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

Block 9 - Disease Processes (2) Flashcards

1
Q

Define parasite

A

Protozoa (unicellular)
Helminth (multicellular)
Arthropods (ectoparasites)

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2
Q

Define concomidant immunity

A

Develop immunity against new infections but cannot get rid of the pathogen that you already have

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3
Q

What do anti-protozoal agents target?

A

Fast growing and young organisms

via their metabolic pathways

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4
Q

What do anti-helminth agenets target?

A

Non-growing and adult organisms

via their metabolic pathways

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5
Q

What are the 4 main malaria parasites?

How are they diatinguished?

A

Plasmodium falciparum, vivax, ovale and malariae

PCR

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6
Q

What is the definite and intermediate malaria host?

A

Definite: Mosquito (sexual reproduction)
Intermediate: Human (no sexual reproduction)

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7
Q

Explain, in detail, the malaria lifecycle

A

1) Mosquito injects SPOROZITES
2) Exo-erythrocytic cycle: Sporozites infect the liver cell which ruptures and releases SCIZONTS that rupture to release MEROZOITES
3) Erythrocytic cycle: Merozoites infect cells forming TROPHOZITES then more schizonts which then rupture and infect more cells
4) Trophozites also form GAMETOCYTES which enter the mosqito (macro = F) (micro = M)
5) The gametocytes form an OOKINETE in the stomach, OOCYST in the midgut which released SPOROZITES which go to the salivary glands

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8
Q

What mosquito carries malaria?

A

The female anapheles mosquito

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9
Q

What are the 3 complications of malaria?

A 
Acodosis (respiratory distress)
Severe anaemia
Cerebral malaria (unarousable coma related to meningitis, convulsions and hypoglycaemia)
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10
Q

What organism causes African Tyranosomiasis?
What is another name for the disease?
How does the organism cause disease?

A

Tyranosoma brucei
Sleeping sickness

  1. Parasite in circulation = no symptoms
  2. Parasite crosses BBB –> CNS infection and death
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11
Q

What organism causes South American Tyranosomiasis?
What is another name for this disease?
How does the organism enter the body?
How does the organism cause disease?

A

Tyranosoma cruzi
Chagas disease

Insect bites and faeces enter through a lesion (also congnital, food, blood transfusion)
Acute = no symptoms
Chronic = heart, GI and neurological problems

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12
Q

What transmits Leishmaniasis?
Where does it reside in the body?
What disease does it cause?

A

Female sandfly
Resides intracellularly often in macrophages
Asymptomatic in the beginning but causes disruption to mucus membranes

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13
Q

What organism causes Toxoplasmosis?

What disease is often caused?

A

Toxoplasma gondii

Mild lymphadenopathy

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14
Q

Give 2 examples of intestinal protozoans
What disease do they cause?

What do they normally cause?

A

Entameba histolytica –> Amoebiasis (intestinal and extra retinal infections)
Giardia Lambila –> Giaraiasis (diarrhoea)

Usually non-pathogenic

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15
Q

WHAT ARE THE 6 EXAMPLES OF PROTOZOANS

A 
Malaria 
African Tyranosomiasis
South American Tyranosomiasis
Leishmaniasis
Toxoplasmosis
Intestinal protozoans
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16
Q

How do helminths cause infection?

What causes the problems in a helminth infection?

A

Infection by larvae/eggs causes problems

Adults are large but do not replicate and do not cause many problems

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17
Q

Give 3 examples of soil transmitted helminths

A

Ascarls (eggs secreted in faeces and human digest)
Hookworm
Whipworm

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18
Q

What causes Taeniasis infection?

How is it transmitted?

A

Larval cysts

Contaminated meat

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19
Q

What is another name for Schistomiasis
How is it transmitted?
Where do the helminths reside and when are symptoms caused?

A

Bilharzia
Spread by water contaminated with urine
Adult worms in blood vessels
Eggs in the bladder and intestine causing symptoms

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20
Q

What is another name for Lymphatic Filriasis
What helminth causes it?
How is it transmitted?
What is the disease mechanism?

