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Principles of disease AM > Formative > Flashcards

Formative Flashcards

1
Q

List the categories of microorganism that cause disease

A 
Bacteria
Viruses
Fungi
Parasites
Prions
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2
Q

What is the role of microscopy in the diagnosis of bacterial infection?

A

Allows for staining and quick detection (but not identification) of bacteria in samples

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3
Q

What is the role of culture in the diagnosis of bacterial infection?

A

Strains can be identified by colonial appearance and growth patterns

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4
Q

What is the difference between sterile and non-sterile sites?

A

Sterile sites contain no microorganisms, commensal or otherwise, while non-sterile sites can contain commensal microbes that may not harm the body but show up in testing

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5
Q

What are some sterile sites? 4

A

Blood
CSF
Bladder
Lungs

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6
Q

What are some non-sterile sites? 4

A

Skin
Nasopharynx
Urethra
Gut

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7
Q

How are viruses detected?

A

Cell line must be innoculated, and electron microscopes used

Antigen election and nucleic acid amplificated used

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8
Q

What is the function of bacterial ribosomes?

A

Protein synthesis

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9
Q

What is the function of the plasma membrane in bacterial cells?

A

Allows diffusion

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10
Q

What is the function of the bacterial cell wall?

A

Cell structure and support

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11
Q

What is the function of the bacterial capsule?

A

Defence mechanism

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12
Q

What is the function of the flagellum?

A

Motility

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13
Q

What is the function of the fimbriae?

A

Allows adherence

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14
Q

What are the main structures of a bacterial cell surface? 4

A

Plasma membrane
Penicillin binding proteins
Peptidoglycans
Lipopolysaccharides (only in gram negative)

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15
Q

What is the function of penicillin binding proteins in the bacterial cell surface?

A

Synthesizes peptidoglycans

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16
Q

What is the function of peptidoglycan in the bacterial cell surface?

A

Give the cell strength and shape

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17
Q

What is the structure of peptidoglycan?

A

Carbohydrate polymers cross linked with amino acids

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18
Q

What are the two shapes bacteria can be in?

A 
Cocci= spherical
Bacilli= bacilli
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19
Q

Wha is the difference in structure between staph and strep?

A 
Staph= clusters
Strep= chains
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20
Q

What can virus families be classified according to?

A

Virion shape/symmetry
Presence/ absence of envelope
Genome structure
Mode of replication

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21
Q

How are viruses cultured?

A

In living cells (cell lines, tissues or intact animals)

Cell lines are grown in a nutrient containing medium with 5% CO2

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22
Q

What respiratory infections are of major importance? 3

A

Influenza A
Rhinovirus
Respiratory syncytial virus

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23
Q

What gastrointestinal virus is of major importance?

A

Rotavirus

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24
Q

What neurological viruses are of major importance? 2

A

Enterovirus

Herpes simplex

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25
Q

What are the 3 classifications of fungi?

A

Basidomycetes
Ascomycetes
Zygomycetes

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26
Q

What are basidiomycetes?

A

Mainly mould and mushrooms, a few yeasts

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27
Q

What are ascomycetes?

A

Moulds and yeasts, some mushrooms

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28
Q

What are zygomycetes?

A

Moulds

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29
Q

What are dermatophytes?

A

Fungi that use keratin as a nutrient source and attack the skin and mucous membranes

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30
Q

What are systemic fungi?

A

Yeasts responsible for oral, skin, nail, and many other forms of infections

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31
Q

What are the main types of parasites? 3

A

Protozoa
Helminths
Ectoparasites

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32
Q

What is a protozoa?

A

A single celled organism that can only multiply in the host

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33
Q

What are helminths?

A

Worm parasites e.g. roundworm, tapeworm

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34
Q

What are ectoparasites?

A

Parasites that live on, as opposed to in, the host e.g. lice

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35
Q

What is active immunisation?

A

Production of antibodies in the immune system in response to the presence of an antigen, creating immunological memory

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36
Q

What is used to immunise in active immunisation?

A 
Attenuated organism
Dead organism
Toxoid
Recombinant
Conjugate
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37
Q

What is passive immunisation?

A

Patient is immunised with antibodies specific to the pathogen, providing immediate protecting but no immunological memory

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38
Q

What are the advantages of using passive immunisation?

A

Easily stored and transported

Safer- can be used on even immunocompromised

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39
Q

What are the gram positive coagulase positive bacteria?

