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ESA 2 Clinical Cases > Pathological Processes > Flashcards

Pathological Processes Flashcards

1
Q

Which conditions can lead to hypercoagulability?

A

Antithrombin III deficiency
Protein C or S deficiency
Factor V Leiden

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2
Q

How can immunohistochemistry be used in cancer?

What colour will proteins show up if present?

A
  1. Antibodies for cytokeratins can be used (family of around 20 intracellular fibrous proteins present in almost all epithelia) - will give information about primary site of cancer e.g. CK7+/CK20- can be present on lung cancer cells
  2. Antibodies for Her2 receptors - growth factor which can be used to predict the response of breast cancer to drug Herceptin

Proteins will show up brown if present

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3
Q

What kind of hypoxia does cyanide poisoning lead to? Why?

A

HISTIOCYTIC HYPOXIA

Cyanide poisoning leads to disabled oxidative phosphorylation.

It blocks the flow of electrons along the electron transport chain which means that H+ can’t flow out of the matrix into the intermembrane space.

This means no proton motive force is established so H+ doesn’t flow through ATP synthase –> no ATP –> needed for respiration in cells

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4
Q

What is ischaemic reperfusion injury? Why is it dangerous?

A

When blood is returned to a damaged but not yet necrotic area of tissue.

  1. FREE RADICALS - Increased production of free radicals with reoxygenation
  2. NEUTROPHILS - Increased neutrophils delivered to reperfused area - inflammation and tissue injury
  3. COMPLEMENT - Delivery of complement proteins and activation of complement pathways
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5
Q

What is graft vs host disease?

A

Pathological apoptosis - following a graft of foreign tissue, the cytotoxic T cells (?) from the graft tissue attack host cells causing them to apoptose

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6
Q

What is a1-antitrypsin deficiency?

What main complication can arise?

A
  • What it is: an autosomal recessive disorder with varying levels of severity
  • Pathophysiology: low levels of alpha-1 antitrypsin, a protease inhibitor which deactivates enzymes released from neutrophils at the site of inflammation. The liver produces a version of the protein α1-antitrypsin that is incorrectly folded. This cannot be packaged by the endoplasmic reticulum and accumulates within this organelle and is not secreted by the liver.
  • Presentation: Breathlessness, jaundice, upper-left quadrant pain
  • Complications: The systemic deficiency of the enzyme means that proteases within the lung can act unchecked and patients with the condition develop emphysema as lung tissue is broken down. Liver disease also occurs as the accumulated abnormal version of the protein causes hepatocyte damage and eventually cirrhosis.
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7
Q

How could you tell whether pleural oedema was due to pneumonia or heart failure?

A 
Transudate = same protein content as blood plasma
Exudate = higher protein content than blood plasma - only occurs in inflammation when vascular permeability is increased

Can take fluid from pleural oedema - if high protein then probably pneumonia.
If normal protein probably heart failure.

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8
Q

Which cytokines are particularly important?

A

IL-1, IL-6, TNFa - stimulate acute phase response = stimulates liver to produce CRP, complement factors, clotting factors, increase erythropoiesis in bone marrow.

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9
Q

Which organisms cause meningitis in different age groups?

A

Neonates (Up to 6 weeks old): group B strep (acquired from mother if she has it present in vagina), E.coli, listeria

Children: Same as young adults, plus haemophilus influenza

Young adults: Neisseria meningitidis, streptococcus pneumoniae

Older adults: Listeria, neisseria, strep pneumoniae

(Say Neisseria meningitidis other than for neonates)

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10
Q

What grading system is used for breast cancer?

A

Bloom-Richardson system grades according to presence of

  1. Tubules
  2. Pleomorphism
  3. Mitoses
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11
Q

Invasion of carcinoma cells involves altered adhesion, stromal proteolysis and motility.

What does altered adhesion involve?
Which proteases are involved in stromal proteolysis?

A
  • Altered adhesion between malignant cells involves a reduction in E-cadherin expression.
  • Altered adhesion between malignant cells and stromal proteins involves changes in Integrin expression.
  • The cells must degrade basement membrane and stroma to invade.
  • This involves altered expression of proteases, notably matrix metalloproteinases (MMPs)
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12
Q

What are the histiological features of TB and sarcoidosis?