A

Elephantitis
Roundworms
Mosquito
Larvae block the lymphatic system

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21
Q

What is another name for Echinoccocosis?

Where is the adult, egg and larvae?

A

Hydarid disease
Adult in definite host (animal)
Eggs in faeces
Larval cysts form in the organs

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22
Q

What is the disease process in Dracunculiasis?

What is the treatment?

A

The worm moves over joints causing pain

Treatment is removal

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23
Q

WHAT ARE THE 6 EXAMPLES OF HELMINTHS?

A 
Soil transmitted
Taeniasis
Schistomiasis
Lymphatic Filriasis
Echinoccocosis
Dracunculiasis
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24
Q

What mite causes scabies?

A

The human itch mite

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25
Q

What is another name for:
Tapeworms
Flukes
Roundworms

A

Tapeworms: Cestodes
Flukes: Trematodes
Roundworms: Nematodes

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26
Q

What is a wood’s lamp used for?

A

Looks for pigments and bacteria by using UVA light

Fluoresces

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27
Q

What do you look for in the skin? (SCAM)

A

Size, Shape, Symptoms
Colour
Associated seconday changes
Morphology, Margin

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28
Q

5 things you palpate for in the skin?

A

Surface, Consistency, Mobility, Tenderness, Temperature

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29
Q

3 clinical features of Lichen Planus

A

Small bites on the wrist
Nail problems
White scarring on mucus membranes

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30
Q

What is the difference between erythema and purpura?

A

Erythema: Redness due to inflammation/vasodilation which disappears on pressure
Purpura: Red/purple bleeding into the skin/mucus membranes which doesn’t disappear on pressure

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31
Q

Define auritis

A

Itching

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32
Q

Define naevus

A

Localised malformation of tissue

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33
Q

Define ecchymoses

A

Large patches on the skin

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34
Q

3 causes of hyper-pigmentation

1 cause of de-pigmentation

A

Pill, pregnancy, drugs

Vitiligo (decreased melanocytes)

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35
Q

What is the treatment of acne?

A

Antibiotics

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36
Q

Give 4 clinical features of acne

A

Seborrhoea: increased oil due to androgens turning on sebaceous glands
Comedomes: non-inflammatory
Papules and pustules: inflammatory
Scarring

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37
Q

What are the 3 types of comedomes and their characteristics?

A

Open: blackhead (large; filled with melanin)
Closed: whitehead (small)
Early-mid-facial (severe)

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38
Q

Give 3 examples of superficial inflamed lesions

A

Macule: Flat
Papule: Raised and red
Pustule: Raised, red and pus

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39
Q

Give 2 examples of deep inflamed lesions

A

Nodule: Solid lesion, not always visible
Cyst: Nodule with fluid

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40
Q

Where do you find eczema in INFANTS?

A

Face and extensors

flexors in children

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41
Q

Give 2 examples of skin findings with atopic eczema

A

Vesicles and bulla

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42
Q

What causes psoriasis

A

Hyperproliferation of keratinocytes and inflammatory cell infiltration

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43
Q

5 clinical signs of psoriasis

A 
Plaque: Palpable raised lesion
Urticaria: Wheals due to histamine
Koebner effect
Nail changes
Joint problems
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44
Q

8 causes of psoriasis

A

Genetic, immune, environment

Trauma, infection, drugs, alcohol, stress

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45
Q

2 complications of psoriasis

A

Erythroderma: A lot of skin affected causing secondary infection, fluid, loss, electroylte imbalance, hypothermia, capillary leak, renal and heart failure

Inflamatory dermatosis: 90% of body affected

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46
Q

Define abscess

A

Accumulation of pus in the dermis

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47
Q

2 benign skin tumours

A

Warts

Seborrheic keratoses

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48
Q

3 examples of fungi which infect the skin

A

Candida, Tinea, Yeast

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49
Q

3 examples of viruses which infect the skin

A

Herpes zoster, HPV, Herpes simplex

50
Q

What is the difference in presentation of a BCC and SCC

A

BCC: Pearly rolled edge with spider veins and a necrotic centre

SCC: Pink and scaly

51
Q

Where is the most common site for a menaloma in a male and female?

