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Phase 2a > Pat > Flashcards

Pat Flashcards

1
Q

what are 5 cardinal signs of infection

A

-rubor (redness)
-dolor (pain)
-calor (heat)
-tumor (swelling)
-loss of function

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2
Q

3 stages of inflammation

A
  1. bradykinin + prostacyclin + NO mediate vasodilation
    2.fluid exudate- vessel becomes leaky and fluid forced out
    3.cellular exudate- neutrophils become abundant in exudate
  2. chemotaxis, more neutrophils move to inflammation site due to chemicals released
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3
Q

neutrophils in acute inflammation

A

-migrate to edge of BV
-adhesion together
-

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4
Q

what is the sequence of acute inflammation

A

-injury/infection
-neutrophils phagocytose and release enzymes
-macrophages phagocytose
-either, resolution OR progression to chronic inflammation

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5
Q

what are the 4 outcomes of acute inflammation

A

-resolution, normal
-suppuration, pus formation
-organisation, tissue replaced with granulation tissue in healing process
-progression to chronic inflammation

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6
Q

what are neutrophil polymorphs

A

-WBCs
-contain lysosomes for phagocytosis
-1st cells at site of inflammation
-lifespan= 2-3 days

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7
Q

what are macrophages

A

-phagocytose debris/bacteria
-transport material 2 lymph nodes + present it to lymphocytes 2 induce secondary immune response
-lifespan= months-years

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8
Q

what is the sequence of chronic inflammation

A

-no/very few neutrophils
-macrophages + lymphocytes
-fibroblasts arrive
-often ends w. repair + scar tissue

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9
Q

what are lymphocytes

A

-lifespan= years
- produce antibodies, B lymphocyte plasma cells
-immunological memory cells
-secondary defence mechanism

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10
Q

what are fibroblasts

A

produce collagenous connective tissue in scarring following some types of inflammation

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11
Q

what are granulomas

A

-particular type of chronic inflammation
-collections of macrophages/histiocytes surrounded by lymphocytes
-may be due to TB or leprosy
-may be seen around foreign material in tissue

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12
Q

2 reasons why blood clots don’t form all the time

A
  1. laminar flow
  2. non sticky endothelial cells
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13
Q

what is thrombosis

A

formation of a solid mass of blood from constituents in an intact vessel in a living person

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14
Q

what is the 1st stage of thrombosis

A

platelet aggregation, clotting cascade, + feedback loop causes formation of fibrin mesh which traps RBCs

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15
Q

3 factors that can cause thrombosis

A
  1. endothelial cell injury (changes vessel wall)
  2. change in blood flow
  3. change in blood constituents
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16
Q

thrombosis risk factors

A

-smoking, harmful chemicals
-diabetes
-hypertension
-lack of activity
-high cholesterol

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17
Q

what is an embolism

A

solid mass of blood is carried thru circulation until it becomes stuck + blocks a vessel

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18
Q

causes of an embolism

A

usually a thrombus
otherwise air, cholesterol crystals, amniotic fluid, fat

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19
Q

what is ischaemia

A

reduction of blood flow , therefore O2, to a tissue

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20
Q

what is an infarction

A

tissue necrosis due to inadequate blood flow to affected area

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21
Q

which organs are less susceptible to an infarction

A

dual arterial supply in:
liver, lung and brain

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22
Q

what is resolution

A

initiating factor removed
tissue undamaged/able to regenerate

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23
Q

what is repair

A

initiating factor still present
tissue damaged + unable to regenerate
- damaged tissue replaced by fibrous tissue
-collagen produced by fibroblasts

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24
Q

look up in notes regeneration

A

and repair

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25
Q

what is atherosclerosis

A

accumulation of fibrolipid plaques in systemic arteries
-reduces blood flow

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26
Q

risk factors for atherosclerosis

A

-hypertension
-hyperlipidaemia
-cigarette smoking
-poorly controlled diabetes

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27
Q

process of atherosclerosis

A

-endothelium damaged
-ulceration of endothelium leads to development of atherosclerosis plaques

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28
Q

what can atherosclerosis cause

A

if plaque completely blocks artery- no blood flow to organ= infarction

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29
Q

what happens when pieces of plaque break off

A

pieces can travel downstream + block smaller vessels causing embolism/small infarcts

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30
Q

what is apoptosis

A

programmed cell death
- prevents cells with genetic damage continuing to divide

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31
Q

which protein detects DNA damage within cells

A

p53

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32
Q

how does a cell apoptose

A

series of proteins, trigger a release of activated enzymes, auto digest cell

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33
Q

2 examples of apoptosis for healthy functioning

A

development, eg webs between fingers

cell turnover, old cells replaced

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34
Q

2 examples of apoptosis in disease

A

-mutations in p53 gene
p53 no longer detects DNA damage, no apoptosis of damaged cells

-HIV virus induces apoptosis in CD4 helper cells = immunodeficient state

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35
Q

what is necrosis

A

destruction of large numbers of cells via an external factor

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36
Q

examples of necrosis

A

-infarction
-frostbite
-toxic venom
-pancreatitis

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37
Q

what does congenital mean

A

disease is present at birth

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38
Q

what is acquired disease

A

caused by non-genetic environmental factors

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39
Q

why do older peoples skin cells divide less than younger people

A

shorter telomeres, cells can divide

40
Q

what is the only definitive method of slowing down ageing

A

calorie restriction

41
Q

effects of ageing on skin

A

wrinkles- dermal elastosis
UV-B light causes cross-linking of proteins, particularly collagen in the dermis

42
Q

effects of ageing on eyes

A

UV-B causes cross-linking of proteins, causes opacity

43
Q

what is osteoporosis

A

loss of bone matrix- predominantly in women after menopause due to lack of oestrogen

can be prevented via hormone replacement therapy + vit D supplements

44
Q

types of dementia and their risk factors

A

alzheimer’s- not fully understood pathogenesis, some genetic factors

vascular dementia= similar risk factors to athersclerosis

45
Q

what happens to muscle in ageing

A

loss of muscle- sarcopaenia
might be caused by reduced levels of growth hormone + testosterone

46
Q

what can causes deafness

A

hair cells in cochlear do not divide, If damaged by high volumes, they will. die and not be replaced

47
Q

what is hypertrophy

A

an increase in the size of an organ due to an increase in the size of its constituent cells

48
Q

in which types of cells does hypertrophy occur

A

in organs where cells cannot divide

49
Q

examples of hypertrophy

A

skeletal muscle in bodybuilders

50
Q

what is hyperplasia

A

increase in the size of an organ due to an increase in the number of its constituent cells

51
Q

in which types of cells does hyperplasia occur

A

organs where cells can divide

52
Q

examples of hyperplasia

A

benign prostatic hyperplasia, endometrial hyperplasia

53
Q

what is mixed hypertrophy/hyperplasia

A

increase in the size of an organ due to an increase in size and number of its constituent cells

54
Q

what cells does mixed hypertrophy/hyperplasia occur

A

cells that can divide

55
Q

examples of mixed hypertrophy/hyperplasia

A

smooth muscle cells of the uterus during pregnancy

56
Q

what is atrophy

A

decrease in the size of an organ due to a decrease in size OR number of constituent cells

57
Q

examples of atrophy

A

Alzheimer’s dementia, quadriceps muscle following knee injuries

58
Q

what is metaplasia

A

change in cell differentiation from one fully differentiated type to another fully differentiated type

59
Q

what usually causes metaplasia

A

a consistent change in the environment of an epithelial surface

60
Q

examples of metaplasia

A

-bronchial epithelium from ciliated columnar epithelium to squamous epithelium, caused by cigarette smoke
-oesophageal squamous epithelium to glandular epithelium, continued acid reflux (barrett’s oesophagus)
-uterine cervix from columnar epithelium to squamous epithelium @ puberty

61
Q

what is dysplasia

A

increase in abnormal cell growth/development
-precancerous but may be seen before procession to development of cancer- neoplasia

62
Q

examples of dysplasia

A

bronchial epithelium in cigarette smokers turns from ciliated to squamous epithelium, then development of dysplasia in squamous epithelium

63
Q

what is carcinogenesis

A

the transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations
-multistep process
-applies to malignant neoplasms

64
Q

what is a neoplasm

A

an abnormal growth of cells (tumour)

65
Q

define carcinogenic

A

cancer causing

66
Q

define oncogenic

A

tumour causing

67
Q

problems identifying carcinogens

A

-interval from first explosion may last decades eg asbestos
-complexity of environment
-ethical constraints eg can’t test carcinogens on humans

68
Q

where is hepatocellular carcinoma common

A

areas with high incidences of hepatitis B/C and mycotoxins

69
Q

what risk is lung cancer associated with

A

smoking

70
Q

what risks is bladder cancer associated with

A

-working in aniline dye and rubber industries
-β-naphthylamine

71
Q

what risks is scrotal cancer associated with

A

chimney sweeping- hydrocarbons in chimneys

72
Q

what experimental evidence is there for carcinogens

A

-incidence of tumours in laboratory animals
-cell/tissue cultures
-mutagenicity testing in bacterial cultures

73
Q

cons of experimental evidence

A

animals/cultures may metabolise agents differently to humans

74
Q

what are 4 classes of carcinogens

A

-chemical
-viral
-ionising and non-ionising radiation
-hormones, parasites and mycotoxins

75
Q

what chemical can caused gut cancer

A

nitrosamines

76
Q

what can cause leukaemia

A

alkylating agents

77
Q

percentage of cancers caused by viruses

A

10-15%

78
Q

chemical carcinogens

A

-no common structural features
-some act directly BUT most require metabolic conversion from pro-carcinogens to ultimate carcinogens

79
Q

name 4 DNA viruses

A

-human herpes virus 8
-epstein barr virus
-hepatitis B virus
-HPV
merkle cell polyomavirus

80
Q

what cancer is Human herpes virus 8 (HHV8) associated with

A

kaposi sarcoma

81
Q

what cancer is associated with Epstein Barr virus (EBV)

A

burrito lymphoma nasopharyngeal carcinoma

82
Q

what cancer is hepatitis B virus (HBV) associated with

A

hepatocellular carcinoma

83
Q

what cancer is human papillomavirus (HPV) associated with

A

squamous cell carcinomas of the cervix,penis,anus and head and neck

84
Q

what cancer is merkle cell polyomavirus (MCV) associated with

A

merkle cell carcinoma

85
Q

name 2 RNA viruses

A

-human T-lymphotrophic virus (HTLV-1)
-Hepatitis C virus (HCV)

86
Q

what cancer is HTLV-1 associated with

A

adult T-cell leukaemia

87
Q

what cancer is hepatitis C associated with

A

hepatocellular carcinoma

88
Q

what does exposure to UVA or UVB increase the risk of

A

increases risk of BCC, SCC and melanoma
-people with xeroderma pigmentosum = more at risk

89
Q

what can increase in oestrogen levels cause

A

increased risk of mammary/endometrial cancer

90
Q

what do anabolic steroids increase the risk of

A

hepatocellular carcinoma

91
Q

what does the mycotoxin , aflatoxin B1 increase the risk of

A

hepatocellular carcinoma

92
Q

what does the parasite chlonorchis sinensis increase the risk of

A

cholangiocarcinoma

93
Q

what does the parasite shistosoma increase the risk of

A

bladder cancer

94
Q

5 host risk factors

A

-ethnicity
-diet/lifestyle
-constitutional factors eg age , gender etc
-premalignant lesions
-transplacental exposure

95
Q
A

Phase 2a (12 decks)

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