exam 2 Flashcards
Essential versus secondary HTN; linked to a disease, sustain incre. Pressure or a complex multigenic?
Essential only sustains incre. P (140/90) and complex multigenic disorder
Secondary is only linked to a dis.
Which multigenic disorders help causes essential HTN
Environmental(stress, obese, smoke, physical attack and increase salt) and Genetic (genetically affecting Na+/fluid reabsorb in kidney)
which disease are linked secondary HTN?
renal dysfunction, endocrine dysfunction cardiac and Neruon
BP equation
CO(Peripheral resistance)
Types of arteriosclerosis
hyaline and hyperplastic
hyaline arteriosclerosis
Narrow lumen: protein deposits=increase sm. eosinophil
Assoc.: Benign hypertension
Damages endoth. yes b/c increase P. and plasma protein leak
hyperplastic arteriosclerosis
Narrow Lumen: onion skin (incre. layer of smo. muscle BsM)
Assoc: severe hypertension
damage endoth.: NO
Is Atherosclerosis a type of arteriosclerosis
yes
what disease is assoc. w/ atheroma
Atherosclerosis
Atherosclerotic plaque
AKA atheroma
Fibrous cap w/ lipid core
More stable=increase fibrous cap and less lipid
-stop thrombus
Lesion w/in Tunica intima=lumen pushed inward
Basic pathogenesis of Atheroma
Endothelial cell dysfunction
formation of atherosclerosis plaque
T cells-MAC interaction
Fracture of the plaque and thrombosis
endothelial cell dysfunction (atheromas)
OCCUR via hemodynamic distrub. or hypercholesterolemia
-Plaque that only form w/in intact endoth. to cause dysfunctional endoth.
LDL oxidize by excess ROS
Fatty streak b/c foamy cell
hypercholesterolemia
Increase LDL while decre. HDL (or abnormal lipoprotein)
Chronic hyperlipidemia
-LDL Accum.=damage T. intima
-MAC cnt remove debris and form foamy cells
Foamy cells directly attack endoth. cells
LDL oxidize by excess ROS
Directly damage endoth. cells Sp. recep. allow MAC digest LDL -incre. accum=foamy cells Activate cytokine/GF/chemokin secretion -monocyte recruit MAC relase ROS to incre. ROS -tissue injury and decre. NO which makes it difficult remove LDL
Does a fatty streak b/c have a fibrous cap?
no fibrous cap
Fibrous cap (atheroma)
Cytokine released during inflammation rxn induce sm. muscle prolif. and ECM prod.
-from intima–>lumen
-sm. muscle cell–>endoth.
Fib. cap form and coer fatty streak
ROS and cytokine cont’ to produce oxidize LDL
T-cell MAC interaction/cell migration
Dysfunction endoth.=adhesive molec.
-leukocyte/Tcell migrate
Via chemokines w/in intima
T cell=chronic inflam.(relase inflamm. cytokine)
Thrombosis(atheroma)
Frag. of plaq. Damage endoth. rovide focal pt. for platelet bind and activate accum platelet producing clots -BV microvess. -inflamm med.
types of MI cuases ischemic heart disease
Necrotic damage to myocardium Biochem changes (incre. lactate and decre. ATP) Necrosis=1st 30min. (reverseible) 12 hrs. (lost)
permeant or temporary occlusions impact myocardiocyte
both
cardiac vascular disease
Hypertension
Atherosclerosis
heart disease
Myocardial infarction Cardiac hypertrophy Conduction disorder s Myocarditis Carcinoid syndrome
Hematopathology
Erythrocytes=anemia
Platelets=thrombocytopenia
Leukocytes=neutropenia
what type of cardiac dis.=ischemic heart dis.
Myocardial infarction
MC of myocardiam ischemia
Decrease Perfusion=increasing need
Affecting E production/Nutrient availability and removing waste
Can necrotic damage occur in myocardial infarction to the myocardium?
yes
Reversible (1st 30min.) and irreversible(12 hrs.)
can see troponin I and CK-MB
Myoglobin is not specific
Which Biochem. changes occur in MI?
increase in lactate and decrease in ATP
why does injury still occur after reperfusion tx?
before tx.=incre. glycolysisi which increase lactic acid–>increase stress and ROS
-this means there is a decrease in anti-oxid.
after perfusion=cells need time to catch up to crease anti-oxidation
salvage
degree to manage the cells that did not die
Is post-ischemic ventricular dysfunction reversible?
