Exam 1 Infection & Inflammation Flashcards

1
Q

In what way is Inflammation a protective response?

A

Eliminates cause of injury, remove damaged tissue, Generates new tissue

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2
Q

What the 2 types of Inflammation and how long do they last?

A

Acute; minutes to days (vascular permeability and neutrophil proliferation)
Chronic; days to years

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3
Q

Causes of acute inflammation

A

Infection physical injury; surgery; cancer; chemical agents; tissue necrosis; foreign body; immune reaction

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4
Q

Stage of Acute Inflammation: Vascular Permeability
What is key behind the permeability ?
Give two types of exudate

A

Inflammatory mediators (histamine) -> make blood vessels dilate and become more permeable -> fluids, WBC, and platelets travel to the site more easily

Purulent exudate(PUS)= rich in protein from WBCs, microbial debris and cellular debris.

Transudate exudate- contains little protein i.e. blister

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5
Q

What are the 5 hallmark signs of inflammation

A

warm, red and swollen , pain, loss of function;

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6
Q

Stage of Acute Inflammation: Cellular chemotaxis

Hint: think of who is sending chemical signals

A

Movement of cell migration towards the site of injury.
Microbial agents, endothelial cells, WBC- send chemical signals -> attract platelets and other WBCs to the site of injury.
WBCs release different inflammatory mediators (like cytokines, prostaglandins(control blood flow and blood clots), histamines

Cytokines- modulate the inflammatory reaction by amplifying or deactivating the process.
- amplify the inflammatory process - some attract more WBCs - some attempt to stop inflammatory process

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7
Q

What is the job Cytokines during inflammation

What organ does it stimulate?

A

Cytokines- modulate the inflammatory reaction by amplifying or deactivating the process.
- amplify the inflammatory process - some attract more WBCs - some attempt to stop inflammatory process
Cytokines: stimulation of the liver to release substances called acute phase protein.
Acute phase protein are proteins that can ↑ or ↓ the response to inflammation

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8
Q

What is FRP and Fibrinogen?

A

C-reactive protein; key acute phase protein and indicates active inflammation If pt has elevated CRP then this implication of active inflammation in the body

A protein converted to fibrin by the thrombin in response to vascular or tissue injury. This is what you will see in blood clot to prevent bleeding

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9
Q

How do histamines work and antihistamines?

A

FIRST MEDIATOR to be released during acute inflammatory reaction- > binds with H 1 receptors of endothelial cells -> dilatation of arterioles and increase permeability of venules.

the drug would bind to the H1 receptor so histamine cant bind and cause inflammation. Doesnt allow dilation of arterioles

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10
Q

What are the types of WBC and their function

A

Neutrophils (AKA polymorphonuclear leukocytes or PMNs)
Appears within 24-48 hours -> phagocytosis, first responders, Short lifespan; hours-days

Lymphocytes- T cells, B cells, Natural Killer Cells - immune response

Eosinophils- increase number in allergic reaction and parasitic infections Ex. Malaria

Basophils (least amount of) involved in allergic and hypersensitivity reaction

Monocytes- largest in size among the WBC activated after 48 hrs, big brother to neutrophils, phagocytosis

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11
Q

Stage of Acute Inflammation: Systemic response (symptoms )

A

Fever, pain, lymphadenopathy, anorexia, lethargy.

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12
Q

What is the most common Systemic response (symptom) of inflammation ?

A

Fever
Pyrogens are fever-causing substances; microbial organisms, bacterial products and cytokines are all pyrogens.

  • A higher body temperature is thought to increase the efficiency of WBCs in phagocytosis.
    Implication: low grade fever can be beneficial in the presence of infection! You dont have to treat in an adult but baby needs treatment ASAP leads to febrile seizure
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13
Q

What is Lymphadenopathy or lymphadenitis?

A
  • enlargement of the lymph nodes.
    Lymphocytes mature in the lymph nodes As response to inflammation, there is a proliferation of
    lymphocytes - > lymph nodes become enlarged and tender. Other systemic response:
    anorexia; lethargy
    this is related to cytokines and other inflammatory mediators
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14
Q

What is the outcome of Acute Inflammation? If the job is done correctly or incorrectly

A

Complete resolution
• Injurious agent is eliminated/ activation of chemical mediators caused the area to look good as new

Healing by connective tissue
Development of fibrous scar tissue/ can happen if there is infection

Chronic, persistent inflammation that does not recede ->
inflammation becomes chronic!

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15
Q

What causes Chronic Inflammation?

What are the Dominant cells in Chronic Inflammation ?

A

bacteria ( TB; Mycobacterium spp.; Treponema; syphillus); parasites, fungi;
prolonged exposure to toxic agents like coal dusts; autoimmune diseases.- RA
predominance of monocytes, lymphocytes and macrophages

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16
Q

Whats the difference between macrophages and monocytes ?

