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MCD > Cell pathology > Flashcards

Cell pathology Flashcards

1
Q

List the EIGHT causes of cell injury.

A 
Oxygen deprivation
Inflammation
Chemical Agents
Genetics
Infection
Nutritional imbalances
Physical Agents
Ageing
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2
Q

What four intracellular mechanisms are particularly vulnerable to cell injury?

A

Cell membrane integrity
Protein synthesis
ATP Generation
Integrity of the genetic apparatus

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3
Q

Define Atrophy.

A

Shrinking in the size of a cell or organ by the loss of cell substance.

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4
Q

Define Hypertrophy.

A

Increase in the size of cells and, consequently, an increase in the size of the organ

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5
Q

Define Hyperplasia.

A

Increase in the number of cells in an organ

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6
Q

Define Metaplasia.

A

A REVERSIBLE change in which one adult cell type is replaced with another

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7
Q

Define Dysplasia.

A

Pre-cancerous cells which show the genetic and cytological features of malignancy but not invading the underlying tissue

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8
Q

Define Ulcer.

A

A local defect, or excavation of the surface, of an organ or tissue, produced by sloughing of necrotic inflammatory tissue

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9
Q

What are the two physiological causes of hyperplasia?

A

Hormonal (e.g. oestrogenic wave of proliferation)

Compensatory

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10
Q

What are two light microscopic changes associated with reversible injury?

A

Fatty change

Cellular swelling

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11
Q

Define Necrosis.

A

Confluent cell death associated with inflammation

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12
Q

What are the four types of necrosis?

A

Coagulative, Liquefactive, caseous and fat

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13
Q

What disease is fat necrosis associated with and why?

A

Acute pancreatitis - release of lipases that break down triglycerides into free fatty acids and glycerol. Free fatty acids associate with calcium deposits.

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14
Q

Describe some uses of apoptosis.

A

Embryogenesis - lumen of intestine
Removal of auto-reactive T and B cells
Cell deletion in proliferating populations

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15
Q

Describe three differences between apoptosis and necrosis.

A

Apoptosis is an active process (required energy)
Apoptosis can be physiological
Apoptosis is not associated with inflammation

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16
Q

Define inflammation.

A

Reactions of living vascularised tissue to sub-lethal injury

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17
Q

What are the three types of inflammation?

A

Acute
Chronic
Granulomatous (type of chronic inflammation)

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18
Q

What are the five cardinal signs of inflammation?

A 
Rubor
Dolor
Calor
Tumor
Functio Laesa
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19
Q

What triggers histamine release and what effect do histamines have?

A

Binding of IgE to the Fc receptor on mast cells
Antigens bind to the IgE and cause cross-linking and mast cell degranulation
Histamines cause: vasodilation + increased vascular permeability

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20
Q

What is an exudate?

A

Fluid with high protein content and cellular debris, which leaves vessels and deposits in tissues or on tissue surfaces, usually as a result of inflammation

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21
Q

What is a transudate?

A

Fluid escape from vessels due to disturbances in hydrostatic and colloid osmotic pressure – NOT CAUSED BY INFLAMMATION

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22
Q

What is the most important difference between exudates and transudates?

A

Exudates are associated with inflammation transudates are not

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23
Q

What are the three types of exudates and how do they differ?

A

Serous – fluid filled – lowest protein content of the three exudates
Fibrinous – high fibrin content – more due to traumatic injury
Purulent – pus filled – fibrin, inflammatory cells, debris and fluid

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24
Q

What is the main histological feature of acute inflammation?

A

Lots of neutrophils

25
Q

What are the three main cell types involved in chronic inflammation?

A

Macrophages
Lymphocytes
Plasma Cells

26
Q

What is an important difference between acute and chronic inflammation?

A

Acute inflammation produces an exudate whereas chronic inflammation doesn’t

27
Q

What are the histological features of granulomatous inflammation?

A

Granuloma – collection of macrophages
You get a collection of macrophages in the middle and they may appear to have fused together
There will be lymphocytes and plasma cells around the outside

28
Q

What is the good outcome of inflammation?

A

Resolution – healing of tissue damage to preserve integrity and function

29
Q

What is ‘Repair’ in terms of wound healing?

A

Replacing normal tissue with scar tissue

30
Q

Give an example of resolution and how it takes place.

A

Pneumococcul lobar pneumonia
Inititally you get exudation
Then you get red hepatisation (erythrocytes move into the alveolar cells)
Grey hepatisation – erythrocytes break down
Provided the basement membrane is still there – the body can remove the problem

31
Q

What are three main complications of repair? Describe each of them.

A

Keloids – excess collagen deposition
Contractures – scar tissue contracts after a while, if the scar tissue is over a joint it can affect joint mobility
Organ Function – if normal functional tissue is replaced with

32
Q

Define Oedema.

A

Abnormal increase in interstitial fluid

33
Q

What three forces determine the movement of fluid between blood vessels and the interstitial space?