A

Staphylococcus aureus

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40
Q

What are the gram positive coagulase negative bacteria?

A

Staphylococcus epidermis

Staphylococcus saprophyticus

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41
Q

What are the gram positive aerobic non spore forming bacteria?

A

Listeria monocytogenes

Corynebacterium diptheriae

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42
Q

What are the gram positive aerobic spore forming bacteria?

A

Bacillus species

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43
Q

What are the gram positive anaerobic spore forming bacteria?

A

Clostridium species

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44
Q

What are the gram positive partially haemolytic bacteria?

A

Streptococcus pneumonia

Viridans streptococci

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45
Q

What are the gram positive completely haemolytic bacteria?

A

Streptococcus pyogenes

Streptococcus agalactiae

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46
Q

What are the gram positive non haemolytic bacteria?

A

Enterococci

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47
Q

What are the gram negative cocci?

A

Moraxella catarrhalis
Neisseria gonorrhoeae
Neisseria meningitidus

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48
Q

What are the gram negative bacilli lactose fermenters that show growth on MacConkey’s?

A

Escherchia coli

Klebsiella species

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49
Q

What are the gram negative bacilli lactose non-fermenters that show growth on MacConkey’s?

A

Proteus species
Salmonella species
Shigella species
Pseudomonas species

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50
Q

What are the gram negative anaerobic bacilli bacteria?

A

Bacteriodes species
Prevotilla species
Porphyromonas species

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51
Q

What are the gram negative curved bacilli?

A

Campylobacter species
Vibrio species
Helicobacter species

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52
Q

What are the gram negative cocci-bacilli?

A

Haemophilus influenzae

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53
Q

What is virulence?

A

A quantitive measure of the likelihood of a pathogen to cause disease

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54
Q

What are some of the virulence factors of bacteria?

A

Colonisation
Immunoevasion
Immunosuppression
Bacterial toxins

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55
Q

What is pathogenesis?

A

The process by which a pathogen causes a disease in the host

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56
Q

What is minimal inhibitory concentration?

A

Minimum concentration of antimicrobial required to inhibit visible growth of an organism

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57
Q

What is the minimal bactericidal concentration?

A

The minimum concentration of the antimicrobial needed to kill the arganism

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58
Q

What is a sensitive organism?

A

An organism that is inhibited or killed by levels of the antimicrobial that are available at the site of infection

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59
Q

What is a resistant organism?

A

An organism that is not killed or inhibited by the concentration of antimicrobial at the site of infection

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60
Q

What is a bactericidal?

A

An antimicrobial that kills bacteria

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61
Q

What is a bacteriostatic?

A

An antimicrobial that inhibits the growth of a bacteria

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62
Q

Explain the term ‘synergy’

A

Two or more structures, agents or processes working together to create a combined action greater than the sum of each acting separately

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63
Q

Explain the term ‘antagonistic’

A

Two or more structures, agents or processed working against each other to create a combined action less than the sum of each acting separately

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64
Q

What are the 3 methods by which antibacterials act?

A

Inhibition of cell wall synthesis
Inhibition of protein synthesis
Inhibition of nucleic acid synthesis

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65
Q

What antibacterials act by inhibiting cell wall synthesis?

A

Penicillin and cephalosporins

Glycopeptides

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66
Q

How to penicillins act as antibacterials?

A

Inhibit cell wall synthesis by inhibiting the enzymes responsible for cross linking carbohydrates to form peptidoglycans
Contain beta lactams

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67
Q

How to glycopeptides act as antibacterials?

A

Inhibit cell wall synthesis by inhibiting production of the peptidoglycan precursor in gram positive bacteria

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68
Q

Give examples of glycopeptide antibacterials

A

Vancomycin and teicoplanin

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69
Q

What types of antibacterials act by inhibiting protein synthesis?

A

Aminoglycosides
Macrolides and tetracycline
Oxazolidiones

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70
Q

What type of bacteria do aminoglycosides act on and give an example of one

A

Gram negative

Gentamicin

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71
Q

What type of bacteria do macrolides and tetracycline act on and give examples

A

Gram positive

Erythromycin and clairithromycin

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72
Q

What infection are oxazolidiones used to treat and give an example

A

MRSA

Linezolid

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73
Q

What types of antibacterials act by inhibiting nucleic acid synthesis?

A

Trimethoprim and sulphamethoxazole

Fluoroquinones

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74
Q

How do trimethoprim and sulphamethoxazole work?

