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Clin Path > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What is inflammation?

A

a cellular process that is responsible for removing injurious agent, removal of cellular debris and the initiation of the healing processing

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2
Q

What is an infection?

A

an injurious contamination of body or parts of the body by bacteria, viruses, fungi, protozoa, and/or by the toxins that they may produce.

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3
Q

List some signs and symptoms of inflammation

A

1) Redness
2) Swelling
3) Heat
4) Pain
5) Loss of function

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4
Q

Describe acute inflammation

A

Onset: rapid
Duration: short (days)
Specificity: non specific
Cardinal signs: present

Cause: Physical or chemical damage, pathogens, tissue necrosis, immune response

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5
Q

Describe chronic inflammation

A

Onset: delayed
Duration: long (weeks, months, years)
Specificity: specific (acquired immunity)
Cardinal signs: absent

Cause: Persistent damage or infection, presence of foreign body, autoimmunity

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6
Q

Which type of inflammation is age related?

A

Chronic inflammation is age related while acute inflammation is not

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7
Q

List the trigger, magnitude, outcomes, and bio markers for acute inflammation

A

Trigger: PAMPs (infection), DAMPs (cellular stress, trauma)
Magnitude: high grade
Outcomes: Healing, trigger removal, tissue repair
Bio markers: IL-6, TNF-α, IL-1β, CRP

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8
Q

List the trigger, magnitude, outcomes, and bio markers for chronic inflammation

A

Trigger: DAMPs (‘exposome’, metabolic dysfunction, tissue damage)
Magnitude: low grade
Outcomes: Collateral damage
Bio markers: Silent—no canonical standard biomarkers

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9
Q

List the phases of wound healing

A

1) Inflammation (4-6 days)
2) Proliferation (4-24 days)
3) Remodeling (21 days - 2 years)

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10
Q

Describe the cellular events in acute inflammation

A

1) increased neutrophilic influx in vessels
2) margination, rolling, adhesion
3) transmigration (diapedesis)
4) opsonophagocytic destruction

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11
Q

Describe the vascular events in acute inflammation

A

1st path

1) arteriolar changes
2) vasodilation
3) hypernemia (redness)

2nd path

1) venular changes
2) increased venular permeability
3) swelling (edema)

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12
Q

What are the types of capillaries?

A

1) continuous
2) fenestrated (dots)
3) sinusoid (holes)

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13
Q

What is Starling force?

A

Governs the passive exchange of water between the capillary microcirculation and interstitial fluid

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14
Q

Describe Starling force in action in a capillary

A

Aretrial end:

1) Blood pressure higher than osmotic pressure so net pressure is out.
2) fluid exits the capillary

Venous end:

1) Osomotic pressure higher then blood pressure so net pressure in
2) fluid enters the capillary

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15
Q

What is the stage of healing?

A

1) Hemostasis
2) Inflammation
3) Proliferation
4) Rmeodeling

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16
Q

List some inflammatory mediators affecting blood flow

A

1) histamine
2) serotonin
3) bradykinin
4) prostaglandis
5) luekotrines

Lead to vasodilation + increased vascular permeability = edema

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17
Q

List some inflammatory mediators attracting cells

A

1) monokines
2) lymphokines
3) lipooxygenase

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18
Q

What marks where the cells need to go?

A

Antigens

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19
Q

Describe cytokine release

A

1st pathway

1) at the phospholipid layer
2) phosphatidylcholine
3) phosphalipase A2
4) Arachnoid acid
5) cyclooxygenase
6) prostaglandis

2nd pathway

1) at the phospholipid layer
2) phosphotidylilonsitol
3) phospholipase c
4) arachnoid acid
5) lipooxygenase
6) leukotrines

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20
Q

What are the types of exudate?

A

1) normal (hydrostatic = osmotic pressure)
2) transudate (decreased osmotic pressure = fluid leakage)
3) exudate (decreased osmotic pressure more = fluid and protein leakage)

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21
Q

What are nociceptors?

A

Pain receptors

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22
Q

List the inflammatory exudates

A

1) Hemorrhagic, sanguineous
2) Serosanguineous
3) Serous
4) Purulent
5) Catarrhal

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23
Q

What is the appearance and significance of hemorrhagic, sanguineous exudate

A

Appearance:
Bright red or bloody; presence of red blood cells

Significance:
Small amounts expected after surgery or trauma. Large amounts may indicate hemorrhage. Sudden large amounts of dark, red blood may indicate a draining hematoma.

24
Q

What is the appearance and significance of serasonguineous exudate

A

Appearance:
Blood-tinged yellow or pink; presence of RBCs

Significance:
Expected for 48-72 hours after injury or trauma to the microvasculature. A sudden increase may precede wound dehiscence (rupture or separation).

