through inhibiting ATP binding to the bcr/abl fusion protein
- Chronic myeloid leukaemia, acute lymphoblastic leukaemia and intestinal stromal tumours

g. Gefitinib (2002)
prevents ATP binding to EGFR

180
Q

What is EGFR?

A

Epidermal growth factor receptor

181
Q

Consequences of binding of EGF:

A
  • Binding of EGF causes receptor dimerisation and activation of enzyme activity
  • Dimerisation means that the active site on each half of the receptor dimer catalyses the phosphorylation of the tyrosine residues in the other half
  • If dimerisation does not occur then phosphorylation cannot take place and signalling is inhibited
  • Important because EGFR is overexpressed in many solid tumours
182
Q

Targeted therapies

Disruption of oestrogen-receptor interaction:

A
  • Breast cancer can be oestrogen-dependent
  • Oestrogen secretion can be reduced by surgery
  • Alternative is use of tamoxifen
  • –>Competitive inhibition of oestrogen binding to its receptor
  • –>FDA approved for advanced breast cancers and primary breast cancer
  • Inhibits expression of oestrogen regulated
    genes
183
Q

Inhibiting MAPK signalling

examples:

A

.g. Dabrafenib and vemurafenib

Used in the treatment of melanoma

Only suitable for patients with a mutation in the B-Raf gene

Approximately 50% of melanomas harbour B-Raf mutations

This mutation makes RAF-ERK signalling constitutively active

Diagnostic test is required to establish this:
- Most common mutation is V600E

184
Q

How can use inflammation as a target therapy?

A

Inflammation can support all aspects of cancer:

  • Initiation
  • Growth
  • Metastasis
  • Response to therapy

Two ways in which we can target inflammation in cancer:

1) Inhibit pro-tumour inflammation
2) Promote anti-tumour inflammation

185
Q

Inhibiting pro-tumour inflammation as a cancer therapy:

A
  • Blocking signalling pathways prevents pro-tumourigenic inflammatory signalling within the tumour
  • Examples of this approach include MAPK inhibitors.
186
Q

Promoting anti-tumour inflammation as a cancer therapy:

A

It relies on endogenous tumour antigens that are released during tumour lysis by treatments such as chemotherapy or local radiation.

These tumour antigens are captured by dendritic cells, activated byGLAAS™technology, to generate an anti-tumour immune response.

Immune system attacks the primary tumour and distal metastases (if present)

187
Q

What is the “checkpoint approach”

A

T cell immune responses (anti-tumour) are controlled through on and off switches, so called ‘immune checkpoints’

These protect the body from potentially damaging immune responses

Developed drugs to target these immune checkpoints

This illicits anti-tumour T-cell-mediated immune responses

e.g. anti-CTLA4 and anti-PD1 or PDL1 therapy

188
Q

What is CTLA4?

A
  • Master switch (checkpoint) for T cell activation is CTLA4
  • CTLA4 is a receptor found on the surface of T cells and its activation inhibits T cell function
  • Therapy - anti-CTLA4 monoclonal antibody (ipilimumab) – binds to CTLA4
  • This blocks CTLA4 signalling, enabling an anti-tumour T cell response
189
Q

What is the PD-1/PD-L1 pathway?

A

PD-1 receptor and its ligand (PD-L1) are expressed on the surface of dendritic cells and macrophages

They are inhibitory factors, which act as a check-point for the dendritic-cell mediated T cell response

Therapy = monoclonal antibodies targeted against PD1 and PD-L1 (Nivolumab) – blocks the PD-1 signal

This releases the inhibitory checkpoint enabling a T-cell response, T-cell proliferation and therefore anti-tumour activity

190
Q

What are the causes of bacterial UTI?

A 
Common pathogens
E.coli (~ 85%)
Staphylococci spp
Proteus spp
Klebsiella spp
Pseudomonas spp
191
Q

Features of UTI (bacterial cystitis) :

A
  • Common in healthy adults, especially women
  • Less common in men due to urethral length

Signs and symptoms

  • Frequency
  • Dysuria
  • Urgency
  • Haematuria
192
Q

What is dysuria?

A

pain, stinging, burning on urination

193
Q

Why are UTI’s more common in women?

A

Women have a short urethra, predisposing to ascending infection with Grm –ve bacteria from the GI tract

194
Q

Management of cystitis in community pharmacy?

A
  • OTC potassium and sodium citrate (alkaline urine less painful to pass)
  • OTC analgesia
  • Public health role–> Differential diagnosis of STI, pregnancy
195
Q

When to refer (UTI) in community pharmacy?

A
  • Pregnancy
  • Recurrent or non-resolving / worsening cystitis
  • Children and men
  • Symptoms suggestive of ascending infection (pyelonephritis)
  • Diabetes
196
Q

Features of UTI (pyelonephritis?

A

Ascending infection causes:

  • Pyelonephritis
  • loin pain
  • fever
  • malaise
197
Q

Pylonephritis–> Hospital treatment needed for:

A
  • Pregnant women
  • Dehydration / unable to keep fluids down
  • High risk of complications e.g. diabetics, immunocompromised
  • Recurrent pyelonephritis
  • Men (in whom there is no obvious cause)
198
Q

Further investigation needed for (UTI’s) when:

A
  • Recurrent UTI
  • 45 years and over with haematuria that persists after UTI treated
  • 60 years and over with unexplained non-visible haematuria and raised WCC
199
Q

Diagnosis of UTI ?

A
  • Symptoms
  • Urine dipstick
  • -> tests for nitrites
  • -> leucocytes
  • -> protein
  • -> blood
  • Mid Stream Sample of Urine (MSSU) to identify organism responsible
200
Q

Recurrent UTI:

A
  • Recurrent UTIs carry an increased risk of renal damage
    • –> Refer for further investigation if more than 3 episodes in one year
  • Investigate repeated episodes
  • Possibility of kidney stones / local obstruction must be eliminated
201
Q

What is complicated UTI?

A
  • Men
  • Structural abnormality
    Indwelling catheter, stent or nephrostomy tube
    Vesicouteric reflux
    Prostatic hypertrophy
    Many more e.g. tumour, cysts, congenital abnormalities
202
Q

What is uncomplicated UTI?

A
  • Women (inc pregnancy)

- Single episode in children

203
Q

Management of UTI?

A
  • Treat when symptomatic and urine dipstick is positive (except in pregnancy)
    Nitrites, leucocytes

Give advice on prevention & symptom control

  • Drink plenty of fluids
  • Avoid caffeine
  • Empty bladder often and ensure full emptying; wipe front to back
  • Empty bladder after sexual intercourse
  • Analgesia
204
Q

Management of UTI’s in pregnancy?

A
  • UTIs are very common and often asymptomatic; risk of progression to pyelonephritis
  • Women are screened for bacteruria at first visit
  • -> Treated with antibiotics even if no symptoms
  • ->Urine culture performed 7 days after antibiotic treatment
  • ->Follow-up with monthly urine cultures
205
Q

Management of UTI - in children?

A

UTIs thought to affect

  • 3.6% boys
  • 11% girls
  • risk of upper tract infection and scarring

Diagnosed in much the same way as for adults
symptoms can be less specific

Treated when dipstick positive

  • ->if cystitis/lower UTI treat for 3 days
  • ->if at risk of pyelonephritis or upper UTI treat for 10 days

Recurrent infections

  • Common
  • Distressing for child (bed-wetting, urinary incontinence)
  • Prophylactic antibiotic indicated
206
Q

Choice of antibiotic therapy for UTI influenced by?

A

Choice of therapy influenced by:

  • Local resistance patterns & formularies
  • Previous exposure
  • Culture results
  • Allergy status / intolerances
  • Renal function
  • Likelihood of interactions
207
Q

Antibiotics used for UTI?

