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Z Medicine Term 1 > Principles of Disease > Flashcards

Principles of Disease Flashcards

1
Q

killed whole organism vaccine

A

organism is heat killed.
effective and easy to manufacture.
booster shots likely required.

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2
Q

Attenuated whole organism vaccine

A

a strain of the organism is made avirulent.
simulates natural infection.
refrigeration required.

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3
Q

subunit vaccine

A

viral nucleic acid is removed (only antigens injected).
very safe.
not very immunogenic

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4
Q

Toxoid vaccine

A

a modified toxin (has antigens but no toxic activity)

only produces immunity against the toxin

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5
Q

active natural immunity

A

infection/ exposure

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6
Q

active artificial immunity

A

vaccination

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7
Q

passive natural immunity

A

placental transfer of IgG

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8
Q

Passive artificial immunity

A

immunoglobulin (antibody) therapy

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9
Q

Computed tomography (CT)

A

x-ray tube rotates around patient with detector opposite.
Iodinated contrast often given.
produces cross-sections/ 3D images

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10
Q

Positron Emission Tomography (PET)

A

isotope bound to ligand is injected.
ligand binds to structure of interest.
isotope produces positrons which collide with surrounding electrons, emitting 2 photons in opposite directions which are detected.

used to distinguish between benign/malignant tumours
prolonged exposure to radiation is bad

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11
Q

Magnetic Resonance Imaging (MRI)

A

a strong magnetic field aligns protons in the same direction.
time taken for them to “relax” to original alignment is recorded - lighter molecules take longer.

no radiation but difficult for patients

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12
Q

X-rays

A

A -ve metal cathode is heated releasing inner-shell electrons by thermionic emmision.
electrons collide with a +ve anode and emit energy (1% as x-rays)

x-rays produce sparks of light on a luminescent screen
silver halide forms clumps after exposure to light

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13
Q

Attenuation

A

stopping (of x-rays) power.
increases with atomic number, density and thickness.

Air

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14
Q

Central self-tolerance

A

deletion of autoreactive T and B cells during maturation

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15
Q

Peripheral self-tolerance

A

inhibits the activity of autoreactive cells that escaped central self-tolerance

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16
Q

telomeres

A

regions of repeated nucleotide sequences at the ends of chromosomes.
some is lost during each DNA replication but then replenished by telomerase reverse transcriptase

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17
Q

Euchromatin

A

region of chromosome with an open structure and active genes

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18
Q

Heterochromatin

A

region of chromosome with a condensed structure and silenced genes.
contains extragenic sequences that don’t code for proteins.

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19
Q

condensed chromosome exists…

A

only during cell replication. the rest of the time chromatin exists jumbled in the nucleus

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20
Q

chromatin

A

non-condensed DNA wrapped around histone proteins in nucleosomes

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21
Q

nucleosome

A

DNA wrapped around a histone protein

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22
Q

factors of pathogenicity

A

infectivity and virulence

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23
Q

factors of virulence

A

invasiveness.
Toxin production.
Evasion of immune system.

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24
Q

Exotoxins

A

toxins released extracellularly by the microorganism

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25
Q

Enterotoxins

A

Act on the GI tract

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26
Q

Endotoxins

A

part of the gram negative cell wall (the bacteria itself is a toxin)

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27
Q

Type I hypersensitivity

A

allergens are engulfed, activate T cells which activate B cells.
B cells produce IgE which binds to mast cells
mast cells release inflammatory mediators.

allergen - T cells - B cells - IgE - mast cells - inflammatory mediators

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28
Q

Type II hypersensitivity

A

IgG/ IgM antibodies bind to surface antigens (exogenous or self) which leads to …

complement activation, Fc mediated damage, ADCC, inhibition/stimulation of target cell function

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29
Q

outcomes of complement activation

A

opsonisation.
ADCC.
byproducts attract neutrophils.

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30
Q

Fc mediated damage

A

Fc receptors on immune cells bind to the Fc region of antibodies (that are bound to a pathogenic/infected cell) which stimulates the immune cell to destroy the pathogen

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31
Q

Antibody dependent cellular cytotoxicity

A

cytotoxic immune cell bound to Fc region of antibody releases cytotoxic factors causing lysis of cell

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32
Q

Type III

A

Pathological immune complexes of an antigen and antibody are formed.
These precipitate out of the blood and into tissues where they cause inflammation.

