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ESA 2 > Mechanisms of Disease > Flashcards

Mechanisms of Disease Flashcards

1
Q

Define apoptosis

A

Programmed cell death by intracellular programmes (degradation of DNA/proteins)

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1
Q

Apart from TB name three other granulomatous infections.

A

-Leprosy -Cat-scratch disease -Syphilis -Chronic fungal infections -Xanthogranulomatous pyelonephritis

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1
Q

Define aplasia

A

Complete failure of a specific tissue or organ to develop

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2
Q

Define arteriosclerosis

A

The thickening of the walls of arteries and arterioles, usually as a result of hypertension or diabetes mellitus

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2
Q

Define atheroma

A

The accumulation of intracellular and extracellular lipid in the intima and media of large and medium sized arteries

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3
Q

Define atherosclerosis

A

The thickening and hardening of arterial walls as a consequence of atheroma

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4
Q

Define disease.

A

The consequence of failed homeostasis with consequent morphological and function disturbances

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4
Q

Define chronic inflammation.

A

Chronic response to injury with associated fibrosis

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4
Q

Define atrophy

A

Shrinkage of a tissue or organ due to an acquired decrease in size and/or number of cells

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5
Q

Define dysplasia

A

Abnormal maturation of cells within a tissue

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6
Q

Define hyperplasia

A

Increase in tissue or organ size due to increased cell numbers.

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7
Q

Define hypertrophy

A

Increase in tissue or organ size due to increased cell size.

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7
Q

Define hypoplasia

A

Incomplete development of a tissue or organ

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8
Q

Define metaplasia

A

Reversible change of one DIFFERENTIATED cell type to another.

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9
Q

Define necrosis

A

Changes after cell death in living tissue

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10
Q

Describe the appearance of caseous necrosis

A

It looks like cheese - contains an amorphous (structureless) debris

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10
Q

Define regeneration.

A

The replacement of dead or damaged cells by functional, differentiated cells

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10
Q

Describe the appearance of an arterial thrombi?

A

Pale, granular, low cell count and lines of Zahn

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10
Q

Describe the appearance of a venous thrombi?

A

Deep red, soft, gelatinous and a high cell count

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11
Q

Describe the basic structure of the collagen molecule

A

-Glycine every third position -3 alpha chains -Left handed triple helix -Mostly hydroxyproline and proline residues in other positions

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12
Q

Describe the differences in the appearance of benign and malignant tumour to the naked eye.

A

-Benign - grow in a confined local area and so have a pushing outer margin -Malignant - irregular outer margin and shape and may show areas of necrosis and ulceration

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13
Q

Describe the features of coagulative necrosis

A

-Histologically the structure is preserved creating “ghost outlines” -After this the tissue goes through acute inflammation and there is a mass immigration of phagocytes and neutrophil polymorphs -Increased eosinophilia of cytoplasm

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14
Q

Describe the features of liquefactive necrosis

A

-Liquefaction of tissues -Massive neutrophil immigration

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15
Q

Describe the four steps of infiltration of neutrophils.

A
  1. Margination - neutrophils line up at the edge of blood vessels along the endothelium 2. Rolling - neutrophils roll and begin to stick 3. Adhesion - fully stick 4. Emigration
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15
Q

Describe the mechanism of fibrous repair.

A

1) Inflammatory cells infiltrate the blood clot (neutrophils digest, macrophages + lymphocytes are recruited)
2) Angiogenesis occurs where capillaries/lymphatics sprout and myo/fibroblasts migrate and differentiate laying down ECM and collagen
3) Cell population falls, collagen increases and the myofibroblasts pull it together - left with a fibrous scar.

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15
Q

Describe the healing of a bone fracture.

A

1) Haematoma - forms from ruptured vessels within marrow cavity and periosteum. Haematoma allows for an invasion of macrophages, endothelial cells fibroblasts and osteoblasts allowing necrotic tissue to be removed and for capillaries develop.
2) Soft callus - bone is laid down in an irregular woven pattern, sometimes with islands of cartilage
3) Hard callus - Woven bone replaced with more organised lamellar
4) Remodelling - the bone is shaped by stresses of different movements N.B. a callus is described as a specialised mixture of cells

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15
Q

Describe the macroscopic appearance of atheroma

A

-Fatty streak (yellow bumpy lipid deposits at the intima) -Simple plaque (irregular outline, raised white/yellow colour) -Complicated plaque (thrombosis, haemorrhage, calcification or aneurysm)

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16
Q

Describe the microscopic appearance of atheroma

A

-Early changes - proliferation of smooth muscle cells, lots of foam cells and extracellular lipids -Later changes - fibrosis, necrosis, inflammatory cells and cholesterol clefts

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17
Q

Describe the normal structure of an artery from inside to outside.