A

Inhibit nucleic acid synthesis by inhibiting different steps in purine synthesis

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75
Q

What is the combined form of trimethoprim and sulphamethoxazole and what is it and trimethoprim individually used to treat?

A

Co-trimoxazole used to treat chest infections

Trimethoprim used to treat UTIs

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76
Q

What type of bacteria are fluoroquinolones effective against?

A

Gram negative

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77
Q

Give an example of a fluoroquinolone and explain why it cannot be used to treat children

A

Ciprofixacin

Interferes with cartilage growth

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78
Q

What types of antifungal are there?

A

Polyenes
Azoles
Allylamines
Echnocandins

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79
Q

How do polyenes act as an anti fungal?

A

Bind to ergosterol and make the cell wall more permeable

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80
Q

Name two polyene antifungals and what they are used to treat

A

Amphotericin B- serious fungal and yeast infections

Nyastatin- candida infections of the skin

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81
Q

How do azoles act as an antifungal?

A

Inhibit ergosterol synthesis

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82
Q

Name two azoles and what they are used to treat

A

Fluconazole- yeast infection

Voriconazole and itraconazole- aspergillosis

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83
Q

How do allylamines work as antifungals?

A

Suppress ergosterol synthesis

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84
Q

What allylamine is in use and what is it used to treat?

A

Terbinafine

Dermatophytes

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85
Q

How do echnocandins act as antifungals?

A

inhibit production of glucan polysaccharide

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86
Q

What organisms combat B-lactam activity and how do they do this?

A

Staph aureus

Produces B-lactamas enzymes to break down penicillins and cephalosporins

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87
Q

What are the causes of acute inflammation?

A 
Microorganisms
Mechanical trauma
Chemical changes
Extreme physical conditions
Dead tissue
Hypersensitivity
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88
Q

What are the cardinal signs of inflammation?

A

Dolor- pain
Calor- heat
Rubour- redness
Tumour- swelling

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89
Q

What are the benefits of acute inflammation?

A

Rapid response
Protects site
Neutrophils deal with damage
Plasma proteina localise process

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90
Q

Describe the change in blood vessel radius during acute inflammation

A

Transient arteriolar constriction followed by local arteriolar dilation (flush and flare)

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91
Q

Describe the change in vessel permeability during acute inflammation

A

Chemical mediators cause the vessel walls to become more permeable, allowing exudation of plasma proteins such as immunoglobulin and fibrinogen

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92
Q

Describe the movement of neutrophils during acute inflammation

A

Neutrophils move from the centre to the endothelial aspect of the lumen- margination
Neutrophils then adhere to endothelium- pavementing
Neutrophils squeeze between endothelium to outside tissue- emigration

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93
Q

List the systemic effects of acute inflammation

A

Pyrexia
General malaise
Neutrophilia
Septic shock

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94
Q

How can acute inflammation be detrimental to the patient?

A

Spread t the bloodstream causing sepsis
Bacteraemia
Septicaemia
Toxaemia

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95
Q

What cell types are involved in chronic inflammation?

A

Lymphocytes
Macrophages
Plasma cells
Fibroblasts

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96
Q

What are the major causes of chronic inflammation?

A

Arising from acute inflammation

Arising as primary lesion

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97
Q

How can chronic inflammation arise from acute inflammation?

A

Large volume of damage
Inability to remove debris
Fails to resolve

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98
Q

How can chronic inflammation arise as a primary lesion?

A

Autoimmune disorder
Material resistant to cellular digestion
Exogenous substances
Endogenous substances

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99
Q

What are the effects of chronic inflammation?

A

Scarring and fibrosis

Granuloma formation

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100
Q

What factors promote healing and repair?

A 
Cleanliness
Apposition of edges
Sound nutrition
Metabolic stability and normality
Normal inflammatory and coagulation mechanisms
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101
Q

What factors impair healing and repair?

A 
Dirty gaping wound
Large haemotoma
Poor nourishment- lack of vitamins A and C
Abnormal CHO metabolism
Inhinition of angiogenesis
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102
Q

What kind of reaction is type I sensitivity?

A

Allergic reaction

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103
Q

Describe the process of a type I hypersensitivity reaction?

A

B cells stimulated to produce IgE to a specific antigen, triggering a mast cell response and sensitising it to the antigen

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104
Q

What is a type II hyper sensitivity reaction?

A

The antibodies bind to antigens on the patient’s own cell surface

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105
Q

What immunoglobulins are involved in type II hypersensitivity?

