intro to clinical sciences Flashcards
1
Q
what is the first cell on the scene in inflammation
A
neutrophil polymorphs
2
Q
how long do neutrophil polymorphs live
A
3-5 days
3
Q
what do macrophages do
A
phagocytose bacteria and debris, can be APCs
4
Q
how long do macrophages live (vague)
A
weeks to months
5
Q
how long do lymphocytes live (vague)
A
years
6
Q
what do lymphocytes do
A
produce chemicals which attract other inflammatory cells, provide immunological memory for antigens
7
Q
where can you find endothelial cells
A
lining capillary blood vessels
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
9
Q
what is the most common type of cell found in connective tissue
A
fibroblasts
10
Q
what do fibroblasts do
A
secrete collagen proteins used to maintain structural framework
11
Q
what shape are fibroblasts
A
spindle shaped
12
Q
tuberculosis (TB) is an example of what kind of inflammation
A
chronic
13
Q
what is TB caused by
A
mycobacteria (which macrophages then ingest)
14
Q
what is a granuloma
A
lump of macrophages surrounded by lymphocytes (at site of inflammation)
15
Q
how do corticosteroids work
A
by suppressing the immune system and up regulating inhibitors of inflammation
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.
17
Q
where are pneumocytes found
A
lining of alveoli
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
19
Q
what causes the white line on a scar
A
collagen
20
Q
what is pus primarily made of
A
dead neutrophils
21
Q
in abrasion, what does the epidermis regrow out of
A
adnexa
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)
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
24
Q
which are the main cells in the body that do not regenerate
A
myocardial cells, neurones
25
which are the main cells in the body that do regenerate
- hepatocytes
- pneumocytes
- blood cells
- gut epithelium
- skin epithelium
- osteocytes
26
causes of inflammation
- necrosis
- infection
- chemical/ physical agents (inc radiotherapy)
- autoimmune reactions (inc hypersensitivity)
27
features of inflammation
- heat
- redness
- pain
- swelling
- reduced functionality/ movement
28
what kind of granuloma is typical of chrons disease
non-caseating
29
treatment for chrons disease
- surgery
- diet
- steroids (note this causes immunosuppression)
- antimetabolites (eg methotrexate)
- biological (eg adalimubab)
30
what is the key symptom of shingles
blistering rash on one side of the face or torso (over a single dermatome)
31
what is post-hepatic neuralgia
lasting pain after the shingles rash
32
what is the most common cause of a lobar chest infection
pneumonia
33
which cells are most commonly seen in the lungs of a patient with pneumonia
neutrophils
34
when should steroids be stopped
during bacterial infection (eg pneumonia)
35
how does c.difficile kill patients
- causes inflammation in colon
- not treatable by antibiotics
- blood loss in colon
- dehydration (no water reabsorbed --> severe diarrhoea)
36
death certificate
1a- what killed them (be specific eg psduedomembranous colitis not C. difficile)
1b- what caused 1a
1c- what caused 1b
2- background / confounding factors
37
iatrogenic meaning
illness caused by the medical treatment eg c.difficile
38
what happens at cell injury
fibrinogen --activation, polymerisation--> fibrin (positive feedback loop)
39
what happens when endothelial cells are injured
- collagen underneath is stick
- disrupts laminar flow
- platelet aggregation (to collagen)
- RBC (some) become attached
- thrombus formed
40
what is a thrombus
solid mass of blood constituents formed within intact vascular system during life
41
what 3 things cause thrombosis
- change in vessel wall
- change in blood flow
- change in blood constituents
42
what can cause endothelial cell injury
- smoking
- atheroma (degeneration of blood vessels)
- trauma
43
what causes varicose veins
damage to valves in veins
44
what forms a teflon coating for endothelial cells
nitrous oxide
45
what is stasis
- slowing or stoppage of blood flow
| - endothelial cells don't receive enough oxygen
46
when might stasis occur
long periods of bed rest
47
how does aspirin work
by inhibiting platelet aggregation
48
what is an embolus
a mass of material in the vascular system that can get lodged in a vessel and block it
49
what is the most common cause of embolus
deep vein thrombosis - bits break off causing embolus
50
what is ischaemia
- reduction in blood flow
- cells furthest from capillaries don't get enough oxygen
- in heart this can cause hibernating myocardium
51
what is infarction
- reduction in blood flow with subsequent cell death
| - hence a subset of ischaemia
52
which parts of the body have dual blood supplies**
- liver (portal venous system and hepatic artery)
- lungs (pulmonary and bronchial arteries)
- brain (circle of Willis)
53
what are the potential outcomes of acute inflammation
- resolution
- progression to chronic inflammation
- suppuration (formation of pus)
- organisation (ingrowth of capillaries and fibroblast action forming more collagen)
54
what is the vascular component of acute inflammation
vasodilation
55
what is the exudative component of acute inflammation
vascular leakage of protein rich fluid
56
how do bacteria cause inflammation
-by releasing exotoxins
OR
-with endotoxins, found in gram-negative bacterial cell walls
57
what is a hypersensitivity reaction
an excessive immune reaction causing tissue damage
58
how does infarct cause inflammation
tissues not getting enough oxygen die (infarction), releasing peptides which cause inflammation
59
what are the physical characteristics of acute inflammation (latin)
-rubor (redness)
-calor (heat)
-tumor (swelling)
-dolor (pain)
(also loss of function)
60
2 causes of calor (heat) in inflammation
- vasodilation/ hyperaemia (increased blood flow to area) eg in cellulitis/ early acute appendicitis
- systemic fever
61
causes of tumor (swelling) in inflammation
- PRIMARILY oedema
- also physical mass of extra inflammatory cells present
- formation of new connective tissue
62
causes of dolor (pain) in inflammation
- stretching/ distortion of tissues due to oedema (particularly pus in an abscess cavity under pressure)
- chemical mediators (bradykinin, prostaglandins, serotonin)
63
causes of loss of/ reduced function in inflammation
- pain
| - swelling
64
what is an atherosclerotic plaque
a build up of cholesterol, fibrous tissue, calcium in arteries
65
distribution of atherosclerotic plaques
found most commonly in high pressure systems (arteries not veins)
66
risk factors for atherosclerosis
hyperlipidaemia, smoking, hypertension, diabetes
67
how does smoking contribute to endothelial cell damage (leading to atherosclerosis)
- free radicals
- nicotine strips teflon layer off endothelial cells
- carbon monoxide
68
how does hypertension contribute to endothelial cell damage (leading to atherosclerosis)
shearing forces increased on endothelial cells
69
how does diabetes contribute to endothelial cell damage (leading to atherosclerosis)
- superoxide anions
| - glycosylation products
70
how does hyperlipidaemia contribute to endothelial cell damage (leading to atherosclerosis)
direct damage to endothelial cells from lipids
71
what are the complications of atherosclerosis
- cerebral infarction
- carotid atheroma
- MI
- aortic aneurisms
- peripheral vascular disease
- gangrene
72
what is apoptosis
programmed cell death
73
action of p53 protein
determines degree of DNA damage - if damage to DNA, will prompt apoptosis
74
when can apoptosis go wrong
-not enough: webbed hands/feet or in cancer
75
what is necrosis
- traumatic cell death (NOT programmed)
| - usually happens in big groups of cells (unlike apoptosis)
76
causes of necrosis
- spider venom
- frostbite
- cerebral infarction
- avascular necrosis (bone)
- pancreatitis
77
what is caseous necrosis likely to be caused by
TB (cheese-like necrosis, form of coagulative necrosis)
78
what is pyrexia
abnormal elevation of body temperature (fever)
79
what is a potential congenital cause of a systolic murmur
ventricular septal defect (VSD)
80
what are homeobox genes
a group of genes that regulate development in multicellular organisms
81
congenital meaning
present at birth (not necessarily genetic)
82
acquired meaning
caused by non-genetic factors
83
inherited meaning
caused by genetic factors
-may not manifest until later in life
84
hypertrophy meaning
increase in size of tissue caused by an increase in SIZE of constituent cells
85
hyperplasia meaning
increase in size of a tissue caused by an increase in NUMBER of constituent cells
86
polygenic inheritance meaning
caused by many genes
87
what causes an enlarged prostate
hyperplasia (more cells not bigger cells) of smooth muscle
88
atrophy meaning
decrease in size of tissue caused by decrease in number of cells or decrease in cell size
89
metaplasia meaning
change in differentiation of a cell from one fully differentiated type to another fully differentiated type (eg in Barretts oesophagus)
90
what kind of metaplasia occurs in the bronchi of smokers
ciliated epithelial --> squamous epithelial (losing cilia- gives smokers cough)
91
dysplasia meaning
- 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
what is the limiting factor to allow cells to divide
telomeres on the ends of chromosomes shorten at each cell division
93
what causes non-dividing tissues to die
- cross-linking DNA or proteins (eg caused by UV light in skin cells)
- damage to mitochondrial DNA
94
what is the hayflick limit
maximum number of times a cell can divide
95
what causes cataracts
UV-B light and protein cross-linking proteins in the eye
96
what is sarcopenia
muscle loss (usually in the elderly)
97
causes of sarcopenia
< GH
< testosterone
> catabolic cytokines
98
what causes deafness in the elderly
permanent to damage to cochlear hair cells
99
what kind of skin tumour is locally invasive but not metastatic
basal cell carcinoma
100
where do carcinomas spread to first
the lymph nodes that drain the site of the carcinoma (eg breast cancer spreads to axillary lymph nodes)
101
which cancers most commonly spread to the bones
- breast
- prostate
- lung
- thyroid
- kidney
102
what test is used to diagnose breast cancer
needle core biopsy
103
adjuvant therapy meaning
extra treatment given after surgical excision of cancer eg radiotherapy to make sure there are no micro metastases
104
what crystals are deposited in joints in gout
uric acid
| note gout is acute inflammation
105
what's the name of calcification in disease (as opposed to normal tissues)
dystrophic calcification
106
which cells produce antibodies
plasma cells
| -lots of cytoplasm and ER (for protein production)
107
what is carcinogenesis
the transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations
108
what does carcinogenesis apply to
malignant neoplasms
109
what does oncogenesis apply to
benign and malignant tumours
110
carcinogen meaning
agents that are known or suspected to cause cancer
111
oncogenic meaning
agents that are known or suspected to cause tumours (tumour= swelling)
112
how much of cancer risk is environmental
85%
113
Chernobyl caused an increase of what kind of cancer and why
thyroid- due to radioactive iodine isotope absorption
114
classes of carcinogens
- chemical
- viral
- ionising and non-ionising radiation
- hormones, parasites, mycotoxins
- miscellaneous / other
115
most carcinogens require conversion from pro-carcinogens to what before they cause cancer
ultimate carcinogens
| -this conversion requires enzymes that can be ubiquitous or confined to certain organs
116
what kinds of cancer does alcohol cause
- oropharynx
- larynx
- oesophagus
- liver
- breast
- colorectal
117
how does alcohol increase chance of oropharyngeal cancer
ethanol makes it easier for cells in oropharynx to absorb other carcinogens
118
how does alcohol increase chance of breast cancer
ethanol increases oestrogen levels (oestrogen is a carcinogen)
119
how does alcohol increase chance of all mentioned cancers
acetaldehyde (metabolite of alcohol) is a mutagen
120
which hormones are carcinogenic
oestrogen, anabolic steroids (esp liver cancer)
121
which mycotoxin is a common carcinogen and for what kind of cancer
aflatoxin B1 --> liver cancer
122
which common parasites cause cancer and which kinds of cancer
chlonoris sinesis (colon), shistoma (bladder)
123
which host factors that increase risk of cancer
- race (genetic and cultural)
- diet
- constitutional factors (age/gender)
- pre-malignant lesions
- transplacental exposure to carcinogens
124
what are the key miscellaneous carcinogens
asbestos (skin cancer), metals
125
what was a common trasnplacental carcinogen used to treat morning sickness
diethylstiboestrol
126
polycyclic aromatic hydrocarbons- what do they cause, where are they found
can cause lung/skin cancer. found in smoking / mineral oils
127
aromatic amines- what do they cause, where are they found
can cause bladder cancer. found in rubber/dyes
128
nitrosamines- what do they cause
can cause gut cancer (proven in animals)
129
alkylating agents- what do they cause
can cause leukaemia, small risk in humans
130
what is a neoplasm
a lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initial stimulus has been removed
131
what is a lesion
a localised abnormality
132
why can't neoplasms cannot arise from erythrocytes
they are anuclear
133
neoplastic cells have a growth pattern related to what
their parent cell
134
what is stroma (re cancer)**
fibrous connective tissue framework
- supports growth of cancer in metastasis, suppresses it before
- contains fibroblasts and blood vessels
135
neoplasm classifications
benign, borderline, malignant OR by cell of origin
136
characteristics of benign neoplasms
- localised
- non-invase
- close resemblance to normal tissues
- circumscribed or encapsulated
- low mitotic activity
- grows on mucosal surfaces
137
how to benign neoplasms cause morbidity and mortality
- pressure on adjacent structures
- obstruct flow
- produce hormones
- transformation to malignant neoplasm (uncommon)
- patient anxiety
138
characteristics of malignant neoplasms
- invasive
- ability to metastasise
- rapid growth rate
- variable resemblance to normal tissue
- poorly defined (margins not clear)
- increased mitotic activity
139
ulceration and necrosis is common in what kind of cancer
malignant
140
describe the nuclei of malignant cancer cells
hyperchromatic, pleomorphic nuclei (variable shape/size)
141
high grade cancer is referred to as
poorly differentiated (very far from normal cells)
142
what is a papilloma
benign tumour of non-glandular, non secretory epithelium
143
what is an adenoma
benign tumour of glandular or secretory epithelium
144
what is a carcinoma
a MALIGNANT EPITHELIAL NEOPLASM (important!!)
145
lipoma
cancer originating in adipocytes
146
chondroma
benign tumour originating in cartilage
147
osteoma
benign tumour originating in bone
148
angioma
benign tumour originating in vasculature
149
rhabdomyoma
benign tumour originating in striated muscle
150
leiomyoma
benign tumour originating in smooth muscle
151
neuroma
benign tumour originating in nerves
152
benign and malignant tumour of adipose tissue NAMES
lipoma (benign)
liposarcoma (malignant)
- OMA: benign
- SARCOMA: malignant
153
what is different about carcinosarcomas
both epithelia and stroma are malignant
