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EMS - JL > 14,15,16 > Flashcards

14,15,16 Flashcards

1
Q

Risk of metastasis of skin tumours

A

low

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2
Q

Risk of metastasis of lung cancers

A

high

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3
Q

what does suffix -osis mean

A

state or conditiosn

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4
Q

what does the suffix -oid mean

A

bears resembrance to

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5
Q

what does the suffix-ectasis mean

A

-dilation

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6
Q

what does the suffix -opathy mean

A

abnormal state

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7
Q

What is involved in the maintenance of a steady cellular state

A

Preserving genetic material
Normal enzyme content
Intact membranes and TM proteins
Adqueate oxygen and substrate supply

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8
Q

What is hyperplasia

A

increased number of cells

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9
Q

what is hypertrophy

A

increased size of cells

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10
Q

physiological hyperplasia

A

increase in bone marrow cells producing RBCs at altitude

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11
Q

physiological hypertrophy

A

skeletal and heart muscle in athletes

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12
Q

pathological hypertrophy

A

left ventricular hypertrophy in systemic hypertension

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13
Q

pathological hyperplasia

A

angiogenesis in wound repair

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14
Q

patholigcal atrophy

A

loss of innervation causing muscle atrophy

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15
Q

physiological atrophy

A

organ formation in embryogenesis

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16
Q

When does atrophy in adrenal gland occur

A

when given corticosteroids

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17
Q

describe metaplasia in barretts oesophagus

A

Change from squamous to columnar glandular due to gastric reflux

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18
Q

describe metaplasia in the cervix

A

Normally squamous epithelium in vagina, columnar in cervix

At puberty the columnar cervical epithelium is pushed into the vagina –> changes to columnar due to the acid

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19
Q

Hypoxia/anoxia cell injury

A

Cuaed due to ischaemia

reperfusion can generate oxygen free radicals causing problems

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20
Q

What does malluscum contagious virus cause

A

skin lesions

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21
Q

what tissue are affected most by irradiation

A

tissues wit high cell turn over rates

Can cause an inflammatory response

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22
Q

Mechanical trauma causes what

A

disruption of cell structure and thrombosis leading to ischaemia

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23
Q

Effects of low ATP on sodium pump

A

Decreases sodium pump
Efflux of Potassium
Influx of Calicum, water and sodium

Causes Cellular/cloudy swelling

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24
Q

Effects of low ATP on glycolysis

A

Increases glycolysis
Decreases glycogen
Decreases pH due to lactic acid produced
Causes clumping of genetic material

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25
Q

Effects of low ATP on ribosomes

A

Low pH causes detachment of ribosomes, decreases protein synthesis hence can’t export lipids

Lipid deposition - called FATTY CHANGE

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26
Q

What is the final effector of cell death

A

free radicals

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27
Q

what are free radicals

A

highly reactive ions/molecules with single unpaired electrons

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28
Q

What detoxifies free radicals

A

Superoxide dismutase and antioxidants (vitamins A,C,E)

Macrophages and neutrophils ill bacteria using superoxide

29
Q

Increased calcium activates which enzymes

A

ATPases
Phospholipases (causes membrane damage)
Proteases (breakdown membrane and cytoskeleton proteins)
Endonucleases (responsible for DNA fragmentation)

30
Q

What is fibrinoid necrosis associated with

A

mallignant hypertension

31
Q

When does cell death occur

A

Irreversible breakdown of energy dependent organised interactions between DNA, membranes and enzymes

32
Q

Types of necrosis

A

Coagulative
Colliquative
Caseous
Gangrenous

33
Q

What happens if coagulative necrosis

A

Typical of ischaemic injury
Denaturation of intracytoplasmic proteins –> dead tissue becomes firm and swollen
Cell contents destroyed but membrane intact
Tissue shows retention of microscopic architectiture
Cellular proteins may leak into blood

34
Q

What happens in colliquative necrosis

A

Necrotic neural tissue liquifies due to loss of collagen framework
Eventually marked by a cyst

35
Q

what happens in caseous necrosis

A

Occurs in TB
Cellular detail destroyed and surrounded by granulomatous inflammation
Appears cottage cheese like in nodule of necrosis

