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Foundations Of Medicine - Mats > PoD Learning Outcomes > Flashcards

PoD Learning Outcomes Flashcards

1
Q

What is a bacterium

A

Single celled prokaryotic organism
round, spiral or rod shaped
Lives in soil, organic matter or the bodies of plants and animals

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2
Q

What is a virus

A

Acellular
Metabolically inert organism
Only replicates within living cells

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3
Q

What is a fungus

A

Saprophytic and parasitic spore-producing eukaryotic
Typically filamentous
Includes moulds, yeasts, mushrooms

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4
Q

List the categories of micro-organism that can cause infection

A

Bacteria, viruses, fungi, parasites, prions

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5
Q

List the common sites that specimen types are collected for culture.

A

Sputum, throat swabs, faeces, blood culture, cerebrospinal fluid (CSF), aspirate of pus, bone, mid stream specimen of urine (MSSU)

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6
Q

Explain the difference between sterile and non sterile sites.

A

Sterile sites:
Brain, heart, liver, kidney
Non-sterile sites:
Mouth, oesophagus, lungs, stomach, intestine

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7
Q

Outline the methods of detecting viruses.

A

Molecular methods (real time/multiplex PCR)
Antigen detection
Serology to determine immunity
Virtually obsolete methods (electron microscopy, cell or tissue culture)

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8
Q

Outline the diagnostic principles in parasitology

A

Microscopy of different life cycle stages:

  • Parasites, cysts and ova in faeces
  • Blood films for malaria
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9
Q

Describe basic infection control measures

A 
F – face coverings
A – avoid crowded places
C – clean your hands regularly 
T – two metre distance 
S – self isolate and book test if symptomatic
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10
Q

What is a Chromosome (bacteria)

A

made of proteins and single strand of DNA

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11
Q

What is cytoplasm (bacteria)

A

gelatinous liquid that fills inside of a cell. Cytoplasmic membrane has proteins embedded

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12
Q

What is cell wall (bacteria)

A

made of peptidoglycan, thick and strong, maintains shape, important for cell division

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13
Q

What is ribosome (bacteria)

A

synthesis of proteins, consist of RNA and associated proteins

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14
Q

What is penicillin binding proteins (bacteria)

A

proteins that bind penicillin and other antibiotics. Generally enzymes. Contribute essential role in bacterial cell wall biosynthesis

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15
Q

What is peptidoglycan (bacteria)

A

major structural polymer in most bacterial walls

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16
Q

What is Lipopolysaccharide (bacteria)

A

only in gram neg. Prevevents peptidoglycan from bile salts in gut

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17
Q

What is capsule (bacteria)

A

polysaccharide layer outside cell envelope, not easily washed off

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18
Q

What is flagella (bacteria)

A

used for locomotion

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19
Q

What is fimbriae (bacteria)

A

adherence

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20
Q

What is plasmid (bacteria)

A

DNA molecule separate from chromosome and replicate independently of that (carry small number of genes – notably some associated with antibiotic resistance)

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21
Q

What is bacteriophage (bacteria)

A

virus that infects bacteria (destroy the host cell)

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22
Q

What are spores (bacteria)

A

involved in reproduction

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23
Q

Explain the classification of and nomenclature used for bacterial species

A 
Phenotypically:
-	Observable physical properties
o	Gram stain
o	Growth requirements e.g. aerobicba, anaerobic, microaerophilic 
Genotypically:
-	Relating to DNA 
o	Ribosomal RNA sequence analysis 
o	Whole genome sequencing
Nomenclature: based on genus followed by species
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24
Q

Describe how bacteria replicate and create genetic variation

A 
-	Replication by binary fission:
o	Identical progeny
-	Genetic variation by:
o	Spontaneous mutation
o	Transfer of DNA
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25
Q

Describe briefly the detection and culture of bacteria

A

Detection
- Individual bacteria can be seen with microscope
- Stains
Culture
- Colonies of individual bacteria can be cultured on solid medium (agar)
- Can be seen by eye

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26
Q

Explain the basic characterisation of viruses

A

Small 20-400nm diameter
Non-cellular – genetic element that cant replicate independently of a living host
- Obligate intracellular pathogens
Most viruses have specific host and only infect specific host cell types (tissue tropism)

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27
Q

What is a virion

A

Extracellular form of a virus – exits outside host and facilitates transmission from one host to another

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28
Q

Basic classification of viruses

A
  • Virion shape/symmetry
  • Presence/absence of envelope
  • Genome structure
  • Mode of replication
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29
Q

Describe examples of human virus infections of major importance.

A 
Blood-borne: HIV, hepatitis B & C
Sexual: HIV, hepatitis B
Vertical: HIV, hepatitis B
Faecal-oral: hepatitis A, hepatitis E, polio
Droplet: influenza, RSV
Airborne: measles, chickenpox
Close contact: herpes simplex, CMV, EBV
Vector-borne: Dengue, yellow fever, chikungunya
Zoonotic: rabies, MERS, Ebola
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30
Q

Describe the structure of viruses

A 
Nucleic acid – containing genetic material
Virion associated polymerase 
Protein capsid 
Lipid envelope 
Spike projections
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31
Q

Describe how viruses replicate

A

Virus attaches to host cell
Uncoating (lipid envelope removed)
Replication of genomic Nucleic acid (mRNA synthesis)
Protein synthesis
Newly synthesised virus proteins are assembled into new Virion
Budding and release – virus gets lipid envelope back

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32
Q

Explain the concept of host range in relation to viruses

A

Some viruses may only infect humans e.g. smallpox
Some may affect other animals/birds
- Can have transmission of a novel virus to humans

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33
Q

Describe the consequences of a viral infection

A

Clearance of a virus
- Can have no (hep C), short or long term immunity (measles)
Chronic infection
- HIV, Hep B & C
Latent infection
- Herpes
Transformation (long term infection with altered cellular gene expression)
- Epstein-Barr virus, human papilloma virus

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34
Q

Explain the concept of viral latency

A

Following primary infection, some viruses lie dormant in the cell
Full viral genome retained in the host cell, but expression is restricted
Reactivation of viral replication can occur
- May or may not cause apparent disease
- More likely to occur and more severe in immunocompromised

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35
Q

Describe the link between viruses and cancer and explain the mechanisms through which this results (+example)

A

Mechanisms
- Modulation of cell cycle control (driving cell proliferation)
- Modulation of apoptosis (prevention of programmed cell death)
- Some viruses cause persistent inflammatory processes which lead to cancer via reactive oxygen species
Examples:
- Human papillomavirus (HPV)
o Cervical, anal, oropharyngeal cancers

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36
Q

Describe the indications for and principles of anti-viral therapy

A

All antiviral agents are virustatic (preventative), none are virucidal (destroy the virus)
Viruses use host cell enzymes to replicate – limited viral proteins for antiviral drugs
Antivirals used for:
- Prophyaxis – prevent infection
- Pre-emotive therapy – evidence of infection/replication detected before symptoms apparent
- Suppressive therapy – keep viral replication below the rate that causes tissue damage in asymptomatic infected patient

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37
Q

Describe how to prevent viral infections

A

Immunisation – vaccination, passive immunisation with immunoglobulin
Prophylactic treatment – post exposure
Infection prevention and control measures – isolation of symptomatic patients, PPE, disposal of sharps
Blood/tissue/organ screening
Antenatal screening

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38
Q

explain how viruses can be eradicated

A

Viruses with certain properties can be eradicated:
- No animal reservoir/ability to amplify in environment
- Clearly identifiable
- No chronic carrier state
- Efficient and practical intervention e.g. vaccine
- Political/social support
Example: small pox & polio

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39
Q

Describe the principles of active immunisation.

A 
Active immunity
Microbial antigen (vaccine or infection) —> challenges infection —> recovery (immunity) 
Specific: yes
Memory: yes
Natural – exposure/infection 
Artificial – Vaccination
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40
Q

Describe the principal of passive immunisation

A 
Serum (antibodies) from immune individual—> administration of serum to uninfected individual —> recovery (immunity)
Specific: yes
Memory: no
Advantages:
-	Gives immediate protection
-	Quick fix
Disadvantages:
-	Short term effect – no immunological memory
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41
Q

Describe the types of vaccine available for active immunisation.

A

Killed whole organism (inactivated): Target organism e.g. polio virus is killed

Attenuated whole organism (live attenuated): strain of target organism isolated but virulence reduced

Subunit vaccines (purified antigen)

Toxoid (inactivated toxin)

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42
Q

Define what is meant by the term vaccination

A

Administration of antigenic material (a vaccine) to stimulate an individuals immune system to develop adaptive immunity to a pathogen

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43
Q

Describe the contra-indications to vaccination

A

Temporary:
Febrile illness
Pregnancy – cannot be given live attenuated vaccines
Permanent:
Allergy
Immunocompromised- cant be given live attenuated vaccines as individuals may develop disease from the vaccine strain

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44
Q

Describe the concept of herd immunity

A

Primary aim of vaccination to protect individual receiving vaccine
Vaccinated individuals less likely to be source of infection to others
Reduces risk of unvaccinated individuals being exposed to infection
Those that cant be vaccinated still benefit from vaccine programmes
Herd immunity – large portion of community becomes immune, making spread of disease from person to person unlikely

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45
Q

Describe the vaccines that may need to be given to travellers

A 
Hepatitis A
Typhoid
Neisseria meningitidis 
Cholera
Yellow fever
Japanese encephalitis 
Tick-borne encephalitis 
Rabies
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46
Q

Describe the main groups of parasites and their life cycles.

A

Protozoa:
Microscopic, single celled organisms
Responsible for malaria – live in the blood transferred via an insect vector
Helmiths (worms):
Cause variety of diseases in variety of body systems
Ectoparasites:
Parasites which live outside the body (most are insects or arachnids and many are vectors of infection)

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47
Q

Describe the common diseases caused by enteric and blood-borne parasites.

A

Malaria – plasmodium species (protozoa)
Amoebic dysentery – entamoeba histolytica invade gut wall (causes cysts in stool)
Cestodes (tapeworms) – eating raw undercooked meat (can form cysts outside of the gut)

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48
Q

Define what is meant by the term ‘parasite’

A

An organism that lives in or on another organism (host) and derives its nutrients at the expense of the host

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49
Q

Describe the diagnostic principles in parasitology

A

Blood microscopy for parasites
Stool microscopy (cysts)
Serology (immune testing)
Rapid diagnostic tests

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50
Q

Explain the difference between gram negative and gram positive bacteria and describe the features of the cell surface in both types

A

Gram negative – surrounded by thin peptidoglycan cell wall, which is also surrounded by outer membrane containing lipopolysaccharide
(Stain pink)
Gram positive – lack outer membrane but are surrounded by layers of peptidoglycan (many times thicker than gram negative)
(Stain purple)

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51
Q

List clinically significant Gram positive bacteria

A

Staphylococcus aureus
Streptococcus pyogenes
Streptococcus pneumoniae
Clostridium difficile

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52
Q

Difference between staphylococci and streptococci/enterococci

A

Staphylococci = clusters

Streptococci & enterococci = chains

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53
Q

What is Staphylococcus aureus

A
  • gram positive
  • commensal carried in nose, axial, perineum
  • Wide range of diseases from boils/abscesses and soft tissue infections to septicaemia and osteomyelitis
  • Commonly penicillin resistant due to production of penicillinase
  • By different mechanism some strains methicillin resistant staph aureus (MRSA)
    o Major problem for infection prevention and control in hospital
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54
Q

What is Streptococcus pyogenes

A

Gram positvie

  • Beta-haemolytic streptococci
  • Pharyngitis
  • Cellulitis
  • Necrotising fasciitis (flesh eating bug)
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55
Q

What is Streptococcus pneumoniae

A

Gram positive

  • Alpha-haemolytic streptococci
  • Pneumonia, meningitis, septicaemia
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56
Q

What is Clostridium difficile

A

Gram positive

  • “difficult to culture”
  • Asymptomatic gut carriage in healthy people (16% in adults 66% of babies)
  • Important cause of diarrhoea, associated with toxin production and potentially fatal
  • Increased risk with antibiotic use and anything else that disrupts normal gut flora
  • Transmitted via spores
  • Detect antigen and toxin in stool sample
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57
Q

List clinically significant Gram negative bacteria

A 
75% of terrible 12 are gram neg.
Escherichia coli 
Salmonella spp.
Salmonella typhi 
Campylobacter spp. 
Helicobacter pylori
Haemophilus influenza
Pseudomonas spp.
Anaerobes
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58
Q

What is Escherichia coli

A
  • Human and animal reservoirs
  • Several virulence mechanisms
  • Ferments lactose
  • Strains vary in disease potential
    o E.g. travellers diarrhoea
    o Bloody diarrhoea
  • Important cause of UTI
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59
Q

What is Salmonella spp.

A
  • Doesn’t ferment lactose
  • Self-limiting enterocolitis with or without bloody diarrhoea
  • Second most common cause of bacterial diarrhoea in UK
  • Can be invasive (enter bloodstream)
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60
Q

What is Salmonella typhi

A
  • Cause of typhoid fever
  • Fever & constipation in early stages
  • Organism can be isolated from blood and faeces
  • Vaccine available
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61
Q

What is Campylobacter spp.

A
  • Likes low O2
  • Source is domestic animals and chickens
  • Spread via faecal-oral route
  • Foul smelling bloody diarrhoea
  • Most common cause of bacterial diarrhoea in UK
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62
Q

What is Helicobacter pylori

A
  • Curved rods
  • Habitat is human stomach
  • Damages mucosa and causes ulcers
  • Risk factor for gastric adenocarcinoma
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63
Q

What is Haemophilus influenza

A
  • Mixed appearance

- Causes respiratory tract infection

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64
Q

What is Pseudomonas spp.

A 
-	Water and soil coloniser 
o	Drains, sinks, mops
-	May contaminate medical equipment 
-	Hospital acquired cause of sepsis 
o	UTI, bacteraemia, pneumonia (rare)
-	Multi-drug resistance mechanisms
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65
Q

List clinically significant bacteria which are not readily identified by Gram staining and outline how they are identified or distinguished

A 
Mycobacterium spp.
-	Visualised by special stains e.g. ZN or auramine 
o	Resistant to decolorisation by acid and alcohol (AAFB)
-	Leprosy 
-	TB
Mycobacterium tuberculosis
-	High HIV prevalence in TB cases
-	9 million new cases/year
Spirochaetes
-	Long, spiral shaped
-	Diseases:
o	Syphilis
o	Lyme disease
o	Leptospirosis
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66
Q

Explain the structure of fungi

A

o Chemo-organotrophic eukaryote that lacks chlorophyll and forms spores
o Cell wall contains polysaccharides (often chitin or glucagon) and absorbs nutrients
o Membrane contains ergosterol as the major sterol

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67
Q

Explain the classification of fungi

A

based on morphology

o Informally refer to major types as moulds, yeasts or mushrooms

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68
Q

Describe the clinically important systemic and dermatophytic fungal infections.

A

Dermatophytes
- Ringworm infections usually called tinea
- Moulds with a predilection to degrade keratin as a nutrient source
Systemic
- Athletes foot: epidermophyton, microsporangia and trichophyton spp.
- Thrush: candida spp.
- Pityriasis versicolor: malassezia spp.

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69
Q

Describe the properties of fungi

A 
Eukaryotic
Reproduce by spores 
Non-vascular 
Non-motile
Heterotrophic organisms 
Lack chlorophyll
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70
Q

Describe the host factors that contribute to the pathogenicity of fungal infections

A
  • Favourable micro-environments (warm + moist areas) encourage growth of fungi on skin and mucous membranes
  • Antibacterial agents reduce competition for epithelial colonisation sites in the gut
  • Immunosuppression creates opportunity for fungal invasion
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71
Q

Describe the diagnostic methods for detecting fungi

A 
Direct detection:
-	Histopathology, high-res CT scans
Direct smear:
-	PAS Staining 
Growth on selective medium
Detection of circulating fungal antigens 
Detection of circulating antibodies to fungi
PCR for fungal DNA
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72
Q

Describe the mechanisms of action of anti-fungal drugs, their route of administration and issues associated with anti-fungal agents

A 
Antifungal drugs:
Echinocandins – target wall
Polyenes – target membrane
Flucytosine – target DNA synthesis
Triazoles & allylamines – target sterols 
Antifungal agents:
Polyenes 
-	Amphotericin B (topical, IV, lozenge, ointment, oral suspension)
-	Nystatin (topical, pastille, oral suspension)
Azoles
-	E.g. miconazole (topical)
-	Fluconazole (oral and/or IV)
Echinocandins
-	Anidulafungin, -fungin (IV)
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73
Q

Describe some of the features of viral pathogenesis.

A
  1. Implantation of virus at portal of entry
  2. Local replication
  3. Spread to target organs (disease sites)
  4. Spread to sites of shedding of virus into environment
    Dependent on:
  5. Accessibility of virus to tissue
  6. Cell susceptibility to virus multiplication
  7. Virus susceptibility to host defences
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74
Q

Define the terms pathogen and commensal.

