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With oxygen--most common type of energy production in the cell. Supplies about
90% of the cells energy. End product: more ATP; waste products: CO2, H2O.
Examples include citric acid cycle, oxidative phophorylation.



 


 
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Epithelial- cover and line the internal and external body surfaces. Found in the
bladder, GI tract, blood vessels. Classified by cell layers and shape. Aid in
absorption, protection, excretion. A single layer makes it easier for substances to
diffuse
Simple squamous- minimal barrier; alveoli, capillaries of kidnyes
Simple cuboidal- less diffusion; secreting substances in glands
Simple columnar- cilia or microvili; thicker so less passive diffusion;
bronchi and GI tract
Stratified epithelium- lots of wear and tear; mouth and skin
Connective-
Loose-holds things like organs in place by elastin and collagin
Adipose-fat for protection and warmth
Dense-ligaments and tendons
Reticular- makes up lymph tissue and bone marrow
Muscle-
Skeletal-attached to bones; aids in movement
Cardiac- heart; contracts
Smooth- GI, bladder, vessels; for propulsion
Nervous-
Neurons are highly specialized that transmit electrical impulses
Atrophy-
Decrease in cell size
Caused by disuse, denervation, lack of endocrine stimulation, decreased
nutrition, ischemia
Hypertrophy-
Increase in cell size
Physiological cause: exercise
Pathologic cause: walls of urinary bladder thickening due to an
obstruction; myocardial or kidney compensation
Hyperplasia-
Increase in the number of cells overall
Only occurs in cells that can divide (so NOT cardiac or nervous)
3 types: compensatory, hormonal, pathologic
Examples: breast enlargement during pregnancy (h); liver regeneration (c);
fibroblasts in wound healing (p); endometrial hyperplasia (p)
Chronic pathologic= nice set up for hyperplasia
Metaplasia-
 When one cell converts to another type of cell
Reversible
Also can cause dysplasia if chronic
Caused by: chronic irritation or inflammation
Ex: squamous cells replacing ciliated columnar cells in smokers
Dysplasia-
Abnormal cell growth of a certain tissue that causes the cells to vary in
size, shape, and appearance
Causes: chronic irritation and inflammation
Sometimes reversible
Strong indicator of developing cancer
Pap smears screen for cervical dysplasia

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Rubor- erythema bc of capillary dilation
Calor- warmth bc increase in blood flow
Tumor- edema for fluid accumulation
Dolor- pain bc of the pressure on the nerves and chemicals being released
(prostaglandins)
Function laesa- alteration in function (ex: swelling at joint²doesn¶t work as well)


 