A

-Endothelium -Sub-endothelial connective tissue -Internal elastic lamina -Muscular media -External elastic lamina -Adventitia

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18
Q

Describe the process of degradation and phagocytosis in apoptosis

A

-Cell breaks into membrane-bound fragments that are taken up by neighbouring cells or phagocytes. -Membrane bound “apoptotic bodies” express proteins on their surface that are essential for phagocytosis by neighbouring cells.

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18
Q

Describe the process of angiogenesis in wound healing.

A

1) Endothelial proteolysis of basement membrane 2) Migration of endothelial cell via chemotaxis 3) VEGF causes endothelial proliferation 4) Endothelial maturation and tubular remodelling 5) Recruitment of periendothelial cells - become the pericytes and smooth muscle tissue of the blood vessel, they are important in maintaining the stability of the blood vessels.

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19
Q

Describe the systemic effects of alcohol abuse.

A
  • Liver - alcoholic cirrhosis and acute hepatitis
  • Nervous system - thiamine deficiency produces degeneration of nerve cells
  • CV system - cardiac muscle degeneration causing cardiomyopathy, hypertension and arrythmias
  • GI system - gastritis/pancreatitis
  • Skeletal muscle - Rhabdomyolysis and chronic myopathy
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20
Q

Describe the three main stages of the change of blood flow during acute inflammation.

A
  1. Transient vasoconstriction 2. Vasodilatation of arteries/capillaries (increased bloodflow/redness) 3. Increased permeability (exudation of protein rich fluid into tissues)
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20
Q

For benign neoplasms which effects of the growth are the most relevant?

A

-Local effects -Hormonal effects

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21
Q

Give a physiological and pathological example of hyperplasia

A

-Physiological causes - proliferative endometrium, bone marrow at altitude -Pathological Causes - thyroid goitre

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22
Q

Give a physiological and pathological example of hypertrophy

A

-Physiological causes - skeletal muscle and pregnant uterus (hypertrophy + hyperplasia) -Pathological causes - ventricular cardiac muscle hypertrophy, bladder smooth muscle hypertrophy

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23
Q

Give an example of one physiological and one pathological role of apoptosis.

A

-Physiological - Web space loss in embryogenesis -Pathological - Graft versus host disease

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24
Q

Give five functions of the extracellular matrix.

A

-Supports and anchors cells -Separates tissue compartments e.g. basement membrane -Sequesters growth factors -Allows communication between cells -Facilitates cell migration

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25
Q

Give the anagram commonly used for collagen synthesis and briefly outline what each letter stand for.

A

CHASPOGRL: -Cleavage of signal peptide -Hydroxylation of proline/lysine residues -Addition of N-linked oligosaccharides -Sulphide bond (di) formation -Procollagen - formation of triple helix -O-linked glycosylation -Golgi then exocytosis -Removal of terminal peptides (procollagen peptidase) -Lateral aggregations to form fibrils

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26
Q

Give two ways in which the immune system can damage cells?

A

-Hypersensitivity -Autoimmune

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27
Q

How are inflammatory cells recruited in fibrous repair?

A

Chemotaxis

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27
Q

How are malignant cells transported to distant sites?

A

1) Blood vessels (via capillaries and venules) 2) lymphatic vessels 3) Fluid in body cavities (pleura, peritoneal, pericardial and brain ventricles)

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29
Q

How can an aspirin overdose cause problems?

A

Stimulates respiratory centre resulting in a respiratory alkalosis. Compensatory mechanisms result in a metabolic acidosis – fall in pH indicates serious poisoning

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30
Q

How can atheroma be prevented?

A

-Stop smoking -Modify diet -Treat hypertension -Treat diabetes -Lipid lowering drugs

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31
Q

How can endothelial injury occur?

A

-Raised LDL -‘Toxins’ e.g. cigarette smoke -Hypertension -Haemodynamic stress

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32
Q

How can you diagnose alcoholic hepatitis?

A

-Elevated serum bilirubin -Elevated aminotransferases -Elevated alkaline phosphatase -Elevated prothrombin time

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33
Q

How can you diagnose someone with excessive alcohol intake?

A

-Elevated MCV - macrocytic (due to damaged bone marrow/folate deficiency) -Raised AST and ALT -Raised Gamma-GT

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34
Q

How do growth factors promote proliferation in the stem cell population?

A

Extracellular signals transduced into the cell. There promote expression of genes controlling cell cycle.

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35
Q

How do malignant cells take advantage of nearby non-neoplastic cells?

A

Form “cancer niches” where the normal cells provide some growth factors and proteases

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36
Q

How do neutrophils move? What chemical mediators are required?

A

Chemotaxis by: -C5a -LTB4 -Bacterial peptides

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38
Q

How does angiogenesis occur in fibrous repair?

A

Platelets, ECM and others produce angiogenic cytokines in response to hypoxia e.g. VEGF, bFGF

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39
Q

How does contact between the basement membranes & adjacent cells control the rate of cell division?

A

Contact inhibition - signalling through adhesion molecules inhibits proliferation in intact tissue. If this contact is lost proliferation occurs.

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40
Q

How does pain and loss of function combat injury?

A

Enforces rest (stops further injury)

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41
Q

How does smooth muscle proliferation occur during atheroma?

A

Endothelial damage leads to increased platelets and PDGF which then leads to smooth muscle proliferation

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43
Q

How does the exudation of fluid combat injury?

A

-Delivers plasma proteins (immunoglobins, fibrinogen, inflammatory mediators) -Dilutes toxins -Increases lymphatic drainage (so it delivers micro-organisms to phagocytes and antigens to immune system)

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43
Q

How does the body go about resolving acute inflammation using chemical mediators?

A

-All chemical mediators of acute inflammation have short half-lives, some can be degraded (heparinase) or inhibitors may bind (anti-proteases) -Chemical mediators may be diluted in the exudate -Lipoxins, endothelin

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43
Q

How does the fibroblast and ECM proliferation occur in fibrous repair?

A

Macrophages produce various pro-fibrotic cytokines, e.g. IL1, TNF alpha, TGF beta

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44
Q

How does the increased smooth muscle cause increased foam cells?

A

Proliferation and migration of smooth muscle takes the lipid with it. Macrophages arrive and phagocytose the fat, becoming foam cells

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45
Q

How does the infiltration of cells combat injury?

A

Removes pathogenic organisms/necrotic debris

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45
Q

How does vasodilatation combat injury?

A

-Increases delivery -Increases temperature

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47
Q

How is the vascular wall made more permeable during acute inflammation?

A

Chemical mediators: -Histamine, leukotrienes cause endothelial contraction which creates gaps -Cytokines IL-1 and TNF cause cytoskeletal reorganisation which creates gaps -VEGF which creates channels across endothelial cytoplasm

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47
Q

How is apoptosis initiated and executed?

A

-Intrinsic - Everything required is in the cell - usually due to the response to DNA damage by p53. Causes mitochondria to be more permeable, release cytochrome c, mixes with caspase 9 and APAF1 to form an apoptosome activates caspases -Extrinsic - an external ligand (TRAIL or Fas) bind to a death receptor resulting in caspase activation

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48
Q

How long can a cell survive hypoxia?

A

Trick question…mwhahaha Some neurones can only stand a few minutes, however, some fibroblasts in the dermis can stand hours.

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48
Q

How might fat necrosis be diagnosed? Why can you use this method?

A

X-rays - free fatty acids released and they react with calcium to form chalky deposits in fatty tissue

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50
Q

In general what is a neoplasm?

A

An abnormal growth of cells that persists after the initial stimulus is removed

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51
Q

In what cell populations can hyperplasia occur?

A

Labile/stable cell populations

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51
Q

In what type of cell population do germ cell neoplasms arise?

A

Pluripotent

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52
Q

In which three ways can chronic inflammation arise?

A

-Take over from acute inflammation (if damage is to severe to be resolved) -Arise anew (by some chronic low level irritation i.e. RA) -Alongside acute inflammation (when there is severe/repeated irritation)

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52
Q

Increasing tumour burden and cytokine release due to secondary neoplastic effects canlead to what presentation?

A

-Reduced appetite and weight loss -Cachexia -Malaise -Immunosuppression (can also be due to direct bone marrow destruction) -Thrombosis.

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53
Q

List five causes of acute inflammation.

A

-Microbial -Tissue necrosis -Hypersensitivity -Physical agents -Chemical agents

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55
Q

List four of the main thrombin inhibitors

A

Anti-thrombin III, Alpha 1 anti-trypsin, Alpha 2 macroglobulin and Protein C/S

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56
Q

List some irreversible changes of hypoxia

A

-Huge cystolic Ca2+ increase -Several enzymes activated resulting in cell death

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57
Q

List some reversible changes of hypoxia

A

-Increased anaerobic respiration producing lactate and therefore lowering pH -Low ATP means Na+ accumulates in cells -Cell swells via osmosis -Detachment of ribosomes which leads to decreased protein synthesis

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58
Q

Name some common causes of cirrhosis? (replacement of liver tissue by fibrosis, scar tissue and regenerative nodules)

A

-Alcohol -Infection with HBV, HCV -Fatty liver disease -Drugs and toxins

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59
Q

Name three types of giant cell and explain in which condition they are commonly seen in.

