Brainscape's Knowledge GenomeTM

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


See full index

NURS 330 - Theoretical Perspectives in Nursing: Adults/Older Adults and Their Families > Module 4 - Infection and Immunity > Flashcards

Module 4 - Infection and Immunity Flashcards

You may prefer our related Brainscape-certified flashcards:
Nursing Mental Health flashcards Nursing Management of Care flashcards NCLEX-PN® flashcards NCLEX-RN® flashcards Nursing Fundamentals flashcards Nursing Pediatrics flashcards Nursing Safety & Infection flashcards Nursing Pharmacology flashcards Nursing Maternity flashcards Family Nurse Practitioner (FNP) flashcards
1
Q

What are the 3 lines of defense?

A
  1. Anatomic barriers
  2. Inflammatory response
  3. Immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the main anatomical barrier and how is it maintained?

A

Intact skin - usually lower than 37 degrees, around pH 3-5, normal flora, and some fatty acids to prevent bacterial growth and defend against invading pathogens

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

How is urine an anatomical barrier?

A

Our constant production of urine helps to flush out toxins (filtered out by the kidneys and excreted during voiding)

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

Which anatomical barriers are found in the respiratory tract? How do they act as barriers?

A

Cilia and circulating macrophages. Cilia can sweep pathogens out of the respiratory tract and macrophages can trap and destroy pathogens before they get into the lungs

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

What is the main anatomical barrier in the GI tract?

A

Gastric acid - very acidic, most pathogens and invading bacteria cannot survive

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

What is an acute inflammatory response?

A

The first response to cellular damage by an invading pathogen, irritant, or chronic health condition. This is usually triggered when our anatomical barriers fail

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

What is the purpose of inflammation?

A

To neutralize, or dilute toxins, remove necrotic tissue, and provide an environment for healing

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

Why is an inflammatory state potentially a bad thing?

A

An inflammatory state can cause further cellular and tissue damage, so if the body is stuck in a chronic inflammatory state, this can lead to more and more damage accumulating.

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

List 3 conditions that can cause inflammation:

A
  • chronic illness (atherosclerosis, arthritis etc)
  • physical trauma (cuts, lacerations,
  • chemical trauma
  • micro-orgaisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens immediately after tissue or cellular damage?

A

Damaged tissues release mediators to start the inflammatory process

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

What is the first mediator in an inflammatory response? What is the role of this mediator?

A

Epinephrine - causes vasoconstriction to restrict the flow of blood and stop the spread of the toxin or reduce bleeding for a short time

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

Which effects are caused by chemotaxic and which are caused by vascular mediator responses?

A

Erythema (redness) is caused by both.

Edema and pain are caused by vascular mediators

Heat is caused by chemotaxic mediators.

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

What do the vascular mediators of the secondary response do?

A

Cause vasodilation and the capillary membranes to become leaky, both of which allow white blood cells to enter the damaged area

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

What do the chemotaxic mediators of the secondary response do?

A

Cause leukocytosis, basically attracting white blood cells to the region - this works in tandem with the vascular mediators

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

During the inflammatory response, what happens to the affected organ?

A

Loss of function

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

Can we diagnose inflammation based on only systemic signs/symptoms? Why or why not?

A

No - the systemic symptoms are applicable to a range of conditions

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

What are the systemic signs/symptoms of inflammation?

A

Malaise - a general feeling of unwell due to metabolic system increase

Nausea and anorexia - irritation of the stomach due to vascular mediators

Tachycardia + tachypnea - increased HR and RR due to epinephrine release

Fever - heat from chemical reactions, increased metabolic system activity to kill pathogens

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

What causes erythema?

A

Blood leaking out of capillaries

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

How does inflammation lead to edema (swelling)?

A

Fluid leaking from the blood vessels into the surrounding tissues

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

How is heat generated from inflammation?

A

Blood vessels near skin dilate, allowing increased blood flow from core

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

How can inflammation cause pain?

A

edema pushing up against skin and/or nerves, chemical mediators irritating nerves

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

How can inflammation cause loss of function?

A

Edema can limit mobility, damage cells, mediators can damage cells

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

What are the main localized signs + symptoms of inflammation?

A

Erythema, edema, pain, heat, loss of function

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

What is an easy way for us to detect inflammation in a patient during an assessment?

A

Look for heat and edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is typically the first test done for inflammation?

A

C Reactive Protein (CRP), released by the liver in response to inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Are the tests for inflammation specific or non-specific?

A

CRP and ESR are non-specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the usual levels for CRP?

A

3-5 mg/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the usual levels for ESR?

A

Females: 0-20 mm/h
Males: 0-10 mm/h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does an ESR work?

A

ESR = erythrocyte separation rate.

When inflammation is present, fibrinogen is released, and causes erythrocytes to stick together. This affects the speed at which these RBCs will separate from plasma, and the higher the number, the more inflammation is present.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Once we identify inflammation, what is our first goal of care? What are the subsequent goals of care?

A

Eliminate the trigger causing inflammation. The next goals are to reduce the edema and support the cellular function in the damaged area.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which comes first for controlling inflammation, ice or heat? Why?

A

Ice first! We need to control the edema, so ice causes vasoconstriction. Heat comes after ice to enhance vasodilation and allow blood flow to the region, along with some muscle relief

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What 3 classes of medications can we give for inflammation?

A

Anti-inflammatory, anti-histamine, and corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the main type of anti-inflammatory medication, and what is one example?

A

NSAIDS –> ibuprofen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the mechanism of action for anti-inflammatory medications?

A

Inhibit prostaglandin synthesis via Cox1/2, which can irritate nerves, exacerbate pain, and cause leaky capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is one of the main risks with NSAIDs? How can we reduce this risk?

A

NSAIDs are acidic, so they leave the patient at risk for gastritis, or exacerbation of kidney issues. To reduce risk, give with food to neutralize acidity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the mechanism of action for anti-histamines?

A

Block histamines, which enhance inflammation/inflammatory response

37
Q

What are 2 examples of anti-histamines?

A

Diphenhydramine (Benadryl) and Ranitidine (Zantac)

38
Q

True or false: anti-histamines should be taken with meals

A

True - anti-histamines can cause stomach irritation

39
Q

What are some signs you should watch for when administering anti-histamines?

A

Dizziness or sedation

40
Q

What is the main mechanism of action of corticosteroids?

A

Inhibit chemical mediators of inflammation

41
Q

What is the effect of high doses of corticosteroids? What is the effect of low doses?

A

High = immunosuppressive

Low = anti-inflammatory

42
Q

Do you need to take corticosteroids with food?

A

Yes - they are also acidic, so patient is at risk for GI bleeding if not taken with food.

43
Q

What are some risks associated with corticosteroids?

A

Infections due to immune system suppression, and hyperglycemia due to glucose release.

44
Q

What are the 3 main components of the immune system?

A
  1. Bone marrow
  2. Lymph system
  3. Thymus
45
Q

What is the role of the bone marrow in the immune system?

A

Produce WBCs like lymphocytes, RBCs, and platelets

46
Q

What is the role of the lymph system in the immune system?

A

To produce, store, and transport immune mediators

47
Q

What is the role of the thymus in the immune system?

A

Produce T Lymphocytes (WBCs)

48
Q

What are the 2 main types of immunity?

A

Active (lifelong immunity) and passive (not lifelong)

49
Q

What are the 2 main mechanisms of immunity?

A

Humoral and cellular

50
Q

What are some examples of active immunity?

A
  • Natural due to pathogen exposure
  • Vaccine acquired due to exposure to weakened or killed form of pathogen
51
Q

What are some examples of passive immunity?

A
  • administration of antibodies
  • via placenta
  • through chest milk
  • administration of immunoglobins
52
Q

How does humoral immunity occur?

A

Through production or administration of antibodies to that pathogen. Helper T cells support B cells to produce antibodies against pathogen’s antigens. These antibodies then destroy or dissolve the affected cell

53
Q

How does cellular immunity occur?

A

Helper T cells release cytokines that allow the T cell to attach to the antigen to become cytotoxic T cells, and lyse the affected cell

54
Q

Why is the elderly population at higher risk for infection?

A

Their immune systems are much more diminished and they tend to have more comorbidities, so they are more susceptible to pathogens multiplying

55
Q

What 3 factors are needed for an infection to occur?

A
  1. Source
  2. Susceptible person
  3. Transmission
56
Q

What are the 4 methods of transmission?

A
  1. Airborne
  2. Droplet
  3. Contact
  4. Puncture
57
Q

List some factors that can influence pathogen survival in the body:

A
  • glucose: promotes bacterial growth
  • water: moist environment promotes growth
  • oxygen: aerobic vs anaerobic vs both environments
  • temperature: warm but not hot or cold
  • pH: usually around 7 to promote growth
  • light: bacteria like dark environments
58
Q

What is an example of a type of pathogen that thrives in an anaerobic environment? An aerobic environment? Both?

A
  • anaerobic = MRSA
  • aerobic = pneumococcal
  • both = E. coli
59
Q

What are the stages of infection, in order?

A
  1. Exposure
  2. Incubation
  3. Prodromal
  4. Illness
  5. Convalescence
60
Q

Will every exposure lead to infection?