A

IgG and IgM

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106
Q

When do type III hypersensitivity reactions occur?

A

When there is an accumulation of immune complexes that cannot be cleared from the circulation

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107
Q

How long do type IV hypersensitivity reactions take to develop?

A

2-3 days

108
Q

How are type IV hypersensitivity reactions mediated?

A

Through CD4 helper T cells

109
Q

What is the process of a type IV hypersensitivity reaction?

A

CD4 cells recognise the antigen and produce cytokines, leading to an inflammatory response

110
Q

What is an early phase response?

A

A response occurring within minutes performed by mast cell mediators

111
Q

What is a late phase response?

A

Takes longer to respond with newly synthesised mediators

112
Q

What is the difference between localised and systemic hypersensitivity?

A

Localised- causes localised inflammation and can be cleared away by macriphages
Systemic- Immune complexes deposited in skin, joints, kidneys, blood vessels etc

113
Q

What is an autoimmune disease?

A

A large group pf clinical disorderes characterised by tissue or organ damage mediated by incorrect immune mechanisms targertted at self-antigens

114
Q

What factors are involved in the aetiology of the immune system?

A

Genetic factors
Immune regulatory factors
Hormonal factors
Environmental factors

115
Q

What pathogenic mechanisms are involved in autoimmune disease?

A 
Cell mediated
Antibody mediated
Antibody+ complement
Immune complex mediated
Recruitment of innate compounds
116
Q

What are the 2 types of autoimmune disease?

A

Organ specific

Non-organ specific

117
Q

What is the difference between organ specific and non-organ specific autoimmune disease?

A

organ specific- immune response directed towards antigens in one organ only
Non specific- attacks antigens in several organs

118
Q

Describe ionisation of drugs and how this affects their uptake

A

Most drugs are weak acids or bases and the degree of dissociation depends on the pH of the environment
Ionised drugs to do not cross the membrane
Unionised drugs diffuse until equilibrium is reached

119
Q

How does lipid solubility affect drug transport across a membrane?

A

For a drug tp be able to cross a membrane, it must be lipid soluble

120
Q

How does the drug structure affect active transport?

A

In order to be able to be absorbed by active transport, the drug must resemble naturally occurring molecules

121
Q

What factors affect the absorption of a drug from the GI tract?

A

Gut motility
Food
Illness

122
Q

How do food and illness affect drug absorption from the GI tract?

A

Food- some food impair or enhance the ability of a drug to be absorbed
Illness- Malabsorption caused by illness can impair the absorption rate of certain drugs

123
Q

What is first pass metabolism?

A

Metabolism of the drug prior to it reaching the site of absorption

124
Q

Where does first pass metabolism mainly occur?

A 
Gut lumen (acid enzymes)
Gut wall (metabolic enzymes)
Liver (hepatic enzymes)
125
Q

How can first pass metabolism be avoided?

A

Using different delivery methods

126
Q

What are the benefits of administering drugs IV?

A

100% bioavailability

Avoids first pass metabolism

127
Q

What are the benefits of administering drugs topically?

A

Controlled, sustained doses of drug

Avoids first pass metabolism

128
Q

What are the benefits of administering drugs via inhalation?

A 
Drug delivered directly to site of action
Rapid effect
Small doses
Little systemic absorption
Reduced adverse effects
129
Q

What is the bioavailability of a drug?

A

Amount of drug which reaches the circulation and is available for action

130
Q

What factors affect bioavailability?

A

Formulation
Drug’s ability to pass physiological carriers
Gastrointestinal effects
First pass metabolism

131
Q

What affects a drug’s ability to pass physiological barriers?

A

Particle size
Lipid solubility
pH and ionisation

132
Q

What factors affect drug distribution?

A 
Tissue perfusion
Membrane characteristics 
Transport mechanisms
Disease/other drugs
Elimination
133
Q

What membrane characteristics affect drug distribution?

A

Blood brain barrier

Blood testes/ovaries barrier

134
Q

What factors does renal filtration depend on?

A

Glomerular filtration
Passive tubular reabsorption
Active tubular reabsorption

135
Q

What is glomerular filtration?

A

All unbound drugs are filtered at the glomerulus provided their size or charge doesn’t prevent this

136
Q

What is passive tubular reabsorption?

A

As the filtrate moves down the kidney tubules, it becomes more concentrated and unionised drugs can be reabsorbed by diffusion

137
Q

What is active tubular reabsorption?

