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Respiratory Disease - Veterinary Internal Medicine > Pulmonary Parenchymal Disease > Flashcards

Pulmonary Parenchymal Disease Flashcards

1
Q

Pulmonary Parenchymal Disease

List potential clinical signs:

A
  • Respiratory Signs:
    1. Cough
    2. Exercise intolerance
    3. Tachypnoea
    4. Excessive panting
    5. Increased respiratory effort
    6. Respiratory Distress
  • Systemic signs:
    1. Weight loss
    2. Lethargy
    3. Fever
    4. Lymphadenomegaly
    5. Distal limb swelling
    6. Reduced appetite
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2
Q

Diagnostic Evaluation of Pulmonary Parenchymal Disease

List useful diagnostic investigations

A
  1. Measurements of oxygenation
    • SpO2
    • PaO2
    • A-a gradient calculation
  2. Screening Tests
    • CBC / biochemistry / urine
      • Rarely specific but may help identify concurrent or potentially causative disease (eosinophilia, uraemia, leukocytosis, other)
    • Faecal floatation / Baerman technique
    • Heartworm antigen testing (in endemic areas)
    • PCR for systmic diseases with respiratory signs
  3. Natriuretic peptides - NT-proBNP
  4. Diagnostic Imaging
    • Thoracic radiographs vs CT
    • Echo to help exclude or define causative or concurrent cardiac disease
  5. Invasive Tests
    • TTW or BAL (with or without bronchoscopy)
    • Bronchoscopy
    • Lung biopsy
    • FNA of peripheral nodules
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3
Q

Discuss brain type natriuretic peptide metabolism and function.

A
  • Natriuretic peptides including BNP are related hormones that affect circulatory homeostasis
  • ProBNP is produced in cardiac myocytes
  • ProBNP production is increased with increased myocyte stress due to increased vetricular blood volume
  • ProBNP is cleaved to BNP and NT-ProBNP (inactive) upon release into the blood stream
  • Through many effects, BNP lowers both preload and afterload
  • BNP effects:
    • vasodilatation
    • Sympathetic nervous system inhibition
    • RASS inhibition (inhibits renin secretion)
    • Natriuresis
    • Diuresis
  • NT-ProBNP can be affected by kidney disease, hyperthyroidism or pulmonary hypertension.
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4
Q

List the various pulmonary parastites

A
  1. Paragonimus kellicotti
  2. Filaroides spp
  3. Aelurostrongylus abstrusus
  4. Crenosoma vulpis
  5. Oslerus osleri
  6. Eucoleus aerophilus
  7. Troglostrongylus spp
  8. Dirofiliaria immitis
  9. Angiostrongylus Vasorum
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5
Q

Aulurostrongylus abstrusis

Discuss lifecycle and pathogenesis of:

A
  • Common feline lungworm
  • Inflammation secondary to worm presence can lead to bronchiolar inflammation
    • cough and wheeze are classical clinical signs
  • Mature worms live in the bronchioles
  • Female is ovoviviparous - eggs hatch within the adult
  • L1 is coughed and swallowed to be passed in the faeces of the host
  • L1 infects the intermediary host - mollusk
    • Rodents, birds, amphibia, reptiles can act as transport hosts
  • L1 develops to L3 in the intermediary or transport host
  • L3 ingested by the cat - penetrates the gut wall and transports to the lung via lymphatics or blood stream
  • Adults have developed by 8-9 days after infection
  • L1 produced by 6 weeks post infection
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6
Q

Paragonimus kellicotti

Discuss lifecycle and pathogenesis of:

A
  • Trematode lung fluke
  • Infects dogs and cats
  • Can form bullae or cysts within the pulmonary parenchyma
  • Infected animals are usually well
    • rupture of cysts or bullae can lead to haemoptysis or pneumothorax
  • Crayfish is the intermediary host
  • Parasite is ingested –> migrates from the intestine –> into the peritoneum –> across the diaphragm –> into subpleural tissues.
  • Eosiophilic and neutrophilic inflammation of the subpleural tissues
  • Ova are released into the airways –> bronchioles –> coughed, swallowed and passed in faeces.
  • Ova can be identified in either faeces or BAL samples
    • sedimentation techniques are preferred for ova identification
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7
Q