A

Male: Trunk
Female: Legs

52
Q

What are the 4 types of melanoma?

Where are they found?
What age do they occur in?
What type of UV exposure causes them?

A

Superficial spreading: Legs, young, intermittent high intensity UV
Nodular: Trunk, young, intermittent high intensity UV
Lentigo maligna: Face, elderly, long term cumulative UV
Acral lentiginous: palms soles and nail beds, elderly, not related to UV

53
Q

Define tumour

A

Swelling

54
Q

Define neoplasm

A

Abnormal mass of cells due to poorly regulated proliferation

55
Q

Define cancer

A

Malignant tumour/neoplasm

56
Q

3 characteristcs of the mutations in a cancer cell

A

They must happen in the genes controlling cell proliferation (tumour suppressor or oncogenes)
Affect a proliferating cell
Accumulate over time

57
Q

What are the 8 hallmarks of cancer

A

1) Self sufficiency in growth signals (oncogenes)
2) Insensitivity to antigrowth signals (tumour supressor)
3) Evasion of apoptosis
4) Replicative immortality (telomerase)
5) Sustained angiogenesis
6) Tissue evasion and metastasis
7) Reprogramming of energy metabolism
8) Evasion of host immune defences

58
Q

What happens in each of the 5 stages of the cell cycle?

A 
G0: Not dividing
G1: Replication of cell contents and machinery 
S: DNA replication
G2: Prepare to divide
M: Division
59
Q

What regulates the cell cycle?

A

cyclin-CDK complexes

60
Q

What are the 4 cell cycle checkpoints?

A

G0-G1: Growth factors ensure more cells are needed

G1-S: DNA damage checkpoint, replication machinery triggered and environment and cell checked for readiness

G2-M: DNA replication checkpoint (has it all been replicated), DNA damage checkpoint, mitosis machinergy triggered and environment checked

M-G1: Mitotic spindle assembly checkpoint and chromosomes checked for alignment

61
Q

Give 4 examples of external signalling mechanisms

A

Growth factors (activate transcription factors)
Receptors
Signal transduction pathway

62
Q

What does DNA damage activate

A

DNA damage activates ATM which can activate

BRACA –> DNA repair
P53 which inhibit CDK complexes
CDK complexes can no longer phosphorylate Rb so DNA synthesis is stopped

63
Q

Which gene causes cancer- oncogenes or proto-oncogenes?

What do the normal genes do? (2)

A

Oncogenes cause cancer

Proto-oncogenes code for normal cell regulatory factors e.g. growth factors, transcription factors

64
Q

How many mutations do you need in oncogenes?

A

1 mutation

65
Q

How can gene amplification cause cancer?

A

The gene coding for oncogenes is amplified

66
Q

How many mutations do you need in tumour suppressor genes?

Why?

A

2 mutations
One in each allele
(one inherited and one acquired)

67
Q

Define the role of a gatekeeper genes

2 examples

A

Loss of the gene leads to increased proliferation

P53 and Rb

68
Q

Define the role of a caretaker gene

1 example

A

Maintain genetic stability e.g. DNA repair

BRACA

69
Q

Explain how p53 works

A

DNA damage checkpoint
P53 is degraded if the DNA is normal
ATM phosphorylates P53 if the DNA is damaged –> inhibition of CDK and prevention of Rb synthesising DNA
If the DNA cannot be repaired, P53 –> puma and apoptosis

70
Q

What instructs Rb to release the transcription factor?

A

CDK phosphorylates Rb when the cell is instructed to proliferate

71
Q

What are the 2 viral oncogenes which the HPV virus produces?

What do they do?

A

E6: Removes p53
E7: Captures Rb

72
Q

What is the process of cell structure change?

