Pathophysiology Study Guide – Test 2

Ch. 15 Concepts of Neurologic Dsfx p 439-466

Decorticate response: flexion of arms, wrists & fingers w/adduction in upper extremities (pulling in to
the core)
 Lesion of upper brainstem
Decerebrate response (worse): All four extremities in rigid extension w/hyperpronation of forearms
& plantar extension of feet.
 Patient who has lost cerebral control of spinal reflexes, usually as a result of an intracranial
catastrophe
Seizure: sudden explosive disorderly discharge of cerebrl neurons charx by sudden transient alteration
in brain fx.
 Can be caused by hypoxia, enzyme & neurotransmitter changes, cerebral lesions, biochemical
disorders, cerebral trauma, and epilepsy.
 Types of seizures:
o Generalized: involving neurons bilaterally, and do not have a local (focal) onset originate
from subcortical/deeper brain focus
o Simple partial seizures: simple, w/o impairment of consciousness, with motor signs
(head turning, jerking, stiffening), special sensory/somatosensory sx (tingling, tinnitus,
visual distort), autonomic sx of signs & w/psychic sx. “Déjà vu”
o Complex partial seizures: typical is w/impairment of consciousness; loss of contact
w/environment & blank stare, lasts seconds (atypical: only noticed in EEG)
Myoclonic: sudden excessive jerking
Atonic: sudden loss of muscle tone
Tonic/clonic: GRAND MAL
Tonic: stiffening associated with loss of consciousness) apnea may be present, phase followed by…
Clonic: jerking phase (contraction/relaxation of muscles)
Aura: sx that is a signal to generalized tonic-clonic seizure…partial seizure
Prodroma: early manifestation that may occur hours to days before a seizure
Agnosia: defect of pattern recognition
Alzheimer’s neurofibrillary tangles & neuritic plaques, abnormal proteins in areas of cell loss in brain,
neurotransmitter changes
 Risk factors: age, genetics, head trauma, MI
 Stages:
I. Early confusion
II. Late confusion
III. Early dementia
IV. Middle dementia
V. Middle-middle dementia

Ch. 16 Alterations of Neurologic Fx p 505-515

Thrombus: Blood clot within a blood vessel
Embolism: Blood clot or other material carried to the brain from another part of the body
 Cerebral embolism: usually younger (usually released from heart)…s/s hemiplegia/ ↓ LOC
Cerebral hemorrhage: rupture of a cerebral blood vessel with bleeding into brain.
 Causes: [#1] hypertension, trauma, aneurysm, transient ischemic attack, . Sx: headache that
progresses
Cerebral thrombosis: most frequent cause of CVA
Patho of CVA: cerebral ischemia and infarction occur when there is a significant ↓ in O2, then
electrical fx occurs & s/s of ischemia. Area of infarction dictates symptomology: [most frequent location
of occlusion: middle cerebral artery)

1
 L sided CVA R sided CVA
Aphasia Disorientation
↓ of verbal skills Impaired judgment
Personality changes ↓ in performance
 skills
Reduced retention of Time orientation
verbal materials problems
Right paralysis Left paralysis or
paresthesia

Embolic stroke: fragments that break from a thrombus formed outside of the brain or in the heart,
aorta, common carotid or thorax
Hemorrhagic stroke (intracranial hemorrhage): third most common cause of CVA.