A
  • Trimethoprim
  • Nitrofurantoin
  • Cephalosporins
  • Co-amoxiclav
  • Quinolones
  • Gentamicin

3-5 days uncomplicated
7-10 complicated

208
Q

Antibiotics used for recurrent UTI?

A

Treat as UTI but consider prophylaxis with trimethoprim

  • 3-6 months
209
Q

Antibiotics used for acute pyelonephritis?

A

2nd-generation

  • cephalosporin
  • Quinolone
  • Gentamicin

14 days

210
Q

Antibiotics used for asymptomatic bacteruria?

A

Pregnancy
1st line: nitrofurantoin (avoid at term)
2nd line: cefalexin

7 days

211
Q

Is tromethroprim used in pregnancy?

A

Trimethoprim contraindicated in 1st trimester – folate antagonist

212
Q

Trimethoprim side effects?

A
  • Blood disorders long term
213
Q

Nitrofurantoin side effects?

A
  • Nausea, GI disturbance
  • Rarely, pulmonary reactions, peripheral neuropathy
  • Contraindicated in renal impairment (see BNF – check eGFR)
214
Q

Cephalosporins / penicillins side effects?

A
  • GI disturbance (allergy, C diff risk)
215
Q

4-quinolones side effects?

A
  • Rarely arthralgia, tendon damage
  • Caution in epilepsy
  • broad spectrum so C diff risk
216
Q

Gentamicin side effects?

A

Nephrotoxic , ototoxic

217
Q

What antibiotics target cell wall synthesis?

A

Vancomycin, penicillins, cephalosporins

218
Q

What antibiotics target DNA gyrase?

A

Quionolones (ciprofloxacin)

219
Q

What antibiotics target 50s protein synthesis?

A

macrolides (erythromycin)

220
Q

What antibiotics target 30s protein synthesis?

A

tetracyclines, streptomycin

221
Q

What antibiotics target folic acid synthesis?

A

trimethoprim, sulphonamides.

222
Q

Definition of antibiotic resistance?

A

The acquired ability of a microorganism to resist the effects of a chemotherapeutic agent to which it is normally sensitive

223
Q

Why have bacteria become

resistant to antibiotics?

A

1,) We keep trying to kill them with antibiotics.

2.) Microbes are extremely versatile and are natural and very successful survivors.

224
Q

What advantage do microbes have over humans?

A

Bacteria generation time = 20-100 minutes

(lower the better) with a very high abundance.

225
Q

How do microorganisms

resist antibiotics?

A
  1. Overproduction/alteration of target
  2. Alternative pathway (bypass)
  3. Decreased influx/
    increased efflux
  4. Drug modification
  5. Drug destruction

(All brought about by generation or acquisition of resistance genes)

226
Q

How do microorganism acquire the ability to resistant antibiotics?

A
  1. Mutation
  2. Horizontal gene transfer
    ‘Spread of resistance’
227
Q

What is horizontal gene transfer?

A

Transfer of genetic material between cells, even of different species, independent of cell replication

228
Q

What is transformation?

A

DNA goes into bacterial cell.

229
Q

What is transduction?

A

transfer by viral delivery

230
Q

What is conjugation?

A

plasmid DNA passes via cell to cell

231
Q

What are plasmids?

A
  • Independent of chromosomal DNA
  • Replication can exist autonomously
  • Carry ‘extra’ genes not strictly necessary for ‘normal’ growth
  • Including resistance genes.

Plasmids can also be transferred through transformation

232
Q

Is biofilm bacteria less susceptible to antimicrobials?

A

Yes

233
Q

How does antibiotics resistance increase?

A

1 Antibiotic use

2. Time

234
Q

Solution for AB resistance?

