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phåse twoå > intro to clinical sciences > Flashcards

intro to clinical sciences Flashcards

1
Q

what is the first cell on the scene in inflammation

A

neutrophil polymorphs

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2
Q

how long do neutrophil polymorphs live

A

3-5 days

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3
Q

what do macrophages do

A

phagocytose bacteria and debris, can be APCs

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4
Q

how long do macrophages live (vague)

A

weeks to months

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5
Q

how long do lymphocytes live (vague)

A

years

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6
Q

what do lymphocytes do

A

produce chemicals which attract other inflammatory cells, provide immunological memory for antigens

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7
Q

where can you find endothelial cells

A

lining capillary blood vessels

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8
Q

what is the role of endothelial cells in inflammation

A
  • become sticky so inflammatory cells can adhere to them
  • become porous to allow inflammatory cells to pass into tissues
  • grow into damaged areas to form new capillary vessels
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9
Q

what is the most common type of cell found in connective tissue

A

fibroblasts

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10
Q

what do fibroblasts do

A

secrete collagen proteins used to maintain structural framework

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11
Q

what shape are fibroblasts

A

spindle shaped

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12
Q

tuberculosis (TB) is an example of what kind of inflammation

A

chronic

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13
Q

what is TB caused by

A

mycobacteria (which macrophages then ingest)

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14
Q

what is a granuloma

A

lump of macrophages surrounded by lymphocytes (at site of inflammation)

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15
Q

how do corticosteroids work

A

by suppressing the immune system and up regulating inhibitors of inflammation

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16
Q

what is the difference between resolution and repair

A

in resolution the initiating factor is removed and the tissue is undamaged or able to regenerate. in repair, the tissue is damaged and unable to regenerate.

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17
Q

where are pneumocytes found

A

lining of alveoli

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18
Q

when there is fibrosis in the lungs, this is what kind of healing (repair or resolution and why)

A

repair (not resolution) because though pneumocytes can regenerate, alveoli may be permanently damaged

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19
Q

what causes the white line on a scar

A

collagen

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20
Q

what is pus primarily made of

A

dead neutrophils

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21
Q

in abrasion, what does the epidermis regrow out of

A

adnexa

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22
Q

what is involved in healing by first intention**

A

bring edges of the wound together to form weak fibrin join. fibroblasts come and produce collagen. strong collagen plug forms (now safe to remove stitches)

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23
Q

what is involved in healing by second intention**

A
  • can’t bring edges of wound together
  • granulation tissue forms
  • organisation: capillary loops form
  • myofibroblast layer produces collagen
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24
Q

which are the main cells in the body that do not regenerate

A

myocardial cells, neurones

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25
Q

which are the main cells in the body that do regenerate

A
  • hepatocytes
  • pneumocytes
  • blood cells
  • gut epithelium
  • skin epithelium
  • osteocytes
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26
Q

causes of inflammation

A
  • necrosis
  • infection
  • chemical/ physical agents (inc radiotherapy)
  • autoimmune reactions (inc hypersensitivity)
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27
Q

features of inflammation

A
  • heat
  • redness
  • pain
  • swelling
  • reduced functionality/ movement
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28
Q

what kind of granuloma is typical of chrons disease

A

non-caseating

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29
Q

treatment for chrons disease

A
  • surgery
  • diet
  • steroids (note this causes immunosuppression)
  • antimetabolites (eg methotrexate)
  • biological (eg adalimubab)
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30
Q

what is the key symptom of shingles

A

blistering rash on one side of the face or torso (over a single dermatome)

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31
Q

what is post-hepatic neuralgia

A

lasting pain after the shingles rash

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32
Q

what is the most common cause of a lobar chest infection

A

pneumonia

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33
Q

which cells are most commonly seen in the lungs of a patient with pneumonia

A

neutrophils

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34
Q

when should steroids be stopped

A

during bacterial infection (eg pneumonia)

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35
Q

how does c.difficile kill patients

A
  • causes inflammation in colon
  • not treatable by antibiotics
  • blood loss in colon
  • dehydration (no water reabsorbed –> severe diarrhoea)
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36
Q

death certificate

A

1a- what killed them (be specific eg psduedomembranous colitis not C. difficile)
1b- what caused 1a
1c- what caused 1b
2- background / confounding factors

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37
Q

iatrogenic meaning

A

illness caused by the medical treatment eg c.difficile

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38
Q

what happens at cell injury

A

fibrinogen –activation, polymerisation–> fibrin (positive feedback loop)

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39
Q

what happens when endothelial cells are injured

A
  • collagen underneath is stick
  • disrupts laminar flow
  • platelet aggregation (to collagen)
  • RBC (some) become attached
  • thrombus formed
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40
Q

what is a thrombus

A

solid mass of blood constituents formed within intact vascular system during life

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41
Q

what 3 things cause thrombosis

A
  • change in vessel wall
  • change in blood flow
  • change in blood constituents
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42
Q

what can cause endothelial cell injury

A
  • smoking
  • atheroma (degeneration of blood vessels)
  • trauma
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43
Q

what causes varicose veins

A

damage to valves in veins

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44
Q

what forms a teflon coating for endothelial cells

A

nitrous oxide

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45
Q

what is stasis

A
  • slowing or stoppage of blood flow

- endothelial cells don’t receive enough oxygen

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46
Q

when might stasis occur

A

long periods of bed rest

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47
Q

how does aspirin work

A

by inhibiting platelet aggregation

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48
Q

what is an embolus

A

a mass of material in the vascular system that can get lodged in a vessel and block it

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49
Q

what is the most common cause of embolus

A

deep vein thrombosis - bits break off causing embolus

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50
Q

what is ischaemia

A
  • reduction in blood flow
  • cells furthest from capillaries don’t get enough oxygen
  • in heart this can cause hibernating myocardium
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51
Q

what is infarction

A
  • reduction in blood flow with subsequent cell death

- hence a subset of ischaemia

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52
Q

which parts of the body have dual blood supplies**

A
  • liver (portal venous system and hepatic artery)
  • lungs (pulmonary and bronchial arteries)
  • brain (circle of Willis)
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53
Q

what are the potential outcomes of acute inflammation

A
  • resolution
  • progression to chronic inflammation
  • suppuration (formation of pus)
  • organisation (ingrowth of capillaries and fibroblast action forming more collagen)
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54
Q

what is the vascular component of acute inflammation

A

vasodilation

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55
Q

what is the exudative component of acute inflammation

A

vascular leakage of protein rich fluid

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56
Q

how do bacteria cause inflammation

A

-by releasing exotoxins
OR
-with endotoxins, found in gram-negative bacterial cell walls

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57
Q

what is a hypersensitivity reaction

A

an excessive immune reaction causing tissue damage

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58
Q

how does infarct cause inflammation

A

tissues not getting enough oxygen die (infarction), releasing peptides which cause inflammation

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59
Q

what are the physical characteristics of acute inflammation (latin)

A

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

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60
Q

2 causes of calor (heat) in inflammation

A
  • vasodilation/ hyperaemia (increased blood flow to area) eg in cellulitis/ early acute appendicitis
  • systemic fever
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61
Q

causes of tumor (swelling) in inflammation

A
  • PRIMARILY oedema
  • also physical mass of extra inflammatory cells present
  • formation of new connective tissue
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62
Q

causes of dolor (pain) in inflammation

A
  • stretching/ distortion of tissues due to oedema (particularly pus in an abscess cavity under pressure)
  • chemical mediators (bradykinin, prostaglandins, serotonin)
63
Q

causes of loss of/ reduced function in inflammation

A
  • pain

- swelling

64
Q

what is an atherosclerotic plaque

A

a build up of cholesterol, fibrous tissue, calcium in arteries

65
Q

distribution of atherosclerotic plaques

A

found most commonly in high pressure systems (arteries not veins)

66
Q

risk factors for atherosclerosis

A

hyperlipidaemia, smoking, hypertension, diabetes

67
Q

how does smoking contribute to endothelial cell damage (leading to atherosclerosis)

A
  • free radicals
  • nicotine strips teflon layer off endothelial cells
  • carbon monoxide
68
Q

how does hypertension contribute to endothelial cell damage (leading to atherosclerosis)

A

shearing forces increased on endothelial cells

69
Q

how does diabetes contribute to endothelial cell damage (leading to atherosclerosis)

A
  • superoxide anions

- glycosylation products

70
Q

how does hyperlipidaemia contribute to endothelial cell damage (leading to atherosclerosis)

A

direct damage to endothelial cells from lipids

71
Q

what are the complications of atherosclerosis

A
  • cerebral infarction
  • carotid atheroma
  • MI
  • aortic aneurisms
  • peripheral vascular disease
  • gangrene
72
Q

what is apoptosis

A

programmed cell death

73
Q

action of p53 protein

A

determines degree of DNA damage - if damage to DNA, will prompt apoptosis

74
Q

when can apoptosis go wrong

A

-not enough: webbed hands/feet or in cancer

75
Q

what is necrosis

A
  • traumatic cell death (NOT programmed)

