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► Med Misc 39 > *Pathology 1 - Lectures 1, 2 and 3 > Flashcards

*Pathology 1 - Lectures 1, 2 and 3 Flashcards

1
Q

What are all diseases caused by a problem with one of?

A 
Vascular
Infection/ inflammatory
Neoplastic
Drugs/ toxins
Intervention/ Iatrogenic
Congenital/ development
Autoimmune
Trauma
Endocrine/ metbaolism
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2
Q

What chemical is used to fix and preserve biological specimens when the first arrive at the lab?

A

Formalin (formaldehyde)- then dehydrated and prepared for histology by paraffin

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3
Q

What must occur before the paraffin can be added to specimens?

A

Must be dehydrated

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4
Q

What histological stains are used to look at specimens? - colour of these

A

Eosin (red)

Haematoxylin (blue)

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5
Q

Why do environmental changes result in changes at the organ and cellular level?

A

To adapt and help maintain homeostasis (alterations can become abnormal = pathological)

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6
Q

What cellular changes can increased demand lead to?

A

Hyperplasia

Hypertrophy

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7
Q

What cellular change can decreased demand lead to?

A

Atrophy

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8
Q

What cellular change can altered demand lead to?

A

Metaplasia

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9
Q

What is hyperplasia?

A

Increase in cell number

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10
Q

What is hyperplasia due to?

A

Always due to an external stimulus (will regress on withdrawal of the stimulus)

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11
Q

Is hyperplasia physiological and/or pathological

A

Can be physiological or pathological

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12
Q

Give 2 examples of hyperplasia?

A

Changes in breast tissue at puberty
Hyperplasia of endometrial lining at pregnancy
(both stimulated by hormones)

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13
Q

What type of hyperplasia occurs due to loss of tissue?

A

Compensatory (reactive) hyperplasia e.g. in liver and bone marrow (if bleeding a lot)

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14
Q

What are the mechanism behind hyperplasia? (3)

A

Production of increased growth factors
Increased growth factor receptors
Switch on of genes encoding cell cycle regulators to promote new cell growth

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15
Q

Pathological hyperplasia examples caused by hormones?

A

Excess oestrogen leads to endometrial hyperplasia and abnormal menstrual bleeding (often post-menopausal)
Hormonally induced prostatic hyperplasia in response to androgens

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16
Q

Pathological hyperplasia example caused by infection?

A

Lymph nodes become hyper plastic in response to an infection

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17
Q

What happens when the stimulus causing hyperplasia is withdrawn?

A

The hyperplasia will regress (cancer keeps growing in the absence of a stimulus)

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18
Q

Is hyperplastic tissue at risk of developing cancer?

A

Yes e.g. endometrial cancer is much more common in obese individuals

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19
Q

What is hypertrophy?

A

Increase in cell size

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20
Q

What 2 cellular changes often occur together?

A

Hyperplasia and hypertrophy

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21
Q

In what type of cells does hyperplasia normally occur in isolation in?

A

Non-dividing cells e.g. cardiac myocytes and skeletal muscles

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22
Q

What type of stress tends to cause hypertrophy?

A

Mechanical stress

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23
Q

When does hypertrophy in the heart become pathological?

A

When the heart can no longer function and requires more blood supply, etc. that it is supplied (same principle for skeletal muscle)

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24
Q

What is atrophy?

A

Reduction in cell size

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25
Q

Is atrophy pathological and/or physiological?

A

Can be pathological or physiological

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26
Q

Examples of physiological atrophy? (2)

A 
Embryological structures (can remain = pathological)
Uterus undergoes rapid atrophy after parturition
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27
Q

Causes of pathological atrophy? (7)

A

Decreased workload e.g. cast for broken limb
Loss of innervation
Blocked blood supply
Ageing (usually in cells that have no replicating ability)
Inadequate nutrition
Loss of hormonal stimulus (e.g. post-menopausal uterus)
Pressure (e.g. can be seen in normal tissue adjacent to tumours)

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28
Q

Mechanisms of atrophy? (3)

A

Reduced cellular components

Protein degradation- “digestion” in lysosomes and degraded

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29
Q

What is the name of the pathway which leads to atrophy by digestion in lysosomes?

A

The ubiquitin proteasome pathway (principle mechanism of protein catabolism in the mammalian cytosol and nucleus

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30
Q

Example of 2 hormones that promote degradation and atrophy?

A

Gucocoritoids

Thyroid hormone

31
Q

Example of a hormone that promotes growth?

A

Insulin

32
Q

What is metaplasia?

A

Reversible change from one mature cell type to another

33
Q

What is metaplasia caused by?

A

A change in signals to stem cells causing them to differentiate down a different line

34
Q

What is metaplasia often in response to?

A

Mat be cytokines, growth factors and other chemicals in the cells microenvironment
Commonly in response to a noxious stimulus

35
Q

What do other epithelia metaplastically change to in response to injury?

A 
Squamous epithelium (covers your skin and is very resistant to a range of noxious stimuli)
Therefore lung and salivary ducts commonly change to it in response to injury e.g. smoking
36
Q

What metaplasia occurs at the bottom of the oesophagus in response to acid?
Called?

A

Squamous epithelium -> glandular epithelium

37
Q

Is metaplasia reversible?

A

Yes

38
Q

Is metaplastic tissue an at risk site for development of cancer?

A

Yes, it is sometimes associated with progression to malignancy (despite there being no squamous epithelium in the lung, lung squamous cell cancer is quite common)
(adenocarcinoma is common in the oesophagus despite there being no glandular epithelium)

39
Q

What 2 cellular adaptions increase chance of cancer?

A

Hyperplasia
Metaplasia
(not hypertrophy)

40
Q

What are the main causes of inflammation? (5)

A 
Infection
Trauma
Foreign bodies
Immune reactions
Necrosis of any cause
41
Q

What 4 factors does the response to injury involve?

A

Vascular changes
Cellular changes
Chemical mediators
Morphological patterns

42
Q

What are the vascular changes involved in the formation of inflammation due to tissue injury? - 2 main groups and explanation

A

Changes in flow and vessel caliber:
Initially vasoconstriction
Followed by vasodilation
Results in increased heat (callor) and increased redness (rubor)
As well as increased blood flow, there is a gradual slowing of circulation through inflamed tissue
Changes in vascular permeability:
Endothelium becomes more permeable to plasma proteins (leaky vessels = loss of proteins)
Changes in osmotic pressure as water follow protein = swelling

43
Q

In vasodilation during inflammation, does the capillary beds or arterioles vasodilator first?

A

Arterioles

44
Q

What mediates vasodilation of blood vessels during inflammation? (2)

A

Histamine

Nitric Oxide

45
Q

Why do vessels become more leaky? (5)

A

Endothelial contraction in response to inflammatory mediators
Direct injury (e.g. toxins, burns)
Leukocyte-mediated injury (through release of cytotoxic agents)
Transcytosis
New vessel formation

46
Q

What inflammatory mediators cause the vessels to become leaky due to endothelial contraction? (4)

A

Histamine
Bradykinin
Substance P
Leukotrienes

47
Q

What is transcytosis?

What is it mediated by?

A

Transcellular transport

VEGF (vascular endothelial growth factor)

48
Q

How does new vessel formation cause vessels to become leaky?

A

Due to VEGF which makes new cells but also causes leakiness

49
Q

What cellular changes (broad) lead to inflammation?

A 
Stasis (slowing down)
White cell margination
Rolling
Adhesions
Migration
50
Q

What is white cell margination and rolling?

A

As the rate of blood flow decreases, cells are able to move to the peripherally (especially WBCs)
The WBCs roll along the surface and become increasingly adherent to the endothelial wall

51
Q

What causes rolling?

A

Due to expression of various proteins on the lumenal surface that have matching protein on white cell surface:

52
Q

What are the specific molecules expressed on the endothelial surface that cause rolling? (3)

A

Selectins
Vascular cell adhesion molecules (VCAM)
Intercellular cell adhesion molecules (ICAM)

53
Q

What are expressed on the leukocyte wall that allow them to bind to the epithelium during rolling? (2)

A

Integrins

Selectins

54
Q

Why is binding fast during rolling?

A

The integrin/selectin interaction is of low affinity

55
Q

What inflammatory cells increase selection expression? (2)

A

Histamine

Thrombin

56
Q

What inflammatory cells increase endothelial cell expression of VCAM and ICAM?

A

TNF

Interleukin-1

57
Q

What do chemokines from the site of injury do in terms of adhesion?

A

They bind to proteoglycans on the endothelial cell surface

These proteoglycans then increase affinity of ICAMSs and VCAMs for integrins making them more likely to stick

58
Q

What happens after the leukocytes attach to the endothelium?

A

Leukocytes pass through adjacent endothelial cells and exit from the circulation

59
Q

How do leukocytes which have exited the circulation migrate towards the site of injury?

A

By chemotaxis (cells follow a chemical gradient and move along it)

60
Q

What 3 important molecules act as chemotaxins in the inflammatory process?

A

Complement
Leukotrienes
Interleukins (cytokines)

61
Q

What are the 3 phases of phagocytosis?

A

Recognition and attachment
Engulfment
Killing and degradation

62
Q

What do bacterial surface glycoproteins and glycolipids have on them that makes them recognised by macrophages?
What is used to recognise them?

A 
Mannose residue (no present on mammalian cells)
Mannose receptors
63
Q

What is another type of receptor involved in recognition and attachment during phagocytosis?

A

Scavenger receptors

64
Q

What can be added to an antigen to mark it for an immune response?
What is an example of an opsonin?

A

An opsonin

IgG

65
Q

During phagocytosis, what are the names of the temporary projections of the cytoplasm that captures prey?

A

Pseudopods

66
Q

Name of vesicle formation within a phagocyte?

Name when the vesicle joins with lysosome?

A

Phagosome

Phagolysosome

67
Q

What are the 2 options for killing of bacteria by a phagocyte?

A

Oxygen dependant

Oxygen indépendant

68
Q

Oxygen dependant killing of bacteria?

A

NADPH oxidase causes oxygen to gain an electron from NADPH = superoxide (O2-) which can be converted to hydrogen peroxide

69
Q

Oxygen indépendant killing of bacteria by a phagocyte?

A

Nitric oxide synthase can combine NO with superoxide to form ONOO (peroxynitrite) (many other cytotoxic granules)

70
Q

What are 5 clinical features of inflammation?

A 
Rubor (redness)
Calor (heat)
Tumor (swelling)
Dolor (painfull)
Loss of function
71
Q

What causes rubor, calor and tumor?

A

Increased perfusion, slow flow and increased permeability

72
Q

What cause dolor?

A

Prostoglandins and bradykinin

73
Q

What is the inflammatory cell that characterises acute inflammation?
Other names? (2)
Characteristic features?

A 
Neutrophils
Polymorph
Granulocyte
Many lobes to nucleus
Phagocytic and cytotoxic abilities

► Med Misc 39 (38 decks)

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