Structure & Fx of Digestive System Ch. 37 p.1231-1257

Fx: Digestion, ingestion, absorption, elimination
GI: innervated by PNS
Enteric/Intrinsic NS: coordinates motor & secretory activities (hormones & enzymes)
25%-30% of cardiac output: venous blood goes from GI tract into portal vein & perfuses the liver
GI mvmt: propulsion & mixing accomplished by peristalsis & segmentation
Walls of GI tract: submucosa, mucosa, tunica muscularis & serosa (adventitia)
Gastric secretions: (stimulated by vagus nerve, gastrin & histamine)
Gastrin: facilitates relaxation…stimulates gastric glands to secrete HCL & pepsinogen
Motliin:  gastric motility, stimulated by acid & fat in duodenum
Secretin: delays gastric emptying; stimulates pancreas to secrete alkaline panc. Juice & liver to
secrete bile; ↓ GI motility, stimulated by chyme in duodenum
CCK: delays gastric emptying; stimulates gallbladder to eject bile & pancreas to secrete alkaline
fluid, ↓ gastric motility; stimulated by presence of chyme in duodenum
Acids: (main fx: dissolve food fibers, bactericide against organisms & convert pepsinogen to pepsin)
Parietal cells: hcl & intrinsic factor…stimulated by Ach…”breed & feed”
Chief cells: pepsinogen which converts to pepsin…stimulated by Ach/gastrin/secretin
Mucus: prostaglandins & NO protect mucosal barrier by stimulating secretion of mucus & bicarbonate,
and inhib acid secret.
Small intestine: 5 meters long
 Stomach  pyloric sphincter  duodenum  jejunum  ileum  ileocecal valve  large
intestine
 Peritoneum: serous membrane surrounding organs of abdomen & pelvic cavity (visceral
over organs, parietal: wall
of abd cavity)
 Absorption of h20 (85 to-90%), lytes, carbs/proteins (proximal area of intestine)/fats (lacteals…
emulsification, lipolysis, micelle formation, absorption, resynth of triglycerides &phospholipids))/minerals/vitamins
via brush border
Emulsification: process by which emulsifying agents (fatty acids, monoglycerides, lecithin, chol,
protein, bile salts) in the intestinal lumen cover the small fat particles & prevent them from reforming
into fat droplets
 Liver: hepatocytes synthesize cholesterol to form primary bile salts (cholic acid &
chenodeoxycholic (chenic) acid and secondary bile acids, deoxycholic acid & lithocholic acids
 Both forms (primary & secondary) are conjugated with amino acids (glycine or taurine) in the
liver to form bile salts
 Conjugation makes bile acids more H20 soluble this restricting their diffusion from the
duodenum & ileum
 Bile salts: conjugated bile acids
2
Large intestine: 1.5 meters long (cecum, appendix, colon, rectum, anal canal)
Continued absorption of substances, but majority have already absorbed into GI
Haustral segmentation: localized, rhythmic contractions of circular smooth muscles (occurs
more freq than peristalsis)
Peristaltic movements: short segments of longitudinal muscle
Distention of ileum w/chyme causes the gastrocolic reflex, or mass propulsion of feces to rectum
Liver: largest organ, secretes bile, metabolizes bilirubin, stores lg volumes of blood, metabolizes
nutrients & stores min/vit
Fx unit: hepatocytes, which form the lobules of the liver
Bile canaliculi: conduct bile, which is produced by the hepatocytes, outward to bile ducts & drains into
common bile duct
Kupffer cells: part of the mononuclear phagocyte system; remove bacteria from portal blood; destroy
int bacteria & prev infx
Secretion of bile: 700-1200mL/day (alkaline bitter, yellowgreen fluid that contains bile salts)
Bilirubin: byproduct of destruction of aged RBC p1250
Detoxification: endogenous & exogenous chemicals i.e. RX, hormones, etc….aka metabolic
detoxification or biotransformation
Gall bladder: on inferior surface of liver; stores & concentrates bile
 Bile flows from liver to R or L hepatic duct into COMMON hepatic duct & meets resistance
@ sphincter of Oddi which controls flow into duodenum and prevents reflux of duod
contents into pancreobiliary system
 Bile then flows to the cystic duct into the gallbladder where it is concentrated & stored
DX tests for GI
Abdominal xray Ultrasound
CT MRI
Stool study Upper GI (barium
swallow)
Serum Lower GI (barium
enzymes/proteins enema)
Alterations of Digestive Fx Ch. 38
Vomiting triggers:
 Ipecac or copper salts
 Severe pain or distention of stomach/duodenum
 Torsion or trauma affecting ovaries, testes, uterus, bladder or kidney
 Activation of CTZ
 5-Hydroxytryptamine (5-HT aka Seratonin) stimulates emetic center & is released from
enterochromaffin cells in intestinal wall and possibly from neurons in brain stem
Retching: deep inspiration, glottis closes, intrathoracic pressure ↓ & esophagus distends…abd muscles
contract & creates a pressure gradient from abd to thorax. The lower eso sphincter & body of stomach
relax but duodenum & antrum spasm. The reverse peristalsis & pressure gradient force chyme from
stomach & duodenum up into the esophagus
Vomiting: duodenum and antrum of stomach produce retrograde peristalsis while body of the stomach
& eso relax…when stomach is full, diaphragm is forced high into thoracic cavity by strong contractions
of abd muscles. The  intrathoracic pressure causes the eso sphincter to open & chyme is expelled.
Diarrhea (loose stools  frequency)
 Causes:
 ↓ fluid absorption or  fluid secretion
 Motility disturbances
 Acute, from infx…cramping, N/V; malaise, febrile or…
 Chronic, persisting ~ two weeks…lyte/dehydration probs
Dx: HX, labs (wbc, parasites, mucus, blood)…either upper or lower GI
Manged by: assessment, AD meds, antiperistaltics or antibiotics
Major mechanisms of diarrhea:

3
O smotic diarrhea: a nonabsorbable substance in the intestine draws water into the lumen by
osmosis…the excess H20 & nonabsorbable substance cause large volume diarrhea (LACTASE
DEFICIENCY most common cause)

S ecretory diarrhea: caused by excessive mucosal secretion of fluid & lytes or inhibition of sodium
chloride absorption.
 Cause: bacterial enterotoxins, i.e. E. coli & neoplasms, gastrinoma or thyroid carcinoma
major cause
 LG VOLUME: Cause: excessive motility, i.e. lesion that impairs autonomic control of
motility, such as diabetic neuropathy
 SM VOLUME: inflammatory disorder of int, such as ulcerative colitis or Chron disease

M otility diarrhea: caused by resection of small intestine, surgical bypass of an area of int or
fistula formation between loops of intestine…food is not mixed properly & there is impaired
digestion &  motility
Disorders of motility:
Dysphagia: difficulty swallowing; can result from mechanical obstruction or disorder that impairs
esophageal motility  likely from a neural or muscular disorder that interferes w/voluntary swallowing
or paralysis
Achalasia: denervation of smooth muscle in (middle/lower) esophagus  from neural dysfx, probably a
↓ in the number of myenteric ganglion cells & atrophy of smooth muscle cells
GERD (reflux of chyme from stomach to esophagus)
 LES is weakened, relieved when sitting up
 1-2 hours after meal
 Vomiting, coughing, lifting contribute to pressure
 Eso wall: hyperemia,  cap perm, edema, tissue fragility, erosion, ulcerations, fibrosis & basal
cell hyperplasia & elongation of papillae are common
 “heartburn” sensation
 symptoms can exist when no acid is in esophagus or ↓ eso motility results in dysphagia
 alcohol & citrus fruits cause discomfort during swallowing
 endoscopy = edema & erosion
Hiatal Hernia (type of diaphragmatic hernia…protrusion of upper part of stomach thru the
diaphragm & into thorax)
1. Sliding (most common): stomach slides or moves into thoracic cavity thru eso hiatus
(opening for vagus nerves)
2. paraesophageal (rolling) the membrane becomes thinned out or defective, allowing a true
peritoneal sac to protrude into the posterior mediastinum where negative intrathoracic
pressure causes it to enlarge.
 ASYMPTOMATIC: difficult to distinguish, manifestations include gastroesophogeal reflux,
dysphagia, heartburn & epigastric pain…regurgitation & discomfort after eating are common
Pyloric Obstruction (narrowing or blocking of opening between
stomach/duodenum)
 vague epigastric fullness…more distressing after eating & later in the day
 s&s: nausea, fullness, anorexia, weight loss, distention, succession splash (rolling or
jarring of abd prod sloshing sound)
 Vomiting = undigested food but no bile (cardinal sign of obstruction)
Intestinal Obstruction (ANY condition that prevents flow of chyme thru
int. lumen)
Simple: mechanical blockage of lumen by lesion (ie fibrous adhesions, most common type)
Fx: failure of motility (ie paralytic ileus)Can’t absorb h20 easily, h20 in lumen, gas buildup & absorption of lytes ↓
s&s: colicky pain followed by vomiting, sweating, n/v, distention and dehydration, metabolic alkalosis if @
pylorus or high in sm intestine (excessive loss of H+ ions OR metabolic acidosis if in lower intestine because
bicarb from panc & bile can’t be resorbed) TX: OR
Gastritis (inflammatory disorder of gastric mucosa)

4
Causes: injury from drugs, alcohol, chemicals, h. pylori, antiinflamatory rx such as aspirin, ibuprofen,
naproxen, indomethacin (b.c they inhibit prostaglandins…which NORMALLY stimulates secretion of
mucus) also H. Pylori!!!!
S&s: bleeding may be only sign!!!, tenderness, pain, n/v…
Tx: smaller bland meals, cimetidine (tagamet)
Peptic Ulcer Disease (PUD: break in mucosal lining…5 million people!)
Causes: H. pylori, NSAIDS, genetics, STRESS
Chronic intermittent pain, worse when stomach is empty
Duodenal Ulcer (younger people, type O blood)
Cause: H. pylori, Hypersecretion of acid & pepsin…inadequate secretion of bicarb, rapid gastric
emptying,  number of parietal cells, failure of feedback mechanism whereby acid in gastric antrum
inhibits gastrin release)
Ulcerative Colitis (inflammatory bowel disease)
o Common @ 20-40 yrs of age, Jewish descent, family hx
o Disease is most severe in rectum & sigmoid colon, mucous layer thinner than normal
 Bleeding, pain, diarrhea (large volumes, watery), fluid loss & urge to defecate (purulent
mucus/blood passed in stool)
o Patho lesions of inflammation on LG intestine
o Immunologic factors (anticolon antibodies)
o Dx by lower GI study (barium enema?)
Chron Disease (idiopathic inflammatory disorder effecting any pt. of int.
tract)
o 4-10% of population, greater in Caucasian & Jewish
o Genetic (20-40%)
o S&s: Pt claims “irritable bowel”…diarrhea most common sign w/passage of blood/mucus
o PAIN after meals, weight loss & insidious onset
o Environmental, pesticides, additives, tobacco, radiation)
o  T cells & alterations in IgA
o continues for life
o Begins in submucosa  int wall  mucosa/serosa …MOST common site = ileocolon
o “skip lesions” discontinuous inflammation affects some haustral segments but not others
o Tx: steroids, antiD, antiB, psychotherapy or removal of inflammed bowel 
Diverticulitis
Diverticulum: outpouching of mucous membrane that lines the bowel & goes out through the muscle,
anywhere in GI tract, but 95% in sigmoid colon
o Most common over 60 yrs….high refined food diet
o More common in men (congenital predisposition)
o Sx: cramps, LLQ pain, constipation before disease s&s irregularity/diarrhea
o Tx: surgery…rest bowel w/meds
IBS (Irritable Bowel Syndrome)
o Relatively common 1:6, but 3:1 women vs. men
o Onset 20-30yrs
o Cause…???
o Disorder of int. motility, CNS alterations to motor & sensory fx of bowel
o  peristaltic intensity,  secretion of mucus in color but NO inflammed tissue
o s&s:  abd. Pain, bouts of diarrhea/constipation, change in bowel patterns & stimulated by
certain foods and STRESS!
o Dx: rule out other GI…nursing dx=pain, ineffective coping, diarrhea/constipation…assess
what stimulates the condition & work with the PT to rule out those factors i.e. bulk diet
o Rx: Anticholinergics to interfere w/PNS; antiD, antisposmodics, herbal remedies (peppermint,
sage, anise)

5
Structure & Fx of the Pulmonary System Ch. 31 (Fx: ventilate alveoli,
diffuse gases in & out of blood, perfuse lungs so organs and tissues
receive 02 rich blood)
Neurochemical control of ventilation
o Respiratory center: in brain stem, composed of several groups of neurons located
bilaterally…
 DRG: dorsa respiratory group  sets basic automatic rhythm of respirations also receives
impulses from peripheral chemoreceptors in carotid & aortic bodies
 VRG: ventral respiratory group (in medulla)…contains both inspiratory & expiratory
neurons
 The pneumotaxic & apneustic centers

