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Medicine - Year 2 > Block 9 - Disease Processes (1) > Flashcards

Block 9 - Disease Processes (1) Flashcards

1
Q

What is disease a consequence of?

A

Failed homeostasis

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2
Q

What are the two types of morphological changes?

A

Microscopic changes which eventually turn macroscopic

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3
Q

Which is the acidic and basic dye in the haematocyclin-eosin stain?

A 
Haematocyclin = basic (purple)
Eosin = acidic (pink)
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4
Q

4 main disease targets in a cell?

A

Cytoskeleton, Ionic channels, Membrane, Mitochondria

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5
Q

Define autophagy

A

The cell ‘eats’ itself

Triggered by calcium influx

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6
Q

Define karyorrhexis

A

Large fragments

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7
Q

Define atrophy

A

Decrease in cell size and number

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8
Q

What are the three stages of necrosis?

A

Coagulative –> Colliquative/Liquefaction –> Caesating

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9
Q

Define coagulative necrosis

A

Cell death but structure retained

Pale cytoplasm, decreased nuclei

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10
Q

Define colliquative/liquefaction necrosis

A

Hydrolytic enzymes from dying cells degrade tissue

Fluid-filled cavity of necrotic cells

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11
Q

Define caesating necrosis

A

Accumulation of inflamamtory cells

Structure lost but not fluid

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12
Q

3 structural chromosome abnormalities

A

Break, reattach, inverted incorrectly

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13
Q

Define PLOIDY

A

Additional chromosome

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14
Q

Definer restituation

A

When the opposite DNA strand is used as a template

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15
Q

Define dysplasia

A

Abnormal cell apperance

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16
Q

Define metaplasia

A

The cell differentiates into a different type of cell

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17
Q

Define immunopathology

A

The damage from the immune system becomes more clinically significant than the thing it was defending

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18
Q

Type 2 hypersensitivity:
What antibodies are involved?
Two types of tissue cytotoxicity?
6 examples

A

IgG or IgM

Antibody or complement dependent cytotoxicity

Goodpasture, Myasthenia gravis, Grave’s disease, Rhesus disease, Drug allergies, Drug induced haemolytic anaemia

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19
Q

Type 3 hypersensitivity:
What antibody is involved
3 examples

A

IgG

Arthur’s reaction (vaccination)
Serum sickness
Lupus

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20
Q

Type 4 hypersensitivity:
Explain the primary and secondary response
What is a Hapten?
What class of diseases also come under this?
4 examples

A

Primary: Sensitisation and memory cell production when APC presents Haptens (sensitising agents that bind to self-proteins in the epidermis –> neoantigens)

Secondary: APC with hapten presents to CD4+ cells –> T cell and macrophage activation

Autoimmune diseases

Contact sensitisation, Rheumatoid arthritis, MS, Allergen skin tests

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21
Q

What layer of skin is found in thick skin but not in thin skin?
2 characteristics

A

Stratum lucidium

Thin, transparent layer between the granulosum and corneum

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22
Q

What is different about the stratum corneum and hypodermis in thick skin?

A

Corneum is thicker

Hypodermis has more angualtion

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23
Q

What epithelium is the skin?

A

Stratified squamous

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24
Q

What are the 4 layers of the epidermis?

A

Stratum corneum –> Stratum granulosum –> Stratum spinosum –> Stratum basale

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25
Q

What happens at the stratum corneum?
How are the cells arranged?
What is the main property of the cells?

A

Apoptosis
Tight junctions form a barrier
Lipids and insoluble proteins = hydrophobic

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26
Q

What two things are found in the stratum granulosum?

A

Lamellar bodies: Lipids for hydrophobic barrier

Reratohyalingranules: Proteins which bind to keratin

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27
Q

How many layers are in the stratum spinosum?
What pigment is present?
What protein structures are present?

A

Many layers
Keratin
Tonofibrils: Cytoplasmic protein structures that meet at desmosomes

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28
Q

What 2 cells are found in the stratum basale?