A

Some drugs are actively secreted into the proximal tubules of the kidneys for excretion

138
Q

What is drug metabolism?

A

Biochemical modification of pharmaceutical substances by living organisms usually through specialised enzymatic activity

139
Q

What 3 reactions can be involved in phase 1 metabolism?

A

Oxidation
Reduction
Hydrolysis

140
Q

What is the process of phase 1 metabolism?

A

Polar groups are exposed on or introduced to a molecule, providing an active site for phase 2

141
Q

What enzymes carry out phase 1 metabolism?

A

Cytochroms P450

142
Q

What reaction is involved in phase 2 metabolism?

A

Conjugation

143
Q

How does conjugation metabolise the drug?

A

Attaches glucuronic acid, glutathione, sulphate or acetate to the metabolite generated in phase 1

144
Q

What does conjugated the drug achieve?

A

Increases water solubility, enhancing excretion

Usuall results in activation of the drug

145
Q

What factors inhibit or induce drug metabolism?

A 
Other drugs/substances
Genetics
Hepatic blood flow
Liver disease
Age
Sex
Ethnicity
146
Q

How do other drugs and substances affect drug metabolism?

A 
Many drug metabolising enzymes can be induced by other substances (alcohol and smoking), decreasing drug effect 
Other drugs (e.g. clairythromycin) inhibit enzymes through a number of mechanisms
147
Q

How do genetics affect drug metabolism?

A

Drug metabolising enzymes are often expressed in different forms so differences in the individual’s gene expression can vary
Can cause absences or deficiencies of certain enzymes, leading to toxicity

148
Q

How does age affect drug metabolism?

A

Metabolising enzymes often absent or reduced in foetuses or premature babies, renal disruption common

149
Q

What are the advantages and disadvantages of using drugs in solution or suspension?

A

Absorbed rapidly
Can be given to young or elderly
Can be given to those with issues swallowing
May be given via nano-gastric or PEG tube
Absorption depends on gastric emptying
First pass metabolism

150
Q

What are the advantages and disadvantages of using drugs in tablet or capsule form?

A 
Convenient
Accurate does
Easy to reproduce
Stability
Ease of mass production
Absorption depends at the rate the tablet breaks down
First pass metabolism
151
Q

What are the types of adverse drug reaction?

A 
Augmented
Bizarre
Chronic
Delayed
End of treatment
Failure of treatment
152
Q

Describe what is meant by an augmented adverse drug reaction

A

Predictable, dose dependent reaction that resolves when the drug is stopped

153
Q

Describe what is meant by a bizarre adverse drug reaction

A

Unpredictable, rare reaction that can cause serious illness or death

154
Q

Describe what is meant by a chronic adverse drug reaction

A

Semi-predictable reaction related to the dose and length of treatment

155
Q

Describe what is meant by a delayed adverse drug reaction

A

Occurs years after treatment in patient or children of patient

156
Q

Describe what is meant by an end of treatment adverse drug reaction

A

Effects caused when drug treatment is stopped

157
Q

Describe what is meant by a failure of treatment adverse drug reaction

A

Common reaction frequently caused by drug interactions

158
Q

What are the common mechanisms of drug-drug interactions?

A 
Pharmacodynamic 
Pharmacokinetic
Distribution
Metabolism
Elimination
159
Q

When do pharmacodynamic drug interactions happen?

A

When drugs act on the same or interrelated receptors, resulting in additive, synergistic or antagonistic effects

160
Q

What are pharmacokinetic drug interactions?

A

Interactions affecting absorption, distribution, metabolism or excretion

161
Q

When are pharmacokinetic drug interactions important?

A

When drug has a short half life or rapid results are needed

162
Q

What are distribution drug interactions?

A

Interactions that cause an alteration in the distribution of the drug

163
Q

What are metabolism drug interactions?

A

One drug influencing the metabolism of another

164
Q

What are elimination drug interactions?

A

Interactions between drugs that cause alterations in their elimination from the system

165
Q

What factors predispose a patient towards drug interactions?

A 
Higher number of drugs
Age
Critical illness
Undergoing surgery
Chronic underlying conditions
166
Q

What are the uses of a clinical study?

A

Provide evidence
Test efficacy
Test safety

167
Q

What are the basic considerations involved in clinical trial design?

A 
Time scale
End point
Choice of control drug
Choice of patients
Exclusion criteria
Drug used
168
Q

What are the types of clinical trial? 12

A 
Double blind
Single blind
Randomised
Placebo controlled
Prospective
Retrospective
Cross over
Sequential
Parallel
Factorial
Large simple
169
Q

What are single blind trials?

A

The patient doesn’t know what treatment they are receiving but the doctor does

170
Q

What is a randomised trial?

A

Patients are assorted to groups randomly to prevent bias

171
Q

What is a placebo controlled trial?

A

Half of patients are given a placebo and half given the treatment and comparisons made

172
Q

What is a retrospective trial?

A

The data is collected from past records and does not follow patients

173
Q

What is a prospective trial?

A

Participants differ with certain respects under study and differences in outcome monitored

174
Q

What is a cross over trial?

A

Participants receive a sequence of different treatments

175
Q

What is a sequential trial?

A

A trial where the sample size is not fixed in advance

176
Q

What is a parallel study?

A

Two groups of participants are given two different drugs

177
Q

What are factorial clinical trials?

A

More than one factor is evaluated

178
Q

What is a large simple trial?

A

Deals with fewer aspects in a larger sample size

179
Q

What is the structure of DNA?

A

2 chains of nucleotides bound in a double helix structure

180
Q

What is the structure of a nucleotide?

A

Deoxyribose pentose sugar, phosphate and a base

181
Q

Briefly describe the process by which DNA is replicated

A

DNA helices unzips double helix by breaking H bonds between bases
New nucleotides added in 5’ to 3’ direction using DNA polymerase
In lagging strand, short Okazaki fragments are made using a primer then linked together by DNA ligase

182
Q

Why can DNA synthesis be described as semi-conservative?

A

One half of each new strand of DNA id ‘old’

183
Q

Describe the process of transcription

A

The strand is unzipped by DNA helices and methionine acts as a start codon for the beginning of transcription
The sequence is read in codons and transcribed into mRNA until a stop codon is reached
Introns are then spliced out of the copy and a cap added to each end of the strand to protect it from being broken down by other enzymes

184
Q

Describe the process of translation

A

tRNA attaches to the mRNA molecule and reads it a codon at a time
tRNA brings the correct amino acid correlating to that codon and begins the polypeptide chain
The rRNA moves along the mRNA coding of the amino acids until a stop codon is reached

185
Q

What are the different kinds of DNA mutation?

A

Silent
Missense
Nonsense
Frameshift

186
Q

What are silent mutations?

A

One base change that does not result in a change of amino acid

187
Q

What are missense mutations?

A

The wrong amino acid is coded for

188
Q

What are nonsense mutations?

A

A stop codon is coded for prematurely, resulting in a small protein

189
Q

What are frameshift mutations?

A

Insertion or deletion mutations that result in the whole sequence being changed

190
Q

What is the polymerase chain reaction used for?

A

Forensic medicine
Genetic identification
Detections of mutations
DNA cloning

191
Q

What does gel electrophoresis do?

A

Separates DNA fragments by size using an electric field

192
Q

What are the advantages of gel electrophoresis?

A

Quick
Easy to use
Robust
Sensitive

193
Q

What is restriction fragment length polymorphism analysis?

A

Bacterial cells that cut DNA at known sites used to get required sections of DNA for gel electrophoresis

194
Q

What is amplification refraction mutation system?

A

Normal and mutant primers used with strands of DNA to detect a mutation

195
Q

Describe the basic structure of a chromosome

A

Centromere connecting the two sides
Telomere on the tips of arms
DNA is tightly packaged around positively charged histone proteins to form nucleosomes which coil into a chromosome

196
Q

Describe the difference between heterochromatin and euchromatin

A 
Euchromatin= open structure, being expressed
Heterochromatin= dense, tightly bound structure not being used
197
Q

Describe the structure of a nucleosome

A

146 negative base pairs wrapped around 8 positive histone proteins

198
Q

What are the stages of mitosis?

A 
Interphase
Prophase
Metaphase
Anaphase 
Telophase
Cytokenesis
199
Q

Describe the steps of prophase

A

Chromosomes condense
Nuclear membrane disappears
Spindle fibres form from centrioles

200
Q

Describe the steps of metaphase

A

Chromosomes align at the cell equator and attach to spindle fibres

201
Q

Describe the steps of anaphase

A

Sister chromatids separate longitudinally at centromere

Move to opposite poles of the cell

202
Q

Describe the steps of telophase

A

New nuclear membrane forms and each cell has 46 chromosomes

203
Q

Describe the steps of cytokenesis

A

Cytoplasm separates and 2 new daughter cells form

204
Q

How do the first and second divisions of meiosis differ?

