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Nadim Phase 2A > ICS > Flashcards

ICS Flashcards

1
Q

2 good scenarios of inflammation, 2 bad scenarios of inflammation

A

good: infection and injury
bad: autoimmunity (where body starts to attack its own cells and tissues), hypersensitivity

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2
Q

differences between acute and chronic inflammation

A

Acute:
–Sudden onset
– Short duration
– Usually resolves

Chronic:
– Slow onset or sequel to acute
– Long duration
– May never resolve

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3
Q

5 types of cells involved in inflammation

A
  1. Neutrophil polymorphs
  2. Macrophages
  3. Lymphocytes
  4. Endothelial cells
  5. Fibroblasts
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4
Q

Neutrophil polymorphs
1- lifespan
2- sequence in acute inflammation
3- roles in inflammation

A

1: short lived (hours)
2: usually first on scene of acute inflammation
3: roles:
- cytoplasmic granules full of enzymes that kill bacteria
- usually die at the scene of inflammation
- release chemicals that attract other inflammatory cells such as macrophages

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5
Q

macrophages
1- lifespan
2- roles in inflammation (4)

A

1- long lived (weeks to months)

2- phagocytic properties, ingest bacteria/debris may carry debris away, may present antigen to lymphocytes

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6
Q

lymphocytes
1- lifespan
2- roles in inflammation

A

1- long lived (years)

2- produce chemicals which attract in other inflammatory cells, immunological memory for past infections and antigens

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7
Q

Endothelial cells
1- location
2- 3 roles in inflammation

A

1- line capillary blood vessels in areas of inflammation

2-

(1) become sticky in areas of inflammation so inflammatory cells adhere to them
(2) become porous to allow inflammatory cells to pass into tissues
(3) grow into areas of damage to form new capillary vessels

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8
Q

Fibroblasts
1- lifespan
2- role in inflammation

A

1- long lived cells

2- form collagen in areas of chronic inflammation and repair

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9
Q

Acute inflammation example

  • cell
  • blood vessels
  • inflammation of… and effect
  • outcomes
A

Acute appendicitis:

  • unknown precipitating factor
  • neutrophils appear
  • blood vessels dilate
  • inflammation of serosal surface occurs, pain felt
  • appendix either surgically removed or inflammation resolves or appendix bursts with generalised peritonitis and possible death
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10
Q

Chronic inflammation example

  • what doesn’t occur?
  • cells involved
  • what then occurs?
A

Tuberculosis

  • no initial acute inflammation
  • myobacteria ingested by macrophages, which often fail to kill the myobacteria
  • lymphoccytes and macrophages appear
  • fibrosis occurs
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11
Q

what is a granuloma?

A

mass of granulation tissue which is usually produced in response to infection/inflammation/ presence of a foreign substance. epithelioid histiocytes

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12
Q

3 steps of acute inflammation

Potential outcomes of acute inflammation

A

(1) vascular component- dilation of vessels
(2) Fluid Exudative component- vascular leakage of protein-rich fluid due to increased vascular permeability
(3) Cellular exudative component- Neutrophil polymorph is the characteristic cell recruited to the tissue

Outcomes possible; resolution, suppuration (e.g. abcess), organisation or progression to chronic inflammation

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13
Q

6 main causes of acute inflammation

A

(1) Microbial infections- e.g. pyogenic bacteria, viruses, fungal etc. Bacteria release exotoxins (chemicals synthesised by them that specifically initiate inflammation) or endotoxins (associated with their cell walls). Some microorganisms cause immunologically mediated hypersensitivity reactions e.g. parasitic infections and tuberculosis
(2) Hypersensitivity: inappropriate/excessive immune reaction which damages tissues
(3) Physical agents e.g. trauma, ionising radiation, heat, cold
(4) Chemicals
(5) Bacterial toxins
(6) Tissue necrosis- death of tissues from lack of oxygen/nutrients resulting from inadequate blood flow (infarction) or a potent inflammatory stimulus. Often shows acute inflammatory response (resumably in response to peptides released from the dead tissue)