A

Capillary hydrostatic pressure
Plasma hydrostatic pressure
Plasma oncotic pressure

34
Q

What are the four broad causes of oedema?

A

Increased capillary hydrostatic pressure
Decreased plasma oncotic pressure (e.g. nephrotic syndrome)
Inflammation
Lymphatic Obstruction

35
Q

What is a common cause of pulmonary oedema?

A

Increased plasma hydrostatic pressure in the pulmonary capillary bed
Left Ventricular Failure – build up of pressure in left atrium leading to back pressure into the capillaries – this pushes water into the tissues
This is cardiogenic pulmonary oedema

36
Q

What is non-cardiogenic pulmonary oedema?

A

Caused by increased permeability
ARDS – Acute Respiratory Distress Syndrome
Often caused by Sepsis, Shock and Trauma

37
Q

What are the four types of cerebral oedema?

A

Vasogenic – physical breakdown of the blood-brain barrier – commonly due to trauma or tumours
Interstitial – breakdown of the CSF-brain barrier – commonly due to obstruction of the flow of CSF (Obstructive Hydrocephalus)
Cytotoxic – derangement of the sodium-potassium pumps leads to a build up of intracellular sodium causing intracellular oedema (common with ischaemic strokes)
Osmotic – increase in plasma osmolality – commonly caused by Syndrome of inappropriate ADH secretion (SIADH) that is commonly caused by small cell lung cancer

38
Q

What are the possible serious consequences of cerebral oedema?

A

Rise in intracranial pressure, which could cause herniation

39
Q

What are two common causes of generalised oedema?

A

Left Ventricular Failure

Nephrotic Syndrome

40
Q

What is a consequence of oedema in a peripheral setting?

A

Impaired wound healing

41
Q

What are the three main factors affecting thrombus formation?

A

Hypercoagulability
Vessel Wall Injury
Stasis

42
Q

What is cardiac thrombosis caused by and what is an important complication?

A

Stasis – e.g. atrial fibrillation

Complication – systemic embolisation

43
Q

What is arterial thrombosis caused by?

A

Vessel Wall Injury

44
Q

What is venous thrombosis caused by and what is an important complication?

A

Stasis and Hypercoagulability

Complication – pulmonary embolism

45
Q

What are the four fates of a thrombus?

A

Propagation – thrombus accumulates fibrin and grows
Embolisation – thrombus dislodges and moves somewhere else
Dissolution – thrombus is dissolved by fibrinolytics
Organisation and Recanalisation – thrombus becomes fibrotic and is remodelled, lumen appears again allowing blood flow

46
Q

Where do most arterial thromboemboli originate?

A

Carotid Arteries

47
Q

Define haematoma.

A

A localised mass of extravasated blood that is relatively or completely confined within an organ or tissue

48
Q

What are the three classes of haemorrhage based on size?

A 
Petechiae = 1-2mm
Purpura = >3mm
Ecchymoses = 1-2cm
49
Q

What is shock characterised by?

A

Hypotension

50
Q

What two equations are used to evaluate the effects of changes in various vascular factors?

A 
MAP = CO x SVR
CO = HR x SV
51
Q

What are the five types of shock?

A 
Cardiogenic
Hypovolaemic
Anaphylactic
Neurogenic
Septic
52
Q

Describe each of the five types of shock and its causes and effects.

A 
Cardiogenic -impaired cardiac function
Causes include cardiac tamponade
Reduced SV
Hypovolaemic – loss of blood volume
Causes include: trauma, haemorrhage
Low SV leads to Low MAP
Body tries to compensate with tachycardia
Anaphylactic – IgE mediated hypersensitivity
Causes vasodilation and increased permeability
Reduced SVR leads to Reducer MAP
Neurogenic – injury to sympathetic pathways
Normally happens after trauma
Widespread vasodilation and reduced SVR
Septic – result of inflammatory response
Causes vasodilation
Reduced SVR leads to Reduced MAP
53
Q

Define infarction.

A

Tissue necrosis due to unresolved ischaemia

54
Q

What are the two types of infarct and how are they different?

A

Red – haemorrhagic – affects organs with a dual blood supply

White – anaemic – affects solid organs that have one blood supply

55
Q

How can the rates of development of the occlusion affect the infarction?

A

If the occlusion develops slowly then there may be enough time for collateral vessels to form

56
Q

What are the two types of myocardial infarction?

A

Transmural – across the whole wall of the heart

Subendocardial – just the layer under the endocardium

57
Q

Describe the process of atherosclerosis.

A

Endothelial damage
Macrophage infiltration and release of cytokines
Cytokines recruit LDLs
LDLs become oxidised and hence become pro-inflammatory and drive progression of plaque
Smooth muscle cells migrate from the tunica media to the lesion and deposit a collagen-rich matrix, which forms a protective fibrous cap

58
Q

What are the two types of atherosclerotic plaque and how are they different?

A

Stable – thick fibrous cap – less likely to rupture

Unstable – thinner fibrous cap – more likely to rupture

MCD (7 decks)

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