25
Q

What is the appearance and significance of serous exudate

A

Appearance:
Thin, clear yellow, or straw-colored; contains albumin and immunoglobulins

Significance:
Occurs in the early stages of most inflammations; common with blisters, joint effusion with rheumatoid arthritis, viral infections (e.g., skin vesicles caused by herpesvirus); expected for up to 1 week after trauma or surgery. A sudden increase may indicate a draining seroma (pocket of serum within tissue or organ).

26
Q

What is the appearance and significance of purulent exudate

A

Appearance:
Viscous, cloudy, pus; cellular debris from necrotic cells and dying neutrophils (PMNs)

Significance:
Usually caused by pus-forming bacteria (streptococci, staphylococci) and indicates infection. May drain suddenly from an abscess (boil).

27
Q

What is the appearance and significance of catarrhal exudate

A

Appearance:
Thin, clear mucus

Significance:
Seen with inflammatory process within mucous membranes (e.g., upper respiratory infection).

28
Q

What happens to nociceptors during inflammation?

A

Lowered depolarization threshold (to activate nociceptors). More sensitive to pain

29
Q

Relate the cardinal signs of inflammation to what causes them

A

1) (heat & redness) vasodilation and increased BF
2) (swelling) exudation and leukocyte infiltration into extracellular space
3) (pain) direct trauma, chemical mediators, swelling of nerve endings
4) (loss of function) ICF model

30
Q

What are these

A

1) Margination
2) Rolling
3) Adhesion

31
Q

What does margination do (in order)?

A

1) Increased permeability
2) Increased cell concentration
3) Hemoconcentration
4) slows blood flow

32
Q

What is chemotaxis?

A

“Cell movement” letting other cells know where to go by chemokines

33
Q

List the steps of phagocytosis

A

1) chemotaxis and adhesion of microbe to phagocyte
2) ingestion of microbe by phagocyte
3) formation of phagosome (vesicle like around microbe)
4) fusion of lysosome with phagosome to form phagolysosome
5) Digestion of microbe until only indegisteable stuff is left
6) discharge of waste material from phagocyte

34
Q

What is systemic inflammatory response syndrome (SIRS)?

A

It is a widespread inflammatory reaction covering multiple systems

Stages:
1) SIRS
2) Sepsis (infection + SIRS)
3) Severe Sepsis (sepsis + end organ damage)
4) Septic shock (severe sepsis + hypotension)
5) Death

35
Q

What is immunology?

A

The study of physiologic mechanisms that allow the body to differentiate between self and non self and how it reacts when a non self component is encountered

36
Q

What is the immune system?

A

The bodily systems that protects the body from foreign substances by producing an immune response

37
Q

What does the immune system do?

A

1) highly adaptable and generates diversity for protection
2) after “threat” detection it triggers an effector response to eliminate the threat

38
Q

What are the phases of adaptive immune response?

A

1) recognition phase (differentiation)
2) amplification phase (colonial expansion, differentiation)
3) effector phase (elimination of antigens)
4) termination phase (apoptosis)
5) memory (surviving cells)

39
Q

What are antibodies?

A

AKA immunoglobulins, (Immunogenic, binds to antigens)

1) PROTEINS produced by the body (mainly plasma B) to fight foreign pathogens
2) activate the complement system
3) activating anaphylaxis by releasing histamine
4) stimulate antibody mediated hypertension

40
Q

What are antigens?

A

(Immunogenic “potentially”, reactive to antibodies)

1) any substance foreign to the body that evokes an immune response either alone or after forming a complex with a larger molecule

41
Q

Describe blood type with antigen/antibody

A

Blood A:
1) A antigens
2) anti B antibodies

Blood B:
1) B antigens
2) anti A antibodies

Blood AB (universal recipient):
1) antigens A and B
2) no antibodies

Blood O (universal donor):
1) no antigens
2) antibodies A and B

41
Q

What is MHC/HLA?

A

1) membrane proteins that function to present antigenic peptides for recognition by T cells

All nucleated proteins present MHC I (self-antigens)
Antigen presenting cells (APC) contain MHC II.

42
Q

What are the most common (#1 and #2) cells of the immune system?

A

1) Neutrophils (50-70%)
2) Lymphocytes (20-35%)

43
Q

Describe the primary function and classification of the cells of the immune system

A

1) Basophil:
Classification: granulocyte
Function: release chemicals that mediate inflammation and allergic response

2) neutrophil:
Classification: granulocyte, phagocyte
Function: ingest and destroy invaders

3) Eosinophils:
Classification:granulocyte, phagocyte, cytotoxic cell
Function: destroy invaders specifically parasites

4) monocytes:
Classification: phagocytes, (antigen presenting cell)
Function: ingest and destroy invaders

5) Lymphocyte:
Classification: cytotoxic cell “some”, (antigen presenting cell)
Function: specific response to invaders including antibody production

6) Dendritic cell:
Classification: (antigen presenting cell)
Function: recognize pathogens and activate other immune cells by antigens presentation

44
Q

From the immune cells, what are the non specific innate and what are specific/adaptive/aquired

A

Specific/adaptive/aquired:

1) Lymphocyte

Non specific innate:

1) neutrophils
2) eosinophil
3) basophil
4) macrophage
5) dendrite cell

45
Q

Innate immune reaction steps

A

1) inflammatory chemicals
2) margination
3) diapedisis (transmigration)
4) chemotaxis
5) phagocytosis

46
Q

Describe natural killer cells

A

Kills tumors and infected cells

1) innate (non specific)
2) needs activating ligands
3) and absence of inhibitory signal (MHC I)

47
Q

Describe T cells and types

A

cell mediated immunity

1) CD4+ (T helper) “gets help”
2) CD8+ (T cytotoxic) “kills cell”

48
Q

Describe B cell

A

Humoral immunity

1) Becomes either a “memory” B cell or plasma cell

49
Q

What does the complement system do?

A

1) Opsonization for phagocytosis

2) Cell lysis by membrane attack complex (MAC)

3) Chemotactic factors (C3a, C5a)

50
Q

Describe the mechanism of activation and give and example for hypersensitivity types

A

Type I:

Mechanism: Allergen-specific IgE antibodies bind to mast cells via their Fc receptor. When the specific allergen binds to the IgE, cross-linking of IgE induces degranulation of mast cells.
Example: allergy anaphylaxis, asthma

Type II:

Mechanism: IgG or IgM antibody binds to cellular antigen, leading to complement activation and cell lysis. IgG can also mediate ADCC with cytotoxic T cells, natural killer cells, macrophages, and neutrophils.
Example: cytotoxic reaction to self antigen

Type III:
Meachanism: Antigen-antibody complexes are deposited in tissues. Complement activation and cytotoxic T cells. provides inflammatory mediators and recruits neutrophils. Enzymes released from neutrophils damage tissue.
Example: Immune complex disease

Type IV:

Mechanism: TH1 cells secrete cytokines, which activate macrophages and cytotoxic T cells
Example: Delayed cell mediated

51
Q

Explain Type I

A

EX: Allergy

Stimulus: exogenous
Immune response: allergic, inflammatory response
Mediator process: IgE antibodies
Timing: immediate
Previous exposure increases B cell sensitivity & may worsen response
Epinephrine: opposite effect

52
Q

Explain Type II

A

EX: Cytotoxic reaction to self, Myathenia Gravis

Stimulus: exogenous or endogenous
Immune response: cytotoxicity
Mediator process: IgG and IGM antibodies, complement system, NK cells
Outcome: Cell lysis, phagocytosis, impaired cell function

EX: MG
Voluntary muscle weakness & fatigue
Disruption in the normal communication between nerves and muscles
No cure for MG
PT for safe mobility and function.

53
Q

Explain Type III

A

EX: Immune Complex, Rheumatoid Arthritis

Stimulus: exogenous or endogenous
Immune response: Excessive antibody complex, complement system
Mediator process: IgG and IgM antibodies, complement system
Outcome: Cell lysis

EX: RA

chronic inflammatory disorder
May affect joints, skin, eyes, lungs, heart and blood vessels.
No cure for RA
PT to maintain function & mobility

54
Q

Explain Type IV

A

EX: Delayed cell mediated, Type I diabetes

Figure 5-23. Type IV Hypersensitivity Reactions: the Mechanisms and Roles of T Lymphocytes.

The pathogenesis of a type IV hypersensitivity is centered on activation of CD4+ (T helper lymphocyte type 1) lymphocytes leading to activation of CD8+ lymphocytes and the production of cytokines, resulting in tissue injury and cell killing.

A. delayed-type hypersensitivity

B. T-lymphocyte-mediated cytolysis. APC, Antigen-presenting cell; CTL, cytotoxic T lymphocyte.

Ex: Type I diabetes

Chronic condition in which the pancreas produces little or no insulin

the body’s own immune system mistakenly destroys the insulin-producing (islet, or islets of Langerhans) cells in the pancreas.

No cure for t1dm

No prevention method

Exercise help improve glucose control.

55
Q

What is immunodeficiency

A

Immunodeficiency, the immune response is absent or depressed as a result of a primary or secondary disorder.

1) Primary immunodeficiency: reflects a defect involving T cells, B cells, or lymphoid tissues.

2) Secondary immunodeficiency: results from an underlying disease or factor that depresses or blocks the immune response. Like HIV, aging, malnutrition, cancer, autoimmune disease

56
Q

Describe HIV

A

1) HIV-1 infects T cells and macrophages directly
2) viral replication in both T cells and macrophages continues unabated
3) A gradual erosion of CD4+cells by productive infection
4) CD4+cell numbers decline, and the patient develops clinical symptoms of full-blown AIDS

Clin Path (12 decks)

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