A

No, only becomes infection if there’s a portal of entry and all 3 barriers fail

61
Q

What is the incubation period?

A

The time between exposure and onset of symptoms, where a person is considered infectious. Can last 1-21 days.

62
Q

What is the prodromal period?

A

The time between general symptoms and the symptoms specific to the illness. Can last 1-7 days

63
Q

What is the illness stage?

A

When symptoms occur that are specific to that disease. Can last days-weeks-months-years

64
Q

What is the convalsecence stage?

A

The time when symptoms start to subside and the body starts to recover from the illness. Can last days-weeks-months-years, or even fail

65
Q

What are the local signs/symptoms of an infection?

A

Erythema, edema, pain, heat, induration (thickening/hardening of soft tissues), loss of function, exudate (fluid leakage)

66
Q

What are the systemic signs and symptoms for a local infection?

A

Fever, tachycardia and tachypnea, hypertension, headache, nausea, vomiting, diarrhea

67
Q

True or false? Bacterial infections lead to a high grade fever?

A

False. Bacterial infections lead to a low grade fever, viral infections lead to high grade

68
Q

Why does our blood pressure increase during an infection?

A

To promote blood flow to the area to hopefully bring in white blood cells to clear the infection. The elevated blood pressure may cause the headache.

69
Q

What are some systemic signs and symptoms of a systemic infection, like sepsis?

A

Fever or hypothermia, tachycardia or bradycardia, tachypnea, hypotension, alterations to level of consciousness, oliguria (not a lot of pee)

70
Q

Why can sepsis cause either fever or hypothermia?

A

Fever caused during immune response, hypothermia caused by a lack of immune response (ie. in an elderly person)

71
Q

Why is oliguria a dangerous symptom?

A

It indicates that the kidneys are not perfused, which tells us that the rest of the body is not receiving enough O2.

72
Q

What will likely be the first sign that an elderly person has an infection?

A

Changes to LOC

73
Q

What are the 3 main assessments for infection?

A

Complete blood count (CBC), Culture and Sensitivity (C+S), and Blood Cultures

74
Q

What does a CBC tell us?

A

Nonspecific, just tells us which stage of infection we’re at based on what WBCs are present

75
Q

If lymphocytes are present but not neutrophils or moncytes, what stage of infection are we at?

A

Middle of infection.

Neutrophils indicate start, monocytes indicate late stage.

76
Q

How does a C+S work?

A

Take culture of the pathogen from the site of infection (urine, wound, sputum) and test it against different antibiotics to determine which bacteria is present

77
Q

How does the Blood culture work?

A

Take a blood sample to test if a pathogen is present in the blood stream.

78
Q

Why is providing fluids important to prevent infection?

A

Ensures adequate blood volume and allows for leaky capillaries

79
Q

What are some of the dangers of lack of mobility when considering infection?

A

If they sit still, their bladders are not emptied as often, they risk skin pressure injuries, and typically do not cough as often.

80
Q

How can antibiotic resistance arise?

A

If the wrong antibiotics are prescribed, if antibiotics are prescribed when they aren’t needed, or if antibiotics aren’t taken properly

81
Q

What is the most common group that develops resistance?

A

Enterococci, which are typically found in the gut and on the skin

82
Q

What is MRSA?

A

Methicillin resistant staphylococcus aureus, a strain of bacteria that is resistant to penicillin and tends to live on the outside of the skin

83
Q

What is the mortality rate with MRSA?

A

~20%

84
Q

What is Vancomycin Resistant Enterococcus?

A

Strain of bacteria that is resistant to vancomycin, lives in the GI tract and urinary tract

85
Q

What condition can VRE cause? What is the mortality rate with this strain of bacteria?

A
  • can cause bacteremia and endocarditis
  • ~40%
86
Q

What is carbapenem resistant enterobacterales?

A

Strain of bacteria that is resistant to the carbapenems (imipenem and meropenem). This strain is always acquired in hospital settings, not at home.

87
Q

Why is CRE so dangerous? What is the mortality rate?

A
  • the carbapenems are considered the last line of defense, some of the strongest antibiotics that can be given. Resistance to these can leave a patient with very few options.
  • mortality rate around 50-60%
88
Q

What are some examples of CREs?

A
  • E. coli
  • Klebsiella pneumoniae
89
Q

What are some antibiotics that we are seeing new resistance to?

A
  • Clarithromycin (H pylori)
  • Fluoroquinolone (resp infections, UTIs)
  • Cephalosporin (skin, antibiotic resistance, resp infections, meningitis)

NURS 330 - Theoretical Perspectives in Nursing: Adults/Older Adults and Their Families (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions