Dr. D.'s Overhead Lecture Notes                                Section 3 - REPLACE PAGE NUMBERS WITH PAGES FROM SIXTH EDITION3
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Cerebrovasular disease
   - most common cause of neurological disease

CNS (brain) O₂ needs
   Approx. 2% of body weight / 20% of O₂ needs
       - high and continuous O₂ demand
   - decr. O₂ supply -> immediate cell injury -> immediate neurological malfunction (reversible)
   - prolonged decr. O₂ -> cell death -> prolonged neurological deficit
       - no neuron reproduction/replacement
       - possible compensation by remaining neurons

Brain blood supply = brain O₂ supply (pp. 780, 781, 852, 853, 855)
           Cerebral arterial supply, angiogram
           8. Cerebral arterial circulation and aneurysms, diagram
   - depends most on cardiac output, not systemic BP - "me first"
   - regulated by self regulating vessels
       1. based on O₂, CO₂, pH
         decr. O₂/incr CO₂/decr. pH -> vasodilation -> ??
         incr O₂/decr. CO₂/incr pH -> vasoconstriction -> ??
       2. based on cerebral BP
         decr. cerebral BP -> vasodilation -> ??
         incr. cerebral BP -> vasoconstriction -> ??
               - protects against edema
       NOTE: opposite systemic vessels
       - assures brain function by shifting blood to or from brain

   - influenced by intracranial pressure
         Increased Intracranial Pressure = IIP
       - not a regulatory process
         incr. intracranial pressure -> vessel compression -> decr. blood flow -> ??

       - causes of IIP = incr. volume in skull (sketch)
           - edema, hemorrhage, tumor, incr.  CSF

Stroke = cerebrovascular accident = CVA
   causes - usually from atherosclerosis
           Normal coronary artery, microscopic *
           Mild coronary atherosclerosis, microscopic *
           Severe calcific coronary atherosclerosis, microscopic *
           Aorta, lipid streaks, gross
           Aorta, lipid streaks, gross
           Aortas with mild, moderate, and severe atherosclerosis, gross
           Aorta, atheromatous plaque, medium power microscopic *
           Aorta, atheromatous plaque, high power microscopic *
           Aorta, atheromatous plaque, high power microscopic *
           Aorta, atherosclerotic aneurysm, gross

   1. thrombus (p. 853) = most common cause (sketch)
       - atheroma -> thrombus -> blockage -> ischemia
           34. Internal carotid artery, thrombosis, recent, gross [ANGIO]
                    This image shows blockage of an artery to the brain.
           31. Cerebrum, coronal section, acute cerebral infarct, gross
                    This image shows infarction from ischemia.
           39. Cerebrum, acute infarction, microscopic *
                    This image shows infarction from ischemia and the development of edema from the inflammatory response.

   2. embolus - usually from atherosclerosis (sketch)
           e.g., M.I. -> thomboembolus
           e.g., carotids -> thromboembolus, plaque
      - embolus moves to brain -> blockage in brain -> ischemia
           35. Cerebral artery, thromboembolus, microscopic *
                    This image shows blockage of an artery to the brain.
           38. Cerebrum, coronal section, hemorrhagic infarct, from arterial embolus, gross
                    This image shows infarction from ischemia. There is also slight hemorrhaging from the necrotic region.
           37. Cerebrum, coronal section, hemorrhagic infarct, from arterial embolus, gross
                    This image shows infarction from ischemia followed by significant hemorrhaging in the necrotic region. Note the development of edema from the inflammatory response.
           Liquefactive necrosis, cerebral infarction, gross
                    This image and the next seven images show the liquefaction of infarcted brain regions.
           Liquefactive necrosis, cerebral infarction, gross
           Liquefactive necrosis, cerebral infarction, microscopic *
           44. Cerebrum, remote infarct, microscopic *
           Liquefactive necrosis, cerebral infarction, microscopic *
           29. Pons, lacunar infarct, gross
           30. Lacunar infarct, microscopic *
           45. Cerebrum, coronal section, remote infarct, gross
   3. hypertensive hemorrhage
       - hemorrhage -> injury from Hb and volume of blood
            - i.e., chemical and physical damage from blood
           2. Basal ganglia hemorrhage with hypertension, gross [CT]
           3. Basal ganglia hemorrhage with hypertension, gross [CT]
        - hypertensive hemorrhage usually -> more hemorrhage the ruptured aneurysm

       - effects from hypertensive hemorrhage (p. 96) (sketch)

           1. ischemia from local decr. BP
           2. spurting blood hitting neurons
           3. hematoma -> local pressure on neurons
           4. hematoma -> IIP -> pressure on all neurons
           5. Hb injures neurons (chemical damage)
           6. injury -> inflammation -> edema -> IIP -> incr. neuron injury
               47. Cerebrum, coronal section, edema, gross
                        This image and the next five images show how edema from ischemic strokes and hemorrhagic strokes can cause additional brain injury due to pressure, shifting, and herniation.
               52. Pons, Duret hemorrhages, gross
               27. Pons, Duret hemorrhages, gross
           7. IIP (hematoma, -> vessel compression -> diffuse ischemia
           8. hematoma -> brain shifting -> injury to neurons and vessels
           9. IIP -> herniation through skull openings -> injury to neurons
               49. Cerebrum, uncal herniation from edema, gross
               50. Cerebrum, uncal herniation from edema, gross
               51. Cerebellum, tonsillar herniation from edema, gross
               52. Pons, Duret hemorrhages, gross
               27. Pons, Duret hemorrhages, gross

   4. aneurysm - atherosclerosis, congenital, trauma (p. 855)
       - aneurysm -> hemorrhage -> injury from Hb and volume of blood
            - i.e., chemical and physical damage from blood
           8. Cerebral arterial circulation and aneurysms, diagram
           10. Circle of Willis with multiple berry aneurysms, gross
                    This image and the next four images show "berry" aneurysms, so names because they appear like berries attached to arteries. Aneurysms can lead to strokes by being sites of thrombus formation and by hemorrhaging.
           11. Berry aneurysm, sectioned, gross
           9. Ruptured intracranial berry aneurysm, gross
           12. Subarachnoid hemorrhage, base of brain, from ruptured berry aneurysm, gross
           13. Subarachnoid hemorrhage from ruptured berry aneurysm, gross
           18. Vascular malformation, microscopic [CT] *
                    Aneurysms like these within the brain tissues can cause hemorrhagic strokes just as berry aneurysms do.
           17. Intracerebral and intraventricular hemorrhage from ruptured vascular malformation, gross
                    Here is an example of a hemorrhaging stroke from an aneurysms within the brain.

Effects from ischemia
   ischemia -> decr. O₂/incr. CO₂/decr. pH/decr. nutrients/incr. wastes  -> cell injury/cell death -> brain malfunction
   consequences vary based on;
       1. regions affected (area of specialization)
       2. amount of injury
            a. partial versus complete ischemia
             b. rate of onset - thrombus versus embolus
            c. duration
               - vasodilation -> incr. blood flow
               - dissolving the thrombus -> incr. blood flow
        3. rate of recovery of neurons

Types of strokes based on timing
   1. TIA = transient ischemic attack
       - all S&S gone by 24 hours (may recur)
       - long term = no S&S remain (transient)
   2. RIND = residual ischemic neurological deficit
       - S&S last more than 24 hours
       - long term = some S&S improve quickly and some S&S improve slowly or not at all (residual)
       NOTE: if some S&S develop later = "progressive stroke" = "stroke in evolution"
           e.g., more emboli forming
   3. completed stroke
       - almost all S&S develop quickly
       - long term = little or no improvement in S&S

Causes of TIA, RIND, completed strokes

thrombus usually -> TIA (but may -> RIND or completed stroke)

embolus usually -> RIND (but may -> TIA or completed stroke)

aneurysm usually -> RIND (but may -> TIA or completed stroke)

hypertensive hemorrhage usually -> completed stroke (but may -> TIA or RIND)

S&S (p. 851+ but ignore specific vessels)

Reasons for different S&S
   1. regions affected
       - have different functions
   2. amount of injury in each area
       - mild to severe
   3. rate of recovery of neurons
       - fast, slow, none (reversible versus irreversible damage)

Epilepsy
   - second to CVA as CNS disorder in adults
   - definition
       - excessive
       - uncontrolled
       - synchronous
       - paroxysmal
       - local
       - discharge
       - cerebral neurons (usually in the cortex)
   - causes = other cerebral pathologies
       e.g., stroke, trauma, meningitis, alcoholism
            Epilepsy may develop as a new disease or it may develop as a complication from almost any brain pathology.
           15. Brain, parietal lobe, vascular malformation, gross [ANGIO]
           18. Vascular malformation, microscopic [CT] *
           60. Cerebrum, cysticercus cyst, microscopic *
   - petit mal = loss of consciousness
       - partial or complete
       - brief (moment to seconds)
   - grand mal = loss of consciousness + tonic spasms (tension), then clonic spasms (movement)

Multiple sclerosis (MS) = many scars/much scarring
   - cause = idiopathic
   - ?second exposure to virus? -> autoimmune response to CNS myelin
           Multiple sclerosis is an autoimmune disease characterized by intermittently progressive destruction of myelin in the CNS.
   - pathogenesis

Myasthenia gravis (pp. 869, 870) (sketch)

Brain trauma (traumatic injury)
   Normal conditions for brain (pp. 778, 780, 783, 793, 889)
       - NOTE: skull (cranium), meninges, brain, CSF, vessels, intracranial pressure
   Causes and immediate effects
       1. penetration or laceration (sketch)

Secondary effects of brain trauma
   1. hemorrhage outside brain (only physical damage from blood)
           6. Bridging veins from dura, gross
       a. epidural hematoma (pp. 887, 890) (sketch)
           - hematoma between dura mater and skull
           - usually from artery
               - rapid and high pressure bleeding
               4. Epidural hematoma, gross [CT]
       b. subdural hematoma (p. 890) (sketch)
          - hematoma between dura mater and pia mater
          - usual from vein
             - slow, gradual incr. pressure
                - acute = problems within 24-48 hours
                - subacute = problems continue 48 hours - 2 weeks
                - chronic = problems for more than 2 weeks
           5. Subdural hematoma, acute, gross [CT]
           7. Subdural hematoma, bilateral, chronic, gross [CT]
           59. Infected subdural hematoma, gross
       - effects from epidural / subdural hematoma
                (only physical damage from blood)
           - enlarging hematoma -> (sketch)
            1. local pressure on neurons ->
            2. **IIP -> pressure on all neurons ->
            3. **IIP -> vessel compression -> ischemia (p. 885) ->
            4. brain shifting -> injury to neurons and vessels ->
            5. **IIP -> brain herniation -> injury to neurons ->
                                   yields
                          neuron injury/neuron death
                                   yields
                          brain malfunction
   2. inflammation
           neuron injury/neuron death -> inflammation -> edema ->
                IIP ->
                1. neuron injury
                2. shifting
                3. vessel compression
                4. herniation

           - may include brain cell swelling (hydropic change) -> shifting and IIP -> etc.
           - limited compensation for IIP
               - CSF shifts from cranium to scalp &/or spinal cord
                     (sketch)
   3. vessel damage from trauma
           vessel damage -> reduced vessel autoregulation (chemicals, BP) ->
                                    yields
         a. inappropriate vasoconstriction -> ischemia ->
         b. inappropriate vasodilation -> hyperemia -> IIP ->
                                    yields
                   neuron injury/neuron death
                                     yields
                         brain malfunction

Causes of increased intracranial pressure (IIP)
   1. hemorrhage (inside brain or outside brain)
   2. inflammation
   3. brain cell swelling
   4. tumors
   5. excess CSF production
   6. inadequate CSF removal
           65. Cerebrum, coronal section, hydrocephalus, gross
   7. passive congestion (e.g., tumor on vein)

Damage from IIP
   1. neuron injury
   2. shifting
   3. vessel compression
   4. herniation
        47. Cerebrum, coronal section, edema, gross
        48. Cerebrum, external view, edema, gross
        49. Cerebrum, uncal herniation from edema, gross
        50. Cerebrum, uncal herniation from edema, gross
        52. Pons, Duret hemorrhages, gross
        27. Pons, Duret hemorrhages, gross
        51. Cerebellum, tonsillar herniation from edema, gross

S&S from brain trauma - like S&S from stroke
   - depends upon
       1. regions affected
       2. amount of injury
       3. rate of neuron recovery

Spinal cord trauma (traumatic injury)
   Normal conditions for spinal cord (p. 793)
       NOTE: vertebrae, adipose, meninges, cord
   Causes and immediate effects
       1. penetration or laceration
               - physical objects contact cord -> ??
       2. excessive flexion/extension/rotation
               - bending/twisting -> ??