A

Pathogen – organism which can cause disease
Commensal – organism which is part of normal flora e.g. E. coli in the gut

Distinction between both not always clear

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75
Q

Describe in outline the human defence mechanisms of innate and acquired immunity.

A

Innate
- Non-specific immunity – natural barriers (skin and mucosa) and secretions
Acquired
- Immune system responds to foreign substance/microorganism
o Adaptive – response to being infected with or vaccinated against a microorganism
o Passive – person receives antibodies to a disease or toxin rather than making them through own immune system

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76
Q

Explain meaning of colonisation

A

presence of bacteria on body surface (skin, mouth, intestines) without causing disease in the person

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77
Q

Explain the meaning of latent

A

Latent – residence in the body of a specific infectious agent without any manifestation of symptoms

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78
Q

Explain the meaning of asymptomatic infection

A

organism has invaded the body but not yet caused any symptoms

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79
Q

Explain the meaning of infection

A

invasion of organisms body tissues by disease causing agents, their multiplication, and the reaction of the host tissues to the infectious agent and toxins produced

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80
Q

Describe the features of clinical infection

A
  • Inflammation
  • Low temperature
  • Tachycardia
  • Constipation
  • Increased white cell count
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81
Q

Define pathogenicity and describe the concepts of infectivity and virulence

A

Pathogenicity – capacity of a micro-organism to cause an infection
- Requires:
o Infectivity – ability to become established on or within a host
o Virulence – ability to cause harmful effects (disease) once established

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82
Q

Describe the features of pathogenic toxins and their effects (exotoxins, enterotoxins, endotoxin)

A

Exotoxins – released intracellularly by the micro-organism
Enterotoxins – exotoxins which act on the GI tract
Endotoxin – structurally part of the gram negative cell wall

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83
Q

Describe the sites of viral entry

A 
Conjunctiva
Respiratory tract
Skin
Scratch/injury
Arthropod
Alimentary tract
Urinogenital tract
Anus
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84
Q

Describe the features of enterovirus infection with the use of examples

A

Virus acts on the gut – if they enter the bloodstream (viraemia) and act on neuronal tissue = paralysis
Examples:
poliomyelitis – Poliovirus
Aseptic meningitis – many enteroviruses
Respiratory infections – many enteroviruses

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85
Q

Describe how virus can induce tumours with the use of examples

A

Papillomaviruses – cervical carcinoma

Retroviruses – lymphomas and leukaemias

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86
Q

Describe humoral and cell mediated immunity

A

Humoral – process of adaptive immunity manifested by production of antibodies by B lymphocytes
- B cells triggered to proliferate into plasma cells which produce antibodies

Cell mediated – doesn’t involve antibodies
- Driven by mature T cells, macrophages and release of cytokines in response to antigen

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87
Q

What is hypersensitivity

A

Hyper-response from the immune system that may produce tissue injury and cause serious disease

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88
Q

Contrast the mechanisms of Type I,II,III and IV hypersensitivity

A

Type I, II (V), and III are antibody mediated

Type IV is T cell mediated

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89
Q

Type I mechanism

A

Type I = IgE (soluble antigen)
Predisposition to Allergy (e.g. eczema)
Activated mast cell – leads to vasodilation, bronchoconstriction, inflammation, vascular congestion, tissue damage

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90
Q

Type II mechanism

A

Type II = IgG (cell or matrix antigen)

Rheumatic fever

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91
Q

Type III mechanism

A

Type III = IgG (soluble antigen)

Rheumatoid arthritis

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92
Q

Type IV mechanims

A

T-cell mediated
Type IV = TH1 (soluble antigen), TH2 (soluble antigen), CTL (cell antigen)
Inflammatory cytokines
Type 1 diabetes, MS

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93
Q

Understand how allergens can induce immediate immune responses during early phase allergy

A
  • IgE mediated effects (vasodilation, vascular leak, bronchoconstriction, inflammation, tissue damage, intestinal hypermotility)
    o Through amines (histamine), lipid mediators, cytokines, enzymes

(Late reaction
- Eosinophils, neutrophil and T cell infiltrates
o Killing of parasites and host cells, tissue damage)

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94
Q

Define atopy

A

Predisposition to allergy – through exaggerated IgE-mediated immune response (all atopic disorders are type 1 hypersensitivity disorders)

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95
Q

Understand the differences between type II and III antibody mediated hypersensitivity

A

The difference between type II and type III is the location of the antigens

  • Type II – the antigens are cell bound
  • Type III – the antigens are soluble

Type II
Antibody-mediated immune reaction in which antibodies IgG or IgM are directed against cellular or Extracellular matrix antigens with resultant tissue injury
Type III
Mediated by antigen-antibody complexes in the circulation which may be deposited in tissues causing damage.

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96
Q

Define and explain immune tolerance

A

Immune tolerance: state of unresponsiveness to a specific antigen (self of foreign)
- Prevents adaptive responses that are damaging
- Can be exploited by microbes and tumours
- Important to understand because:
o Allows us to understand why autoimmune diseases develop
o Intervene with novel therapeutics based on immune tolerance mechanisms to treat or cure many diseases
o Replacement of long-term immunosuppression with short term therapeutic strategies with less toxicity

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97
Q

Define and explain automimmune disease

A

Autoimmune disease: a failure or breakdown of immune system that maintains tolerance to self tissues
- Genetic pre-disposition
- Environmental impact
o Prior infection, trauma, drugs, food

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98
Q

Define and explain immune tolerance

A

Immune tolerance: state of unresponsive news to a specific antigen (self of foreign)

  • Prevents adaptive responses that are damaging
  • Can be exploited by microbes and tumours

(Important to understand because:
o Allows us to understand why autoimmune diseases develop
o Intervene with novel therapeutics based on immune tolerance mechanisms to treat or cure many diseases
o Replacement of long-term immunosuppression with short term therapeutic strategies with less toxicity)

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99
Q

Contrast systemic and organ specific autoimmune disease.

A

Systemic

  • Autoimmune processes diffuse throughout the body
  • Affects more than one organ (nor necessarily the same ones in different individuals)

Organ specific
- Autoimmune process directed against one organ
o Type 1 diabetes – pancreas

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100
Q

Explain the terms MIC/MBC, sensitive/resistant, bacteriocidal/bacteriostatic, synergy/ antagonism.

A

Sensitive: organism is sensitive if it IS inhibited or killed by the antimicrobial available at the site of infection
Resistant: organism is resistant if it is NOT killed or inhibited by the antimicrobial available at the site of infection
Bactericidal: antimicrobial that kills bacteria
MBC: (Minimal bactericidal concentration) minimum concentration of antimicrobial needed to kill a given organism
Bacteriostatic: antimicrobial that inhibits growth of bacteria
MIC: (minimal inhibitory concentration) minimum concentration of antimicrobial needed to inhibit growth of given organism

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101
Q

Describe mechanisms of action of antibacrterial drugs: inhibition of cell wall synthesis

A

Penicillins and cephalosporins (beta-lactams) – bactericidal antibiotics
Most effective against Gram-positive bacteria
Disrupt the peptidoglycan (cell wall component) synthesis by inhibiting the enzymes (penicillin-binding proteins) responsible for cross-linking the carbohydrate chains

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102
Q

Describe mechanisms of action of antibacrterial drugs: inhibition of protein synthesis

A

Aminoglycosides – concentration dependent bactericidal antibiotics
Useful in treatment of serious gram-negative infection
Differences between bacterial and mammalian mRNA at ribosome allows selective targeting of bacterial protein synthesis
- Leads to inaccurate translation and premature termination of the bacteria

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103
Q

Describe mechanisms of action of antibacrterial drugs: inhibition of nucleic acid synthesis

A

Inhibition of purine synthesis – bacteriostatic when combined with bactericidal antibiotics
Inhibition of DNA synthesis directly, or indirectly by interrupting supply of precursors for DNA synthesis

104
Q

Spectrum of action used in antibacterial drugs

A

Inhibition of wall synthesis - Disrupt the peptidoglycan (cell wall component) synthesis by inhibiting the enzymes (penicillin-binding proteins) responsible for cross-linking the carbohydrate chains
Inhibition of protein synthesis – inhibits protein synthesis by selectively targeting bacterial protein synthesis and preventing translation + addition of amino acids to peptide chains
Inhibition of nucleic acid synthesis – directly or indirectly inhibits DNA synthesis by interrupting supply of precursors for DNA synthesis

105
Q

List the factors to be considered in choosing suitable antimicrobial agents to prevent or treat infection.