A

Macrophages are like monocytes but monocytes are in the blood vessels in the blood moving around from place to place
Macrophages reside in one place

17
Q

What is the name of the area where macrophages are aggregated and are transformed into epithelial-like cells

A

Granuloma (small area of inflammation) seen in xRays like TB Granuloma
Surround foreign bodies and causes inflammation ex. suture tools in body, asbestos, sutures
1-2 mm lesion - there is a mass of macrophages surrounded by lymphocytes.

18
Q

How are injured tissues repaired?

A

regeneration of parenchymal cells or by connective tissue repair –> scar formation

19
Q

Explain the 3 phases of wound healing

A

Inflammation
The process of inflammation is essential in wound healing

Proliferation, granulation tissue formation, and epithelialization
The key cell: fibroblast- connective tissue that synthesizes and secretes collagen; Fills wound space
Final component of this phase: epithelialization; form the surface layers similar to the ones destroyed

Wound contraction and remodeling
Here, there is simultaneous production and lysis of collagen as the scar tissue is remodeled.

20
Q

Explain:

Primary intention (or primary union)

Secondary intention

Tertiary intention

A

The edges are clearly demarcated, cleanly lacerated. Example- surgical wound •

There is an extensive loss of tissue; regeneration of the same cells are not possible. Scar formation

The wound is missing large amount of tissue and is contaminated;
Needs to be cleaned and left open before closure; wound packing may be necessary; • May require skin graft, Large bed sores

21
Q

What are factors that affect wound healing ?

A

Nutrition- proteins and minerals
CHON, CHO, Fats, Vitamins A,C, B • Oxygenation

Circulation
Adequate blood supply to bring nutrients and WBC; to remove waste products

Immune Strength - fights infection

Contamination
Can result to healing by tertiary intention; animal bite higher chance of infection especially cats

Obesity
Adipose tissues do not heal efficiently

Age
Decreased inflammatory response, general slowing processes.

Protein and fibroblast

22
Q

Vitamins A,C, B

A

A- stimulates and supports epithelialization
C- collagen formation
B- enzyme reactors

23
Q

What are some Complications of Wound Healing?

A

Keloid; There is hypertrophic scar due to excessive accumulation of epithelium and collagen

Contractures- permanent tightening of the muscles, tendons, skin
Wound contraction normally happens without issue.
It can become exaggerated- > deformity burns and joint surfaces Stricture- type of contracture that happens on bodily ducts, canals, or tubes–> GERD

Fistula; Abnormal connection between 2 different organs
Ex: recto-vaginal fistula tube connecting the two leads to lots of UTI’s

Adhesions-a band of scar tissue that joins two internal body surfaces that are not usually connected
Abnormal bands of scar tissues •

Wound rupture- dehiscence; evisceration
• Tension on the wound can cause this
• Dehiscence- previously closed wound open up
• Evisceration- internal organs extrude from the open wound.
Encourage post-op pts to cough to prevent pneumonia, use pillow to cover the area

24
Q

What is infection ?

A

invasion, colonization and multiplication of pathogens

within the host

25
Q

What causes lyme disease ?

A

Borrelia burgdorferi bacteria

26
Q

What is colonization?

A

Microorganism doesnt affect host ex. staph aureus is on the skin when cut it goes in the skin can cause inflammation and infection

27
Q

What are the 5 types of pathogens

A

Bacteria- can be beneficial or harmful to humans
Ex: Staphylococcus aureus; Treponema pallidum syphillus ; Streptococcus pyrogenes

Viruses-
Microorganisms that depend on host cellular processes for their life cycle and
replication. • Ex: Adenovirus, Influenza virus, Hepatitis A, B, C virus, HIV

Fungi
Mold-like microorganisms that live on human tissue; mycoses- fungal infection; can be superficial or systemic infection • Dermatophytes- tinea infections (T. cruris (ringworm), T. pedis (athlete’s foot); • Candida albicans infection- can happen to immunocompromised individual

Prions- infectious agents capable of causing brain diseases in humans and animals. Lacks nucleic acid can withstand conventional means of sterilization
• Mad cow disease; in human- Creutzfeldt- Jakob Disease (CJD) and the Variant
Creutzfeldt Jakob Disease (VCJD)- human encephalopathy transmitted
through infected beef; • Mad Cow Disease- result from ingestion by humans of prions in infected meat • IP: about 10 years (more or less) but it can lie dormant for ages; • CA- > pass the BBB- > deposited in brain tissue -> degeneration of brain

  • Parasite- protozoa, helminths
  • Protozoa- Trichomonas vaginalis; Giardia lamblia
  • Helminths- Taenia saginata tape worms; Enterobius vermicularis human worms are
28
Q

What is the chain of infection ?

A
Pathogen 
Reservoir 
portal of exit 
Modes of transmission Direct; cough, Indirect; fomite
portal entry 
Susceptible host