A
  • Antimicrobial stewardship
    (Use them carefully)
  • Combination therapy
    (where indicated)
  • Develop new antibiotics
    (easier said then done…)
235
Q

What is the chlamydia screening test?

A

Screening for U25’s = free

  • Simple and painless
  • Swab or urine sample
  • Results in 7-10 days
  • 1 in 10 people affected
236
Q

Chlamydia treatment?

A

azithromycin 1g
7 day doxycycline 100mg BD
14 days erythromycin 500mg BD

237
Q

What are the two emergency contraceptives?

A

Levonelle one step 1500mg (no later than 72 hours, contains progesterone)

Ellaone 30mg has to be taken within 120 hours.

238
Q

Levonelle mode of action?

A

Prevents ovulation by delaying the release of egg ovulation.

239
Q

Ellaone mode of action?

A

stops progesterone working delaying the release of an egg.

240
Q

How many adult teeth were extracted by the NHS in 15/16?

A

3.1m

241
Q

How many baby teeth (deciduous) are there?

A

20 of them

242
Q

How are teeth numbered?

A 
1-2 = sizers
3 = canine 
4+5 = pre molar 
6+7 = molar
243
Q

What are teeth made up of?

A

crown and root

244
Q

What are the different layers of teeth?

A

Enamel (hard part)
Dentin (softer and made of tubules)

Pulp

245
Q

What is plaque?

A

Polymicrobial shiny biofilm

Gum disease can loosen the fibres that keep teeth in place

Peridontal can be broken down by flossing, smoking etc plaque can form in these gaps.

246
Q

What is fluoride?

A

Found in water and toothpaste

  • Held in enamel and plaque for a while after it enters mouth
  • When pH drops during an acid attack the reservoir acts as an efficient source of free fluoride ions
  • Calcium fluoride is then incorporated into the enamel as hydroxyfluoropatitie as part of the demineralisation process.
247
Q

What fluoride toothpaste can be prescribed for over 16’s?

A

81000 ppm F

21800 for over 10 y/o

248
Q

What causes carries?

A
  • Bacteria are involved in the formation of lesions on their function
249
Q

What bacteria are best at being acidoduric and acidogenic?

A

Mutans streptococci

Lactobacili

250
Q

What is the ecological plaque hypothesis?

A
  • Explains polymicrobial nature of caries.
  • Explains how bacteria associated with disease can be present at healthy sites
  • Disease is a result of the shift in balance of resident microflora.
251
Q

What ecological changes can cause caries?

A

Sugar, low pH, reduced salivary flow

252
Q

What ecological changes can cause periodontal disease?

A
  • Increased GCF
  • Inflammation
  • immune suppression
253
Q

What is gingival crevice?

A
  • Anaerobic

- Abundance of protein in environment

254
Q

What are the main periodontal diseases?

A
  • Gingival diseases
  • chronic periodontitis
  • Necrotising periodontal disease
  • Aggressive periodonitis
255
Q

What is gingivitis?

A
  • Reversible inflammation of the gums due to poor dental hygiene
  • Hormonal disturbances
  • Drug therapies
  • Smokers
  • Precursor for periodontal disease .
256
Q

What is chronic periodontitis ?

A

Major cause of tooth loss 1/3 adults

Loss of attachment occurs

Alveolar bone loss may also occur

257
Q

Where does the bacteria come from (periodontitis)

A
  • Some peridontopathogens can attack the mucosa and have been isolated from the tongue biofilm.

Tongue piercings = risk

258
Q

What is necrotising periodontal disease?

A

Underlying systemic infection

  • Bad breath = halitosis
  • Grey pseudomembrane on the gingivae
  • A true infection
259
Q

What is aggressive periodonitis?

A
  • Rare
  • Usually occurs in adolescents
  • Inherited condition
  • Rapid loss of attachment
  • Associated with high levels of aggregatibacter aa leukotoxin
  • Tetracyclines/metrondiazole/amoxycillin
260
Q

What other periodontal diseases are there?

A
  • Pregnancy gingivitis
  • Group A streptococcal gingivitis
  • Diabetes gingivitis –> inflammation impaired healing may increase insulin resistance
  • HIV periodontal disease - characterised by the presence of opportunistic pathogens.
261
Q

Inflammatory response to plaque?

A

1) Flow of GLF increases
2) Delivery of nutrients
3) Proteolytic bacteria proliferate
4) Local pH increase and redox reduces
5) Up regulation of bacterial virulence factors

262
Q

Is there an association between oral health and systemic health?

A

Yes periodontal disease is associated with:

  • CVD
  • Respiratory disease
  • Diabetes
  • Risk of premature labour
  • Risk of low birth weight

WHY? inflammation related to G-ve species results in toxic metabolites and increased LP’s

Oral bacteria can also enter blood stream

263
Q

What are caries?

A

areas of deminierlisation

264
Q

Why is it essential for antimicrobials to bind to the oral mucosa?

A

There is a short contact time in the mouth

265
Q

What is substantivity?

A

Idea that once the agents are adsorbed to the mouth they are released slowly back into the oral environment

They are then re-distributed around the mouth.

266
Q

What is chlorhexidine?

A
  • Bisbiguanide
  • The “gold standard” of oral antimicrobials
  • Mouthwash/gel/varnish only
  • Broad spectrum
  • Reduces plaque, caries and gingivitis
  • Long term use can cause staining and mucosal irritation
  • Substantive – binds to surfaces well
  • Mutans streptococci are highly sensitive
267
Q

What is Triclosan?

A
  • Most commonly used agent in paste
  • Broad spectrum
  • Phenol
  • Selectively inhibits obligately anaerobic gram negative bacteria
  • Substantive
  • Multiple mode of action
  • Inhibits acid production, reduces inflammation, inhibits bacterial fatty acid metabolism
  • Can be enhanced by formulation with a co-polymer or zinc citrate
  • Concerns over widespread use
268
Q

Enzymes and Essential oils as plaque control?

A
  • Dextranases and glucanases to modify plaque matrix
  • Glucose oxidase and amyloglucosidase to boost salivary peroxidase system
  • Menthol, thymol and eucalyptol can penetrate plaque
  • Oils disrupt cell membranes and inhibit enzymes
  • Plant extracts – recently fashionable
269
Q

What are Quaternary Ammonium Compounds (QACs)?

A
  • Cetyl-pyridium chloride
  • Broad spectrum
  • Substantive (cationic)
  • Binds to bacterial cell membranes and disrupts integrity
  • Inhibits glucan synthesis and co-aggregation
  • Formulation – mouthwash only
270
Q

How can metal ions be used in plaque mediated disease?

A
  • Usually zinc or stannous salts
  • Zinc salts inhibit bacterial glycolysis
  • May be synergistic with other antimicrobials
  • Zinc lactate inhibits VSC production
  • Stannous fluoride inhibits caries formation
    Reduces dental hypersensitivity
271
Q

Surfactants in plaque mediated disease?

A

e.g. Sodium Lauryl Sulphate (SLS)

  • Detergent properties – disrupts lipids
  • Bactericidal – inactivates bacterial enzymes
  • Formulation issues with enzymes
  • Foams to coat the teeth
  • Removes organic matter to bulk phase
  • Some people may be allergic
272
Q

Arginine in plaque mediated disease:

A

Arginine salts increase the pH

Arginine is metabolised to ammonia containing end-products by oral bacteria

This raises the pH in the mouth, keeping it above critical caries levels

Arginine additional is a sensitivity agent (blocks dental tubules)

273
Q

Sugar Substitutes in plaque mediated disease:

A
  • Dietary sweeteners proposed to prevent caries
  • No acid challenge
  • Examples include aspartame and saccharin
  • Not metabolised by plaque bacteria
  • Sorbitol, mannitol and lactitol in sugar free chewing gums
274
Q

The Future of plaque mediated disease:

A

Oral Probiotics?

