Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1.2.5. Pathological Processes > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What generic name do we give chemical messengers that can trigger an inflammatory reaction?

A

Inflammation mediators

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

Cell types in chronic inflammation?

A 
Plasma cells, 
Lymphocytes, 
Macrophages, 
Eosinophils,
Fibroblasts/myofibroblasts,
Giant cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cell types in acute inflammation?

A

Neutrophil polymorphs

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

Give an example of when the body’s acquired immune response is triggered without the innate response being triggered first

A

Viral infection

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

What are the major causes of acute inflam?

A 
Microbial infections, 
acute phase hypersensitivity reactions, 
physical agents, 
chemicals, 
tissue necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the biological purpose of acute inflam?

A

Eliminate initial cause of cell injury,

clear out necrotic cells and tissues damaged from original insult and inflam process,

initiate tissue repair.

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

What are the characteristic signs of acute inflam?

A

Rubor, calor, tumour, dolor, loss of function

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

How are the tissue changes brought about?

A

Vascular flow (vasoconstriction then dilation, increases viscosity = stasis), formation of fluid exudate, neutrophil emigration

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

What is fluid exudate and how is it formed?

A

Protein rich fluid from blood vessels and into nearby tissues with an increase in vascular permeability,

composed of serum, fibrin, and white blood cells = oedema = increases lymph drainage

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

How do neutrophils emigrate?

A

Margination: stasis = line up at vessel edge.

Rolling: roll and stick intermittently.

Adhesion: stick more avidly.

Emigration: through inter-endothelial cell junctions / digestion of basement membrane

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

Why do the tissue changes in inflam constitute an effective response to injury?

A

Delivery of nutrients = oxygen, cells, plasma proteins such as antibodies, inflammatory mediators, fibrinogen,
Dilution of toxins,
Maintenance of temperature,
Stimulation of immune response,
Destruction and removal of dead or foreign material,
Pain and loss of function enforcing rest

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

How do neutrophils kill microorganisms?

A

Contact, recognition via opsonins, phagocytosis

1) O2 dependent = superoxide/hydrogen peroxide.
2) O2 independent = lysosomes

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

How do neutrophils move?

A

Chemotaxis: movement along conc gradient of chemoattractant

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

Name the important mediators in acute inflam

A

Histamine, bradykinin, prostaglandin, complement system, cytokines

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

What is the function of histamine?

A

One of the first chemical mediators, in response to damage C3a C5a IL-1, from mast cells, basophils, platelets

vascular dilation, increased vascular permeability, pain

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

What does bradykinin do?

A

Vasodilation

17
Q

What are the local complications of acute inflam?

A 
Damage to normal tissue, 
Obstruction of tubes, 
compression of vital structures, 
Loss of fluid, 
Pain and loss of function
18
Q

What are the systemic consequences of acute inflam?

A

Fever,

leucocytosis,

acute phase response (decreases appetite, raise pulse, changes CRP),

shock (sepsis, damage in response to infection = dangerously low BP and abnormalities in cellular metabolism)

19
Q

How is acute inflam resolved?

A

Vascular changes stop,
exudate drains to lymph,
fibrin degraded,
neutrophils die,
damaged tissue might be able to regenerate,
all mediators have short half-lives, can be deactivated

20
Q

Outline the sequelae of acute inflam?

A

Abscess, chronic inflam, fibrous repair, death

21
Q

What are some clinical examples of acute inflam and causative organism?

A

Lobar pneumonia = acute pneumonia involving one or more lobes of the lung (Strep pneumoniae),

Acute appendicitis = acute inflammation of the appendix (c.diff, e.coli),

Bacterial meningitis = inflam of meninges around brain and spinal cord (Strep pneumoniae, Neisseria meningitides)

22
Q

Give examples of inherited disorders of acute inflam

A

Hereditary angio-oedema,
Alpha-1 antitrypsin deficiency,
Chronic granulomatous disease

23
Q

What does pyogenic mean?

A

Pus forming

24
Q

What is the difference between an exudate and a transudate?

A

Transudate = fluid pushed through capillary due to high hydrostatic pressure, low protein content.

Exudate = fluid that leaks around the cells of the capillaries caused by inflam, high protein content.

25
Q

What are the phases of acute inflam?

A

Vascular phase: changes in blood flow (vasodilation, permeability), chemical mediators, exudation, delivery of plasma proteins (fibrin),

Cellular phase: neutrophil infiltration

26
Q

What is the primary WBC involved in acute inflam?

A

Neutrophil (granulocyte)

27
Q

How can neutrophils cause damage?

A

Activated neutrophils may release toxic metabolites and enzymes causing damage to host tissues

28
Q

Name the chemical mediator that increase blood flow

A

Histamine, prostaglandins

29
Q

Name the chemical mediator that increase vascular permeability

A

Histamine, leukotrienes

30
Q

Name the chemical mediator that cause neutrophil chemotaxis

A

C5a, LTB4, bacterial peptides

31
Q

Name the chemical mediator that causes phagocytosis

A

C3b

32
Q

What are the hallmarks of acute inflam?

A

Exudate of fluid (oedema), infiltrate of cells (inflammation)

33
Q

Discuss lobar pneumonia

A

pathological stages = congestion, red hepatisation, grey hepatisation, resolution

compare bronchopneumonia = lobar is the lobe of lung, broncho is inflam of bronchi/br

MO = strep pneumoniae

complications = bacteremia, diff breathing, pleural effusion, lung abscess

34
Q

Discuss acute appendicitis

A

macroscopic = swelling, odema

microscopic = infiltration of neutrophils, ulceration ( break in epithelium)

cause = c.diff, e.coli

complications = bursting, peritonitis, abscess, fistula

35
Q

Discuss bacterial meningitis

A

macroscopic = pus, exudate in sulci

microscopic = infiltration of neutrophils

cause = Strep pneumoniae, Neisseria meningitides

complications = increase pressure, DIC, encephalitis, seizures, under devel of brain

36
Q

What are the complications of gallstones?

A

obstruct common bile duct = jaundice

inflam gallbladder

acute pancreatitis

gallbladder cancer

37
Q

Discuss ascending cholangitis and its link with gallstones

A

link with gallstones = infection of the bile duct, tends to occur if duct is already obstructed by gallstones

cause = tumours, clostridium,

complications = renal failure, resp failure, heart failure, shock, death

38
Q

what is chronic granulomatous disease and how does it present?

A

immune system has diff forming the reactive oxygen compounds for killing = formation of granulomata in many organs

present = pneumonia, abscesses of the skin, tissues, and organs, suppurative arthritis, osteomyelitis

1.2.5. Pathological Processes (11 decks)

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