fever and SIRS/sepsis II Flashcards
1
Q
fever (pyrexia or febrile response)
A
- temp rising above the normal (97.9-98.6)
- 104-105 dangerous –> CNS damage
- 101 F (38.3 C) defined as fever**
- variation depending on where you check it
2
Q
diurnal variation
A
- variation of 1 degree F between 6a.m.-6pm
- lowest temp at 6 am
3
Q
ovulation cycle
A
-1 degree F lower before ovulation, 1 degree F increase after ovulation until menses
4
Q
chills and sweats
A
-shiver/chills when the temp is rising, sweats when the temp is falling
5
Q
temp control
A
- controlled by prep-optic region of anterior hypothalamus (also the dorsomedial part)***
- a pyrogen (prostaglandin E2) can act on hypothalamus –> systemic response*
- TNF-a, IL-1,6, IFN-g –> cross blood-brain barrier to reach hypothalamus*
- afferent impulses from PNS also transmit signals from tissues to hypothalamus to regulate temp.*
6
Q
Diencephalic fits/seizures (“central fevers”)**
A
- usually after brain injury or hemorrhagic stroke
- have fevers, tachycardia, tachypnea, autonomic dysfunction –> don’t regulate temp well
- hyperthermia in hot room, hypo in cold room
7
Q
heat stroke (aka sun stroke)**
A
- produce way more heat than your body can dissipate*
- beta blocker or alcoholics are risk factors*
- temp >104F –> CNS problems, lack of sweating
- treat: physical cooling, IV
8
Q
malignant hyperthermia**
A
- autosomal dominant (genetic)**
- exposed to succinylcholine or anesthetic gas***
- high fevers, metabolic acidosis, tachycardia, muscle rigidity (from high Ca2+) –> Hyperkalemia and rhabdomyolysis**
- treat: dantrolene (inhibits Ca2+ release from SR)***
9
Q
malignant neuroleptic syndrome**
A
- neuroleptic meds depress the nervous system
- rxn to neuroleptic anti-psychotic or anti-nausea meds* (life-threatening)
- fever, altered mental status, muscle rigidity/tremors, sweating, hyporeflexia
- treat: dantrolene, bromocriptine, diazepam***
- haloperidol** most commonly leads to syndrome
- takes days to occur
10
Q
serotonin syndrome**
A
- use of 2 or more serotonergic meds** –> excess serotonin on CNS
- SSRIs are common
- hyperthermic, tachycardia, shiver/sweat, dilate pupils, myoclonus, hyperreflexia*
- treat: benzodiazepines, cyproheptadine
- risk factors: linezolid + SSRI*** –> febrile
- occurs quickly
11
Q
drug fever**
A
- meds that can cause fevers and dissipate after discontinuation
- don’t look toxic (septic), but have a high fever***
- caused by antimicrobials or anticonvulsants
12
Q
lipopolysaccharide (LPS)**
A
- lipid A endotoxin
- pro-inflammatory cytokine**
- gram neg bacteria (and others) –> release LPS –> release of other cytokines (IL-1,TNFa) –> fever***
other cell walls that cause fever with pro-inflammatory cytokines: peptidoglycan and lipoteichoic acid (Gram-positive organisms) mannan in fungi, lipoarabinomannan in mycobacteria.
13
Q
pulse-temp. dissociation (Faget’s sign)**
A
- high fever, but low pulse rate (opposite)**
- pulse should increase by 10 with each 1 temp raise
- seen in SALMONELLA infections**
- also in Legionnaires, mycoplasma, Psittacosis**
14
Q
fever with night sweats**
A
- sever night sweats
- also seen in liver and lung abscesses
- due to TB and lymphoma**
15
Q
noninfectious causes of fever*
A
- usually in ICU patients
- seen in autoimmune, neoplasms (lymphoma, hypernephroma*, anything metastatic to the liver), gout, stroke, MI
16
Q
fever patterns
A
- intermittent: temp rises, falls back to normal each day –> bactermia, lymphoma
- remittent: temp rises and falls back down each day (but above normal) –> endocarditis**, ricketssia
- continuous/sustained: 0.5F change in 24 hr. period (temp rises but doesn’t come down) –> pneumonia, meningitis**
- relapsing: fever for few days, returns to normal, fever again days later –> relapsing fever, malaria, Hodgkin’s lymphoma (pel-ebstein fevers)***
- hectic fevers: big temp deviation with chills/sweats –> abscesses and pyogenic infections
- quotidian: once every 24 hr. (falciparum malaria)
- double quotidian: 2 spikes daily (endocarditis)
- tertian**: 1 spike every 24 hr (ovale and vivax)
- quartan**: 1 spike every 72 hr (malariae)
17
Q
fever suppression
A
- NSAIDs and many others
- do to be comfortable, decrease morbidity (risk of high HR, CHF, arrhythmia, stroke, angina)
- studies show that suppressing fever in someone with sepsis increase mortality/morbidity rate*
- stillwell treats it only when it rises above 103F or if associated with other morbidities*
18
Q
the host response**
A
- innate immune system –> recognized PAMPs and DAMPs with their PRRs**
- PAMP examples: LPS on gram neg rods, lipoteichoic acid and peptidoglycan** on gram +, flagellin on flagella, *lipoarabinomannan in AFB/mycobacterial cell walls, *mannan in the wall of fungi**, *unique bacterial and viral nucleic acids.
- PRR examples: toll like receptors (1-3)**, also NOD and RIG1
- DAMPs (aka alarmins): released during an inflammatory rxn due to cell injury
19
Q
binding of PRRs
A
- binding of PRR to DAMPs and PAMPs release cytokines/chemokines (ex. TNFa, IL-1)** –> inflammatory response
- neutrophils also activated and recruited to site of injury*
20
Q
normal/abnormal responses to infection - duality of man***
A
- mixture of pro-inflammatory (TNF-a, IL-1 to recruit neutrophils/Macs)** and anti-inflammatory mediators/cytokines released when invaded by pathogen**
- anti-inflammatories released for balance and to keep body from destroying itself
- IL-6, 10 have both pro and anti-inflammatory functions
21
Q
when does sepsis and septic shock occur?**
A
- when the pro-inflammatory overruns the anti-inflammatory mediators leading to dysregulation (lose balance)**
- septic shock when all regulation is lost
22
Q
body’s response to sepsis
A
- kill bacterial cell wall and mediators released - get worse before getting better
- cytokines cause problems - TNFa can lead to septic shock (anti-TNFa antibodies prevent lethal effects of LPS)
- compliment activated - recruit more inflammatory cells and opsonize pathogens
- microcirculatory lesions from activating coagulation and fibrinolysis systems –> ischemia and multi organ failure
- pro-inflammatory mediators damage mitochondria