                               yields
                  neuron injury/neuron death
                                yields
                    cord malfunction

     systemic effects
           1. decr. voluntary motor function (descending tracts)
           2. decr. conscious sensory function (ascending tracts)
           3. decr. BP from decr. sympathetic tone (descending tracts and gray matter)
           4. decr. reflexes below site of injury (descending tracts and gray matter) (sketch)
                   - decr. brain facilitation of reflexes
                   - spinal shock
           1 & 2 are often permanent
           3 & 4 are usually temporary
           - types, degree, and duration of effects depends upon (like the brain)
                  1. regions affected
                  2. amount of injury
                  3. rate of neuron recovery

CNS tumors (neoplasia)
   - "primary" from CNS connective tissue
           - neurons do not reproduce
   - "metastatic" from metastasis (e.g., lung, breast)
           141. Cerebrum, coronal section, metastasis, gross
   glioma (glioblastoma)
       - usually malignant
       - most common primary brain cancer
       - rapid & invasive -> poor prognosis (death in <1yr. from diagnosis)
           134. Brainstem, sagittal section, glioma, gross
           135. Cerebrum, coronal section, glioma, gross [MRI]
           136. Glioma, low power, microscopic  *
           133. Brainstem, external view, glioma, gross
           132. Cerebrum, coronal section, glioma with mass effect, gross [MRI]
           138. Cerebrum, coronal section, glioblastoma multiforme, gross
           140. Gliolbastoma multiforme, high power, microscopic [IPX] *
   meningioma
       - usually benign
       - usually dura mater or arachnoid
       - usually slow growing, easily removed by surgery
       112. Meningioma, parasagittal, gross
        113. Meningioma, parasagittal, gross
        114. Meningioma with cerebral compression, gross [MRI]
        115. Meningioma, sphenoid ridge, gross
            The meningioma in this image is in the upper left region. It is not in the upper right region as stated under the image.
        116. Meningioma, resected, gross
        120. Posterior fossa, sagittal section, fourth ventricle with ependymoma, gross [MRI]
        121. Cerebrum, horizontal section, fourth ventricle with ependymoma, gross
        128. Acoustic nerve schwannoma, gross [MRI]

   pathological effects possible (sketch)
    1. local pressure on neurons -> ??
    2. local pressure on vessels -> ischemia -> ??
    3. local pressure on veins -> IIP from passive congestion & blocked CSF removal -> ??
           65. Cerebrum, coronal section, hydrocephalus, gross
    4. local pressure on CSF passages -> IIP -> ??
    5. weak vessels -> hemorrhage -> ??
    6. general IIP -> ??
    7. competition for O₂ & nutrients (malignant neoplasia) -> ??
                          yields
             neuron injury/neuron death
                            yields
                  brain malfunction

   classic S&S from brain tumors
       1. headache from pressure on meninges, vessels, cranial nerves
       2. vomiting from pressure on medulla
       3. papilledema (swelling of optic disc) from IIP and passive congestion

Alzheimer's disease
     For more details, go to the tutorial on CNS degenerative diseases.
   Brain atrophy
        Alzheimer's disease, gross.
        Alzheimer's disease, gross.
        Alzheimer's disease, gross.
   Plaques
        97. Cerebrum, Alzheimer's disease, plaque, microscopic, Bielschowsky silver stain
        98. Cerebrum, Alzheimer's disease, plaque, microscopic, Bielschowsky silver stain *
        100. Cerebrum, Alzheimer's disease, plaque, microscopic, Bielschowsky silver stain *
        99. Cerebrum, Alzheimer's disease, plaque, microscopic, Congo red stain *
   Neurofibrillary tangles
        101. Cerebrum, Alzheimer's disease, tangle, microscopic, H&E stain *
        Neurofibrillary tangles, Alzheimer's disease, microscopic
        103. Cerebrum, Alzheimer's disease, tangle, microscopic, Bielschowsky silver stain *

For more images and other nervous system diseases, go to the SSU network from on-campus computers at the following URL.