A

-Langhans cells - TB -Foreign Body cells - any foreign body, commonly sutures -Touton cells - fat necrosis

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61
Q

Neoplasms originating in what area most commonly metastasise to the bone?

A

-Breast -Bronchus -Kidney -Thyroid -Prostate

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62
Q

Other than pancreatitis, what else can cause fat necrosis?

A

Also can occur after direct trauma to fatty tissue (for example breast tissue)

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63
Q

Other than thrombosis suggest other causes of embolism

A

-Nitrogen -Air -Amniotic fluid -Medical Equipment -Tumour cells

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64
Q

Suggest some common sites for blood borne metastasis.

A

-Lung -Bone -Liver -Brain

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65
Q

Suggest some common sites of atheroma

A

-Abdominal aorta -Coronary arteries -Carotid arteries -Cerebral arteries -Leg arteries

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66
Q

Suggest some miscellaneous systemic effects of neoplasms.

A

-Neuropathies affecting the brain and peripheral nerves -Skin issues (pruritis and abnormal pigmentation) -Fever -Myositis

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67
Q

What abnormal accumulations are seen under a light microscope during cell injury in alcoholic liver disease?

A

-Keratin deposition (Mallory’s hyaline) -Fat deposition

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69
Q

What are acute-phase proteins? Give examples of some of these proteins.

A

Proteins that concentrations increase or decrease in response to inflammation. For example: C-reactive protein, a1 antitrypsin, haptoglobin, fibrinogen etc.

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71
Q

What are blastomas?

A

Occur mainly in children and are formed from immature precursor cells

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71
Q

What are amyloidosis?

A

A variety of conditions where normally soluble proteins become insoluble and are deposited in the extracellular space of various organs or tissues, disrupting normal function.

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73
Q

What are cells with no resemblance to any tissue called?

A

Anaplastic

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74
Q

What are giant cells? When does it usually occur?

A

Multinucleate cells made by fusion of macrophages, usually occurs during frustrated phagocytosis.

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75
Q

What are initiators of mutation? Give some of the main examples

A

Mutagenic agents - chemicals, infections, and radiation are the main initiators

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76
Q

What are neutrophils?

A

Neutrophils are a type of granulocyte and are the primary type of white blood cell involved in inflammation.

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77
Q

What are paraneoplastic syndromes?

A

Indirect systemic effects of neoplasms. (e.g. includeeffects of increasing tumour burden, secreted hormones etc.)

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79
Q

What are plasma cells?

A

Differentiated antibody-producing B lymphocytes

80
Q

What are sarcomas?

A

Stromal malignant neoplasm

82
Q

What are some of the complications of fibrous repair?

A
  • Excessive fibrosis - Insufficient fibrosis - Excessive contraction
82
Q

What are small clusters of malignant cells that lodge at secondary sites but fail to grow called?

A

Micrometastases

83
Q

What are the 4 types of hypoxia?

A

-Ischaemic -Anaemic -Hypoxaemic -Histiocytic

84
Q

What are the common effects of venous thrombi?

A

-Congestion -Oedema -Ischaemia -Infarction

85
Q

What are the effects of aspirin over use?

A

-Acute erosive gastritis producing GI bleeding -Inhibits platelet cyclo-oxygenase producing decreased platelet aggregation which results in petechaie

85
Q

What are the five possible outcomes of thrombosis?

A

-Lysis (breakdown) -Propagation (progressive spread of thrombosis, distally in arteries, proximally in veins) -Organisation (reparative process with ingrowth of fibroblasts and capillaries. ) -Recanalisation (blood flow starts again, little holes in the thrombus) -Embolism (breaks off and ends up obstructing a vessel)

86
Q

What are the folds of the brain called?

A

Gyri

88
Q

What are the four main changes in tissue during acute inflammation?

A

-Vasodilation -Exudation of fluid -Infiltration of cells -Pain…and loss of function

89
Q

What are the four main effects of chronic inflammation?

A

-Fibrosis -Impaired function -Atrophy -Stimulation of an immune response

90
Q

What are the four main types of necrosis?

A

-Coagulative -Liquefactive -Caseous -Fat necrosis

90
Q

What are the four possible consequences of acute inflammation?

A

-Complete resolution -Continued acute inflammation with some chronic inflammation = abscess -Chronic inflammation and fibrous repair -Death

92
Q

What are the functions of lymphocytes?

A

-B lymphocytes differentiate to produce antibodies -T lymphocytes are responsible for control and some cytotoxic functions

92
Q

What are the functions of fibroblasts/myofibroblasts?

A

Recruited by macrophages to make collagen which can tighten and pull damage together.

94
Q

What are the functions of macrophages in chronic inflammation?

A

-Phagocytosis -Processing and presentation of antigen to immune system -Synthesis of cytokines, complement component, blood clotting factors and proteases -Control of cells via cytokine release

95
Q

What are the grooves of the brain called?

A

Sulci

96
Q

What are the main causes of cell injury and death?

A

-Hypoxia -Toxins -Physical agents (trauma, temperature pressure etc.) -Radiation -Micro-organisims -Immune mechanisms -Dietary insufficiencys/excesses

97
Q

What are the main cells involved in the chronic inflammatory response?

A

-Macrophages -Lymphocytes -Plasma cells -Eosinophils -Fibroblasts/myofibroblasts

99
Q

What are the most lethal features of a malignant neoplasm?

A

Invasion and metastasis

100
Q

What are the three types of cells with different regeneration ability? Give an example of each.

A

-Labile (active cells with the normal state being cell division - high proliferation) i.e. epithelial or haematopoietic cells -Stable (resting state at G0 with varying speed of proliferation) hepatocytes, osteoblasts, fibroblasts -Permanent (unable to divide - have exited the cell cycle) neurones, cardiac myocytes

100
Q

What are the two main factors controlling regeneration?

A

-Growth factors -Contact between basement membranes & adjacent cells

100
Q

What are the three components of Virchow’s triad?

A

-Changes in blood flow -Changes in vessel wall -Changes in blood components

101
Q

What are the two types of gangrene? Which is more serious and why?

A

-Dry (coagulative necrosis) -Wet (liquefactive necrosis) Wet is worse as it is caused by infection which can spread into the blood causing septicaemia

103
Q

What are the two types of gangrene? Which is more serious and why?

A

-Dry (coagulative necrosis) -Wet (liquefactive necrosis) Wet is worse as it is caused by infection which can spread into the blood causing septicaemia

104
Q

What are the two types of infarct? Where are they common

A
  • White (common in the kidney and spleen - end arteries)
  • Red (bowel, lung, intestines)
106
Q

What are the two types of O2 dependent killing mechanism?

A

-Superoxide and hydrogen peroxide -H2O2-Myeloperoxidase-halide system - produces HOCl.

107
Q

What can be given to reverse the effects of paracetamol overdose? How does it work?

A

N-acetylcysteine which increases availability of hepatic glutathione

108
Q

What changes does invasion into other tissues by carcinoma cells require?

A

-Altered adhesion -Altered stromal proteolysis -Altered motility

110
Q

What complication can follow the perforation of an inflamed appendix?

A

Infection in the abdomen - peritonitis

111
Q

What cytoplasmic changes are seen under a light microscope during cell injury? Are they reversible or irreversible?

A

-Initially reduced pink staining due to water accumulation (reversible) -Later, increased pink staining due to ribosome detachment and denaturation of proteins (irreversible)

112
Q

What disease is commonly associated with caseous necrosis?

A

Tuberculosis

114
Q

What disease is commonly associated with caseous necrosis?

A

Tuberculosis

115
Q

What do blood vessels do to aid haemostasis?

A

Constrict to reduce the blood flow and therefore prevent blood loss

116
Q

What do platelets do to aid haemostasis?

A

They adhere to the vessel wall and each other forming a platelet plug to stop blood flowing out.

116
Q

What do foam cells secrete? What does this lead to?

A

Secrete cytokines causing further smooth muscle cell stimulation and recruitment of other inflammatory cells

117
Q

What do we mean by the term in-situ and what is the inverse of that term?

A

No invasion of epithelial basement membrane , the opposite of this being invasive

118
Q

What does a granuloma in Crohn’s disease consist of? How is it different to one in tuberculosis?

A

Epithelioid macrophages and giant cells surrounded by a cuff of lymphocytes. These are distinguished from those in TB by not having any central caseous necrosis.

119
Q

What does altered adhesion between malignant cells and stromal proteins require?

A

Changes in Integrin expression

120
Q

What does altered adhesion between malignant cells require?

A

Reduction in E-cadherin expression

121
Q

What does successful haemostasis depend on?

A

-Vessel wall -Platelets -Coagulation System -Fibrinolytic System

123
Q

What does the term hemiplegia mean?

A

The paralysis of one side of the body - trunk, arm and leg of one side

124
Q

What event may trigger acute inflammation of the appendix?

A

Blockage of the appendix lumen: -Faecoliths -Lymphoid hyperplasia (lots of lymphoid tissue) -Tumours

125
Q

What four things are the local effects of neoplams due to?