A

Single layer of cuboidal cells

Stem cells which proliferate in a 40 day cycle

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29
Q

What are the four cells found in the skin?
Which is the most abundant?
What are their roles?

A

Keratinocytes - most abundant, more in high layers
Langerhans - Dendritic APC
Merkel - Fine touch
Melanocytes - more in low layers

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30
Q

What causes scaling

A

Imbalance between loss and renewal

Shedding of the cornified layer

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31
Q

What causes blisters

A

Breakage of the cell-cell junctions

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32
Q

3 roles of the dermis?

A

Protection
Thermoregulation
Touch

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33
Q

Papillary dermis:
Thickness
Type of connective tissue
3 properties

A

Thinnest
Loose connective tissue
Fine collagen and elastin
Squiggles to provide blood

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34
Q

Reticular dermis:
Thickness
Type of connective tissue
2 properties

A

Thickest
Dense and irregular connective tissue
Thick collagen fibre
Immune cells and cell appendages

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35
Q

How are nails produced?

What is their structure?

A

Nail root cells in the basal layer proliferate to form the nail matrix
Similar to the straum corneum and contains keratin

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36
Q

Where is hair produced?

A

Hair follicle from the acini in the basal layer

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37
Q

What is the structure of hair?

A

Medulla - Cortex - Cuticle

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38
Q

What are the three phases of hair growth?

A

Anagen - Growth phase
Catagen - Transition phase
Telogen - Resting phase

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39
Q

What type of glands are sebaceous glands?
What do they secrete?
How do they secrete?

A

Branched acinar
Secretes sebum: A lipid which keeps hair soft and waterproof
Holocrine secretion: Increased lipid concentration causes rupture of cell membrane

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40
Q

What type of glands are eccrine and apocrine glands?
Where are they?
How do they secrete?

A

Coiled tubular
Reticular dermis
Merocrine secretion: Secrete directly onto skin

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41
Q

Which glands become active in puberty?

A

Apocrine

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42
Q

What are the 5 stages of healing of deeper wounds?

A 
Haemostasis: Fibrin clot
Inflammation
Fibroplasia: Fibroblasts --> collagen
Epithelialisation: Keratinocytes create new layers
Remodelling
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43
Q

2 examples of liquid-filled lesions

Where are they found?

A

Blister, pustule

Epidermis

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44
Q

3 examples of solid lesions

3 causes

A

Plaque, nodule, wheal

Increased epidermal thickness, tumour, oedema

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45
Q

2 examples of lesions in skin colour

2 causes

A

Patch, erythema

Changes in blood flow, melanocytes

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46
Q

What causes a callus?

A

Hyperplasia of the epidermis following pressure/friction

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47
Q

What causes an ulcer?

A

Loss of epidermis and papillary dermis

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48
Q

3 requirements of fluid homeostasis

A

Intact vessels, osmolarity and constant pressure

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49
Q

How much blood do you need to lose to go into hypovolemic shock?

A

20%

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50
Q

What are the three stages of haemostasis?

A

Haemorrhage: Bleeding
Thrombosis: Clotting
Fibrinolysis: Clot dissolution

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51
Q

2 causes of a decrease in plasma proteins

A

Liver cirrhosis

Malnutrition

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52
Q

4 causes of lymphatic obstruction

A

Parasitic worm
Malignancy
Surgery
Radiation therapy

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53
Q

What causes the formation of a thrombus?

A

Inappropriate haemostasis caused by endothelial injury, abnormal blood flow and hypercoagulability

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54
Q

Main component of an arterial and venous thombus

A

Arterial: Platelets
Venous: Fibrin and electrolytes

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55
Q

2 reasons why there is an increase in blood flow to a tissue

A

Hyperaemia

Congestion

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56
Q

When does hyperaemia occur?

What are the two types?