Signs you see throughout the body even if the injury is local
Lymphadenopathy-enlarged lymph node bc of filtering the excess fluids
(exudates) that are present in the tissues; exudate is used to dilute infecting agents
Lymphangitis-inflammation of lymphatic vessel
Lymphadentis-inflammation and localized infection of lymph nodes
Fever- pyrexia²endogenous pyrogens (the things that reset your natural
thermometer in the hypothalamus) are produced by macrophages and eosinophils
and all this causes an increase in temperaturerincrease in blood flow to site of
injuryrless than optimal environment for bacterial to proliferate; tachycardia
(1ºF=10bpm)
Mechanism- acts on hypothalamus to reset the body¶s natural thermostatr body
initiates heat saving measures like vasoconstriction, piloerection (goose bumps),
and shivering all trying to raise body temperature
ESR- erythrocyte sedimentation rate- is elevated if there is an infection
somewhere; it¶s the rate at which RBCs settle in a test tube; doesn¶t specify where
the infection is but it does help determine if there is an inflammatory process
going on internally
Leukocytosis- elevation of WBC count; the different types of WBC indicate what
kind of infection there is; order CBC to get differentiation
Neutrophil- pyogenic bacteria
Eosinophil- parasitic worm or allergen
Lymphocytes- virus
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"  - B lymphocytes mature into plasma cells and those plasma cells make
specific anti-bodies. Steps: antigen is recognized by a cellr antigen is presented
to T-cellr t-cell activates b-cellr plasma cells produce thousands of antibodies
(aka immunoglobulins) to the specific antigen. B cells made up of 2 heavy chains
(same for all Igs) and 2 light chains (specific for whatever antigen they¶re looking
for with specific binding site)
Antibodies- neutralize bacterial toxins, neutralize viruses, and activate
inflammatory response²basically attach to the antigen and lock it up so they
can¶t attack anything else- it¶s still floating around but its disabled (like a prison)
IgG- 80% of Abs; found in body fluids and tissues; protects against
viruses and bacteria toxins; passes through placenta barrier and in breasts
milk; slow rise in primary but most effective in secondary response
IgM- largest Ig; first one produced during infection; peaks 1-2 wks;
highest during primary response; increase in chronic infections; activates
complement cascade
IgA- found in blood stream but is more concentrated (allows for faster
immune response) in saliva, sweat, tears, mucus, bile (GI tract),
colostrums (initial milk 2, 3 days for baby); increased in chronic
infections/inflammation; doesn¶t let pathogens bind to mucosal surfaces
IgE- hypersensitivity rxn; low conc in serum; binds to mast cells; when it
reacts with antigens the mast cells are degranulated (which is what causes
the inflammatory response); allergic rxns/parasites
Primary- 6 days after antigen introduced; IgM detectable; IgG at 10 day mark and
it stays with you as memory cells
Secondary- IgG development immediate; AB is specific; doesn¶t have to
redevelop Abs only has to work on mass production
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Overactivation of IgE and degranulation of mast cells; rxn of body depends on
where the mast cells degranulate
Ex: anaphylaxis (degranulated in blood stream), asmtha (lungs), allergic rhinitis
(nose), food allergy (GI tract)
When mast cells degranulate they release histamines causes widespread
vasodilation (drop in BP) and bronchoconstriction
Tx: epinephrine- opens blood vessels and vasoconstriction
First exposure: lots of IgE produced that binds to basophils and mast cells but no
rxn
Second exposure: IgE signals mast cells to release the chemicals and causes s/s
S/S: wheezing, sneezing, runny eyes, itching; edema of airways, thick secretions
in airway, bronchoconstriction; dyspnea, tachypnea, anxiety
 Chemicals released when mast cells degraded: histamine, prostaglandins,
leukotrienes, serotonin, bradykinin

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3 stages:
Primary- flu-like symptoms, lymphadenopathy, fever, night sweats; may last 2-4
weeks; slight decrease in CD4+ count but still somewhat normal; you are
contagious but you might
Latency-asymptomatic;CD4+ cells decline slowly; getting sick more but no AIDS
defining illnesses; viral and AB load detectable; last up to 10-20 years with meds
Overt Phase- CD4+ count above 200 (really high) or AIDS defining illness onset

 




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- same osmotic pressure between cell and ECF so cell stays the same size
"

- solution has higher pressure than cell; cell shrinks bc water flows out of
cell trying to dilute the solution
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- solution has lower pressure than cell; cell will swell bc water flows into
cell trying to dilute the cell

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GERD²when stomach acid and contents come back up bc of poor
gastroesophageal tone (stomach pH= 2, esophagus=7)
S/S: heartburn, coughing, throat clearing, congestion (bc body is making
excess mucus in response to food in esophagus), ear infections (kids); may
result in asthma, atopy, Barrett¶s esophagus, strictures
Risk factors: hiatal hernia, obesity, family hx
Dx: Hx, pH probe, UGI, Endoscopy
Tx: diet change (no acidic foods, caffeine, alcohol, thickening foods in
kids, eating upright); medication (antacids, PPI- protein pump inhibitors,
H2 blockers- make stomach less acidic); Nisssen fundoplication (where
they tie off the top part of the stomach); increase promotility (less time in
stomach=less chance to come back up)
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Upper²mouth, esophagus, stomach; mechanical and initial chemical digestion,
Middle²small intestines (duodenum, jejunum, ileum); chemical digestion and
absorption of nutrients and water
Lower²cecum, colon, rectum; water absorption and fecal elimination
Accessory organs²Salivary glands, Pancreas, Liver, Gallbladder; Produce
digestive enzymes
Chemical digestion- chemicals that digest food released from salivary glands,
pancreas, liver, and gallbladder