A

1) Direct invasion and destruction of normal tissue 2) Ulceration at a surface leading to bleeding 3) Compression of adjacent structures 4) Blocking of tubes and orifices.

126
Q

What general factors influence wound healing?

A
  • Age - Drugs - General/specific dietary deficiencies - State of health - Cardiovascular status
127
Q

What helps distal axons reconnect after being severed?

A

Neurotrophic hormones (growth factors) produced by Schwann cells which guide axonal regeneration

128
Q

What irreversible changes are seen under an electron microscope during cell injury?

A

-Nuclear changes (shrinkage, dissolution and fragmentation) -Lysosome rupture (membrane damage) -Myelin figures (defects in the membrane) -Lysis of the ER (due to membrane damage)

130
Q

What is a fistula?

A

An abnormal connection between two epithelium-lined organs

130
Q

What is a councilman body?

A

A hepatocyte that is undergoing necrosis - an eosinophilic globule often surrounded by normal parynchyma found in the liver of individuals suffering from viral hepatitis, yellow fever, or other viral syndrome.

131
Q

What is a granuloma? Why does it form?

A

A collection of lymphocytes and epitheloid histiocytes (modified, immobile macrophages). Granulomas form when the immune system attempts to wall off substances that it perceives as foreign but is unable to eliminate.

133
Q

What is a malignant neoplasm?

A

an abnormal growth of cells that persists after the initial stimulus is removed AND invades surrounding tissue with potential to spread to distant sites

135
Q

What is a metastasis?

A

A malignant neoplasm that has spread from its original site to a new non-contiguous site.

136
Q

What is a monoclonal cell population?

A

A collection of cells that all originated from a single founding cell

137
Q

What is an apotosome made from?

A

Cytochrome c, APAF1 and caspases 9 form an apoptosome

139
Q

What is an embolism?

A

The blockage of a blood vessel by a solid, liquid or gas at a site distant from its origin

140
Q

What is an infarct?

A

Ischaemia that results in necrosis

141
Q

What is dysplasia?

A

A pre-neoplastic alteration in which cells show disordered tissue organisation. It is not neoplastic because the change is reversible.

142
Q

What is fat necrosis in breast tissue commonly confused with?

A

Breast cancer - due to the scar left mimicing a nodule of breast cancer

143
Q

What is fibrinolysis?

A

Breakdown of fibrin by plasmin

144
Q

What is gangrene?

A

Necrosis that you can see

145
Q

What is granulomatous inflammation? (this is as easy as it sounds)

A

Chronic inflammation with granulomas

146
Q

What is healing by primary intention?

A

An incised wound with apposed edges, the epidermis regenerates and the dermis undergoes fibrous repair with minimal clot and granulation tissue. Minimal contraction and scarring as the granulation tissue turns to scar tissue.

146
Q

What is haemostasis?

A

The body’s response to stop bleeding and loss of blood

147
Q

What is healing by secondary intention?

A

Large wounds with unapposed edges, forms a scab (eschar) with the epidermis regenerating from the base up and a shitload of granulation tissue. This therefore produces a lot of contraction and a big ass scar.

149
Q

What is hypoxaemic hypoxia?

A

A low amount of arterial oxygen due to: -Reduced absorption -Reduced oxygen at high altitudes

149
Q

What is histiocytic hypoxia?

A

Hypoxia caused by the inability to utilise oxygen by oxidative phosphorylation (like in cyanide poisoning)

151
Q

What is leukaemia?

A

Malignant neoplasm of blood-forming cells arising in the bone marrow

152
Q

What is lymphoma?

A

Malignant neoplasms of lymphocytes, mainly affecting lymph nodes

153
Q

What is passage beyond the R point of the cell cycle governed by?

A

The phosphorylation of the Retinoblastoma Protein (pRb)

155
Q

What is Rheumatoid arthritis?

A

An autoimmune disease where there is a localised and systemic response. The localised chronic inflammation leads to joint destruction and the systemic immune response can affect other organs and cause amyloidosis.

155
Q

What is pleomorphism?

A

Worsening differentiation of individual cells have increasing nuclear size and nuclear to cytoplasmic ratio, more mitotic figures and increasing variation in size and shape of cells and nuclei.

157
Q

What is streptokinase?

A

A fibrinolytic therapy used to active plasminogen

158
Q

What is the importance of endothelial cells in fibrous repair?

A

Angiogenesis

159
Q

What is the clinical appearance of acute inflammation? (those 4 words)

A

-Rubor (redness) -Tumor (swelling) -Calor (heat) -Dolor (pain) and loss of function

160
Q

What is the function of an apotosome?

A

Part of the initiation phase of apoptosis. The apoptosome leads to caspase activation and ultimately to apoptosis

161
Q

What is the function of Bcl-2 in apoptosis?