A

A change in environment
Reactive: Vasodilation due to decreased oxygen or increased waste
Active: Vasodilation due to exercise

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57
Q

What is congestion?

What are the two types?

A

Decreased blood removal due to impaired venous return
Local: Vessel compression
Systemic: Heart failure, oedema

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58
Q

How does shock cause cell injury and damage?

A

Decreased blood flow (systemic hypoperfusion) due to decreased cardiac output causes decreased nutrients to cells

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59
Q

Define cardiogenic shock

3 examples

A

Failure of the heart to pump sufficient blood to damage

e.g. MI, Arrhythmia, Pulmonary oedema

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60
Q

Define neurogenic shock

A

CNS damage –> loss of systemic stimulation of blood vessels –> blood pooling

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61
Q

Define sepsis

A

Uncontrolled systemic reaction to the infection causes organ dysfunction

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62
Q

Define septic shock

A

Profound circulatory, cellular and metabolic abnormalities which increase mortality

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63
Q

Pathophysiology of sepsis

A

> Bacteria activate neutrophils and macrophages
Systemic release of cytokines causes systemic vasodilation, hypotension and vascular leakage
Oedema decreases blood pressure more and decreases blood flow to organs, decreasing nutrient exchange
Complement activated
Dysregulation of immune and haemostatic systems causes respiratory distress and multiple organ failure

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64
Q

Are parasites eukaryotes or prokaryotes?

A

Eukaryotes

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65
Q

What are the two classes of prokaryotes?

A

Archaea: Virus and prion

Bacteria

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66
Q

3 ways to classify bacteria?

A

Cell wall
Morphology
Nutritional and biochemical properties

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67
Q

What is found on the peptidoglycan layer?

A

Tecchoic acid

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68
Q

What do you use to stain Gram+ and Gram- bacteria?

A

Crystal violet
Retained in Gram+, lost in Gram -
Stain with counterstain
Not seen in Gram+ but seen in Gram-

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69
Q

Which class of bacteria can make spores?

A

Gram positive

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70
Q

Define microaerophilic

A

Requires some oxygen but not a lot

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71
Q

How do you identify bacteria?

A

PCR and genome sequencing

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72
Q

What are the 4 methods of horizontal gene transfer?

A

Transformation: DNA released into environment and taken up
Transduction: Phage transfers non phage DNA
Conjugation: Bacteria have sex
Transposons: Genetic units which jump

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73
Q

What are the 4 phases of bacterial replication?

A
  1. Lag phase: Bacteria make the right conditions
  2. Growth phase: Optimum multiplication
  3. Stationary phase: Nutrients decrease (can remain here for a while)
  4. Death: Non nutrients
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74
Q

What bacteria causes Lyme disease?

A

Borrella burgdorferi

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75
Q

What is in tears which provides a barrier to infection?

A

Lysozyme

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76
Q

Microbe free areas? (7)

A

Blood, Urine, CSF

Muscles, glands, inner ear, brain

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77
Q

What are the three types of pathogen?

A

Overt/Strict: Disease causing
Opportunistic: Causes disease when they end up where they’re not supposed to be
Faculative: Survives in host normally

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78
Q

What is the role of virulence factors?

A

Facilitate colonisation, growth, spread and immune evasion

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79
Q

Give 5 examples of virulence factors and their roles

A 
Adhesions: Fimbriae, pili, membrane proteins
Flagella: Mobility and penetrate mucin
Capsule: Prevents phagocytosis 
Type 3 secreted molecules
Toxins
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80
Q

What 3 diseases does streptococcus pneumoniae cause?