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14
Q

5 macroscopic appearances of acute inflammation

A

(1) Rubor (redness)- due to dilation of blood vessels in damaged area
(2) Calor (heat)- temp increase due to hyperaemia and resultant vascular dilation (and also systemic favour)
(3) Tumor (swelling)- result from oedema and physical mass of inflammatory cells migrating into area; progression of inflammation response leads to formation of new connective tissue contributes to the swelling
(4) Dolor (pain)- stretching and distortion of tissues due to inflammatory oedema and pus under pressure in abcess cavity. Also some chemical mediators of inflammation (bradykinin/prostaglandin/serotonin- involved in acute) are known to induce pain
(5) Loss of function

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15
Q

chemical mediators of acute inflammation- effects

A

(1) injured tissue releases chemical substances following injury into uninjured areas- leads to spread of acute inflammatory response
(2) early in immune response, histamine and thrombin released by original inflammatory stimulus cause up-regulation of adhesion molecules on the surface of endothelial cells. Overall effect of molecules is the firm neutrophil adhesion to the endothelial surface
(3) endogenous chemical mediators cause vasodilation, emigration of neutrophils, chemotaxis, increased vascular permeability, itching and pain

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16
Q

Plasma enzymatic cascade systems

A

(1) complement
(2) kinin
(3) Coagulation
(4) Fibrinolytic

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17
Q

what is the best known chemical mediator in acute inflammation?

A

Histamine

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18
Q

list 3 medications for inflammation

A
  1. Aspirin
  2. Ibuprofen
  3. Paracetamol
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19
Q

what do macrophages do?

A

ingest bacteria n debris
may carry debris away
may present antigen of lymphocytes

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20
Q

what do lymphocytes do?

A

produce chemicals which attract other inflammatory cells

have an immunological memory for past infections and antigens

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21
Q

where are inflammatory cells?

A

in bone marrow, released into blood

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22
Q

outcomes of acute inflammation

A

(1) Resolution
(2) Suppuration- if there is excessive exudate, leads to pus production
(3) organisation (due to exessive necrosis or suppuration)
(4) Progression to chronic inflammation

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23
Q

Systemic effects of inflammation

A
  • pyrexia
  • constitutional symptoms
  • weight loss
  • reactive hyperplasia of the reticuloendothelial system (the enlargement of an organ or tissue caused by an increase in the reproduction rate of its cells,)
  • heamatological changes
  • amyloidosis (abnormal protein produced in bone marrow builds up in organs and can be deposited in any tissue or organ)
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24
Q

causes of chronic inflammation (4)

A

(1) primary chronic inflammation
(2) transplant rejection
(3) Progression from acute inflammation
(4) recurrent episodes of acute inflammation

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25
Q

macroscopic appearances of chronic inflammation

A

(1) chronic ulcer
(2) chronic abscess cavity
(3) thickening of the wall of a hollow viscus
(4) granulomatous inflammation
(5) fibrosis

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26
Q

1- what is healing?

2- what regulates healing and repair?

A

1- healing involves regeneration and migration of specialised cells. Repair consists of angiogenesis (formation of blood vessels), fibroblast proliferation and collagen synthesis resulting in granulation tissue

2- growth factors which bind to specific receptors on cell membranes and trigger a series of events culminating in cell proliferation

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27
Q

two types of lymphocytes

A

1- B lymphocytes- on contact with antigen become progressively transformed into plasma cells, which are cells specially adapted for the production of antibodies

T Lymphocytes- responsible for cell-mediated immunity. On contact with antigen, T lymphocytes produce a range of soluble factors called cytokines, with important activities such as recruitment and activation of other cell types

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28
Q

what is resolution? (2)

A

(1) initiating factor removed

(2) tissue undamaged or able to regenerate

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29
Q

what can a paracetamol OD result in?

A

liver failure

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30
Q

how does alcoholism impact regeneration in liver?

A

bc of ongoing damage which results in abnormal architecture (cirrhosis)

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31
Q

which cells lining the alveoli can regenerate?

A

pneumocytes

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32
Q

what are the most superficial skin wounds & an example?

What happens during this type of injury?

A

abrasion eg road rash from cycling

only top cell layer is removed, leaving the bottom layer/follicles/glands for scab to form and for the epidermis to eventually be regenerated

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33
Q

what are the 2 types of skin would healing?

