Patho Exam Deuce

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Patho Exam Deuce
2013-08-01 21:06:00
Patho exam

Patho exam 2
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  1. 2 objectives of all living organisms
    survival and reproduction
  2. What vitamin do Microflora produce and why?
    Vit. K to prevent colonization of other microbes
  3. Prions
    • have no dna/rna
    • don't illicit an immune response
    • lack metabolic and reproduction functions is what antibodies attack
    • not even radiation, chemo, etc., can kill them
    • create abnormal proteins
    • affect the CNS
  4. virus
    • single celled
    • cannot reproduce w/o host
    • have no metabolic enzymes of their own

    viral replication is NOT cell division
  5. bacteria
    • single celled
    • live in colonies
    • produce endo and exo toxins
  6. endotoxin
    part of bacteria cell wall which causes immune rxn
  7. exotoxin
    proteins made and released by the bacteria to damage or kill host cells
  8. spriochetes


    rickettsiae and chlamydiea
    S= spiral shaped anaerobes

    M= lack cell walls, commensals

    R & C= have to live inside cells to metabolize or reproduce
  9. 2 infectious pathways
    direct and indirect contact
  10. direct contact with infectious agent

    types of contact
    ingestion, inhalation, penetration

    • zoonosis = animals
    • nosocomial infection
    • fomite = doorknobs
  11. 5 stages of infection
    • 1. incubation
    • 2. prodromal
    • 3. acute
    • 4. convalescent
    • 5. resolution
  12. incubation stage
    active replication w/o symptoms
  13. prodromal stage
    generalized symptoms
  14. acute stage
    • specific symptoms
    • max impact of the infection
  15. convalescent stage
    • getting over the "hump"
    • feelng better
  16. ending "-emia"
    presence of bacteria in the blood (with symptoms)
  17. lectins
    ligands that bind to carbs to bind to sources of energy
  18. hemagglutinins
    part of infectious agents (especially viral), bind to Carb Receptors to enter the cell and replicate
  19. virulence factor
    likelihood that they can cause disease
  20. 4 virulence factors
    • toxins
    • adhesion factors
    • evasive factors
    • invasive factors
  21. 2 adhesion factors 
    lectins and hemagglutinins
  22. 3 evasive factors

    Alpha Toxin
    • encapsulation
    • leukocidin C= causes membrane damage to host cell, but does not lyse it
    • coagulase= release prothrombim which increases clotting

    Alpha= can cause septic shock
  23. 2 invasive factors
    • production of enzymes
    • penetrate host membranes and tissue
  24. 2 diagnositics
    • culture
    • serology= measure antibody titers
  25. antibody IgG
    important b/c it can pass through the placenta
  26. 4 ways that antibiotics kill bacteria
    • target:
    • cell wall synthesis
    • protein synthesis
    • nucleic acid synthesis
    • bacterial metabolism
  27. 4 ways that bacteria fight back (in relation to antibiotics)
    • inactivating antibiotics
    • changing antibiotic binding sites
    • using different metabolic pathways
    • mutate cell wall to keep antibiotic out
  28. Target Site of antibacterial agents:

    cell wall
  29. Target Site of antibacterial agents:

  30. Target Site of antibacterial agents:


    S= folic acid synthesis

    Q= DNA synthesis
  31. 3 reasons for antibiotic resistant organisms
    • mutation and conjugation
    • inappropriate use
    • incomplete treatment
  32. 3 ways antivirals kill
    • block viral RNA or DNA synthesis
    • block viral binding to cells
    • block production of protein coats (capsids) of new viruses
  33. **Immune systems consists of...**

    • WBC
    • cell mediators
    • lymphatic system
  34. **antigen
    molecule that stimulates an immune response
  35. Innate immunity
    • born with it
    • does NOT distinguish between
  36. 3 mechanisms of the complement immunity
    • Opsonization= flag it
    • Chemotaxis= chem signal to attract cells
    • Membrane attack complex= lyse the cell
  37. Adaptive/Acquired Immunity

    2 types of:
    specific cell attacks specific antigen

    • Humoral
    • Cell-mediated
  38. humoral immunity

    cell-mediated immunity
    H= B-cell/Antibody mediated

    C= T-cell mediated
  39. What is the trigger for B and T-cell activation?
    recognition of the antigen on the surface receptors of the APC
  40. Lymphatic system is all over the body.

    List 8 highlighted ones:
    • thymus
    • intestine
    • Peyers Patches
    • appendix
    • bone marrow
    • adenoids
    • tonsils
    • spleen
  41. cytokines
    signalling compounds that are associated with both types of immunity
  42. MHC I
    • Self identifier
    • Found on Every cell
  43. MHC II
    • non-self identifier
    • APC show this to CD8 cells to be destroyed
  44. CD4 cells
    • T-helper cells
    • master regulator of the immune system

    **release cytokins to call other WBC's to the site
  45. CD8 cells
    • T-cytotoxic cells
    • kill invaders that have been "flagged"
  46. cytokines
    ***proteins and peptides used by organisms as a messenger system
  47. How are B-cells activated?
    ONLY by interaction with a CD4 T-cell
  48. 5 antibodies
    • Ig G
    • Ig A
    • Ig M
    • Ig E
    • Ig D
    • "GAMED"
  49. Ig G
    can cross the placenta
  50. Ig M
    • 1st antibody that a baby can self produce
    • 1st to respond to the initial exposure to injury
  51. Ig E
    • allergic response
    • Mast cells are part of this response

    "Iggie the allergic elephant"
  52. vaccination produce what kind of response?
    A primary response because we are introducing the actual antigen into the body
  53. B-cells do not require T-cell interaction for a secondary immune response
    B-cells do not require T-cell interaction for a secondary immune response
  54. Universal blood donor
  55. O can only receive O blood
    O can only receive O blood
  56. A bld rxn from transfusion mismatch is a cellular rxn
    A bld rxn from transfusion mismatch is a cellular rxn
  57. 1st stage on inflammtion
    Acute or Vascular stage
  58. Acute/Vascular stage
    prostagladins and leukotrienes are released to vasoconstrict arterioles and venules dilate and become more permeable to allow proteins, globulins, and liquid through

    Exudate is released followed by the proteins
  59. the acute vascular stage is intiiated by...
    ***momentary vasoconstriction, followed by vasodilation to cause localized congestion.
  60. 4 WBC in inflammation
    • Basophils (H &H)
    • Eosinophils (allergic and parasitic)
    • Neutrophils (largest # and primary phagocyte)
    • Monocytes ****(largest and longest living phagocyte)
  61. shift to the left
    more WBCs are being produced than normal

    dtermined by the # of band cells present
  62. 4 steps of leukocyte response to injury (basic)
    • 1. recognize cytokines via Chemotaxis
    • 2. attach to blood vessel wall via Margination
    • 3. squeeze out bewteen cells via Diapedisis
    • 4.follow chemotaxis to injury
  63. 5 WBC inflammatory mediators
    • Histamine and serotonin
    • platelet growth factor
    • cytokins
    • nitric oxide
    • acid metabolites
  64. bradykins (kinins)
    brochoconstrictor, increse capillary permeability

    ***also involved in pain. Release for ARTERIOLES not venules like histamines
  65. Acute-phase response (inflammation)
    • is actually System
    • comes on suddenly and doesn;t last long

    • WBC release IL and TNF
    • see fever and lethargy
  66. granulation tissue
    generation of new vessels old ones
  67. 1st intention vs. 2nd intention tissue healing
    2nd has tissue lost while 1st does not (surgical incision)
  68. hypersensitivity

    4 types:
    • excessive and/or inappropriate activation of the immune system
    • the body is damaged during the immune response

    • Type:
    • 1 Allergic/anaphylatic
    • 2 antibody mediated
    • 3 immune complex mediated
    • 4 t-cell mediated
  69. type 1 hs
    • commonly called allergic rxns
    • **very rapid, w/n minutes of exposure
    • **Ig E meditated
    • ** Mediators are released be mast cells
  70. mechanism of Type 1 hs
    • Ig E to mast cells
    • Atigen attaches to Ig E
    • Mast cells degranulate
  71. anaphylaxis
    system response to inflammatory mediateors of type 1

    give Epi to patient
  72. Type 2 hs
    • is cytotoxic rxn
    • Ig G or Ig M attack antigens on cell surface
  73. a blood transfusion mismatch is what type of rxn?
    Type 2 hypersensitivty
  74. type 3 hs
    • "serum sickness"
    • creation of insoluble antibody/antigen compounds that can adhere to small vessels

    penicillin, food, drug, and insect bite rxns when it is NOT an autoimmune disorder
  75. Type 4 hs

    delayed-type hs
    • cell mediated cytotoxicity
    • only class to be triggered by antigen specific cells

    • D= allergic contact dermatitis
    • EX: positive TB skin test
  76. transplant rejection

    3 types
    rejection is an immune response

    • Hyperacute= immediate Type 3 response
    • Acute= weeks to years
    • Chronic
  77. primary immunodeficiency
    born without an immune system
  78. more blood in veins than arteries b/c venous system is a reservoir for blood
    more blood in veins than arteries b/c venous system is a reservoir for blood
  79. what if the rate of the Right side of the heart is less that the Left side?
    blood accumulates in the Left side
  80. volume and pressure relationship in the venous system?
    P and V have an inverse relationship

    decrease P, increase V
  81. resistance to cardiac output
    peripheral OR systemic vascular resistance of ***ARTERIES not veins***
  82. cardiac output
    amount of blood pumped per minute

    CO=HR X SV
  83. larger cross-section equals?
    lower velocity
  84. turbulence causes and noted by:
    cause= increased velocity, decreased diameter, low viscosity

    noted by= thrills, murmur, bruits
  85. Laplace Law
    pressure needed to overcome wall tension increases the as radius decreases
  86. wall tension
    • is affected by wall thickness
    • wall tension increases as the wall becomes thinner and vice versa

    wall thickens in HTN
  87. regulation of cardiac performance:
    The ability to alter CO depends of what 4 factors?
    • Preload
    • Afterload
    • Contractility
    • Heart Rate
  88. how does nitro affect the capillaries?
    it inhibits platelet agranulation and vasodilates everything
  89. what is the last anatomical structure of the peripheral vascular system?
  90. where does the lymph derive from?
    interstitial fluid
  91. 3 centers for ANS control of circulation
    • Medulla Oblongata
    • Vasomotor center
    • cardioinhibitory center
  92. medulla oblongata
    this is the control center for circulation
  93. vasomotor center
    SNS: increase HR and vasonconstrict
  94. cardioinhibitory center
    PNS: decrease HR
  95. HIV transmission via...
    • sexual contact
    • breast milk
    • blood-to-blood contact
    • vaginal and c-section birth
  96. Largest growing HIV population?
    Eastern Europe and Central Asia
  97. HIV in US
    1.2 million people living with AIDS
  98. HIV in Sub-Sahara Africa
    24.7 million living with AIDS
  99. Teaching objectives in HIV/AIDS
    • 1st symptom--Flu-like
    • Keep on medication therapy, even with lots of side effects
    • Keep viral load below 500 and CD4 above 5000
  100. Drug therapy for HIV
    • HIV fusion inhibitors (blocks entry of HIV to CD4)
    • Reverse transcriptase inhibitors
    • Protease inhibitors (prevents maturation but destroys Tcells)
  101. Pulmonary artery carries...
    de-oxygenated venous blood
  102. Systemic venous flow
    • more blood in veins than arteries
    • venous system a reservoir for blood
    • works against gravity=more pressure than pulm
  103. Blood moves from..
    • high pressure to low
    • pressure inverse to volume
  104. In diastole, what happens
    • Ventricles relax
    • AV valves open
    • blood fills heart
  105. Systole, what happens
    • Ventricles contract
    • blood rushes out of semilunar to aorta/pulm arteries
  106. Coronary artery perfusion is
    • holes (orifaces) in heart that allows blood to flow into cardiac veins not arteries
    • repairable
    • sometimes congenital

    **only occurs during daistole while vent is at rest because contract with vent does
  107. Peripheral vascular resistance
    • When arterioles are not able to completely relieve pressure in arteries and resistance to cardiac output.
    • arterioles end of pvr
  108. Pressure, Resistance and flow
    • Flow depends on vessel pressure
    • width controls pressure
    • inc hematocrit=inc pressure
  109. Vascular endothelium
    • semipermeable membrane that controls molecular transport 
    • controls platelet adhesion & blood clots
    • regulates hormones which regulate heart rate
  110. Artherosclerosis
    • Lipids in arteries which create plaque
    • causes inc blood flow d/t dec diameter
  111. unstable plaque
    • thin shelled with a large fatty core and rupture easily.
    • rupture causes damage to bld vessel wall by letting the fat out=MI and CVA
  112. Intermittent claudication/exercise induced pain
    • AKA Chronic arterial insufficiency or Arterio-sclerosis in legs
    • thickening, dec elasticity and calcification of arterial walls in legs.
  113. Treatment of intermittent claudication
    • Pts MUST walk more to reroute arteries
    • pts may have diminished or absent pedal pulses
  114. Arteriosclerosis streatment
    • angiography
    • peripheral vasodilators
    • dec lipid levels by statins and diet changes
    • Aspirin or anticoagulant therapy
  115. Primary varicose veins
    congenital or unknown caused
  116. Secondary varicose veins
    D/t identifiable condition that's treatable
  117. Secondary varicose veins cause
    • Stasis dermatitis, hard to treat
    • sit>stand
    • pressure hose before feet hit the ground
  118. Chronic arterial insufficiency
    • in head=strokes/CVA
    • in heart=Heart attack
    • in legs=intermittent claudication
  119. Lowering LDL
    • Statin medications
    • diet changes such as inc fiber and omega-3, dec fat
  120. Pericardial effusion
    Abnormal fluid in pericardial cavity.  Can be bacterial, viral or other disease pathways.

    Dec Stroke Volume and Dec Cardiac Output
  121. Cardiac tamponade
    • Squeezing of heart caused by pericardial effusion.
    • Heard by change in breath strength on both insp and exsp.
  122. Consequences of Pericardial Effusion
    • Left ventricle doesn't accept enough blood-dec CO-dec BP then shock
    • Right ventricle doesn't accept enough blood-Inc VP and jugular distension
  123. Angina
    The pain of decreased O2 levels to the heart
  124. Coronary artery disease
    Atherosclerosis that blocks coronary arteries
  125. Heart problems d/t CAD
    Angina, MI, Cardiac arr(dys)hythmias, conduction deficits, heart failure d/t muscle damage and sudden death
  126. 3 types of angina
    • stable--pain w/ exercise, treatable
    • variant-occur at rest, in sleep
    • silent-no pain in chest but other symptoms, DMII causes this.
  127. When angina is reversible
    Within 30 min or less with ischemia, treat with aspirin and lifestyle changes

    After 30, not reversible d/t infarction
  128. Treatment for CAD
    • Thrombolysis---TPA
    • PTCA-percutaneous translumenal coronary angioplasty
    • PTCS with stents
    • CABG-coronary artery bypass graft
  129. Valvular Heart Disease
    • Stenosis when valves can't open all the way
    • or
    • regurgitation when they don't close
  130. Stenotic valvular heart disease
    • Valves fuse---creaky gate
    • #1 is aortic then mitral valve
    • CO decreased causing heart to work harder
    • S1 heart murmur
  131. Regurgitative valvular heart disease
    • When valves don't shut all the way
    • ejected blood flows backwards
    • caused by rheumatic heart disease
    • S2 heart murmur
  132. aortic regurgitation--diastolic murmur
    • From incompetent aortic valve
    • Left ventricle has vol overload d/t inc preload
    • hypertrophy and dilation occurs
    • need valve replacement
  133. Primary/essential hypertension
    • AKA idiopathic HTN
    • no known cause
    • treat with beta blocks, diuretic, CA channel blockers
  134. Secondary HTN
    • treat underlying disorder then hypertension
    • caused by kidney disorders, endocrine disorders, co-arcitation of aorta, phaeochromocytoma, pregnancy, estrogen and BCP's, steroids.
  135. Heart Failure
    Inability of heart to pump adequate supply of blood to meet the metabolic demands of the body
  136. Preload
    amount of blood in ventricles at the end of diastole
  137. Afterload
    Amount of force needed to eject blood into circulation
  138. Contractility
    ability of heart muscle to contract during systole
  139. Left-sided heart failure
    blood backs up into atrium then into pulm veins causing lung congestion
  140. Left-sided heart failure signs/symptoms
    • Pink frothy foamy cough
    • fatigue, oliguria, inc HR, restlessness, confusion, anxiety
  141. Right-sided heart failure
    right ventricle can't pump blood through the pulm system so it backs up in systemic circulation
  142. Right-sided heart failure signs/symptoms
    Hepatomegaly, ascites, splenomegaly, anorexia, jugular vein distension, leg edema
  143. Hypovolemic shock
    • Acute intravascular blood loss.  Usually from burns or bleeding out. 
    • Dec in bld volm, bld pressure, CO= heart attack, tissue death and death
  144. Anaphlylactic shock
    A severe type of allergic reaction that involves 2+ body systems
  145. Type I alvolar cells
    Larger and limited
  146. Type II alvolar cells
    • Smaller
    • Found at corners of Type I
    • Makes surfactant
  147. Lung surfactant
    Decreases surface tension and modulates immune function in the lungs.  Allows alvoli to open
  148. Lung Functions
    • Moves O2 to blood, removes CO2
    • Blood storage
    • Regulates vasoconstriction substances like bradykinin, angiotension II and heparin.
  149. Do the lungs make heparin?
    Yes, because the blood in our lungs are introduced to air which will lead to clots
  150. Perfusion
    • Capillary blood flow provided for gas exchange.
    • affected by position and gravity
  151. TB
    • #1 cause of death from infectious agent causing 26% of avoidable deaths
    • caused by mycobacterium tuberculosis hominis
  152. TB Infection
    Inhaled infection--macrophages present pathogen to T cells---T cells kill pathogen
  153. Ghon complex
    Nodules in lungs and lymph tissue that encapsulate Tb infection
  154. Small cell lung cancer
    • Very aggressive and fast.
    • Metastasizes very easily.
    • D/t smoking
  155. Non-small cell lung cancer
    • Large cell carcinoma
    • squamous cell
    • adenocarcinoma-most common lung CA
  156. Adenocarcinoma
    • Most common lung cancer
    • d/t smoking and 2nd hand smoke
    • most common for nonsmokers and 45 yo or younger.
  157. Respiratory Distress Syndrome
    • Neonates born before surfactant is made in lungs
    • Protein-rich fluid leaks into alveoli blocking O2 uptake
    • Tx with mechanical ventilation and synthetic surfactant
  158. Pleural Effusion
    • Fluid in the pleural cavity
    • Hydrothorax (serous fluid)
    • Empyema (hardest to treat)
    • Chylothorax (Lymph)
    • Hemothorax (blood)
  159. Pneumothorax
    Deflated lung, can be partial (open pneumothorax)
  160. Empyema
    • AKA pleural empyema, pyothorax or purulent pleuritis
    • Pus in lung cavity mostly caused by pneumonia
  161. Atelectasis
    • Incomplete expansion of lung or portion of lung.  
    • Can be an obstruction, compression, pleural effusion or lack of surfactant caused by infection or burst alveola
  162. COPD
    Chronic obstructive pulmonary disease
  163. Disease that make up COPD
    • Chronic bronchitis
    • Emphysema
    • Asthma
  164. Extrinsic asthma
    • External environment causing 
    • Type I hypersensitivity reaction
    • Mast cells mediators cause acute response within 10-20 minutes
    • Use inhaled steroids to dec allergic response
  165. Intrinsic Athma
    • Irritant causing Asthma (not allergy related)
    • Respiratory infections, exercise, hot or cold air, inhaled irritants
    • Treat with aspirin/NSAIDS and inhaled steroids
    • Hard to control
  166. Mechanisms of COPD
    • Inflammation and fibrosis of bronchial wall
    • Excess mucus which obstructs airflow
    • Dec surface area for gas exchange d/t loss of alveolar tissue
    • Loss of elastic lung fibers which causes airway collapse, obstructed exhalation and air trapping
  167. COPD
    • Recurrent obstruction of airflow accompanied by airway hyperresponsiveness
    • Partially reversible
    • Caused by smoking
  168. Emphysema
    Enlargement of airspaces distal to bronchial spaces
  169. Mechanisms of emphysema
    • Increased neutrophils d/t inhaled irritants which secrete trypsin and damage alveoli
    • Can be d/t a genetic factor
  170. Chronic bronchitis
    Sputum production on most days for three months for two years.
  171. Mechanism of chronic bronchitis
    • Chronic irritation of airways causing in increased number of mucus cells/hypersecretion
    • Productive cough
    • Hyperplasia and hypertrophy of goblet cells
  172. Pink Puffer
    • Emphysema
    • Increase in respiration to maintain o2
    • Dyspnea
    • skinny d/t increase metabolism to keep o2 in body
  173. Blue bloater
    • Chronic bronchitis
    • Cannot inc respiration enough to maintain o2
  174. Chronic bronchitis causes______ side heart failure d/t ?
    Right side d/t scaring of lungs pushing on heart
  175. Hypercapnia
    High CO2
  176. Acute Respiratory Distress Syndrome
    • Swelling of alveoli and interstitial lungs.
    • Surfactant destroy by lung inflammation and/or injury causing septic shock (pneumonia, aspiration vomit etc)
  177. Mechanisms of ARDS
    • Exudate enters alveoli blocking gas exchange making inhalation more difficult
    • Neutrophils enter alveoli releasing inflammatory mediators and release proteolytic enzymes
  178. key cells of innate immunity
    • Neutrophils
    • macrophages
    • NK cells

    all phagocytic