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Pathophysiology 2.0 > Week 3 - Tutorial - Immunopathology > Flashcards

Week 3 - Tutorial - Immunopathology Flashcards

1
Q

List 3 types of chronic inflammation which can lead to cancer. (provide specifics of both the inflammation & cancer)

A

Could be any 3 of the following

  • Chronic Ulcerative Colitis = Colon Cancer
  • Chronic Hepatitis B or C = Liver Cancer
  • Chronic Obstructive Pulmonary Disease (COPD) or asthma = lung cancer
  • Chronic Cystitis = Bladder Cancer
  • Sjogren syndrome = lymphoma
  • Chronic Thyroiditis = lymphoma
  • Fibrocystic breast disease = breast cancer
  • Benign Prostatic Hyperplasia = prostate cancer
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2
Q

How does chronic inflammation develop into a tumour?

A

(can enter at any stage)

  1. Cells transform
  2. Primary growth
  3. Metastasis
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3
Q

What does a loss in gut bacteria cause? (could be one of 3 reasons)

A
  • loss in gut bacteria =
  1. loss of barrier function
    • increase commensal penetration
    • increase inflammation
    • = enhanced tumour growth
  2. Pathobiont-mediated tumorigenesis
    • potentially pathogenic commensal strains enhance tumorigenesis
    • use TH17 cells
    • inflammation
  3. Dysbiosis-mediated inflammation
    • loss of host-related innate sensing platforms
    • = pertubation of microbiota composition and function
    • = tumour growth enhanced
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4
Q

How do Inflammatory Cells help tumour cells?

A

Inflammatory cells release;

  1. Growth Factors
    • TNF
    • IL-1
  2. Survival Factors
    • TNF
    • IL-1
    • IL-6
    • CXCL8
    • VEGF
    • CSF1

Which alter the gene expression of the cell & thus promotes its survival & makes it flourish (specifically through action of IL-2)

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5
Q

What are the primary sources of Chronic Liver Disease?

A
  • 26% Hepatitis C Virus
  • 24% Alcohol
  • 17% Unknown
  • 14% Hepatitis C virus and Alcohol
  • 11% Hepatitis B Virus
  • 5% Other
  • 3% Hepatitis B virus & alcohol

aka Hepatitis B & C main

although data was taken in Alabama

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6
Q

What are the main causes of Hepatitis C?

A
  • 60% Injecting Drug use
  • 15% Sexual
  • 10% Transfusion (occurred before screening)
  • 10% Unknown
  • 4% Occupational
  • 1% other (Nosocomial, iatrogenic, prenatal)
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7
Q

What does iatrogenic mean?

A

Means diseases that occurred due to a harmful complication, or other ill effects by any medical activity, including diagnosis, intervention, error, or negligence.

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8
Q

What is the progression of Chronic Liver Disease (CLD)?

A
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9
Q

How quickly can the liver regenerate itself?

A

~2 months

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10
Q

What is the prognosis of CLD?

A

1 in 4 die (aka v bad)

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11
Q

What is the progression of a healthy liver to liver cancer? Describe the 4 stages. (hint 2 have been said)

A
  1. Healthy liver
    • normal
  2. Fibrotic Liver
    • continuous inflammation
    • if caused by Hep B
    • lead to fibrosis aka HEALING WITH SCARRING
    • ie formation of scar tissue
  3. Cirrhotic liver
    • scar tissue replaces normal, healthy tissue
    • blocks flow of blood through liver
    • prevents norm function
  4. Liver Cancer
    • formation of malignant tumours in liver
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12
Q

What does HCC stand for?

A

Hepatocellular carcinoma

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13
Q

How is Chronic liver disease diagnosed?

A
  • Computed Tomography
    • aka ultrasound
    • to see if there are any visible lesions
  • If yes, a percutaneous biopsy of lesions
  • examination under microscope to compare morphology
    • diagnose stage & prognosis
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14
Q

What are some factors that may cause liver inflammation?

A
  • HBV & HCV (more so HCV as there is no vaccine)
  • Non-Alcoholic Steatohepatitis (NASH)
  • Alcohol
  • Diabetes
  • Aflatoxins
  • abnormalities in TGF-β1 pathway
  • p53 family abnormalities (as v important in killing cancer)
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15
Q

Which one is healthy? What is the other? Why do you think this?