- usually happens in big groups of cells (unlike apoptosis)

76
Q

causes of necrosis

A
  • spider venom
  • frostbite
  • cerebral infarction
  • avascular necrosis (bone)
  • pancreatitis
77
Q

what is caseous necrosis likely to be caused by

A

TB (cheese-like necrosis, form of coagulative necrosis)

78
Q

what is pyrexia

A

abnormal elevation of body temperature (fever)

79
Q

what is a potential congenital cause of a systolic murmur

A

ventricular septal defect (VSD)

80
Q

what are homeobox genes

A

a group of genes that regulate development in multicellular organisms

81
Q

congenital meaning

A

present at birth (not necessarily genetic)

82
Q

acquired meaning

A

caused by non-genetic factors

83
Q

inherited meaning

A

caused by genetic factors

-may not manifest until later in life

84
Q

hypertrophy meaning

A

increase in size of tissue caused by an increase in SIZE of constituent cells

85
Q

hyperplasia meaning

A

increase in size of a tissue caused by an increase in NUMBER of constituent cells

86
Q

polygenic inheritance meaning

A

caused by many genes

87
Q

what causes an enlarged prostate

A

hyperplasia (more cells not bigger cells) of smooth muscle

88
Q

atrophy meaning

A

decrease in size of tissue caused by decrease in number of cells or decrease in cell size

89
Q

metaplasia meaning

A

change in differentiation of a cell from one fully differentiated type to another fully differentiated type (eg in Barretts oesophagus)

90
Q

what kind of metaplasia occurs in the bronchi of smokers

A

ciliated epithelial –> squamous epithelial (losing cilia- gives smokers cough)

91
Q

dysplasia meaning

A
  • morphological changes seen in cells which are precursors to cancer (disorganised as opposed to organised metaplasia)
  • can be used to refer to developmental (orthopaedic) abnormality
92
Q

what is the limiting factor to allow cells to divide

A

telomeres on the ends of chromosomes shorten at each cell division

93
Q

what causes non-dividing tissues to die

A
  • cross-linking DNA or proteins (eg caused by UV light in skin cells)
  • damage to mitochondrial DNA
94
Q

what is the hayflick limit

A

maximum number of times a cell can divide

95
Q

what causes cataracts

A

UV-B light and protein cross-linking proteins in the eye

96
Q

what is sarcopenia

A

muscle loss (usually in the elderly)

97
Q

causes of sarcopenia

A

< GH
< testosterone
> catabolic cytokines

98
Q

what causes deafness in the elderly

A

permanent to damage to cochlear hair cells

99
Q

what kind of skin tumour is locally invasive but not metastatic

A

basal cell carcinoma

100
Q

where do carcinomas spread to first

A

the lymph nodes that drain the site of the carcinoma (eg breast cancer spreads to axillary lymph nodes)

101
Q

which cancers most commonly spread to the bones

A
  • breast
  • prostate
  • lung
  • thyroid
  • kidney
102
Q

what test is used to diagnose breast cancer

A

needle core biopsy

103
Q

adjuvant therapy meaning

A

extra treatment given after surgical excision of cancer eg radiotherapy to make sure there are no micro metastases

104
Q

what crystals are deposited in joints in gout

A

uric acid

note gout is acute inflammation

105
Q

what’s the name of calcification in disease (as opposed to normal tissues)

A

dystrophic calcification

106
Q

which cells produce antibodies

A

plasma cells

-lots of cytoplasm and ER (for protein production)

107
Q

what is carcinogenesis

A

the transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

108
Q

what does carcinogenesis apply to

A

malignant neoplasms

109
Q

what does oncogenesis apply to

A

benign and malignant tumours

110
Q

carcinogen meaning

A

agents that are known or suspected to cause cancer

111
Q

oncogenic meaning

A

agents that are known or suspected to cause tumours (tumour= swelling)

112
Q

how much of cancer risk is environmental

A

85%

113
Q

Chernobyl caused an increase of what kind of cancer and why

A

thyroid- due to radioactive iodine isotope absorption

114
Q

classes of carcinogens

A
  • chemical
  • viral
  • ionising and non-ionising radiation
  • hormones, parasites, mycotoxins
  • miscellaneous / other
115
Q

most carcinogens require conversion from pro-carcinogens to what before they cause cancer

