Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PRINCIPLES > Pathology > Flashcards

Pathology Flashcards

(80 cards)

Start Studying
1
Q

What does VINDICATE(M) stand for?

A

Vascular, inflammatory, neoplasia, drugs, iatrogenic, congenital, autoimmune, trauma, endocrine, (metabolic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What aspect of health does VINDICATE not take into account?

A

Psychiatry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Immediately after the invasion by a pathogen, which two immune signals are released?

A

Cytokines and histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the purpose of cytokines?

A

To regulate inflammation by recruiting other cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the purpose of histamine?

A

Causes vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which two proteins are involved in white cell margination?

A

Integrins and selectins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe briefly ‘white cell rolling’.

A

Weak bonds formed with selectins, which break and reform regularly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the term for when a white cell moves across the membrane?

A

Diapedesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Leaky vessels mean more white cells are transferred across the membrane. Which factors can cause this?

A

Trauma, chemical burns, change in osmotic gradient, loss of vascular protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a chemotaxi?

A

Immune cells following a chemical gradient to reach inflammatory site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the three stages of phagocytosis?

A

Recognition, engulfment, degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which things can help a phagocyte recognise bacteria?

A

Mannose receptors, opsonins, coatings, and immunoglobulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which two structures are formed by phagocytes during engulfment?

A

Pseudopod, vesicle -> phagolysosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which chemical degrades pathogens within phagocytes?

A

Reactive oxygen/nitrogen species - I.e. NAPDH oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is meant by rubor, calor, tumour, and dolor?

A

Redness, heat, swelling, pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which words can be used for redness, heat, swelling, and pain?

A

Rubor, calor, tumour, dolor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which immune components can cause dolor (pain)?

A

Bradykinins, prostaglandins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which immune cell characterises inflammation?

A

The neutrophil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Once a monocyte reaches the site of inflammation, what is it then called?

A

A macrophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Inflammation can ‘end’ in four main ways. What are these?

A

Resolution, suppuration, organisation repair and fibrosis, and chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which factors contribute to 1. resolution of inflammation?

A

Good vascular supply and quick removal of immune agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which factors contribute to 2. suppuration?

A

A walled off area (i.e. empyema) with no blood supply. Requires surgery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is suppuration?

A

Pus filled fluid, or abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

During 3. fibrosis, what happens?

A

Scarring, necrosis, buildup of fibrin, and a collagen/smooth muscle plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Chronic inflammation is NOT related to time/severity. What is the marker of 4. chronic inflammation?
The lymphocyte.
26
Before the lymphocyte is recruited in 4. chronic inflammation, which immune cells are utilised?
Neutrophil 'shock troops', macrophage 'tanks'
27
Define the granuloma.
Aggregate of epitheliod histiocytes.
28
Describe why calcium buildup is bad in myocardial infarct.
Stimulates caspase proteins, like ATPase, phospholipase, protease, nuclease, and mitochondrial permeability.
29
After what time period will thrombolytic drugs not work on MI?
30 minutes.
30
Describe the early resolution of MI in terms of cells.
Always pathological. Pyknosis (cell shrinking), complement cascade, and neutrophils.
31
After the inital 'mopping up' of cells in MI by neutrophils, what occurs?
Neutrophils replaced by macrophages, which are replaced by fibroblasts, which lay down collagen
32
What is hypertrophy?
Increase in cell size
33
What is atrophy?
Decrease in cell size
34
What is metaplasia?
Change in cell type
35
What is hyperplasia?
Increase in number of cells
36
What is dysplasia?
Decrease in number of cells.
37
What is the main difference between necrosis and apoptosis?
Necrosis is ALWAYS pathological, apoptosis can be physiological
38
What are the three main types of necrosis?
Coagulative, liquefactive, caseous
39
When can apoptosis be physiological?
Removing autoimmune cells, for growth (i.e. making foramen)
40
When is apoptosis typically pathological?
Radiation, chemotherapy, hepatitis, cancer, grafts
41
Describe the intrinsic method of apoptosis.
Growth factors -> Bak/Bax -> increased mitochondrial permeability -> capase cascade
42
Describe the extrinsic method of apoptosis.
FAS-ligand binds to death domain (FAS) and activates TRADD and FADD.
43
Which is the main death protein in intrinsic apoptosis?
Cytochrome C
44
What are the four main stages of the cell cycle?
G1, S, G2, M
45
Where do the checkpoints of the cell cycle occur? What are they assessing for?
G1 - growth and proteins, G2 - correct duplication of DNA (p53), M - anaphase, ensuring correct attachment
46
Which cyclins are released during each stage of the cell cycle? Note - at the G1 checkpoint there are unique cyclins.
G1 - CD4, CD6. G1c - CE, CDK2. S - CA, CDK1. M - CB. CDK1.
47
Describe how the threshold for progression through G1 (not G0) is reached.
CD4, CD6 bind to E2F/Rb, which dissociates E2F and Rb. E2F is then free to bind to DNA and produce protein
48
Which telomere provides terminal differentiation?
TTAGGG
49
What is the Hayflick Limit's value?
50-70 replications
50
Describe neoplasia.
A new growth which can occur anywhere, except the lens of the eye. Can be benign, premalignant, or malignant. Not equivalent to cancer.
51
Describe the difference between hyperplasia and dysplasia, in terms of cancer risk.
Hyperplasia 'looks normal'. Dysplasia looks abnormal and disordered, and is pre-cancer.
52
How may inherited predisposition increase risk of cancer?
Affects the cell cycle in some way, for example a mutation in the gene that produces Rb
53
Describe the two hit hypothesis.
A mutation is required in both alleles of tumour supressor genes.
54
How can virus lead to cancer?
Removal of cell cycle components, like E2F and Rb
55
Describe specifically how HPV can cause anal and penile cancer.
E6 gene destroys p53, and E7 stops Rb
56
Which two viruses most predispose to cancer?
HPV, EBV
57
Which lifestyle activity predisposes most to cancer and why?
Smoking. Initiators and promoters of genes present. Over 40 carcinogens.
58
How may chronic inflammation lead to cancer?
Over production of lymphocytes, which can lead to errors in production, making lymphomas.
59
Describe how obesity may predispose to cancer.
Hyperplasia steroids are mimicked by cholesterol. Affects the mTOR pathway of the cell cycle.
60
What is the most important thing about obesity in relation to cancer?
Distribution - all around the midriff is more risky
61
There are eight Weinberg Hallmarks of Cancer. What are they?
Activating invasion and metastasis, evasion of the immune system, disordered repair mechanisms, angiogenesis, avoiding apoptosis, unlimited replication potential, loss of suppression, sustained growth signals
62
What are oncogenes?
Genes that accelerate cancer. They bypass prevention mechanisms.
63
What are tumour supressors?
Genes that 'brake' cancer.
64
Which DNA repair mechanism, if faulty, can lead to cancer?
Mismatch repair complex
65
How may a mutation in the gene B-raf cause cancer?
Removes need for phosphorylation - i.e. sustained growth signal.
66
How may a mutation in the gene HER2 cause cancer?
Produces too many receptors - sustained growth signal
67
Describe the genesis of the Philadelphia chromosome.
Translocation of genes causes a hyperactive fusion protein - a sustained growth signal.
68
What is the difference in appearance of benign and malignant tumours?
Benign - structured and ordered, slow growth. Malignant - irregular, infiltrative and destructive.
69
What are the three hallmarks of malignant tumours when looking at a biopsy?
High N/C ratio, hyperchromasia, pleomorphism
70
Which pathological tools can be used to help diagnose a cancer?
Morphology, genetics, staging and grading (tumour/cells)
71
Describe why cancer metabolism causes cachexia.
Rapid energy consumption which increases basal metabolic rate.
72
Why is there no such thing as a benign brain tumour?
No space for the tumour to go. Affects HR and RR. Causes pressure and seizures.
73
Why is a tumour of the pancreas or ovary generally less dangerous? When may this change?
Plenty of space to grow. When the tumour presses on i.e. the ovary.
74
Which three anatomical places may a tumour directly invade which will cause significant problems?
Nerves (loss of function), blood vessels (haemorrhage), bone marrow (loss of folate, WBCs, anaemia)
75
What is paraneoplasty?
When hormones from the tumour travel and affect secondary structures.
76
Why may infection be particularly dangerous in cancer patients?
Immunosuppression - cancer 'distracts' immune system
77
How may metastasis cause arrhythmia?
Affects bone growth, and calcium release
78
How may hypermethylation of DNA cause cancer?
It may block tumour supressors
79
How may hypomethylation of DNA cause cancer?
May activate oncogenes
80
Which results may cancer testing yield?
+/-/variant of unknown significance.

PRINCIPLES (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions