1
Q
What are the 2 steps of the nursing process for infection?
A
- Assess to diagnose
2. Get pathogen-specific
2
Q
What 4 things to consider first when assessing?
A
- “where is the illness”:
- Sign and symptoms
- Portal of entry
- Immunity of the host (health history)
3
Q
LATER SNAPS
A
Location Associated signs and symptoms Timing (onset, duration, constancy) Environmental/exposure factors Relieving or alleviating factors
Severity/quantity Nature/quality Aggravating factors Perspective of client Significance to client
4
Q
What are the three lab works to do next after the assessment?
A
- Culture from source
- CBC (complete blood count)
- Antibody analysis
5
Q
What to do after the culture result is out?
A
Identify the pathogen + classify the bacteria by iodine staining
6
Q
E-coli, Klebsiella, Pseudomonas, Salmonella, Hib, Cholera, Syphillis, Gonorrhea, Nisseria M.
are examples of gram ____ bacteria
A
negative
7
Q
Staphylococci, Streptococci (Pneumococci), Enterococci, Listeria, C-dif
are examples of gram ____ bacteria
A
positive
8
Q
Empiric treatment is based on _______ bacteria
A
suspected (estimated pathogen, decision of antiinfection)
9
Q
Why is it important to treat ASAP?
A
sepsis, severe infection, exhausted host
10
Q
What are some considerations when treating infection?
A
- administration and distribution
2. patient’s complaints
11
Q
4 side effects of antibiotics
A
- GI
- superinfection
- drug to drug interaction
- allergy
12
Q
How is immunotherapy beneficial?
A
supply host with immunity
13
Q
Immunotherapy has high efficacy for ______ infection
A
viral
14
Q
Is immune globulin a biologic?
A
yes (antibiotics from donor)
15
Q
Is immune globulin passive or active immunity?
A
passive
16
Q
When should immune globulin be given?
A
shortly after exposure
17
Q
What is the most common route for immunotherapy
A
IV (IVIG) (interferon alpha-2)
18
Q
Immune globulin and cytokine are examples of
A
immunotherapy
19
Q
What is the function of cytokines?
A
immune mediators that stimulate immune system (WBC synthesis, T cell stimulation)
20
Q
Which is the main antibody found in breastmilk?
A
IgA
21
Q
igA is specialized against?
A
intestinal infection
22
Q
which is the main antibody that transfers readily from the other’s blood across the placenta?
A
igG
23
Q
elderly have minimized ________
A
thymus gland
24
Q
when does the thymus gland begin to atrophy (degenerate)
A
adolescence
25
elderly have decreased _____ and _____
WBC synthesis and specificity (B cells decreased differentiation --> autoimmune)
26
immunization is the administration of _____
antigen (dead or alive attenuated減弱的)
27
what do we want immunization to develop?
development of B cell antibodies
28
how does booster help?
increase recognition
29
what was the 1st successful immunization
smallpox virus
30
what are the 4 treatments for infections?
1. prevention: immunization, boosters
2. anti-infective therapy: antibiotic, antifungal
3. immunomodulation: IVIG, cytokines
4. surgery: removal of infected tissue
31
immune response occurs _____ to ____ and _____ to ____.
local to systemic (shock state)
| general to specific (antigen-specific response)
32
is maternal-infant a passive or active immunity
passive
33
active immunity is ______ term and passive immunity is _____ term
long term; short term
34
how does infection lead to inflammation?
the infection leads to tissue damage --> acute inflammation
35
how fast is acute inflammation after infection?
within minutes
36
What's the average maximum day for infection?
10 days
37
chronic inflammation can lead to _______ and _____
organ dysfunction and necrosis
38
why can inflammation lead to hypotension?
leakage of blood volume into tissues --> hypovolemia --> hypotension
39
what does inflammation response activate?
endothelial cells, WBC, connective tissue cells, platelet
40
septicemia means
pathogen is present in the blood
41
A systemic inflammatory response can lead to
Sepsis
42
what is sepsis
infection from any body part that causes an extreme inflammatory response
43
sepsis is ______ a medical emergency
ALWAYS (shock if untreated)
44
sepsis is pathogen in ____ or ____
blood or tissue
45
sepsis causes vaso____
dilation
46
what kind of infection causes 50% of sepsis?
respiratory infection
47
meningitis, UTIs, skin infection, abdominal infection, surgical incisions, IV line contamination can cause
sepsis
48
common pathogen for sepsis (state - or + and kind)
gram +, fungal, ANY pathogen can
49
septic shock is presence of _______ and organ _____ in a septic patient
hypotension; hypoperfusion
50
how does septic shock lead to overall ischemia (lack of o2 in blood)
hypotension --> hypoxia --> hypoxemia --> overall ischemia
51
renal failure, disseminated intravascular coagulation, hyperglycemia
are often result from
septic shock
52
distributive shock is also known as
vasodilatory shock or normovolemic shock
53
distributive shock leads to ____ response, vaso
| ____, and ____shift.
1. inflammatory response
2. vasodilation
3. fluid shift (plasma out --> swelling)
54
what are the three types of distributive shock?
1. septic (most common)
2. anaphylactic
3. neurogenic
55
best treatment against sepsis & septic shock
empiric antimicrobial therapy
56
in septic shock, mortality rises _____% per hour without antibiotics treatment
10
57
mortality in septic shock is ____%
80
58
＿＿＿＿ are pinpoint, round spots that appear on the skin as a result of bleeding.
Petechiae
59
Things to consider when doing physics assessment on skin
Rash?
When did it start?
What’s the distribution?
What does it look like?
60
What are the 8 ways to treat septic shock?
1. Antimicrobial therapy (emperical to focal)
2. Fluid resuscitation 500ml adult and 20ml/kg peds)
3. Adrenergic/ inotropes: treat hypotension MAP>60mmHg (norepi, dopamine, dobutamine)
4. O2 therapy: maintain >92% saturation
5. Source control (e.g. appendectomy)
6. Analgesia: tylenol, ibuprofen, opioids
7. Treat complication
8. Isolation
61
are all sepsis caused by bacteria?
no; 70% failure rate
62
what are the complications for sepsis/septic shock?
```
renal failure
metabolic acidosis
GI
Hyperglycemia
DIC
Fever
```
63
why there is a renal failure in sepsis/septic shock?
hypotension and organ hypoperfusion --> renal ischemia
64
In humans, the kidneys together receive roughly __% of cardiac output.
20% of cardiac output
65
how many minutes of ischemia can start to affect renal function?
15-20
66
s&s of renal failure?
oliguria 少尿 (aka. less than 0.5 mL/kg/h)
67
treatment of renal failure
1. catecholamines (dopamine): improve renal blood flow and glomerular filtration rate
2. fluid resuscitation: have enough fluid to be circulated
68
______ _____ occurs when lactic acid production exceeds lactic acid clearance, caused by impaired tissue oxygenation.
Lactic acidosis
69
s&s of metabolic acidosis
```
Kussmaul respiration (hyperventilation)
headache
decreased BP
hyperkalemia
muscle twitching
warm flushed skin (vasodilation)
N&V, diarrhea
changes in LOC
```
70
normal pH is ____ to ____
7.35 to 7.45
71
how is pH balanced?
bicarbonate and hydrogen ions (H+)
72
What happens intracellularly and to the lungs and renals when there is a failure to regulate pH?
intracellular: inflammatory reactions and cellular hypoxia increase anaerobic cellular metabolism (lactic acid as a byproduct)
lungs: increased in CO2
renal: decreased renal clearance of H+
73
_____ and _____ are byproducts made for cellular metabolism
H20 and C02
CO2 reacts with water to produce a hydrogen ion.
74
how to treat pH imbalances?
1. ABCs
2. underlying cause
3. optimize oxygenation and ventilation to decrease C02
4. check electrolytes (K can increase due to potassium shifts from cell)
5. sodium bicarbonate (BUT can lead to fluid shift)
75
What is responsible for fever in sepsis?
pyrogen and inflammation mediators in circulation (e.g. Cytokines)
stimulate hypothalamic thermoregulation
76
how does sepsis lead to hyperglycemia?
hypotension --> tissue hypoxia --> decreased cellular metabolism and transport of glucose to cells
stress situation --> release cortisol and catecholamines --> hepatic glucose production = hyperglycemia
77
how to treat hyperglycemia in sepsis
insulin IV and enteral nutrition
78
why nutrition is given enterally not parenterally to treat hyperglycemia in sepsis
parenteral causes a further fluid shift
79
how does sepsis lead to DIC?
tissue injury leads to activation of coagulation and decreased hepatic perfusion (aka. function)
80
what is the function of the liver with regards to coagulation
produce plasmin for clot lysis and form coagulation factors
81
how to treat DIC in sepsis?
1. anticoagulants to inhibit thrombin (heparin, LMWH)
| 2. blood products (whole blood, platelets, vitamin K for clotting factors)
82
why is there a risk of bleeding in sepsis?
widespread coagulation --> depletion of platelets and clotting factors --> risk of bleeding
83
treatment of GI in sepsis
1. nasogastric feeding
2. PPI and H2 receptor antagonist
3. antiemetics
84
s&s of GI ischemia
N&V
abdominal pain
bowel necrosis
acute hemorrhage (2-10 days post)
85
how does meningitis progress to shock?
meningitis --> meningcoccemia --> septic shock
86
s&s of meningitis
NON SPECIFIC PRODROME
| - headache, joint pain, vomiting, cough, sore throat
87
s&s of meningeal bacteremia
rash (50% common) and seizure
88
s&s of septic shock
cool extremities
hypotension
tachycardia
89
GI ischemia will lead to ______________________, which increases GI acidity.
SNS activated mucosal vasoconstriction
NURS216B
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