A

ultimate carcinogens

-this conversion requires enzymes that can be ubiquitous or confined to certain organs

116
Q

what kinds of cancer does alcohol cause

A
  • oropharynx
  • larynx
  • oesophagus
  • liver
  • breast
  • colorectal
117
Q

how does alcohol increase chance of oropharyngeal cancer

A

ethanol makes it easier for cells in oropharynx to absorb other carcinogens

118
Q

how does alcohol increase chance of breast cancer

A

ethanol increases oestrogen levels (oestrogen is a carcinogen)

119
Q

how does alcohol increase chance of all mentioned cancers

A

acetaldehyde (metabolite of alcohol) is a mutagen

120
Q

which hormones are carcinogenic

A

oestrogen, anabolic steroids (esp liver cancer)

121
Q

which mycotoxin is a common carcinogen and for what kind of cancer

A

aflatoxin B1 –> liver cancer

122
Q

which common parasites cause cancer and which kinds of cancer

A

chlonoris sinesis (colon), shistoma (bladder)

123
Q

which host factors that increase risk of cancer

A
  • race (genetic and cultural)
  • diet
  • constitutional factors (age/gender)
  • pre-malignant lesions
  • transplacental exposure to carcinogens
124
Q

what are the key miscellaneous carcinogens

A

asbestos (skin cancer), metals

125
Q

what was a common trasnplacental carcinogen used to treat morning sickness

A

diethylstiboestrol

126
Q

polycyclic aromatic hydrocarbons- what do they cause, where are they found

A

can cause lung/skin cancer. found in smoking / mineral oils

127
Q

aromatic amines- what do they cause, where are they found

A

can cause bladder cancer. found in rubber/dyes

128
Q

nitrosamines- what do they cause

A

can cause gut cancer (proven in animals)

129
Q

alkylating agents- what do they cause

A

can cause leukaemia, small risk in humans

130
Q

what is a neoplasm

A

a lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initial stimulus has been removed

131
Q

what is a lesion

A

a localised abnormality

132
Q

why can’t neoplasms cannot arise from erythrocytes

A

they are anuclear

133
Q

neoplastic cells have a growth pattern related to what

A

their parent cell

134
Q

what is stroma (re cancer)**

A

fibrous connective tissue framework

  • supports growth of cancer in metastasis, suppresses it before
  • contains fibroblasts and blood vessels
135
Q

neoplasm classifications

A

benign, borderline, malignant OR by cell of origin

136
Q

characteristics of benign neoplasms

A
  • localised
  • non-invase
  • close resemblance to normal tissues
  • circumscribed or encapsulated
  • low mitotic activity
  • grows on mucosal surfaces
137
Q

how to benign neoplasms cause morbidity and mortality

A
  • pressure on adjacent structures
  • obstruct flow
  • produce hormones
  • transformation to malignant neoplasm (uncommon)
  • patient anxiety
138
Q

characteristics of malignant neoplasms

A
  • invasive
  • ability to metastasise
  • rapid growth rate
  • variable resemblance to normal tissue
  • poorly defined (margins not clear)
  • increased mitotic activity
139
Q

ulceration and necrosis is common in what kind of cancer

A

malignant

140
Q

describe the nuclei of malignant cancer cells

A

hyperchromatic, pleomorphic nuclei (variable shape/size)

141
Q

high grade cancer is referred to as

A

poorly differentiated (very far from normal cells)

142
Q

what is a papilloma

A

benign tumour of non-glandular, non secretory epithelium

143
Q

what is an adenoma

A

benign tumour of glandular or secretory epithelium

144
Q

what is a carcinoma

A

a MALIGNANT EPITHELIAL NEOPLASM (important!!)

145
Q

lipoma

A

cancer originating in adipocytes

146
Q

chondroma

A

benign tumour originating in cartilage

147
Q

osteoma

A

benign tumour originating in bone

148
Q

angioma

A

benign tumour originating in vasculature

149
Q

rhabdomyoma

A

benign tumour originating in striated muscle

150
Q

leiomyoma

A

benign tumour originating in smooth muscle

151
Q

neuroma

A

benign tumour originating in nerves

152
Q

benign and malignant tumour of adipose tissue NAMES

A

lipoma (benign)
liposarcoma (malignant)

  • OMA: benign
  • SARCOMA: malignant
153
Q

what is different about carcinosarcomas

A

both epithelia and stroma are malignant

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