  • Potential life-long protection
  • Popular with consumers
  • Safety concerns?
  • Examples include non pathogenic mutans streptococci
275
Q

Saliva in dental caries?

A

Acts as a buffer that neutralises acid

276
Q

What is haematology?

A

Haematology is the study of blood which is composed of plasma (~55%), and the formed elements

277
Q

What are the different elements of blood?

A
  • Plasma: the liquid part of blood which is similar in composition with serum except that the serum does not contain clotting factors of blood (fibrinogen).

The erythrocytes (RBCs) (~45%)

  • Contain haemoglobin
  • Function in the transport of O2 and CO2

The Leukocytes (WBCs) and platelets (thrombocytes) (~1%)

  • Leukocytes are involved in the body’s defense against the invasion of foreign antigens.
  • Platelets are involved in haemostasis which forms a barrier to limit blood loss at an injured site.
278
Q

Significance of haematology?

A
  • Haematology is primarily a study of the formed cellular elements.
  • Alterations in the formed elements in the blood are usually a result of disease rather than being the primary cause of disease.
279
Q

What is an Anticoagulant?

A

an agent that prevents the clotting of blood

Examples are EDTA, Citrate and Heparin

280
Q

What is a capillary:

A

small blood vessel that connects arterioles and venules

281
Q

What is Haemoglobin?

A

the oxygen carrying molecule of red blood cells

282
Q

What is haemolysis?

A

the breakdown of red blood cells, with the release of hemoglobin into the plasma or serum

283
Q

What does Lipemic mean?

A
  • Having abnormally high level of fat.

- Milky looking samples

284
Q

What is plasma?

A

pale yellow part of whole blood; contains all clotting factors

285
Q

What is Serum?

A

liquid portion of blood which does not contain one of the clotting factors, the protein fibrinogen

286
Q

What is serology?

A

the study of antigen – antibody reactions using laboratory tests

287
Q

What is Haematopoiesis?

A

is a term describing the formation and development of blood cells.

288
Q

Homeostasis to maintain amount of blood cells in blood:

A
  • Proliferation of progeny stem cells
  • Differentiation and maturation of the stem cells into the functional cellular elements
  • In normal adults, the proliferation, differentiation, and maturation of the hematopoietic cells (RBCs, WBCs, and platelets) is limited to the bone marrow and the widespread lymphatic system and only mature cells are released into the peripheral blood.
289
Q

Primary site of haematopoiesis:

A

The bone marrow

290
Q

What is bone marrow?

A

– is located inside spongy bone

- The bone marrow contains both Erythroid (RBC) and leukocyte (WBC) precursors as well as platelet precursors

291
Q

Hematopoietic cells can be divided into three types based on maturity:

A
  • Pluripotent stem cell capable of self-renewal and differentiation into all blood cells
  • Committed progenitor stem cells destined to develop into distinct cell lines
  • Mature cells with specialized functions
292
Q

Replacement of peripheral hematopoietic cells is a function of the pluripotent (totipotent) stem cells found in the bone marrow. True or false?

A

True

  • Pluripotent stem cells can differentiate into all of the distinct cell lines with specific functions and they are able to regenerate themselves.
  • The pluripotent stem cells provide the cellular reserve for the stem cells that are committed to a specific cell line.
293
Q

Function of the blood?