Filaroides spp

Discuss lifecycle and pathogenesis of:

A
  • Uncommon parasites of dogs
  • Adults reside in the alveolar spaces and terminal bronchiole
  • Ovoviviparous - direct faecal oral transmission
  • Can lead to transmission between infected dam and pups or between pups in a litter
  • Repeat infection or autoinfection is also possible - can lead to super-infection
  • Dogs are usually healthy while infected but can develop severe or even fatal disease
  • Young and immunocompromised are most susceptible
  • Can see diffuse bronchointerstitial or alveolar granulomatous infiltrates in reaction to dead/dying worms
  • Ova/larva can be detected via BAL or in faeces
    • Faecal detection has a poor sensitivity due to intermittent shedding
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8
Q

Oslerus (Filaroides) osleri

Discuss lifecycle and pathogenesis of:

A
  • Direct trasmission without an intermediate host
    • L1 is infective
  • Mature adult lives in the distal trachea or proximal bronchi
  • Can cause granulomatous mucosal nodules
  • Usually a subclinical infection
  • Cough is the primary sign
  • Decreased or impaired mucocilliary clearance can lead to secondary bacterial infection
  • Airway obstruction or pneumothorax can occur in rare cases
  • Zinc sulphate centrifugal faecal floatation can identify larvae
  • Mature worms can be visualised during bronchoscopy
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9
Q

Angiostrongylus vasorum

Discuss lifecycle and pathogenesis of:

A
  • “French heartworm”
  • Adults reside in the right heart, pulmonary arteries or pulmonary arterioles
  • Eggs laid into the vessels are transported to the pulmonary capilliaries where they hatch.
  • L1 migrate into the alveoli and are coughed and swallowed
  • L1 infects intermediary (mollusk) or paratenic host (eg. frog)
  • Baerman technique faecal exam or BAL identification
  • Affected dogs can be healthy, show respiratory signs or a bleeding diathesis
  • Bleeding may be due to a consumptive coagulopathy
  • Bleeding may occur with or without respiratory signs
  • Severe pulmonary hypertension and cor pulmonale occasionally occurs
  • Pneumothorax is rare
  • Thrombosing pulmonary arteritis can be severe
  • Most common clinical presentation is chronic cough and ill-thrift
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10
Q

List the broad clinical signs seen with bacterial pneumonia

A

Respiratory Signs

  1. Cough (often soft and productive)
  2. Tachypnoea
  3. Respiratory distress
  4. Nasal discharge
  5. Increased / decreased bronchovesicular lung sounds
  6. Cyanosis

Systemic signs

  1. Lethargy and Anorexia
  2. Reduced body condition
  3. Variable fever
  4. Exercise intolerance
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11
Q

Discuss diagnostic screening tests for a patient with suspected bacterial pneumonia

A
  1. CBC - non specific and inconsistent changes
    • neutrophilia +/- left shift
    • lymphopenia
    • mild anaemia
  2. biochemistry, urinalysis - screening for concurrent disease
  3. Faecal analysis - primarily to assess for concurrent parasitic infection
  4. Thoracic radiographs
    • Classic - alveolar pattern with predominantly ventral distribution
    • Lobar consolidation
    • Dorso-caudal distribution may predominate in haematogenously spread pneumonia
    • Less severe - interstitial changes only
  5. SPO2 or arterial blood gas
    • Hypoxaemia is common - severity dependent
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12
Q

Discuss how bacterial pneumonia is diagnosed considering presumptive and definitive diagnosis and clinical implications

A
  • Presumptive diagnosis is based on history, clinical signs, and results of screening tests including radiographs
  • Definitive diagnosis requires identification of pulmonary sepsis - bacteria within neutrophils - on airway sampling together with a positive bacterial culture
  • Note: a study (Proulx 2014) identified 26% of dogs for which empircal treatment was inappropriate. Further, 65% who had received antibiotics in the preceding 4 weeks had resistance to empirical antibiotics.
  • Cultures can be negative even with definitive pneumonia
  • Anaerobic culture should be considered when there is lobar pneumonia or consolidation.
  • Mycoplasma PCR (or culture) should also be considered

Clinically, dogs with severe pneumonia are often unstable precluding the use of anaesthesia for collection of airway samples. If unstable, empirical antibiotic treatment as per ISCAID guidelines would be advised.

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13
Q

Discuss the various treatments utilised for bacterial pneumonia

A
  1. Antimicrobials
    • Based on culture results ideally. Empircal treatment should be commenced after airways sampling with a view to altering the regime as required.
      • Mild: monotherapy with amoxicillin/clavulanate, enrofloxacin or trimethoprim sulfonamide
      • Moderate: Monontherapy or combination therapy - amoxicillin/clavulanate AND fluoroquinolone or Clindamycin AND fluoroquinolone
      • Severe: monotherapy - imipenem, ticarcillin or combination with beta-lactam AND fluoroquinolone or aminoglycoside
  2. Oxygen supplementation
  3. Fluid therapy
  4. Physical therapy including coupage
  5. Nebulisation (saline)
  6. Bronchodilators
  7. Mucolytics
  8. Nutritional support
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14
Q

List viral causes of pneumonia in dogs and cats

A

Canine:

  1. Canine herpesvirus
  2. Canine infectious hepatitis (CAV-1)
  3. Canine parainfluenza
  4. Canine adenovirus type 2
  5. Canine respiratory coronavirus
  6. Canine influenza - uncommon

Feline

  1. Feline calicivirus
  2. Feline Herpesvirus
  3. Feline coronavirus (FIP)
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15
Q

Bordatella Bronchiseptica

Brief notes on pathogenesis and transmission:

A
  • Airborne transmission
  • Highly contagious
  • Incubation period - 2-10 days
  • Mild to severe clinical signs (more severe if lower respiratory tract is involved)
  • Organism can be shed for 1 month or up to several months
  • Adhesion molecules use to adhere bacteria to respiratory cilia
  • Virulence factors including O antigen - outer capsule that protects from complement mediated lysis or phagocytosis
    • Type III secretion systems - allow colonisation
    • exotoxins - epithelial cell necrosis
    • adenylate cyclase toxin
  • Colonisation triggers altered epithelial cell function and over-production of mucus - this further impairs the immune system and can lead to secondary infections
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16
Q

Mycoplasma cynos:

Brief notes on pathogenesis and transmission:

A
  • Commensal organisms
  • Role in pneumonia and respiratory disease is not clear
  • Isolated from lungs or trachea of ~ 25% healthy adult dogs (Randolf - 1993)
  • Uncertain if primary or secondary pathogen
  • Experimental infection results in clinical pneumonia
  • Transmitted via aerosols
  • Infection within 2-3 weeks of exposure
  • Young more susceptible
  • Can be shed/persist in the airways for ~ 3 weeks following infection
17
Q

Streptococcus equi subspecies zooepidemicus

Brief notes on pathogenesis and transmission:

A
  • B-haemolytic streptococcus
  • Commensal of the upper respiratory tract of horses
  • Outbreaks of severe haemorrhagic pneumonia reported in group housed dogs
  • History of contact with horses is not always present
  • Mild signs initially - cough and nasal discharge
  • Rapid progression within 24-48 hours
    • Fibrinosuppurative, necrotizing and haemorrhagic bronchopneumonia
  • Exotoxin genes trigger disease similar to toxic shock syndrome
  • In experimental models, coinfection with CIV was important at producing disease. Experimental infection with Strep. equi alone did not produce disease (Larson 2011)
18
Q

Canine adenovirus type 2

Brief notes on pathogenesis and transmission:

A
  • Non-enveloped, double stranded DNA virus
  • Infects non-ciliated bronchiolar epithelial cells, epithelial cells or the nasal mucosa, pharynx and tonsillar crypt., mucus cells in the trachea and bronchi
  • clinical signs typically mild - sneezing, nasal discharge and dry cough
  • Virus can shed for 1-2 weeks post infection
  • Virus can surviv in the environment for weeks to months
19
Q

Canine Herpes virus:

Brief notes on pathogenesis and transmission:

A
  • Enveloped, double stranded DNA virus
  • CHV-1 most often associated with reproduction failure in bitches or severe illness in neonates
  • High seroprevalence in dogs housed in kennel situations
  • Experimental infection can cause
    • Rhinitis
    • Tracheobronchitis
    • Ocular signs - keratitis and conjunctivitis
  • Infects the epithelial cells of the upper respiratory mucosa
  • Incubation 6-10 days
  • Can become latent in neurological tissue with re-activation at times of stress or immunosuppression
  • Intermittent shedding throughout life
20
Q

Canine Influenza Virus

Brief notes on pathogenesis and transmission:

A
  • Enveloped, segmented negative-sense RNA virus
  • Subtyped based on haemagglutin (H) and neuraminidase (N) genes
  • H3N8 - first identified in a population of raciing greyhounds in Florida in 2004. Spread through the US, particularly in kennels. Thought to be extinct by 2015
  • H3N2 outbreak in Chicago in 2015 - likely mutated from an avian influenza virus - now common throughout the USA
  • Generally mild respiratory clinical signs, occasionally more severe and can cause pneumonia
  • Virus shedding reduces markedly by ~ 1 week. Virus can be isolated still at 3 weeks post infection.
21
Q

Canine parainfluenza virus

Brief notes on pathogenesis and transmission:

A
  • Enveloped single stranded negative-sense RNA virus
  • Highly contagious and present worldwide
  • Prior to vaccines - isolated from ~ 50% of dogs with respiratory disease in a kennel situation
  • Spread via respiratory secretions / droplets
  • Virus infects the respiratory epithelial cells
  • No signs or mild clinical signs
    • Dry, harsh cough for 2-6 days +/- pyrexia, +/- nasal discharge
  • Clinical signs are worse with co-infections
  • Virus shedding decreases 1-2 weeks after infection
  • Susceptible to inactivation by disinfectants
22
Q

Canine Respiratory Coronavirus:

Brief notes on pathogenesis and transmission:

A
  • Enveloped RNA virus
  • First identified in shelter dogs in the UK in 2003
  • Infection is associated with mild respiratory signs - nasal discharge, cough, sneezing
  • Virus affects mosty respiratory tissue and respiratory associated lymphoid tissue
  • Infection causes damage to or loss of respiratory cilia
  • Virus shedding detected fro up to 10 days
23
Q

Pneumocystis Carinii

Brief notes on pathogenesis and transmission:

A
  • Saprophytic fungus
  • Not highly virulent
  • Infection is most often seen with immunocompromise
  • Dachshund and CKCS pre-disposed
    • Dachshund - common variable immunodeficiency
    • CKCS - IgG deficiency
  • Infects young dogs and most present for progressive lower respiratory tract disease
  • Absence of fever despite severe pneumonia is common
  • Fungus not easily recovered on BAL - lives in the alveoli and cause thickening of the alveolar septum and minimal inflammation
  • Special stains required for organism visualisation
  • Potentiated sulfonamides appear to be most affective treatment
24
Q

Aspiration pneumonia

List conditions that predispose to aspiration

A
  1. Impaired conscious protection of the airways
    • anaesthesia, sedation, seizures
  2. Impaired unconscious protection of the airways
    • laryngeal paralysis, post-laryngeal surgery, MG
  3. Impaired swallowing
    • CN X, CN IX, maxilliary nerve (from CN V), achlasia
  4. Regurgitation
    • megaoesophagus, motility disorder, botulism etc
  5. Gastric overdistension
  6. Vomiting
  7. Forced feeding
25
Q

Aspiration pneumonia

Discuss the pathogenesis post aspiration event

A
  • Largeley dependent on the material aspirated and the volume
  • Aspiration of food stuffs can cause physical obstruction
  • Aspiration of liquids including gastric acid can cause chemical injury
  • Hypertonic solutions such as for bowel cleansing can draw excessive water into the airspaces
  • Aspiration can trigger an acute airway response followed by a secondary inflammatory response
  • Primary airway damage can lead to inflammation and secondary bacterial infection. Alternatively, bacteria may be present in the aspirated material leading to direct innoculation
  • Gravity dependent lobes are most likely to be affected - right middle, left cranial (caudal portion), right cranial.
  • Radiographic changes will lag behind clinical signs, especially those due to chemical lung injury
26
Q

Discuss microvascular fluid movement within the lung

A

In health:

  • minute quantites of fluid leave the vascular space via tiny gaps between the endothelial cells –> enter interstitium
    • Tight junctions between alveolar epithelial cells prevent fluid movement into the air spaces
  • Interstital fluid moves through to the peribronchovascular space
  • Fluid is returned to the circulation via lymphatics
  • Fluid movement from into the interstitium is dictated by 4 major factors
    • Vascular hydrostatic pressure
    • Lymphatic hydrostatic pressure
    • Oncotic pressure
    • Vascular endothelial integrity
27
Q

Compare and contrast cardiogenic pulmonary oedema and non-cardiogenic pulmonary oedema

A

Cardiogenic pulmonary oedema

  • Caused by volume overload and an increase in capilliary hydrostatic pressure
  • The fluid is low-protein
  • Responds rapidly to changes in circulating volume as treated by diuretics

Non-cardiogenic pulmonary oedema

  • Triggered by an increase in capillary vascular permeability
  • Leakage of relatively protein-rich fluid
  • Protein-rich oedema fluid alters oncotic pressure gradients
    • Retention of interstital fluid
    • Further increases vascular fluid leak
  • Removal of fluid requires active Na and Cl transport - water moves passively
    • Endothelial damage can impede the transport of Na and Cl leading to oedema refractory to treatment.

Both:

  • Reduced pulmonary compliance and airway compression from fluid accumulation
  • Increased pulmonary vascular resistance
28
Q

Non-cardiogenic pulmonary oedema

Discuss the proposed pathogenesis of neurogenic pulmonary oedema formation.

A
  • Triggered by a significant insult to the central nervous system
    • Any cause of an abrupt, rapid, extreme elevation in ICP
    • Neuronal compression, damage or necrosis triggers a catecholamine surge
  • Proposed to be due to massive catecholamine surge
  • Intense pulmonary vasoconstriction together with inflammation
  • Numerous mechanisms have been described but not proven at the vascular/alveolar level.

Examples

  • seizures - status epilepticus
  • electrocution
  • head trauma
  • spinal cord injury
29
Q

Non-cardiogenic pulmonary oedema

Discuss mechanism of formation in post-obstructive pulmonary oedema

A
  • Caused by inhalation against obstruction
  • Marked increase in negative intra-thoracic pressure
  • Increased right ventricular preload and afterload leading to increased capilliary hydrostatic pressure
  • Negative airway pressures further drive fluid from the interstitium
  • Hypoxia also drives vasoconstriction and disrupts vascular wall integrity
  • Hyperadrenergic state (sympathetic stimulus) redistributes blood flow to the pulmonary circulation compounding the above.
30
Q

Non-cardiogenic pulmonary oedema

Discuss the systemic causes of pulmonary oedema and their proposed mechanisms of action

A

pancreatitis, uraemia, sepsis

systemic inflammation causes vascular endothelial changes

31
Q

Non-cardiogenic pulmonary oedema

Discuss the formation of oedema following direct pulmonary injury

A

alterations in vascular permeability together with local inflammation

Examples:

  • aspiration
  • smoke inhalation
  • pneumonia
32
Q

Non-cardiogenic pulmonary oedema

List other causes of pulmonary oedema

A
  • Lymphatic obstruction
    • More typical to see pleural effusion - especially chylothorax
  • hypoalbuminaemia
    • Other signs tend to predominate - ascites, pleural effusion, subcutaneous oedema
  • vasculitis
  • drowing
  • phaeochromocytoma
  • air embolus
  • high altitude
33
Q

Acute Respiratory Distress Syndrome

Discuss definition (in humans)

A
  • Berlin definition in humans
  • An acute, diffuse, inflammatory lung injury, leading to increase pulmonary vascular permeability, increased lung weight and loss of aerated tissues
    • With hypoxaemia
    • Bilateral radiographic opacities
    • decreased pulmonary compliance
  • Severity is despendent on the PaO2:FiO2 while receiving PEEP +5 mmHg
    • Mild - 200-300 mmHg
    • Moderate - 100-200 mmHg
    • Severe - < 100 mmHg
34
Q

Interstitial Lung Disease

Define ILD and list broad causes

A

Heterogeneous group of non-infectious, non-neoplastic pulmonary disorders that can only bhge diagnosed by histopathological means

The changes focus on the space between the basement membrane of the alveolus and the capilliary endothelial cells including vasculature and lymphatics

Characterised by inflammation, fibrosis +/or accumulation of lipid or protein. They cause restriction to lung volume and compliance

Causes:

  1. inhalation of toxicants, allergens, irritants (mineral fibres)
  2. Systemic exposure to drugs or toxins
  3. Mostly considered to be idiopathic.
35
Q

Lipid pneumonia - basic overview

A
  1. Exogenous lipid pneumonia - triggered by aspiration of lipid such as mineral oil
  2. Endogenous lipid pneumonia
    • pneumocyte injury (often associated with obstructive disease) –> Cellular degeneration –> release of cholesterol and over-production of cholesterol rich surfactant –> lipid is phagocytosed by pulmonary macrophages –> lipid-laden macrophages accumulate in the alveolar space
    • Can be seen in association with atypical mycobacterial infection in cats
    • Rare - typically diagnosed on autopsy
    • Concurrent disease is common on autopsy
    • Serum lipaemia not assessed
    • The idiopathic disease in humans has been reported to respond to corticosteroids
36
Q

Smoke inhalaton

Describe the pathophysiological mechanisms that lead to lung injury

A
  • Upper airway obstruction can occur secondary to bronchospasm or larygeal swelling - due to thermal and chemical injury - peak within ~ 24 hours
  • Inflammation of lower airways/alveoli
  • Inflammatory mediator release
  • Inactivation of surfactant
  • Airway oedema
  • Atelectasis
  • ARDS
  • Exfoliation of damaged epithelium and soot can lead to delayed obstruction –> respiratory compromise is dynamic for up to a week post exposure
  • Impaired local and systemic defence mechanisms - marked susceptibility to secondary bacterial infection
37
Q

Lung Lobe Torsion

Pathophysiology, presenting signs and investigation

A
  • Afghan Hounds and Pugs predisposed
  • Torsion usually on the long-axis of the lung
    • Compression of the bronchus and vein, while muscular artery remains partly open
    • Congestion of the lung and fluid fills the bronchus/alveoli
    • Fluid eventually leaks from the surface to cause a pleural effusion
    • Note: pleural effusion may predispose to torsion
  • lethargy, anorexia and tachypnoea are common presenting findings
  • May see cough, haemoptysis, collapse, fever
  • Clinical exam may reveal cyanosis, variable lung sounds, muffled heart sounds, prolonged CRT, variable pulses
  • Peripheral neutrophilia is common
  • Pleural effusion - blood tinged modified transudate with neutrophils and lymphocytes. Chylous effusion is possible
  • Note: 8/26 dogs had a positive bacterial culture in one study

Respiratory Disease - Veterinary Internal Medicine (5 decks)

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