Pathology Flashcards

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

A

ICAM VCAM`

18
Q

white cells

A

leukocytes

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
Q

killing and degradation

A

reactive oxygen and nitrogen species

26
Q

calor

A

heat

27
Q

dolor

A

pain

28
Q

rubor

A

redness

29
Q

tumor

A

swelling

30
Q

functiono laesa

A

loss of function

31
Q

the main cell of acute inflammation

A

neutrophil

32
Q

neutophils

A

most abundant white blood cell

33
Q

suppuration

A

pus formation

34
Q

resolution

A

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
Q

organisation

A

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
Q

granulation tissue

A

new connective tissue and microscopic blood vessels that form on the surface of a wound during healing
deposits collagen and smooth muscle cells

37
Q

scarring

A

loss of function
in heart: doesnt contract well
in skin: v tight
in liver: small regenerative capacity but if overwhelmed cant filter toxins

38
Q

chronic inflammaion

A

persists if:

  • suppration
  • autoimmune eg organ rejection
  • foreign body
  • infectious agent e.g virus
39
Q

granuloma

A

mass of granulation tissue

40
Q

granulomatous inflammation

A

collection of macrophages

41
Q

causes of granulomatous inflammatin

A

keratin
talcum powder
foreign bodies