BoD Exam I

interaction of epithelial cells w mesenchymal tissue including blood vessels

interaction of epithelial cells w mesenchymal tissue including blood vessels

gas exchange fxn of respiratory tract is achieved by:

• gas exchange

• nourishment of pulmonary structures

pulmonary blood serves 2 purposes

mechanical defense of airways

• Particles become entrapped in mucus and gases become dissolved in mucus

• Mucus is moved mechanically by beating cilia, sneezing and coughing, moved to the pharynx, then swallowed

broncho-alveolar junction

the most vulnerable area in respiratory system

BALT

makes Abs to inhaled Ags

IgA

Humoral immunity is based on ___ in upper airways

IgG

humoral immunity is based on ____ in lower airways

macrophages

main defense in alveoli

surfactants

important opsonins in alveoli

Ruminants, horses, pigs, & cats

spps w PIMs (pulmonary intravascular macrophages)

sneezing

induced by irritation of the uppermost respiratory tract

coughing

induced by irritation in the trachea and/or bronchi

congenital ciliary dyskinesia, environmental, infectious

3 main causes of ciliary dysfunction

scarring

result if the basement membrane is damaged in URT

repair

if the basement membrane is intact, the ciliated epithelium will ___

goblet cell hyperplasia, fibrosis, squamous metaplasia

effects of chronic upper respiratory damage

Type I

Alveolar cells very vulnerable to damage

phagocytosis by kupffer cells and splenic macrophages

defense against blood-borne agents in dogs

phagocytosis by pulmonary intravascular macrophages

defense against blood-borne agents in ruminants, cats, pigs, & horses

atelectasis

collapse or incomplete expansion of alveoli (typically on margins)

congenital atelectasis

failure of lungs to expand at birth

acquired atelectasis

• Compression - pressure on lungs (air, fluid, viscera)

• Obstructive - alveoli distal to airway obstruction collapse as gas is gradually resorbed

emphysema

ruptured alveoli leading to trapping of air, trapped air may extend into the interstitium

epistaxis

blood may originate from within the nasal cavity or distal to the nasal cavity

aerogenous

• most common route

• leads to cranioventral distribution

• bacteria, mycoplasma, viruses, toxic gases, foreign particles

hematogenous

• common in septicemia and viremia

• leads to diffuse non-collapsing lung

• viruses, bacteria, and parasites

direct extension

penetrating injury, migrating airways, bites, esophageal rupture

rhinitis

inflammation of the nasal mucosa

• acute viral

• acute allergic

• acute bacterial

• foreign bodies

• chronic

causes of rhinitis

acute viral rhinitis/sinusitis

sero-mucoid, mild epithelial cell degeneration

• ex: “red nose”, malignant catarrhal fever, atopic rhinitis

acute allergic rhinitis/sinusitis

serous discharge (±mucus) - IgE, eosinophils, and mast cells

acute bacterial rhinitis/sinusitis

purulent to mucopurulent discharge, usually secondary to mucosal damage (viral, trauma, dental, dehorning)

• ex: murine respiratory mycoplasmosis, “snuffles” in rabbits

foreign body induced rhinitis

discharge is mucopurulent, often bloody

chronic rhinits

from progression of untreated acute disease, or fungal agents

• ex: nasal & nasopharyngeal polyps, chronic granulomatous rhinitis, sinonasal neoplasia

potential sequelae of sinusitis and rhinitis

• Bronchopneumonia and pulmonary abscesses

• Osteomyelitis and turbinate atrophy (atrophic rhinitis, pigs)

• Meningitis

• Otitis +/- vestibular syndrome and polyp formation

Equine Recurrent airway obstruction (COPD or "Heaves")

• Likely allergic

• Diffuse bronchiolitis

• Cough, tachypnea, expiratory dyspnea, exercise intolerance

• Wt loss & "HEAVE LINE" (bc atrophy of abd mm)

• Epithelial hyperplasia, mucus

atopic rhinitis

• Disease of swine

• Predisposing factors: infectious (bacteria +/- viral), environmental genetics, nutrition

• Bordetella bronchiseptica + Pasteurella multocida, type D

• Toxins from Pasteurella stimulate osteoclasts and inhibit osteoblasts => degeneration and remodeling of nasal turbinates (predisposed to bronchopneumonia)

• Don’t see scrolls!

nasal & nasopharyngeal polyps

• From chronic inflammation

• Composed of a myxomatous matrix, fibroplasia covered w nasal epithelium

• Control of inflammation will reduce size, but lesion is persistent

sinonasal neoplasia

• Most common in dogs

  • Most are malignant & are carcinoma or adenocarcinoma

  • Chondrosarcoma & other tumors sometimes occur

• Other spp

  • Squamous cell carcinomas - cat/horse

  • Retroviral enzootic nasal carcinoma - sheep

clinical signs of sinonasal disease

• Sneezing, foul odor, facial deformity, nasal discharge, noisy breathing, epistaxis, increased resp effort

• If coughing is a feature, then there is involvement of more proximal respiratory tract structures

clinical signs of disease of pharynx, larynx, guttural pouch, trachea

• Stridor, cough, ptyalism, changes in voice/vocalization, nasal discharge, inspiratory dyspnea and cyanosis, dysphagia, head/neck extension

  • Inspiratory stridor => airway obstruction above the glottis

  • Expiratory stridor => tracheal obstruction

brachycephalic airway syndrome

• Stenotic nares, elongated soft palate, everted laryngeal saccules & hypoplastic trachea

• Bulldogs & other brachycephalic breeds

• Laryngeal edema & saccule eversion is secondary to forceful respiration

• Stridor (& snoring)

• Exercise intolerance

• +/- dyspnea & cyanosis

diseases of the pharynx & larynx

"calf diphtheria”, “roaring” in horses

developmental anomalies

• Palatoschisis/cleft palate

• Choanal atresia

  • Usually seen in lamb

  • Commonly seen in camelids (obligate nasal breathers)

Guttural pouch TYMPANY

distention w fluid and gas

Guttural pouch EMPYEMA

distention w purulent exudate

Guttural pouch MYCOSIS

fungal necrotizing infxn (Aspergillus sp)

CAN HAVE ACUTE FATAL BLEEDING DUE TO EROSION OF CAROTID ARTERY

major potential consequence of guttural pouch mycosis

non-productive, honking cough

primary sign of Canine infectious tracheobronchitis ("Kennel Cough")

collapsing trachea

• Dorsal ligament gets loose

• Small breed dogs

• Dry, honking cough

• Dyspnea (worse w stress/exercise)

• +/- secondary pneumonia

pneumonia

inflammation of the lung

fibrin

sign of acute severe injury in alveolar response to pneumonia

cranioventral distribution

bronchopneumonia, injurious agent arrived via AIRWAYS (aerogenous)

origination of inflammation at the broncho-alveolar junction

hallmark of bronchopneumonia

bronchopneumonia

• Necrosis of type I pneumocytes

• Type II pneumocytes hyperplasia leading to epithelialization

• Recruitment of leukocytes & other exudes - type depends on cause and severity

predisposing factors for bronchopneumonia

• The site of deposition of small particles

• No mucociliary blanket - no alveolar macrophages

• Bottleneck of clearance from alveoli

Suppurative bronchopneumonia

• Obstructive - due to exudates

• Usually bilateral, cranioventral (lobar), lobular

• ACUTELY the lungs are swollen and consolidated (filled w exudate)

  • Exudate flood & fill bronchoalveolar ducts and adjacent alveoli

• May progress to healing w early & effective tx, potential for scarring

• May proceed to fibrosis or abscessation if no tx

• Necrosis & hemorrhage is common

  • If necrotic tissue is walled off by fibrous tissue, an abscess or necrotic sequestrum will result

FIBRINOUS bronchopneumonia

• Usually MORE severe (and more serious)

• Usually ACUTE to PERACUTE - hemorrhage, fibrin, necrosis

• Multiple coalescent lobules affected - LOBAR pattern

• "MARBLED" appearance of lung

• Prototypical example is SHIPPING FEVER IN CATTLE

• Can be caused by aspiration

• Secondary pleuritis common

• Necrosis and pulmonary sequestra also common

• COMPLETE RESOLUTION IS UNCOMMON

pleuropneumonia

common name for fibrinous bronchopneumonia

bronchiolitis fibrosa obliterans

adverse outcome of fibrinous bronchopneumonia

diffuse distribution

Interstitial pneumonia, injurious agent arrived HEMATOGENOUSLY, also pulmonary edema is diffuse

interstitial pneumonia

• TYPICALLY DIFFUSE, BUT CAN BE DORSOCAUDAL

• Aerogenous: primary EPITHELIAL damage

• Hematogenous: primary ENDOTHELIAL damage

• If you cut the lung and it looks like tuna

• Lung fails to collapse, rubbery to meaty texture

• In ACUTE disease there is edema and emphysema

• Chronic disease is characterized by fibrosis

dorsocaudal distribution

interstitial pneumonia, VERMINOUS (parasitic) pneumonia

multifocal distribution

most often EMBOLIC via the blood stream, can be via AIRWAYS, also common w granulomatous pneumonia

embolic pneumonia

• HALLMARK IS RANDOM MULTIFOCAL DISTRIBUTION

• Septic emboli lodge in pulmonary vessels, infxn spread into interstitium

• Most common sources

  • Hepatic abscesses

  • Infected jugular thrombus

  • Valvular endocarditis

Granulomatous Pneumonia

• CHARACTERIZED BY THE TYPE OF INFLAMMATORY RESPONSE (NOT PORTAL OF ENTRY OR SITE OF LESION)

• Well circumscribed, variable sized, firm nodules

• May be mineralized (caseous necrosis)

• Random distribution

• May be aerogenous or hematogenous

• THE MAIN DIFFERENTIAL IS NEOPLASIA

Causes of granulomatous pneumonia

• Fungi: Cryptococcus, Coccidioides, Histoplasma, Blastomyces

• Higher bacteria: Mycobacterium, Rhodococcus

• Foreign material: grass, ET tube, contrast media

• Migrating parasites

• FIP - granulomatous inflammation secondary to Ag-Ab complexes

Actinobacillus pleuropneumonia, aspiration pneumonia, hypostatic congestion (prolonged recumbency)

causes of irregular distributions on lungs

pulmonary hypertension

• Increased pulmonary vascular resistance

  • Vasoconstriction of pulmonary arteries

  • Vascular obstruction

  • Volume overload

• lead to congestion & edema

• If long standing, fibrosis can occur

• Almost all euths and natural deaths have this bc agonal breathing

• Increasingly common in fed cattle and chickens

• Cardiac disease: L heart failure, L to R shunts

• Lung disease: hypoxia from high altitude, pulmonary fibrosis

• Thromboembolism

• Hypervolemia: IV fluids, etc

Pulmonary edema

• May be inflammatory or cardiogenic

• Fluid accumulates in interstitium 1st

  • RESTICTS LUNG INFLATION

• Fluid in alveoli later - occurs abruptly

  • OBSTRUCTS VENTILATION

• Increased rate and depth of respiration

• Loud lung sounds initially - crackles

• W severe effects lung sounds may be diminished

Restrictive respiratory failure

• Anything that takes up space in chest cavity

• Lesions in pleural cavity, mediastinum, thoracic wall

  • Pleural effusion

    • Hydrothorax, Hemothorax, Pyothorax, Chylothorax

  • Pneumothorax

  • Masses

Obstructive respiratory failure

• Pathology that results in REDUCED VENTILATION of the lungs

• Can be caused by

  • Obstruction of movement of air in airways or alveoli

  • Reduced elasticity of the lung parenchyma

• RAPID, DEEP RESPIRATIONS => HYPOXIA, HYPERCAPNIA

• Obstruction of movement of air in airways or alveoli

  • EXUDATIVE PNEUMONIA - exudates fill alveoli (common w bronchopneumonia)

  • Pulmonary edema - when edema is in alveoli

  • Bronchitis or bronchiolitis - exudates, mucous, and hyperplastic epithelium obstruct airways

• Ex: Feline asthma

ARDS (acute respiratory distress syndrome)

• SYNDROME OCCURRING SECONDARY TO MANY OTHER DISEASE CONDITIONS

• Diffuse alveolar damage following

  • Sepsis, Burns, Pancreatitis, Major trauma/sx, Aspiration, Drugs, Inhaled toxins

diffuse damage to alveolar wall

basic lesion of ARDS

move sufficient volume of blood to all organs in the body

role of cardiovascular system

epicardium

outermost layer of cardiac wall

myocardium

thick muscular middle layer of cardiac wall

endocardium

innermost layer which is continuous w the tunica intima of the great vessels entering and leaving the heart

epicardium, myocardium, endocardium

3 layers of the the cardiac wall

SA node

node that has the most frequent rate of depolarization and is therefore dominant

mural & valvular endocardium, myocardium, pericardium

3 broad anatomic divisions of the heart

valvular insufficiency

failure to seal or close completely

valvular stenosis

narrowing, failure to open

Increased VOLUME loading during DIASTOLE (PRELOAD)

valvular insufficiency results in:

Increased SYSTOLIC workload characterized by increased PRESSURE load during contraction (AFTERLOAD)

valvular stenosis results in:

Vegetative ENDOCARDITIS

• More common lesion of myocardium

  • Bacteria seeded out on endothelium (cause ulcer=> clot)

    • Fibrin forms, leukocytes

      • Thickens valves, cause incompetency

• May result in embolism

• Scarring can distort valve leading to insufficiency or stenosis

• Gross lesion: ROUGH, YELLOW/TAN/GREY/RED, FRIABLE LESIONS ON VALVE, SOMETIMES ALSO MURAL ON VENTRICULAR WALL

• Histo lesion: fibrin, leucocytes, bacteria

• Pathogenesis: BACTEREMIA => endothelial injury/turbulence/hypercoagulability => bacterial adherence to valve, clot material forms => proliferative inflammatory lesions

ENDOCARDIOSIS

• common in dogs

  • Small or medium breed dogs

  • Males > females

• Degenerative thickening of the valve typically produces incompetency w regurg and leads to CHF

• Leads to incompetence

• Left AV valve is most commonly affected

• NOT febrile

• Gross lesion: THICK, SMOOTH, WHITE, OPAQUE NODULES

• Histopath lesion: myxomatous degeneration

• Regurgitation => L atrial dilation & ventricular dilation => ECCENTRIC hypertrophy

• LV dilation worsens due to decrease CO => increase RAS => increase blood volume which increases preload

• Can have tendon chordae rupture

responses of the myocardium to injury

myocardial infarction, change in mm mass or dimension, replacement fibrosis, dysrhythmia, dilated ventricular lumen accompanied by a nx to thin ventricular wall, increase in ventricular wall thickness or mass

Dilated ventricular lumen accompanied by a nx to thin ventricular wall

• Commonly reflects increased preload on the heart

• Due to AV or semilunar valvular insufficiency or a vascular shunt

• In the absence of an inciting cause, dilated cardiomyopathy should be considered

• Myocardial contractility diminishes

increase in ventricular wall thickness or mass (hypertrophy)

• Associated w increased afterload

• Due to stenotic valve, shunt btwn chambers or great vessels, or increased peripheral resistance

• Commonly secondary to hyperthyroidism in cats

• If no obvious cause for hypertrophy then primary myocardial disease, such as hypertrophic cardiomyopathy, should be considered

DISTURBANCES OF IMPULSE FORMATION OR IMPULSE CONDUCTION

• Arise from injury to atrial and ventricular MYOCYTES

  • Causes include electrolyte disturbance, coronary arterial thrombosis or embolism, nutritional deficiencies, bacterial and viral infxns, and toxins esp plant toxins

  • ECTOPIC PACEMAKERS often arise from cells in close proximity to necrotic/apoptotic myocytes

    • Irritable myocytes that are adjacent to area of injury, they develop a rhythm of depolarization that is different than the SA node

• The predominant alteration in HR and rhythm are an increased rate and an erratic rhythm (TACHYARRHYTHMIAS)

• Resulting from diseases of sinus node, conducting fibers - the intra-atrial conduction pathways, AV node, common bundle, R and L bundle branches, purkinje fibers

  • Can result in a decrease or an absence of impulse conduction

  • Manifest as various forms of bradyarrhythmias (heart block)

depression in cardiac output

arrythmia due to these disturbances causes erratic filling and contraction , leading to a _______

depressed myocardial contractile strength

Decrease in ventricular myocardial contractile critical mass

• Eg massive myocardial necrosis

Ineffective contraction w sufficient ventricular myocardial mass

• Eg dilated cardiomyopathy, esp in dogs and cats

impeded blood flow

• Occurs w stenosis (narrowing) of the AV or semilunar valves

• Results in either a restriction of blood flow form one chamber to another (atrium to ventricle), or from a ventricle to the major arteries

• Results in increased systolic workload (afterload) on the affected chamber

• Stenotic valves can also be mildly regurgitant/insufficient

• Stenosis can either be congenital or acquired

  • Distorting fibrosis secondary to scarring of valvular endocarditis is a common form

regurgitant blood flow

• Due to effaced AV and semilunar valve structure (INSUFFICIENT)

• There is backflow of blood from ventricle to atrium or from a great vessel back to its ventricle

• Increased diastolic load (preload)

• Can be

  • Congenital (eg congenital mitral insufficiency)

  • Acquired (eg healed endocarditis or endocardiosis)

abnx pattern of blood flow (shunted blood flow)

• Commonly congenital in origin

  • Patent ductus arteriosus

  • Patent foramen ovale/atrial septal defect

  • Ventricular septal defect

• Pathophysiology is complicated

  • May result in variable changes in both preload and afterload

response to reduced cardiac output

• Compensatory mechanisms work to maintain tissue perfusion

  • Changes in mm mass & HR

  • Peripheral vascular changes mediated by the renin-angiotensin-aldosterone system

    • Maintains tissue perfusion by

      • Increasing blood volume, via renal retention of Na & water

      • Increased peripheral resistance via arterial constriction

stroke volume and HR

Cardiac output dependent upon:

myocardial contractility, preload, and afterload

Stroke volume dependent upon

Activation of neuro-hormonal mechanisms due to decreased cardiac output

• Increased sympathetic tone

  • Increased HR

  • Stronger contractions

  • Peripheral vasoconstriction

• Renin-Angiotensin System

  • Peripheral vasoconstriction

  • Increase ADH => water retention

  • Increase aldosterone => Na (and water) retention

• W excessive or prolonged response, increased workload and CARDIOGENIC EDEMA can result