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33
Q

physiological immune complexes

A

travel dissolved in the blood to the liver/spleen and are destroyed.

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34
Q

Type IV hypersensitivity

A

A hapten/ microorganism binds to a protein carrier.
this compound is phagocytosed.
this activates Th1 cells which produce cytokines.
the cytokines cause inflammation.

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35
Q

action of chemical carcinogens

A

chemical carcinogens react with DNA to form DNA adducts.

Adduct formation at particular chromosome sites can cause cancer.

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36
Q

Cancer initiation

A

a mutation caused by a chemical, physical or viral carcinogen

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37
Q

Cancer promotion caused by…

A

mutated oncogenes, growth factors or tumour suppressor genes (e.g. P53)

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38
Q

cancer progression

A

Metastasis

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39
Q

types of metastasis

A

local.
lymphatic.
by blood.
trans-coelomic (to body cavities)

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40
Q

factors which allow for cancer metastasis

A

degradation of the ECM by enzymes
altered cell-cell and cell-ECM adhesion

(cells must detach to move to other sites)

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41
Q

Effects of benign tumours

A

all are local:

pressure, obstruction

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42
Q

Local effects of malignant tumours

A 
pressure,
obstruction,
tissue destruction,
bleeding (from damage to blood vessels),
pain (pressure on/invasion of nerves),
effects of treatment
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43
Q

systemic effects of malignant tumours

A

Weight loss (cachexia)
secretion of hormones (normal or abnormal/inappropriate)
paraneoplastic syndromes
effects of treatment

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44
Q

paraneoplastic syndromes

A

neuropathy (loss of nerve function) and/or
myopathy (loss of muscle function)

caused by humoral immune response

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45
Q

Stages of acute inflammation

A
  1. transient (temporary) arteriolar constriction
  2. local arteriolar dilation (vasodilation)
  3. relaxation of vessel smooth muscle (increases permeability)
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46
Q

results of relaxation of vessel smooth muscle in acute inflammation

A
  1. exudation (causes oedema/swelling)
  2. this increases viscosity in the capillary so the rate of flow slows causing a change in flow characteristics
  3. causes the emigration of neutrophils
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47
Q

exudation

A

a net movement of plasma from capillaries into the extravascular space
(happens in acute inflammation as a result of increased vascular permeability)

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48
Q

emigration of neutrophils

A
  1. Margination - neutrophils move towards the endothelial cells of the capillary wall
  2. Pavementing - neutrophils adhere to the endothelium
  3. Emigration - neutrophils squeeze between endothelial cells to extravascular space
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49
Q

abnormalities on chromosome number (aneuploidy)

A

Trisomy - an extra copy of a chromosome, e.g. triploidy 21 = down syndrome

Monosomy - only one copy of a chromosome

Sex chromosome aneuploidy syndromes

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50
Q

Types of structural chromosomal abnormalities

A

Translocation (balanced or unbalanced)
Deletions
Insertions
Inversions

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51
Q

Reciprocal chromosome translocation

A

2 chromosomes mix and form 2 new chromosomes
balanced = no missing genetic info
unbalanced = some info missing, some doubled

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52
Q

Acrocentric chromosomes

A

All functional DNA is on the q arm or the chromosome

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53
Q

Robertsonial chromosome translocation

A

fusion of 2 acrocentric chromosomes

unbalanced translocation leads to whole chromosomes being missing or doubled

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54
Q

mutational transitions

A

purine-purine / pyrimidine-pyrimidine

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55
Q

mutational transversions

A

purine-pyrimidine

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56
Q

silent mutations

A

e.g. CGC(arg) - CGA(arg) amino acid is unchanged = no effect

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57
Q

missense mutations

A

amino acid changes. has varying effects

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58
Q

nonsense mutations

A

mutation codes for a stop codon. has varying effects

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59
Q

frameshift mutations

A

caused by insertions/ deletions. very serious effects

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60
Q

functions of fibroblasts

A
  1. synthesise collagen (forms granulation tissue)

2. secrete growth factors that induce angiogenesis

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61
Q

Fibrosis

A
  1. synthesis of stronger better arranged collagen
  2. capillaries thin out

results in scar tissue

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62
Q

Statistical power

A

the probability that a test will reject a null hypothesis

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63
Q

purpose of statistical tests

A

to show if differences are due to chance

p<0.05 is statistically significant

64
Q

a small p value means…

A

strong evidence against the null hypothesis

high statistical power

65
Q

clinical significance

A

the practical importance of a treatment effect

small statistical differences may not be meaningful to patients

66
Q

Glomerular filtration

A

(metabolised or unmetabolised) unbound, uncharged, small drug particles are filtered out of the blood at the glomerulus

67
Q

Passive tubular reabsorbtion

A

lipid soluble drugs are reabsorbed

metabolism makes drugs more polar to prevent this

68
Q

Active tubular secretion

A

charged drugs (that could not be filtered out at the glomerulus) are actively secreted into the proximal tubule from the blood

69
Q

radiotherapy

A

Treats inoperable lesions.
Maintains function and appearance.
Given in stages to maximise tumour damage but minimise healthy tumour damage
P53 mutants are more sensitive to radiation.
Cells are more sensitive at specific cell cycle phases

70
Q

Programmed cell death pathway

an immune cancer therapy

A

PDL1 on cancer cell surface deactivates T cells by binding to PD1 on T cell surface.
blocking this interaction allows T cells to recognise cancer cells

71
Q

Monoclonal antibodies

an immune cancer therapy

A

antibodies (e.g. herceptin) bind to antigens on cancer cells. Immune cells can then recognise the cancer cells

72
Q

CAR (Chimeric Antigen Receptor) T cell Therapy

an immune cancer therapy

A

T cells from a healthy person are mixed with an attenuated virus
This makes the T cells produce CARs which can recognise cancer cells
The T cells are then injected into the patient.

This is non-patient specific

73
Q

causes of type A adverse drug reactions

A

pharmacodynamic abnormalities (e.g. an excess effect such as insulin induced hypoglycaemia)

pharmacokinetic abnormalities (abnormalities in ADME) caused by disease or pharmacogenetics

74
Q

pharmacodynamics

A

a drug’s effects

75
Q

types of drug-drug interactions

A

pharmaceutical interactions
pharmacokinetic interactions
pharmacodynamic interactions

76
Q

pharmaceutical interactions

A

mixing 2 drugs in the same solution

77
Q

Absorbtion

A

The rate at which a drug enters the blood

78
Q

Factors affecting absorption

A 
Gut motility
other drugs
food/drink
illness
gastric emptying time
site of absorption
lipid solubility/ionisation
79
Q

Bioavailability

A

The amount of drug which is absorbed and is available for action

80
Q

factors affecting bioavailability

A

Ability of drug to pass physiological bariers
first pass metabolism
drug interactions

81
Q

Distribution

A

The rate at which a drug moves from the blood to the site of action

82
Q

factors affecting distribution

A 
capillary permeability
blood flow : tissue mass ratio
plasma protein binding
transport mechanisms available
characteristics of tissue membranes (e.g. blood-brain and blood-testes/ovaries barrier
83
Q

Glandular tumours

A 
Benign = adenoma
Malignant = edeno-carcinoma
84
Q

Squamous tumours

A 
Benign = squamous papilloma 
Malignant = squamous carcinoma
85
Q

Bone tumours

A 
Benign = Osteoma
Malignant = Osteo-sarcoma
86
Q

Fat tumours

A 
Benign = Lipoma
Malignant = Lipo-sarcoma
87
Q

Fibrous tissue Tumours

A 
Benign = Fibroma
Malignant = Fibro-sarcoma
88
Q

White Blood Cell Tumour

A

Malignant = Leukaemia

89
Q

Lymphoid Tissue Tumour

A

Malignant = Lymphoma

90
Q

Melanocyte tumour

A 
Benign = Naevus
Malignant = melanoma
91
Q

Central nervous system tumours

A

Astrocytoma

92
Q

Peripheral nervous system tumours

A

Schwannoma

93
Q

Germ cell tumours

A

Teratomas

ovarian-usually benenign
testicular-usually malignant

94
Q

Diseases that affect how drugs work

A

Hepatic impairment - drugs are often metabolised in the liver so impairment can lead to toxic levels building up
Renal impairment - drugs are often excreted by the kidneys so impairment can lead to toxic levels building up
Oedema - reduces drug absorption from the gut