A

In the second division, the chromosomes are not copies and haploid cells are created

205
Q

What are the main differences between spermatogenesis and oogenesis?

A 
Spermatogenesis= meiotic cycle takes roughly 60 days, undergoes many divisions (greater chance of mutation)
Oogenesis= Each meiotic cycle produces 1 ovum and 3 polar bodies that develop into ova
206
Q

What us meant by a trisomy abnormality?

A

There are 3 copies of a chromosome instead of 2

207
Q

What condition occurs from trisomy 21 and give symptoms

A

Downs syndrome

Distinct facial characteristics and IQ less than 50

208
Q

What condition occurs from trisomy 13 and give symptoms

A

Patau syndrome

Multiple dysmorphic features, few live beyond first year

209
Q

What condition is caused by trisomy 18 and give life span

A

Edwards syndrome

1 month-1 year

210
Q

What condition would have 46, X?

A

Turner syndrome

211
Q

What condition would have 46, XXY?

A

Klinefelter syndrome

212
Q

What is a Robertsonian translocation?

A

One chromosome has the two long arms while the other has the two short arms

213
Q

What is a chromosomal deletion?

A

Sections of the chromosome ‘disappear’ from one or both of the arms

214
Q

What is a chromosomal inversion?

A

A section of DNA is inverted

215
Q

What are the 2 types of chromosomal inversion and what are they?

A 
Paracentric= a section of DNA on the arm of the chromosome is inverted
Pericentric= a section of DNA around the centromere is inverted
216
Q

What are the three types of sex linked abnormalities?

A

X linked recessive
X linked dominant
Y linked

217
Q

What is non-mendelian inheritance?

A

Inheritance that doesn’t follow Mendel’s laws

218
Q

What are Mendel’s laws?

A

Law of segregation- Alleles from each gene segregate so gamete only carries one
Law of independent assortment- genes for different traits can segregate independently
Law of dominance- Some alleles are dominant while others are recessive

219
Q

Give examples of non-mendelian inheritance

A

Anticipation- Huntington’s, Myotonic dystrophy, fragile X syndrome
Mitochondrial disease- maternal inheritance

220
Q

What is the Hardy-Weinberg principle?

A

Allele and genotype frequencies will remain constant from generation to generation in the absence of mutation or selective pressures

221
Q

What factors affect the Hardy-Weinberg principle?

A 
Mutation
Migration
Population
Mating
Selective pressures
222
Q

Where are the gene mutations in myotonic dystrophy and Duchenne muscular dystrophy?

A

Myotonic- autosomal genes

Duchenne- X chromosome

223
Q

What are photo-oncogenes?

A

Genes that code for cell growth and regulation

Mutations can turn these into oncogenes

224
Q

What are oncogenes?

A

Genes that accelerate cell growth, forming a tumour

225
Q

What are tumour suppressor genes?

A

Genes that inhibit the cell cycle and/or promote apoptosis

226
Q

How many mutations are needed to cause cancer in a photo-oncogene and tumour suppressor genes?

A

Proto-oncogenes= 1

Tumour suppressor= 2

227
Q

What are benign and malignant tumours of the squamous epithelia called?

A 
Benign= squamous papilloma
Malignant= squamous carcinoma
228
Q

What are benign and malignant tumours of the glandular epithelia called?

A 
Benign= adenoma
Malignant= adenocarcinoma
229
Q

What are benign and malignant tumours of the bone called?

A 
Benign= osteoma
Malignant= osteosarcoma
230
Q

What are benign and malignant tumours of theft called?

A 
Benign= lipoma
Malignant= liposarcoma
231
Q

What are benign and malignant tumours of the fibrous tissue called?

A 
Benign= fibroma
Malignant= fibrosarcoma
232
Q

What is cancer of the lymphoid tissue called?

A

Lymphoma

233
Q

What are tumours of the gremlin cells called?

A

Teratomas
Ovary usually benign
Testes usually malignant

234
Q

What are the differences between benign and malignant cells’ growth pattern?

A 
Benign= non invasive
Malignant= invasive
235
Q

What are the differences between benign and malignant cells’ capsules?

A 
Benign= usually encapsulated
Malignant= no capsule, or capsule has been breached
236
Q

What are the differences between benign and malignant cells’ cell shape?

A 
Benign= cells similar to normal
Malignant= cells abnormal
237
Q

What are the differences between benign and malignant cells’ function?

