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Phase 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

Definition of Inflammation

A

A reaction to injury/infection that involved cells such as neutrophils and macrophages

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2
Q

Is infectious mononucleosis chronic or acute?

A

Chronic from the start

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3
Q

Characteristics of acute inflammation

A

Sudden onset, short duration and usually resolves. Cells include neutrophils.

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4
Q

Characteristics of chronic inflammation

A

Slow onset, long duration and may never be resolved. Cells include macrophages and lymphocytes

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5
Q

Neutrophil polymorphs characteristics

A

Lots of enzymes in vacuoles in cytoplasm. Can phagocytose. Short lived and first cells on scene of acute inflammation. Usually die at scene (yellow pus) and release cytokines that attract other inflammatory cells

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6
Q

Macrophage characteristics

A

Non-discript nucleus with bags of enzymes in cells. Long lived and can phagocytose. APC cells

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7
Q

Lymphocyte characteristics

A

Long lived and have immunological memory

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8
Q

What are endothelial cells coated with?

A

Nitric acid

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9
Q

What do fibroblast do?

A

Make collagen - contain ER and are long lived

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10
Q

What are granulomas?

A

Lump of macrophages surrounded by lymphocytes. Occurs in sarcoidosis, leprosy and TB

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11
Q

Definition of resolution?

A

Where damaging factor is removed, tissue is undamaged and able to regenerate eg LIVER
IT GOES AWAY

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12
Q

Definition of repair

A

Damaging factor is present but there is tissue damage this tissue cannot regenerate

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13
Q

Can pneumocystis regenerate?

A

Type 2 pneumocystis are known to produce surfactants and regenerate alveolar epithelium after injury

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14
Q

Healing by 1st intentions steps?

A

Incision, no tissue loss, fibrinogen release, edges joined by fibrin and replaced by collage (little scar tissue) - structure and functions restored

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15
Q

Healing by second intention steps?

A

Loss of tissue, gap filled with it granulomatous tissue and edges don’t come together. Fibrosis formation which leads to a big scar

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16
Q

Inadequate wound healing characteristics?

A

Por blood supply, poor nutrition, wound infection, immunosuppression, diabetes and old age

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17
Q

Excessive wound healing characteristics?

A

Hypertrophic scars due to excessive collagen, stays within wound site. Keloid scars -> excessive granulation tissue that expands beyond wound edges

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18
Q

What tissues regenerate?

A

Hepatocytes, pneumocytes, blood cells, gut cells, skin cells and oesteocytes

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19
Q

Non regenerating cells?

A

Heart cells, brain cells and spinal cord

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20
Q

types of autopsy

A

hospital

medico-legal

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21
Q

hospital autopsy %

A

<10%

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22
Q

medico-legal autopsy % and types

A

> 90%
coronial autopsy - where death is not due to unlawful actions
forensic autopsy - where death is unlawful eg, murder

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23
Q

why deaths are referred to coroner

A

when death is presumed natural (cause not known), presumed iatrogenic and presumed unnatural

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24
Q

external examination for autopsy

A

look for any ID, diseases and treatments, injuries and then perform evisceration

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25
Q

what is evisceration

A

Y shaped (from behind ears down to clavicles and then down midline incision) where al body cavities are opened and examined. Brain is also removed.

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26
Q

suppuration definition

A

pus formation eg, abscess

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27
Q

why does rubor occur in inflammation?

A

due to dilation of small blood vessels within damaged area

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28
Q

why is calor seen in inflammation?

A

hyperaemia (increased blood flow) and vascular dilation delivers warm blood to area
also systemic fever can result due to chemical mediators of inflammation

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29
Q

why is there dolor in inflammation?

A

pain from stretching and distortion of tissue due to inflammatory oedema and pus
some chemical mediators eg, bradykinin, PG and serotonin can induce pain

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30
Q

vascular changes in acute inflammation

A

pre-capillary sphincters relax and this increases blood flow through capillaries causing rubor and calor
arteriole dilate and causes increased vascular permeability (fluid exudation)

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31
Q

stages of neutrophil polymorph emigration

A

1 - margination of neutrophils
2- adhesion of neutrophils
3- neutrophil emigration
4- diapedesis

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32
Q

what does histamine do

A
  • chemical mediator in acute inflammation
  • causes vascular dilation and increases basilar permeability
  • able to have immediate affect due to it being stored in granules (mast cells)
  • histamine release is stimulated by C3a and C5a
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33
Q

what are the 4 systems of chemical mediators

A

complement, kinins, coagulation factors and fibrinolytic systems

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34
Q

what is the kinin system activated by?

A

factor XII and plasmin activate conversation of prekalilkin to kallikrenin. This then stimulates conversion of kinonogens to kinins eg, bradykinin

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35
Q

what do IL-1 and TNF alpha do?

A

causes endothelial cells, fibroblasts and epithelial cells to secrete MCP1 (chemotactic protein) to attract neutrophil polymorphs

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36
Q

which cell is present first at the sight of inflammation?

A

macrophages

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37
Q

why can acute inflammation be bad?

A
  • enzymes such as collagensases and proteases may digest normal tissue
  • inappropriate swelling
  • inappropriate inflammatory responses (hypersensitivity reactions)
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38
Q

what is organisation in acute inflammation.

A

Organisation of tissues is their replacement by granulation tissue
(tissue forming in response to injury, contains many new blood vessels (TGF beta) and, in its later stages, large numbers of fibroblasts (produces collagen and other fires) as part of the process of repair (so possible scar formation)

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39
Q

what is amyloidosis?

A

long standing chronic inflammation where there is elevated serum amyloid A protein (abnormal
protein, that builds up in organs/tissues and can eventually lead to
their failure). This is deposited in various tissues

40
Q

most common acute -> chronic inflammation

A
  • suppurative

- pus forms an abscess cavity that is deep-seated so drainage is delayed/inadequate

41
Q

main cells in chronic inflammation

A

lymphocytes, plasma cells and macrophages (multinucleate giant cells)

42
Q

what is granuloma

A

epithelium histiocytes

43
Q

epithelium histiocytes

A

have large vesicular nuclei, have plentiful eosinophilic cytoplasm, elongated, show little phagocytic activity, have ACE enzyme and this is the enzyme that is measured as a marker for systemic granulomatous diseases eg, sarcoidosis

44
Q

granulation tissue?

A

combination of capillary loops and myofibroblasts

45
Q

thrombosis definition?

A

solidification of blood contents that forms within the vascular system during life

46
Q

thrombosis v clot

A

clot is when blood coagulated outside of vascular system compared to thrombosis which is within vascular system

47
Q

why doesn’t thrombus form all the time?

A
  • laminar flow

- endothelial cells are not sticky when healthy

48
Q

what do platelets contain?

A
  • alpha granules; eg, fibrin

- dense granules; eg ADP causing aggregation

49
Q

platelet activation?

A
  • change shape and extend pseudopodia
50
Q

Virchows triangle?

A
  • three factors that can cause thrombosis

- change in vessel wall, blood flow and change in blood constituents

51
Q

thrombus formation process in arteries?

A
  • slightly raised fatty streak on intimal surface of vessel
  • plaque grows and protrudes into lumen causing turbulence in blood flow
  • turbulence results in loss of intimal cells
  • fibrin deposition and platelet clumping occurs
  • platelets is first layer of thrombus and RBC become trapped forming another layer
  • platelet derived GF (alpha granules) causes proliferation of arterial smooth muscle
  • structure protrudes more, causing more turbulence, more platelet deposition
52
Q

propagation?

A
  • thrombi grow in direction of blood flow
53
Q

venus thrombus?

A
  • most thrombi begin at valves as valves have a natural degree of turbulence
  • atheroma’s due not occur due to low BP
  • 95% occur in leg as DVT
54
Q

embolism?

A

mass of material in the vascular system able to lodge in a vessel and block its lumen

55
Q

pulmonary embolism?

A

If an embolus enters the venous system it will travel to the vena cava,
through the right side of the heart and will lodge somewhere in the
pulmonary arteries

56
Q

Ischaemia?

A

A reduction in blood flow to a tissue or part of the body caused by constriction
or blockage of the blood vessels supplying it

57
Q

Infaraction?

A 
The death (necrosis) of part or the whole of an organ that occurs when the
artery supplying it becomes obstructed
58
Q

plaque composition?

A

The fully developed plaque is a lesion with a central lipid core with a cap of fibrous tissue covered by
the arterial endothelium
- Connective tissues in the cap, mainly collagens, provide the structural strength of the plaque
and are produced by smooth muscle cells (SMCs)
- Inflammatory cells, including macrophages, T lymphocytes and
mast cells, reside in the fibrous cap - they are recruited from the arterial
endothelium or, in advanced plaques from newly formed micro vessels
present at the base of the atheroma
- They are rich in cellular lipids and cellular debris

59
Q

foam cells?

A
  • macrophages that have phagocytosed oxidised lipoproteins -

they have large amounts of cytoplasm with a foamy appearance

60
Q

how many steps is plaque formation?

A

2 step; first step is endothelial damage and 2nd step is the tissue response

61
Q

process of plaque formation?

A
  • early lesion
  • endothelial dysfunction → injury to endothelial cells (caused by LDL deposition on tunica intima and become oxidised)
  • these activated endothelial cells release chemoattractants from site of injury
  • the chemicals attracts leukocytes that accumulate and migrate to vessel wall
  • leukocytes then allow migration of monocytes and T-helper cells
  • monocyte → macrophage within the intima layer of vessel wall

intermediate lesion

  • macrophages ingest oxidised LDL then become foam cells
  • foam cells promote smooth muscle migration from tunica media to intima and proliferation of SMC
  • there is also adhesion and aggregation of platelets to vessel wall

fibrous plaques

  • SMC allows synthesis of ECM eg collagen and elastin → this hardens and forms fibrous cap
  • death of foam cells releasing lipid content → causing the plaque to grow, build pressure and rupture.
  • foam cells release IL1, IL6 and IFN gamma are key inflammatory cytokines and DNA

plaque rupture

  • plaque is still growing
  • The fibrous cap needs to be resorbed and redeposited in order to be maintained
  • If balance shifts e.g. in favour of inflammatory conditions (increased
    enzyme activity) then the cap becomes weak and the plaque ruptures
  • Basement membrane, collagen and necrotic tissue exposure as well as haemorrhage of vessel within the plaque
  • thrombosis → plaque ruptures, blood coagulation and impedes blood flow
61
Q

process of plaque formation?

A
  • early lesion
  • endothelial dysfunction → injury to endothelial cells (caused by LDL deposition on tunica intima and become oxidised)
  • these activated endothelial cells release chemoattractants from site of injury
  • the chemicals attracts leukocytes that accumulate and migrate to vessel wall
  • leukocytes then allow migration of monocytes and T-helper cells
  • monocyte → macrophage within the intima layer of vessel wall

intermediate lesion

  • macrophages ingest oxidised LDL then become foam cells
  • foam cells promote smooth muscle migration from tunica media to intima and proliferation of SMC
  • there is also adhesion and aggregation of platelets to vessel wall

fibrous plaques

  • SMC allows synthesis of ECM eg collagen and elastin → this hardens and forms fibrous cap
  • death of foam cells releasing lipid content → causing the plaque to grow, build pressure and rupture.
  • foam cells release IL1, IL6 and IFN gamma are key inflammatory cytokines and DNA

plaque rupture

  • plaque is still growing
  • The fibrous cap needs to be resorbed and redeposited in order to be maintained
  • If balance shifts e.g. in favour of inflammatory conditions (increased
    enzyme activity) then the cap becomes weak and the plaque ruptures
  • Basement membrane, collagen and necrotic tissue exposure as well as haemorrhage of vessel within the plaque
  • thrombosis → plaque ruptures, blood coagulation and impedes blood flow
62
Q

aneurysm?

A

A localised permanent dilation of part of the vascular tree

63
Q

apoptosis

A

A physiological cellular process in which a defined and programmed
sequence of intracellular events leads to the removal of a cell WITHOUT the
release of products harmful to surrounding cells

64
Q

inhibitors of apoptosis?

A

GF, ECM, sex steroids and some viral proteins

65
Q

inducers of apoptosis?

A
  • GF withdrawal, loss of matrix, glucocorticoids, free radicals, ionising radiation, DNA damage and some viruses
66
Q

pathways of apoptosis

A

2 pathways; extrinsic and intrinsic

67
Q

intrinsic pathway of apoptosis?

