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Cell pathology Flashcards

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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?

Study These Flashcards
A

Lots of neutrophils

25
What are the three main cell types involved in chronic inflammation?
Macrophages Lymphocytes Plasma Cells
26
What is an important difference between acute and chronic inflammation?
Acute inflammation produces an exudate whereas chronic inflammation doesn’t
27
What are the histological features of granulomatous inflammation?
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
What is the good outcome of inflammation?
Resolution – healing of tissue damage to preserve integrity and function
29
What is 'Repair' in terms of wound healing?
Replacing normal tissue with scar tissue
30
Give an example of resolution and how it takes place.
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
What are three main complications of repair? Describe each of them.
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
Define Oedema.
Abnormal increase in interstitial fluid
33
What three forces determine the movement of fluid between blood vessels and the interstitial space?
Capillary hydrostatic pressure Plasma hydrostatic pressure Plasma oncotic pressure
34
What are the four broad causes of oedema?
Increased capillary hydrostatic pressure Decreased plasma oncotic pressure (e.g. nephrotic syndrome) Inflammation Lymphatic Obstruction
35
What is a common cause of pulmonary oedema?
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
What is non-cardiogenic pulmonary oedema?
Caused by increased permeability ARDS – Acute Respiratory Distress Syndrome Often caused by Sepsis, Shock and Trauma
37
What are the four types of cerebral oedema?
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
What are the possible serious consequences of cerebral oedema?
Rise in intracranial pressure, which could cause herniation
39
What are two common causes of generalised oedema?
Left Ventricular Failure | Nephrotic Syndrome
40
What is a consequence of oedema in a peripheral setting?
Impaired wound healing
41
What are the three main factors affecting thrombus formation?
Hypercoagulability Vessel Wall Injury Stasis
42
What is cardiac thrombosis caused by and what is an important complication?
Stasis – e.g. atrial fibrillation | Complication – systemic embolisation
43
What is arterial thrombosis caused by?
Vessel Wall Injury
44
What is venous thrombosis caused by and what is an important complication?
Stasis and Hypercoagulability | Complication – pulmonary embolism
45
What are the four fates of a thrombus?
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
Where do most arterial thromboemboli originate?
Carotid Arteries
47
Define haematoma.
A localised mass of extravasated blood that is relatively or completely confined within an organ or tissue
48
What are the three classes of haemorrhage based on size?
``` Petechiae = 1-2mm Purpura = >3mm Ecchymoses = 1-2cm ```
49
What is shock characterised by?
Hypotension
50
What two equations are used to evaluate the effects of changes in various vascular factors?
``` MAP = CO x SVR CO = HR x SV ```
51
What are the five types of shock?
``` Cardiogenic Hypovolaemic Anaphylactic Neurogenic Septic ```
52
Describe each of the five types of shock and its causes and effects.
``` 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
Define infarction.
Tissue necrosis due to unresolved ischaemia
54
What are the two types of infarct and how are they different?
Red – haemorrhagic – affects organs with a dual blood supply | White – anaemic – affects solid organs that have one blood supply
55
How can the rates of development of the occlusion affect the infarction?
If the occlusion develops slowly then there may be enough time for collateral vessels to form
56
What are the two types of myocardial infarction?
Transmural – across the whole wall of the heart | Subendocardial – just the layer under the endocardium
57
Describe the process of atherosclerosis.
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
What are the two types of atherosclerotic plaque and how are they different?
Stable – thick fibrous cap – less likely to rupture | Unstable – thinner fibrous cap – more likely to rupture

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