A
  • Antimicrobials should only be used when indicated and in minimum dose and duration to achieve efficacy
-	Factors considered:
o	Age
o	Renal function
o	Liver function
o	Pregnancy 
-	Antibiotic chosen should be effective against known/likely organism
106
Q

List the side effects commonly associated with the major groups of drugs.

A

Allergic reactions (commonly with beta-lactams)
Immediate hypersensitivity - anaphylactic shock (IgE mediated)
Delayed hypersensitivity – hours or days to develop
Gastrointestinal side effects – nausea and vomiting are common
Thrush – suppression of normal flora leads to overgrowth of resistant organisms
Liver toxicity
Renal toxicity
Neurological toxicity

107
Q

Explain the role of the laboratory (and Clinical Microbiologists) in influencing antimicrobial usage in clinical practice.

A

Medical microbiologists – advice on urgent treatment of infection before organism is isolated, identified and antibiotic sensitivity tested
Laboratory – ensure therapeutic levels achieved + ensure levels aren’t so high they are toxic

108
Q

Describe the classification and nomenclature of tumours.

A

Tumour (neoplasm) = abnormal growing mass of tissue

  • Growth is uncoordinated with surrounding tissue
  • Growth continues after removal of any stimulus
  • Irreversible change
109
Q

Define benign, dysplastic, malignant

A

Benign – lacks ability to metastasise – rarely or never become cancerous
Dysplastic – benign but could progress to malignancy. Cells show abnormalities of appearance and cell maturation (pre-malignant)
Malignant - able to metastasise

110
Q

Epithelial tumours: benign + malignant glandular

A

Benign – adenoma

Malignant – adenocarcinoma

111
Q

Epithelial tumours: benign and malignant squamous

A

Benign – squamous papilloma

Malignant – squamous carcinoma

112
Q

Tissue tumours: benign and malignant Bone

A

Benign – osteoma

Malignant – osteo-sarcoma

113
Q

Tissue tumours: benign and malignant Fat

A

Benign – lipoma

Malignant – lipo-sarcoma

114
Q

Tissue tumours: benign and malignant fibrous tissue

A

Benign – fribroma

Malignant – fibro-carcoma

115
Q

Blood cells: benign & malignant white blood cells

A

Benign – N/A

Malignant – leukaemia

116
Q

Lymphoid tissue: benign and malignant lymphoid tissue

A

Benign – N/A

Malignant – lymphoma

117
Q

Melanocytes: benign and malignant melanocytes

A

Benign – Naevus

Malignant – melanoma

118
Q

Cancers of the neural tissue: central nervous system

A

Astrocytoma

119
Q

Cancers of the neural tissue: peripheral nervous system

A

Schwannoma

120
Q

Germ cell tumours (benign and malignant in which)

A

teratomas (develop in ovaries and testies)
Ovarian = usually benign
Testicular = usually malignant

121
Q

Characteristics of benign tumours

A
  • Non-invasive growth pattern
  • Usually encapsulated
  • No evidence of invasion
  • Not metastases
  • Cells similar to normal
  • Well-differentiated
  • Function similar to normal tissue
  • Rarely cause of death
122
Q

Characteristics of malignant tumours

A

Malignant = cancer

  • Invasive growth pattern
  • No capsule or capsule breached by tumour cells
  • Cells are abnormal
  • Poorly differentiated
  • Loss of normal function
  • Often evidence of spread of cancer (metastasis)
  • Frequently cause death
123
Q

Define the properties of cancer cells. (Tumour suppressor genes, oncogenes, cellular function)

A 
Loss of tumour suppressor genes:
-	Adenomatous polyposis (APC)
-	Retinoblastoma (Rb)
-	BRCA1
Gain of function of oncogenes:
-	B-raf
-	Cyclin D1
-	ErbB2
-	C-Myc
-	K-ras, N-ras
Altered cellular function
-	Loss of cell-to-cell adhesion
-	Altered cell-to-matrix adhesion
Cells capable of independent growth 
Tumour biomarkers (tumour-related proteins)
124
Q

Define the spread of cancer

A

Fundamental property of cancer
- Invasion and metastasis
Clinical problem is formation of metastatic (secondary) tumours
- Prognosis dependent on cancer spread

125
Q

Explain the mechanisms of cancer spreading

A
  • Local spread
    o Into connective tissue
  • Lymphatic spread
    o Adherence to lymph vessels then into lymph nodes
  • Blood spread
    o Adherence to blood vessels then invasion into tissue
  • Trans-coelomic spread
    o Spread of tumour cells across body cavities e.g. pleural
    o Often in tumours of lung, stomach, colon, ovary
126
Q

State the common/uncommon sites for cancer to metastasise to

A 
Common sites of metastasis 
-	Liver
-	Lung 
-	Brain
-	Bone 
o	Axial skeleton 
-	Adrenal gland 
-	Omentum/peritoneum
Uncommon:
-	Spleen
-	Kidney
-	Skeletal muscle 
-	Heart
127
Q

List the local affects of benign tumours

A
  • Pressure

- Obstruction

128
Q

List the local effects of malignant tumours

A
  • Pressure
  • Obstruction
  • Tissue destruction
    o Ulceration/infection
  • Bleeding
    o Anaemia
    o Haemorrhage
  • Pain
    o Pressure on nerves
    o Perineural infiltration
    o Bone pain from pathological fractures
  • Effects of treatment
129
Q

List the systemic effects of cancer

A

Malignant

  • Weight loss-cancer cachexia
  • Secretion of hormones
  • Normal/ abnormal (inappropriate)
  • Paraneoplastic syndromes
  • Effects of treatment
130
Q

Identify the concepts of dysplasia and intra-epithelial neoplasia.

A

Early detection = better prognosis
- Detection of pre-invasive stage
o Identification of dysplasia/intraepithelial neoplasia
Dysplasia:
- Pre-malignant change
- Identification in epithelial
- No invasion
- Disorganisation of cells (increased nuclear size, increased mitotic activity)
ABNORMAL CELLS FOUND ON THE SURFACE OR IN THE TISSUE THAT LINES AN ORGAN

131
Q

Understand some of the key molecules in the cell cycle – e.g. the retinoblastoma gene product

A
  • Applies break to cell cycle
  • Carcinogenesis = failure of cell cycle control
  • P53 and D-pRb-E2F pathway often disrupted
    o P53 mutants don’t G1 arrest or repair damaged DNA
  • Frequently Mutated regulating genes:
    o Cyclin D
    o CDK4
    o P16
    o Rb
132
Q

Describe how aetiological agents cause abnormalities in regulators of the cell cycle.

A

Environmental:
- Chemicals
o Target purine and pyrimidine bases in DNA
- Radiation
o Purine and pyrimidine bases in DNA are targets
- Oncogenic viruses
o Cause proto-oncogene over expression
o HPV
Inherited factors:
Tumour suppressor genes (anti-oncogenes):
- Protect a cell from forming cancer

133
Q

Identify that tumour formation is a multi-step process.

A

Two-hit hypothesis
- Tumour suppressor alleles usually recessive
- Loss of both normal allelic copies gives rise to cancer
Mutations accumulate with time
Mutation = loss of function
Genes negatively regulating mitosis – Rb, INK4A family
Genes regulating apoptosis – p53

134
Q

Explain the importance of genetic changes in cancer.

A

Accounts for 5-10% of cancer

Genetic predisposition to cancer

135
Q

List the causes of acute inflammation.

A

Micro-organisms – bacteria, fungi, viruses, parasites
Mechanical – trauma – injury to the tissue
Chemical – upset stable environment
Physical – extreme conditions
Dead tissue
Hypersensitivity

136
Q

Recognise the benefits of acute inflammation.

A
  • Rapid response to non-specific insult
  • Cardinal signs and loss of function
    o Protection of inflamed area
  • Neutrophils destroy organisms and denature antigen for macrophages
  • Plasma proteins localise process
  • Resolution and return to normal
137
Q

Describe the sequence of microvascular changes in inflammation

A

Phases:

  • Margination – neutrophils move endothelial aspect of lumen
  • Pavementing – neutrophils adhere to endothelium
  • Emigration – neutrophils squeeze between endothelial cells – active process – to extravascular tissues
  • (Diapedesis – passage of blood cells through intact walls off the capillaries)
  • (WHITE BLOOD CELLS ON THE OUTSIDE OF VESSELS AND EMIGRATING OUT, RED BLOOD CELLS IN CENTRE)
138
Q

List the local effects of acute inflammation.

