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004 - Systemic Pathology > 05 - Developmental Abnormalities (cont) > Flashcards

05 - Developmental Abnormalities (cont) Flashcards

1
Q

(Bronchiectasis) (ectasia = dilation of tubulular structure)

  1. What is this? due to what?
  2. Associated with what?
  3. inflammatory cells damage what?
  4. Results in increased turbulence of airflow: due to what three things?
  5. Most common in what?
A
  1. Dilation of bronchi beyond normal (due to wall destruction)
  2. chronic bacterial bronchitis
  3. the wall
  4. increased resistance

impaired mucociliary clearance

deeper penetration of lung by infectious agents

  1. cattle
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2
Q

(Canine Primary Ciliary Dyskinesia)

  1. Congenital disorders of mucus-propelling cilia in what four locations?
A
  1. nasal cavity

bronchi

sperm flagella

brain ependyma

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3
Q

(Bronchitis and Bronchiolitis)

  1. The infectious causes are what?

(Viral)

  1. Generally see what type of lesions?
A
  1. viral and bacterial
  2. necrotizing epithelial lesions
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4
Q

(Bronchitis and Bronchoiolitis)

(Infectious Causes: Bacterial)

  1. usually what type of inflammaton?
  2. If chronic injury can get what two things?
  3. What organisms associate with Cilia?
A
  1. suppurative
  2. bronchiectasis

mucous cell hyperplasia

  1. mycoplasma sp. (continued neutrophil infiltration and submucosal lymphocyte proliferation)
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5
Q

(Bronchitis (main passages) and Bronchiolitis (smaller ones))

(Parasitic)

  1. what type fo inflammation?
  2. what spp. in ruminants and horses?
A
  1. suppurative to eosinophilic
  2. dictyolcaulus spp.
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6
Q

(Bronchitis and Bronchiolitis)

  1. Inhaled gases (like what?) are directly toxic?
  2. Ingested toxins resulting in what?
  3. What occurs at low dose?
  4. at high dose?
A
  1. NO2
  2. Clara cell and type I pneumocyte necrosis

(L-tryptophan (lush pasture) –> 3-methylindole in rumen)

(4-ipomeanol (moldy sweat potatoes)

  1. epithelial necrosis, mild inflammation
  2. pulmonary edema, damage to septa
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7
Q

(Bronchitis and Bronchiolitis)

(Type I, IgE-mediated Hypersensitivity)

  1. What in stabled horses due to environmental antigens (molds, spores, hay dust)?

2-3 what other two things do you see?

A
  1. “Heaves”; chronic obstructive pulmonary disease
  2. excersise intolerance, coughing, expiratory dyspnea
  3. external abdominal oblique hypertrophy (heave line)
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8
Q

(Equine Heaves)

(Type I, IgE-mediated Hypersenstivity)

(Gross)

  1. mucus where? due to what?
  2. peribronchiolar fibrosis - bronchiolitis #1
  3. +- emphysema due to what?
  4. +- what in mucus?
A
  1. in bronchioles, (goblet cell hyperplasia)
  2. mucus blockage
  3. eosinophils
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9
Q

(Bronchitis and Bronchiolitis)

(Type I, IgE-mediated Hypersensitivity)

(“Feline allergic bronchitis, feline bronchial asthma”)

  1. Episodic wheezing, cough, airway constriction –> ?
  2. Allergic or non-allergic triggers?
  3. Increase responsiveness of airways to what?
  4. Chronic eosinophilic bronchiolitis, airway plugs
A
  1. dyspnea
  2. either
  3. to stimuli (Bronchoconstriction, mucus secretion)
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10
Q
  1. Feline Asthma = ?
  2. Mediators (what are they?) are released to induce…

3-6 what four things?

A
  1. allergic bronchitis
  2. histamine, leukotriencs, eosinophil chemotactic factor
  3. chemotaxis of eosinophils
  4. increased permeability of blood vessels - edema
  5. contriction of smooth muscle - bronchoconstriction
  6. hypersecretion of mucus by goblet cells
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11
Q

(Pathology of the Lung)

(congential abnormalities)

1-3. What are three?

(Lung Lobe Torsion)

  1. what types of dogs get this?
  2. what lung lobes are involved?
  3. What is the cause?
A
  1. lung hypoplasia
  2. hamartoma (benign, focal malformation that resembles a neoplasm in the tissue of its origin)
  3. accessory lung
  4. deep-chested breeds
  5. right middle/left cranial
  6. usually idiopathic (trauma, neoplasm, pneumonia, pneumothorax)
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12
Q

(Pulmonary Atelectasis)

  1. what is this?
  2. how do affected areas look/feel?
  3. Can involve whole lungs, lobes, lobules
  4. will congenital survive birth?
  5. what are two forms of acquired?
A
  1. incomplete expansion or collapse of lung
  2. depressed and red, not firm
  3. no
  4. Compressive vs. Obstructuive
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13
Q

(Emphysema)

  1. Define it

2 most important as human disease

  1. What is alveolar emphysema?

(Interstital emphysema)

  1. gas present in what?
  2. forced expiration –> ?
  3. Affects species with what?
A
  1. enlarged gas-filled spaces in tissues
  2. destruction of alveolar walls with resulting enlargement of airspaces
  3. pulmonary interstitium
  4. wall rupture, dissection of gas into interstitum
  5. prominent interlobular septa (cattle)
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14
Q

(Pulmonary Edema)

  1. What is this?
  2. What happens to lung complicance?
  3. interfere with what?
A
  1. abnormal accumulation of transudate/fluid in alveoli and interstitium
  2. decreases (decreased elasticity)
  3. surfactant production oand gas exchange
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15
Q

PULMONARY

A

EDEMA

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16
Q

(Pulmonary Edema)

1 Histologically, edema fluid is what?

A
  1. eosinophilic, homogenous, faintly granular material filling the alveoli
17
Q

1-5 WHAT ARE THE FIVE CAUES OF PULMONARY EDEMA?

A
  1. increased venous hydrostatic pressure
  2. increased permeability of the alveolar barrier
  3. impaired active transport of fluid from distal airways
  4. reduced oncotic pressure
  5. lymphatic obstruction

(there is some table on p38 i guess)

18
Q
A

A (i think…)

19
Q
A

don’t know this one - i’ll come back

20
Q
A

B (i think…)

21
Q

(Pulmonary Thrombosis/Thromboembolism)

1-3. What are the three mechanisms?

A
  1. vasculitis (bacteremia, dirofilariasis, mycoses)
  2. hypercoagulability (DIC, renal disease, neoplasia)
  3. changes in vascular flow (torsion)
22
Q

yep

A
23
Q

(Pulmonary Thrombosis/Thromboembolism)

(Hypercoagulabilty)

1-6 Many reasons for this - name 6

A
  1. hyperadrenocorticism
  2. liver disease
  3. renal disease (protein losing nephropathy)
  4. intestinal disease (protein losing enteropathy)
  5. neoplasia
  6. Disseminated intravascular coagulation (DIC)
24
Q

yep

A
25
Q

(Pulmonary Thrombosis/Thromboembolism)

(Consequences)

  1. poor perfusion of lung –> ?
  2. infarction rare (large artery + inadequate collateral flow)
  3. pulmonary hypertension
  4. painful
A
  1. hypoxia (if widespread)
26
Q

(Pulmonary Hemorrhage)

1-5. What are five causes?

A
  1. inherited coagulopathies (eg Von Willebrands, factor IX deficiency)
  2. exogenous anticoagulants (eg brodifacoum, rodenticide)
  3. Trauma
  4. abscess with eroision of pulmonary vessel
  5. aerosolized toxin
27
Q

(Exercise-induced pulmonary hemorrhage (EIPH) in horses)

  1. Affects what percentage of horses during vigorous exercise?
  2. Epistaxis in what percentage of affected horses…. related to what?
  3. Marked elevation of what blood pressures during exercise?
  4. Bronchoalveolar lavage indicates that EIPH occurs in what percentage of racehorses during vigorous exercise?
A
  1. 100% (usually subclinla and does not effect performance)
  2. < 2.5%; age-related
  3. pulmonary arterial and capillary pressures
  4. 100%
28
Q

(Tetrahydrofluorocarbons)

  1. Overheating of pans, skillets space heater elements, light bulbs etc. coated with Teflon
  2. THFC become aerosolized and when inhaled cause what? leads to what?
A
  1. necrosis of capillary endothelium in lung

peracute to acute pulmonary hemorrhage and suffocation withough premonitory signs

004 - Systemic Pathology (24 decks)

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