A 
Benign= function similar to normal tissue
Malignant= loss of function
238
Q

What are the differences between benign and malignant cells’ differentiation?

A 
Benign= well differentiated
Malignant= poorly differentiated
239
Q

What are the properties of cancer cells?

A

Altered genetics
Altered cellular function
Abnormal structure
Cells capable of independent growth

240
Q

What are the mechanisms of cancer spread?

A

Local spread
Lymphatic spread
Blood spread
Trans-coelomic spread

241
Q

What is the mechanism of local spread of tumours?

A

Malignant tumour invades surrounding connective tissue and into the lymph/blood vessels

242
Q

What is the mechanism of lymphatic spread of tumours?

A

Tumour cells adhere to lymph vessels, penetrate, then pass to the lymph nodes forming metastases

243
Q

What is the mechanism of blood spread of tumours?

A

Tumour invades blood vessels and then out of the vessels into the tissues

244
Q

What is the mechanism of trans-coelomic spread of tumours?

A

Tumour invades the peritoneal, pleural, pericardial or subarachnoid spaces and spreads

245
Q

What are common sites of metastases?

A 
Liver
Lungs
Brain
Bone
Adrenal gland
246
Q

What are the local effects of benign tumours?

A

Pressure

Obstruction

247
Q

What are the local effects of malignant tumours?

A 
Pressure
Obstruction
Tissue destruction
Bleeding
Pain
Effects of treatment
248
Q

What are the systemic effects of malignant tumours?

A

Secretion of hormones- normal (produced by correct organ but abnormal control) or abnormal (produced by wrong organ)
Weight loss
Effects of treatment

249
Q

What is dysplasia?

A

Pre-malignant change that indicates a tumour is becoming malignant
Features- disorganisation of cells but no invasion

250
Q

What is an intra-epithelial neoplasia?

A

A tumour in the epithelium that is developing and will form a malignant tumour if left unchecked or untreated

251
Q

What are the phases of the cell cycle?

A

M, G1, S, G2

252
Q

What occurs during the G1 phase of the cell cycle?

A

Cell growth

Synthesis of components for DNA synthesis

253
Q

What happens during the S phase of the cell cycle?

A

DNA synthesis

254
Q

What happens during the G2 phase of the cell cycle?

A

Cell growth

Preparation for mitosis

255
Q

What two pathways are most affected by carcinogenesis?

A

Cyclin pRb pathway

Protein p53 pathway

256
Q

How is the pRb cycle disturbed by carcinogenesis?

A

pRb usually acts as the cell cycle brakes, and mutation prevents this, allowing for uncontrolled growth and proliferation

257
Q

How is the protein p53 pathway disturbed by carcinogenesis?

A

p53 normally stops the cell cycle upon damage, allowing for repair, and mutation stops this function and the cell cycle continues with these mutations, leading to cancer

258
Q

What are the major causes of cancer?

A

Inherited predispositions
Proto-oncogene to oncogene
Viruses
Chemicals

259
Q

What is the scientific basis of an MRI?

A

Magnetic field makes all of the protons spin in the same direction. A radio frequency pulse then distorts the protons and takes pictures by displaying the protons going back to their original positions

260
Q

Explain the process and use of using contrast agents in MRIs

A

Galdolinium DPTA causes changes in the magnetic field, altering the tissue signals
Allows vascular lesions and some tumours to be seen very clearly

261
Q

What factors are involved in staging cancer?

A 
Position of tumour
Depth of penetration of tumour
Relationship of adjacent structures
Involvement of regional lymph nodes
Presence of metastases
262
Q

What are the classes of anti-tumour therapeutics?

A 
Alkylating agents
Antimetabolites
Vinca alkaloids
Texans
Antimitotic antibiotics
263
Q

How do alkylating agents fight cancer?

A

Alkyl groups attach to guanine and prevent the DNA strands from separating during replication, preventing it from taking place

264
Q

How do antimetabolites fight cancer?

A

Antimetabolites integrate themselves into the nuclear membrane or irreversibly bind with vital enzymes to prevent mitosis

265
Q

How do vinca alkaloids fight cancer?

A

Prevent metaphase by preventing spindle formation

266
Q

How do takahes fight cancer?

A

Promote spindle formation and then freeze mitosis at this stage

267
Q

How to anti mitotic antibiotics fight cancer?

A

Anthracyclins and non-arythracyclins intercalate to prevent DNA and RNA synthesis

Principles of disease AM (16 decks)

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