A
  • Triple response: flush, flare, wheel (increased local tissue blood flow = observed redness + heat)
    1. Transient arteriolar constriction (protective)
    1. Local arteriolar dilation (active hyperaemia)
    1. Relaxation of smooth muscle

Change in permeability of the vessel wall – exudation

  • Plasma from capillaries to extravascular space
  • Exudate = fluid rich in protein, plasma, includes immunoglobulin and fibrinogen
  • Leads to oedema formation
139
Q

List the systemic effects of acute inflammation.

A

Pyrexia – raised temperature
Fell unwell - Malaise, anorexia, nausea
Neutrophilia – raised white cell count
Septic shock – inability to perfume tissues

140
Q

Describe the complications of acute inflammation.

A

Pus formation – dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris
Pyogenic membrane surrounds pus – walls off pus
Abscess – collection of pus under pressure

141
Q

Summarise the mediators of acute inflammation.

A

Cytokines and chemokines (produced by macrophages, lymphocytes, endothelium) in response to inflammatory stimuli

142
Q

Recognise how the process of acute inflammation can be altered to the detriment of the patient

A

Lymphadenopathy- regional lymph node enlargement
Weight loss – catabolic process
Spreads to blood-stream – patient become septic
Shock is rapidly fatal

143
Q

Define chronic inflammation

A

inflammation in which the cell population is especially lymphocytes, plasma cells, macrophages
- Features tissue or organ damage, (necrosis), loss of function

144
Q

List the cells involved in chronic inflammation

A

Lymphocytes – immune response and immune memory (B+T cells)
Plasma cells – differentiated B-cell – antibody production
Macrophages – remove debris, antigen presenting cell
Fibroblasts – make and assemble structural proteins (collagens)

145
Q

Role of T-cell in inflammation

A

produce cytokines + damage a lyse other cells and destroy antigens (granule proteins)
o Attract and hold macrophages
o Activate macrophages

146
Q

Major causes of chronic inflammation

A 
Arising from acute inflammation
-	Follows on from acute
-	Large volume of damage
-	Inability to remove debris 
-	Fails to resolve 
Arising as a primary lesion 
-	No preceding acute phase 
-	Only see chronic changes
147
Q

Describe the effects of chronic inflammation.

A

Granulation tissue (pink tissue round the edge of wound containing new connective tissue and capillaries)
- Capillaries grow into inflammatory mass with access to plasma proteins
- Fibroblasts lay down collagen to repair damaged tissue
- Collagen replaces inflammatory exudate
- Patches tissue defects
- Contracts and pulls together
New vessel formation – angiogenesis
Fibrosis and formation of scar

148
Q

Describe the adverse effects of tissue scarring.

A

Fibrous tissue = scar

- May be a problem if in the bowel – adhesions between loops of bowel following peritonitis

149
Q

List factors involved in promoting healing and repair.

A 
Cleanliness
Apposition of edges (no haematoma)
Sound nutrition
Metabolic stability and normality 
Normal inflammatory and coagulation mechanisms 
Local mediators
150
Q

Define the role of angiogenesis in healing and repair.

A

Angiogenesis – formation of new vessels (capillary buds)

151
Q

List the factors that impair healing and repair.

A

Dirty, gaping wound, large haematoma
Poorly nourished, lack of vitamins C, A
Abnormal CHO metabolism, diabetes, corticosteroid therapy
Inhibition of angiogenesis

152
Q

Sequence of events in wound healing

A
  • Phase of acute inflammation
  • Granulation tissue formation
  • Local angiogenesis
  • Fibrosis and scar formation
  • (Larger defects = lots of granulation, miofibroblasts move in and lay down collagen)
153
Q

Describe the principles of ‘staging’ in cancer.

A

Where is the cancer (examination + imaging)

What kind of cancer (pathology/cytology (study of individual cells))

154
Q

Explain the importance of genetic changes in cancer.

A

Somatic mutations – most common and is acquired
Germline mutations – hereditary
Oncogene = mutated gene giving rise to tumour formation in dominant fashion
Tumour suppressor gene – inhibits tumour formation (usually recessive)

155
Q

Describe the preventive measures of cancer therapy

A
  • Environment/behaviour change
  • Diet
  • Screening
    o Smear tests
  • Genetics
    o BRCA1/2 for breast cancer
  • Medication/vaccination
    o HPV/Hep B vaccines
  • Regular exercise
156
Q

Describe the treatment therapies for cancer

A
  • Surgery (local therapy, cured about 50%)
  • Radiotherapy (local therapy, can treat inoperable lesions or make surgery possible, can maintain function/appearance)
  • Systemic therapy (chemotherapy)
    o Beneficial for widespread disease, can result in widespread toxicity
  • Immunotherapy
157
Q

Describe classes of anti-cancer therapeutics. (Types of chemotherapy)

A

Alkylating agents and platinum drugs – form DNA adducts blocking DNA replication (all phases of cell cycle)
Antimetabolites – structurally mimic essential molecules required for cell division (S phase)

158
Q

Describe classes of anti-cancer therapeutics. (Personalised systemic therapies)

A

Hormonal therapies – anti-oestrogen (breast cancer - tamoxifen), aromatase inhibitors (breast cancer – blocks conversion of androgens to oestrogen)
Targeted therapies – EGF, VEGF, CDK 4/6
- Growth inhibitors, prevent passage of cells through phases of cell cycle
Immunotherapy – PD 1, PD-L1, CTLA-4

159
Q

Describe the origin of platelets in terms of anatomical site, precursor cell type, and method of production

A

Produced in bone marrow from precursor cell called megakaryocyte (large cell with many nuclei)
Platelets bud off as tiny fragments from cytoplasmic extensions of the megakaryocyte – form thrombi when there are breaks in vessel wall

160
Q

Explain the role of platelets in forming a thrombus in relation to trauma or tissue damage

A

Trauma to vessel = exposure of platelets to interstitial collagen
Platelets adhere together to try to form a bridge to close the gap
Thrombus formation occurs in flowing blood and consist of platelets and mesh like network to fibrin strands

161
Q

Describe role of plasminogen in thrombuses

A

Plasminogen converts to plasmin and cuts up fibrin into smaller fragments as a way of removing fibrin, both in clots and thrombi (thrombolysis)

162
Q

Explain the main site of production of certain key clotting factors

A

Mainly produced in the liver but also by endothelial cells

163
Q

Discuss the mechanism of action of certain key clotting functions, particularly the production of fibrin (from fibrinogen) in producing clots and thrombi

A

Clotting factors are part of an amplification system resulting in thrombin production
- Thrombin in turn converts soluble fibrinogen into insoluble fibrin – which forms mesh of strands

164
Q

Define thrombi and clots

A

Thrombi are platelets admixed with fibrin and form in flowing blood
Clot is fibrin admixed with red blood cells and forms in stagnant blood

165
Q

Describe the difference between clot and thrombus formation

A

Thrombus formation occurs in flowing blood and consist of platelets and mesh like network to fibrin strands – vessel contracts and thrombus stops the bleeding
Clot is fibrin admixed with red blood cells and forms in stagnant blood

166
Q

Describe Virchow’s triad

A

Pathological thrombosis

  • Changes in the intimacy surface of a vessel
  • Changes in the pattern of blood flow
  • Changes in the blood constituents

All 3 situations may occur and lead to coronary artery thrombosis (bad)

  • Complete obstruction = no flow beyond blockage
  • Partial obstruction leads to decreased flow beyond blockage = tissue supplied by artery receives less blood
167
Q

Define pathological thrombosis

A

thrombosis in the absence of acute or trauma

168
Q

Virchow’s triad: explain Changes in the intimacy surface of a vessel

A

o High lipid content can also rupture through the intimal surface (due to atheroma = build up of materials adhering to arteries) – the platelets and fibrin are now exposed to abnormal substance (lipid and collagen) and are deposited

Thrombus forms in the flowing blood blocking lumen of the coronary artery
Clot forms behind the thrombus in the stagnant blood

169
Q

Virchow’s triad: explain Changes in the pattern of blood flow

A

o High lipid in the blood can build up under the intimal surface of the arteries making the artery narrower leading to both slow and turbulent flow

170
Q

Virchow’s triad: explain Changes in the blood constituents

A

o Smoking makes platelets more sticky Making it more likely that a thrombosis occurs (platelets aggregate)

171
Q

Explain the terms ischaemia, hypoxia, anoxia, necrosis and infarction, and discuss a common example of each.

A 
Ischaemia = stoppage or restraint of blood
Hypoxia = insufficient oxygen supply to maintain adequate homeostasis 
Anoxia = extreme form of hypoxia. Part of body e.g. the brain has insufficient oxygen
Necrosis = death of body tissue 
Infarction = localised area of dead tissue resulting from a failure of blood supply (as a result of ischaemia)
172
Q

Understand why ischaemia often leads to hypoxia.

