Pathology Flashcards

(41 cards)

1
Q

homeostasis

A

stable state closely maintained

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2
Q

hypertrophy

A

cells get bigger

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3
Q

hyperplasia

A

more cells

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4
Q

atrophy and the mechansim

A

tissues waste away

via protein degradation

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5
Q

metaplasia

A

abnormal change in the nature of a tissue

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6
Q

what can influence more cell division?

A

inc groth factors

inc growth factor receptors

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7
Q

categories of growth hormone receptor

A

transmembrane G protein coupled receptor
receptors with intrinsic tyrosine kinase receptors
receptors without intrinsic tyrosine kinase receptors

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8
Q

what regulates each stage of the cell cycle

A

cyclin dependent kinase

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9
Q

what cells enter Go and why

A

neurons rbc

because fully differentiated and do not divide

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10
Q

p53

A

checks for DNA faults and induces apoptosis if faults

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11
Q

telomere

A

cap at the end of a chromosome to protect, prevent degradation and prevent fusion

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12
Q

what can cause pathological hyperplasia

A

excess oestrogen

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13
Q

why would a lymph node undergo hyperplasia?

A

infection

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14
Q

what causes inflammation

A

INJURY by

  • trauma
  • foreign bodies
  • immune reactions
  • necrosis
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15
Q

vascular changes to injury

A

vasodilation
mediated by histamine and NO
inc heat and redness

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16
Q

cellular changes to injury

A

stasis
white cell margination
migration

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17
Q

integral membrane proteins involved in attaching to white cells

18
Q

white cells

19
Q

what increases expression of selectins and where do they come from?

A

histamine and thrombin from inflammatory cells

20
Q

what increases endothelial expression of VCAM and ICAM

A

tumour necrosis factor and interleukin 1

21
Q

phagocytosis

A

ingestion of bacteria by a phagocyte

22
Q

3 stages of phagocytosis

A

recognition and attachment
engulfment:
killing and degradation

23
Q

receptors involved in recognition and attachment

A

mammose receptors
scavenger receptors: recognise low density lipoprotein
opsonins: bind to microorganisms making them more susceptible to phagocytosis

24
Q

how is the bacteria englufed

A

phagosome: a vacuole is formed with the phagocytosed particle in it
phagolysosome: phagosome fuses with a lysosome to release digestive enzymes

25
killing and degradation
reactive oxygen and nitrogen species
26
calor
heat
27
dolor
pain
28
rubor
redness
29
tumor
swelling
30
functiono laesa
loss of function
31
the main cell of acute inflammation
neutrophil
32
neutophils
most abundant white blood cell
33
suppuration
pus formation
34
resolution
complete restoration of the tissue to normal after removal of the inflammatory components depends on tissues repair mechainsms: gi tract reguarly replaces endothelium but CNS cannot regernerate
35
organisation
Mucosa where damage goes beyond the basement membrane favours healing by organisation and repair and not resolution Erosions and abrasions describe injury with basement membrane intact.
36
granulation tissue
new connective tissue and microscopic blood vessels that form on the surface of a wound during healing deposits collagen and smooth muscle cells
37
scarring
loss of function in heart: doesnt contract well in skin: v tight in liver: small regenerative capacity but if overwhelmed cant filter toxins
38
chronic inflammaion
persists if: - suppration - autoimmune eg organ rejection - foreign body - infectious agent e.g virus
39
granuloma
mass of granulation tissue
40
granulomatous inflammation
collection of macrophages
41
causes of granulomatous inflammatin
keratin talcum powder foreign bodies