Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

ΩΩ 2a Bateman - Introductory Clinical Sciences > Inflammation, ischaemia, normal and abnormal development > Flashcards

Inflammation, ischaemia, normal and abnormal development Flashcards

1
Q

What is inflammation?

A

A reaction to injury or infection involving cells such as neutrophils and macrophages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When is inflammation good?

A

Infection or injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

When is inflammation bad?

A

Autoimmunity or when an over-reaction to a stimulus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is inflammation classified?

A

Acute and Chronic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens in acute inflammation?

A

Sudden onset

Short duration

Usually resolves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the steps in acute inflammation?

A

Initial reaction of tissue to injury

Vascular component: dilatation of vessels

Exudative component: vascular leakage of protein-rich fluid

Neutrophil polymorph is the characteristic cell recruited to the tissue

Outcome may be resolution, suppuration (e.g. abscess), organisation, or progression to chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the causes of acute inflammation?

A

Microbial infections, e.g. pyogenic bacteria, viruses

Hypersensitivity reactions, e.g. parasites, tubercle bacilli

Physical agents, e.g. trauma, ionising radiation, heat, cold

Chemicals, e.g. corrosives, acids, alkalis, reducing agents,

Bacterial toxins

Tissue necrosis, e.g. ischaemic infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the essential characteristics of acute inflammation?

A

Rubor (red due to blood vessels)

Calor (heat due to blood vessels)

Tumor (swelling due to oedema)

Dolor (Pain due to sweeling and stretching, bradykinin, prostaglandin and serotonin also cause pain)

Loss of function is also characteristic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens in chronic inflammation?

A

Slow onset or sequel to acute

Long duration

May never resolve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What cells are involved in inflammation?

A

Neutrophil polymorphs

Macrophages

Lymphocytes

Endothelial cells

Fibroblasts

Plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are neutrophil polymorphs and what are their function?

A

Short lived cells

First on the scene of acute inflammation

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are macrophages and what are their fuction?

A

Long lived cells (weeks to months)

Phagocytic properties

Ingest bacteria and debris

May carry debris away

May present antigen to lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are lymphocytes and what are their function?

A

Long lived cells (years)

Produce chemicals which attract in other inflammatory cells

Immunological memory for past infections and antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are endothelial cells and what happens to them in inflammation?

A

Line capillary blood vessels in areas of inflammation

Become sticky in areas of inflammation so inflammatory cells adhere to them

Become porous to allow inflammatory cells to pass into tissues

Grow into areas of damage to form new capillary vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are fibroblasts?

A

Long lived cells

Form collagen in areas of chronic inflammation and repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is an example of acute inflammation?

A

Acute pancreatitis

Empyema of the gall bladder

Fibrinous pleuricy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is involved with acute pancreatitis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is an example of chronic inflammation?

A

Tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is involved with tuberculosis?

A

No initial acute inflammation

Mycobacteria ingested by macrophages

Macrophages often fail to kill the mycobacteria

Lymphocytes appear Macrophages appear Fibrosis occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the difference between an exudate and a transudate?

A

Exudates have a high protein content due to increased vascular permeability whilst transudates have a low protein content due to a normal vascular permeability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is a granuloma?

A

An aggregate of epithelioiod histiocytes and a feature of some-specific chronic inflammatory disorders.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is granulation tissue?

A

Granulation is an important component of healing and comprises small blood vessels in a connective matrix with myofibroblasts (A myofibroblast is a cell that is in between a fibroblast and a smooth muscle cell in phenotype)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are histiocytes?

A

Specialised macrophages e.g. Kupffer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is fibrin?