A

Stoppage or restraint of blood (ischaemia) leads to insufficient blood to tissues downstream. Blood carries oxygen, therefore no blood = no oxygen = hypoxia

173
Q

Explain the term embolism, understand its consequences, and discuss one common example.

A

Embolism = mass of material moving in vascular system that’s able to become lodged in a vessel and block its lumen (mainly derived from thrombi or clots which break off and go elsewhere in circulation)
Thromboembolism = embolism as a result of thrombi/clot
Example:
Knife to neck air enters the vein and embolises to heart = air embolism

174
Q

What is shock

A

“Profound circulatory failure causing poor perfusion of vital organs” = low blood pressure and its physiological consequences

175
Q

3 majour causes of shock

A
  • Hypovolaemic
  • Septic
  • Cardiogenic
176
Q

Explain hypovolaemic shock

A

low blood pressure reflects severe reduction in amount of blood in circulation. High pulse reflects physiological response to low BP
o Example: Injury leads to ruptured spleen losing 3L blood into abdominal cavity
o As blood flows out of damaged spleen not enough blood in vessels so they collapse, vena cava also collapses so venous pressure = basically 0
o Now almost no blood enters right side of heart, very little blood goes through lungs, brain and rest of body
o Leads to drop in systemic pressure so carotid sinuses sense this and upregulate sympathetic nervous system

Patient feels very ill, rapid breathing, tachycardia, pale and sweaty
BP 60/40

177
Q

Explain septic shock

A

infection in blood causing generalised vasodilation and shock
o Example: UTI infection leading to kidney infection then bacteria go into blood (SEPTICAEMIA)
o Molecules released cause generalised vasodilation
o Leads to pooling of blood in veins (e.g. in legs)
o Not enough blood gets back to heart due to low venous pressure and filling
o Therefore not enough blood to rest of body

178
Q

Explain cardiogenic shock

A
  • Cardiogenic: not due to blood loss – venous pressure is normal or sometimes increased
    o Example: heart disease – heart starts failing and eventually can no longer pump enough blood to maintain BP
179
Q

Explain the physiological mechanisms which normal pressure relies on

A
  • Enough blood in system (~5L)
    o If no blood in vessel it will collapse
  • Smooth muscle in vessels having a certain tone
    o If tone decreased the vessel will dilate, if enough vessels affected the blood pressure will fall
  • Heart pumping blood
    o If it doesn’t pump enough blood then pressure will fall
180
Q

Explain the physiological mechanisms which try to maintain blood pressure in shock.

A

2 carotid bodies + sinuses on either side of neck – bifurcation (splitting) of the artery into internal and external carotid arteries
2 carotid bodies detect partial pressure of oxygen
2 carotid sinuses respond to blood pressure – sense drop in blood pressure and respond by nervous signals to brain stem
- Brain stem tells heart to pump harder and faster via nerve signals
Sympathetic nervous system – increased vascular tone in legs and abdomen push blood to chest and head (keeps lungs and brain alive), also secretes adrenaline to make the heart pump even faster and harder

181
Q

Discuss the organ damage, which occurs in shock, with reference to 2 main examples.

A

Brain: decreased perfusion (ischaemia) of brain – initially reversible but then permanent (infarcts)
Kidney: decreased perfusion of kidneys, initially reversible, then more severe (ischaemic necrosis of renal tubules)

182
Q

Describe the basic structure and packaging of chromosomes.

A

Level 1 = nucleosome
Level 2 = chromatin fibre
Level 3 = fibre-scaffold complex
Level 4 = chromosome

183
Q

Describe a nucleosome

A

DNA packaged with histone (positive charge) proteins to form chromatin
- Looks like beads on a string

184
Q

Describe the 2 types of chromatin

A
  • Heterochromatin = condensed structure (silenced genes)

- Euchromatin = open structure (active genes)

185
Q

Describe the characteristics of Mendelian inheritance, both autosomal and sex-linked.

A

Autosomal dominant: 1 affected parent, each child 50% chance inheriting mutation, no skipped generations, transmitted equally by men and women
Sex-linked: only males affected, can skip generations, unaffected women and affected men can transmit condition, no male-male transmission

186
Q

Explain mitochondrial inheritance

A

maternal inheritance

187
Q

Describe the double-helical structure of DNA.

A 
DNA = chain of nucleotide monomers (nucleotide = sugar + base + phosphate group)
The double helix has major and minor groove 
Complementary pairing (Adenine – thymine, Guanine – cytosine)
188
Q

Describe the process by which DNA is replicated.

A 
Mitosis:
-	Prophase 
o	Chromosome condense 
o	Nuclear membrane disappears 
o	Spindle fibres form the centriole 
-	Metaphase 
o	Chromosomes aligned at equator of cell
o	Attached by fibre to each centriole 
o	Maximum condensation of chromosome 
-	Anaphase 
o	Sister chromatids separate longitudinally at centromere 
o	Move to opposite ends of the cell
-	Telophase 
o	New nuclear membranes form
o	Each cell contains 46 chromosomes (diploid)
-	Cytokines 
o	Cytoplasm separates
o	2 daughter cells
189
Q

Describe how a base-sequence of DNA is transcribed into a base-sequence in RNA.

A

Requires 2 strands of DNA to separate to allow enzymes access to template
DNA replication is semi-conservative (one half of each molecule of DNA is old and one is new) and bi-directional

190
Q

Describe in outline the post-transcriptional processing of RNA.

A

DNA is transcribed into mRNA
tRNA (transfer RNA) has major role to translate mRNA sequence into amino acid sequence
rNA (ribosomal RNA) combine with proteins to form ribosome

191
Q

Describe the types, effects and nomenclature of mutations

A

Chromosomal abnormalities: numerical, structural, mutational
Non-coding
Coding

192
Q

Describe types of coding mutations

A
  • Silent mutations (synonymous – make no change to amino acid encoded for)
  • Missense (single base substitution encoding for different amino acid)
  • Nonsense (single base substitution leading to a stop codon being encoded)
  • Frameshift (insertion/deletion so that base pairs are no longer divisible by 3 = amino acid not used)
193
Q

Describe the application of molecular genetic technology to identify genetic mutations associated with disease.

A 
Polymerase chain reaction (PCR)
-	Denature, anneal, extend
Gel electrophoresis
-	Separates DNA fragments by size 
Restriction fragment length polymorphism (RFLP) analysis 
Amplification refractory mutation system (ARMS)
DNA sequencing 
-	Gold standard method
194
Q

Describe the types, effects and nomenclature of mutations

A

Somatic mutations – occur in non-germline tissues, non-inheritable
Germline mutations – present in egg or sperm, are heritable, cause cancer family syndromes
Proto-oncogene – normal gene that codes for proteins to regulate cell growth and differentiation
- Mutations can turn a proto-oncogene into an oncogene
- Oncogenes can accelerate cell division

195
Q

Describe the application of molecular genetic technology to identify genetic mutations associated with disease.

A

Carried out routinely on certain cancers to identify familial mutations
E.g. breast and ovarian cancer (BRCA1/2, TP53 and more), colorectal cancer (MLH1, MSH2/6)

196
Q

Discuss the clinical relevance of population selection pressures

A

Fitness = relative ability of organisms to survive long enough to pass on their genes
Natural selection = process by which biological traits become more or less common in population
Negative selection = reduces reproductive fitness, decreases the prevalence of traits, leads to gradual reduction of mutant allele
Positive selection = increases reproductive fitness, increases prevalence of adaptive traits, heterozygous advantage

197
Q

Discuss the clinical relevance of ethnic genetic variation.

A
  • Dominant:
    o Hereditary breast cancer gene mutations BRCA1/2 (Jewish, polish, Scandinavian)
  • Recessive
    o North-west European Celtic cystic fibrosis mutation
198
Q

Know of the different roles of staff in clinical genetics services

A 
Clinical geneticist
Genetic counsellor 
Hospital doctor
GP
Nurse
199
Q

Describe the general principles of methods for testing of DNA and the interpretation of genomic variation

A

Next generation sequencing - interpretation of variants takes long time +requires scientist

200
Q

Describe mechanisms of non-Mendelian inheritance.

A

Non-Mendelian = several variants in several genes acting together
Mechanism:
Environmental factor/genetic modifiers = incomplete penetrance
Variants from parents = genomic imprinting
Mitochondria mutations = extranuclear inheritance
Triplet repeat expansion = anticipation
Multi-genic risk = complex

201
Q

Describe what is meant by penetrance.

