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PRINCIPLES > Pathology > Flashcards

Pathology Flashcards

1
Q

What does VINDICATE(M) stand for?

A

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

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2
Q

What aspect of health does VINDICATE not take into account?

A

Psychiatry

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3
Q

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

A

Cytokines and histamine

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4
Q

What is the purpose of cytokines?

A

To regulate inflammation by recruiting other cells

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5
Q

What is the purpose of histamine?

A

Causes vasodilation

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6
Q

Which two proteins are involved in white cell margination?

A

Integrins and selectins

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7
Q

Describe briefly ‘white cell rolling’.

A

Weak bonds formed with selectins, which break and reform regularly

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8
Q

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

A

Diapedesis

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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

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10
Q

What is a chemotaxi?

A

Immune cells following a chemical gradient to reach inflammatory site

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11
Q

What are the three stages of phagocytosis?

A

Recognition, engulfment, degradation

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12
Q

Which things can help a phagocyte recognise bacteria?

A

Mannose receptors, opsonins, coatings, and immunoglobulins

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13
Q

Which two structures are formed by phagocytes during engulfment?

A

Pseudopod, vesicle -> phagolysosome

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14
Q

Which chemical degrades pathogens within phagocytes?

A

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

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15
Q

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

A

Redness, heat, swelling, pain.

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16
Q

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

A

Rubor, calor, tumour, dolor

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17
Q

Which immune components can cause dolor (pain)?

A

Bradykinins, prostaglandins.

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18
Q

Which immune cell characterises inflammation?

A

The neutrophil

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19
Q

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

A

A macrophage

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20
Q

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

A

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

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21
Q

Which factors contribute to 1. resolution of inflammation?

A

Good vascular supply and quick removal of immune agents

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22
Q

Which factors contribute to 2. suppuration?

A

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

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23
Q

What is suppuration?

A

Pus filled fluid, or abscess

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24
Q

During 3. fibrosis, what happens?

A

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

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25
Q

Chronic inflammation is NOT related to time/severity. What is the marker of 4. chronic inflammation?

A

The lymphocyte.

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26
Q

Before the lymphocyte is recruited in 4. chronic inflammation, which immune cells are utilised?

A

Neutrophil ‘shock troops’, macrophage ‘tanks’

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27
Q

Define the granuloma.

A

Aggregate of epitheliod histiocytes.

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28
Q

Describe why calcium buildup is bad in myocardial infarct.

A

Stimulates caspase proteins, like ATPase, phospholipase, protease, nuclease, and mitochondrial permeability.

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29
Q

After what time period will thrombolytic drugs not work on MI?

A

30 minutes.

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30
Q

Describe the early resolution of MI in terms of cells.

A

Always pathological. Pyknosis (cell shrinking), complement cascade, and neutrophils.

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31
Q

After the inital ‘mopping up’ of cells in MI by neutrophils, what occurs?

A

Neutrophils replaced by macrophages, which are replaced by fibroblasts, which lay down collagen

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32
Q

What is hypertrophy?

A

Increase in cell size

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33
Q

What is atrophy?

A

Decrease in cell size

34
Q

What is metaplasia?

A

Change in cell type

35
Q

What is hyperplasia?

A

Increase in number of cells

36
Q

What is dysplasia?

A

Decrease in number of cells.

37
Q

What is the main difference between necrosis and apoptosis?

A

Necrosis is ALWAYS pathological, apoptosis can be physiological

38
Q

What are the three main types of necrosis?

A

Coagulative, liquefactive, caseous

39
Q

When can apoptosis be physiological?

A

Removing autoimmune cells, for growth (i.e. making foramen)

40
Q

When is apoptosis typically pathological?

A

Radiation, chemotherapy, hepatitis, cancer, grafts

41
Q

Describe the intrinsic method of apoptosis.

A

Growth factors -> Bak/Bax -> increased mitochondrial permeability -> capase cascade

42
Q

Describe the extrinsic method of apoptosis.

A

FAS-ligand binds to death domain (FAS) and activates TRADD and FADD.

43
Q

Which is the main death protein in intrinsic apoptosis?

A

Cytochrome C

44
Q

What are the four main stages of the cell cycle?

A

G1, S, G2, M

45
Q

Where do the checkpoints of the cell cycle occur? What are they assessing for?

A

G1 - growth and proteins, G2 - correct duplication of DNA (p53), M - anaphase, ensuring correct attachment

46
Q

Which cyclins are released during each stage of the cell cycle? Note - at the G1 checkpoint there are unique cyclins.

