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
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2
Q

diurnal variation

A
  • variation of 1 degree F between 6a.m.-6pm

- lowest temp at 6 am

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3
Q

ovulation cycle

A

-1 degree F lower before ovulation, 1 degree F increase after ovulation until menses

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4
Q

chills and sweats

A

-shiver/chills when the temp is rising, sweats when the temp is falling

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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.*
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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
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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
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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)***
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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
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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
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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
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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.

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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**
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14
Q

fever with night sweats**

A
  • sever night sweats
  • also seen in liver and lung abscesses
  • due to TB and lymphoma**
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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

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16
Q

fever patterns

A
  1. intermittent: temp rises, falls back to normal each day –> bactermia, lymphoma
  2. remittent: temp rises and falls back down each day (but above normal) –> endocarditis**, ricketssia
  3. continuous/sustained: 0.5F change in 24 hr. period (temp rises but doesn’t come down) –> pneumonia, meningitis**
  4. relapsing: fever for few days, returns to normal, fever again days later –> relapsing fever, malaria, Hodgkin’s lymphoma (pel-ebstein fevers)***
  5. hectic fevers: big temp deviation with chills/sweats –> abscesses and pyogenic infections
  6. quotidian: once every 24 hr. (falciparum malaria)
  7. double quotidian: 2 spikes daily (endocarditis)
  8. tertian**: 1 spike every 24 hr (ovale and vivax)
  9. 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
  1. innate immune system –> recognized PAMPs and DAMPs with their PRRs**
  2. 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.
  3. PRR examples: toll like receptors (1-3)**, also NOD and RIG1
  4. 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
  1. kill bacterial cell wall and mediators released - get worse before getting better
  2. cytokines cause problems - TNFa can lead to septic shock (anti-TNFa antibodies prevent lethal effects of LPS)
  3. compliment activated - recruit more inflammatory cells and opsonize pathogens
  4. microcirculatory lesions from activating coagulation and fibrinolysis systems –> ischemia and multi organ failure
  5. pro-inflammatory mediators damage mitochondria