Monica - Week 3 - Exam 1 Flashcards

1
Q

Stem cells from the bone marrow can differentiate further into which two categories of WBC?

A

Granulocytes and Agranulocytes

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2
Q

What WBC are considered granulocytes?

A

Basophils, Eosinophils, and Neutrophils

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3
Q

What WBCs are considered agranulocytes?

A

Monocytes and Lymphocytes

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4
Q

What type of cells are WBCs?

A

Disease fighting cells - protect from infections - bodies defense mechanism

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5
Q

What are the normal range for WBCs?

A

4,500 - 10,000 cell/mct

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6
Q

T/F: all WBC are the same

A

FALSE. Agranulocytes and Granulocytes

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7
Q

Characteristics of Granulocytes

A

contain granules within cytoplasm; multi-lobed nuclei - 2-5 segmented lobes connected by strands; appear in the initial stages of infection

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8
Q

What is the role of granulocytes?

A

To release their granules, which are anti microbial products, to help us kill off those pathogen

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9
Q

What is the most common type of granulocyte?

A

Neutrophils (50 - 70%), also known as “segs”; MATURE WBCs

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10
Q

What are “bands”?

A

Another type of neutrophil; horseshoe shape; IMMATURE neutrophils released into circulation during an acute infection

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11
Q

Range of “bands”

A

0-5%; could be greater if the acute infection is severe enough

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12
Q

What are the ranges of the eosinophil and basophils?

A

Eosinophils (2-4%)

Basophils (<2%)

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13
Q

What are eosinophils and basophils involved in?

A

Allergic reactions; they don’t respond to bacterial or viral infections

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14
Q

Characteristics of agranulocytes

A

contains no granules; mononuclear (one nucleus)

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15
Q

What are the two types of agranulocytes and their ranges?

A

Lymphocytes (30-40%) and Monocytes (4-8%)

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16
Q

what is the job of neutrophils?

A

they respond to bacterial infections through phagocytosis - because they have granules with anti-microbial properties

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17
Q

What stimulates neutrophil production?

A

Acute bacterial infections

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18
Q

T/F: Neutrophils have a short life span.

A

TRUE. once they engulf a pathogen, they die within 1-2 days.

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19
Q

In the presence of infection, if there is not enough neutrophils to fight infection d/t short life span, they will promote the release of ____?

A

Bands - immature neutrophils

Neutrophils stimulate the band cell production in acute bacterial infections - secondary force behind neutrophils

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20
Q

What is an increase in band cells called?

A

“a left shift”

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21
Q

What is the second line of defense in bacterial infections and foreign substances after neutrophils?

A

monocytes

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22
Q

characteristics of monocytes

A

slower to respond, but stronger than neutrophils; can transform into macrophages; assist in phagocytosis (ingest bacteria); clean up debris (help healing); longer lifespan

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23
Q

when do monocytes arrive on site?

A

3-7 days after the onset of inflammation

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24
Q

As macrophages, what do monocytes have the ability to do?

A

ingest large masses of matter and help clean up dead cells/tissue debri in order to help healing to commence

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25
Q

T/F Because they have a longer shelf life, monocytes are able to stay in places that need healing for weeks.

A

TRUE

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26
Q

what are the two different types of lymphocytes and which type of immunity are each?

A

B cells (humoral immunity) and T cells (cell mediated immunity)

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27
Q

what is the job of B cells?

A

humoral production and secretion of antibody bodies, specific to antigen; prevent the spread of infection; memory cells - remember our antigens and when they encounter again it remembers and sends specific antibodies to attach and destroy the antigen

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28
Q

what is the job of T cells?

A

recognize and attack foreign substances - upon recognition of something that doesn’t belong, they release

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29
Q

what do T cells release upon recognition of something that doesn’t belong?

A

they release large amounts of cytokines - cell signaling molecules - “cell to cell communication for immune response” - raise alarm to kill foreign organisms

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30
Q

Cytokines named _____ promote inflammatory response

A

Interleukins

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31
Q

What type of infections can lymphocytes fight against?

A

chronic bacterial infections and acute viral infections

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32
Q

C Reactive Protein is present with what?

A

produced by the liver in response to 0

tissue injury and acute inflammation (runny nose, feeling sick) - in the absence of inflammation, our levels are 0%

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33
Q

When does C Reactive Protein appear and when is the peak??

A

6 - 10 hr after inflammatory response; peak is 48 - 72 hours

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34
Q

Can C Reactive Protein tell us what kind of inflammation or infection?

A

No. It is a non-specific inflammatory marker; it tells us when there is an inflammatory response present.

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35
Q

T/F: CRP has also been used as a diagnostic for cardiac disease.

A

TRUE. CRP has been used to evaluate the risk for cardiac disease or cardiac event. plague formation causes inflammation.

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36
Q

what is a culture and sensitivity diagnostic test?

A

Culture: identifies the bacteria/pathogen that is making us sick
Sensitivity: identifies what antibiotic/treatment is gong to work on it (antibiotic sensitivity)

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37
Q

When would we want to identify the pathogen ideally?

A

We would want to identify the pathogen first, prior to antibiotic therapy

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38
Q

What would be the second best ideally?

A

to collect the specimen even before we started antibiotic therapy - if obtained after therapy has started, might harbor false positive results.

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39
Q

what types of specimens can be collected for C+S?

A

urine, blood, sputum, stool, wounds

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40
Q

how long does it take to identify the pathogen?

A

2 - 3 days

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41
Q

How does the lab test which antibiotics the pathogen is susceptible to?

A

the pathogen is exposed to antibiotic discs on an agar plate

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42
Q

what does the zone of inhibition indicate on a culture plate?

A

It means that the pathogen is susceptible to the antibiotic - that it will kill the pathogen - the wider the diameter, the more susceptible the antibiotic

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43
Q

What are the 3 different results?

A

susceptible, intermediate, resistant

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44
Q

what does intermediate mean?

A

it means it may work but it will require a higher dose in order for the antibiotic to be effective

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45
Q

C+S will also show a MIC. What is a MIC?

A

minimal inhibitory concentration - lowest concentration of drug that will inhibit the growth of the organism. lower MIC = lower dose; ideal; more effective and less cost to the patient

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46
Q

what is urinalysis used to diagnose?

A

UTI, kidney function, and metabolic diseases like diabetes

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47
Q

what are the characteristics of urine that indicate infection?

A

clarity, odor, nitrite, and leukocyte esterase

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48
Q

How does infection affect “clarity”?

A

infection causes urine to be cloudy, indicating presence bacteria or pus; if collected, quickly take it to lab → if sits, it will become cloudy.

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49
Q

how does infection affect “odor”?

A

bacteria causes an ammonia-like odor. a sweet syrup odor may indicate congenital metabolic disorder.

50
Q

how does infection alter “nitrite” results?

A

Nitrite is used to test for bacteriuria. Increased presence of nitrite forming bacteria yields an abnormal, positive result.

51
Q

how does infection alter “leukocyte esterase” results?

A

enzyme present in neutrophils; indicates an infection. leukocytes are increased in bacterial infection, calculus formation, fungal/parasitic infection, glomerulonephritis, interstitial nephritis, or tumor.

52
Q

If any of these tests come back abnormal or there is RBCs in the urine, what occurs?

A

a microscopic urine culture. we want to find out what kind of bacteria is in the urine.

53
Q

T/F: in the ER, they dip their own urine in order to identify it. If + for nitrite, leukocyte esterase, or RBC, it will be sent to the lab. They will also dip it for protein/glucose for DKA.

A

TRUE

54
Q

what is gram staining used for?

A

it is used to categorize the bacteria that is potentially growing; in the lab, they will stain it.

55
Q

what is gram positive bacteria?

A

they have a thick cell wall peptidoglycan layer; retains purple color; ex: staphlococcus, streptococcus, enterococcus

56
Q

what is gram negative bacteria?

A

they have a THINNER, complex peptidoglycan layer; doesn’t retain purple, has a reddish, pink tone; structure of this bacteria’s cell wall makes it HARDER to treat; drugs → harder time penetrating through capsule

57
Q

what are the 3 anti-infective principles?

A

empiric, definitive, and prophylactic

58
Q

what is empiric therapy?

A

*aka broad spectrum therapy; is given when pathogen is unknown; when we’re not sure if its gram +/- or anaerobic (GI, Vaginal, cavity)

59
Q

why do we give empiric therapy?

A

in an emergency, we don’t want our patient to die; prevent patient from getting more sick; can have more adverse effects ***IMPORTANT TO GET A SPECIMEN BEFORE START OF THERAPY TO ID PATHOGEN

60
Q

once we find out the C+S results, what is it important that we do and why?

A

It’s important to start the patient on a narrow spectrum (definitive) antibiotic that is for sure susceptible to the drug. It reduces cost, resistance of antibiotics, and toxicity d/t adverse effects.

61
Q

what is definitive therapy?

A

narrow spectrum agent once pathogen has been ID’d

62
Q

what is prophylactic therapy?

A

preventative therapy against possible pathogens; narrow spectrum (tissue infection, bone infection) given when infective organism likely to occur in the OR before first incision and surgeries longer than 3 hrs (2nd dose) ex q8hrs for 3 doses

63
Q

what are the 4 mechanisms that anti-infective fight bacteria?

A

cell wall synthesis interference, disruption of metabolic reactions, interference of nucleic acid replication, and protein synthesis interference.

64
Q

how does cell wall interference work? which drugs use this mechanism?

A

antibiotic will interfere with the creation of the cell wall; it doesn’t allow it to form or become mature and contents leak out; drugs include beta lactams, vancomycin

65
Q

how does disruption of metabolic reactions work? which drug uses this mechanism?

A

disruption of metabolic process inside the bacteria - example is folate synthesis, needed for protein synthesis (NA, DNA, amino acids); drug includes sulfonamides

66
Q

how does interference of nucleic acid replication occur? which drugs use this mechanism?

A

DNA/RNA inhibition - prevents the replication process of pathogen; drugs include quinolones and Rifampin; Rifampin - tx of TB

67
Q

how does protein synthesis interference work? what drugs use this mechanism?

A

affects/interrupts process of RNA transfer, changes the shape of ribosome (protein builders), and interferes with pathogen’s ability to be effective; drugs include macrolides, tetracycline, and aminoglycosides

68
Q

what is the structure of beta lactams?

A

beta-lactam RING structure

69
Q

what do beta-lactams do?

A

inhibit the peptidoglycan cell wall; ability to stop construction of antigen cell wall, doesn’t allow it to become effective

70
Q

which two drugs fall into the beta-lactams category?

A

penicillin and cephalosporins → bactericidal

71
Q

d/t antibiotic resistance, bacteria can now secrete an enzyme called __________ which ______________

A

beta-lactamase; hydrolyzes the B-lactam ring in penicillins and celphalosporins → inhibits the anti-infective qualities of the drug

72
Q

d/t resistance, beta-lactamase inhibitors were created. what are the 3 beta lactamase inhibitors? type of penicillin + a B-L inhibitor

A

amoxicillin + clavulanic acid (Augmentin), piperacillin + tazobactuam (Zosen), and ampicillin + sulbactam (Unicem)

73
Q

three characteristics of penicillin

A

bactericidal;
narrow-spectrum against GRAM + (streptococcal and staphylococcal infections);
can be given prophylactically

74
Q

what are the indications of penicillin?

A

pneumonia, gonorrhea, and syphilis strains

75
Q

what are the adverse effects of penicillin?

A

CAUTION in patients with hypersensitivity to cephalosporins (same beta lactam ring structure)

76
Q

should we know what type of reaction the patient had to a penicillin?

A

YES; if it was severe, like anaphylaxis - dont give

if it was a small rash, etc, we could give and watch for effects.

77
Q

What is the drug to drug interaction of penicillin

A

may ↓ effectiveness of oral contraceptives.

78
Q

how many generations of celphalosporins are there?

A

5 generations

79
Q

Celphalosporins have a cross-sensitivity with _____. What does this mean?

A

Penicillin. This means that it is not recommended for patients with a history of penicillin anaphylaxis. `

80
Q

3 characteristics of celphalosporins

A

bactericidal; broad spectrum coverage including gram +/- AND anaerobic; perioperative prophylaxis (3 doses after surgery)

81
Q

T/F: level of gram negative coverage increases with each successive generation.

A

TRUE

82
Q

which generation is effective against MRSA?

A

the 5th generation

83
Q

what are the adverse effects of cephalosporins?

A

Steven-Johnson syndrome, C. Diff associated diarrhea.

84
Q

what is the sulfonamides combination drug?

A

trimethoprim/sulfamethoxazole

85
Q

what spectrum drug is it and what is it’s mechanism? (sulfonamide)

A

it is a broad spectrum drug (gram+/-) and it works by inhibiting folic acid synthesis within the antigen

86
Q

what is the sulfamethoxazole part of the combo drug?

A

a bacteriostatic - stops growth → immune system can take over

87
Q

what is the trimethoprim part of the combo drug?

A

bactericidal - kills the pathogen

88
Q

what are the indications of sulfonamides (trimethoprim/sulfamethoxazole)?

A

UTI prophylaxis, UTI, bronchitis, otitis media

89
Q

when is trimethoprim/sulfamethoxazole contraindicated?

A

pt with megaloblastic anemia because it inhibits folic acid synthesis; contraindicated in pregnancy

90
Q

what are the adverse effects of trimethoprim/sulfamethoxazole?

A

S-J syndrome, crystaluria (crystals in urine) → drink lots of water ( 1L -1.5L /day)

91
Q

what are the drug to drug interactions of trimethoprim/sulfamethoxazole?

A

may ↑ hypoglycemic and anticoagulant effects, hyperkalemia with concurrent K+ sparing drugs, like spironolactone

92
Q

what are the 3 characteristics of tetracycline?

A

broad spectrum (gram +/-) including anaerobic, bacterostatic - stops growth; inhibits protein synthesis prevents the addition of amino acids

93
Q

what are the indications of tetracycline?

A

gonorrhea and syphilis treatment for PCN allergic pts; prevent chronic bronchitis exacerbations; acne

94
Q

what are the adverse effects of tetracycline?

A

SJ syndrome; photosensitivity - more susceptible to sunburns

95
Q

what are the drug-food-drug interactions of tetracycline?

A

dairy, calcium products, and iron supplements reduce absorption by 50% or more; recommended to wait 1-2 hrs b/t to take drug.

96
Q

what are the two macrolides?

A

erythromycin and azithromycin

97
Q

what are the indications of erythromycin?

A

resp. infections, skin/skin structure infections, pertussis, syphilis or gonorrhea (hypersensitivity to PCN)

98
Q

how does erythromycin work?

A

inhibits bacterial protein synthesis; works against strept/staph strains like penicillin

99
Q

what are the 2 characteristics of azithromycin?

A

longer half life; short duration of therapy (3-5 days); compared to 10 day tx

100
Q

what are the indications of azithromycin?

A

lower and upper respiratory infections like bronchitis and pneumonia

101
Q

what is the name of the older generation fluroquinolones?

A

ciprofloxacin (gram - pathogens)

102
Q

what are the names of the two newer generation fluroquinolones?

A

levofloxacin and moxifloxacin (gram + pathogens)

103
Q

what are the indications of fluroquinolones?

A

UTI, gynecologic infections, respiratory tract infections, skin/skin structure infections, bone/joint infections
- can be given to pt with hypersensitivity to penicillin and cephalosporins

104
Q

what is the name of the aminoglycoside drug?

A

gentamicin

105
Q

what principle does gentamicin fall into? (spectrum)

A

narrow spectrum reserved for serious systemic infections for patients allergic to penicillin

106
Q

what are characteristics of vancomycin?

A

bactericidal; mechanism - disrupt bact. cell wall; active against gram + pathogens; seen for MRSA and septicemia

107
Q

IV form is given for: _____? what happens if it infiltrates?

A

septicemia and MRSA - can cause necrosis and extravasation if infiltrates

108
Q

What is PO Vancomycin used for?

A

Clostridium difficile - goes to GI tract unlike IV

109
Q

what are adverse effects of vancomycin only?

A

red-man syndrome and hypotension if IV quickly infused

110
Q

what are the adverse effects of both vancomycin and gentamicin?

A

assess kidney function (renal pt, CKF pt doses ↓) 90% excreted by kidneys (except PO vancomycin - stool) - can cause toxicity;

can cause nephrotoxicity (assess BUN, Creatinine, I+O, GFR; urine pink/cloudy, foster hydration and kidney function) or ototoxicity (hearing loss, ringing ears, can be irreversible00000000000000000000000000)

**if any pain caused by IV, a new IV should be started - midline = ↓ risk of necrosis

111
Q

Red man syndrome is a result of what ?

A

massive histamine release when vancomycin given too fast - benedryl as tx

112
Q

what is a trough?

A

our way of monitoring how well kidneys are clearing the drug (renal clearance); it is lowest concentration of the drug in the blood stream.

113
Q

what are 3 ways to prevent infections?

A

immunizations, hygiene care of catheters, and hand hygiene

114
Q

what are 3 ways to identify and treat infection?

A

culturing organisms, limiting use of broad spectrum agents, and patient teaching (finish antibiotics, dont share, dont save for later)

115
Q

what are 3 ways to prevent nosocomial infections?

A

hand hygiene, PPE practices (isolation) and prevention of recurrent infections

116
Q

when should a trough be taken and why?

A

prior to administering the next dose because it lets us know renal clearance and how therapeutic the drug is (assures therapeutic levels between doses)

117
Q

what occurs when the trough level is low?

A

↑ in dose and/or dosing frequency

118
Q

what occurs when the trough level is high?

A

↓ in dosage or hold dose until next trough

119
Q

what are the “ok” trough levels for gentamicin?

A

trough NTE 2 mcg/ml

120
Q

what are the “ok” trough levels for vancomycin?

A

trough NTE 10 mcg/ml mild to moderate infection

sever infections: 15 - 20 mcg/ml