Describe them?

A

1st and 2nd intention healing

1st intention:
- edge to edge healing (heals w/ reasonable scar)
both ends are sealed together
- the slight gap is filled w blood, fibrin etc which holds together a little w stitches
- epidermis regrows, fibroblasts produce collagen
- scar line is stronger than surrounding tissue as more blood vessels are grown

2nd intention= traumatic wound where u can’t bring 2 edges together
granulation –> epithelium slowly grows in from edges (depending on wound size)

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34
Q

define repair

A

replacement of damaged tissue by fibrous tissue

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35
Q

what is collagen prod by?

A

fibroblasts

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36
Q

after a MI, what is there where dead heart tissue was?

A

a fibrous scar

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37
Q

what type of scar does MF (myocardial fibrosis) result in?

A

a dense white fibrous scar (patient may live for a few months but may die after)

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38
Q

if healing by 2nd intention, we don’t want infection… what may be done to reduce this?

A

artificial skin dressings to keep the skin moist so it doesn’t dry out - sometimes may have growth factors in them

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39
Q

what is fibrosis in the brain called?

A

Gliosis

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40
Q

how does stroke recovery happen?

A

only the injured (not dead tissue) around the edge of the infarct gets better, with plasticity involved

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41
Q

list some cells that regenerate (5)

A
  1. hepatocytes
  2. pneumocytes
  3. all blood cells
  4. gut and skin epithelium
  5. osteocytes
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42
Q

what are some cells that don’t regenerate? (2)

A
  1. Myocardial cells

2. Neurones

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43
Q

Why are clots rare in normal blood flow? (2)

A
  1. Laminar flow (endothelial cells travel in the centre of arterial vessels and don’t usually touch the sides)
  2. Endothelial cells are not sticky when healthy.
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44
Q

Define thrombosis

A

the formation of a solid mass from BLOOD CONSTITUENTS in an intact vessel of a living person.

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45
Q

3 steps of thrombosis

A
  1. Platelet aggregation (due to exposed collagen)
  2. Chemicals released during aggregation lead to further aggregation and also begin the clotting cascade of proteins in the blood (POSITIVE FEEDBACK LOOPS)
  3. Clotting cascade results in formation of FIBRIN (large protein molecule) which makes a mess in which red blood cells can become entrapped.
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46
Q

What is the thrombosis triad? (VIRCHOW’S TRIAD)

A

The three main factors which result in thrombosis- usually a combination of two or three

  1. Changes in the vessel wall
  2. change in blood constituents
  3. change in blood flow
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47
Q

What is an embolism? What causes it?

A

Embolism= process of solid mass in blood being carried through circulation to a place where it gets stuck and BLOCKS VESSEL
Usually due to thrombus but can also be due to air (due to iv/bloods), cholesterol crystals (due to atheromatous plaques), tumor, amniotic fluid. fat (severe trauma with multiple fractures)

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48
Q

What is ischaemia?

A

reduced blood flow to a tissue without other implications

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49
Q

What is infarction? What causes it? Why are most organs susceptible to infarction?

A

Reduction in blood flow to a tissue which is so severe that it cannot even support maintenance of the tissue cells, resulting in them dying.
Usually caused by thrombosis of a supplying artery.
Most organs are susceptible because most organs are only supplied by a single artery (end artery supply), so very susceptible to infarction

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50
Q

Which organs are less susceptible to infarction and why?

A

Some organs are less susceptible to infarction because they have dual artery supply so if there is thrombosis in one, they have supply from another. These include;

  • liver (portal venous & hepatic artery)
  • lung (pulmonary venous & bronchial)
  • brain (circle of willis)
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51
Q

what does occlusion of a coronary artery result in?

A

death of heart muscle due to lack of blood flow (MI)

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52
Q

what does occlusion of a cerebral artery result in?

A

death of brain tissue due to a lack of blood flow (CI)

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53
Q

what is a stroke aka?

A

cerebral infarction (CI)

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54
Q

why does thrombosis in the veins most commonly occur?

A

due to slow blood flow within those veins eg when a patient is lying in bed for long periods of time after a major op

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55
Q

list some preventions of DVT (deep vein thrombosis) in hosp (3)

A
  1. early mobilisation
  2. use of small doses of anti-coagulants eg heparin
  3. venous stocking to prevent leg veins being full of blood
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56
Q

what is heparin?

A

an anti-coagulant

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57
Q

if an embolus enters the venous system, where will it lodge?

A

it will travel to the vena cava –> through RHS of heart –> &will lodge in pulmonary arteries

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58
Q

why can’t an embolus in the venous system get through to arterial circulation?

A

bc the blood vessels in the lung split down to capillary size so lung acts as a filter for any venous emboli
(aka lung acts as a FILTER for venous emboli)

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59
Q

what happens if an embolus enters the arterial system?

A

it can travel anywhere downstream of its entry point eg a mural thrombus overlying a myocardial infarct in LV can go anywhere in systemic circulation

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60
Q

What can injury to endothelial cells result in?

A

exposure of sub-endothelial collagen

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61
Q

what does fibrinogen get activated by?

A

chemicals the platelets release

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62
Q

an LAD CA thrombus can led to an MI. how will this present on ecg?

A

ST elevation on chest leads

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63
Q

how does cigarette smoke change vessel walls?

A

kills endothhelial cells

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64
Q

why does CO inhalation result in an increased risk of thrombosis?

A 
inhaling lots of CO
--> more rbc production
--> more cells
= blood more turgid
--> can thrombus more easily
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65
Q

how does atherosclerosis disrupt laminar flow?

A

atherosclerosis= disease which causes plaque build-up in arteries
Causes arterial walls to become sticky

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66
Q

what is aspirin in low doses daily good for?

A

inhibits platelet aggregation

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67
Q

what is the most common cause of an embolus?

A

broken off thrombus travelling in the bloodstream

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68
Q

what is significant about IV drug abusers?

A

street heroin is often cut with talcum powder which isn’t v soluble

  • -> injected emboli into veins
  • -> usually filtered in lungs, sometimes liver
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69
Q

above what ml of air can cause an embolus?

A

150

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70
Q

what is the diff btwn ischaemia and infarction?

A 
ischaemia = any reduction in blood flow
infarction = death of cells due to severe lack of blood flow
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71
Q

What is atherosclerosis? what causes it?

A

Condition where arteries become clogged with plaque.

Caused by atheromas (pathology of arteries in which there is deposition of lipids in the arterial wall with surrounding fibrosis and chronic inflammation)

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72
Q

what is the predominant cause of myocardial infarction?

A

atherosclerotic plaques

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73
Q

list 3 risk factors for atheromas

A
  1. raised serum lipids
  2. hypertension
  3. diabetes mellitus
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74
Q

what is the linkage between high serum lipids and atherosclerosis?

A

lipids cause endothelial damage

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75
Q

what is the major process after endothelial damage (and with which cells)?

A

chronic inflammation - with macrophages/fibroblasts

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76
Q

name 3 factors that can reduce endothelial damage

A
  1. reduced lipids
  2. lowered BP
  3. stopping smoking
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77
Q

which drug can reduce the amount of platelet aggregation at the site of endothelial damage?

A

taking low dose aspirin

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78
Q

define atherosclerosis

A

narrowing of arteries due to plaque formation

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79
Q

what is the diff btwn atherosclerosis and arteriosclerosis?

A
  • athero = narrowing of arteries due to plaque formation

- arterio = hardening of arteries

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80
Q

can u have a genetic predisposition to atherosclerosis?

A

Yes

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81
Q

when is complicated atherosclerosis usually seen?

A

later in life

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82
Q

what is significant about atherosclerosis?

A

it is mostly based on incremental episodes of endothelial cell damage over a LONG period of time eg decades

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83
Q

what is in a plaque? (3)

A
  1. quite a lot of fibrous tissue
  2. lipids
  3. lymphocytes (maybe also inflammation)
84
Q

name 3 risk factors for atherosclerosis

A
  1. smoking
  2. hypertension
  3. diabetes
85
Q

why does vaping have adv over smoking?

A

free radicals in cig smoke/CO/nicotine kills endothelial cells, vaping has fewer free rads and no CO

86
Q

list the journey from smoking –> chest pain

A

smoking

  • -> endothelial cell damage
  • -> thrombus
  • -> heals bc endothelial cell layer grows over
  • -> small bump
  • -> not much impact
  • -> repeated endothelial damage
  • -> cycle continues w/o symptoms
  • -> symptoms may finally begin after years eg slight chest pain OR still asymptomatic
87
Q

what are the symptoms of atherosclerosis in coronary arteries?

A
  • vomiting
  • anxiety
  • angina
  • coughing
  • feeling faint
88
Q

what can atherosclerosis in coronary arteries result in?

A

ischaemia of cardiac muscle cells

89
Q

list some symptoms of atherosclerosis in carotid arteries

A
  • weakness
  • dyspnea (shortness of breath)
  • facial numbness
  • paralysis
90
Q

which disease can atherosclerotic plaque also cause?

A

peripheral vascular disease

91
Q

what are some symptoms of peripheral vascular disease?

A
  • hair loss
  • erectile dysfunction
  • weakening of area
92
Q

what are some symptoms of atherosclerosis in renal arteries?

A
  • reduced appetite
  • hand swelling
  • renin release can be increased –> BP may be sig increased
93
Q

high or low amounts of circulating LDL can lead to endothelial dysfunction?

A

high

94
Q

Describe the mechanism of plaque formation in atherosclerosis (8 steps)

A
  1. irritant (e.g. smoking/hypertension/hyperlipidemia) –> endothelial dysfunction
  2. increased LDL deposits in the tunica intima & becomes oxidised, activating endothelial cells which then begin expressing adhesion molecules for WBCs (leukocytes)
  3. Adhesion of leukocytes to activated endothelial cells allows monocytes and T helper cells to move into the tunica intima layer of blood vessels
  4. Monocytes and T helpers become macrophages which take up oxidised LDLs, becoming foam cells.
  5. Foam Cells promote the migration of smooth muscle cells from the tunica media to the tunica intima and smooth muscle proliferation
  6. Increased SMC proliferation leads to increased collagen production, which leads to hardening of plaque
  7. The foam cell dies, unleashing lipid content -> this drives growth of the plaque
  8. Growth of the plaque builds pressure and can cause rupture of the plaque itself. This can lead to thrombosis, where coagulation happens to stop the plaque from spilling its contents into the lumen, forming a thrombus which can impede blood flow and cause serious complications
95
Q

how can you prevent/treat atherosclerosis?

A

smoking cessation, control of BP, weight reduction, regular exercise, dietary modifications, cholesterol-lowering drugs (e.g. Statins) and surgical interventions to reduce sizes of arterial lesions/remove thrombus/bypass severely narrowed or occluded arteries

96
Q

define apoptosis

A

programmed cell death of a single cell

97
Q

define necrosis

A

unprogrammed death of a large number of cells due to an adverse event

98
Q

list some examples of adverse events that could result in necrosis?

A

infarction
burns
frostbite

99
Q

which type of cell death is important in the normal function of the human body?

A

apoptosis (works alongside mitosis for renewal of cells)

100
Q

why is apoptosis important in embryogenesis?

A

apoptosis removes cells that are no longer needed as organs develop eg tissue btwn fingers/toes so we dot s so that we dont end up w webbed feet n hands

101
Q

What is the internal pathway?

What is the external pathway?

A

Both means of regulating apoptosis

Internal: BCl2 family; BCl2 inhibits apoptosis, Bax induces apoptosis

Extrinsic: activation of apoptosis characterised by ligand-binding at ‘death receptors’ on a cell e.g. TNFR gene family. Ligand-binding at these receptors promotes clustering of receptor molecules on a cell’s surface and the resultant initiation of a signal transduction cascade resulting in the activation of caspases

102
Q

what can an aging or ill cell do besides apoptose?

A
  • autophagy
  • closing down protein synthesis
  • cell cycle arrest
103
Q

when can abomal apoptosis occur?

A

in a variety of situations inc:

drugs
graft vs host disease after bone marrow transplantation
neurodegeneration

104
Q

what are condensed bodies in apoptosis aka

A

apoptic bodies

105
Q

are there any accompanying inflammatory reactions with apoptosis?

A

no (probably because cell membrane remains intact)

106
Q

what does p53 protein detect?

A

DNA damage in dividing cells

107
Q

why do cancers get bigger?

A

bc apoptosis is lacking (often bc of a mutation in p53 gene so dna damage is not recognised)

108
Q

why is apoptosis switched off in HIV?

A

as p53 is switched on to kill myphocytes

109
Q

what happens to the contents of cells in necrosis?

A

swelling and disintegration of small bodies of cell

110
Q

list some examples of necrosis

A

frostbite
CI
avascular necrosis of bone
pancreatitis

111
Q

where do autosomal diseases occur?

A

non-sex chromosomes

112
Q

what is a congenital disease?

A

a disease that someone is born with (mostly genetic but can be acquired)

113
Q

what is an acquired disease?

A

one that occurs after birth (often due to env, can be genetic)

114
Q

name 2 prenatal factors, other than genetic abnormalities that can contribute to disease risk?

A

transplacental transmission of env agents eg FA

nutritional deprivation

115
Q

what is a genetic disease?

A

1 that occurs primarily from a genetic abnormality

116
Q

what causes sickle cell anaemia?

A

a point mutation in the beta-globin chain of Hb

117
Q

in sickle cell anaemia, when do the RBC deform/sickle?

A

when oxygen saturation is low

118
Q

single gene disorders are typically classified into what?

A

dominant or recessive

119
Q

how else can single gene disorders be classified?

A

autosomal (non-sex chromosomes)

sex-linked (parts of x chromosome that dont have a corresponding region on y chromosome)

120
Q

what type of disorder is breast cancer an example of?

A

polygenic disorders (bc BRCA1/BRCA2 do have a large individual efffect but mostly risk is composed of incremental rises in risks by 100s of unrelated genes)

121
Q

what is E4 epoprotein associated with?

A

high risk of ischaemic heart disease due to atheroma

3x higher in pop of papa new guinea than caucasians

122
Q

what is spina bifida occulta?

A

malformation of 1+ vertebrae

123
Q

Growth Hormone excess is usually due to what?

A

pituitary tumour - adenoma

124
Q

define adenoma

A

benign tumour formed from glandular structures in epithelial tissue

125
Q

what does hungtington’s disease result in?

A

death of brain cells

early symptoms - subtle with mood/mental abilities

general lack of coordination and unsteady gait often follow

126
Q

what type of disorder is huntingtons?

A

inherited - autosomal dominant - gene called huntingtin (HTT) on chromosome 4… ≥36

127
Q

increased cell growth is caused by which 2 processes?

A

hypertrophy and hyperplasia

128
Q

define hypertrophy

A

when the SIZE of an individual cell/tissue/organ is increased by an increase in the SIZE OF THE CELLS without the increase number of cells

129
Q

define hyperplasia

A

increased growth of cell/tissue/organ because of an INCREASE IN NUMBER OF CELLS. often accompanied by increase in cell size

130
Q

bodybuilders prefer what? hypertrophy or hyperplasia

A

hypertrophy - increase in size of cells (appearance)

131
Q

athletes prefer what? hypertrophy or hyperplasia?

A

hyperplasia - increased number of cells (or myofibrils in each cell, strength)

132
Q

which 2 factors contribute to hypertrophy?

A
  1. sarcoplasmic hypertrophy - focuses more on increased muscle glycogen storage
  2. myofibrillar hypertrophy - focuses more on increased myofibril size
133
Q

how does hypertrophy/hyperplasia present in pregnancy?

A

hyperplasia - breast epithelial cells respond to increased demands

uterus - both hypertrophy and hyperplasia

134
Q

define atrophy

A

decrease in the size of cells caused by a decrease in NUMBER of cells OR decrease in SIZE

135
Q

why might pathological atrophy happen?

A

bc of loss of blood supply, loss of innervation, pressure, lack of nutrition, lack of hormonal stimulation or bc of hormonal stimulation

136
Q

define metaplasia

A

reversible transformation of 1 mature cell type in another fully differentiated cell type

137
Q

what is an example of metaplasia in smokers?

A

transformation of normal pseudostratified columnar ciliated epithelium of bronchi into squamous epithelium after repeated exposure to cig smoke

138
Q

what is dysplasia?

