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pathology Flashcards

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1
Q

define risk factor

A

Social or individual factor which increases the likelihood of you getting a disease

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2
Q

Defin aetiology

A

causes of the disease

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3
Q

Define pathogenesis

A

sequence of events from healthy state to clinical disease

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4
Q

Define sequelae

A

the range of possible outcomes of a disease process

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5
Q

Define necrosis

what does this elicit?

A

Death of tissues, pathological and elicits adjacent tissue response

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6
Q

Define coagulative necrosis

A

proteins coagulate, preservation of cell outline - MI

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7
Q

Define colliquative necrosis

A

necrotic material becomes softened and liquified (pus) - Brain necrosis

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8
Q

define caseous necrosis

A

Cheese like - TB!

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9
Q

Define gangrenous necrosis

A

cell death by necrosis and infection on top - anaerobic bacteria have the potential to grow

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10
Q

fibrinoid necrosis?

How can malignant hypertension cause this?

A

Fibre deposition - damage to blood vessel in malignant hyper tension

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11
Q

Fat necrosis? - provide an example

A

something like acute pancreatitis

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12
Q

Define apoptosis

What are the two things it can be?

A

Programmed cell death

can be either physiological or pathological

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13
Q

What can happen if p53 is lost?

What is this most likely to be?

A

can lead to the development of cancer which is most likely to be resistant to treatment

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14
Q

What is the role of p53?

What happens if mistakes are found?

A

Bit like a spell checker (G1), if mistakes are found cell cycle is paused then repair attempted

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15
Q

What are the three checkpoints of p53?

What happens at each checkpoint?

A

G1 - apoptosis can occur if DNA is damaged

G2 - mitosis will not occur if DNA is damaged or not replicated

M - mitosis will not occur if chromosomes are not aligned properly

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16
Q

If DNA can not be repaired what does P53 stimulate?

A

caspases and induces apoptosis

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17
Q

Why are chromosomes capped?
What happens to the number of repeats every division?

What does telomerase do and how is cancer caused?

A

Chromosomes are capped to prevent further degradation and fusion

Every division the number of repeats gets smaller

Telomerase adds on TTAGGG after its lost preventing cells from dying

cancer reactivates telomerase and can become immortal

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18
Q

What are free radicals produced by?

A

drugs, O2 toxicity, reperfusion injury

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19
Q

How are we protected from free radicals?

A

Protection by anti-oxidants ( scavenge free radicals)

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20
Q

What is a metabolic disorder?

How can this cause end organ damage?

A

Biochemical abnormality which may itself be deleterious, but which also causes target organ damage mostly due to the accumulation of a toxic agent

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21
Q

What kind of genetic mutation is a metabolic disorder

what does the gene encode?

A

autosomal recessive, gene encodes enzyme in metabolic pathway

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22
Q

What happens during the vascular phase and

exudative and cellular phase of inflammation?

A

vascular phase - dilation and increased permeability of blood vessels (first is arteriole)

exudative and cellular phase - fluid and cells escape from permeable venules

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23
Q

What are some positive effects of acute inflammation?

A

toxin dilution, entry of antibodies, drug transport

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24
Q

What are some harmful effects of inflammation?
digestion…
tumour
type 1 hypersensitivity

A

Digestion of normal tissues, swelling and inappropriate inflammatory response - type 1 hypersensitivity

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25
What are some characteristics of chronic inflammation?
redness - due to dilation of small vessels heat - increased blood flow through region swelling - accumulation of fluid in extravascular space pain - distortion of tissues loss of function - inhibited by pain or swelling
26
What are acutely inflamed organ surfaces usually covered in?
Fibrin
27
What is the process of neutrophils getting to the site of inflammation? margination, rolling, pavementing and diapedesis
1) Margination - loss of intravascular fluid and increased plasma viscosity allows neutrophils into plasma 2) rolling - WBC’s are still moving along the vessel wall 3) Pavementing - white blood cell’s bind tightly and flatten against the vessel wall? 4) diapedesis - is the movement of WBC’s through the vessel wall.
28
What is chemotaxis?
Locomotion orientated along a chemical gradient
29
Why is histamine important in chronic inflammation? what is it released by? What stimulates its release?
vascular dilation, released by mast cells, eosinophils, and basophils release stimulated by C3a, C5a and lysosomal proteins (released by neutrophils)
30
What can serotonin do in inflammation?
Increase vascular permeability
31
What do chemokines do?
attract various leukocytes to site of inflammation
32
What chemical mediator is involved in type 1 hypersenstivity
leukotrienes
33
prostaglandins? what do they increase and what do they stimulate?
increase vascular permeability - simulted platelet aggregation
34
What is required for recognition of a microorganism in inflammation?
To be coated in opsonins
35
What is suppuration? what is contained in this?
Formation of Pus - neutrophils, bacteria, cellular debris
36
What is resolution | what does it occur after?
complete restoration of tissues to normal after episode of acute inflammation
37
What cells are involved in chronic inflammation?
plasma cells, lymphocytes and macrophages
38
Detail some macroscopic appearances of chronic inflammation TB, breach in mucosa,
chronic ulcer - breach in mucosa, thickening of wall by fibrous tissue granulomatous - chrons / TB
39
When do B lymphocytes become plasma cells?
on contact with antigen
40
What do T lymphocytes produce in chronic inflammation?
cytokines
41
Detail some examples of reversible damage of cells | lipids, tumour, pump, respiration
Reduced aerobic respiration/ increased anaerobic membrane pump fails cell swelling accumulation of lipids
42
What is some irreversible damage done to cells? | membranes, leak, nuclear
Severe damage to cell membranes and mitochondria leakage of enzymes nuclear changes - ATP changes, cell membrane damage
43
What is the progression of repair?
Injury and damage attempted repair complete (regeneration/ restitution) incomplete (scarring)
44
Where are labile(cells that multiply throughout all of life) cells found?
GI tract, bone marrow
45
Where are stable cells found? | What are they?
Hepatocytes, endothelium These cells can multiply to replace lost cells
46
Where are permanent cells found?
neurones and skeletal muscle Regeneration of these are not possible
47
What can pluripotent stem cells differentiate into?
Most cell types
48
What is granulation tissue
a tissue that undergoes organisation to form fibrous scar
49
What is a granuloma?
Chronic inflammation, collection of macrophages (in response to foreign bodies)
50
What is wound contraction caused by?( healing response that reduces the size of the tissue defect and decreases the amount of damaged tissue that needs repair.)
caused by the action of myofibrils
51
Define differentiation
Acquisition of specialised function
52
define Hyperplasia
increase in cell number
53
define hypertrophy
increase in cell size
54
Define atrophy
Reduction in cell size and number in an organ that was of normal size
55
What is hypoplasia?
reduced size of an organ that never fully developed to normal size
56
What is metaplasia?
One type of cell becomes another form of cell in response to stress (at risk site for cancer)
57
What is neoplasia? what does neoplastic material being monoclonal mean
NEW abnormal mass of tissue, growth which exceeds and is uncoordinated with that of normal tissues neoplastic cells are monoclonal = derived from a single common ancestor
58
What are the signs of benign neoplastic activity
No necrosis, nucleus to cytoplasm ratio normal, minimal pleomorphosm ( change in size or shape) diploid
59
What are some examples of benign neoplasms?
Adenoma or papilloma
60
What are the signs of malignant neoplasms?
Necrosis, N:C ratio increased, pleomorphic, aneuploidy
61
What are some examples of malignant neoplasms?
Carcinoma - cancer of epithelial cell carcinoma in situ - not invading other tissues, confined to site of origin sarcoma - cancer of mesenchymal cell
62
What is dysplasia?
Disordered growth | Pre-malignant process
63
What is angiogenesis?
formation of new, abnormal blood vessels Successful tumours will develop their own blood supply
64
What is metastasis?
Formation of tumour in a place discontinuous with its primary legion
65
What are the two routes of metastasis?
lymph - carcinoma haematogenous = sarcoma
66
What is the double hit hypothesis?
one working gene is enough, one faulty gene puts person at increased risk... Two faulty mutated genes will result in a functional problem
67
What is stepwise progression of malignant mutations?
Initiation - 1st mutation promotion - further accumulation of mutations persistence - unregulated abnormal growth that could possibly become malignant
68
Detail some examples of oncogenes that are effected by mutations (RAS, BRAF, MYC, P13K)