A

Prevents cytochrome c release from mitochondria, therefore inhibits apoptosis

162
Q

What is the importance of inflammatory cells in fibrous repair?

A

-Removal of debris (by neutrophils and macrophages) -Chemical mediators (lymphocytes and macrophages)

163
Q

What is the main difference between Crohn’s disease and Ulcerative colitis? (both types of inflammatory bowel disease)

A

-Crohn’s disease is transmural so results in strictures and fistula -Ulcerative colitis is superficial and results in diahorrea and bleeding

164
Q

What is the main target for radicals? What does this result?

A

Lipids in the membrane - results in lipid peroxidation and autocatalytic chain reaction (creates more radicals)

165
Q

What is the process early in female embryogenesis whereby one allele is randomly inactivated in each cell?

A

Lyonisation

166
Q

What is the process of malignant cells leaving a vessel called?

A

Extravasation

168
Q

What is the process that affects distal nerve fibres that have been severed called?

A

Wallenian degeneration

169
Q

What is the purpose of acute inflammation?

A

This is the response of living tissue to limit damage/injury to tissue

170
Q

What is the risk of increased intercranial pressure?

A

Intercranial haematoma (bleed in the brain) leading to cerebral oedema.

171
Q

What is the role of thrombin in the clotting cascade?

A

Positively feeds back on factors V, VIII and XI

173
Q

What is the significance of the hydroxyproline residues in the collagen molecule? How are they formed?

A

Formed from hydroxylation of proline (Prolyl Hydroxylase) and forms many interchain H-bonds

174
Q

What is the significance of the proline residues in the collagen molecule?

A

Prevents the peptide moving into a different structure than the extended α-chain conformation

175
Q

What is the spread of malignant cells via fluid in the body cavities known as?

A

Transcoelomic spread

176
Q

What is tuberculosis caused by? How does it cause disease?

A

Mycobacteria (especially M. tuberculosis) which causes disease by persistence and induction of cell-mediated immunity

178
Q

What local complications can be caused by swelling?

A

Blockage of tubes (in the bile ducts, intestine etc.)

178
Q

What local complications can be caused by excessive exudate?

A

-Compression (cardiac tamponade etc.) -Serositis

179
Q

What local factors influence wound healing?

A
  • Type/size/location of wound - Apposition/movement - Blood supply - Infection - Foreign material - Radiation
180
Q

What main things cause granulomas to arise?

A

-Hypersensitivity to mildly irritant foreign material -Infections (e.g. mycobacteria in TB/leprosy) -Sarcoidosis -Wegener’s granulomatosis -Crohn’s disease

180
Q

What must malignant cells do to get from a primary site to a secondary site?

A

1) Grow and invade at the primary site 2) Enter a transport system 3) Grow at the secondary site to form a new tumour. N.B. At all points the cells must evade destruction by immune cells.

182
Q

What nuclear changes are seen under a light microscope during cell injury? Are they reversible or irreversible?

A

-Clumped chromatin (reversible) -Shrinkage (pyknosis), fragmentation (karryohexis) and dissolution (karryolysis) - (irreversible)

183
Q

What often covers areas of acute inflammation? (fancy word for pus)

A

Fibropurulent exudate

185
Q

What reversible changes are seen under an electron microscope during cell injury?

A

-Swelling (due to messed up Na+/K+ pump) -Clumped chromatin (due to low pH) -Autophagy (due to needing more energy) -Ribosomes pop off (no energy to keep them) -Cytoplasmic blebs (cell swelling)

186
Q

What structural changes that you can see under a light microscope accompany apoptosis?

A

-Single cells or small clusters -Intensely eosinophilic -Dense nuclear fragments -Cell shrinkage -Chromatin condensation -Nuclear fragmentation -Phagocytosis by macrophages NO INFLAMMATION

187
Q

What structural changes that you can see under an electron microscope accompany apoptosis?

A

Cytoplasmic blebs - producing fragmentation into membrane-bound apoptotic bodies NO INFLAMMATION

188
Q

What three processes make up apoptosis?

A

-Initiation -Execution -Degradation and phagocytosis

189
Q

What two things are required for Prolyl Hydroxylase to function correctly?

A

-Vitamin C -Fe 2+ ions

190
Q

What two things determine the site of a secondary tumour?

A

1) Regional drainage i.e. lymphatics to the lymph nodes, blood to the next capillary bed and for transcoelomic spread this is predictably to other areas in the coelomic space or to adjacent organs 2) Cross-talk between malignant neoplasms and organ microenvironments (Stephen Paget)

191
Q

What type of cell is mainly present in chronic gastritis?