o Lung receptors: send impulses from lungs to DRG: (lungs are innervated by ANS)
 Irritant receptors: found in epi of conducting airways…sensitive to noxious aerosols,
gases, etc & cause bronchoconstriction and  ventilatory rate (proximal airways mostly)
 Stretch receptors: located in smooth muscles of airways & are sensitive to size/volume
of lungs….these are responsible for ↓ ventilatory rate & volume when stimulated
 J receptors: sensitive to  pulm cap pressure & initiate rapid, shallow breathing,
hypotension & bradycardia
o Chemoreceptors: monitor pH, Paco2, Pao2 of arterial blood
 Central chemoreceptors: monitor arterial blood, by sensing changes in pH of CSF…pH in
the CSF reflects Paco2 because unlike H+, co2 in arterial blood diffuses across blood-brain
barrier
o Co2 that enters CSF combiners with H20 to form carbonic acid, which disassociates
into H ions & stimulate central chemoreceptors…VERY SENSITIVE to small changes
in pH.
 Peripheral chemoreceptors: located in aortic & carotid bodies, the aortic arch
o Primarily sensitive to o2 levels in arterial blood & responsible for all the  in
ventilation that occurs in response to arterial hypoxemia…sends signals to resp
center to  ventilation
BARORECEPTORS: located in aortic arch & carotids: respond to BP & changes in ventilation
PROPRIOCERPTORS: in peripheri…respond to body mvmt and  ventilation
Alveolar surface tension:
o Law of Laplace: The pressure (P) required to inflate a sphere is = to 2x the surface tension
divided by the radius or
o P=[2T/r] …as the radius of the sphere becomes smaller, more and more pressure is required
to inflate it. RELATES TO PRESSURE!
Elastic recoil: tendency of the lungs to return to normal state after inspiration
Compliance: measure of lung and chest wall distensibility; it represents the relative ease with which
these structures can be stretched. C =(v/p)
One half to two thirds of airway resistance occurs in the nose! p.1092
Physiologic dead space: amojnt of air that remains in alveoli & tracheobronchial tree between
breaths
Oxygen content of blood: depends on the amount of O2 combined w/hemoglobin, as well as that
dissolved in the blood
 Must know: 1) hemoglobin concentration available to bind with O2 (hb in gr/dL) and 2) O2
sat or % of available hemoglobin bound to O2 (SaO2) …and 3) the partial pressure of O2
(paO2)
Oxyhemoglobin Association & Disassociation
 When hemoglobin binds w/O2, oxyhemoglobin is formed. Binding occurs in the lungs and is
called oxyhemoglobin association or hemoglobin saturation curve.

6
  Shift to the RIGHT  depicts hemoglobins ↓ affinity for O2 or an increase in the ease in which
oxyhemoglobin dissociates and O2 moves into the cells…i.e. acidosis (low pH) & hypercapnia
( PaCo2) and hyperthermia
 Shift to the LEFT  depicts hemoglobins  affinity for O2, which promotes assoc in the lungs
and inhibits disassociation in the tissues…i.e. alkalosis (high pH) & hypocapnia (↓PaCo2)
and hypothermia
 The shift byh changes in Co2 & H+ concentration is called the Bohr effect.
 Oxyhemoglobin curve is shifted also by changes in body temp and  or ↓ levels of 2,3-DPG, a
substance normally present in RBCs (hyperthermia to RIGHT, hypothermia to LEFT)
Carbon dioxide transport:
Co2 equilibrates with carbonic acid & must be eliminated to prevent acidosis
Acid base balance…. CO2 + H20 H2CO3 H+ + HCO3-
Tests of Pulmonary Fx
Spirometry: measures forced expiration…measures volume & flow
Restrictive lung disease: restricts lungs VOLUME…lungs are unable to expand normally, diminishing the
amt of gas that can be inspired. (ARDS, viral infx, cancer of lung, TB)
Obstructive lung disease: affect gas flow, airflow into &
out of lungs is obstructed (COPD, emphysema,
bronchitis, asthma)

VC = TV + IRV + ERV
VC (Vital Capacity): max volume of air that is
exhaled after full inspiration
TV (Tidal Volume): volume of air normally inhaled or
exhaled
IRV (Inspiratory Reserve Volume): max volume of
air that can be inhaled after normal inhalation
ERV (Expiratory Reserve Volume): max volume of
air that can be exhaled after normal exhalation
RV (Residual Volume): volume of air in the lungs
after max exhalation
TLC (Total Lung Capacity): volume of air in lungs after max inhalation
FRC (Functional Residual Capacity): volume of air in lungs at resting & exhalation
 Diffusing capacity: measure of 02 & Co2 exchange
 Perfusion: actual blood flow through pulmonary circulation…greater pressure = greater
perfusion
 Route of blood thru lungs: right ventricle  pulmonary artery  supplies BOTH lungs
 Shunting: normally about 2% of blood pumped by right ventricle does not perfuse alveolar
caps and does not have gas exchange…the HIGHER the amount of shunted blood, the MORE
the HYPOXIA
Alterations of Pulmonary Fx Ch. 32 p.1105
Dyspnea: sensation of uncomfortable breathing, or unable to get enough air…usually caused by
extensive pulmonary disease
Orthopnea: pulmonary congestion that causes dyspnea by the vertical position, b/c body water is
redistributed & abd contents exert pressure on diaphragm and  the efficiency of the respiratory
muscles
Obstructed breathing: occurs if airways are obstructed as in COPD…slow vent rate, large TV, 
effort & prolonged inspiration or expiration
Restricted breathing: pulm fibrosis, or disorders that stiffen the lungs or chest wall and 
compliance…small TV & rapid vent rate (tachypnea)
Hypercapnia (Co2): most causes are a result of decreased drive to breathe or inadequate ability to
respond to vent stim:
o Depression of resp center by drugs
o Diseases of medulla; infx of CNS or trauma

7
 o Abnormalities of the spinal conduction pathway; i.e. poliomyelitis
o Diseases of the nm junction or the resp muscles, i.e. MG (myasthenia gravis) or muscular
dystrophy
o Large airway obstruction; tumors or sleep apnea
o  work of breathing or physiologic dead space as in emphysema
Hypoxemia ( o2 of arterial blood): Causes:
1.  o2 content of inspired gas
2. hypoventilation; i.e. unconscious person…sedation, and COPD
3. diffusion abnormalities
4. abnormal vent-perfusion ratios MOST COMMON CAUSE:
5. pulmonary RIGHT to LEFT shunt (when blood passes through portions of cap bed that
receive no vent, b/c alveoli are collapsed or filled w/fluid & cellular debris…blood flows
thru pulm circ without being oxygenated which results in  systemic Pa02 & hypoxemia.
Hypoxemia resulting from shunting does NOT respond to  in supplemental inspired O2
(i.e. nasal cannula) b/c a portion of the pulm cap bed is never exposed to the o2 gas…
this makes hypoxemia resulting from shunting VERY difficult to treat; i.e. ARDS & RDS of
newborn…High V/Q (look on pg 1109 table 32-2) = most common cause is pulmonary
embolus
Hypoxia: (↓ o2 of tissues) Causes:
1. Low CO
2. cyanide poisoning\
Acute Respiratory Failure: inadequate gas exchange…can result from direct injury to lungs, airways
or chest wall or indirectly due to another body system such as brain (resp centers)
Pulmonary edema: excess h20 in the lung…MOST COMMON CAUSE is HEARTDISEASE
(when left ventricle fails, filling pressures on left side of heart  and cause a concomitant
 in pulm cap hydrostatic pressure…when this pressure exceeds oncotic pressure, fluid
moves into interstitial space)
o Another cause of pulmonary edema=cap injury that  cap permeability…i.e. ARDS or
inhalation of toxic gases such as ammonia
o Another cause of pulm edema: obstruction of lymphatic system
o Sx: dyspnea, orthopnea, hypoxemia,  work of breathing…crackles & dullness over lung
bases
o Cardiomegaly {}…severe = pink frothy sputum 
Aspiration: passage of fluids/solid particles into lung (commonly caused in individuals whose normal
swallowing mechanism & cough reflex are impaired by a  LOC or CNS abnormality)
o Substance abuse, sedation, anesthesia, seizure disorder, CVA, myasthenia gravis (nm
disorder) & Guillain-Barre syndrome (inflammation of nerves)
o In children: tracheoesophageal fistula
o SEVERE PNEMONIA can result….50% will death rate from aspiration pneumonia
Atelectasis: Collapse of lung tissue…two common types: Compression & absorption
1. Compression: ext pressure by tumor, fluid, or air in pleural space, or by abd distention
pressing on lung causing alveoli to collapse
2. Absorption: removal of air from obstructed/hypovent alveoli or from inhalation of
CONCENTRATED O2 or anesthetic agents
s&s: dyspnea, cough, fever, leukocytosis…tends to occur post OP, pain, shallow breathing, reluctant to change
positions & viscous secretions produced…DEEP breathing (spirometer) beneficial! b/c it promotes ciliary clearance
and stabilizes alveoli by redistributing the surfactant, and permits collateral vent thru pores of Kohn in alveolar
septa (which open only during deep breathing & allows you to pass air from well vent alveoli to obstructed
alveoli…minimizing their collapse.
COPD: inflammation, edema, fibrosis of bronchial wall, loss of elastic fiber, loss of
alveolar tissue, loss of elastic fibers which impairs expiratory flow  SOB
w/exertion, sputum in a.m., cough w/sputum, fatigue

8
*pursed lip breathing ><can help relieve dyspnea (p 1125) ..teach, nutritional counseling, resp hygiene, early
s&s of infx

Type A COPD: Emphysema Type B COPD: Chronic Asthma

Bronchitis
Dry hack Bronchioles inflammed: SOB ( Causes: immunologic &
loss of elastic recoil: reduces exercise tol) nonimmuno.
volume of
air that can be expired passively
Loss of lung elasticity (by proteases) Hypersecretion of mucus  Wheezing &
dyspnea
Cough (little) accessory musc. for Cough with sputum ID allergens
ventilation
Destruction of alveoli S02  90% Acute: nasal o2, IV
aminophylline
02 sats better (vs type B) No lung tissue damage Severe: intubate,
hospitalize, IPPB
Permanent elg of air spaces with Causes: smoking/environmental Chronic: oral steroids,
destruction to alveolar walls inhaler &
Symptom control
Two types: Centrilobular: affects Tx: bronchodilators/steroids Chest tightness,
bronchioles in center part of resp lob coughing at night
Panacinar: involves peri alveoli Dx: chest xray, ABG, sputum More acute &
extends intermittent
to more central bronchioles (damage
randomly distributed)
Causes: hereditary (in younger ppl… Dyspnea common Expiratory flow
alpha Prolonged expiration always
Antrypsin is  ) & smoking… present 
Central chemoreceptors no longer Forced exp volume
macrophages in alveolar walls which
act as Forced vital capacity
attracts Neutrophils
primary stimuli for breathing… FRC & ttl lung
 inflammation
taken over by perichemoreceptors capacity 
Malnutrition major concern Hyperventilation
Barrel chest triggered by
Prolonged expiration Lung receptors
Tx: inhaled Anticholinergics, b-adr responding to
agonists & bronchodilators lung volume &
obstruction
Pink Puffer (not as many O2 Blue Bloater (more o2 Result = early
changes!!!) changes) hypoxemia w/o CO2
retention

ARDS (form of resp failure characterized by acute

Lung inflammation & diffuse alveolocapillary injury
Patho: leakage of fluid into alveolar interstitial spaces
And alterations in the capillary bed  pulm edema (increased
Capillary permeability is hallmark of ARDS) which  lung compliance,
Result of injury to lung by numerous unrelated causes;
i.e. trauma, sepsis, burns, aspiration, pneumonia, o2 toxicity
smoke, or noxious gas inhalation
Massive inflammatory response by lungs (stiff lungs) …shunting in lungs, small airway
closure

9
Progressive respiratory distress, severely ill, LOC 
Tx: Trach, suctioning, semi fowlers or prone positioning, psych support vent, PEEP, IV, enteral feeding,
high 02 concentration, partial liquid ventilation, sedation to  02 consumption, drugs to  CO….HIGH
mortality 
Rapid, shallow breathing, resp alkalosis; dyspnea,  lung compliance;
Hypoxemia unresponsive to o2 tx & diffuse alveolar infiltrates on chest radiographs

Clinical course of progression: (p.1120)

Hyperventilation  respiratory alkalosis  dyspnea & hypoxemia 
Metabolic acidosis  resp. acidosis  further hypoxemia  hypotension &  CO  DEATH