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Purposes for gas exchange
1. obtain O₂  - for energy
2. eliminate CO₂   - for chemical balance and to prevent acidosis
3. regulate pH   - to remove CO₂ to incr. pH or retain CO₂ to decr. pH
        - compensates for pH changes from other sources (e.g., food, metabolism)
Note: must occur just fast enough to balance O₂ use, CO₂ production, and pH changes

Requirements for proper gas exchange
    1. proper ventilation (breathing)
        a. open airways
            - normal - open airways and spaces
                 2. Normal lung, cross section, gross
                 4. Normal lung, microscopic*
            - abnormal - filled air spaces
             5. Lung, edema, microscopic*
             17. Lung, bronchopneumonia, low power microscopic*
             115. Lung, interstitial fibrosis, microscopic*
        b. proper pressure changes
        c. proper lung compliance
            - elasticity
            - surface tension (surfactant)
    2. proper perfusion (blood flow)
        a. open vessels (p. 561)
        b. many capillaries near alveoli (p. 557)
            - normal - thin alveolar walls containing capillary networks
                 2. Normal lung, cross section, gross
                 4. Normal lung, microscopic*
            - abnormal - fibrosis replaces the capillary network in the alveolar membrane
             115. Lung, interstitial fibrosis, microscopic*
       c. proper heart function (p. 559)

    shunt unit = low ventilation/good perfusion (p. 564)
    dead space unit = low perfusion/good ventilation (p. 564)

    3. proper diffusion
        a. large surface area
        b. thin surface (respiratory membrane)
        - normal - large amount of thin surfaces
             2. Normal lung, cross section, gross
             4. Normal lung, microscopic*
        - abnormal - thick membranes and filled air spaces
             29. Lung, interstitial pneumonitis, microscopic*
             5. Lung, edema, microscopic*
             17. Lung, bronchopneumonia, low power microscopic*
             115. Lung, interstitial fibrosis, microscopic*

Major types of respiratory diseases
    1. acute infection
        9. Lung, bronchopneumonia, gross
        17. Lung, bronchopneumonia, low power microscopic*
    2. chronic respiratory disease
        a. chronic obstructive pulmonary disease (COPD)  - expiration is main problem
        b. restrictive pulmonary disease  - inspiration is main problem
    3. cancer
        80. Lung, squamous cell carcinoma, gross [XRAY]
        87. Lung, bronchioloalveolar carcinoma, microscopic*

Results from inadequate gas exchange

Hypoxemia vs tissue hypoxia

    (1) hypoxemia = low dissolved O₂ in blood = low PaO₂ = low arterial blood O₂
        PaO₂  = dissolved O₂ in arterial blood (from arterial blood gas analysis)
        - measured in mmHg (pressure)
        - depends upon proper ventilation only (not on pH, temp. or Hb)

    (2) tissue hypoxia = low O₂ supply to cells

        - most O₂ in the blood (95%) is carried bound to Hb as HbO₂
        - each Hb can bind up to four molecules of O₂ -> actually up to Hb4O₂
    (i.e., Hb, HbO₂, Hb2O₂, Hb3O₂, Hb4O₂)
        - therefore, amount of O₂ available from HbO₂ depends mostly upon amount of Hb, condition of Hb (e.g., sickle cell anemia, carbon monoxide poisoning), pH, and  temp. (p. 565)


   

    - good Hb carries much O₂ to capillaries near cells, bad Hb carries little
    - decr. pH, or incr. temp. (all from cell metabolism) -> O₂ leaves Hb,  goes to cells
            (opposite conditions and effects in lungs to help bind O₂ to Hb) 
           (To see conditions in lungs, click here.)

    - usually only part of O₂ from HbO₂ is used
    - unused HbO₂ remains in blood unless extra O₂ is needed by cells
    - therefore, HbO₂ is reservoir for O₂ , and can supply more if pH drops or temp. rises
                    (e.g., high cell metabolism or cell need)

    - therefore, since the amount of O₂ available for cells depends on (1) PaO₂, (2) amount of Hb, (3) condition of Hb, (4) pH, and (5) temp. (p. 567), it is possible to have low PaO₂ (hypoxemia) and not have hypoxia


       

    - and since the PaO₂ supplies only a small portion of the O₂ for cells, it is possible to have a good PaO₂  (no hypoxemia) and still have hypoxia


       

       
    Therefore, to evaluate hypoxemia and hypoxia, you must know;
    1. PaO₂ (for hypoxemia = low arterial blood O₂)
    2. ** amount of Hb in blood
    3. ** condition of Hb
    4. ** pH
    5. ** temperature
        (** for hypoxia)

Development of pulmonary edema (sketch)
 

 (sketch)
     - normal lung
           - much thin membranous surface area and open clear airways and spaces
        - normal - much thin membranous surface area and open clear airways and spaces
             2. Normal lung, cross section, gross
             4. Normal lung, microscopic*
     - abnormal lung from pulmonary edema (sketch)
          - thick membranes
                         29. Lung, interstitial pneumonitis, microscopic*
          - fluid-filled air spaces
                       - thick membranes and fluid-filled air spaces
                         5. Lung, edema, microscopic*
          - infection in fluid-filled air spaces
                        - infection in fluid-filled air spaces
                         17. Lung, bronchopneumonia, low power microscopic*
          - fibrosis
                        - thick membranes and fibrosis
                         115. Lung, interstitial fibrosis, microscopic*

Resistances to ventilation
    nonelastic resistance
        - narrow airways inhibit flow
        - highest during expiration
            - airways collapse during expiration
        - overcome by elastic recoil (passive) or muscles (active, uses O₂, makes CO₂)
    elastic resistance
        - elastic recoil (from tissue elasticity and surface tension) and tissue stiffness
        - highest during inspiration
        - overcome by surfactant (passive) and muscles (active, uses O₂, makes CO₂)

Obstructive disease   =  incr. nonelastic resistance
    - main problem is expiration
Restrictive disease   =  incr. elastic resistance
    - main problem is inspiration

Work of breathing   =  O₂ used for ventilation
    - usually less than 5% of O₂ taken in -> >95% available for body cells

See charts for Asthma, Chronic bronchitis, and Emphysema

Asthma
    causes
        - external cause  =  extrinsic asthma
             - e.g., dust, pollen, cold air
        - internal cause  =  intrinsic asthma
            - e.g., emotional upset, stress
        - either external or internal cause  =mixed asthma (most common)
    pathogenesis  (p. 591, 137, 138) (sketch)
  

    S & S  =  dyspnea, difficult expiration, wheeze

Chronic bronchitis
    causes  =  smoking, any air pollution
        (pp. 592-594)

        pathogenesis (sketch)
 

    S & S  =  dyspnea, chronic cough, incr. sputum (p. 553)

Emphysema - Centrilobar emphysema (CLE) (sketch)
    - gross views
        2. Normal lung, cross section, gross
        66. Lung, centrilobular emphysema, gross
    - microscopic views
        4. Normal lung, microscopic*
        68. Lung, emphysema, microscopic*

    causes  =  smoking, any air pollution
            (pp. 592-594)
    pathogenesis (sketch)
 

    S & S  =  dyspnea, cough, incr. sputum, low FEV₁

Emphysema - Panlobar emphysema (PLE) (sketch)
    causes  =  air pollution, genes, "aging", ??
         (pp. 592-594)
      pathogenesis (sketch)
 

    S & S  =  dyspnea, barrel chest, low FEV₁ (p. 553)

Interrelatedness among obstructive diseases (p. 591) (sketch)

Complications form COPD
    bleb  ->  pneumothorax (compression atelectasis = pressure collapses lung)  ->  decr. inspiration (p. 593, 604) (sketch)
        65. Lungs, bullous emphysema, gross
    bulla (large air-filled space in lung) ->  collapsed airway   ->  permanent collapse of region served (absorption atelectasis = removal of air collapses lung) (p. 593) (sketch)
    cor pulmonale (sketch)
        - right-sided heart failure from pulmonary hypertension (p. 619)
    pneumonia = inflammation in the lung (sketch)
        - pulmonary edema, incr. mucus, decr. clearing   ->  incr. risk of infection
    pulmonary edema (sketch)
 

1.  decr. ventilation	2. decr. pulmonary vessels
yields	yields
decr. O2, incr. CO2 in lungs
yields
pulmonary vasoconstriction
yields                                        yields
pulmonary hypertension
yields
pulmonary edema     5. Lung, edema, microscopic*      6. Lung, passive congestion, microscopic*      122. Lung, thickened peripheral pulmonary artery with pulmonary hypertension, microscopic*
yields
etc., etc.

Problems from O₂ therapy with COPD

    - therefore

Restrictive respiratory diseases
    - main effect is decr. inspiration with incr. elastic resistance
    extrapulmonary types  - abnormality is outside the pleural cavity
        neurological causes
             causes - strokes, drugs, head trauma, high cervical fracture
             mechanisms - inhibits stimulation of diaphragm and other respiratory muscles
        anatomic causes
             causes - kyphoscoliosis, trauma, obesity
             mechanisms - inhibits movement of thoracic components

    intrapulmonary types - abnormality is inside the pleural cavity
        - pleural effusion  =  fluid in pleural cavity outside lung  (p. 604) (sketch)
             causes - congestive heart disease, hypoproteinemia, inflammation of lung surface, hemothorax (blood in thorax)
                 126. Pulmonary atelectasis, gross [XRAY]
                 127. Hemothorax, gross
                 128. Chylothorax, gross [XRAY]
             mechanisms - fluid puts pressure on lung and takes up space
                fluid  ->  pressure on lung  ->  partial lung collapse (compression atelectasis) -> decr. compliance -> decr.inspiration -> decr. ventilation -> decr. O₂,  incr. CO₂,  decr. pH -> cell injury/cell death  -> body malfunction
            S & S  =  dyspnea, altered sounds and motion, x-ray (p. 604)
        - pneumothorax  =  air in pleural cavity outside lung (sketch)
            causes - trauma, bleb bursts, surgery
               -  closed pneumothorax = trapped air can be absorbed
               -  open pneumothorax = more air enters with each inspiration
            mechanisms - air puts pressure on lung and takes up space
                air ->  pressure on lung + decr. pressure changes -> partial lung collapse + decr. compliance + decr. pressure changes  ->  decr.  inspiration   ->  ->  ->  -> body malfunction
             S&S  =  dyspnea, altered sounds and motion x-ray
        - pneumonia  = pneumonitis  =  inflammation of the lung
            causes and mechanisms
               - microorganisms  (p. 608)
                    - bacteria ->  exudate blocks airways -> decr. ventilation (sketch)
                            - bronchopneumonia
                             7. Lung, bronchopneumonia, gross [XRAY]
                             8. Lung, bronchopneumonia, gross
                             18. Lung, bronchopneumonina, high power microscopic*
                             20. Lung, abscessing pneumonia, low power microscopic*
                            - lobar pneumonia
                             11. Lung, lobar pneumonia, gross
                             12. Lung, lobar pneumonia, gross
                             13. Lung, empyema, gross
                            - pulmonary abcess
                             14. Lung, abscesses, gross
                        S&S  =  dyspnea, productive cough, altered sounds, chills, fever, x-ray
                    - viruses -> edema  -> decr. diffusion (sketch)
                             29. Lung, interstitial pneumonitis, microscopic*
                          S&S  =  dyspnea, dry cough, fever
                    - TB and fungi -> necrosis of lung tissue ->  (decr. ventilation,  decr. perfusion, decr. diffusion) (sketch)
                        - TB
                             34. Lung, tuberculosis with granulomatous inflammation, gross
                             35. Lung, tuberculosis with granulomatous inflammation, gross
                             36. Lung, granulomatous inflammation and caseation, gross
                             39. Lung, Ghon complex with primary tuberculosis, gross
                             40. Lung, granulomas, low power microscopic*
                             41. Lung, granulomas, low power microscopic*
                             42. Lung, granulomas, medium power microscopic*
                             44. Lung, M. Tuberculosis, acid fast stain, high power microscopic*
                             45. Lung, miliary tuberculosis, gross
                             46. Lung, miliary tuberculosis, gross
                        - fungal infections
                             47. Lung, Aspergillus, gross
                             48. Lung, fungal granuloma, gross
                             49. Lung, extensive fungal granulomas, gross
                          S&S  =  dyspnea, productive cough, hemoptysis, x-ray, skin test
               - aspiration of gastric contents  -> blockage, inflammation, necrosis, and abscess of airways and lung
                             4. Larynx with aspiration of food, gross
                             14. Lung, abscesses, gross
                             15. Lung, abscesses, gross
                      - S&S  =  dyspnea, choking, cough, fever
                - dusts  -> chronic inflammation -> scar formation (pulmonary fibrosis) -> decr. elasticity (decr. compliance)  (p. 612)
                         110. Farmer's lung, scene
                         111. Silo filler's disease, scene
                         101. Fibrous pleural plaques, gross
                         102. Fibrous pleural plaque, low power microscopic*
                         99. Asbestos body, microscopic*
                         100. Lung, ferruginous bodies, iron stain, microscopic*
                         103. Lung, silicotic nodule, low power microscopic*
                         104. Lung, anthracosis, microscopic*
                         105. Lung, silicosis, polarized light microscopic*
                         115. Lung, interstitial fibrosis, microscopic*
                         116. Lung, interstitial fibrosis, Trichrome stain, microscopic*
                      - S&S  =  dyspnea
        - reduced surfactant
            - causes
                - hyaline membrane disease (premature birth)
                - adult respiratory distress syndrome  =  ARDS
            - mechanisms
                - increases surface tension
                    - decr. surfactant  ->  incr. surface tension -> decr. compliance
                - edema (with ARDS)
                note: ARDS has decr. surfactant + edema
                 118. Lung, diffuse alveolar damage, gross
                 119. Lung, diffuse alveolar damage, microscopic*
             - S&S  =  dyspnea, straining to inspire

Cor pulmonale
    causes (p. 619)
        - chronic bronchitis, emphysema, pulmonary embolism, pulmonary fibrosis -> decr. ventilation ->  pulmonary vasoconstriction -> pulmonary hypertension ->  overworked right ventricle ->  dilation and hypertrophy ->  right CHF (cor pulmonale) (p. 617) (sketch)
        - decr. number/size of vessels  ->  blocked flow  ->  pulmonary hypertension  ->  overworked right ventricle  ->  dilation and hypertrophy  ->  right CHF (cor pulmonale) (sketch)

respiratory failure
    hypoxemic respiratory failure (p. 624)
        - from problems other than ventilation
        - low O₂ but normal (or low) CO₂
    hypercapnic respiratory failure (p. 624)
        - from decr. ventilation (+ other problems)
        - low O₂ + high CO₂
    respiratory insufficiency
        - decr. O₂ or incr. CO₂ during exercise
    respiratory failure
        - PaO₂ 50 mmHg (normal  =  85-100)
        - PaCO₂ 50 mmHg (normal  =  35-44)

pulmonary malignant neoplasms
    - i.e. lung cancer (p. 113 fig. 8-7)
    - risk factors (causes)
        - for primary lung cancer  -  air pollution (smoking)
             79. Lung, squamous cell carcinoma, gross [CT]
             80. Lung, squamous cell carcinoma, gross [XRAY]
             81. Lung, squamous cell carcinoma, gross [XRAY]
             85. Lung, peripheral adenocarcinoma, gross
             86. Lung, bronchioloalveolar carcinoma, gross
             87. Lung, bronchioloalveolar carcinoma, microscopic*
             88. Lung, oat cell carcinoma, gross
             89. Lung, oat cell carcinoma, gross
             97. Lung, mesothelioma, gross
        - for metastatic lung cancer
            - all systemic blood goes to heart and then the lungs
             94. Lung, metastatic carcinoma, gross [XRAY]
             93. Lung, metastatic carcinoma, gross [XRAY]
    - S&S  =  dyspnea, hoarseness, difficulty swallowing, chronic cough, hemoptysis, digital clubbing, x-ray
    - effects (sketch)
        - decr. ventilation (blocks airways)
        - decr. perfusion (blocks/replaces vessels)
        - decr. diffusion (thickens/replaces surface {i.e., respiratory membrane})

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