95
Q

Anti-metabolites

A

e.g. fluorouracil

bind to and inhibit essential enzymes, inhibiting DNA synthesis

96
Q

Alkylating agents

A

e.g. cisplatin

bind anti-parallel DNA strands together so they can’t be unzipped

97
Q

mechanisms of resistance of cancer cells (to alkylating agents)

A
  1. decreased entry/increased exit of agent from cell
  2. inactivation of agent in cell
  3. enhanced DNA repair
98
Q

intercalating agents

A

interfere with transcription and DNA replication

99
Q

Antimitotic antibiotics

A

e.g. Doxobubicin

inhibit DNA/RNA synthesis during mitosis

100
Q

Spindle Poisons

A

e.g. Vinca Alkaloids

blocks microtubule formation during mitosis

101
Q

mitotic inhibitors

A

e.g. Etoposide

breaks down DNA strands during mitosis

102
Q

Examples of anti-cancer hormone therapy

A

Tamoxifen - blocks oestrogen receptors to decrease risk of breast cancer

Anti-androgens - block testosterone production for prostate cancer

103
Q

Parallel clinical trial design - pros and cons

A

prevents confounding results from carry over effects
good for disorders with likely progression

groups may be unbalanced

104
Q

Cross-over clinical trial design

A

reduces confounding variables
requires fewer subjects

carryover between treatments confounds results
bad for curative treatments or rapidly changing conditions

105
Q

Type A ADRs

A

Augmented

e.g. hypoglycaemia with insulin
bradycardia (slow heart rate) with beta blockers

106
Q

Type B ADRs

A

Bizarre

e.g. drug allergy hypersensitivity reactions

107
Q

Type C ADRs

A

Chronic

e.g. steroid induced osteoporosis
opiate dependence

108
Q

Type D ADRs

A

Delayed

e.g. Teratogenesis (damage to embryo/ foetus)
carcinogenesis

109
Q

Type E ADRs

A

End of Treatment

e.g. withdrawal seizures from anti-epileptics
MI when beta blockers are stopped

110
Q

Type F ADRs

A

Failure of treatment

e.g. failure of OCP (oral contraceptive pill) when administered with antibiotics

111
Q

Hypostasis

A

The settling of blood after death due to gravity with areas of pallor in areas under pressure

112
Q

Putrefaction

A

degradation of the body by microorganisms

113
Q

Autolysis

A

Degradation of the body by endogenous enzymes

114
Q

saponification

A

Fatty acids and ionic solutions form soaps in the body months after death.

115
Q

diagnosis of bacterial infection by microscopy

A

quick but insensitive detection but not identification

116
Q

diagnosis of bacterial infection by culture

A

strains can be identified by colonial appearance and growth patterns

117
Q

sterile sites

A

blood
CSF
bladder
Lungs

118
Q

non-sterile sites

A

skin
nasopharynx
urethra
gut

119
Q

detection of viruses

A

a cell line must be inoculated.
electron (not light) microscopy
serology

most common: antigen detection and nucleic acid amplification

120
Q

fimbrae

A

features of bacterial cells, used for adherance

121
Q

causes of acute inflammation

A 
microorganisms
mechanical trauma to tissue
chemical changes
dead tissue
hypersensitivity
122
Q

systemic effects of acute inflammation

A

pyrexia
malaise
neutrophilia
septic shock

123
Q

causes of chronic inflammation

A

failure of acute inflammation to resolve
autoimmune disorder
exogenous substances
endogenous substances

124
Q

localised type III hypersensitivity reaction

A

causes localised inflammation that can be resolved by macrophages

125
Q

systemic type III hypersensitivity reaction

A

complexes deposited in many organs

126
Q

IV administration

A

100% bioavailability

avoids first pass metabolism

127
Q

Topical administration

A

can achieve local or systemic effects
doses can be controlled and sustained
avoids first pass metabolism

128
Q

inhaled administration

A 
drug delivered directly to site of action
rapid effect
little systemic absorption
small doses can be used
reduced adverse effects
129
Q

Meiosis

A

Meiosis I - same as mitosis except that non, sister chromatids cross over forming chiasmata where they exchange DNA sequences, resilting in variation

Meiosis II - same as mitosis except chromosomes are not copies so 4 haploid cells are produced

130
Q

Prophase

A

chromosomes condense
nuclear membrane disappears
spindle fibres form from centrioles

131
Q

Metaphase

A

chromosomes align at equator
microfilaments attach to centrioles
maximum condensation of chromosomes

132
Q

Anaphase

A

sister chromatids separate and move to opposite ends of the cell

133
Q

Telophase

A

new nuclear membranes form

134
Q

proto-oncogenes

A

code for cell growth and regulation.
mutations can turn them into oncogenes which can accelerate growth, causing a tumour.
One mutation is enough to cause cancer

135
Q

Tumour-suppressor genes

A

inhibit the cell cycle/promote apoptosis.
cancer only arises when both copies of the gene are mutated.
If a mutation is in a germline cell, the child will only need one mutation as they already have one.

136
Q

common sites of metastasis

A 
liver
lung
brain
bone
adrenal glands
137
Q

Dysplasia

A

a pre-malignant change that can indicate a tumour is becoming malignant.

Features include…
increased nuclear size
increased mitotic activity
abnormal mitosises

138
Q

P53 pathway

A

P53 normally stops the cell cycle to allow DNA repair or trigger apoptosis after damage.

mutations in P53 prevent the cell cycle from stopping so mutations are replicated leading to cancer.

139
Q

Commensal

A

Normal members of the microbial flora

140
Q

ELISA

A

measures antibody / antigen

141
Q

epigenetic factors

A

affect the phenotype without changing the genotype

142
Q

examples of non-mendelian Inheritance

A

Incomplete penetrance

Genomic imprinting - gene expressed from only one chromosome (the other is switched off)

Extracellular inheritance - e.g. mitochondrial DNA

Anticipation - disease presents at an earlier age/ is more severe with each succeeding generation

143
Q

PCR

A
  1. DNA is denatured
  2. primers anneal
  3. replication by heat resistant DNA polymerase

*repeated 20-30 times
followed by analysis by gel electrophoresis

144
Q

ARMS - amplification refractory mutation system

allele specific PCR

A

like PCR, used to detect single base pair mutations

run first with normal primers, then with mutant primers

amplification will only occur if the primer matches.

145
Q

Restriction fragment length polymorphism

A

restriction endonucleases cut DNA at a specific site
this creates restriction fragments

fragments are analysed by gel electrophoresis

146
Q

DNA sequencing

A

PCR using chemically altered terminator bases (dideoxynucleotides) that stop replication at different points - this creates many fragments of different lengths

fragments are analysed by gel electrophoresis

the fluorescent tags on the dideoxynucleotides are “read” by a computer as they pass a point on the gel.

the shortest fragments reach the point first so the order read by the computer gives the base sequence. (each base has a different tag)

147
Q

Causes of acute inflammation

A 
Infection
Trauma (even sterile injuries)
chemical upset
Physical factors (heat, cold, ionising radiation)
dead tissue
hypersensitivity
148
Q

breast tumours commonly metastasise to…

A

bone

149
Q

prostate tumours commonly metastasise to…

A

bone

150
Q

colorectal tumours commonly metastasise to…

A

liver

151
Q

ovary tumours commonly metastasise to…

A

omentum

152
Q

Cys64Arg

A

64th amino acid changed from Cys to Arg

153
Q

662-42C>T

A

42 nucleotides before 662, C changed to T

154
Q

M252X

A

252nd amino acid changed from an M to a STOP codon

155
Q

IVS2+12insG

A

in the second intron, after 12 nucleotides, insertion of a G

156
Q

1294del40

A

at position 1294, 40 nucleotides deleted

157
Q

1298A>G

A

at position 1298, single base mutation of A to G

Z Medicine Term 1 (8 decks)

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