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Hematology > Sepsis, Hemorrhagic Fever, and EBV > Flashcards

Sepsis, Hemorrhagic Fever, and EBV Flashcards

1
Q

Define SIRS (systemic inflammatory response syndrome)

A
  • clinical response arising from a nonspecific insult manifested by 2 or more of the following:
  • temperature outside range of 98.6-100.4
  • HR>90 beats/min
  • respirations>20/min
  • WBC count > 12,000 or 10%bands (young neutrophils)
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2
Q

Define infection.

A
  • Organisms found in normally sterile sites
  • inflammatory response to microorganisms
  • invasion of normally sterile tissues
  • bacteremia: cultivatable bacteria in the blood stream
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3
Q

Define sepsis.

A

SIRS plus infection

-systemic response to infection

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4
Q

Define hypotension.

A

-systolic blood pressure 40mmHg from baseline

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5
Q

Define Severe Sepsis.

A

Sepsis with:
-dysfunction of organ(s) distant from site of infection
-hypotension
-hypoperfusion
May include lactic acidosis, oliguria (decreased output of urine), altered mental status, acute lung injury

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6
Q

Define septic shock.

A

Sepsis plus hypotension despite fluid resuscitation

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7
Q

What is the pathophysiology of shock?

A

cellular level: oxygen demand greater than supply

  1. Initial stage: hypoperfusion–>hypoxia
    - lactic acidosis
  2. Compensatory “cold shock”
    - hyperventilation (decrease CO2)
    - vasoconstriction
    - low urine output
  3. Progressive “warm shock”
    - compensatory mechanisms fail
    - leakage of protein and fluid into tissues
    - ischemia of organs
  4. Refractory
    - organ failure
    - shock can’t be reversed
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8
Q

What are the causes of shock?

A
  1. Hypovolemic shock
    - dehydration or blood loss
    - most common cause
  2. cardiac shock
    - MI
    - cardiomyopathy
  3. Obstructive shock
    - pulmonary embolism, aortic stenosis, tension pneumothorax, cardiac tamponade
  4. Distributive shock
    - septic, anaphylactic, neurogenic
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9
Q

What causes sepsis?

A
  • triggered by infection
  • used to be mainly gram neg bacteria, but now gram positive make up at least >30% of bacterial infections that cause sepsis
  • Gram positive: teichoic acid, lipoteichoic acid, peptidoglycan
  • Gram neg: lipopolysaccharide (LPS)
  • viral: viral dsRNA
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10
Q

Describe the pathological host response to infection.

A

-microcirculatory and mitochondrial dysfunction
-activation or injury of vascular epithelium
-pro-inflammatory cytokines: TNF, Il-1
-complement activation: repression of anticoag and fibrinolysis
+activation of coagulation cascade–>coagulopathy
-immunosuppression
-shunting of blood flow and micro thrombosis–> disordered blood flow–>organ failure

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11
Q

What are the clinical manifestations of sepsis?

A

-systemic: fevers and chills
-hemodynamic: tachycardia, hypotension
Organ system dysfunction
-clotting system: endothelial damage, microvascular thrombosis, DIC
-heart: depressed myocardial contractility (decreased cardiac output), tachycardia (increased cardiac output)
-lung: capillary endothelial damage–> fluid leaking into interstitium and alveoli, inadequate air exchange, ARDS
-acute renal failure
-liver: jaundice
-hemorrhagic necrosis from ischemia
-CNS: confusion, delirium, stupor, coma

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12
Q

What are the therapeutic approaches to sepsis?

A
  • Goal-Directed therapy
  • Achieve adequate oxygenation: nasal O2 or intubation
  • achieve adequate blood pressure and end organ perfusion: fluid resuscitation and vasoactive agents
  • transfusion therapy for anemia
  • rapid eradication of microbes: IND, effective antimicrobial agents,
  • corticosteroids in low doses
  • modulation of harmful inflammatory response
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13
Q

Describe the features of classical FUO (fever of unknown origin).

A
  • fever >101 F (38.3 C) on several occasions
  • duration of fever >3 weeks
  • no diagnosis after 1 week after intensive and intelligent investigation or after 2 outpatient visits or 3 days in the hospital
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14
Q

What are the etiologies or classic FUO?

A

In the order of most common to least common

  • infections
  • neoplasms
  • CT disease
  • Misc
  • undiagnosed
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15
Q

What are infectious causes of classic FUO?

A
  • abscess: classic hiding place in retroperitoneal area
  • endocarditis
  • granulomatous disease: disseminated Tb, hitoplasmosis, coccidioidomycosis, blastomycosis
  • viral infections: CMV, EBV, HIV, parvo, Hep
  • Zoonoses: brucellosis, leptospirosis, lyme
  • typhoid fever
  • malaria
  • leshmaniasis
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16
Q

What are the diagnostic possibilities in the investigation of classic FUO?

A

-History
-physical exam
-Lab studies
CBC with differential
ESR/CRP
Liver panel
Urinalysis and culture
Blood cultures (at least 3)
Chest X-ray
PPD
-Non-invasive Studies
CT scan of abdomen/pelvis, chest
Labeled WBC scan (Indium or 99mTc)
Gallium scan (particularly effective in imaging chronic infections)
Venous duplex imaging of lower extremities
-Specialized studies
Serologic tests: Salmonella, Brucella, rickettsia. Lyme, RPR
Antigen detection: Cryptococcus
Malaria smears
O&P
Rheumatologic panels
-Invasive procedures
Biopsies (average of 2.8 to 4.6 biopsies per case)
Liver, lymph node, temporal artery
Exploratory laporotomy (rare today)
Lumbar puncture

17
Q

What is the prognosis of FUO?

A
  • 8% remain undiagnosed

- most of cases resolve spontaneously without sequelae

18
Q

Define viral hemorrhagic fever.

A
  • Severe multisystem syndrome
  • Overall vascular system is damaged, and self-regulation is impaired
  • Accompanied by hemorrhage
  • Some types can cause relatively mild illnesses, but many cause severe, life-threatening disease
19
Q

What is the mechanism behind viral hemorrhagic fever?

A

-Capillary leak
-Bleeding diathesis
DIC
Hepatic damage
Consumptive coagulopathy
Primary marrow dysfunction
-Hemodynamic compromise leading to shock

20
Q

What are the causes of viral hemorrhagic fever?

A
  • all enveloped RNA viruses
  • geographically restricted
  • humans not natural reservoir for any of these viruses: infected when they come into contact with infected host
  • human cases or outbreaks occur sporadically and irregularly
21
Q

What is the clinical presentation of viral hemorrhagic fever?

A
  • fever and bleeding diathesis (predisposition)
  • symptoms: marked fever, malaise, myalgias, exhaustion, headache, dizziness, vomiting, and diarrhea
  • physical exam: flushing of face and chest, edema, petechiae, frank bleeding, hypotension and shock
  • severe cases: signs of bleeding under skin, in internal organs, body orifices
  • shock
  • nervous system malfunction, coma, delirium, seizures
  • some types of VHF are associated with renal failure
22
Q

Describe Yellow fever.

A

Yellow fever:

  • In Africa and South America
  • transmitted by mosquitos, replicates in lymph nodes, have widespread petechial hemorrhages and bleeding (liver damage–>decrease clotting factors, intravascular coat, thrombocytopenia, endothelial damage), hepatocellular damage (jaundice)
23
Q

What are some specific organisms/diseases that cause viral hemorrhagic fever?

A
  • flaviviridae: dengue, yellow fever
  • Arenaviridae: lassa fever
  • filoviridae: ebola, marburg
  • bunyaviradae: hantavirus
24
Q

Describe Lassa Fever.

A
  • West Africa
  • Mastomys species complex
  • rodent to human transmission
  • secondary human to human transmission with potential for nosocomial outbreaks with high fatality
  • pathogenesis: endothelial cell damage/capillary leak, platelet dysfunction, suppressed cardiac fxn, cytokines other mediators of shock and inflammation
  • clinical: gradual onset fever, headache, malaise. Also pharyngitis, myalgias, retrosternal pain, cough, GI. Minority have: bleeding, neck/face swelling, shock
  • deafness common sequela
  • Tx: supportive measures, ribavirin
25
Q

Describe Ebola.

A

-central africa
Transmission
-Close contact with the blood, secretions, organs or other bodily fluids of infected animals.
-Chimpanzees, gorillas, fruit bats, monkeys, forest antelope and porcupines
-Health-care workers have frequently been infected
Clinical
-incubation period 2-21 days
-sudden onset: fever, intense weakness, muscle pain, headache, sore throat
-vomiting, diarrhea, rash, impaired kidney and liver function
Tx:
-supportive care
-strict airborne and contact precautions

26
Q

Describe the properties of Epstein-Bar Virus.

A
  • belongs to gamma herpes virus subfamily
  • Linear dsDNA
  • protein core, icosohedral nucleocapsid
  • enveloped
  • Viral genome forms circular episomes that reside in host nucleus, doesn’t integrate into DNA
27
Q

Understand the epidemiology of EBV infection

A

90-95% of adults have EBV Abs

  • 50% of population in US has seroconversion before age 5
  • humans only reservoir
  • in oropharyngeal secretions of asymptomatic people
  • not very contagious, need large viral load to transmit
28
Q

Understand the pathophysiology of EBV infection

A
  • Primary infection from exposure to oral secretions of seropositive individuals: kissing, food sharing, anything that shares oral secretions
  • Infects B cells and nasopharyngeal epithelial cells
  • EBV receptor: C3d gp=CD21=CR2
  • Infected B cells cause cytotoxic T cell response
  • most cleared but quiescently infected B cells remain as life long reservoir
  • Latent infection: no viral production, viral DNA is present, gene products convert B lymphocytes into immortalized lymphoblastic cells capable of continuous growth
  • First genes expressed:EBNA1, 2, 3A, 3B, 3C, LP, EBNA2 essential for transformation of B lymphocyte
  • latent: LMP1 dominant transforming gene in latent infection
29
Q

Describe the symptoms of acute EBV infection

A

children: asymptomatic, FUO
teens and adults: 30-50% chance of infectious mononucleosis (IM) with acute infection
clinical presentation of IM:
-incubation 4-6 weeks
-self limited disease
-Triad: fever, lymphadenopathy, pharyngitis
Also: heptaosplenomegaly (week 2 of illness)
-periorbital edema, jaundice, rash less common

30
Q

Discuss the chronic conditions associated with EBV infection

A
  • symptoms up to 4 months

- may progress to lymphoproliferative diseases, lymphoma

31
Q

How does the host immune system respond to EBV infection?

A

-challenge for immune system: up to 20% of B cells in circulation express EBNA
-Cell mediated response: CD8 and CD4 CTLs, NK cells
-Humoral response: IgM against VCA, IgG VCA (viral capsid antigen)
-

32
Q

What are diseases associated with EBV?

A 
Infectious Mononucleosis
Chronic infectious mononucleosis
Fever of Unknown Origin (FUO)
AIDS associated: Oral hairy leukoplakia , Chronic interstitial pneumonitis (LIP)
Burkitt's lymphoma
Nasopharyngeal carcinoma
Lymphoproliferative disease: Lymphoma in the immunosuppressed, Hemophagocytic lymphohistiocytosis 
X-linked lymphoproliferative syndrome
33
Q

What is the differential diagnosis of infectious mononucleosis?

A
  • Acute EBV
  • Acute CMV
  • acute toxoplasmosis
  • Acute retroviral syndrome: HIV
34
Q

What are the laboratory findings in infectious mononucleosis?

A

Hematologic:
-lymphocytosis: >50% circulating mononuclear cells
-atypical lymphoctyes, cytotoxic T cells directed against infected B cells
Mild Hepatis
-elevated ALT/AST
-ocasional jaundice
Positive heterophile antibody test: monospot test, agglutination rxn to Ags of horse RBCs, represents nonspecific B cell activation

35
Q

What is the therapy for EBV infection?

A

Supportive care
No antivirals effective
Avoid ampicillin/amoxicillin: often causes a rash in patients with EBV/acute IM
Corticosteriods for complications

36
Q

What are serious complications of EBV infection?

A

serious complications are rare

  • splenic rupture
  • meningoencephalitis
  • pharyngeal obstruction

Hematology (29 decks)

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