A
  • Uses the pro- and anti-apoptotic members of the Bcl-2 family:
    • Bcl-2 can inhibit many factors that induce apoptosis
    • Bax forms Bax-Bax dimers which enhance apoptotic stimuli
  • uses p53 which induces cell cycle arrest and initiates DNA damage but if damage is too difficult to repair p53 can induce apoptosis via pro-apoptotic bcl2 family
68
Q

extrinsic pathway of apoptosis?

A
  • ligand-binding at receptors of cell surfaces
  • eg, TNFR gene family like FAS or TNFR1
  • Ligand binding at these receptors promotes clustering of receptor
    molecules on the cell surface, and the initiation of a signal transduction cascade resulting in the activation of CASPASES (cell death enzymes)
69
Q

what are caspases?

A
  • proteases that degrade cytoskeletal framework and nuclear proteins
70
Q

necrosis?

A

Traumatic cell death which induces inflammation and repair

71
Q

hypertrophy?

A

Increase in cell size without cell division

72
Q

hyperplasia?

A

increase in cell number by mitosis

73
Q

metaplasia?

A

the change in differentiation of a cell from one fully differentiated cell type to a different fully differentiated cell type

74
Q

dysplasia?

A

Imprecise term for the morphological changes seen in cells in the progression
to becoming cancer

75
Q

telomeric shortening?

A

At the tip of each chromosome, there is a non-
coding randomly repetitive DNA sequence - this is
the telomere
- telomeric sequences are not fully copied during DNA synthesis prior to
mitosis - as a result a single-stranded tail of DNA is left at the tip of each
chromosome; this is excised and, with each cell division, the telomeres are
SHORTENED
- Eventually the telomeres are so short that DNA polymerase is unable to
engage with it and thus the cell is incapable of further replication
- Only in germ cells and in embryos are telomeres replicated by the enzyme
telomerase
- Telomere length is inherited from your FATHER

76
Q

carcinogenesis?

A

The transformation of normal cells to neoplastic cells through permanent
genetic alterations or mutations

77
Q

neoplasm?

A

A lesion resulting from the autonomous or relatively autonomous abnormal
growth of cells which persists after the initiating stimulus has been removed - a new growth

78
Q

tumours?

A

any abnormal swelling

79
Q

What factors induce angiogenesis?

A

VEGF - vascular endothelial growth factor

80
Q

ways to classify tumour?

A
  • behavioural and histogenesis
81
Q

behavioural classification?

A

benign v malignant

82
Q

benign tumour classification?

A
  • localised, slow growth, non-invasive, close resemblance to normal tissue, rare necrosis, enveloped by thin layer -> so encapsulated
83
Q

malignant tumour classification?

A

-invasive, metastasis, rapidly growing, have irregular borders, hyperchromtaic nuclei (stain darkly), increased mitotic activity and invade underlying tissue

84
Q

histogenesis classification?

A
  • specific cell or origin of a tumour
85
Q

benign epithelial cell tumour, how to name?

A

suffix -oma

86
Q

benign connective tissue and other mesenchymal tumours, how to name?

A

suffix -oma

eg, leiomyeoma - SMC tumour

87
Q

lymphoid tumour name?

A
  • only give rise to malignant neoplasma

- lymphomas or leukaemia’s

88
Q

histological grading?

A

grade 1 - well differentiated
2 - moderately
3- poorly differentiated

89
Q

papilloma?

A

benign tumour of non-glandular, non-secretory epithelium

benign

90
Q

adenoma

A

Benign tumour of glandular or secretory epithelium

benign

91
Q

carcinoma

A

Malignant tumour of epithelial cells

92
Q

adenocarcinoma

A

Malignant tumour of glandular epithelium

93
Q

intraepithelial neoplasia - carcinoma in situ

A

• Carcinoma in situ refers to an epithelial neoplasm exhibiting all the cellular features associated with malignancy, but which has not yet invaded through the epithelial basement
membrane separating it from potential routes of metastasis e.g.
blood vessels and lymphatics

94
Q

malignant connective tissue and other mesenchymal tumours, how to name

A

suffix sarcoma

eg, leiomyosarcoma - SMC

Phase 2a (12 decks)

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