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ESA Revision > MOD > Flashcards

MOD Flashcards

1
Q

Define neoplasia

A

Abnormal growth of cells that persists after the initial stimulus has been removed.

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2
Q

How may growth control be altered?

A

With increased cell proliferation- more cells enter cell cycle, reduced cell death/ longer life span- cell may be resistant to apoptosis e.g. abnomal expression of bcl-2 gene which inhibits cytochrome C release from mit., altered GFs/hormones and receptors- VEGF induces angiogenesis, angiostatin/endostatin- opposes VEGF action and altered cell-cell interactions- lack of E-cadherin- adhesion molecule.

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3
Q

Name 2 products of endothelium which impede platelet adhesion and activation, and so haemostasis.

A

Prostacyclin and NO

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4
Q

What cofactor is important for anti-thrombin activity?

A

Heparin

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5
Q

How is vitamin K obtained by the body?

A

From intestinal bacteria and food, so disorders of fat absorption or liver disease can cause vit.K deficiency and defective clotting.

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6
Q

Which clotting factors require vit K for their correct synthesis?

A

II(prothrombin), VII, IX and X

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7
Q

Define a thrombus

A

A solid mass of blood that forms within the circulatory system, during life.

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8
Q

Describe the look of a venous thrombus

A

Soft, gelatinous, deep red, higher cell content

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9
Q

Where do most venous thrombi begin?

A

At valves- natural degree of turbulence as protrude into vessels lumen and may be damaged by trauma, stasis or occlusion.

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10
Q

Histological appearance of coagulative necrosis, and name 3 other types of necrosis

A

‘Ghost outline’ of cells, with cellular architecture preserved.
Liquefactive, caseous and fat necrosis

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11
Q

What colour infarct would you expect an MI to be and why?

A

White infarct as coronary arteries occluded are functional end arteries, providing the sole source of blood supply to areas of the heart.

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12
Q

Nuclear changes in necrotic cells with light microscope

A

Pyknosis- nuclear shrinkage, Karyolysis-nuclear dissolution and Karyohexis- nuclear fragmentation

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13
Q

Why does the cell cytoplasm swell in ischaemia and list other reversible cell changes in ischaemia.

A

Ischaemia- blood supply hence oxygen supply cut off to cells, so insufficient O2 for oxidative phosphorylation which produces ATP, so deficit of ATP required for Na+/K+/ATPase to function normally, Na+ not pumped out of cell so remains inside cell, so H20 influx as Na+ is an osmotically active ion.
Chromatin clumping, reduced eosinophilic staining of cytoplasm

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14
Q

Irreversible cell changes in ischaemia

A

Pyknosis, Karyolysis, Karyohexis, lysosomal rupture, ER lysis, membrane defects.

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15
Q

Define necrosis

A

The morphologic changes that follow cell death in a living tissue, largely due to progressive degradative action of enzymes on cell.

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16
Q

Define apoptosis

A

Active process of programmed cell death of single cells.

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17
Q

Pathological and Physiological example of apoptosis

A

Pathological: graft versus host disease
Physiological: limb development- digit sculpting

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18
Q

List 4 histological features where necrosis different from apoptosis

A

Necrosis Apoptosis
Death of contiguous Single cell
groups of cells death
Adjacent inflammation None
Cell size increases but shrinkage in apoptosis.
Pyknosis, Karyohexis and Karyolysis but fragmentation of nucleus into nucleosome size fragments in apoptosis.

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19
Q

4 clinical features of acute inflammation

A

Rubor, Calor, Dolor, Tumor

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20
Q

Define disease

A

Consequence of failed homeostasis with consequent morphological and/or functional disturbances.

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21
Q

When does cell injury become irreversible?

A

Massive cytosolic accumulation of Ca2+, espec. from stores in organelles e.g. ER and mit. Array of potent enzymes activated: ATPases, Phospholipases, Endonucleases, Proteases and protein Kinases.

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22
Q

Name 2 local mediators important for increased vascular permeability in inflamed tissues

A

Histamine and leukotrienes

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23
Q

Name 2 endogenous pyrogens responsible for fever in acute inflammation

A

TNF-alpha and IL-1

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24
Q

What is the molecular abnormality in inherited angio-oedema?

A

Absence of the inhibitor of the first component of complement- C1 esterase inhibitor. This causes tissue swelling, especially of the face.

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25
Q

Name the bacterium implicated in gastric ulceration and explain why the gastric ulcer will heal with a scar.

A

Helicobacter pylori. Imbalance between acid production and mucosal defence, and collagen framework destroyed.

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26
Q

Name the 3 main cells involved with chronic inflammation.

A

Lymphocytes, Macrophages and Plasma cells.

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27
Q

Name 2 complications of chronic inflammation

A

Fibrosis, atrophy, stimulation of an immune response

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28
Q

Name an AI disease that causes hyperthyroidism. What other mechanism, apart from autoimmunity, involves the immune system causing cell injury?

A

Grave’s disease

Hypersensitivity reactions.

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29
Q

Name 2 complications of granulomatous inflammation that might occur in the bowel

A

Strictures, fistulae

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30
Q

Name 3 types of multinucleated giant cells

A

Langhans’ giant cell, Touton giant cell and foreign body giant cell.

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31
Q

Name the principal cellular constituents of granulation tissue

A

Fibroblasts, myofibroblasts, endothelial cells- capillaries and lymphatics

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32
Q

What is DIC?

A

Disseminated intravascular coagulation: widespread activation of the clotting cascade with subsequent consumption of clotting factors, with resultant increased risk of bleeding as increase in time it takes for blood to clot. A combination of haemorrhage and thrombosis complicates another disorder. Increased PTT and APTP. Must treat identifiable cause e.g. fracture/infection. Can give fresh frozen plasma which contains clotting factors.

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33
Q

What clinical features seen on a patient may suggest hyperlipidaemia?

A

Xanthelasma, Corneal arcus, Xanthoma

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34
Q

Why is an inflammatory response absent in apoptosis?

A

Plasma membrane remains intact.

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35
Q

How can a paracetemol overdose cause liver damage?

A

Paracetemol normally undergoes phase II drug met. but at an excess dosage, these pathways become saturated and it instead undergoes phase I metabolism, producing the toxic metabolite NAPQI- toxic to hepatocytes as binds to sulphydryl groups on their membranes, causing nercrosis and liver failure. NAPQI undergoes phase I met. with glutathione, depleting cells of this important anti-oxidant for protection against ROS.

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36
Q

What could be used to treat a paracetemol OD and explain how this works?

A

N-acetyl cysteine, this increases the availability of hepatic glutathione, an important defence against anti-oxidants and necessary as glutathione depleted in drug OD.

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37
Q

Which three cancers are there national screening programmes in place for in the UK?

A

Breast, bowel and cervical

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38
Q

Define a protooncogene

A

signal transducers that act to regulate normal cell division and growth. If mutated, form oncogenes-causes cellular transformation.

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39
Q

What do the G1 and G2 phases in the cell cycle allow?

A

Time for cell growth and cell cycle checkpoints so that incorporation of DNA damage is prevented before a cell undergoes division.

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40
Q

Which phase of the cell cycle do permanent cells reside in?

A

The terminal differentiation phase, from G0.

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41
Q

How do GFs regulate cell proliferation?

A

They bind to specific cell surface receptors, which are generally transmembrane proteins with cytoplasmic tyrosine kinase domains. Activation of tyrosine kinase causes phosphorylation of receptor on specific cytoplasmic domains creating sites for protein-protein interactions, so recruitment and activation of signalling enzymes or adaptor molecules, which are signal transducers, can occur. These transducers serve as enzyme modulators for signalling enzymes.
GF stimulation induces proteins such as CDKs and cyclins.

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42
Q

Name 2 tumour suppressor proteins

A

p53 and retinoblastoma. These are most frequently disrupted in cancer cells.

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43
Q

Describe familial adenomatous polyposis, referring to the gene involved, and then explain how mutations in this gene can cause carcinomas of the colon and rectum.

A

FAP is a rare condition characterised by inactivating germline point mutations in the APC gene-a tumour suppressor gene, resulting in numerous growths of adenomas in the colon These mutations are uncommon, but somatic mutations are more frequent. APC protein binds to beta catenin, and acts to promote the degradation of beta-catenin protein, a protein which drives transcriptional activation, so in APC-mutated cells, beta-catenin accumulates and binds and activates transcription factors, causing deregulated growth control and cancer.

44
Q

Name a tumour marker for hepatocellular carcinoma.

A

alpha-fetoprotein

45
Q

What tumour is carcino-embryonic antigen a marker for?

