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Principles 2018 > Pathology > Flashcards

Pathology Flashcards

1
Q

What does VINDICATE stand for?

A 
V – Vascular
I – Infectious/inflammatory
N – Neoplastic
D – Drugs/toxins
I – Intervention/iatrogenic
C – Congenital/developmental
A – Autoimmune
T – Trauma
E – Endocrine/metabolic
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2
Q

What is an example of vascular pathology?

A

Blood vessels- inflammation, clot, blockage

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3
Q

what is neoplasia?

A

New growth

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4
Q

What is iatrogenic?

A

Caused by doctor

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5
Q

Describe adaptation?

A

Increased demand- hyperplasia, hypertrophy

Decreased demand-atrophy

Altered stimulus- metaplasia

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6
Q

What is hyperplasia?

A

Increase in cell number

-response to external stimulus

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7
Q

What does hyperplasia result in?

A

Will regress on withdrawal of stimulus

Increased organ volume

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8
Q

Describe hormonal hyperplasia?

A

Puberty- breast tissue

Pregnancy- hyperplasia of lining of uterus

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9
Q

When does compensatory hyperplasia occur?

A

After loss of tissue

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10
Q

Where does compensatory hyperplasia occur?

A

Liver

Bone Marrow

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11
Q

Describe the mechanism of hyperplasia?

A

Production of increased growth factors- locally or from distant site. Hormone may be a growth factor itself.

Increased growth factor receptors

Switch on genes encoding growth factors and cell cycle regulators to promote new cell growth.

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12
Q

Describe hormonally induced pathological hyperplasia?

A

Excess oestrogen- endometrial hyperplasia and abnormal bleeding

Prostatic hyperplasia in response to androgens

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13
Q

What happens in lymph nodes as a result of infection?

A

Hyperplasia

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14
Q

Is hyperplasia reversible?

A

Yes, reverse on withdrawal of stimulus

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15
Q

What is the risk of hyper plastic tissue?

A

Risk site for development of cancer

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16
Q

What is hypertrophy?

A

increase in cell size

Not cell number

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17
Q

When does hypertrophy occur?

A

In conjunction with hyperplasia

In isolation in non-dividing cells e.g. cardiac myocytes, skeletal muscle

In response to mechanical stress

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18
Q

When does hypertrophy of cardiac myocytes become pathological?

A

When heart can no longer function and requires more than is supplied

Muscle becomes less functional

Results in HF

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19
Q

What is atrophy?

A

Reduction in cell size

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20
Q

What are examples of physiological atrophy?

A

Embryological structures

Uterus after parturition

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21
Q

What can pathological atrophy be a result of?

A

Decreased workload

Malnutrition

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22
Q

Describe pathological atrophy?

A

Loss of inervation

Loss of function after nerve supply is removed

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23
Q

What causes atrophy in the brain?

A

Blocked blood supply

In association with atherosclerosis

Ageing (also in heart)

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24
Q

What causes atrophy of the kidneys?

A

Pressure

Due to endogenous or exogenous structures

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25
Q

Describe the mechanism of atrophy?

A

Reduced cellular components

Protein degradation

Digested in lysosomes and degraded in many cases by ubiquitin proteasome pathway

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26
Q

Which hormones promote atrophy?

A

Glucocorticoids

Thyroid hormone

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27
Q

Which hormones oppose atrophy

A

Insulin

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28
Q

Define metaplasia

A

Reversible change from one mature cell type to another

29
Q

What does metaplasia represent

A

Change in signals delivered to stem cells causing them to differentiate down a different line

30
Q

What is metaplasia in response to?

A

Cytokines (chemical messengers, growth factors and other chemicals in the cells microenvironment)

Noxious stimuli

31
Q

What is squamous metaplasia a result of?

A

Response to injury

32
Q

what is the risk of metaplasia?

A

Metaplastic site is at risk for cancer development

33
Q

Which metaplasia cancer is common in the lung?

A

Squamous cell

34
Q

Which metaplastic cancer is common in the oesophagus?

A

Adenocarcinoma (glands)

35
Q

What does stress on cells cause?

A

Adaptation

36
Q

What are the causes of inflammation?

A 
Infection
Trauma
Foreign bodies
Immune reaction
Necrosis
37
Q

What is the response to injury?

A

Vascular changes
Cellular changes
Chemical mediators
Morphologic patterns

38
Q

Describe vascular changes in response to injury?

A

Changes in flow and vessel caliber

Vasodilation

First involves arterioles and then capillary beds

39
Q

What mediates vascular changes?

A

Histamine

Nitric oxide

40
Q

What are the clinical manifestations of vascular changes?

A

Increased heat (calor)

Redness/erythema (rubor)

41
Q

What are the cellular changes in response to injury?

A 
Stasis
White cell margination
Rolling
Adhesions
Migration
42
Q

What are selectins?

A

Expressed on a variety of white cells and bind cell adhesion molecules (CAMs) on endothelial surface

43
Q

What are integrins?

A

Over 30 types

Bind to vessel walls, cell matrix and other cells

44
Q

What increases selectin expression?

A

Histamine and thrombin

45
Q

What increases endothelial cell expression of VCAM and ICAM?

A

TNF and interleukin 1

46
Q

What is the role of chemokines?

A

Chemokines from the site of injury bind to proteoglycans on endothelial cell surface

47
Q

What is the role of proteoglycans?

A

Increase the affinity of VCAMs and ICAMs for intergrins

48
Q

What happens in increased vascular permeability?

A

Leaky vessels- loss of protein

Change in osmotic pressure

Water follows protein- swelling (tumour)

49
Q

What causes Endothelial contraction?

A

Histamine, bradykinin, substance P, leukotrienes

50
Q

What causes leaky vessels

A 
Endothelial contraction
Direct injury
White cells
Transcytosis
New vessel formation
51
Q

What causes direct injury to vessels?

A

Toxins

Burns

52
Q

What do white cells do to vessels?

A

Self harm

53
Q

What is transcytosis mediated by?

A

VEGF

54
Q

What forms new vessels?

A

VEGF

55
Q

What is chemotaxis?

A

Cells follow a chemical gradient

56
Q

What causes chemotaxis?

A

Bacterial components

Complement

Leukotrienes

Cytokines- interleukins

57
Q

What are the three phases of phagocytosis?

A

Recognition and attatchment

Engulfment

Killing and degradation

58
Q

What is responsible for recognition and attachment?

A

Mannose receptors

(Bacterial surface glycoproteins and glycolipids contain terminal mannose residues)

Scavenger receptors

Opsonins

59
Q

What does not contain mannose receptors?

A

Mammalian glycoproteins and glycolipids do not

60
Q

What are opsonins?

A

Coating proteins making bacteria stand out

Include components of the complement cascade as well as IgG

61
Q

What vesicle is formed during engulfment?

A

Phagosome

62
Q

What is it called when a phagosome joins with lysosome?

A

Phagolysosome

63
Q

What is responsible for killing and degradation?

A

Reactive oxygen species

NADPH oxidase- oxygen gains an electron from it and becomes superoxide

Reactive nitrogen species

Nitric oxide synthase combines NO with superoxide and produces ONOO

Many other cytotoxic granules

64
Q

What are the five pillars of inflammation?

A 
Heat
Redness
Swelling
Pain
Loss of function
65
Q

Define rubor?

A

Redness

> Increased perfusion. Slow flow. Increased permeability of vessels.

66
Q

Define calor?

A

Heat

> Again – increased perfusion, slow flow rate, increased vascular permeability

67
Q

Define tumour?

A

Literal translation- swelling

Due to vascular changes

68
Q

Define Dolor?

A

Pain

Mediated by prostaglandins and bradykinin

69
Q

What are the microscopic changes in inflammation?

A 
Neutrophils
-polymorph
Many lobes to nucleus 
Granulocyte
Phagocytic and cytotoxic abilities

Principles 2018 (34 decks)

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