A

an imprecise term for the morphological changes seen in cells in the progression to becoming cancer

it’s a premalignant condition characterised by increased growth, cellular atypia and decreased differentiation

139
Q

why does hearing loss occur in older age?

A

hair cells in the cochlear don’t regenerate

140
Q

list some examples of illnesses associated w/ ageing

A

osteoporosis

cataracts

dementia

sarcopaenia (lack of muscle)

deafness

141
Q

what is the generic term for a malignant tumour?

A

cancer

142
Q

how does basal cell carcinoma of the skin act?

A

only invades localy - can be locally excised and cured !

143
Q

most carcinomas spread to where?

A

lymph nodes that drain the site of the carcinoma

144
Q

what are 5 common tumours that spread to bone?

A

breast

prostate

lung

thyroid

kidney

–

212
what is the easiest way to confirm breast cancer?

small needle biopsy

145
Q

what is the easiest way to confirm breast cancer?

A

small needle biopsy

146
Q

what is a lumpectomy?

A

breast conserving surgery / partial masectomy / wide excision

147
Q

what is the most widely used cancer staging system and what does it mean?

A

T = extent of tumoour

M = presence of metastases

N = spread to lymph nodes

148
Q

what is the TNM staging converted to?

A

0 = carcinoma in situ

1-3 = size of cancer/nearby spread

4 = metastatic disease

149
Q

define carcinogenesis

A

process which results in the transformation of normal cells to neopalstic cells due to permanent genetic alterations (mutations)

150
Q

what does carcinogenesis only strictly apply to?

A

malignant tumours

151
Q

what are carcinogens?

A

agents known/suspected to participate in the causation of tumours

152
Q

what type of process is carcinogenesis? and why?

A

multistep - may require initiating and promoting agents - often resulting in a latent period btwn exposure to carcinogen and clinical recognition of a tumour

153
Q

what is the diff btwn carcinogenic and ongogenic?

A

carcinogenic = cancer causing

oncogenic = tumour causing

154
Q

list some classes of carcinogens

A
  1. chemical
  2. viral
  3. ionising and non-ionising radiation
  4. Biological agents: hormones, parasites and mycotoxins
  5. miscellaneous
155
Q

what are some host factors for carcinogens?

A

race

diet

constitutional factors eg age/gender

premalignant lesions

transplacental exposure

156
Q

what is a neoplasm?

A

a lesion resulting from the autonomous growth of cells which persists after the initiating stimulus has been removed

157
Q

what are benign neoplasms like ?

A

generally slow growign

closely resemble parent tissue

remain localised

158
Q

what are malignant neoplasms like?

A

have the capacity to invade surrounding tissues

grow more rapidly

show variable resemblance to parent tissue

159
Q

all neoplasms are designated by which suffix?

A

“-oma”

160
Q

benign connective tissue neoplasms have a prefix denoting what?

A

cell of orgin

eg lipoma - benign neoplasm arising from adipocyte

161
Q
  1. malignant epithelial tumours = ?

2. malignant connective tissue neoplasms = ?

A
  1. Carcinomas

2. sarcomas

162
Q

what are neoplasms made up of?

A

neoplastic cells and stroma

163
Q

what is a stroma?

A

supporting networking cells

164
Q

define angiogenesis

A

recruiting blood vessels to help and grow

165
Q

how can neoplasms be classified behaviourally?

A

benign, borderline, malignant

166
Q

why should we worry about “benign” neoplasms?

A

they cause morbidity and mortality through:

  • pressure on adjacent structures
  • obstruct flow
  • produce hormones
  • transform to malignant neoplasms
  • anxiety
167
Q

how can neoplasms be classified histogenetically?

A
  • specific cell of origin of a tumour
  • histopathological exam
  • specifieis tumout type
168
Q

what is a papilloma?

A

benign tumour of non-glandular, non-secretory epithelium

prefix with cell type of origin eg squamous cell papilloma

169
Q

what is an adenoma?