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Inspiration- size of chest cavity increases; diaphragm contracts and lowers;
intercostals muscles contract; oxygen enters the body when air moves from area of
greater pressure (outside) to area of less pressure (lungs); airways and alveolar ducts
increase in size
Expiration- decrease in chest cavity size; diaphragm relaxes and moves upward
leaving less room for lunges and that forces air out of the lungs; intercostal muscles
relax; rib cage returns to its resting stage; carbon dioxide is exhales; airways and
alveolar ducts decrease in size
 
 



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Ventilation- the exchange of air between the lungs and the atmosphere; actual
movement of air and how well lungs get air into them; involves both the ability to
bring in oxygenated air and expire CO2 concentrated air
Perfusion- the flow of blood through the capillaries surrounding the alveoli;
movement of air into lungs does no good if blood isn¶t there to pick up the O2 rich
blood and drop off the CO2 concentrated air


 V/Q; V=alveolar gas flow, 4L/min; Q=capillary blood flow, 5L/min;
these two numbers allow for the normal V/Q ratio to be 0.8; main purpose of this
ratio is to help determine what the problem is with why the patient isn¶t getting
enough O2 into the tissues²is it blood not moving or is it not enough air is moving
into the lungs?
V/Q mismatch- occurs when the ratio is not 0.8- a change in either the V or the Q
Low V/Q ratio- most common; means impaired ventilation so less than 4L/min of air
is moving into the lungs but the areas are still well supplied with blood; causes:
asthma, pulmonary edema, pneumonia; treatment: increase FIO2 (amount of inspired
oxygen²use O2 masks)
Very low V/Q ratio- when ventilation is completely blocked; causes: ARDS
(acute/adult respiratory distress syndrome²very high mortality rate); treatment: does
NOT respond to FIO2, may be able to use PEEP (mechanical) ventilation which
keeps the alveoli open
 High V/Q ratio- occurs when air is moving in successfully but there is an inadequate
blood supply to pick up the O2; causes: pulmonary embolus (clot caught in lung
capillary and prevents blood from flowing to distal areas); diagnosed by V/Q scan
(nuclear diagnostic test that helps identify pulmonary embolisms by giving good
reading of V/Q ratio

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airway obstruction is caused by chronic inflammation of major
and minor airways; same restriction as in emphysema so CO2 cannot be released
from the lungs; edema of airways and lung tissue; no problems with recoil,
hyperplasia of goblet cells (cells that produce mucus= increase in mucus); prolong
smoker, blue bloater (cyanotic especially around lips), excessive bronchial secretions,
mismatch of V/Q; don¶t compensate by increasing ventilation, lots of mucus and
edema; profusion not affected, ventilation affected; chronic cough and bronchosplasm
  
 when the elasticity in the lungs is lost; alveoli should
be able to expand and then go back to normal size but when the elasticity dies it has
the effect of an over inflated balloon²there is a permanent enlargement of the air
spaces and the alveolar wall along with the capillary beds are destroyed; decrease in
surface area and gas effusion that can occur; loss of elasticity is caused by chronic
irritation of lungs results in the constant inflammatory response; in the inflammatory
response the body will break down elastin and that causes poor recoil and when the
balloon doesn¶t shrink back down like it should you¶re left with hyper inflation in
lung space and all this air is dead air (o2 is used up from it) and air that does have O2
in it cannot get into the lungs; contributing factors: smoking (most common);
deficiency of alpha-1 antitrypsin which is an enzyme that helps protect the recoil
factor (elasticity); prolong smoker; ³pink puffer´; pursed lips (comes from having to
actively blow out air); ³barrel chest´- compensation

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Pneumonia- inflammation of lungs and airways into the lungs (alveoli and
bronchioles); usually related to some type of infection; 6th leading cause of death in
the US²doesn¶t cause death in healthy people but does in those really old or really
young
Causes- viral or bacterial infection; community acquired vs. hospital acquired; has
high rates with bacteremia because infection in alveoli and alveoli is only a single cell
ayer thick separating blood stream from infection so that is not hard to penetrate and
bacteria can easily get through
Community- 40,000 deaths each year; streptococcus pneumoniae most common
cause, mycoplasma or ³walking´- not really that serious, do not have to be
hospitalized
Hospital- acquired 48 hours after admission; highest risk with intubated patients
(because you¶re immune system is already compromised); many strands that develop
in hospital setting are antibiotic resistant (because the patient is most likely already on
antibiotics and the infection is already surviving in that environment)
Pneumocystis Carinii Pneumonia- most common infection in AIDS; caused by a
protozoan so its different than bacterial or virus so it has to be treated differently
 Results of infection- acute respiratory failure, septicemia- infection in blood stream
symptoms lead to septic shock; septic shock- vascular system is supposed to be a
sterile place, bacteremia is when cultures are grown on your blood (not supposed to
happen) and this means that there is bacteria in the blood stream and an infection is
starting; if bacteremia starts showing symptoms then patient can become septicemia
(basically your blood is full of crap) and there is a very high mortality rate
Treatment- antibiotic therapy (ideal to have sputum so you can choose proper meds²
sputum is something you cough up from deep in the chest, have to be old enough to
do this and have to have enough to run tests on); hydration, nutritional support
(patients with pneumonia usually don¶t want to eat); mucolytics (³breaking up´);
respiratory rate can also get dangerously low; get blood cultures 1st and sputum
cultures 2nd; while waiting for cultures (cultures take 48 hours) set the patient on the
antibiotics you think will work and if they aren¶t getting any better then you use the
antibiotics that the culture indicates


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Hematopoiesis refers to blood formation. In the fetus blood cells are formed in
bone marrow, liver, and the spleen but in adults all blood cells are formed in the
bone marrow

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Leukemia- cancer of WBCs; bone marrow makes WBCs that do not mature correctly
and continue to reproduce themselves; generally characterized by huge numbers of
WBCs that are defective; normally cells reproduce only when there is enough space
for them to fit but with leukemia these cells do not respond with signals telling them
to stop reproducing even when there is not more space (bone marrow loses the ability
to say ³we have enough WBCs!´²no negative feedback!) because the bone marrow
is concerned with making WBC¶s it doesn¶t make RBCs and platelets like its
supposed to be; blood becomes viscous with WBCs; become immune deficient; they
don¶t function like mature leukocytes²don¶t phagocytize; symptoms: fatigue
(decreased O2 caarrying capacity of RBC), palor (loss of color in face), weight loss,
repeated infections (decreased immune response), easy bruising (decreased platelet
count), nosebleed, hemorrhage, CNS involvement (leukostasis²can cause stasis in
the bloodstream); treatment- chemotherapy, irradiation (radiate the bone marrow to
keep it from making any more WBC), bone marrow transplant once other marrow is
killed off; testing of bone marrow is used to confirm diagnosis; bone marrow is given
through IV and those cells find their way into bone marrow (all fatty parts of marrow
are filtered out and its only hemopoietic cells are in the IV); killing off all WBCs can
affect electrolytes and some patients go on short term dialysis; can become acidotic


 



 1
 
 

0A decrease in circulating platelets. 100,000
asymptomatic; 50,000 ecchymosis/prolonged bleeding; 30,000 petechiae; 20,000
mucosal, deep tissue, intracranial bleeding
Immune-mediated platelet destruction within the RES.
May follow a viral infection
Platelet count less that 20,000
Bone marrow crowded with megakaryocytes( bone marrow cells).
Usually a spontaneous recovery.

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Intrinsic coagulation- injury to vessel itself; inside of the vessel is exposed; slow;
HEPARIN- run laboratory test aPTT- elevated in patients receiving heparin; antidote:
protamine sulfate- if we give too much heparin this helps to increase the intrinsic
pathway; in patient- shot
Extrinsic coagulation- injured tissue releases tissue thromboplastic which interacts
with Factor VII to directly activate Factor X; faster; generally if the tissue is damaged
the vessel is damaged too; COUMADIN- run laboratory test PT/INR; normal:1-2, on
Coumadin 2-3, 5-10; if levels get too high give antidote of Vitamin K; outpatient-
long term


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BodyrVena Cavarempties into R AtriumrTricuspid ValverR VentriclerPulmonic
ValverPulmonary ArteryrLungs (pulmonary vascular) r picks up O2r Pulmonary Veinr
L Atriumr Mitral Valver L Ventricler Aortar Body



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$Death to part of the myocardium. Myocardial cells begin to die
about 20 minutes after the blood flow is cut off
What happens- body is trying to deal with the necrotic tissue so within about 24 hours
leukocytes get to damaged tissue and release enzymes and also a hormone that is
released causes an increase in blood sugar which causes an increase in insulin within
about 1,2 weeks and then collagen forms and then scar tissue forms at about the 6
week mark
Manifestations/Symptoms- pain that varies with intensity and location (women
complain more about GI issues than chest pain); dyspnea (difficulty breathing²
elderly complain more about this than pain); nausea, vomiting, epigastric pain;
fatigue and weakness esp in limbs; tachycardia (SV is going down to HR increases to
compensate CO); anxiety, restlessness, feelings of doom (because low O2); skin is
pale, cool, moist/diaphoretic; dysrhythmias (disruption of rhythm of heart²why most
people with MI¶s die)
Dx- based on S/S; EKG; biggest clue is the serum cardiac markers (measures
enzymes released by dying tissue²the only problem is that these take a little while to
 show up); use lab test like ESR, elevated creatine kinase (CK), elevated LDH,
troponin, LDH2 >LDH1
Tx- thrombolytic agents, bed rest (to decrease the demands of the heart), pain relief,
vasodilation (watch out for dilating vessels too much!), O2 so that the blood that does
get through to the tissues is oxygenated, beta blockers, diet, stool softeners (avoid
vagal nerve stimulation which decreases HR)
Complications- ventricular wall is weakened, decrease in CO, dysrhythmias, rupture,
death within 1 hr of MI, ventricular fibrillations
Risk Factors- older than 65, previous angina or MI, hypotension, cardiogenic shock,
systolic htn

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 (lower) ± inflammation of the bladder; risk factors²female, sexual activity,
pregnancy, indwelling catheters, diabetes mellitus, prostatitis neuromuscular
disorders; manifestations²frequency, urgency, dysuria, suprapubic and lower back
pain; symptoms²kids: fever only, vomiting, irritability, elderly: personality changes,
dementia; treatment²antibiotics, water, cranberry juice, prevention (frequent
voiding, post-coital voiding)
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(upper)²infection of renal pelvis and interstitum; caused by
advancing UTI¶s, vesicoureteral reflux; usually only one kidney is involved; acute
manifestations²V
, chills, myalgia, flank pain, nausea, vomiting, frequency,
urgency, tenderness at costovertebral angle; chronic manifestations²chronic
inflammation of renal interstitum, dialated or atrophic renal rubules, casts, scarring of
interstitium and renal tubules, atrophic kidney; diagnosis: U/A, IVP, ultrasound


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3 Classifications of Shock
Hypovolemic- most common; absolute loss of blood (loss of blood from vascular
space) 
Cardiogenic- heart loses ability to pump; no blood is lost but the pressure behind
it is
Distributive-widespread vasodilation; relative loss of blood (normovolemic);
there is bad distribution of the blood that is in circulation because of the
vasodilation
Anaphylactic- vasodilation caused by release of histamines signal smooth
muscle cells on the blood vessel walls to relax
Neurogenic- SNS is responsible for vasoconstriction and neurogenic shock
causes the SNS to lose tone and therefore vasodilation occurs
Septic-vasodilation caused by toxins that are released by bacteria

More detail on shock«

Hypovolemic
Usually a 15-20% blood loss; blood loss creates a low blood vol rresults in low venous
return r results in low COrresults in poor tissue perfusionrresults in cell death
Causes- hemorrhage, internal bleeding (when blood moves into the 3rd spacing
and is no longer in the blood vessels), AGE
Symptoms- tachycardia (body trying to compensate for decrease CO by
increasing HR), low UOP (urinary output²body is dehydrated), weakening
pulse; hct/hgb levels vary
Compensation- SNS increasing HR to increase CO; blood shunted away from
abdomen and given to brain and heart; fluid is taken from interstitum (fluid
around tissue cells) and put into cells; kidneys retain H20 and NaCl (BP); angio-
aldosterone system triggered
Nursing Intervention- check vital signs²as heart rate slows body is going give up
on compensation; hct/hgb levels; blood gas levels (looking for signs of acidosis)
Tx- goal is to maintain BP- push fluids (IV, whole blood, crystalloids, colloids);
MAST (where they put pressure cuffs on the legs to try to circulate the blood back
to the heart); raise legs; O2; vasoconstrictors and dopamine
Cardiogenic
Heart loses ability to pump which causes a decrease in CO
Causes- some sort of infarction or ischemia (most common is MI); structural ;
dysrhythmias
Symptoms- tachycardia when body is compensating but as body loses ability to
compensate bachycardia sets in; decrease in UOP
Tx- treat the underlying cause (MI, dysrhythmia, etc); positive inotropes (increase
the contractility of the heart); increase volume (to increase BP even though the
volume would be adequate if the heart were pumping normally); O2
Anaphylactic
Mast cells are degranulated and histamine is released. Rule to remember: what
happens in lungs and blood is opposites. So, if blood vessels are being dilated,
bronchioles are being constricted.
Causes- immediate IgE hypersensitivity reaction; foods, dyes, latex, drugs,
venom, environmental agents, biological agents, etc
Symptoms- bronchoconstriction (wheezing), laryngeal edema/angioedema (face
and neck), tachycardia, pruritis (pus like fluid coming from any sort of skin
lesion), erythema (redness of skin), urticaria (whelps), anxiety, apprehension,
decrease LOC, hives
Tx- remove antigen, intubation, O2, ventilator, epi-pen, Benadryl, corticosteroids
Neurogenic
Loss of SNS tone, aka spinal shock
Causes- most common cause is a spinal cord injury above T6; also caused by
spinal anesthesia (epidural), drug OD, severe emotional stress (mercy dr when
wife died), pain
Compensation- can¶t increase HR like you do with other types of shock because
the HR increase is related to SNS control so compensation is dependent on the
types of medication we can administer to cause vasoconstriction and increase in
HR
 What happens- SNS tone is lost, vasodilation, baroreceptors are inhibited (they
sense BP changes), decrease in afteloadrdecrease in preloadrdecrease in SV and
CO
Symptoms- BRADYCARDIA (only kind of shock at doesn¶t have tachycardia);
there is a transition stage so not as immediately threatening as some other types of
shock
Tx- give fluids to treat relative hypovolemia (increase blood volr BP); positive
inotropes to treat low BP (increase contractility of LV); O2, deep breathing, clean
the airway to treat hypoxia; pace-makers or atropine to treat bradycardia
Septic
Widespread infection; most common in people who are already
immunocompromised; 40-60% mortality rate
Compensation- if you¶re healthy and you have bacteria in your blood stream
(even though it¶s not supposed to be there) you can deal with it but if your
immune system is already not working like it is supposed to then the bacteria able
to reproduce and go crazy!
What happens- its triggered by some sort of infecting agent that releases
endotoxinsr cytokines are released and inflammatory response startsr this causes
lots of damage to endothelium the microvascular arearallows proteins and fluids
to escape from the vascular spacer hyotensionrpoor perfusion OR widespread
clotting
Symptoms- either high or low temp; high HR, RR, WBC; low BP; low UOP
(because of decreased blood flow to the kidneys); CNS changes
Warm Phase- aka hyperdynamic phase; preload (venous return) falls so HR
increases (to try to increase CO); PP widens; vasodilation causes skin to be warm
and pink; In the warm phase the body is still compensating
Cold Phase- hypodynamic; compensation mechanisms are failing; heart muscle is
starting to die so ventricles are failing to pump blood and this results in ischemia,
acidosis, and an increase in afterload; skin becomes cold and clammy and has a
mottled (spotted) appearance; HR increases but SV and CO still fall



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