A

GI tract tumours

46
Q

What name is given to the staging method used for colorectal cancer?

A

Dukes’ staging

47
Q

What grading system is used for breast carcinoma?

A

Bloom-Richardson system

48
Q

What name is given to the cell which characterises Hodkin’s lymphoma?

A

reed-sternburg cell- big nuclei, paired cells

49
Q

Which tumour markers are of value in the diagnosis of testicular tumours?

A

Human chorionic gonadotrophin and alpha-fetoprotein

50
Q

How is Hodkin’s disease staged and what name is given to this type of staging?

A

Stage 1- lymphoma in a single nodal region
Stage 2- 2 separate regions on 1 side of diaphragm
Stage 3- spread to both sides of diaphragm
Stage 4- diffuse or disseminated involvement of 1 or more extra-lymphatic organs e.g. BM or lungs.

Ann-Arbor staging

51
Q

What is tumour staging a measure of?

A

The overall burden of a malignant neoplasm. It is a powerful predictor of survival.

52
Q

What is tumour grading a measure of?

A

The degree of differentiation of a neoplasm. Tumour grade is more important for planning treatment and estimating prognosis in certain types of malignancy e.g. lymphomas, breast and prostate cancer, soft tissue sarcoma and primary brain tumours.

53
Q

What does the Bloom-Richardson system assess?

A

Tubule formation, nuclear variation and number of mitoses.

54
Q

Describe how tamoxifen is used in the treatment of breast cancer.

A

Tamoxifen=oestrogen receptor modulator. It binds to oestrogen receptors, preventing oestrogen from binding and so can be used in the treatment of hormone receptor-positive breast cancer.

55
Q

Which hormone therapy is used for prostate cancer?

A

Androgen blockage

56
Q

Define adjuvant treatment

A

Treatment given after surgical removal of a primary tumour to elimiante subclinical disease.

57
Q

Define neoadjuvant treatment

A

Treatment given to reduce the size of a primary tumour prior to surgical excision.

58
Q

Describe how radiation therapy kills proliferating cells in the treatment of cancer?

A

X-rays or other types of ionising radiation are used which kill rapidly dividing cells, espec. in G2 of cell cycle, as a high dosage causes either direct or free-radical induced DNA damage detected by cell-cycle checkpoints, triggering apoptosis. Double-stranded DNA breakages cause damaged chromosomes that prevent M phase from completing correctly.

59
Q

How does chemotherapy affect proliferating cells?

A

Antimetabolites: mimic normal substrates involved in DNA replication e.g Fluorouracil
Alkylating and platinum-based drugs: cross-link the 2 strands of the DNA helix e.g. cisplatin.
Antibiotics: can causes double-stranded DNA breaks e.g. bleomycin.
Plant-derived drugs: block microtubule assembly and interfere with mitotic spindle formation e.g. vincristine.

60
Q

What would be the difference in colonic appearance between FAP and hereditary non-polyposis colon cancer? What happens in HNPCC?

A

FAP: lots of polyps in the colon, not lots of polyps in colon for HNPCC.

HNPCC: Mutation of DNA mismatch repair gene

61
Q

Describe basic causes of cell injury

A
  • hypoxia: ischaemic, histiocytic, anaemic, hypoxaemic
  • chemicals e.g. toxins
  • physical agents e.g. direct trauma, temp.extremes, pressure changes.
  • radiation
  • microbes
  • nutritional
  • immune mechanisms e.g. hypersensitivity and AI.
62
Q

Define chronic inflammation

A

chronic response to injury with assoc. fibrosis.

63
Q

When does chronic inflammation arise?

A
  • resistance of infective agent to phagocytosis and IC killing e.g. TB, leprosy
  • endogenous materials e.g. necrotic AT, uric acid crystals
  • exogenous materials e.g. asbestos fibres
  • AI diseases
  • specific diseases of unknown cause e.g. chronic inflammatory bowel disease.
  • primary granulomatous diseases e.g. Crohn’s, sarcoidosis
  • transplant rejection
64
Q

What factors are involved in predicting outcome for a patient with a malignant neoplasm?

A
  • age
  • general health status
  • availability of effective treatments
  • type of tumour
  • tumour grading
  • tumour staging
  • tumour site
65
Q

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

A

TNM staging system:
T=tumour size, T1-T4
N= extent of regional node metastasis, N0-N3
M=extent of distant metastatic spread, M0-M1

66
Q

What range of stages might a malignant neoplasm be classed as?

A

Stages I-IV

67
Q

Describe Dukes staging for colorectal carcinoma.

A

A: invasion into but not through bowel wall
B: invasion through bowel wall
C:lymph node involvement
D: distant metastases

68
Q

Describe general grading of malignant neoplasms.

A

G1-well-differentiated
G2- moderately differentiated
G3-poorly differentiated
G4-undifferentiated/anaplastic

69
Q

Why is chemotherapy classed as non-specific?

A

It targets all rapidly proliferating cells.

70
Q

What problems can screening for cancers have?

A

Lead-time bias: bias that occurs when two tests for a disease are compared, and one test (the new, experimental one) diagnoses the disease earlier, but there is no effect on the outcome of the disease — it may appear that the test prolonged survival, when in fact it only resulted in earlier diagnosis when compared to traditional methods, over-diagnosis and length bias: this can give the impression that detecting cancers through screening causes cancers to be less dangerous, when the reality is that less dangerous cancers are simply more likely to be detected by screening.

71
Q

What happens in Kelloid?

A

CT disorder where abnormal amounts of collagen produced, causing scars to appear on the skin.

72
Q

What occurs in systemic sclerosis?

A

CT disorder where all organs of body have an excessive accumulation of collagen (excessive fibrosis).

73
Q

How does xeroderma pigmentosum occur?

A

mutations in base-excision repair enzymes.

74
Q

What is the difference between a transudate and an exudate? Which is produced when streptococcus pneumoniae invades the lungs?

A

a transudate is a fluid produced solely as a result of changes in hydrostatic pressure, whereas an exudate is a protein rich fluid that is formed as a result of a gradient of oncotic pressure.
Exudate

75
Q

Describe features of benign neoplasms

A

Confined to site of origin
Well-defined, regular outline, Pseudocapsule- compressed tissue around tumour as pushing of outer margin due to growth in confined areea
Well-differentiated, cellular and nuclear pleomorphism minimal
low mitiotic activity
slow growth rate

76
Q

Describe features of malignant neoplasms

A

Potential to metastasise
Irregular outer margin and shape, infiltraative growth edges
Well to poorly differentiated-anaplastic
High mitotic activity, may be abnormal mitoses
Relatively rapid growth rate
Increasing nuclear size, increased nuclear to cytoplasmic ratio, more mitotic figures and increasing variation in size and shape of cells and nuclei, so pleomorphism. Usually hyperchromatic so nucleus stains more darkly
Necrosis central from defective vascular perfusion
Ulceration on skin or mucosal surfaces, may break causing haemorrhage and leading to anaemia

77
Q

Example of a physiological apoptosis?

A

Limb morphogenesis

78
Q

Example of a pathological apoptosis?

A

Graft versus host disease

79
Q

Why are infarcts to the lung typically haemorrhagic?

A

as the lung receives a dual blood supply

80
Q

Are infarcts ever a manifestation of apoptosis?

A

No, infarcts refer to ischaemic necrosis, with the death of many cells, whereas apoptosis is the death of single cells

81
Q

Describe how H2O2 produced by neutrophils is used in the oxygen dependent killing pathway of phagocytosed material

A

H2O2 is a substrate for myeloperoxidase. They react in the presence of a halide e.g. Cl-, to produce HOCL- which is a potent microbicidal agent.

82
Q

What do blood monocytes respond to in order to become tissue macrophages?

A

Interferon gamma- produced by T helper 1 cells

83
Q

DVT prophylaxis?

A 
TED stockings (thromboembolicdeterrent)
SC heparin- cofactor for antithrombin III- binding activates ATIII
84
Q

How is thrombosis prevented by the normal endothelium?

A

Production of prostacyclin
Production of thrombomodulin- binds to any locally formed thrombin and activates protein C
*

85
Q

When might atrophy occur?

A

Loss of innervation
Lack of muscle use
Loss of blood supply
Poor nutrition

86
Q

why is inflammation not associated with apoptosis?

A

because the plasma membrane of cells remains intact

87
Q

how do nerves repair themselves?

A

Axon distal to the cut degenerates and the axon above the cut begins to sprout new axons. One of these axons becomes the replacement axon by inserting through the axon tube distally and the other sprouting axons degenerate.
Regeneration occurs at a rate of 2-3mm a day, so slow recovery

88
Q

how do platelets adhere to damaged blood vessels?

A

subendothelial material exposed- collagen and vWF- both bind receptors on platelets, become activated, release pro-aggregatory factors e.g. ADP, 5HT

89
Q

factors that inhibit thrombin?

A

proteins C and S
antithrombin iii- requires heparin as a cofactor
alpha 1 antitrypsin- deficiency can cause empysema*

90
Q

most common cause of fat emoblism?

A

fracture of long bones-fat released from BM, can lead to confusion and coma

and breakdown of lots of AT

can result from pancreatitis with lipases acting on FA producing fat necrosis

91
Q

DVT RFs?

A

post-op
post-partum
OCP
limb immobilisation/bed rest

92
Q

what can be used to increase platelet production in thrombocytopenia?

A

corticosteroids

93
Q

3 processes in acute inflammation?

A

blood flow changes
exudate
inflammatory cell infiltration

94
Q

type of cell death in hepatitis?

A

apoptosis

95
Q

how does shock occur in acute pancreatitis?

A

inflammation- mediators e.g. histamine and prostaglandins- arteriolar and capillary vasodilatation so decrease in TPR and arterial BP, so reduced perfusion, exudate formation- increased viscosity of blood, possible blood clots- maybe DIC- reduced perfusion to vital organs

96
Q

when do pathological Q waves start to develop after MI and why do they develop?

A

Q wave begins hrs-day1/2 after MI, deeper within first few days, persists even after ST and T normalised wks later
cardiac myocytes= permanent cells= unable to regenerate, so healing is by fibrosis- scar tossue deposited- collagen- CHAADTATECLA. waves more than 2mm in depth and more than 0.04s(1 small square) wide. Result as necrotic area creates ‘window’ so lead sees through area, and views back of heart so sees downward Q wave rather than upward R wave. Once Q wave developed, it is usually permanent. ST elevation- opposite to angina- ST depression, cells no longer able to maintain integrity of membranes so break down, get short circuit and injury currents, so flow throughout systole results in changes in electric field.

97
Q

why does liquefactive necrosis occur in brain after infarct?

A

cells heal by gliosis, and lack support of robust collagenous matrix

98
Q

disorders complicated by DIC?

A

infections (e.g. septicaemia- meningococcal meningitis- treat with ceftriaxone as can cross inflamed BB barrier), neoplasm, tissue trauma (e.g. burns

99
Q

blood results of DIC?

A

Fibrinolytic system activated in DIC and plasmin is generated- may attack fibrinogen and coagulation factors V and VIII aswell as fibrin. Fibrinogen and fibrin degradation products produced which have anti-coagulant and anti-platelet effect, contributing to haemorrhagic diathesis. Low blood platelet count, prothrombin time- marker of extrinsic pathway, and activated partial thromboplastin time prolonged. Fibrinogen concentration reduced.

100
Q

what cell characterises liquefactive necrosis?

A

neutrophils- release proteases*emphysema

101
Q

how does insulin regulate phosofructokinase?

A

activates a phosphatase enzyme, and so dephosphorylates, which increases the amount of active enzyme so stimulates glycolysis

102
Q

2 factors controlling collagen formation?*

A

TNF alpha, TGF beta

103
Q

3 key features of healing and repair?

A

cell migration- phagocytsosis, endothelial cells, fibroblasts- chemotaxis
angiogenesis- VEGF e.g. from platelets
EC matrix production and remodelling- collagen, fibroblasts and myofibroblasts- control via TGF beta

blood clot replaced by granulation tissue

104
Q

describe skin repair

A 
Primary intention- small incision, well apposed edges, good blood supply
○ Minimal clot and granulation tissue
○ Epidermis regenerates
○ Dermis undergoes fibrous repair
○ Minimal scarring
● Secondary Intention
○ Large clot to form eschar
○ More granulation tissue
○ More extensive scarring
105
Q

examples of physiological atrophy?

A

vaginal atrophy at menopause due to reduced oestrogen
vagina only completes development at puberty: lactobacilli arise, due to increase in oestrogen
Lbacilli: convert glycogen into lactic acid, maintaining low pH, prevents candida albicans overgrowth, in oesophagus= oesophageal candidiasis- cause of odynophagia

ESA Revision (15 decks)

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