A

Metaplasia - Dysplasia - Neoplasia

73
Q

Define parenchyma

A

Proliferating cells

74
Q

How does H.pylori cause a reduction in the stomach pH

A

Produces urease –> CO2 –> ammonia –> decreased pH

75
Q

Benign and malignant tumour of the surface epithelia

A

Benign: Papilloma
Malignant: Carcinoma

76
Q

Benign and malignant tumour of the glandular epithelia

A

Benign: Adenoma
Malignant: Adenocarcinoma

77
Q

Benign and malignant tumour of the adipose tissue

A

Benign: Lipoma
Malignant: Liposarcoma

78
Q

Benign and malignant tumour of the smooth muscle

A

Benign: Leiomyoma
Malignant: Leiomyosarcoma

79
Q

Benign and malignant tumour of the skeletal muscle

A

Benign: Rhabdomyoma
Malignant: Rhabdomyosarcoma

80
Q

What are lymphoid malignancies?

A

Malignancies of the lymphoid lineage of the blood cells

81
Q

Define choristoma

A

A tumour arising from a germ layer foreign to the site of the tumour

82
Q

Define hamartoma

A

A benign tumour which resembles a neoplasm in its tissue of origin

83
Q

What can tumours form in veins?

A

Embolisms

84
Q

Define anaplasia

What 3 things do cells experience?

A

Malignant neoplasm made from undifferentiated cells

Pleomorphism (variation in size and shape)
Abnormal nuclear morphology
Atypical mitosis

85
Q

Define paraneoplastic syndrome

What can it be mistaken for?

A

Symptoms due to local or distant spread of the tumour
Includes hormone production by tissues

Can be mistaken for metastasis

86
Q

Define tumour grade

A

The degree of differentiation

87
Q

Define menschymal malignancy

A

Soft tissue malignancy

88
Q

How is tumour grade assessed?

A

Tubuleacinar/glandular formation
Nuclear changes (atypical) and pleomorphism
Frequency of mitosis

Each component is graded from 1-3 to give an overall score
Grade 1 = 3-5
Grade 2 = 6-7
Grade 3 = 8-9

89
Q

Define tumour stage

A

The extent of spread

90
Q

How is tumour stage assessed?

A

T0-T4
N0-N3
M0-M1

91
Q

Give 5 examples of DNA damage

A 
Pyrimidine dimers (UV)
DNA cross-links
Base oxidation, hydrolysis and free radicals
Single/double strand breaks
Replication errors
92
Q

Explain how biotransformation can cause DNA damage

A

Biotransformation is the enzymatic process which transforms chemicals to excretory products which can cause DNA damage

e.g. CP450 enzymes add aflatoxin –> damage

93
Q

What happens in spontaneous deamination?

A

One base is changed for another

94
Q

Give 4 methods of DNA repair

A

Direct reversal
Base/nucleotide excision repair
Mismatch repair
Double strand break repair

95
Q

What does the direct reversal repair system repair?

How?

A

Alkylation damage

O-6 methylguanine-DNA methyltransferase (MGMT) ‘picks up’ the alkyl group from the DNA

96
Q

What does the base excision repair system repair?

How?

A

Removes damaged bases

DNA glycoslyases remove damaged bases and AP endonuclease repair the gap

97
Q

What does the double strand break repair system repair?

How?

A

Ionising radiation damage

End binding, processing and ligation

98
Q

What cancers can be treated with alkylating agents?

A

Cancers with decreased MGMT expression

99
Q

What does the nucleotide excision (mismatch) repair system repair?
How?

A

DNA damage not recognised by the base excision repair system (bulky lesions)

XP DNA damage complex binds to the DNA
XP helicases separate the DNA
XP endonueleases cut the damage and remove an oligonucleotide fragment along with the damaged base
DNA polymerases repair the fragment

100
Q

What mutation means that you have a high sensitivity to sunlight?

A

Defect in the XP proteins

101
Q 
What gene is involved in Familial Adenomatous Polyposis?
What class of gene is it?
How does it cause cancer?
A

APC gene
Tumour suppressor - Gatekeeper

APC gene blocks beta catenin (a transcription factor)
APC gene mutated = beta catenin released = proliferation

102
Q 
What gene is involved in Hereditary non polyposis colon cancer?
What class of gene is it?
A

hMSH1 and 2
Tumour suppressor - Caretaker

Genes normally repair replication errors and DNA damage
Mutations cause mutations, expansion of mutated sequences, DNA instability

103
Q

Which colon cancer affects the right colon?

What is the usual age of onset?

A

HNPCC

Early

104
Q

Which colon cancer has an increased cancer risk?

A

HNPCC

105
Q

What are the two methods of damaging DNA in radiotherapy?

A

Indirect action: Photon produces a free radical which attacks the DNA
Direct action: Radiation attacks the DNA

106
Q

Give an advantage and disadvantage of bradytherapy

A

Continuous low dose rate –> higher overall rate

Cannot be used if at risk of metastasis

107
Q

How is external beam radiation given?

A

Linear accelerator

108
Q

What does the timing of acute tissue reactions in chemotherapy depend upon?
2 examples

A

The timing depends on the stage of the cell cycle

Epithelial reactions - heals after treatment
Mucositis - mucosal membrane disruption

109
Q

What limits the maximum dose of radiotherapy?
How long does it take to develop and how long does it last?
What cells are impacted?

A

Late tissue reactions
Takes months - years to develop and is permanent
Cells with low turnover rates are affected

110
Q

Give 6 examples of late tissue reactions

A

> Xerostomia: dry mouth - dental decay
Skin fibrosis
Soft tissue necrosis: mucus ulcers, vessel and bone damage
Ocular: cataracts, neuropathy
Otolotic: otis media
Nerve tissue damage: spinal cord damage (paraplegia), transverse myelitis, brain necrosis, dementia, Sompolence syndrome (CNS effects)

111
Q

What cells does acute and long-term toxicity affect?

A

Acute: Self-limiting damage to normal cells

Long-term: Organ damage

112
Q

How can chemotherapy cause neutropenic sepsis?

A

Decrease in WBC, RBC and platelets

113
Q

Define neoadjuvant and adjuvant in regard to chemotherapy

A

Neoadjuvant: Pre-surgery
Adjuvant: Post-surgery

114
Q 
What can chemotherapy cause to happen to the:
Lung
CNS
Heart
Endocrine
A

Lung: fibrosis
CNS: dementia
Heart: cardiomyopathy
Endocrine: decreased growth

115
Q

How can cancer cells build up resistance to cytotoxic drugs?

A

Increased expression of MDR-1 gene which causes drug efflux

116
Q

How do cancer cells become resistant to methotrexate?

A

Decreased sensitivity and binding to the target

Increased permeability of transporters decreases drug accumulation

117
Q

How do cancer cells become resistant to cisplatin?

Which mechanism is also used for resistance to doxorubicin?

A

Increased permeability of transporters decreases drug accumulation
Chemicals which trap the drug (doxorubicin)
Increased nucleic acid repair

118
Q

Who did the tyrosine kinase inhibitors work best in?

A

People who had a deletion in 19 and a point mutation in 21

Deletion in 19 - the receptor prefers to bind to the drug rather than ATP

119
Q

How does growth factor binding to EGFR cause cell proliferation?
What is special about these pathways?

A

P13K –> AKT –> mTOR
RAS –> RAF –> MAP2K

All of these can be inhibited!

120
Q

What are the receptors called on tumour cells and T cells?
What antibodies overcome this?
Problem with them

A

Tumour cell: Programmed death receptor ligand 1
T cell: Programmed death receptor 1

PDL-1 and PD-1 antibodies can overcome this (immune checkpoint inhibitors)
Can cause autoimmune issues

121
Q

Explain how PABP inhibitors can be used as a cancer treatment

A

Damage to DNA = PABP repairs the damage

Inhibit PABP = no repair and apoptosis

Medicine - Year 2 (19 decks)

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