A

Penetrance = frequency with which a trait is manifested by individuals carrying the gene

202
Q

Appreciate the role of the environment in genetic disease

A

Lifestyle, diet, smoking, alcohol, drugs, stress, air pollution, chemicals, infection, etc.

203
Q

Discuss the physico-chemical factors that affect the transfer of drugs across cell membranes.

A

Pharmaceutical process – get the drug into the patient
Pharmacokinetic process – get the drug to the site of action
Pharmacodynamic process – produce the correct pharmacological effect
Therapeutic process – produce the correct therapeutic effect

204
Q

Explain the ADME of pharmacokinetics

A

A - absorption
D – distribution
M – metabolism
E – elimination

205
Q

Discuss the factors that affect absorption of a drug from the GI tract

A

Gut motility:
- Speed of gastric emptying will affect speed at which drug reaches site of absorption (most drugs absorbed in small intestine)
- Can be affected by other drugs, food/drink and illnesses (especially pain)
Food:
- Can I handle or impair rate of absorption
Illness:
- Malabsorption (e.g. coeliac diseases) can increase or decrease rate of absorption
- Migraine reduces rate of stomach emptying and therefore rate of absorption of analgesic drugs

206
Q

Discuss the medical importance of first pass metabolism.

A

First pass metabolism = metabolism of drug prior to reaching systemic circulation (drugs tend to need to reach systemic circulation to reach target tissues)

207
Q

What is drug distribution

A

reversible transfer of a drug between the blood and the extravascular fluids and tissues of the body (e.g. fat, muscle, brain)

208
Q

Explain why binding of drug to plasma proteins is important.

A

Many drugs bind to plasma proteins – only unbound drugs are biologically active
- Important if the drug is >90% bound and tissue distribution small, if more drug unbound then may result in toxicity

209
Q

Define terms: Apparent volume of distribution (Vd), Clearance (Cl), Half-life (t1/2)

A

Apparent volume of distribution (Vd) – volume of plasma that would be necessary to account for total amount of drug in body
Clearance (Cl) – theoretical volume from which a drug is completely removed over a period of time (measure of drug elimination)
Half-life (t1/2) – time taken for the drug concentration in the blood to decline to half of the current value
- Knowledge of half life used to calculate how often drug needs administered

210
Q

Explain drug elimination

A

Drug elimination – removal of active drug and metabolites from the body
- 2 parts:
o Drug metabolism (usually in liver)
o Drug excretion (usually in kidney but also in biliary system/gut, lung, milk)

211
Q

Explain drug excretion

A

kidneys are primary organ for drug excretion
- 3 mechanisms
o Glomerular filtration (190L of fluid/day
o Passive tubular re absorption
o Active tubular secretion
- Renal damage/impairment often = drug toxicity

212
Q

Define drug metabolsim

A

Drug metabolism = biochemical modification of pharmaceutical substances by living organisms usually through specialised enzymatic activity

  • Makes libid soluble and non-polar compounds water soluble and polar so they can be excreted
  • Purpose is to deactivate compounds and increase water solubility (aid excretion)
  • However some drugs need activation by metabolism (prodrugs)
213
Q

Discuss processes of phase 1 & 2 metabolism

A

Phase 1: activation/inactivation
Oxidation
Reduction
Hydrolysis
Phase 1 increases polarity of compound and provides active site for phase 2 metabolism
- Cytochrome P-450 enzymes are most important super family of metabolising enzymes
Phase 2: conjugation products
Glucuronidation
Conjugation increases water solubility and enhances excretion of metabolised compound (usually inactivation of the drug)

214
Q

Discuss the role of cytochrome P450.

A

Cytochrome P-450 enzymes are most important super family of metabolising enzymes
Drug specificity determined by isoform of cytochrome P-450

215
Q

Explain enzyme induction

A

Enzyme induction – requires increased enzyme synthesis and therefore increased activity
Molecule e.g. drug induces the expression of an enzyme thus increasing the enzymes activity

216
Q

Discuss factors, including drugs, which may inhibit or induce drug metabolism with medically relevant examples.

A
  • Most common enzyme inducers are alcohol and smoking
    Enzyme inhibition – many commonly used drugs, herbal medicines and food stuffs may inhibit drug metabolising enzymes (may be reversible/irreversible binding to enzyme)
    Genetics
    Liver disease
    Pregnancy
217
Q

Discuss, briefly, the importance of pharmacogenetics

A

Variation in response to drugs between individuals
May lead to therapeutic failure or adverse reaction
Lack or decreased activity if an enzyme often results in increased drug toxicity

218
Q

Discuss the uses of a clinical study.

A

Provide evidence

219
Q

Types of clinical study

A

Pilot study – not to estimate outcome but to test study design
Trials may be:
- Double blind – patient/doctor blinded
- Single blind – patient blinded
- Prospective – protocol decided before hand (participants decided then followed forward in time)
- Retrospective – less good as open to bias (uses existing data which has been recorded for reasons other than research – allows for formulation of ideas about possible relationships)
- Randomised control clinical trial – patients assigned at random to either treatment or control – GOLD STANDARD

220
Q

Phases of a clinical trial

A

Preclinical – testing of drug in non-human to gather efficacy, toxicity and pharmacokinetic information
Phase 0 – pharmacokinetics, particularly oral bioavailability and half-life of drug
Phase 1 – dose-ranging on healthy volunteers for safety
Phase 2 – testing of drug on participants to assess efficacy and side effects
Phase 3 – testing of drug on participants to assess efficacy, effectiveness and safety
Phase 4 – post marketing surveillance in the public

221
Q

Discuss the basic considerations involved in trial design.

A

Regulated by the MHRA

222
Q

Discuss the strengths and weaknesses of parallel and cross-over design.

A

Parallel:
100 patients, 50 active drug and 50 placebo – compare outcome in the two groups
Another 100 patients, 50 active drug and 50 comparative therapy – compare is active drug better than comparative therapy
- GOLD STANDARD
o Disadvantages:
o subjects may not represent patient population
o Tend to be better at complying
o Twice as many new patients needed for study
o Some patients will refuse (want to know their treatment)
Cross-over design:
50 study drug, 50 compared drug. Cross patients over at set number weeks
Compare outcomes of both drugs within patient

223
Q

Define superiority and non-inferiority

A 
Superiority = shows new treatment better than the control or standard (or even a placebo)
Non-inferiority = show new treatment is not worse than the standard by more than certain margin + would have beaten a placebo if included (regulatory)
224
Q

Discuss why some studies have statistical significance but lack clinical significance.

A

P0.05 = 5% chance (considered the minimum borderline of statistical significance)

225
Q

Discuss the factors which affect the bioavailability of a drug.

A

Drug delivery system: dose, frequency, timing, desired speed of onset

226
Q

State the different routes of administration via the GI tract.

A

Oral
Buccal (dissolved in mouth)
Sublingual
Rectal

227
Q

Discuss oral administration by solutions and suspensions

A
  • Useful for those who cant swallow, young and elderly
  • Drugs absorbed rapidly
  • Absorption dependent on gastric emptying and most rapid from small intestine
  • (Suspensions = coarse drug particles in liquid phase)
228
Q

Discuss oral administration by tablets and capsules

A
  • Most common formulation
  • Dissolution or tablet/capsule breakdown is rate limiting step in absorption
  • Advantages: convenience, accuracy of dose, reproduction of dose, drug stability, easy mass production
229
Q

Discuss oral administration by modified tablets-enteric coated

A
  • Delays disintegration of tablet until it reaches small intestine
  • Enteric coated to: protect drug from stomach acid (omeprazole), protect stomach from the drug (aspirin)
230
Q

Discuss oral administration by buccal and sublingual

A
  • Ideal for drugs with extensive pre-systemic or first pass metabolism
  • Small and dissolve slowly under tongue or in Buccal cavity
231
Q

Discuss rectal route administration of medication

A
  • Treat local conditions
  • Achieve systemic absorption
  • Useful in young or old, or patients unable to swallow
  • Bypass pre-systemic metabolism
232
Q

Discuss the strengths and weaknesses, with examples, of locally administered medication (topical, inhaled).

A

Topical:

  • Transdermal drug delivery:
  • Skin patches – allow release of drug from reservoir into the skin then into systemic circulation
  • Makes it possible to obtain controlled, sustained blood levels of the administered drug

Inhalation:

  • Deliver drugs directly to the lung for local effect (salbutamol inhalers) or to achieve systemic effect (inhaled anaesthetics)
  • Advantages: delivered directly to site of action, rapid effect, small dose, little systemic absorption, reduced adverse effects
233
Q

Discuss the medical importance of drug interactions in terms of morbidity and mortality.