A

Transporting fluids such as:

  • -> Nutrients from digestive tract
  • -> O2 from lungs
  • -> Waste from cells
  • -> Hormones

Aids in heat distribution

Regulates acid-base balance

294
Q

Composition of the blood: Erythrocytes

A

Red blood cells are responsible for:

  • Transport of oxygen and nutrients
  • Removal of waste and CO2 from the cells
  • Distribution of heat
  • Haemoglobin: the O2 carrying potential
295
Q

Composition of the blood: Leukocytes

A

White Blood Cells are responsible for:

  • Phagocytosis – to engulf and absorb waste material and harmful microorganisms in the blood stream and tissues
  • Synthesis of antibody molecules
  • Inflammation process
  • Production of heparin – component found in lung and liver tissue which have the ability to prevent clotting of blood.
    • ->Heparin used in the treatment of thrombosis
296
Q

Composition of the blood: Thrombocytes

A
  • Platelets – the smallest of the solid components of the blood
  • Responsible for the coagulation (clotting) process
  • Embolism: a blood clot which is moving through the body
297
Q

Anaemia: different types?

A

more than 400 types of anaemia, which are divided into three groups:

1) Anaemia caused by blood loss
2) Anaemia caused by decreased or faulty red blood cell production
3) Anaemia caused by destruction of red blood cell

298
Q

Anaemia caused by blood loss:

A

Red blood cells can be lost through bleeding, which often can occur slowly over a long period of time, and can go undetected.

This kind of chronic bleeding commonly results from the following:

  • Gastrointestinal conditions such as ulcers
  • Use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin or ibuprofen, which can cause ulcers and gastritis
  • Menstruation and childbirth in women, especially if menstrual bleeding is excessive and if there are multiple pregnancies.
299
Q

Anaemia due to decreased or faulty red blood cell production:

A

With this type of anaemia, the body may produce too few blood cells or the blood cells may not function correctly.
In either case, anaemia can result. Red blood cells may be faulty or decreased due to abnormal red blood cells or a lack of minerals and vitamins needed for red blood cells to work properly.

Conditions associated with these causes of anaemia include the following:

  • Sickle cell anaemia
  • Iron-deficiency anaemia
  • Vitamin deficiency
300
Q

Anaemia caused by destruction of red blood cells:

A

When red blood cells are fragile and cannot withstand the routine stress of the circulatory system, they may rupture prematurely, causing haemolytic anaemia.

Haemolytic anaemia can be present at birth or develop later. Sometimes there is no known cause.

301
Q

What is coagulation?

A

Coagulation is the formation of fibrin meshwork (threads) to form a clot
• Coagulation of blood depends on the balance between pro-coagulants and anti-coagulants
• Prothrombin is the inactive form of thrombin
• The liver depends on vitamin K in the production of factor 2,7,9 and 10
• Thrombin changes fibrinogen to fibrin and it activates factor V, VIII and XIII
• Blood Clot is composed of a meshwork of fibrin fibers running in all directions and entrapping blood cells, platelets, plasma
• Fibrinolysis is the break down of fibrin by naturally occurring enzyme plasmin therefore prevent intravascular blocking
• Plasmin is controlled by: Anti-activators and Antiplasmin
• Prevention of blood clotting in the normal vascular system occurs by: Endothelial surface factors, Fibrin fibers, Antithrombin III and Heparin
• Conditions that cause excessive bleeding include: Vitamin K Deficiency, Haemophilia and Thrombocytopenia.

302
Q

What is factor V Leiden Thrombophilia?

A
  • The name of a specific gene mutation that results in the development of the most common type of thrombophilia which is an inherited genetic disorder characterized by increased tendency to form abnormal blood clots.
  • People with factor V Leiden thrombophilia have a higher than average risk of developing a type of blood clot called a deep venous thrombosis (DVT).
303
Q

What is International Normalized Ratio?

A

To assess how well the blood clots the World Health Organization has proposed an international reference which is called International Normalized Ratio (INR).

The time it takes for the blood to clot is called prothrombin time (PT) and the INR is an international standard for the PT that facilitates the determination of the dose of blood thinners, also called anti-clotting medicines or anticoagulants.

304
Q

The INR has two major advantages:

A
  • It allows comparison between results obtained from different laboratories, and
  • it allows investigators to standardize anticoagulant therapy in clinical trials and scientific publications.

The Public Sem 2 (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions