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PathoPhys > Tutorial 3 - Inflammation, cancer & case studies > Flashcards

Tutorial 3 - Inflammation, cancer & case studies Flashcards

1
Q

chronic hepatitis leads to? % probabilities?

A
  1. fibrotic liver (fibrous scar tissue),
  2. liver cirrhosis (25% chance), which can then lead to
  3. liver cancer (3-5%)
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2
Q

state main causes of chronic liver disease?

A

hepatitis C 26%
alcohol 24%
hepatitis C with alcohol 14%
hepatitis B 11%

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3
Q

t/f: spontaneous regression of HCC is a rare phenomena where it basically just goes away

A

true

HCC = hepatocellular carcinoma; liver cancer

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4
Q

possible causes spontaenous regression?

A
  1. ischaemia

2. immunologic mechanisms

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5
Q

what is Trans-catheter arterial chemoembolization (TACE)?

A
  • restrictive blood supply tumor
  • minimally invasive
  • chemotherapy + embolization = chemoembolization
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6
Q

how does TACE work?

A

small embolic particles coated in therapeutic drugs injected selectively through a catheter into an artery which supplies the tumor

these particles block blood supply and induce cytotoxicity

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7
Q

most tumors in liver supplied by which artery?

A

hepatic proper

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8
Q

by attacking the hepatic proper artery, how does this fight off the tumor (TACE)?

A

prevents nutrient delivery over time until neovascularisation can take place

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9
Q

what is (typically) the limiting factor for chemotherapy?

A

systemic exposure

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10
Q

state the 2 mechanisms by which TACE works?

overall effect of this on physiological level?

A
  1. block arterial blood supply until neovascularisation
  2. focused chemotherapy of higher dose. This effect augmented as chemotherapeutic drug not washed out tumor vascular bed by blood flow (as its blocked). This means a higher contact time of tumor and drug

embolization -> ischaemic necrosis -> failure of transmembrane pump, resulting -> greater absoprtion by tumor cells

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11
Q

how was it proven that TACE targets tumor in liver, not liver overall?

A

tumor 40x more agent then rest of liver. This proven as if inject into hepatic portal vein, only 1/10 of intra-tumoral concentration

so using hepatic artery proper gives 10x higher [drug]

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12
Q

where does ulcerative colitis start?

A

starts in rectum, may extend for variable distance along colon

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13
Q

define proctisis

A

anal canal inflamed

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14
Q

how severe can ulcerative colitis (UC) be - how much of colon can be affected?

A

all of colon and all colonic mucosa can be affected in highly severe cases

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15
Q

symptoms of UC?

A

diarrhea, blood/ mucus/ pus in faeces

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16
Q

aetiology of UC?

A

not clear, several hypothesis:

  1. psychosomatic - stress induced
  2. infective - enteropathological form e.coli induce
  3. autoimmune - lymphoid cells cause inflammation

unified explanation: infection triggers inappropriate immune response leading to destruction colonic mucosa

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17
Q

in active UC, the ulcerated areas are _____

A

hemorrhagic, leading to bloody diarrhoea

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18
Q

explain histology of active UC?

A
  • in-tact mucosa sits above areas of ulceration as islands
  • edema
  • increased lymphoid cells & plasma cells in lamina propria
  • neutrophils in lamina propria and gland epithelium
  • neutrophils migrate through walls of glands forming crypt abscesses in gland lumen
  • depletion goblet cells
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19
Q

t/f: UC has only local, no systemic effects

A

false - both

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20
Q

direct local complications of UC?

A

blood and fluid loss from extensive ulceration

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21
Q

natural history of patients with UC?

A

10% develop severe disease, need surgery
10% have persistent active disease despite treatment
80% have chronic quiescent colitis with infrequent episodes

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22
Q

In chronic UC, regeneative changes to colonic mucosa leads to?

A

dysplasia and risk of carcinoma development in colon

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23
Q

There is more risk of dysplasia/ carcinoma development in chronic UC if?

A
  1. disease very severe (total colitis)

2. disease duration long (had for 10 years)

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24
Q

In trying to kill cancer, how are most cancer cells killed?

A

apoptosis is stimulated by drugs given

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25
Q

necrosis means death by?

A

O2 deprivation

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26
Q

contrast necrosis and apoptosis in terms of:

cell size change

A

necrosis - cell swells

apoptosis - cell condense

27
Q

contrast necrosis and apoptosis in terms of:

membrane

A

necrosis - membrane broken

apoptosis - membrane in tact

28
Q

contrast necrosis and apoptosis in terms of:

ATP

A

necrosis - no ATP needed

apoptosis - ATP needed

29
Q

contrast necrosis and apoptosis in terms of:

how cell destroyed

A

necrosis - cell lyses

apoptosis - cell phagocytosed

30
Q

contrast necrosis and apoptosis in terms of:

DNA

A

necrosis - random DNA fragmentation/ smearing

apoptosis - ladder-like DNA fragmentation

31
Q

contrast necrosis and apoptosis in terms of:

in vivo, what area affected?

A

necrosis - whole areas or tissue

apoptosis - individual cells

32
Q

contrast necrosis and apoptosis in terms of:

effect on inflammation?

A

necrosis - inflammation triggered

apoptosis - minimal macrophage activation

33
Q

contrast necrosis and apoptosis in terms of:

which needs protein function?

A

necrosis - nil, passive

apoptosis - requires protein use, active

34
Q

discuss relationship between inflammation and age.

A

age increases inflammation and inflammatory processes age the body (goes both ways)

35
Q

describe the relationship between chronic inflammation and cancer?

A

chronic inflammation contributes toward/ causes cancer, as the chemical mediators released during inflammation stimulate cancerous growth (assumed)

36
Q

chronic inflammation causing cancer; state the disease (which lead to inflammation) behind the following cancer: colon cancer

A

chronic ulcerative colitis

37
Q

chronic inflammation causing cancer; state the disease (which lead to inflammation) behind the following cancer: Liver cancer

A

chronic hepatitis B or C

38
Q

chronic inflammation causing cancer; state the disease (which lead to inflammation) behind the following cancer: Lung cancer

A

COPD, chronic asthma

39
Q

chronic inflammation causing cancer; state the disease (which lead to inflammation) behind the following cancer: bladder cancer

A

chronic cystitis

40
Q

chronic inflammation causing cancer; state the disease (which lead to inflammation) behind the following cancer: lymphoma

A

chronic thyroiditis, sjorgen syndrome

41
Q

chronic inflammation causing cancer; state the disease (which lead to inflammation) behind the following cancer: breast cancer

A

fibrocystic breast disease

42
Q

chronic inflammation causing cancer; state the disease (which lead to inflammation) behind the following cancer: prostate cancer

A

benign prostate hyperplasia

43
Q

expand acronym HCC

A

hepatocellular carcinoma

44
Q

main sources infection hepatitis C

A

inject drug 60%
sexual 15%
transfusion 10%

45
Q

t/f: gut normal flora can migrate across a degenerated gut mucosa (epithelium) and stimulate inflammation

A

true

46
Q

survival factors (cytokines) released by inflammatory cells, promoting tumor growth are?

A

SOD2
BFL1
BCL-Xl
GADD45beta

47
Q

describe the relationship between IL-6 and IL-1

A

they both cause more of each other to be produced (loop)

48
Q

cirrhosis?

A

late stage of fibrosis; the progression

hep c (or others) –> fibrosis –> cirrhosis –> cancer development

49
Q

how would colon of someone with UC in quiescent phase look?

A

pale and rough

50
Q

t/f: inflammation triggers regeneration and repair

A

true (wow)

51
Q

discuss the relationship between MHC class 1 and natural killer cells?

A

if a cell does not possess MHC class 1, natural killer cells will attack

(Major Histocompatability protein has protective, ‘self recognising’ effect TO NK CELLS)

52
Q

non-IgE asthma is driven by which cells (mainly)?

A

ILC2’s and eosinophils

53
Q

Consider IgG and IgM, and IgE.

a. ) Which are likely to be present in the early phase of infection?
b. ) Which are likely to be present in the late phase of infection?

A

a. ) IgM, IgE

b. ) IgG

54
Q

which antibodies are the “memory antibodies”?

A

IgG

55
Q

multiple sclerosis is a type _ hypersensitivity?

A

4

56
Q

state the targets of the autoimmune response in multiple sclerosis?

A

myelin, schwann cells, oligodendrocytes

57
Q

ulcerative colitis is a major cause of ____ ____.

A

colon cancer

58
Q

t/f: apoptosis requires protein synthesis

A

true

59
Q

state 3 growth factors which control tissue repair post inflammation?

A

TFGbeta, VEGF, PDGF

60
Q

state 3 cancers linked to chronic inflammation?

A

colon, liver, lung

61
Q

state cardinal signs of acute inflammation?

A

heat, swelling, pain, redness

62
Q

state chemical mediators in the vascular inflammatory response?

A

serotonin, histamine, prostoglandins, leukotrienes

63
Q

Th2 cells are (MCQ):

a. ) main player pathogenesis asthma
b. ) main player cytotoxic T cell response
c. ) attract macrophages
d. ) lyse other cells

A

a.

64
Q

what type of hypersensitivity is an anaphylactic episode?

A

type 1

PathoPhys (25 decks)

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