36
Q

Gangrenous necrosis

A

Wet and dry gangrene

Dry gangrene in diabetes rarely spreads

37
Q

What causes dry gangrene

A

Hypoxia and sometimes the cold

38
Q

What makes wet gangrene

A

Necrosis occurs and then it is infected

39
Q

Is necrosis passive or active

A

passive

40
Q

Is apoptosis active or passive

A

active

41
Q

What causes extrinsic apoptosis

A

Stimulator binds to cell surface e.g. TNF or Fas

Activates capsizes destroying proteins

42
Q

What causes intrinsic apoptosis

A

Cytochrome C and apoptosis inducing factor normally sequestered –> once activated releases caspases

43
Q

What is P53

A

the guardian of the genome –> causes tumours

44
Q

What is the bcl-2 gene

A

The gene that sequesters cytochrome C –> mutations in bcl-2 causing its overexpression means that cells don’t die

45
Q

is there an inflammatory reaction in apoptosis

A

No

46
Q

What happens to the nucleus in apoptosis

A

Fragmentation - apoptic bodies

47
Q

Components of acute inflammation

A

Cellular
Vascular
Exudative

48
Q

Purpose of acute inflammation

A

Clear away dead tissue
Locally contain infection
Allow access of immune system

49
Q

Signs of inflammation

A

Dolor
Tumour
Rubor
Calor

50
Q

Types of inflammation

A

Serous –> i.e. pleural cavity and pericardium. Produced by mesothial cells of serous membranes
Fibrinous –> increase in vascular permeability allowing fibrin to pass through
Purulent –> get large amounts of pus

51
Q

Systemic effects of inflammation

A

Pyrexia

Acute phase reaction –> cRP goes up and ESR increases!

52
Q

What happens to vasculature in acute inflammation

A

Microvascualr dilation! increases dlwo but initially decreases.
Fluid leaks out due to high hydrostatic pressure

53
Q

Mediated causes of vascular reaction

A

histamine, bradykinin, NO, leukotriene B4, complement components

54
Q

Non-mediated causes of vascular reaction

A

Direct damage to the endothelium e.g. toxins and physical agents

55
Q

Characteristics of the exudative reaction

A 
Protein rich (50g/l) *immunoglubulins and fibrinogen
Constantly turning over --> dilutes noxious agents, transports to lymph nodes, supply of nutrient, spread of inflammatory mediators antibodies and drugs
56
Q

What happens in the cellular reaction

A

Accumulation of neutrophils in the extracellular space

In severe cases the accumulation of neutrophils, cellular debris and bacteria causes pus to form

57
Q

What do neutrophils display in the cellular reactions

A

directional chemotaxis

58
Q

O2 dependent myeloperoxidase

A

H202, Cl, O2, OH, produce free radicals

59
Q

Oxygen dependent

A

lysozyme, lactoferrin, cationic proteins

60
Q

Stored mediators of acute inflammation: cell derived

A

Histamine

61
Q

Synthesised mediators of acute inflammation: cell derived

A

Prostaglandins, leukotrienes, PAF, cytokines (IL1,8 TNF), NO, Chemokines

62
Q

mediators of acute inflammation: Plasma derived

A

Kinin system
Clotting pathway
Thrombolyitc pathway
Complement Pathway

63
Q

mediators of acute inflammation: vascular dilation

A

histamine, NO, PGE2, I2

64
Q

mediators of acute inflammation: increased permeability

A

histomine, NO, bradykinin

65
Q

mediators of acute inflammation: neutrophil adhesion

A

IL-1, IL-8, TNF, C5a

66
Q

mediators of acute inflammation: neutrophil chemotaxis

A

IL-8, chemokines

67
Q

Endothelial activation

A

Tissue damage, activates neutrophils, surface adhesion molecules expressed, endothelial activation

68
Q

Progression of acute inflamation

A

Minimal tissue damage - resolution
Some tissue damage - fibrosis
Marked neutrophil reaction with tissue damage - suppuration/abscess
Damaging agent persis - chronic inflammation

EMS - JL (10 decks)

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