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20 Cards in this Set

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Cardiovascular and Lymphatic System anatomy review
-Blood vessels transport blood bi-directionally. Spleen contains high concentrations of WBC that filter microbes from blood.
-Lymph vessels transport lymph AWAY from extremities. Lymph nodes contain high concentrations of WBC that filter microbs from lymph.
Cardio Defenses
Rich in lymphocytes and phagocytes.
5,000-10,000 per ml of blood
No normal microbiota reside here.
Lymphatic Defenses
All types of WBC reside here.
No normal microbiota reside here.
Presence of microbes in the blood (terminology)
-Bactermia
-Fungemia
-Viremia
Septicemia (terminology)
When bacteria/fungi flourish and grow in bloodstream.
-strong immune reaction
-causes drop in blood pressure and organ failures (septic shock
Endocarditis (terminology)
Inflammation of the endocardium.
Microbes that cause endocarditis (ACUTE/SUBACUTE)
-Acute: Staph. aureus, Strep. pyogenes (Gram+ cocci)
-Subacute: Strep. oralis, Strep. mutans (Gram+cocci) OFTEN ORAL BACTERIAL
What is acute endocarditis?
Bacterial infection of normal/healthy heart valves
-bacteria usually introduced via trauma or surgery
-if untreated, almost always fatal.
Acute Endocarditis Pathogenesis (Same as subacute)
-Bacteria form biofilms on heart valves, which interfere with valve functions.
-Biofilms form emboli.
-Covered with host fibrin/platelets.
Acute endocarditis
Diagnosis: blood culture and biochemical test
Transmission: via injury/trauma/incisions
Prevention: prophylactic antibiotics prior to surgery, clean hospital.
Treatment: IV antibiotics
-long treatment required because biofilms are less susceptible to drugs.
Signs/symptoms: critically ill (fever, anemia, abnormal heartbeat, shortnes of breath, chest pain) and petechiae
What is more detrimental? Acute or Subacute endocarditis?
Acute. Subacute is less pathogenic.
What is subacute endocarditis?
Bacterial infection of DAMAGED heart valves (most often occurs in elderly or people with heart disease)
-bacteria are less pathogenic than those that cause acute endo.
-disease is fatal is left untreated.
Subacute Endocarditis
Signs/symptoms; same as acute. take longer to develop.
Pathogenesis: same as acute.
Diagnosis: blood culture
Transmission: via dental procedures, vigorous brushing.
Prevention: good oral hygiene* avoid gingivitis.
-antibiotics before procedure
Treatment: IV antibiotics (similar to acute)
Septicemia
-Microbes are actively multiplying in bloodstream (fatal if untreated)
-Virulence factors: cell wall or membrane components
-Treatment: broad spectrum antibiotics first, then specific antibiotics once culture results obtained.
Lyme Disease
Transmitted by deer ticks. (apparent red rash ring)
Virulence factors: antigen shifting, adhesins.
Treatment: lengthy treatment with tetracycline or cephalosporins.
Mononucleosis: Signs/symptoms
(arise 30-50 days post exposure)
-severe sore throat with white exudate on tonsils.
-high fever, cervical lymphadenitis
-fatigue that can last for weeks+
-leukocytosis
-enlarged spleen
Monoculeosis: Pathogenesis
-EBV invades oropharynx epithelial cells, replicates and lyses cells.
-Virus infects B-cells and spreads to spleen.
-Causes B-cell proliferation into plasma cells. Plasma cells produce lots of antibodies, but antibodies are not specific for EBV. (heterophile antibodies reach with proteins of other species)
-Virus becomes latent in B-cells)
Mononucleosis
Potential sequelae: Hodgkins lymphoma (cancer of lymph nodes)
Diagnosis: monospot test- agglutination reaction that detects heterophile antibodies.
Transmission: person-to-person via saliva
Prevention:hygiene, common sense.
Mononucleosis: Virulence factors and Treatment
Virulence factors: latency, ability to incorporate into host DNA.
Treatment: supportive, treat symptoms of fever and sore throat. bedrest.
HIV/AIDS
Virulence factors: attachment, syncytia formation, reverse transcriptase, high mutation rate.
Treatment- HAART (reverse transcriptase inhibitors plus protease inhibitors), fuzeon, nonnucleoside RT inhibitors.

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