NO
2 types of infarction occur in ischemic reperfusion injury?
Hemorrhagic infarction
Microscopic infarction
-hem.
-contraction band=hypereosinophilic, cross-striation, due to Ca2+ influx (ischemia)
Causes of cardiac hypertrophy?
Increase. wrkload=incre. BP b/c moving incre. vol. which damage wall
Increase number of sarcomeres in myocardiocytes
MI
cardiac hypertrophy effects
Incre. heart size/mass
Incre. prot. synth.=heart fail, arrhythmia and neur/hormal stim. `
conduction disorder
Arrythmia
2 types of arrythmia
Tachycardia=classified by QRS
-wide=supraventricular w/ conductance issues
-narrow=supraventricular (AV node) w/ atrial fib/flutter or sinus tachy
Bradycardia
-decre. SA node activity
slower pacemaker for contraction
cause=age, drug(Ca2+ channel blocker, beta-blocker),
sleep, fainting (vagus N. hypertension)
-block conduction=link to dis. and ~ cuases as above
define myocarditis
heart inflammation infection
MC of myocarditis
viral infection–>coxsockie A/B and Enterovirus
what type of non-infections causes myocarditis?
autoimmune/drug hypersent.
is carcinoid syndrome a cardiac dis.?
yes
what does the hormones cause in the in carcinoid synd. cancer?
fibrotic lesion
thick endocardium
what type of disorder is considered anemia
Erythrocyte disorder
does anemia increase or decr. RBC
decre. RBC
Causes of anemia
lost blood, hemolysis, decre. erythropoiesis, or sickle cell
types of bleeding causes iron def. anemia
mensuration, GI bleed, and assoc. w/ prego.
iron sources
Dietary absorption in intestines
Iron recycled from aged RBC by MAC in spleen
-MAC=brsk dwn RBC from Hb
S/S of decre. Hb synth. and what type of anemia is it assoc. with
Iron def. anemia
Wkness
Fatigue
Malaise
decre. Hb. Synth. s/s and assoc. anemia
Iron def. Anemia Rbc=decre. Hb content Lower O2 level induce erythrop. Stim. BnM=Platellets RBC become microcytic -smaller/varied size -hypochromic (decre. color b/c Hb) -varied shape
Pernicious anemia also known as
megaloblastic anemia
type of vitamin needed for pernicious
Vit. B12 for thyamidine synth.
-failure of DNA synth. affect hematopoiesis
what does the blood look like histologically for megablastic anemia
megaloblastic=abnormal lrg blood cells and precursors
what does the PMN look like in megablastic anemia
hypersegmented
What part of the stomach is affected in megaloblastic anemia and why?
fundic glands b/c of absorption of vit. B12 for intrinsic factors
-parietal cells have fundic glands
what affect does autoimmune attack on gastric mucosa do within megaloblastic anemia?
Parietal cells are lost(primar) AntBd blocks (secondary) -binding IF -binding to Recp. -H+ pump
What type of disorder is thrombocytopenia and function?
Platelet disorder and causes a decrease in platelet
Causes of Thrombocytopenia
decrease in production -Vit. B12 def and hereditary decrease survivial -immune-med./drug Associa. immune thrombocytopenia -thrombotic thrombocytopenia purpura
Immune mediated/drug assoc. immune thrombocytopneia
Drug(quinine, quinidine, vancomycin)
-bind platele glycoprotein
-create antGN recog. by antiBD
Heprin I(direct) or II(venous/arterial thrombotic)
which heprin disorder causes thrombocytopenia
Heprin-induced Thrombocytopenia (HIT)
- aggregation=thrombosis(low risk w/ low MW heparin)
- clots in lrg arteries=vascular insuf., DVT, emboli (cuases fatal lung dis.)
def. of what in thrombotic thromboccyhtopenic purpura?
Def. ADAMTs13 def.=abnormal vwf complex adering to platelets
- thrombotic clots in microcirc.
- accum. of clots damages endoth.
types of symp. in thrombocytopenic purpura
Episodic
- unknown factors contirb.
- hemolytic anemia b/c shear stress on RBC
type of dis. is leukopenia and what does it caus
leukocyte dis.
lack of WBC=agranulocytosis
-depletion of PMN
-incre. bact/fungal infection
2 mech. in leukopenia
Infective/inhib. granulopiesis
incre. removal/destruction of granulocyte from blood
types of Neutropenia
Absolute neutropenia
Agranulocytosis (granulocyte def.)
Cyclic neutropenia
Infective/inhib. granulopiesis
Inhib. hematopoietic stem cel -accompanied by stem cells :accompanied by anemia/thrombocytopenia Detective precursors due in marrow -megaloblastic anemia Congenital disorder -inherit detect prevent proper differentiation Drug exposure
type of drug exposure in leukopenia
Chemotherapeutic agent
-alkylating agent/anti-metabolites
-predictable cuases, does depend destruction of hemeatopotic cause
-general effect=anemia and thrombocytopenia
Idiosyncratic effect of many drugs
-toxic effect on precursors =phenothiazines(chlorpromazones)
-AntBD-induced destruction of mature leukoctye=certain sulfonamides
PMN Removal
Immunologic -idiopathic -assoc. w/ immune dis. (SLE) -drug exposure splenomegaly -incre. sequestion -anemia/thrombocytopenia Incre use by bact, fungal, rickett. infect.
types of neutropenia
Absolute neutropenia
Agranulocytosis (granulocyte def.)
cyclic neutorpenia
genetic onset for cyclic neutropenia
childhood onset
- rare/spontaneous mutation in adults
- autosomal dominant
mutation in cyclic neutropenia
Neutrophil elastase
- w/in primary azurophilic granules of PMN and monocyte
- mutation is excessively inhib causing excessive trough in production
PMN oscillation
PMN in blood are normal
Mature explains opposing cyclicity of peripheral PMN and monocyte
PMN elastase inhib. myeloblastic diff.
PMN hematopoiesis
2 wks to mature peripheral survival=12 hrs. precursors in marrow PMN productions occurs in waves -negative feedback inhib. PMN production -"oscillations"
Non-specific lung dis.
Clear=cough/mucociliary escalator
-beat up mucus(anything attach to it (dust particles)
Secretions=tracheobronchial(mucus), Alveolar(surfactant), cellular component (RBC)
Cellular defense=not immune but +cytok.
-non-phagocytic (epith.)
-phagocytic (alveolar Mac)
:attack anything =nonspecific attack
Biochem. defense
-proteinase inhib.
-antioxidant(protect lung w/ inhalation sm. etc.)
-ej=transferrin, lactoferrin, glutathione albumin
Specific lung defense
AntiBD med -secretory IgA(meningitis) \:complement/opsonization \:Serum Ig AntGn presentation to lymphocytes -MAC and monocyte/DC/Epith. cells Cell mediated(T-lymphocyte-dependent) immunologic Response -Cytokine mediated -direct cellular cytoxicity Non-lympho cell immune reponse -mast cell/eosinophil dependent
Infectious Rhinitis, sinusitis, pharyngitis/tonsillitis type of respiratory tract infection?
acute upper resp.
Pathogens infectious rhinitis
Rhinoviruses
Others=flu, coronavirus, adenoviruses, enterovirus
potential complication of infectious rhinitis
Bact. infect. b/c swelling, fluid accum
Otitis media
Sinus infection sinusitis
swelling and fluid for infections rhinitis
congestion and discharge
type of infections in sinusitis
bacterial and viral infections
complications in sinusitis
Infected neighboring structures(eye, skull, brain)
Usually discomfort
For sinusitis the impairment of sinus drainage causes
Mucosal edema to inflammation
Obstruction might complete blockages
-result in accum. of infected mucus(suppurative exudate)=empyema
Acute–>chronic
viral or bacterial infections in pharyngitis/tosilitis
viral
S/s of pharyngitis/Tonsillitis
redness, edema, enlargment of tonsils/lymph nodes
Acute upper resp. tract infection
Infectious Rhinitis
Sinusitis
Pharyngitis/Tonsilitis
Define Atelectasis
Colapse prev. inflated lung 3 types -reabsorb(block airway) -compression (accum. in pleural space) -contraction (fibrosis)
Define S/S atelectasis
hypoxemia
increase infection
reversible (except in fibrosis)
neonatal atelectasis
Incomplete expansion
Vascular resp. dis.
Pulmonary embolism Pulmonary Infarction Pulmonary HTN Goodpasture Syndrome Pulmonary Edema
Pulmonary obstructive dis.
Emphysema
Asthma
Cystic Fibrosis
Pulmonary Restrictive dis.
Pneumoconiosis Granulomatous disorder(Hypersensitivity Pneumonitis) Sarcoidosis
Pleural dis.
Pleural effusion
pneumothorax
Pulmonary Embolism and caused by
Blocks lung vessel
casued by=blood clot(MC), air bubble, fat deposits and other debris
Blockage of pulmonary embolism
ischemia downstream and incre. P. upstream
consequences of pulmonary embolism
pulmonary infarction
pulmonary infarctions consequences
Large block=quick kill -no lung patho. -incre. heart P. damage(Rt side heart failure=Cor pulmonale) Signals to body control syst. to lower BP -decre. CO Lung cn collapse b/c -lack of surfactant -reduce movement in response to pain
Tx of pulmonary infarction
Anticoagulant (heparin)
Thrombolytic (incre. hemm and should only be in hospital)
Pulmonary HTN-vascular changes
Medial hypertrophy -muscular and elastic arteries in lung -vital fibrosis in T. intima Plexiform lesion -advanced hypertension -Tuft cap. -dilated thin-walled arteries
Pulmonary HTN-pathogenesis
Chronic obstructive/ interstitial lung dis. (both incre. pulmonary BP) -destroy alveolar cap. -incre. pulmonary vascular R Heart dis. -lft side damage goes back to lung arteries Recurrent emboli=incre. upstream P. Obstructive sleep Apnea Idiopathic=80% gene
Pulmonary HTN S/S
Detectable only when advanced
Dyspnea and fatique
Chest pain (rare)
Severe resp. distress and cyanosis (end stage)
Pulmonary HTN-Tx
Secondary dis.=Primary tx
Autoimmune/refractory=vasodilaters
Lung transplant
Goodpasture synd. Criteria
Pulmonary hemorrhage syndrome
AutoBD against type IV collagen(autoimmune dis.)
-Type IV collagen is in BsM (vasculature)
Kid. and lung Injury
-only affects kid=anti-glomerular BsM dis.
Inflam. mediated destruction of alveolar BsM
-environm. damage=expose deeply embedded protein epitopes(deep in memb.)
-epitope recog. by antBD
-genetic predeposition linked to certain HLA(complex dis.)
GPS pathology-S/S
Hemoptysis -Xray=focal consolidation -death=renal involvement -tx: plasmapheresis to remove autantBD w/ immunosuppression Lung=red/brown consolidations
GPS-histology
Intra-alveolar hemorrhage
Focal necrosis in alveolar walls
Mac accum. heme
GPS-late stages
Septal fibrosis (thickened)
Type II pneumocyte hypertrophy
Blood in alveolar spaces
Pulmonary edema and caused by
Leakage of fluid into. alveolar space Hemodynamic disturbances -incre. P. (MC) -decre. P Increased cap. permeability -damage to microvascularture -infection, gas inhalation, liq. aspiration -drug/chem. -shock, trauma, radiation transfusion
what type of heart failure causes pulmonary edema?
congestive heart failure
microvascular injury PULMONARY edema
Damage to cap. bed -primary to vasc. endoth. cells OR to alveolar sq. pneumocytes Leakage of fluid and protein -interstitial space-->restrictive dis. -alveoli-->pneumonia Acute Resp. distress syndrome(ARDS) -b/c diffuse edema
ARDS=severe acute lung injury
Abrupt onset of hypoxemia
Bilateral pulmonary infiltrates
No cardiac failure
ARDS multiple causes
Mech. trauma Near drowning Sepsis(bact.) Barbituates overdose Gastric aspiration
ARDS-inflammatory dis. that produce diffuse alveolar damage (DAD)
Incre. pulmonary vascular permeability
Edema
Epith. cell death (type 1 pneumocyte)
ARDS pathogenesis
Stress
Initiate by MAC
-endoth.
-pneumocytes
PMN invade and debris accum(hylinzation=hyaline memb.)
Healing starts when MAC produces TGFB and PDG(activate fibroblast)
ARDS causes which pneumocytes loses?
sq. (I)
-incre. permeability (alveolar wall to blood and immune cell)
Cuboidal(II)
-incre. surfactant
-alveolar collapse
ARDS S/S
Lung=heavy and filled w/ fluid (wet)
Stiff lungs=lost surfactant
Dyspnea/tachypnea
Cyanosis/Hypoxemia
ARDS-tx
Oxygen
Mech. ventilation
Underlying causes (sepsis)
where does the fluid come from for pleural effusion?
resorbed(min. amount)
drained (chest tube)
Accum. of pleural fluid is caused by pleural effusion?
Increased hydrostatic P. (CHF) Incr. vascular permeability (pneumonia) Decr. Osmotic P. (renal dis.) Incr. intrapleural Neg. P. (atelectasis) decreased lymphatic Drainage
Pneumothorax is gas/air or fluid?
air/gas
Causes of pneumothorax?
Spontaneous -Idiopathic -Rupture of an alveolus/abcess cavity Traumatic -injury to the chest wall that allows air in Tension Pneumothorax -flap valve=allow air in but not expire -accum of air can cuase compression of structure
S/s pneumothorax
resp. distress(due to compression, collapse, atelectasis of lung)
Pneumoconioses that being a fibrosing disorders?
foreign particles that cnt be eliminated
dis. under pneumoconioses?
Coal workers pneumoconiosis (CWP)
Silicosis
Anthracosis
Asbestosis
Coalworker pneumoconioses aka
black lung
CWP can be complicated
yes and progressive massive fibrosis
S/S of CWP
Pulmonary dysfunction
Pulmonary hypertension
Cor Pulmonale
Silicosis
Incr. susceptibility to TB
2x risk of lung cancer
Asbestosis
Dyspnea
Incr. risk of lung cancer and mesothelioma
Anthracosis
Innoculos CWP
w/in urban dweller and tobacos smoke
Which disorder is hypersensitivity pneumonia?
granulomatous disorder(AKA=allergic alveolitis)
allergic alveolitis histology
Patchy infiltrates in interstitium
Loose granuloma w/o necrosis
Cell lymphocyte, plasma cells epith alveoli MAC
What does inflamm. alveoli in hypersensitvity cause?
decre. diffusion capacity, lung compliance and total lung vol.
Acute attack in granulomatous disorders. S/S
Result=inhale antGN dust
Fever
Dyspnea/cough
Leukocytosis(incre. WBC)
Chronic exposure in granulomatous disroders
progressive resp. failure
Dyspnea/cyanosis
Decre. lung capacity/complience
Which dis. is a granulomatous restrictive dis.
Sarcoidosis
Organs affected in sarcoidosis
Lung Spleen/liver BnM Skin lesion Eyes and muscle
What is etiology in Sarcoidosis
unknown
Charact. in Sarcoidosis
non-necrotizing granuloma
Freq. giant cells
Chromic=scar
Sarcoidosis-lung changes
Granuloma w/in lymphatics
-around bronchi/BV in alveoli and pleura
Lung lesion might heal=fibrotic/hylinized
-interstitial fibrosis
Lymph node involv MC
-hilar and mediastinal
-develop calcification
-tonsils are freq. affected
Clinical course=location, size, and number of granulomas
-lung=progressive fibrosisi and cor pulmonale
-spont. remission/steriod therapy
Emphysema can occur w/ which dis.
Chronic bronchitis and COPD
What occurs in the smaller airspaces in COPD
Permanent enlarged
- destroy the smaller air spaces walls
- no fibrosis
patterns of emphysema
Dis. in acinuc
Assoc. w/ tobacco smoke inhale
Major s/s=dypnea (trouble w/ reg. breathing)
Emphysema-destruction of Pathogenesis
Direct damage from toxing(tobacco smoke/alveolar walls)
Inflam. response
-MAC/epith. cell response release leukotrienese, IL-8, TNF
-Chemotaxis, inflam., structural changes (act as GF)
Protease relased from cell
-def. in protease inhib.
:alpha-1 anti-trypsin inhib. elastase
:genetic component to emphysema
-damage CT elastic fibers
Infection =not a major role=exacerbate inflamm. damage
Asthma a complex gen. dis.?
Yes
Genetic w/ provoked of Adenosin/exercise/ For. particles
Charac. of Asthma
Episodic bronchoconstric.
Bronchial wall inflam.
Incr. mucus secretion
Asthma types
Atopic Classic hypersensitivity rxn IgE
Drug Induced(Asprin/Nsaids) affecting balance of COX acitvity
Occupational
how can asthma be chronic inflam. airway dis.?
recurrent episodes=wheez, breathlessness, chest tight, cough
Asthma IMMUNO. CELL triggers
B/T lympohcytes, IgE, Mast and Eosinophils
Asthma and mast cells
Sm. muscle constriction
Incre. mucus secretion
Vasodilation
-Endoth. Leakage and local edema
Asthma and epith./cytokines
leukotrienes
prostaglandins
Asthma and eosinophil
Major basic protein -AKA prostoglycan 2(PRG2) -Cellular toxin (bact. mammalian) -Possible by disording cell memb. Eosinophil cationic pain -AKA ribonuclease 3 -bind to cell suface heparan sulfate proteoglycan (endocytosis) -Apoptosisi via casp. 8 -Necrosis depend
Cystic fibrosis- viscus mucus cuases
Obstruct passages
Glandular tissue
Digestive tract causing block
cystic fibrosis and channel mutation cuases
Chronic lung dis. -incre. infection risk -chornic bronchitis Pancreatic insuf. -steatorrhea(plug pancreatic duct) -malnutrition Hepatic necrosis Interstial obstruction Male infert.
CFTR
Cystic fibrosisi conductance regulator
Impaired secretion of Cl- ion impair w/ Na secretion
-no ionic balance
-decre. osmosis
Pneumonia infections
bact. Virus, myoplasm or fungi
- lymphatic infiltrate in alveoli
- produce pulmonary edema
pneumonia causes
Suppress cough reflex/inhib.
-coma, anesthesia, neuromuscular disorder
Mucociliary apparatus damage
-cig. smoke, hot gas, viral, genetic
Secretion Accum.
-cystic fibrosis, bronchial obstrusction
Decre. MAC activity
-alcohol, tobacco, anoxia and O2 intox. (not enought or too much)
Edema/cong.
Aspiration Pneumonia
Necrotizing Pneum. -often fatal -Chem :low pH of gastric Acid damaging airway/alveoli :tissue necrosis/ inflam. -Bact. :oral flowa-->more areobes than anerobes :inflam. Microaspiration -need pre-existing dis.(asthma, interstial fibrosis or transplant regjection) -MC w/ GERD -may exacterbate w/
Typical vs. Atypical pneumonia
bact.=typical
virus=Atypical
Bact. Pneumonia
Bronchopnemonia -opaque spot -patchy consolidation -distract area of acute inflamm. Lobar -opaque lobe -lung consolidaiton (hepitzaiton) -fibrin/infection fill alveoli
Clinical response of bact. Pneumonia
Rapid onset=fever, chils, cough/muchs(infection)
Fibrinosuppurative pleuritis
-lung well=PMN infiltrates, fibrin aggregates
-Pleuritic pain/pleural friction rub(lung rub parietal)
acute pneumonia in stages
stg. 1=infection Stg. 2=early red hepatizaiton -PMN infiltrate -Congestion of septal cap. Stg 3.=gray hepatizaiton -alveolar exudate in air spaces Stg 4=resolution -fibromyxoid masses -MAC fibroblasts
Viral Pneumonia
Corona virus from china
Transmission via resp. secretion
Incubation 2-10dys
Viral pnuemonia aka
Server acute resp. syndrom=SARS
S/S of viral pneumonia
Malasie Myalgia Dry cough Fever/chills Virus infect Pneumocytes
complication of Covid-19(SARS-CoV-2)
pneumonia/trouble breathing Organ fialure Heart prob. Acute resp. distress synd. Blood clot AKI addi. bact/viral infect.
Histoplasmosis-infection
w/ histoplasma capsulation
- demorphic fungi
- T-cell mediated response containing infection
Histoplasmosis-clinical
Acute pulm. infection
Chronic infect. (granulomatous)
Disseminated miliary dis. (millary lesion=mellet seed)
histoplasmosis-path.
MAC aggregate filled w/ yeast
Colonize by lymph node
Eventually granuloma w/ giant cells -develop fibrosis/calcification (lymphoma/leukemia)
Gross appearance=perihilar mass lesion
diff. tissue affected and function test for obst. vs. restric lung dis.
Obstructive -partia/complete obstruc -incre. R air flow :decre. lung inflam. -pulm. fuction test=decre foreced exp. vol. Restrictive -reduced parenchyma expansion -decre. total lung capacity -pulm. funciton test=decre. FEV and vital cap.
community acq. pneumonia
typical and atypical
hospital acqp. pneuonia
mechanical ventialaiton
aspiration pneumonia
Markedly debilitated pt./stroke vict.
Abnormal gag/swallowing reflex
chronic pneumonia
localized lesion
immunocomp. pt.