RAS (GTP binding) BRAF - downstream (50% of melanoma are RAF mutated) Myc (supposed to be nuclear transcription factor promoting DNA replication) P13K most common mutated kinase in cancer - located inside the nucleus @ transcription
69
What is p53, what is it activated by? and what can it do? regulate, cycle, death
p53 - guardian of the genome, transcription factor, activated by cell stress regulates transcription of downstream target genes cell cycle arrest - G1/s and G2/M cell death - apoptosis
70
What are the different visual appearances of malignant and benign cancers
malignant - rough and nasty looking benign - rough and smooth
71
What cancers are present in | epithelium(malignant), glands(benign and malignant) and in squamous cells (benign and malignant)
epithelium - carcinomas glands - adenoma vs adenocarcinoma (malignant) Squamous - papilloma vs squamous cell carcinoma
72
What type of cancer is a sarcoma?
MALIGNANT
73
What is a paraneoplastic syndrome?
Rare disorders that are triggered by an altered immune system response to a neoplasm clinical syndromes involving non-metastatic systemic effects that accompany malignancy
74
Detail some examples of an acquired metabolic disease what are the complications of these
type 1 and 2 diabetes obesity (central or periperal) complications - ketoacidosis, hypoglycaemia
75
What is the progression of atheroma?
fatty streak, fibrofatty plaque, proliferative atheroma and then complicated atheroma
76
What are can cause atheroma?
endothelial injury - response to injury, macrophage + platelets, lipid accumulation and then smooth muscle proliferation
77
What are the complications of atheroma? | TADEI
Thrombosis, aneurysm, dissection, embolism and ischaemia
78
What are the consequences of left ventricular hypertrophy?
Increased LV load, poor perfusion, interstitial fibrosis,
79
What is a thrombus?
Solid mass of blood constituents formed within a blood vessel
80
What is vircow's triad?
Vessel wall - loss of endothelial surface, inflammation blood flow - stasis/ turbulence blood constituents - platelets, coagulation proteins
81
What is venous thrombosis casued by? what is hyper coagulability caused by?
blood stasis - immobilised hypercoagulability - inherited, drugs and trauma
82
Define embolism
Mass of material in vascular system moving from its site of origin to lodge in vessels in a distant site
83
When is a DVT most likely to occur?
Post op, bed bound, travel, oedema, pain
84
# Define infarction Why is reperfusion injury possible? How long do neurones have to live if starved of oxygen?
zonal necrosis due to a sudden occlusion of blood supply due to lack of oxygen and nutrient supply reperfusion injury possible due to formation of free radicals neurones in brain die if starved of oxygen for longer than 3 mins
85
``` What is: neo-adjuvant treatment? adjuvant treatment palliative treatment radical treatment ```
Neo-adjuvant treatment is given before surgery to shrink the tumour for surgical removal. Adjuvant treatment is given after surgery, aimed at reducing the risk of recurrence. Palliative treatment is non- curative and simply aims to improve symptoms and quality of life. Radical treatment is intended to be curative.
86
What are proto-oncogenes and when do they change in cancer?
Proto-oncogenes are normal genes that stimulate cell division. In cancer, these proto-oncogenes are changed to oncogenes which enable uncontrolled cell proliferation. .
87
What are tumour suppressor genes? When can cancer develop in accordance to these?
Tumour suppressor genes are normal genes that inhibit cell division - loss of both copies of a tumour suppressor gene can allow cancer to develop
88
What are telomeres? - what happens when cancer is present?
Telomeres are repeats in genetic code in normal cells that mean they can only divide a certain number of times as each time they divide telomere repeats decrease. In cancer there is often a mutation that reactivates telomerase resulting in cells gaining unlimited replicative potential.
89
What are psammamoma bodies? If these are found what is the most likely cause?
collections of calcium | found in biopsy samples of mesothelioma,
90
What types of HPV virus causes cervical cancer?
types 16 and 18
91
What is protective against breast cancer ?
Breastfeeding
92
Where is cardiac muscle nuclei found?
In the centre of the fibre
93
What is a carcinoma?
Malignant epithelial neoplasm
94
Sarcoma?
Malignant neoplasms of connective tissue
95
Glandular neoplasms?
adenocarcinomas - malignant Adeomas - benign
96
Squamous cell carcinoma Benign squamous cell neoplasm?
malignant neoplasms of squamous cell papilloma = benign
97
What are the three growth receptors?
rectors with intrinsic tyrosine kinase activity 7 transmembrane G protein coupled receptors receptors without intrinsic tyrosine kinase activity
98
What is each step in the cell cycle controlled by?
cyclin dependant kinases that activate each other
99
When is retinoblastoma important?
Normal cell growth and in malignancy
100
Why is P53 important?
Check for mistakes, mistakes are found then cell cycle is paused, repair attempted
101
What are telomeres?
Chromosomes are capped - provides protection and stops chromosome ends from degrading
102
Does hyperplasia need a stimulus?
yes it needs to be in response of something results in increased organ volume
103
Why is PDL1 important?
inhibits T-cell proliferation which can switch off immune system so is targeted for cancer treatment
104
What is Myc?
Myc is a nuclear transcription factor that promotes growth – DNA replication etc. Common in lymphoma, neuroblastoma, small call carcinoma of lung

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