Tuberculosis (infx caused by mycobacterium tuberculosis, efx lungs &

other body systems)
o On the rise since 1986, virulent disease involving lungs, lymph, GU,
bone, joint, meninges
o s&s: inflammatory lesions, cough (nonproductive), hemoptysis (coughing
up blood  ), pleuritic chest pain
o tx: multiple rx therapy…UV rays kill bacteria, adhere to regimen! antiBi
therapy
o Transmitted via  droplets…lodge in lymph nodes where they encounter lymphocytes &
initiate the immune response  Neutrophils/macrophages seal off the colonies of bacilli
forming a granulomatous lesion called a tubercle…infected tissues within the tubercle die
forming cheeselike material called caseation necrosis…scar tissue grows around tubercle,
completing isolation of the bacilli…immune response complete in 10 days preventing
further multiplication.
o Can be asymptomatic until disease is advanced except in immunosuppressed
individuals.
o Graded on a 0-5 scale, with 0=no TB, exposure or infx & 5=TB suspected.
Chest trauma:
Typical causes:
 Flail chest: fracture of several consecutive ribs in more than one place, or fracture of the
sternum + several consecutive ribs…result in instability of a portion of chest wall causing
paradoxic movement of chest w/breathing: inspiration=unstable portion moves inward,
expiration=it moves outward (impairs gas exchange)
 Tx: pain relief, o2-ation
 Pneumothorax: (pleural abnormality): presence of air or gas in pleural
space caused by a rupture in visceral or parietal pleura & chest
wall…the air separates the visceral & parietal pleura and DESTROYS
the negative pressure of the pleural space (disrupting equilibrium
that normally exists between elastic recoil forces of lung & chest
wall)

Lung Cancer (arise from epithelium of respiratory tract)

 Second leading cause of death, rising in women…80% caused by smoking
 s&s…cough, sputum streaked w/blood, chest pain, recurring pneumonia or
bronchitis
 dx: by sx
 tx: prevention, surgery, radiation, chemo

10
Review:
1. Review first unit, hypo/hypercorticoids, adrenal medulla, humoral & cell

mediated response, know what B & T lymphocytes are responsible for. OK

2. Know active, acquired, passive immunity OK

3. Review basic products of immunization, HLA etc. OK

4. Hypo/hyperthermia, signs & symptoms, heat stroke? Heat exhaustion? OK

5. Nervous system…know R & L hemi CVA s&s, one vs. the other…know common

causes, emboli, intercranial hemorrhage, etc. OK

6. Seizure activity: tonic, clonic, grand mal seizure. OK

7. N.S.: decorticate, decerebrate posturing…which one is worse? Better? OK

8. What is unique in the GI scenerios for a PT dx with these disorders: pyrosis,

GERD, ulcerative colitis, crohns, hiatal hernia, etc. OK

9. Review physiology of gastric secretions, parietal cells, pepsin, etc. OK

10. Bile & bile absorption…describe conjugated vs. unconjugated. OK

11. Nausea & CTZ center, physiologically what activates, cellularly with the

pathways in the CTZ OK

12. Constipation and diarrhea, secretory…types, osmotic etc. OK

11
13. Respiratory conditions: TB, resp, overall category for restrictive vs. obstructive

disorders OK

14. What makes chronic bronchitis vs. emphysema different? OK

15. Control mechanisms for respiratory system: chemoreceptors, baroreceptors,

peripheral receptors…what substances cause them to make the changes that

they do? OK

16. Asthma, immunological vs. nonimmunological …

17. Know the deoxyhemoglobin (S-curve) disassociation curve…what does a shift to

RIGHT mean, what does shift to the LEFT mean? OK

18. MEMORIZE: lung volumes…tidal, IRV, ERV, etc. OK

19. Laplaces Law, what does it refer to? Resistance? Plasticity? OK

20. o2 therapy & admin of O2, overload & toxicity to o2, typical sx? Symptoms
similar to ARDS, occurring with o2 conc 50-75%  in 24 to 48 hrs…severe
inflammatory response, mediated by 02 radicals, damage to alveolocapillary
membranes, disruption of surfactant production, insterstitial and alveolar
edema, in compliance
21. review section on shunting of blood & what it refers to OK

22. corpulmanal (??)…more freq in chronic bronchitis, enlargement of R side of

heart …???

23. Know type A COPD, type B COPD OK

24. ARDS: review tx & progression of sx OK
25. IBS, ulcerative colitis, chrons, compare how PT has sx…how is IBS, ulcerative
colitis differentiated? OK

12