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FA17 Infectious Disease > Infection, SIRS, Sepsis > Flashcards

Infection, SIRS, Sepsis Flashcards

1
Q

How do viruses cause infection?

A

Invade host cells and take over their cellular machinery

Lyse host cells, remained latent incorporated into genome, oncogenic change

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2
Q

Why is it hard to kill viruses (5)

A
  1. Intracelluar so evade humeral immune system
  2. Easily mutate
  3. Can disguise themselves
  4. Target our own immune cells for destruction
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3
Q

How do prions cause diseaSe?

A

Produces progressive wasting of CNS

Progressive non inflammatory neuron degeneration causing ataxia, dementia, and death

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4
Q

Bacteria infectious agents (6)

Specific family groups

A
  1. Mycoplasma
  2. Spirochetes
  3. Chlamydiae
  4. Rickettsiae
  5. Mycobacteria
  6. Nocardia/Actinomyces
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5
Q

Mycoplasma

A

No cell wall, cause disease w/o invasion

Common cause of GU disease, atypical pneumonia

Sensitive to e-mycin, tetracycline, quinolone

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6
Q

Spirochetes

A

GNR, motile, corkscrew

Cause syphilis, GI disease, Lyme disease

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7
Q

Chlamydiae

A

Obligate intracelullar

GU infection and atypical pneumonia

Treate with tetracyclines, macrolides, quinolone ABX

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8
Q

Rickettsiae

A

Spread by insect vector

Cause vascular cell infection/vasculitis

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9
Q

Mycobacteria

A

acid fast

Slow growing intracellular parasites of macrophages

Cause TB, MAC, leprosy

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10
Q

Nocardia/actinomyces

A

Slow growing and often produce severe infection/access

Esp in patient with cell immune dysfunction

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11
Q

Gram + rods

Family

A

Uncommon

Diphtheria, coryneabacteria, listeria

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12
Q

Gram + cocci (4)

A

Enterococcus
Streptococci
Staph Epidermidis
Staph aureus

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13
Q

Gram -

General

A

Cell walls with lipopolysaccaraide

Strongly induces cytokines

Therefore likely to cause DIC, septic shock

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14
Q

How do anaerobes cause infection?

A
  1. Contamination of usually sterile sites with heave load of anaerobes
  2. Infection of tissues with poor vascular supply and low tissue oxygen concentration (diabetic ulcers, pressure sores)
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15
Q

Clues to the presence of anaerobes

A
  1. Very could odor
  2. Presence of gas
  3. Mixed GN and GP
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16
Q

Common fungal pathogens (6)

A
  1. Candida
  2. Histoplasmosis
  3. Coccidiomycosis
  4. Cryptococcus
  5. Aspergillus
  6. Pneumocystis jiroveci
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17
Q

Immune systems primary role

A

Distinguish between self and non self

Eliminate foreign substances or cells

Specific and non specific

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18
Q

Non specific defense (5)

A
  1. Mucociliary clearance
  2. Skin epithelium (tight junctions)
  3. Phagocytic cells (PMNs, eosinophils)
  4. TLRs
  5. Complement
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19
Q

phagocytic cells in innate immunity

A

polymorphoneuclear leukocytes (PMNs/neutrophils)

eosinophils

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20
Q

toll like receptors

A

family of evolutionary conserved membrane receptors

recognize different components of microbes

part of the innate immune system

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21
Q

complement function

A

innate immune complex (Ag and Ab) or by microbial surface protein

enhances opsonization, phagocytosis and lysis of the invader

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22
Q

complement cascade activation causes (4)

A
  1. deposition of complement on microbe surface – easier for phagocytic cells to see
  2. induces local inflammation and leaky capillaries
  3. drills pores in microbial surface = lysis
  4. recruits WBC
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23
Q

what is the innate humoral response ?

A

complement cascade

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24
Q

innate cellular immune responses cells (3 classes)

A
  1. monocytes/macrophages
  2. Granulocytes
  3. Lymphocytes
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25
Q

macrophages role in innate immunity

A
  1. phagocytosis and presentation of ingested Ags to T and B cells
  2. secretion of proteolytic enzymes, oxygen radicals, and cytokines (further inflammation)
  3. cellular debris clean up
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26
Q

granulocytes of innate immunity (3)

A
  1. PMN cells/neutrophils
  2. eosinophils (parasites, allergies)
  3. basophils (hypersensitivity)
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27
Q

PMN

A

cellular innate immunity

actively phagocytic (non specific)

release cytoplasmic granules w/proteolytic enzymes

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28
Q

lymphocytes of innate immunity

A

natural killer cells

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29
Q

NK cells

A

recruited to inflammatory sites to destroy cells identified by Abs

defend against VIRAL pathogen

ability to recognize and kill tumor cells, abnormal cells and cells infected with intracellular pathogens

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30
Q

lymphocytes of the adaptive immunity, secretion

A

B and T lymphocytes

secrete cytokines (IL, TN - activators of inflammation and immune response)

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31
Q

b lymphocytes mature?

A

in bone marrow

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32
Q

t lymphocytes mature?

A

in the thymus

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33
Q

finishing school for immature B and T cells

A

bone marrow and thymus

only the ones who appropriately mature are allowed to leave (recognize self from non self)

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34
Q

B lymphocytes function

A

circulate body

hoping to run into Ag invader that they recognize

after recognition of Ag causes cell proliferation and ramps up Ig production (humoral immunity)

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35
Q

t lymphocyte function

A

Ag receptor that recognize protein Ags on MHC

if identified, they seek out and kill invader or cells infected by pathogen

(cellular immunity)

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36
Q

five types of immunoglobulins

A 
IgG
IgM
IgE
IgD
IgA
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37
Q

function of Igs

A
  1. recognition of and binding to microbe to inactivate it
  2. binding to microbe and facilitating phagocytosis
  3. recognition of foreign proteins on a body cell surface then killing body cell
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38
Q

IgG

A

smaller Ab

remains elevated for long time (takes a while to proliferate)

principal Ab in response to many infection

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39
Q

IgM

A

large Ab

elevates quickly in acute infection, initial exposure

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40
Q

IgE

A

concentrations are increased in allergic individuals

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41
Q

IgA

A

produced by Ab forming cells in respiratory GI mucosa

combines harmful injected or inhaled Ags – therefore they can’t be absorbed and body is not sensitized to them

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42
Q

IgD

A

found on cell membrane of B lymphocytes

present in minute quantities of blood

43
Q

two types of t lymphocytes

A

CD4
CD8

Helper T cells and Cytotoxic T cells

recognize foreign antigens on body cell surface and kill body’s cells that have been invaded thru apoptosis

44
Q

helper T cells

A

help B lymphocytes produce antibodies and help phagocytic cells

lyse invested bacteria

45
Q

cytotoxic T cells

A

kill or lyse intracellular microbes they specifically recognize

46
Q

following invasion… (6 steps)

A
  1. recognition and processing of Ag, presentation by macrophages and dendritic cells
  2. proliferation of B cells (takes one week)
  3. destruction of Ag by responding to lymphocytes
  4. Some Ags retain memory and are saved
  5. Memory is passed on
  6. later contact with same Ag provokes stronger and faster reaction
47
Q

Peripheral lymphoid tissues

A

spread where we will encounter Ags

spleen, lymph nodes, tonsils, appendix, MALT

48
Q

Lymph node function

A

lymph enters node via afferent channel, carrying Ags from tissues, sampled and removed by T cells

T cells present Ags to the B cells after phagocytosis, B cells pump out Abs into efferent lymph flow

49
Q

filtration of blood stream occurs?

A

spleen

50
Q

which lymphoid tissue provides first look

A

MALT, appendix, tonsils

51
Q

newborns get immunity via

A

maternal Abs transmitted across the placenta

stored in fetal tissue remain functional in first months of life

also get colostrum and breast milk (IgA)

52
Q

what about premies immunity?

A

they do not get the transfer, more susceptible

aslo true for mothers with chronic disease

53
Q

4 types of anaphylactic reactions (4)

A
  1. anaphylactic
  2. cytotoxic
  3. immune complex
  4. delayed hypersensitivity
54
Q

anaphylactic hypersensitivity reaction

A

severe and immediate inflammation mediator release from mast cells and basophils to a normally harmless Ag

55
Q

anaphylaxis

A

generalized, severe IgE mediated reaction

fall in blood pressure, severe respiratory distress

Type I

56
Q

cytotoxic hypersensitivity reaction

A

Abs bind to cell or tissue antigens

results in complement-mediated lysis of the cells or other membrane damage

Type II

57
Q

immune complex hypersensitivity reaction

A

Abs combine with Ags and then they are deposited in tissues

they then activated the tissue which causes localized tissue damage

Type III

58
Q

delayed hypersensitivity reaction

A

T lymphocytes (sensitized and activated on second contact)

they then induce inflammation and activated macrophages

59
Q

which medications do we use to suppress drugs

A

cytotoxic drugs
anti metabolic drugs
corticosteroids
immune globulins

60
Q

cytotoxic drugs

A

suppress growth of lymphocytes

heavy immunosuppression

61
Q

anti metabolic drugs

A

inhibit cell metabolism and proliferation

moderate suppression

62
Q

corticosteroids

A

suppress immune response, phagocytosis, Ab formation, and lymphocyte proliferation

light suppression

63
Q

immunodeficient means this immune response

A
  1. defects in humoral immunity (increased infection from encapsulated organisms)
  2. Decreases in neutrophil number/function (bacterial and fungal infection)
  3. Defects in T cell immunity (pathogens that replicate within host cells)
64
Q

non specific response to agent that causes cell injury

A

inflammation

65
Q

characteristic signs of inflammation

A
  1. calor (heat)
  2. dolor (pain)
  3. rubor (redness)
  4. tumor (swelling)
66
Q

local effects of inflammation

A

capillary dilatation (increased Bf, warmth, red)

increased capillary permeability (swelling0

attraction of leukocytes

67
Q

acute inflammatory process

A

mediators release causing systemic effects (fever, ill)

bone marrow accelerates production of leukocytes

liver produces acute phase reactants

pus formation (exudate)

release of proteolytic enzymes causing tissue destruction (worsening inflammation)

68
Q

cytokines

A

regularly proteins hat are essential to immune response

secreted in short births to activate or inhibit actions of local cells of immune system, can cause systemic response

69
Q

SIRS

A

a repost by the body to insult

can cause dysfunction, worsen organ function and causing mulitisystem failure

70
Q

criteria for SIRS

A
  1. heart rate >90 bpm
  2. Tachypnea > 20 breaths/min, pCO2 32mmHG
  3. Temp >100.4 or < 96.8
  4. WBC >12,000 or <4,000 or 10%+ bands
71
Q

significant reduction of systemic tissue production

A

Shock

results in decreased tissue oxygen delivery

72
Q

shock causes (oxygen, general)

A

prolonged oxygen deprivation leads to cellular and systemic derangements

initially reversible, but quickly irreversible

73
Q

four categories of shock

A
  1. distributive (low pipe pressure)
  2. cardiogenic (central pump failure)
  3. hypovolemic (nothing in line)
  4. obstructive (clog)
74
Q

cariogenic shock cause

A

caused by heart problems (heart attack or failure)

75
Q

hypovolemic shock cause

A

low blood volume

i.e. heavy bleeding, dehydration (n/v/d)

76
Q

vasodilatory shock cause

A

changes in blood vessels

i.e. sepsis, anaphylaxis

77
Q

obstructive shock caus

A

PE

78
Q

pre shock stage

A

warm/compensated shock

increased RR, HR and BP

attempt to vasoconstrictor and compensate for diminished tissue perfusion

**sweating

79
Q

shock stage

A

compensatory mechanisms are overwhelmed and organ dysfunction appears

tachycardia, dyspnea, restlessness, diaphoresis, metabolic acidosis, oliguria, cool clammy skin

80
Q

End stage shock

A

end organ dysfunction = irreversible damage and death

urine output declines (anuria, acute organ failure)

acidemia decreases cardiac output

agitation, obtundation, coma

81
Q

mc cause of ICU death

A

septic shock

82
Q

pathogenies of sepsis

A

endotoxin (GN) or cell wall product (GP) induces pro-inflammatory cytokines (IL-1 and TNF-a)

damage the endothelium and make it leaky

activates coagulation pathways leading to widespread micro thrombi, tissue ischemia and depletion of natural anticoagulants

83
Q

S/s of sepsis

A

increased HR, RR

decreased urine output

alter mental status

BP initially rises then drops

84
Q

cardiopulmonary manifestations fo sepsis (3)

A

CV function is sub-optimal

vasodilator and BP falls, leading to end organ hypoperfusion

ARDS (increased fluid, soggy membrane)

85
Q

hematologic manifestations of sepsis (5)

A

leukocytosis (left shift)

leukopenia (alcoholics/elderly)

thrombocytopenia

coagulopathy

can develop DIC

86
Q

additional sepsis manifestations

A

renal dysfunction
GI bleeding
hypoglycemia

87
Q

general steps in treating patient

A
  1. choose appropriate empiric antimicrobial
  2. IV fluids (1-2L/10 min)
  3. Low BP - pressor, if BP raises - more fluid

also check for other causes

88
Q

sepsis empiric ABX if pseudomonas is NOT concern

A

Vanco +

  1. cephalosporin (ceftriaxone, cefotaxime)
  2. Beta-lactam inhibitor (pip-tazo, amp-sulbac)
  3. Carbapenem
89
Q

sepsis empiric ABX if pseudomonas is concern

A

vancomycin + 2:

  1. anti-pseudo cephalosporin
  2. anti-pseudo carbapenem
  3. anti-pseudo beta lactam
  4. fluoroquinolone
  5. amino glycoside
  6. monobactam
90
Q

pathogens most likely on:

skin

A

staph, strep

91
Q

pathogens most likely on:

DM ulcers

A

staph/strep

gram negatives, anaerobes

92
Q

pathogens most likely on:

burns

A

staph, strep, pseudomonas

93
Q

pathogens most likely on:

urine

A

E. coli, klebsiella

enteric gram -

94
Q

pathogens most likely on:

Lungs/CAP

A

strep pneumo

klebsiella

95
Q

pathogens most likely on:

lungs/atypical pneumo

A

legionella, mycoplasma, kelbsiella

96
Q

pathogens most likely on:

lungs: HAP/VAP

A

pseudomonas other gram - (atypical)

97
Q

pathogens most likely on:

lines

A

gram positive (strep/staph)

98
Q

pathogens most likely on:

heart

A

strep/staph

NO ANAEROBES

99
Q

pathogens most likely on:

abdomen

A

anaerobes, gram -

100
Q

pressors used in shock

A

levophed (vasoconstriction, distributive/vasodilation)

dobutamine (cardiogenic, heart squeezes harder)

vasopressin (additional, 2nd line)

101
Q

febrile neutropenia

ANC level

A

< 1500

typical s/s of infection that doesn’t coincide with low neutrophil level

102
Q

febrile neutropenia

high risk for which pathogens

A

bacterial nd fungal

commonly in skin, perirectal, and genital mucosa

103
Q

febrile neutropenia work up (5)

A
  1. blood cultures
  2. urinalysis w/culture sensitivity
  3. wound/catheter discharge culture
  4. Sputum
  5. Stool check for C. diff
104
Q

febrile neutropenia treatment (5)

A
  1. general care (skin, oral care, avoid rectal interaction)
  2. neutropenic precaution
  3. broad spectrum abx
  4. failure to improve 4-5 days, add anti fungal
  5. GSF giving

FA17 Infectious Disease (9 decks)

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