A

benign tumour of glandular/secretory epithelium

prefix with cell type of origin eg thyroid adenoma

170
Q

name 2 benign epithelial neoplasms:

  1. non-glandular, non-secretory
  2. glandular or secretory, & 2 examples
A
  1. papilloma

2. adenoma- e.g. colonic or thyroid

171
Q

name 2 malignant epithelial neoplasms

A

carcinoma

adenocarcinoma

172
Q

what is the diff btwn carcinoma and adenocarcinoma?

A

carcinoma - malignant tumour of epithelial cells

adenocarcinoma - carcinomas of glandular epithelum

173
Q

all carcinomas are caused by malignancies of what?

A

epithelium

174
Q

all sarcomas are malignancies of what?

A

connective tissue

175
Q

what is invasion of tumours dependent upon?

A

decreased cellular adehesion

abnormal (increased) cellular motility

prod of enzymes w/ lytic effect on surrounding tissues

176
Q

what is metastasis?

A

process by which a malignant tumour spreads from its primary site to prod secondary tumours at distant sites?

177
Q

metastasis is dependent upon what?

A

a chain of events known as metastatic cascade (detachment, invasion, intravasion, evasion of host defences, arrest, extravasation, vascularisation)

178
Q

what is the diff btwn carcinoma in situ and invasive carcinoma?

A

carcinoma in situ = can’t metastasise, can be locally removed

invasive carcinoma = worry of spreading

179
Q

breast cancer is a malignant tumour arising from what?

A

the epithelial cells lining the ducts and lobules of the breast

180
Q

name a popular anti-oestrogen drug?

A

tamoxifen

181
Q

what are 2 ways of increasing tumour size?

A

cell division

lack of cell death (apoptosis)

182
Q

T cells originate from what and mature where?

A

originate from stem cells in bone marrow

mature in the thymus

travel to blood and lymph

183
Q

does innate immunity depend on lymphocytes?

A

no, adaptive does

184
Q

polymorphonuclear leucocytes are mainly involved in what?

A

allergic reactions

185
Q

when are neutrophils important and what for?

A

innate immunity

phagocytosis

186
Q

what are eosinophils mainly associated w?

A

parasitic infections and allergic reactions

187
Q

what are basophils similar to? what are they mainly involved in?

A

mast cells

immunity to parasitic infections/allergic reactions

188
Q

when are monocytes important n what for ?

A

innate and adaptive immunity

phagocytosis

189
Q

how are monocytes and macrophages linked?

A

monocytes –> macrophages

once a monocyte leaves blood, it matures into a wandering/fixed macrophage

190
Q

what do T cells expresss

A

CD3 - T cell receptor complex

191
Q

what are complements?

A

group of ≈20 serum proteins that need to be ‘activated’ to be functional

192
Q

what is epitope?

A

part of the antigen that binds to the antibody/receptor binding site

193
Q

what is the most common Ig?

A

IgG

194
Q

what are cytokines?

A

proteins secreted by immune and non-immune cells

195
Q

what are interferons? (IFN)

A

induce a state of antiviral resistance in uninfected cells

limit spread of viral infection

IFNa&b - prod by virus infected cells

196
Q

what are interleukins? (IL)

A

produced by many cells

can be pro-inflammaotry (IL1) or anti-inflammatory (IL-10)

can cause cells to divide, differentiate and secrete factors

197
Q

what are tumour necrosis factors (TNF)

A

mediate inflammation and cytotoxic reactions

potent

198
Q

list examples of cytokines

A

IFN

IL

TNF

199
Q

what 3 things does innate immunity include?

A
  1. physical/chemical barriers
  2. phagocytic cells (neutrophils and macrophages)
  3. serum proteins (complement, acute phase)
200
Q

what is inflammation?

A

a series of reactions that brings cells/molcules of immune system to sites of infection or damage

201
Q

how is bacteria/funghi generally responded to?

A

phagocytosis

killing

202
Q

how are viruses generally handled?

A

cellular shut-down

self-sacrifice

cellular resistance

203
Q

what is pattern recognition

A

recognition of microbes/viruses depends on seeing ancient, conserved features of them

families of receptors exist to detect these in fluids, cell surfaces and compartments and intracellularly

204
Q

4 qualities of a neoplasm

A

Autonomous, abnormal, persistent, new growth

205
Q

maximum tumor growth without tumor’s own blood supply

A

2mm

Nadim Phase 2A (18 decks)

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