A

Deposited in blood vessels and tissues or on surfaces as a result of the action of thrombin or fibrinogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What does fibrous mean?
Describes the texture of non-mineralised tissue of which the principal component is collagen.
26
What happens in the early stage of acute inflammation?
In the early stages, oedema fluid, fibrin and neutrophil polymorphs accumulate in the extracellular spaces of the damaged tissue. The presence of the cellular component, the neutrophil polymorph, is essential for a histological diagnosis of acute inflammation.
27
What are the three processes of acute inflammation? (In relation to vessels and formation of product)
Changes in vessel calibre and, consequently, flow Increased vascular permeability and formation of the fluid exudate Formation of the cellular exudate – emigration of the neutrophil polymorphs into the extravascular space.
28
How is the cellular exudate formed?
The accumulation of neutrophil polymorphs within the extracellular space is the diagnostic histological feature of acute inflammation. The stages whereby leucocytes reach the tissues are shown in the next figure.
29
What do the endogenous chemical mediators cause?
Vasodilatation Emigration of neutrophils Chemotaxis Increased vascular permeability Itching and pain.
30
What are the plasma factors?
The plasma contains four enzymatic cascade systems: Complement The kinins, The coagulation factors and the Fibrinolytic system which are interrelated and produce various inflammatory mediators.
31
What are the endogenous chemical mediators of the acute inflammatory response?
32
What causes vascular dilation?
Histamine Prostaglandins PGE2/I2 VIP Nitric oxide PAF
33
What causes increased vascular permeability?
Transient phase – histamine Prolonged phase – mediators such as bradykinin, nitric oxide, C5a, leucotriene B4 and PAF, potentiated by prostaglandins
34
What causes adhesion of leukocytes?
Interleukins.
35
What does the outcome of acute inflammation depend on?
The type of tissue present and the amount of tissue destruction which in turn depend on the nature of the injurious agent.
36
What are the outcomes of inflammation?
Resolution Suppuration (Suppuration is the process of pus forming) Organisation Progression to chronic inflammation
37
What does suppuration involve?
Excessive exudate.
38
What is pyrexia?
Raised body temperature.
39
What are some systemic effects of inflammation?
Pyrexia Constitutional symptoms Weight loss Reactive hyperplasia of the reticuloendothelial system Haematological changes Amyloidosis
40
How can chronic inflammation take place?
Primary chronic inflammation Transplant rejection Progression from acute inflammation Recurrent episodes of acute inflammation
41
What are the macroscopic appearances of chronic inflammation?
Chronic ulcer Chronic abscess cavity Thickening of the wall of a hollow viscus Granulomatous inflammation Fibrosis
42
What are the microscopic appearances of chronic inflammation?
**_Lymphocytes plasma cells and macrophages._** A **_few eosinophil polymorphs_** may be present, but **_neutrophil polymorphs are scarce._** Some of the **_macrophages may form multinucleate giant cells_**. Exudation of fluid is not a prominent feature, but there may be production of **_new fibrous tissue from granulation tissue_**. There may be evidence of **_continuing destruction_** of tissue at the same time as **_tissue regeneration and repair._** **_Tissue necrosis_** may be a prominent feature, especially in granulomatous conditions such as tuberculosis.
43
What is involved with connective tissue proliferation? How are these processes regulated?
The predominant features in repair are **_angiogenesis_** followed by **_fibroblast proliferation_** and **_collagen synthesis_** resulting in granulation tissue. These processes are regulated by low molecular weight proteins called **_growth factors_** which bind to **_specific receptors_** on **_cell membranes_** and trigger a series of events culminating in cell proliferation.
44
What are some examples of chronic inflammation?
**_Chronic peptic ulcer_** of the stomach Gall bladder **_chronic cholecystitis_**
45
How are macrophages involved in chronic inflammation?
Move by **_amoeboid motion_** through tissues. Respond to certain **_chemotactic stimuli._** Ingest a **_wider range of materials_** than polymorphs. **_Harbour viable organisms_** if they are not able to kill them. In the delayed-type hypersensitivity response, they often die, **_contributing to the large areas of necrosis_** by lysozymes. They are part of the mononuclear phagocyte system (**_reticuloendothelial system)._**
46
What else can a granuloma contain?
lymphocytes and histiocytic giant cells.
47
What are epithelioid histiocytes?
Named for vague histological resemblance to epithelial cells, They tend to be arranged in clusters. Little phagocytic activity, adapted to a secretory function. One product of the secretory function is angiotensin converting enzyme. Used as measurement for systemic granulomatous disease, such as sarcoidosis.
48
What does the association of granulomas with eosinophils show?
A parasitic infection.
49
What is a common feature of many of the stimuli that induce granulomatous inflammation?
Indigestibility of particulate matter by macrophages.
50
What is a histiocytic giant cell?
Histiocytic giant cells form where particulate matter that is **_indigestible_** by macrophages accumulates. Histiocytic giant cells form when foreign particles are **_too large_** to be ingested by just one macrophage The multinucleate giant cells develop when **_two or more macrophages_** attempt simultaneously to engulf the same particle. **_Little phagocytic activity_** and no known function.
51
What are the characteristics of Langhans’ giant cells and where are they seen?
Horseshoe arrangement of peripheral nuclei at one pole of the cell. Tuberculosis.
