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
2
Q
Why is it hard to kill viruses (5)
A
- Intracelluar so evade humeral immune system
- Easily mutate
- Can disguise themselves
- Target our own immune cells for destruction
3
Q
How do prions cause diseaSe?
A
Produces progressive wasting of CNS
Progressive non inflammatory neuron degeneration causing ataxia, dementia, and death
4
Q
Bacteria infectious agents (6)
Specific family groups
A
- Mycoplasma
- Spirochetes
- Chlamydiae
- Rickettsiae
- Mycobacteria
- Nocardia/Actinomyces
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
6
Q
Spirochetes
A
GNR, motile, corkscrew
Cause syphilis, GI disease, Lyme disease
7
Q
Chlamydiae
A
Obligate intracelullar
GU infection and atypical pneumonia
Treate with tetracyclines, macrolides, quinolone ABX
8
Q
Rickettsiae
A
Spread by insect vector
Cause vascular cell infection/vasculitis
9
Q
Mycobacteria
A
acid fast
Slow growing intracellular parasites of macrophages
Cause TB, MAC, leprosy
10
Q
Nocardia/actinomyces
A
Slow growing and often produce severe infection/access
Esp in patient with cell immune dysfunction
11
Q
Gram + rods
Family
A
Uncommon
Diphtheria, coryneabacteria, listeria
12
Q
Gram + cocci (4)
A
Enterococcus
Streptococci
Staph Epidermidis
Staph aureus
13
Q
Gram -
General
A
Cell walls with lipopolysaccaraide
Strongly induces cytokines
Therefore likely to cause DIC, septic shock
14
Q
How do anaerobes cause infection?
A
- Contamination of usually sterile sites with heave load of anaerobes
- Infection of tissues with poor vascular supply and low tissue oxygen concentration (diabetic ulcers, pressure sores)
15
Q
Clues to the presence of anaerobes
A
- Very could odor
- Presence of gas
- Mixed GN and GP
16
Q
Common fungal pathogens (6)
A
- Candida
- Histoplasmosis
- Coccidiomycosis
- Cryptococcus
- Aspergillus
- Pneumocystis jiroveci
17
Q
Immune systems primary role
A
Distinguish between self and non self
Eliminate foreign substances or cells
Specific and non specific
18
Q
Non specific defense (5)
A
- Mucociliary clearance
- Skin epithelium (tight junctions)
- Phagocytic cells (PMNs, eosinophils)
- TLRs
- Complement
19
Q
phagocytic cells in innate immunity
A
polymorphoneuclear leukocytes (PMNs/neutrophils)
eosinophils
20
Q
toll like receptors
A
family of evolutionary conserved membrane receptors
recognize different components of microbes
part of the innate immune system
21
Q
complement function
A
innate immune complex (Ag and Ab) or by microbial surface protein
enhances opsonization, phagocytosis and lysis of the invader
22
Q
complement cascade activation causes (4)
A
- deposition of complement on microbe surface – easier for phagocytic cells to see
- induces local inflammation and leaky capillaries
- drills pores in microbial surface = lysis
- recruits WBC
23
Q
what is the innate humoral response ?
A
complement cascade
24
Q
innate cellular immune responses cells (3 classes)
A
- monocytes/macrophages
- Granulocytes
- Lymphocytes
25
macrophages role in innate immunity
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
26
granulocytes of innate immunity (3)
1. PMN cells/neutrophils
2. eosinophils (parasites, allergies)
3. basophils (hypersensitivity)
27
PMN
cellular innate immunity
actively phagocytic (non specific)
release cytoplasmic granules w/proteolytic enzymes
28
lymphocytes of innate immunity
natural killer cells
29
NK cells
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
30
lymphocytes of the adaptive immunity, secretion
B and T lymphocytes
secrete cytokines (IL, TN - activators of inflammation and immune response)
31
b lymphocytes mature?
in bone marrow
32
t lymphocytes mature?
in the thymus
33
finishing school for immature B and T cells
bone marrow and thymus
only the ones who appropriately mature are allowed to leave (recognize self from non self)
34
B lymphocytes function
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)
35
t lymphocyte function
Ag receptor that recognize protein Ags on MHC
if identified, they seek out and kill invader or cells infected by pathogen
(cellular immunity)
36
five types of immunoglobulins
```
IgG
IgM
IgE
IgD
IgA
```
37
function of Igs
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
38
IgG
smaller Ab
remains elevated for long time (takes a while to proliferate)
principal Ab in response to many infection
39
IgM
large Ab
elevates quickly in acute infection, initial exposure
40
IgE
concentrations are increased in allergic individuals
41
IgA
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
42
IgD
found on cell membrane of B lymphocytes
| present in minute quantities of blood
43
two types of t lymphocytes
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
helper T cells
help B lymphocytes produce antibodies and help phagocytic cells
lyse invested bacteria
45
cytotoxic T cells
kill or lyse intracellular microbes they specifically recognize
46
following invasion... (6 steps)
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
Peripheral lymphoid tissues
spread where we will encounter Ags
spleen, lymph nodes, tonsils, appendix, MALT
48
Lymph node function
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
filtration of blood stream occurs?
spleen
50
which lymphoid tissue provides first look
MALT, appendix, tonsils
51
newborns get immunity via
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
what about premies immunity?
they do not get the transfer, more susceptible
aslo true for mothers with chronic disease
53
4 types of anaphylactic reactions (4)
1. anaphylactic
2. cytotoxic
3. immune complex
4. delayed hypersensitivity
54
anaphylactic hypersensitivity reaction
severe and immediate inflammation mediator release from mast cells and basophils to a normally harmless Ag
55
anaphylaxis
generalized, severe IgE mediated reaction
fall in blood pressure, severe respiratory distress
Type I
56
cytotoxic hypersensitivity reaction
Abs bind to cell or tissue antigens
results in complement-mediated lysis of the cells or other membrane damage
Type II
57
immune complex hypersensitivity reaction
Abs combine with Ags and then they are deposited in tissues
they then activated the tissue which causes localized tissue damage
Type III
58
delayed hypersensitivity reaction
T lymphocytes (sensitized and activated on second contact)
they then induce inflammation and activated macrophages
59
which medications do we use to suppress drugs
cytotoxic drugs
anti metabolic drugs
corticosteroids
immune globulins
60
cytotoxic drugs
suppress growth of lymphocytes
heavy immunosuppression
61
anti metabolic drugs
inhibit cell metabolism and proliferation
moderate suppression
62
corticosteroids
suppress immune response, phagocytosis, Ab formation, and lymphocyte proliferation
light suppression
63
immunodeficient means this immune response
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
non specific response to agent that causes cell injury
inflammation
65
characteristic signs of inflammation
1. calor (heat)
2. dolor (pain)
3. rubor (redness)
4. tumor (swelling)
66
local effects of inflammation
capillary dilatation (increased Bf, warmth, red)
increased capillary permeability (swelling0
attraction of leukocytes
67
acute inflammatory process
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
cytokines
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
SIRS
a repost by the body to insult
can cause dysfunction, worsen organ function and causing mulitisystem failure
70
criteria for SIRS
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
significant reduction of systemic tissue production
Shock
results in decreased tissue oxygen delivery
72
shock causes (oxygen, general)
prolonged oxygen deprivation leads to cellular and systemic derangements
initially reversible, but quickly irreversible
73
four categories of shock
1. distributive (low pipe pressure)
2. cardiogenic (central pump failure)
3. hypovolemic (nothing in line)
4. obstructive (clog)
74
cariogenic shock cause
caused by heart problems (heart attack or failure)
75
hypovolemic shock cause
low blood volume
i.e. heavy bleeding, dehydration (n/v/d)
76
vasodilatory shock cause
changes in blood vessels
i.e. sepsis, anaphylaxis
77
obstructive shock caus
PE
78
pre shock stage
warm/compensated shock
increased RR, HR and BP
attempt to vasoconstrictor and compensate for diminished tissue perfusion
**sweating
79
shock stage
compensatory mechanisms are overwhelmed and organ dysfunction appears
tachycardia, dyspnea, restlessness, diaphoresis, metabolic acidosis, oliguria, cool clammy skin
80
End stage shock
end organ dysfunction = irreversible damage and death
urine output declines (anuria, acute organ failure)
acidemia decreases cardiac output
agitation, obtundation, coma
81
mc cause of ICU death
septic shock
82
pathogenies of sepsis
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
S/s of sepsis
increased HR, RR
decreased urine output
alter mental status
BP initially rises then drops
84
cardiopulmonary manifestations fo sepsis (3)
CV function is sub-optimal
vasodilator and BP falls, leading to end organ hypoperfusion
ARDS (increased fluid, soggy membrane)
85
hematologic manifestations of sepsis (5)
leukocytosis (left shift)
leukopenia (alcoholics/elderly)
thrombocytopenia
coagulopathy
can develop DIC
86
additional sepsis manifestations
renal dysfunction
GI bleeding
hypoglycemia
87
general steps in treating patient
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
sepsis empiric ABX if pseudomonas is NOT concern
Vanco +
1. cephalosporin (ceftriaxone, cefotaxime)
2. Beta-lactam inhibitor (pip-tazo, amp-sulbac)
3. Carbapenem
89
sepsis empiric ABX if pseudomonas is concern
vancomycin + 2:
1. anti-pseudo cephalosporin
2. anti-pseudo carbapenem
3. anti-pseudo beta lactam
4. fluoroquinolone
5. amino glycoside
6. monobactam
90
pathogens most likely on:
skin
staph, strep
91
pathogens most likely on:
DM ulcers
staph/strep
gram negatives, anaerobes
92
pathogens most likely on:
burns
staph, strep, pseudomonas
93
pathogens most likely on:
urine
E. coli, klebsiella
| enteric gram -
94
pathogens most likely on:
Lungs/CAP
strep pneumo
| klebsiella
95
pathogens most likely on:
lungs/atypical pneumo
legionella, mycoplasma, kelbsiella
96
pathogens most likely on:
lungs: HAP/VAP
pseudomonas other gram - (atypical)
97
pathogens most likely on:
lines
gram positive (strep/staph)
98
pathogens most likely on:
heart
strep/staph
NO ANAEROBES
99
pathogens most likely on:
abdomen
anaerobes, gram -
100
pressors used in shock
levophed (vasoconstriction, distributive/vasodilation)
dobutamine (cardiogenic, heart squeezes harder)
vasopressin (additional, 2nd line)
101
febrile neutropenia
ANC level
< 1500
typical s/s of infection that doesn't coincide with low neutrophil level
102
febrile neutropenia
high risk for which pathogens
bacterial nd fungal
commonly in skin, perirectal, and genital mucosa
103
febrile neutropenia work up (5)
1. blood cultures
2. urinalysis w/culture sensitivity
3. wound/catheter discharge culture
4. Sputum
5. Stool check for C. diff
104
febrile neutropenia treatment (5)
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