A

Pneumonia, Sepsis, Meningitis

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81
Q

Give 5 virulence factors of streptococcus pneumoniae

A 
Capsule
Surface adhesions
Secretory IgA protease (cleaves IgA)
Neuraminase
Spore formation
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82
Q 
Endotoxin:
Which bacteria release it?
How does it react to heat?
What does it cause? (2)
Toxicity?
A

Gram negative
Heat stable
Fever, D+V
Weak toxicity

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83
Q 
Exotoxin:
Which bacteria release it?
How does it react to heat?
What does it target?
Toxicity?
Intracellular or extracellular?
A 
Gram positive and negative
Heat fluctuation
Specific targets
High toxicity 
Extracellular
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84
Q

Define toxoid

A

Inactivated toxin used as a vaccine

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85
Q

Give 2 examples of enterotoxins

What do they cause

A

Cholera and E.coli

Permeability change and D+V

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86
Q 
What type of bacterium is clostridium botulinum?
Type of respiration?
Spore former or not?
Mechanism of entry?
3 clinical uses of botulinum toxin
A 
Gram positive
Anaerobic
Spore former
Ingestion 
Bladder, migraine, sweat
87
Q

What type of bacterium is lysteria monocytogenes?
Where is it found
2 people at increased risk
What other disease can it cause?

A

Gram positive
Found in food
Pregnancy, immunosuppressed
Can cause meningitis

88
Q

What type of bacterium is vibrio cholerae?
What type of toxin is it?
How does it change the osmotic gradient?

A

Gram negative
Exotoxin
Increased adenylate cyclase and cAMP

89
Q

What type of bacterium is salmonella?

How does it cause cell lysis?

A

Gram negative

Modifies the phagosome pathway

90
Q

Define ‘pathogenicity factors’

A

Extra genome sequences unique to a set of related pathogens

91
Q

What are black holes

A

Deleted information

92
Q

Give 7 strategies for bacterial immune evasion

A

> Stay intracellular
Antigen and phage variation (changing immunogenicity)
Molecular mimicry
Modify/block the host immune response (e.g. IgA, protease, Type 3 factors)
Avoid complement activation
Avoid phagocytosis (capsule, anti-phagocytic toxins, resist killing in the phagocytes via enzymes, pH and toxic O2 metabolites)
Inhibit host signalling

93
Q

Give 6 examples of bacteria which are part of the normal flora

A 
H. influenzae
S. epidermidis
S. aureus
S. pneumoniae
L. species
E. coli
94
Q

4 roles of the microbiome

A

Develops the immune system
Prevents pathogens colonising (directly competes with them for nutrients and room and indirectly induces the immune system)
Metabolises toxins
Produce beneficial nutrients

95
Q

What does more species in the microbiome NOT mean?

A

More genes

96
Q

7 things the microbiome is dependent on

A

Age - Diet - Environment - Immune response - Lifestyle - Host genetics - Microbial co-adaptation

97
Q

3 reasons why the microbiome can cause infection

A

Spread into sterile body parts
Expand their population
Disrupt their normal balance

98
Q

Explain the pathogenesis of C.diff

A

Microbiome bacteria convert 1 –> 2 bile salts
2 bile salts stop c.diff growth
less bacteria mean less 2 bile salts and growth of c.diff

99
Q

What is the technical name for diahorrheoa

A

Pseudomemranous colitis

100
Q

What type of bacterium is Clostridiumm Difficile?

Why is it hard to combat in hospitals?

A

Gram positive

It is a spore former

101
Q

Define dysbiosis

A

Imbalance of the normal gut microbiome composition leading to problems in the host (e.g. metabolism and distribution)

102
Q

Define prebiotics

A

Non-digestable food which helps the microbiome develop healthily and improves host health

103
Q

Define probiotics

A

Living, non-pathogenic organisms used as food to improve host health

104
Q

Define selective toxicity

A

Exploiting differences between prokarytic and eukaryotic cells

105
Q

4 properties of antibiotics

A

Bacterial selective
Kills bacteria (not just inhibits growth)
Slow emergence of resistance
Narrow spectrum

106
Q

Give 2 examples of narrow spectrum antibiotics

A

Older penicillins

Macrolides

107
Q

Give 4 examples of broad spectrum antibiotics

A

Aminoglycosides
Synthetic penicillin
Quinolones
2nd and 3rd generation Cephlasporins

108
Q

What does antibiotic resistance relate to?

A

The sensitivity of a bacterial agent at a certain concentration

109
Q

What are the 4 types of acquired bacterial resistance?

A

Modification of the antibacterial target (e.g. change surface protein shape)
Enzymatic inactivation of the antibiotic (e.g. create enzyme to break antibiotic)
Limited access of antibiotic (e.g. stop entry/efflux)
Bypass pathway

110
Q

Define the MIC

What 3 things does it depend upon?

A

Minimum concentration of antibacterial agent below which bacteria growth is not inhibited
Depends on the species, isolate and drug

111
Q

What are the 3 stages of antibiotic resistance?

A

Resistant - Intermediate - Sensitive

112
Q

2 methods of beta lactam resistance

A

Bacteria produce beta-lactamase to degrade the antibiotic

Bacteria alter penicillin binding proteins

113
Q

7 ways that doctors can decrease antibiotic resistance rates?

A 
Individual patient
Prevent overuse, misuse and abuse
Decrease infection risk 
Improve hygiene
Know local guidelines
Shortest course possible
Single use when possible
114
Q

What are the 3 shapes of viruses?

A

Icosahedral
Spherical
Filamentous

115
Q

Which virus is it harder to find a vaccination for?

A

Non-enveloped

116
Q

How is an enveloped virus transmitted?

117
Q

What protrudes from the surface of an enveloped virus?

What are their roles?

A

Protein structures

Adhesion and enzymes

118
Q

2 examples of non-enveloped viruses

A

Rotavirus

Norovirus

119
Q

3 examples of enveloped viruses

A

Influenza
HIV
Ebola

120
Q

What type of genome does norovirus have?

How is it transmitted?

A

Positive strand RNA

Transmitted though food, water and surfaces

121
Q

What is the genome in:
DNA viruses?
RNA viruses?
Reteroviruses?

A

DNA viruses: single or double strand DNA
RNA viruses: single or double strand RNA
Reteroviruses: single strand RNA / double strand DNA

122
Q

What 3 proteins do viruses make?

A

Proteins for new viruses
Enzymes for genome replication
Proteins to interfere with the immune response

123
Q

5 examples of negative single strand RNA viruses

Where is their lifecycle?

A 
Influenza
Mumps
Measles
Ebola
Rabies

Outside the nucleus

124
Q

3 examples of positive single strand RNA viruses

Where is their lifecycle?

A

Poliovirus
Dengue
Hepatitis C

Outside the nucleus

125
Q

2 examples of double strand DNA viruses

Where is their lifecycle?

A

Rotavirus
Gastroenteritis

Outside the nucleus

126
Q

Define burst size

A

Yield of the infectious virus/cell

127
Q

What does the response to the virus depend upon?

A

The type of cell infected (e.g. liver or skin)

128
Q

Give 2 examples of DNA viruses
Where is their lifecycle?
How do they replicate?

A

Herpes
Epstein-Barr

Inside the nucleus
Use normal cell functions to assemble the virus in the nucleus and release it by cell lysis

129
Q

Give 3 classes of viral drugs

A

Nucleoside analogues (inhibit polymerase)
Nucleoside antimetabolite
Protease and fusion inhibitors

130
Q

Define lytic infection

A

Latent/persistant

131
Q

2 ways by which viruses can cause cancer

A

Introduction of viral oncogenes

Transcribing/translating proteins which have never been used before

132
Q

Give an example of a reterovirus
Where is its lifecycle?
How do they replicate?

A

HIV

Inside the nucleus
Viral genome integrates with DNA, reverse transcriptase used and virus packaged in cytoplasm then released by budding

133
Q

What are the 6 main ways of virus transmission

A 
Respiratory 
Zoonoses (animal)
Enteric
Contact
Percutaneous
Mother - Child
134
Q

What do viruses not infect which bacteria do?

135
Q

Give 5 examples of respiratory viruses

A 
Flu
RSV
Coranovirus
Rhinovirus
Parainfluenza
136
Q

Give 3 examples of rash causing diseases

A

Measles
Rubella
Chickenpox

137
Q

Give 2 examples of respiratory viruses transmitted by saliva

A

Epstein-Barr

CMV

138
Q

Give 3 examples of methods by which viruses can be transmitted by animals

A

Ingestion of meat e.g. Hepatitis E
Bites e.g. Rabies
Insects e.g. Mosquitos or Ticks (tick bourne encephalitis)

139
Q

Define arbovirus

A

Virus transmitted by insects

140
Q

Give 5 examples of viruses transmitted by the faecal-oral route

A 
Hepatitis A
Hepatitis E
Norovirus
Rotavirus 
Gastroenteritis
141
Q

Give 3 examples of contact viruses

How are they actually transmitted?

A

HIV (mucosal)
Herpes simplex (mucosal)
HPV (skin)

142
Q

3 examples of viruses transmitted during pregnancy

3 examples of viruses transmitted during birth

A

CMV, Rubella, Varicella

HIV, Hepatitis B, Herpes simplex

143
Q

3 methods of percutaneous tranmission

A

Arbovirus
Mother - baby
Injection

144
Q

Why is it hard to make anti-viral drugs

A

Hard without host damage

145
Q

Give 3 prevention methods for viruses

A

Physical e.g. condoms and DEET
Passive e.g. antibodies
Active e.g. vaccination

146
Q

What part of the immune system less important for viruses?

147
Q

What leads to the production of interferons?

How do they work?

A

Fibroblasts and leukocytes produce them

Stimulate genes –> Host restriction factors –> NK, macrophages, cytokines

148
Q

What leads to the production of lymphocytes?

How do they work?

A

Early: antigens presented by MHC1 –> CD8+
Late: B cells produce IgM and IgG

149
Q

What is the role of IgM?

A

Aggregation in the initial response

150
Q

What is the role of IgG?

A

Neutralising in the later response

Involved in the secondary infection (immunity)

151
Q

A clinical sign of a reactivated latent virus?

A

Specific T cells to the virus

152
Q

Is HIV latent?

153
Q

What inflammatory cells are seen in chronic inflammation?

A

Lymphocyte, Macrophage, Plasma cells

154
Q

What is the difference between exudate and pus?

A

Exudate: Increased fluid with plasma proteins
Pus: Exudate with dying cells and bacteria

155
Q

Explain the process of the C3 and C5 inflammatory cascade

A

Pathogen binds to C3 causing release of histamine and chemoattractant

C3a and C5a: cell recruitment
C3b: interaction
C5a: cascade producing the membrane attack complex

156
Q

Give 3 examples of cell derived inflammatory mediators
What do they release?

2 other roles of inflammatory cells

A

Platelets –> serotonin
Mast cells and basophils –> histamine
Inflammatory cells –> Lymphokines and monokines

Inflammatory cells also activate arachidonic acid metabolites and platelet activating factor

157
Q

3 examples of plasma derived inflammatory mediators

What system do they arise from?

A

Kinin (kallikrenin system)
D-dimers/fibrin degradation products (clotting and fibrinolytic system)
Complement compnents (complement system)

158
Q

What 3 things produce Hageman factor (XII)

A

Plasmin from the fibrinolytic system
XI from the clotting system
Kallikrenin system

159
Q

What are the two pathways which arachidonic acid is a precursor to?
What do these pathways produce?
What is the role of them?

A

Cyclo-oxygenase pathway produces prostaglandins
Prostacyclin –> platelet aggregation and vasodilation
Thromboxane –> platelet aggregation and vasoconstriction

Lipo-oxygenase pathway produces leukotrines
Increase vascular permeability, vasoconstrict, chemotaxis, neutrophil adhesion and vasodilation

160
Q

What are ‘acute phase reactions’

9 examples

A

Systemic effects of acute inflammation
e.g. fever, rigors, tachycardia, decreased bp, reduced appetite, vomiting, aching, skeletal weakness, altered liver metabolism

161
Q

What are the 5 stages of tissue repair after inflammation?

A

Congestion: Tissue filled with proteins and fibrin (firm)
Consolidation: Inflammatory cells infiltrate (red hepatization)
Grey hepatization: Macrophages digest neutrophils and fibrin
Resolution: Restoration of tissue
Repair/reorganisation: Decreased structural integrity forms a scar

162
Q

What causes fever?

A

Pyrogens reset the temperature control system in the hypothalamus

163
Q

How does the HPA axis cause illness?

A

Alters metabolism

164
Q

Give 5 diseases where there is chronic inflammation

A

Arthritis, Alzheimers, Atherosclerosis, Dementia, Depression

165
Q

Give 4 types of chronic inflammation

A

Chronic suppurative
Autoimmune
Non-specific
Granulomatous

166
Q

Explain what happens in chronic suppurative inflammation
Why is it also acute?
Why is it hard to treat?
2 examples

A

Neutrophils are walled off by fibrin and surrounded by macrophages and fibroblasts
Acute inflammation due to neutrophils but a chronic condition
Hard to treat with antibiotics as poor blood supply –> surgery
e.g. Abscess or osteomyelitis

167
Q

What cell indicates an inflammatory condition

A

Eosinophils

168
Q

When does non-specific inflammation occur?
What is the characteristic of it?
What 2 cells does it contain?

A

After the initial inflammation due to a specific infection
No structure or obvious drive
Plasma cells and lymphocytes

169
Q

Explain what gramulomatous is and what happens
What causes more damage?
Two examples of this

A

The immune systems response to agents which hare hard to destroy
Granulomas form around the agent

The host immune response causes more damage

TB, Chron’s

170
Q

Give two ways how macrophages can have increased numbers of nuclei

A

Fusion of many

Replication without cytokinesis

171
Q

What is the difference between Langerhan giant and Touton giant cells
Which is caused by chronic measles?

A

Langerhan giant: Nuclei in a line

Touton giant: Nuclei in a circle (measles)

172
Q

What is the morphology of Warthin-Finkeldey cells?

What are they caused by?

A

Small dots in the nuclei or cytoplasm

Chronic measles

173
Q

What does immunostaining identify?

How does it work?

A

Identifies cells by molecules not morphology

Uses histochemistry and antibody probes to make coloured images

174
Q

What are the 4 receptors involved in the HIV infection?

A

gp120 (on HIV) binds to the CD4 receptor then the CCR5 co-receptor (on the host)

gp41 is also found on HIV

175
Q

What are the 3 enzymes in HIV?

A

Reverse transcriptase
Integrase
Protease

176
Q

What are the two stages of the HIV infection?

A

Primary infection: Virus localised at infection site then spread to lymph nodes causing CD4+ infection (esp in gut)
Secondary infection: Defects in gut mucus causes apoptosis and bystander killing of non-infected CD4+

177
Q

Give 5 stereotypical HIV infections

A

Karposi’s sarcoma: Cancer caused by herpes (red nodules)
Pneumocytes pneumonia: Thick infiltrates in lungs
CNS toxoplasmosis
CMV retinitis: Necrosis and bleeding
Pneumocystis jiroveci: Fungus cysts in the alveoli

178
Q

Treatment of pneumcystis jiroveci?

A

IV Trimethoprim
Sulphaethoxazole
Steroids

179
Q

How are HIV resistance patterns measured?

A

PCR creates a profile which is compared to a database

180
Q

Define quasi-species

A

Easily resistant as mutations are high

181
Q

Define epitope

A

Proteins which initiate immune response

B and T cells can discriminate between these

182
Q

Which antibodies are transferred via the mothers placenta and milk?

A 
Placenta = IgG
Milk = IgA
183
Q

What are the two methods of giving a living vaccination

A 
Naturally weakened (giving a related strain)
Artificially weakened
184
Q

What is the genome of the smallpox virus?

A

Double strand DNA virus

185
Q

What is the genome of the polio virus?

A

Positive single strand RNA virus

186
Q 
Which vaccination (dead or alive) is better for transport?
Which vaccination (dead or alive) is safer? (for who)
Which vaccination (dead or alive) needs a booster?
Which vaccination (dead or alive) is inactivated/attenuated?
Which vaccination (dead or alive) produces which antibodies?
A

Dead is more stable for transport
Dead is safer for immunodeficient
Dead needs a booster
Dead is inactivated but living is attenuated
Dead produces IgG but living produces IgG and IgA

187
Q

Define a subunit vaccination

What do they need?

A

Made from components of an organism

Need an adjuvant (increases the immune response)

188
Q

2 reasons why there is not a vaccination for HIV?

A

Too many people with it

It cannot leave your body

189
Q

Are fungi acellular or multicellular?

190
Q

How does mould grow?

A

Growth by filaments (hyphae) - asexual

Growth by spores - sexual

191
Q

What is the most common yeast to cause human infection?

A

Candida albicans

192
Q

How does yeast grow?

A

Reproduces by budding

Grows by pseudo-hyphae

193
Q

Where does yeast live?

A

Lives in mucus membranes

Normal flora of the mouth and female GU tract

194
Q

What is the prefix for diamorphic fungi?

A

Coccidiodes

195
Q

How are diamorphic infections acquired?

What are the two stages of the infection?

A

Through spores
Early infection can last a while
Late can cause chronic lung infection and spread to organs

196
Q

Define mycotoxins

A

Byproducts of fungi on food

Causes neurological, renal and hepatic problems

197
Q

Define ergotism

A

Poisoning by eating food contaminated with an ergot

198
Q

Give 2 other examples of superficial mycoses

A

Tinea pedia: Athlete’s foot

Baby’s bottom: urea damages the skin so fungi can easily penetrate

199
Q

Define geophilic
Define zoophilic
Define anthrophilic

A

Geophilic: soil
Zoophilic: animal
Anthrophilic: insect

200
Q

Explain the four levels of fungal infection?

A

Superficial mycoses: Ringworm/Tinea
Subcutaneous mycoses: Fungus invades bone, muscles, nerves and vessels –> amputation
Deep/systemic mycoses: Inhalation of spores –> blood
Mucormycoses: Brain

201
Q

How do you diagnose fungal infections?

A

Yeast: Microscopy on culture plates (fast), PCR and antigen
Mould: Culture plates (slow), Antigen tests, Radio and histopathology

202
Q

What temperature do you have conscious intelligence?

203
Q

What is the most reliable measure of temperature?

When is it used?

A

Oesophagus

ICU/Operations

204
Q

What temperature do we measure?

A

CORE temperature

205
Q

Why do elderly people struggle to shiver?

A

It requires increased oxygen and many have

pneumonia

206
Q

Where in the body are temperature receptors found?

A

Conscious: Skin
Subconscious: Organs, GI tract, Great veins, Hypothalamus

207
Q

What are the two pain neurones?

A 
A delta (myelinated)
C (unmyelinated)
208
Q

What branch of the nervous system causes piloerection?

A

Sympathetic system

209
Q

What are the two neuroendocrine controls of temperature?

A

Catecholamines –> increased metabolic rate –> heat increase
Thyroxine

210
Q

What does acclimatisation do to the production of sweat?

Why is this a problem?

A

Increases production

Huge sodium loss

211
Q

Define hypothermia

When is it severe?

A

Below 35C

Severe below 28C

212
Q

Give an active treatment of hypo/hyperthermia?

A

Cardiac bypass to warm/cool the blood

213
Q

Define PUO

A

Pyrexia of Unknown Origin

Medicine - Year 2 (19 decks)

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