A 
Drug interactions are generally avoided and frequently detrimental 
Drug specific risks for DDI:
-	Narrow therapeutic range
-	Dose
-	Poly pharmacy 
Risk factors for DDI:
-	Advanced age 
-	Comorbidities 
-	Genetic polymorphisms
-	Probability of DDI increases exponentially with number of prescribed medications
234
Q

Discuss factors which may predispose a patient to drug interactions. With medically important examples.

A 
Susceptible patients:
-	Comorbidities 
-	Chronic conditions:
o	Liver disease 
o	Renal impairment 
o	Diabetes 
o	Epilepsy 
o	Asthma
235
Q

Discuss the definition and classification of drug - drug interactions. Direct and synnergistic.

A

Object drug – drug whose activity is altered by interaction
Precipitant – agent which precipitates such an interaction

Direct: direct antagonism – beta-blockers such as atenolol will block the actions of beta agonists such as salbutamol
Synergistic interactions: - two drugs with the same pharmacological effect acting on different receptors are given concurrently
- Effect may be additive or multiplicative

236
Q

Define what an x-ray is.

A

X-ray = electromagnetic packet of energy with an extremely short wavelength 0.1-10 nanometres

237
Q

Recall in general terms the principles of xray generation and image capture.

A

Electrons are accelerated through a tube with a potential difference (voltage drop) and directed to a target material. Target material interacts with the matter either absorbing, scattering or transmitting the x-ray

238
Q

Recall the basic principles of CT

A

CT – ionising radiation (x-rays) coupled with electronic detector array to record a pattern of densities to creat image of a “slice” of tissue
Advantages: short study time, high quality images
Disadvantages: radiation exposure, not as detailed as MRI

239
Q

Recall the basic principles of ultrasound

A

high frequency sound pulses 1-20MHz which are reflected at the surfaces between the tissues of different densities. Reflection is proportional to the difference in impedance
Advantages: no ionising radiation, portable, cheap,
Disadvantages: further education required, high initial costs of education and equipment

240
Q

Recall the basic principles of fluoroscopy

A

real time video of the movements inside the body by passing x-rays through the body
Advantages: live image of internal organs to observe size shape and movement, real time interaction
Disadvantages: radiation, limited by patient mobility and ability to comply

241
Q

Describe the scientific basis of the use of iodinated contrast media.

A

Barium – absorbs more x-ray photons than surrounding tissue
Used in clinical investigation to study GI tract
Swallowed along with meal
Complications – bowel disturbance (very common) colonic perforation at enema (very rare)

242
Q

Describe the scientific basis of the hazards of ionising radiation.

A

Ionising radiation is able to neutral atom or molecule and leave them with a positive or negative charge. This leads to cell damage which may lead to cell repair, death or transformation
Minimise exposure by: distance from source, time exposed, shield used to protect staff and patients

243
Q

Explain the scientific basis of magnetic resonance imaging (MRI).

A

Strong magnetic field aligns the protons in the body in one direction
Radio frequency pulses displace protons and images created by displaying time take for protons to relax back to original alignment

244
Q

Explain the indications, contraindications and application of MRI-specific contrast agents

A 
Advantages:
Excellent bone soft tissue detail
Vessels can be demonstrated 
Brain, spine and musculoskeletal 
Abdomen and pelvis
Cardiac imaging 
Disadvantages:
Claustrophobic and noisy
Motion artefact
Cannot image patients with pacemakers, aneurysm clips
245
Q

Describe the pros and cons of population screening with radiological testing, using breast screening as an example.

A

Diagnose disease at an earlier stage, before symptoms start. Makes the cancer easier to treat and more likely to be curable
NHS screening: breast, bowel, cervix
Screening:
- test should detect disease at an early stage where treatment can alter outcome
- Cause no harm
- High sensitivity and specificity
- Benefit the individual and the population should outweigh cost

246
Q

Explain why different anatomical structures have different appearances on x-ray imaging.

A

Attenuation – process by which radiation loses power as it travels through matter and interacts with it.
Example: air – travels straight through
Bone – cannot travel straight through (more white on image)
Abdomen – can somewhat travel through (grey)

247
Q

What is molecular imaging?

A

Molecular imaging = radionuclide imaging positron emission tomography

248
Q

Properties of an ideal isotope

A

Half-life similar to examination length
Gamma emitter (as opposed to a or b)
Easily bound to pharmaceutical component
Easy to prepare and readily available at hospital site
Radiopharmaceutical should be eliminated in similar half-time to examination duration

249
Q

Single photon emission tomography (SPECT)

A

CT version of nuclear medicine
Gamma cameras rotate around area of interest
Routinely used for brain and cardiac studies (can be applied to any site of interest)

250
Q

Positron emission tomography (PET)

A

Molecular imaging
Uses radionuclides that decay
Image biologically interesting processes (active cells glow red)
All scanners are now PET CT

251
Q

Examples of inflammatory and infectious diseases on PETCT

A

Inflammatory – rheumatoid arthritis (shows bright red on PETCT

252
Q

Radiation risks

A

Radiation risks: inducing fatal cancer (CT of abdomen is 1:1600)
Benefits: diagnosis, management change, treatment. Benefits should always outweigh the costs + risks

253
Q

Understand the definitions and nature of specific blunt and sharp force injuries.

A 
Injury: synonymous with wound 
-	Damage caused by heat, cold, electricity, chemicals & radiation 
Lesion: originally mean injury, now widened to include any area of injury, disease or local degeneration in a tissue causing a change in its structure of function
Physical factors:
-	Degree of force applied
-	Area of application of force
-	Duration of application
-	Direction of application
-	Tissue properties
254
Q

Implications of blunt force injuries

A
  • Abrasions (graze, scratch) – injury to skin surface (epidermis)
    o Clinically trivial, bleeding is slight, heal quickly by forming a scab, leave no scar
  • Bruises (contusions) – burst blood vessels which leak into skin, caused by mechanical impact
    o Size doesn’t indicate severity – accurate ageing is difficult
  • Lacerations (cut, tear) – tear/split of skin due to crushing
    o Impact against flat surface e.g. scalp
    o Impacted by edged or pointed object e.g. brick
    o Ragged margins
    o Associated bruising
    o Slight bleeding
    Can often get combination of blunt force injuries as part of Same injury
    Caused by impact with a blunt object (static or mobile)
255
Q

Implications of sharp force injuries

A

Sharp force:
- Stabs
o Penetrating injury resulting from thrusting motion
o Wound depth greater than length on the surface
o Clean cut, well defined margins
o Full thickness of skin and into underlying tissue
o Sites of accessibility, sites which can be concealed = suicide
o Inaccessible sites, sites of perceived pain = homicide
- Incisions
o Superficial sharp force injury caused by slashing motion
o Injury longer than it is deep
o Clean cut, well defined margins
o No associated bruising or abrasions of wound edge
o No tissue bridges
o Bleeds profusely
o Full thickness of skin
Injury caused by sharp cutting edge – superficial or penetrating

256
Q

Recognition of the natural processes which occur after death. (Hours, days/weeks, months)

A

Somatic (clinical) death —> cellular death
Hours:
Algor Mortis (change in body temperature until ambient temperature matched)
Livor mortis (setting of blood after death in gravity-dependent portions of the body)
Rigor mortis (stiffening of the body muscles due to chemical changes in their myofibrils)
Days/weeks:
Putrefaction (rotting/decay in the body)
Months:
Skeletonisation (last bits of soft tissue have decayed or dried so that the skeleton is exposed)
Mummification (preserving the body by drying or embalming flesh)

257
Q

Recognise the difficulties in ascertaining the timing of death.

A

Algor mortis useful indication of post mortem interval (PMI) in first 24hrs (requires core body temperature – rectal (avoid in sexual cases – contamination of evidence)
- Unreliable and misleading as rate of cooling depends on many factors
Livor mortis – poor indication of PMI – may not be evident at all in some cases, very much affected by natural disease
Rigor mortis – muscle fibre relaxation requires ATP to break actin-myosin bonds
- Oxygen dependent process
- Bonds cant break causing Rigor mortis
- Due to residual ATP in body doesn’t develop immediately until ATP reserve is depleted
- Develops in smaller muscles first (eyelids, jaw and neck, small joints of hands and feet)

Rule of thumb:
Warm & without Rigor = PMI <3hrs
Warm & with Rigor = PMI 3-8hrs 
Cold & with Rigor = PMI 8-36hrs 
Cold & without Rigor = PMI >36hrs

Foundations Of Medicine - Mats (3 decks)

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