A
  • Left = Healthy
    • normal
  • Right = cirrhosis of liver
    • many lymphoid cell infiltration
    • more scar tissue (white)
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16
Q

Which of these is infecter and which is uninfected? What disease could it be & why?

A
  • Left = unifected
  • Right = infected
    • probs HCV as
      • its liver
      • infiltration of lymphocytes is seen
      • and connective tissue is being placed down
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17
Q

What is AFP & what is it a marker for?

A

Alpha-fetoprotein (AFP)

is a marker for some cancers specifically in the liver

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18
Q

If a patient has Hepatocellular Carcinomas (HCC) then they have a 34% chance of getting what disease?

A

HCC leads to pulmonary (lung) metastasis

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19
Q

What are the main treatment options for Liver Cancer?

A
  1. Liver Transplant
  2. Trans-Catheter Arterial Chemobolisation (TACE) - for patients who are not suitable for a liver transplant
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20
Q

What is TACE?

A

Trans-catheter arterial chemobolization

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21
Q

What is the main aim of TACE and how does it work?

A
  • Aim = procedure performed in intentional radiology to restrict a tumour’s blood supply
  • combines chemotherapy with embolization
  • small embolic particles coated with chemotherapeutic drugs are injected selectively through a catheter into an artery that is directly supplying the tumour
  • Particles block blood supply & induce cytotoxicity
22
Q

What are the two main mechanisms that are beneficial to TACE?

A
  1. The typical blood supply of hepatic tumours
  2. The ability to deliver a higher dose of chemotherapeutic drugs
23
Q

How is the blood supply of hepatic tumours beneficial to TACE?

A
  • Most tumours are supplied by the PROPER HEPATIC ARTERY
  • embolisation ideally interrupts the tumours blood supply through the blockage of the vessel
  • this stalls growth until neovascularisation occurs
24
Q

Why can higher doses be given during TACE?

A
  • Higher doses of chemotherapeutic drugs can be given
  • as it is being delivered to a focused area
  • decreases systemic exposure (which is usually the limiting factor of doses)
  • occurs due to increase likeliness that drugs
    • arent washed out from the tumour’s vascular bed
    • higher concentration of the drug to be in contact with tumour for a longer period of time
25
Q

The intra-tumour concentration of chemotherapeutic is 10 times greater in ____ than _____

A

a. proper hepatic artery
b. portal vein

26
Q

What does embolization induce?

A

induces ischemic necrosis of tumour

which causes a failure of transmembrane pump = greater absorption of agents by tumour cells

27
Q

What is Ulcerative colitis?

A

is chronic inflammation of the bowel (colon) or digestive tract which can result in formation ulcers

28
Q

What is 5-ASA and what does it do?

A

5-ASA = 5 amino-salicylate

is used to monitor mild to moderate IBM as it is an anti-metabolite

29
Q

How is ulcerative colitis (UC) diagnosed?

A
  • After diagnosis person has annual colonoscopies to monitor condition
  • If surface of lesion is irregular & margin was unclear
  • Biopsy is taken & cells
    • if surrounding colonic mucosa is pale and rough = quisenct phase of UC activity
    • if lesion biopsy shows well differentiated tubular adenocarcinomas then
  • Computed tomography is done to see extent of swelling of digestive system
30
Q

What is the main problem after a colectomy is performed?

A

Managing every day life as faeces cannot be controlled as you cannot feel them coming out

31
Q

Where does ulcerative colitis begin?

A

Starts at rectum & may extend for a variable distance around the colon

32
Q

What are some of the hypotheses of the aetiology of ulcerative colitis?

A
  1. Psychosomatic cause
    • stress is believed to exacerbate disease in some individuals
  2. Infective Cause
    • adhesive of enteropathogenic E. coli may trigger episodes of inflammation
  3. Immunological cause
    • lymphoid cells participate in inflammation
    • antibodies & immune complexes have been seen in some cases
      • steroids are effective in treatment as they’re anti-inflammatories
    • infection triggers inappropriate autoimmune response = leads to destruction of colonic mucosa
    • p53 involvement
33
Q

In active ulcerative colitis what are the effects of;

(a) ulcerated areas
(b) crypt abscesses

A

a. ulcerated areas are haemorrhagic = bloody diarrhea
b. is a collection of neutrophils = increase lymphoid cells and plasma cells in lamina propria = oedema or swelling

34
Q

What are the local effects of ulcerative colitis?

A

LOCAL

  • blood and fluid loss from extensive ulceration
  • may be severe
  • acute disease may process rapidly to toxic dilation & perforation
  • in long standing disease = dysplasia and neoplastic changes may occur
35
Q

What are the Systemic effects of ulcerative colitis?

A

extra-intestinal manifestations e.g.

fever

inflammation of eyes or joints

ulcers of the mouth

inflamed nodules on the shins.

36
Q

List 3 other conditions which may be associated with ulcerative colitis?

A

Can list any of the following

  1. migratory polyarthritis (pain, swelling & joint stiffness)
  2. sacroiliitis (inflammation of both sacroiliac joints)
  3. ankylosing spondylitis (an inflammatory disease that over time causes vertebrae to fuse)
  4. uveitis (inflammation of the uvea = eye redness, pain & blurred vision)
  5. erythema nodosum (is a panniculitis (skin inflammation) that affects the subcutaneous fat in the skin)
  6. primary sclerosing cholangitis (chronic disease which results in the scarring & inflammation of the gall bladder)
37
Q

What are the 3 natural history (progression of the disease) patterns that patients of ulcerative colitis follow? (state %)

A
  1. 10% = develop severe disease requiring early surgery
  2. 10% = have persistent active disease despite treatment
  3. 80% = have chronic quiescent colitis with infrequent episodes of relapse
38
Q

In diagnosis, what are some diseases that ulcerative colitis must be distinguished from?

A
  1. infective colitis
  2. Crohn’s Disease
  3. Ischemic Colitis
  4. Proctitis caused by sexually transmitted diseases
39
Q

What is total ulcerative colitis?

A
  • when the whole entire large intestine
  • occurs in ~20% of people
40
Q

What checks do patients with total UC do & how often do they occur?

A
  • If patient is over 50 years then;
  • have regular screening coloscopy every 2 years
  • rectal biopsy every 6 months to detect dysplastic changes
41
Q

The development of dysplasia in the rectal mucosa in chronic ulcerative colitis is due to?

A

regenerative changes

42
Q
  • Regenerative changes in rectal mucosa lead to the development of; -1-
  • as well as the potential risk of -2-
  • which is related to -3- & -4-
A
  1. dysplasia
  2. carcinoma of the colon
  3. extent of the disease (high risk for total colitis)
  4. Duration of illness (high risk for disease of over 10 year duration)
43
Q

Which side of the colon is associated with a lower risk of cancer?

A

Left

44
Q

What is Necrosis?

A

Necrosis is the death of most cells in a tissue or organ as a result of disease, injury or failure of blood supply (O2 deprivation)

45
Q

What is Apoptosis?

A

Apoptosis is a form of programmed cell death which occurs in multicellular organisms

46
Q

What are differences in the size of a cell if it has undergone necrosis or apoptosis?

A

Necrosis

  • Cellular swelling
  • Many cells are affected - diffuse

Apoptosis

  • Cellular shrinkage (condensation)
  • One cell is affected (individual)
47
Q

What are differences in the uptake of a cell if it has undergone necrosis or apoptosis?

A

Apoptosis

  • Cells contents ingested by macrophages
  • significant inflammation

Necrosis

  • cell contents ingested by neighbouring cells
  • No inflammatory response
48
Q

What the differences to the membrane of a cell if it has undergone necrosis or apoptosis?

A

Necrosis

  • Loss of membrane integrity (brakes)
  • Cell lysis occurs (elicits inflammatory response)

Apoptosis

  • membrane blebbing but integrity is maintained (intact)
  • apoptotic bodies form
49
Q

What are differences in the organelles of a cell if it has undergone necrosis or apoptosis?

A

Necrosis

  • Organelle swelling and lysosomal leakage
  • fragmentation of DNA is either random or smeared
  • ATP is depleted

Apoptosis

  • Mitochondria release pro-apoptotic proteins
  • chromatin condensation & ladder-like DNA fragmentation
  • requires ATP
50
Q

Is Necrosis or Apoptosis an active process? which one isn’t?

A

Apoptosis is active as it requires ATP

Necrosis is inactive and doesn’t need ATP to occur but does result in the depletion of ATP

Pathophysiology 2.0 (19 decks)

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