A

Lymphocytes

192
Q

What type of cell is mainly present in Leishmaniasis (a protozoal infection)?

A

Macrophages

193
Q

What type of cell is mainly present in rheumatoid arthritis?

A

Plasma cells

194
Q

What type of inflammation is commonly associated with caseous necrosis?

A

Granulomatous

195
Q

What type of necrosis does the brain go under after an infarct?

A

Liquefactive

196
Q

What type of necrosis is common in ischaemic cell death?

A

Coagulative

197
Q

What type of necrosis is common when there are loads of neutrophils? Why?

A

Liquefactive as the neutrophils release shitloads of proteolytic enzymes

199
Q

What type of neoplasm ends in a carcinoma?

A

Malignant

200
Q

What type of neoplasm ends in an -oma?

A

Benign

201
Q

When are free radicals produced?

A

-Chemical/radiation injury -Ischaemic-reperfusion injury -Cellular ageing -High oxygen concentrations

202
Q

When do the changes seen in hypoxia become irreversible?

A

-Huge cystolic Ca2+ increase -Several enzymes activated resulting in cell death Mechanism poorly understood (what’s new?!)

203
Q

When do the symptoms of paracetamol OD usually present?

A

After 36-96 hours

205
Q

Where is liquefactive necrosis commonly seen? Why?

A

The brain as it is a fragile tissue without support from a robust collagenous matrix

205
Q

Which chemical mediator is most important during phagocytosis?

A

C3b

207
Q

Which enzyme converts oxygen radicals to hydrogen peroxide?

A

Superoxide dismutase (SOD)

208
Q

Which enzyme is required to turn ethanol to acetaldehyde? What else is required?

A

Alcohol dehydrogenase with CYPZE1 and catalase

209
Q

Which factor turns fibrin into a cross linked fibrin clot

A

Activated factor xIII (factor 13)

210
Q

Which is the most dangerous (badass) free radical?

A

OH•

211
Q

Which neoplasms do not produce metastases?

A

Benign

212
Q

Why are alcoholics particularly susceptible to paracetamol overdose?

A

Lower reserves of glutathione means it is easier to saturate.

213
Q

Why are skin grafts used?

A

Produces apposed edges - less scaring and granulation tissue

214
Q

Why can metaplasia occur due to smoking? What type of cell change takes place?

A

Change in epithelium to be more suited to new environment, to make it more robust. Pseudostratified Ciliated → Squamous cells (more robust)

215
Q

Why do inflamed appendices appear plumper than usual?

A

Oedema

216
Q

Why do malignant cells have altered protease ability? Which proteases are most notably altered?

A

The cells must degrade basement membrane and stroma to invade. Matrix metalloproteinases (MMPs)

217
Q

Why do you get fibrosis of the gall bladder wall in chronic cholecystitis?

A

Repeated obstruction by gall stones leads to recurrent acute inflammation and therefore fibrosis of the gall bladder wall

218
Q

Why does a red infarct occur? (5 reasons)

A

-Dual blood supply -Rich anatomoses -Loose tissue (shit support for capillaries) -Congestion of tissue (congestive cardiac failure) -Raised venous pressure

219
Q

Why does a white infarct occur?

A

The occlusion of an end artery (the sole source of blood to an area)

220
Q

Why is angiogenesis important for wound healing?

A

-Provides access to the wound for inflammatory cells and fibroblasts -Delivery of oxygen and other nutrients

221
Q

Why is fat necrosis commonly seen in pancreatitis?

A

Pancreatitis causes release of lipases from injured pancreatic acinar cells. Lipases act on fatty tissue of pancreas and fat elsewhere in the abdominal cavity causing fat necrosis.

222
Q

Why is NAPQI a big problem?

A

It binds with sulphydryl groups on liver cell membranes, eventually causes hepatocyte necrosis and liver failure.

223
Q

Why is the transition of a carcinoma cell to one able to invade other tissues called EMT?

A

Epithelial-to-mesenchymal transition (EMT) occurs appears more like a mesenchymal cell than an epithelial cell. This allows it to invade other tissues

224
Q

Why is there oedema during acute inflammation?

A

Increased permeability of the vessel wall leads to proteins flowing into the interstitum

225
Q

Why might the appendix have a fibrous tip in older people?

A

Recurrent abscess formation

226
Q

Why might there be a high white blood cell count (leukocytosis) after acute inflammation?

A

-IL-1 and TNFa produce an accelerated release of WBCs from marrow -Macrophages + T lymphocytes produce colony-stimulating factors

227
Q

Why might there be fever after acute inflammation?

A

Endogenous pyrogens (IL-1 and TNFa) are produced

ESA 2 (5 decks)

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