A

G1 - CD4, CD6. G1c - CE, CDK2. S - CA, CDK1. M - CB. CDK1.

47
Q

Describe how the threshold for progression through G1 (not G0) is reached.

A

CD4, CD6 bind to E2F/Rb, which dissociates E2F and Rb. E2F is then free to bind to DNA and produce protein

48
Q

Which telomere provides terminal differentiation?

A

TTAGGG

49
Q

What is the Hayflick Limit’s value?

A

50-70 replications

50
Q

Describe neoplasia.

A

A new growth which can occur anywhere, except the lens of the eye. Can be benign, premalignant, or malignant. Not equivalent to cancer.

51
Q

Describe the difference between hyperplasia and dysplasia, in terms of cancer risk.

A

Hyperplasia ‘looks normal’. Dysplasia looks abnormal and disordered, and is pre-cancer.

52
Q

How may inherited predisposition increase risk of cancer?

A

Affects the cell cycle in some way, for example a mutation in the gene that produces Rb

53
Q

Describe the two hit hypothesis.

A

A mutation is required in both alleles of tumour supressor genes.

54
Q

How can virus lead to cancer?

A

Removal of cell cycle components, like E2F and Rb

55
Q

Describe specifically how HPV can cause anal and penile cancer.

A

E6 gene destroys p53, and E7 stops Rb

56
Q

Which two viruses most predispose to cancer?

A

HPV, EBV

57
Q

Which lifestyle activity predisposes most to cancer and why?

A

Smoking. Initiators and promoters of genes present. Over 40 carcinogens.

58
Q

How may chronic inflammation lead to cancer?

A

Over production of lymphocytes, which can lead to errors in production, making lymphomas.

59
Q

Describe how obesity may predispose to cancer.

A

Hyperplasia steroids are mimicked by cholesterol. Affects the mTOR pathway of the cell cycle.

60
Q

What is the most important thing about obesity in relation to cancer?

A

Distribution - all around the midriff is more risky

61
Q

There are eight Weinberg Hallmarks of Cancer. What are they?

A

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
Q

What are oncogenes?

A

Genes that accelerate cancer. They bypass prevention mechanisms.

63
Q

What are tumour supressors?

A

Genes that ‘brake’ cancer.

64
Q

Which DNA repair mechanism, if faulty, can lead to cancer?

A

Mismatch repair complex

65
Q

How may a mutation in the gene B-raf cause cancer?

A

Removes need for phosphorylation - i.e. sustained growth signal.

66
Q

How may a mutation in the gene HER2 cause cancer?

A

Produces too many receptors - sustained growth signal

67
Q

Describe the genesis of the Philadelphia chromosome.

A

Translocation of genes causes a hyperactive fusion protein - a sustained growth signal.

68
Q

What is the difference in appearance of benign and malignant tumours?

A

Benign - structured and ordered, slow growth. Malignant - irregular, infiltrative and destructive.

69
Q

What are the three hallmarks of malignant tumours when looking at a biopsy?

A

High N/C ratio, hyperchromasia, pleomorphism

70
Q

Which pathological tools can be used to help diagnose a cancer?

A

Morphology, genetics, staging and grading (tumour/cells)

71
Q

Describe why cancer metabolism causes cachexia.

A

Rapid energy consumption which increases basal metabolic rate.

72
Q

Why is there no such thing as a benign brain tumour?

A

No space for the tumour to go. Affects HR and RR. Causes pressure and seizures.

73
Q

Why is a tumour of the pancreas or ovary generally less dangerous? When may this change?

A

Plenty of space to grow. When the tumour presses on i.e. the ovary.

74
Q

Which three anatomical places may a tumour directly invade which will cause significant problems?

A

Nerves (loss of function), blood vessels (haemorrhage), bone marrow (loss of folate, WBCs, anaemia)

75
Q

What is paraneoplasty?

A

When hormones from the tumour travel and affect secondary structures.

76
Q

Why may infection be particularly dangerous in cancer patients?

A

Immunosuppression - cancer ‘distracts’ immune system

77
Q

How may metastasis cause arrhythmia?

A

Affects bone growth, and calcium release

78
Q

How may hypermethylation of DNA cause cancer?

A

It may block tumour supressors

79
Q

How may hypomethylation of DNA cause cancer?

A

May activate oncogenes

80
Q

Which results may cancer testing yield?

A

+/-/variant of unknown significance.

PRINCIPLES (10 decks)

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