A

TB - granulomas present, including Langhan’s giant cells, lymphocytes, epithelioid histiocytes and CASEOUS NECROSIS at the centre

Sarcoidosis - A granulomatous disease affecting lungs and lymph nodes of young adult women. Granulomas and giant cells present but without caseous necrosis.

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13
Q

Compare Crohn’s and Ulcerative Colitis

A

Crohn’s…

  • Lesions are transmural and have a cobblestone appearance
  • Shows discontinuous distribution (skip lesions)
  • Affects any part of the GI tract (anal lesions therefore often seen – Crohn’s is moth to anus)
  • Granulomas and crypt abscesses often seen
  • Lymphocytes predominate
  • Bowel fistulae more likely than in UC

Ulcerative colitis

  • Inflammation limited to mucosa and submucosa - superficial
  • But inflammation is continuous - many neutrophils present
  • Distorted crypt architecture very common
  • Significantly increased risk of colon cancer
  • Often most severe in distal colon
  • Colectomy often indicated
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14
Q

What does Helicobacter pylori do?
What will gut infected with it look like?
What are some complications of it?

A
  • Role of Helicobacter pylori: Gram negative. Causes chronic gastritis by stimulating production of pro-inflammatory cytokines and by directly injuring epithelial cells and increasing acid secretion.
  • Microscopic appearance
  • Helicobacter pylori organisms present
  • Chronic inflammation (and some acute inflammation) in the lamina propria and superficial epithelium
  • Lamina propria fibrosis
  • Mucosal atrophy
  • Intestinal metaplasia

• Complications
o Gastric adenocarcinoma.
o MALT (mucosa associated lymphoid tissue) lymphoma.

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15
Q

What is scurvy? Why does it occur? What is its main complication?

A

Defect in collagen synthesis due to vitamin C deficiency - required for hydroxylation of procollagen.

Patients unable to heal wounds adequately –> tendency to bleed e.g. Gums

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16
Q

What is Ehlers-Danlos syndrome?

What does it lead to?

A

Type 3 collagen deficiency

  • Skin is hyperextensible, fragile and susceptible to injury, hypermobile joints –> poor wound healing and joint dislocation
  • Can lead to rupture of colon and large arteries, corneal rupture and retinal detachment
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17
Q

What is osteogenesis imperfecta?

What does it lead to?

A

Autosomal dominant condition

  • Type 1 collagen deformity/deficiency - major component in ground substance of bone
  • Too little bone tissue –> extreme fragility –> repetitive fractures and bowed limbs
  • Blue sclerae due to too little collagen, making them translucent
  • Can also have hearing impairment and dental abnormalities
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18
Q

What is Alport Syndrome?

What does it lead to?

A

Usually X-linked
Type VI collagen abnormal
- Disruption of glomerular basement membrane –> haematuria and chronic renal failure
- Dysfunction of cochlear or ear and lens of eye –> neural deafness and eye disorders

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19
Q

What is a transient ischaemic attack? What causes it?

A

Episodes of neurological dysfunction that appear suddenly and last minutes or hours and then disappear.

They are the result of microscopic emboli, usually atheroemboli, to the brain.

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20
Q

What does aspirin do and how?

A

Antithrombogenic.

Prevents platelets from producing thromboxane A2, a powerful platelet aggregator.

Prolongs bleeding time.

21
Q

What does heparin do?

A

Forms irreversible complexes with antithrombin III resulting in its activation

22
Q

What does warfarin do?
How are levels measured?
What is recommended dose and what classes as overdose?

A

Interferes with vitamin K metabolism - vitamin K is required to synthesis clotting factors, so inhibiting it means that clotting time will be prolonged.

INR is used as a measure of dose - ratio of patient’s PT to mean normal PT

Dose should be between 3-9mg/day
If INR >8 give vitamin K orally or IV

23
Q

Why might someone have thrombocytopenia (low platelets?)

A

IMMUNE DESTRUCTION - Immune thrombocytopenic purpura - autoantibodies against glycoproteins on platelets –> petechia - treat with corticosteroids

DIC - Small clots in microcirculation - caused by malignancy, G- sepsis, massive tissue injury e.g. Burns, massive haemorrhage and transfusion. Raised PT/APTT, INR, fibrinogen and D-dimers.

Can lead to haemolytic anaemia as RBCs get damage by fibrin

DILUTION - due to blood transfusion

SEQUESTRATION in spleen

MARROW FAILURE e.g. Chemo, cancer/fibrosis, B12 or folate deficiency, HIV/hepatitis

24
Q

What is haemophilia A? What are its symptoms? How would you test for it? And treat it?

How is haemophilia B different?

A

Haemophilia A is an X-linked condition

  • Congenital lack of factor VIII
  • Symptoms: bleeding into muscles, joints and post-operatively
  • Test: ELISA test for factor VIII
  • Treatment: Recombinant factor VIII or DDAVP to release factor VIII from stores

Haemophilia B
- Similar presentation to A, but due to reduction in factor IX

25
Q

What is Von Willebrand’s Factor and Disease?

A

vWF carries factor VIII and protects it from premature destruction - mediates platelet adhesion to endothelium

Disease:

  • Autosomal dominant - males and females
  • Reduction in vWF production - abnormal platelet adhesion to endothelium, reduced Factor VIII levels
  • Symptoms: Skin and mucous membrane bleeding, prolonged bleeding after trauma, heavy periods NOT spontaneous muscle/joint bleeds like haemophilia
26
Q

What kind of cellular adaptation do you see in the bronchi of smokers? In GI with acid reflux? In spleen when bone marrow damaged?

A

METAPLASIA

Bronchial pseudostratified ciliated epithelium –> stratified squamous

Stratified squamous epithelium of oesophagus –> gastric glandular epithelium (can lead to oesophageal adenocarcinoma)

Spleen becomes bone marrow to undertake haematopoiesis

27
Q

What grading system is used for breast cancer?

A

Bloom-Richardson

Assess presence of:

1) Tubules
2) Mitoses
3) Nuclear pleomorphism

28
Q

Which viruses can lead to Burkett’s lymphoma?

A

EBV and malaria

29
Q

In what disease do you sometimes get Kaposi’s sarcoma?

A

HIV/AIDS - caused by herpes virus

30
Q

How does Human Papilloma Virus (HPV) lead to cervical carcinoma?

A

HPV is a direct carcinogen because it expresses the E6 and E7 proteins than inhibit p53 (activates DNA repair or initiates apoptosis) and pRB (gateway through restriction points - won’t let a damaged cell continue) protein function respectively.

31
Q

What kind of carcinogens are Hep B and C and Helicobacter pylori? How do they lead to malignancy?

A

INDIRECT CARCINOGENS

Hep B and C
- Cause chronic liver cell injury –> requires regeneration which gives opportunities for mutations to occur

Helicobacter pylori
- Causes chronic gastric inflammation, increasing risk of gastric adenocarcinoma

32
Q

How does HIV lead to malignancy?

A

Acts indirectly by lowering immunity and allowing other potentially carcinogenic infections to occur e.g. HERPES virus leads to KAPOSI’S SARCOMA

33
Q

How many alleles of a tumour suppressor gene and an oncogene need to be (in)activated to cause cancer?

A

Both alleles of a tumour suppressor gene must be inactivated

Only one allele of a proto-oncogene (becomes and oncogene) needs to be activated

34
Q

What is Xeroderma Pigmentosum (XP)?

A

Autosomal recessive condition due to a mutation in one of the 7 genes that affect DNA nucleotide excision repair.

Patients are very sensitive to UV damage and develop skin cancer at a young age

35
Q

What is the role of BRCA 1 and 2? What happens when there are mutations in them?

A

Genes important for repairing double strand breaks.

Mutations can lead to breast and ovarian cancer - often familial

36
Q

HNPCC - affects mismatch repair genes

A

-

37
Q

What is the adenoma-carcinoma sequence? What are its stages?

A

An example of cancer PROGRESSION

Step-wise accumulation of mutations (originating from initiator and promoter events) to become a malignant neoplasm e.g. Colon adenoma becoming colon carcinoma

  • Normal epithelium –> mutation in tumour suppressor gene such as APC –> early adenoma/dysplastic crypt
  • Mutation in proto-oncogene such as KRAS –> intermediate adenoma
  • TGF-B (transforming growth factor) response inactivation –> late adenoma
  • Loss of p53 function –> carcinoma –> metastasis
38
Q

What are the six hallmark behaviours of cancer cells?

A

1) Self-sufficient growth signals
2) Resistance to growth stop signals
3) Grow indefinitely
4) Induce new blood vessels
5) Resistance to apoptosis
6) Invade and produce metastases

39
Q

What is the commonest method for assessing the extent of tumour?

A

TNM

T = Tumour size (T1-4)
N = Extent of nodal metastasis (N0-N3)
M = Extent of distant metastatic spread (M0-M1)

I. Small and remains at primary site (T1/2, N0, M0)
II. More locally advanced, no spread (T3/4, N0, M0)
III. Regional metastasis (any T, N>1, M0)
IV. Advanced disease with distant metastasis (any T, any N, M1)

40
Q

What staging system is used for lymphoma? What are the stages?

A

Ann Arbour staging - unique to lymphoma

Stage I - single node region
Stage II - two separate regions on one side of the diaphragm
Stage III - spread to both sides of the diaphragm
Stage IV - dissemination to one or more extra-lymphatic organs e.g. bone marrow or lung.

41
Q

What staging system can be used for colorectal carcinoma?

A

Duke’s staging system (TNM is preferred worldwide)

Dukes’ A: Invasion into but not through the bowel
Dukes’ B: Invasion through the bowel wall
Dukes’ C: Involvement of lymph nodes
Dukes’ D: Distant metastases

42
Q

What are tumour markers? What are they useful for? Give some examples.

A

Substances (hormones, oncofoetal antigens, proteins, mucins/glycoproteins) released by cancer cells into circulation. Role in diagnosis and/or monitoring tumour burden.

  • Carcinoembryonic antigen (CEA) – colorectal and breast cancer
  • Beta-human chorionic gonadotropin – choriocarcinoma and testicular cancer
  • Alpha fetoprotein – liver and germ cell tumours
43
Q

What is the purpose of screening programmes? Which ones exist in the UK and who are they open to?

A

Attempts to detect cancers as early as possible when chance of cure is highest

Cervical - women aged 25 to 49 - every 3 years. Women aged 50 to 64 receive - every 5 years.

Breast - mammograms to identify any densities/calcifications - every 3 yrs from 50-69yrs)

Bowel - All men and women aged 60-74 every 2 years - faecal occult blood (FOB) test by post

44
Q

Which are the four most common cancers in the UK?

A
  1. Breast
  2. Prostate
  3. Lung
  4. Bowel
45
Q

Which are the most deadly cancers in the UK?

A
  1. Lung (22%)
  2. Bowel (10%)
  3. Breast (7%)
  4. Prostate (7%)
46
Q

What is the presentation, microscopic and macroscopic features of rheumatoid arthritis

A
  • Presentation: Pain which often starts in fingers and spreads to wrists and ankles. Symmetrical. Worse in the mornings. Joints are warm, swollen and painful.
  • Microscopic features: Signs of chronic inflammation in the synovial membrane e.g. macrophages, plasma cells (differentiated, antibody-producing T lymphocytes, granulomas), destruction of articular cartilage.
  • Rheumatoid nodules including microscopic appearance: Subcutaneous lumps on the posterior forearm. Appear as fibrinoid necrosis with giant cells surrounding it.
47
Q

How does early first pregnancy affect cancer risk?

A

Lower risk of developing breast carcinoma - breast tissue is not fully mature until lactation has happened - lower risk of cancer if mature

BUT

Increased risk of cervical cancer - sexual intercourse at young age leads to increased risk of abnormalities in cervix

48
Q

What can asbestos exposure lead to?

A

MESOTHELIOMA (lung, peritoneum and pericardium)

Usually 20-40 years after exposure

ESA 2 Clinical Cases (9 decks)

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