52
What are the characteristics of foreign body giant cells and where are they seen?
Large cells with nuclei randomly scattered throughout their cytoplasm. They are characteristically seen in relation to particulate foreign body material.
53
What are the characteristics of Touton giant cells and where are they seen?
Central ring of nuclei, peripheral to which there is lipid material. They are seen when macrophages attempt to ingest lipids, and in xanthomas / dermatofibromasof the skin.
54
How does resolution happen after inflammation?
Initiating factor removed. Tissue undamaged or able to regenerate.
55
How does repair happen after inflammation?
Initiating factor still present. Tissue damaged and unable to regenerate.
56
What can pneumocytes do very well?
Regenerate.
57
What are the two different kinds of wound healing?
1st intention and 2nd intention.
58
How does healing by 1st intention work?
Weak fibrin joint into a strong collagen join.
59
What happens during 2nd intention?
You get granulation tissue formed.
60
What are examples of cells that don't regenerate well?
Myocardial cells Neurones
61
What is repair and what are some examples?
Replacement of damaged tissue by fibrous tissue **_Collagen produced by fibroblasts examples_** Heart after myocardial infarction Brain after cerebral infarction Spinal cord after trauma
62
What is laminar flow?
Normal flow through a capillary.
63
What disrupts the laminar flow?
Endothelial damage.
64
What is a thrombosis?
solid mass of blood constituents formed within intact vascular system during life.
65
What factors contribute to thrombosis?
Change in vessel wall. Change in blood flow. Change in blood constituents.
66
What does aspirin do?
Inhibit platelet aggregation.
67
What is an embolus?
Mass of material in the vascular system able to become lodged within vessel and block it.
68
What is ischaemia?
Reduction in blood flow.
69
What is infraction?
Reduction in blood flow with subsequent death of cells.
70
When will an infarction become a problem?
When blood supplied to a tissue is an end artery supply.
71
What is repercussion injury?
Body produces reactive oxygen species after you give the tissue blood back too fast.
72
What is an example of an end artery?
Kidney. Spleen. Bowel.
73
What is dual artery supplied?
Lungs. Liver. Brain.
74
What is the circle of wills for?
Equalise pressure within the brain.
75
What is a watershed area?
Areas far away from the brain likely to lose blood flow.
76
What does an aorta look like when people get older?
End up with atherosclerosis plaque.
77
What are fatty streaks?
Little lines in the aorta in peoples 30s, start of atherosclerosis.
78
Where do you never find any atherosclerosis?
In pulmonary arteries and low pressure systems.
79
What is in a plaque?
Fibrous tissue. Lipids - cholesterol. (crystals). Lymphocytes.
80
What are the risk factors for atherosclerosis?
Smoking. High blood pressure. Diabetes. Hyperlipidaeima.
81
What is the lipid insudation theory?
Lipid in blood goes into the wall and causes a plaque.
82
What is the theory for predicting plaques?
Endothelial damage theory.
83
What damages endothelial cells?
Free radicals. Nicotine. Carbon monoxide.
84
How does hypertension damage endothelial cells?
Shearing of cells.
85
How does poorly controlled diabetes damage endothelial cells?
superoxide anions glycosylation products.
86
How does hyperlipidaemia damage endothelial cells?
Direct damage to endothelial cells.
87
How does a vessel become occluded?
Thrombus and then endothelial cells form over the top, repeated events like this cause an occlusion.
88
What are some complication of atherosclerosis?
Cerebral infarction. Gangrene. Peripheral vascular disease. Aortic aneurysms.
89
What is apoptosis?
Programmed cell death.
90
How does a cell know to die.
Itself tells itself to die.
91
Why would a cell undergo apoptosis?
DNA damage.
92
What are some examples of DNA damage?
Single strand break. Double strand break. Base alteration. Cross linkage.
93
What is an important part of apoptosis?
p53 gene.
94
What is apoptosis useful for?
In development, webbed hands and feet, cells in the web apoptose. In the gut, cells differentiate until the surface then apopotose.
95
What happens when the cell can no longer apoptose?
Cancer.
96
In what disease is there too much apoptosis?
HIV in destroying T lymphocytes.
97
What is necrosis?
Traumatic cell death.
98
What are some examples of necrosis?
Cerebral infacrtion. Pancreatitis. Frostbite.
99
What are two different types of necrosis?
Coagulative necrosis. Liquifactive necrosis
100
What does caseous necrosis mean?
Cheese like appearance.
101
When do you get the most chromosomal abnormalities?
Before the first month.
102
Hole in heart?
Left into right ventricle.
103
What is congenital abnormality?
Present at birth.
104
What are homeobox genes?
Genes that control development.
105
What is a acquired abnormality?
caused by non-genetic environmental factors.
106
What does inherited mean?
caused by an inherited genetic abnormality.
107
What do Down's syndrome get more of?
Beta amyloid - dementia. Cataracts.
108
What is autosomal abnormalities?
Non-sex chromosomes.
109
What does a pituitary adenoma affect before puberty?
Long bones.
110
What does a pituitary adenoma affect after puberty?
Skull. Hands. Feet.
111
What is Amyloidosis?
Build up of amyloid in your body leading to: Swelling of your ankles and legs Severe fatigue and weakness Shortness of breath Numbness, tingling or pain in your hands or feet, especially pain in your wrist (carpal tunnel syndrome) Diarrhea, possibly with blood, or constipation Unintentional, significant weight loss An enlarged tongue Skin changes, such as thickening or easy bruising, and purplish patches around the eyes An irregular heartbeat Difficulty swallowing

ΩΩ 2a Bateman - Introductory Clinical Sciences (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions