Exam 2 Flashcards
(233 cards)
1
Q
Path of O2 in airway
A
o Alveolar Epithelium ->
o Fused basement membranes ->
o Capillary endothelium ->
o CO2 goes in reverse (20x more diffusible than O2)
2
Q
Normal Structure Alveolar epithelium
A
Pneumocytes o Type 1: • Squamous • little repaire • no regen o Type 2: • Cuboidal, microvilli • Can regen • Produce surfactant
3
Q
Normal structure bronchioles
A
o Clara cells act as stem cells
o Used for enzymatic detox
4
Q
Nutritional Vs Functional blood supply in lungs
A
o Functional
• From R heart for gas exchange
o Nutritional
• From L heart to interstitial tissue in lungs
5
Q
Ventilation / perfusion mismatch
A
o Blood & air are not getting to same place
o Due to block of blood supply or block of airway
6
Q
Acid Base Balance in lungs
A
Respiratory alkalosis
• due to HYPERventilation = blow off CO2
Respiratory Acidosis
• due to HYPOventilation = too much CO2
Metabolic Acidosis
• Respiratory compensation: HYPERventilation
Metabolic Alkalosis
• Respiratory compensation: HYPOventilation
7
Q
Define: tachypnea, dyspnea, cyanosis, hemoptysis, epistaxis, stridor, stertor
A
o Tachypnea- rapid breathing o Dyspnea - labored breathing o Cyanosis - blue skin due to decreased blood O2 or circulation o Hemoptysis – coughing blood o Epistaxis – nose bleed o Stridor - harsh grating sound o Stertor - snoring
8
Q
delete card
A
delete
9
Q
3 Routes of entry of organisms into lungs, & natural defenses for those routes
A
Inhalation (airborne) • Sneezing, coughing, bronchoconstriction • Mucociliary clearance • Phagocytosis by alveolar macrophages • Hyperplasia = chronic resp Dz
Hematogenous (blood borne)
• Intravascular macrophages
Direct Extension (penetrating)
10
Q
Primary Ciliary Dyskinesia
A
o Genetic defect in ciliary morphology ->
o Defective ciliary movement ->
o Defective mucociliary clearance ->
o Predisposition to infection
11
Q
Defenses against blood-borne respiratory agents in dogs & rodents Vs ruminants, cats, pigs, horses
A
Dogs, rodents, humans
• phagocytosed by Kupffer cells and splenic macrophages
ruminants, cats, pigs, horses
• pulmonary intravascular macrophages
12
Q
4 Main Causes of Impairment of Respiratory Defenses
A
Viral:
• Destruction of cilia,
• impaired pulmonary alveolar macrophage function
• often predisposes to bacterial infection
Bacterial:
• Inhibit cilia,
• survival and replication in macrophages
• can predispose to other bacteria
Toxic gasses:
• Direct injury to tracheal/bronchial epithelial cells and pneumocytes
Immunodeficiency:
• not very common
13
Q
Cellular Response to Acute & Chronic Mucosal Damage in Respiratory Tract
A
Acute Mucosal damage:
• Decreased cilia + increased goblet cells
• Inflammation - hyperemia, edema, neutrophils
• Impaired mucociliary clearance
• Ciliated epithelium will repair IF basement membrane is intact or scar if not
Chronic Mucosal Damage • Goblet cell hyperplasia • Fibrosis • Squamous metaplasia • Decreased clearance and increased airway resistance
14
Q
Cellular Response to Smooth Muscle, Alveoli, & Interstitium Damage in Respiratory System
A
Smooth Muscle
• Hyperplasia/hypertrophy of smooth muscle = increased airway resistance
Alveoli
• Type II pneumocyte hyperplasia = reduced gas exchange
Interstitium
• Interstitial fibrosis = reduced ventilation of alveoli
15
Q
Developmental Abnormalities of the nasal cavity & sinuses
A
brachycephalic dogs:
• Noisy inspiration
• May have obstruction w/ cyanosis and collapse during exercise
• Elongation of soft palate causing obstruction of glottis -> increased inspiratory effort.
Cleft palate
• Milk and food from nostrils = sneezing, nasal discharge
• Associated with aspiration pneumonia.
16
Q
Atrophic Rhinitis: predisposing factors, offending agents, pathogenesis
A
Predisposing factors: • infectious (bacteria +/- viral), • environment, • genetics, • nutrition
Agent
• Bordatella bronchiseptica + Pastuerella multocida
Pathogenesis:
• Toxins from Pasteurella stimulate osteoclasts & inhibit osteoblasts -> degeneration and remodeling of nasal turbinates
17
Q
Epistaxis: 3 places it may originate & causes
A
Blood may originate from w/in nasal cavity
• Causes: Trauma, inflammation, ethmoid hematoma
Blood may originate distal to the nasal cavity
• Causes: Guttural pouch mycosis, neoplasia, pneumonia, exercise-induced pulmonary hemorrhage in horses
Blood may not necessarily be due to local disease
• Causes: Platelet / coagulation defects
18
Q
Nasal Cavity Neoplasias: most common types in dogs, cats, & sheep
A
Most common in dogs & most are malignant
• nasal carcinoma/adenocarcinoma
Cats
• squamous cell carcinoma, lymphoma
Sheep
• Enzootic nasal carcinoma (retrovirus)
19
Q
Non-neoplastic Nodules in Nasal Cavity
A
- Nasal polyps (cat/horse)
* Cysts (horse)
20
Q
Equine pharyngeal lymphoid hyperplasia: basics, signs, gross lesions, histo
A
- Most common cause of partial upper airway obstruction in horses (esp 2-3 yr old racehorses, 30- 60%)
- Regress with age
- Etiology unknown: likely chronic bacteria + environment
Signs
• Stridor, changes in voice, dysphagia, cough, dyspnea in severe cases
Gross Lesions
• White foci in dorsolateral pharynx
Histo
• Lymphoidnodules
21
Q
Brachycephalic airway syndrome
A
- Stenotic nare and elongated soft palate -> laryngeal edema
- Can have severe upper airway obstruction
- Common in Bulldogs, boxers, boston terriers, pugs, Pekinese
- Signs: Sturdor (snoring), exercise intolerance, +/- severe dyspnea, cyanosis
22
Q
Necrotic Laryngitis
A
- Aka laryngeal necrobacillosis or calf diphtheria
- Calves: damage to laryngeal mucosa (feed, balling gun) - > Secondary bacterial infection -> Local inflammation/necrosis, risk of pneumonia, risk of local airway obstruction
23
Q
Laryngeal hemiplagia
A
• AKA roaring
Horses
• Atrophy of dorsal and lateral cricoarytenoid muscles
• Denervation due to primary or secondary disease of left recurrent laryngeal nerve -> affects L side
Dogs
• Laryngeal paralysis
24
Q
Neoplasia affecting pharynx/larynx
A
Dogs: very rare tonsilar squamous cell carcinoma
25
Issues w/ guttural pouch
Guttural pouch Tympany
• distention with fluid and gas
Guttural Pouch Empyema
• distention with purulent exudate
Guttural pouch Mycosis
• fungal infection
26
Guttural Pouch Mycosis: entry, lesion, signs
* fungal infection
* Most common problem with the guttural pouch
* Usually unilateral
Entry
o Inhalation of mold spores from feed/environment
Lesion
o Fibrinonecrotic exudate- necrosis and inflammation
Signs
o Epistaxis- Unilateral or bilateral, acute or intermittent
o Nerve damage
27
Disease & Other Causes of inflammation in trachea
* Canine Infectious tracheobronchitis
* Herpes viruses - Infectious Bovine Rhinotracheitis, Equine Rhinopneumonitis
* Secondary to collapsing trachea, other trauma
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Signs of tracheal inflammation
* Non-productive honking cough
| * Obstruction (in birds)
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Tracheal anomalies
* Agenesis
| * Hypoplasia (bulldogs)
30
Tracheal collapse: cause & signs
* Wide dorsal tracheal membrane
* Small breed dogs
Causes:
• Trauma, obesity, masses may exacerbate
```
Signs
• Dry, honking cough
• Dyspnea (worse with stress/exercise)
• Cyanosis
• +/- secondary pneumonia
```
31
Restrictive Respiratory Failure
* Pathology that results in restriction of inflation of the lungs
* Intrapulmonary
* extrapulmonary
```
Pathophysiology
• Restriction of lung inflation limits ventilation ->
• Low O2
Normal CO2 ->
• Rapid, shallow respirations ->
• Low CO2 ->
• respiratory alkalosis
```
32
Intrapulmonary Restrictive Respiratory Failure
```
Lesions in alveolar and interlobular septa
o Interstitial edema
o Interstitial pneumonia
o Alveolar Fibrosis
o Type II pneumocyte hyperplasia
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• Effect is less compliant walls
33
Extrapulmonary Restrictive Respiratory Failure
Lesions in pleural cavity, mediastinum, thoracic wall
o Pleural effusion (fluid in pleural cavity)
o Pneumothorax
(air in pleural cavity)
o Deformities (or masses)
34
Obstructive Respiratory Failure: pathophysiology & mechanisms
• Pathology that results in reduced ventilation of the lungs
```
Pathophysiology
• Obstruction of air flow in lungs reduces ventilation ->
• Low O2 & High CO2 ->
• Rapid/deep respiration ->
• Low O2 High CO2 ->
• respiratory acidosis
```
Mechanisms
• Obstruction of movement of air in airways or alveoli
• Exudative pneumonia- exudates fill alveoli
• Pulmonary edema – edema in alveoli
• Bronchitis or bronchiolitis- exudates, mucous, hyperplastic epithelium obstructs airways
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Recurrent Airway Obstruction (RAO, Heaves)
* Horses
* Likely allergic
* Diffuse bronchiolitis - epithelial hyperplasia, mucous
```
Signs
o Cough
o Tachypnea
o Wheeze
o Exercise intolerance
o Dyspnea- Expiratory -> “heave line”
o Weight loss
```
36
Feline Asthma: pathogenesis, respiratory signs, other signs
Pathogenesis
o Obstruction of small airways
->
o Bronchiolar smooth muscle hyperplasia and constriction
o Hypertrophy/hyperplasia of mucous glands
Respiratory signs
o Normal at rest
o Coughing to severe respiratory distress when stressed
o Lung sounds normal to crackles and wheezes
Other signs:
o Anorexia, weight loss
o Peripheral eosinophilia in 30%
37
Pulmonary Edema: Pathogenesis & mechanisms
Pathogenesis:
• Fluid accumulates in the interstitium restricts lung inflation
for variable length of time
->
• Fluid in alveoli occurs abruptly
->
• Increased rate and depth of respiration
->
• Loud lung sounds initially (quiet with severe edema)
Mechanisms
• Increased permeability
• Increased hydrostatic pressure or Decreased oncotic pressure
• Impaired lymphatic drainage
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Increased Permeability leading to pulmonary edema
* cytokines -> inflammation ->
* damage to pneumocytes & endothelium ->
* leaky vessels -> high protein fluid
39
Hemodynamics of pulmonary edema
Increased Hydrostatic Pressure
o Left heart failure - cardiogenic edema
o Hypervolemia/fluid overload
Decreased Oncotic Pressure
o Hypoalbuminemia
40
Impaired Lymphatic drainage in pulmonary edema
* Least common mechanism
| * Neoplasia blocking lymphatics
41
Acute Respiratory Distress Syndrome (ARDS): symptoms, pathogenesis
• Diffuse damage to alveolar wall
Symptoms
o Sudden onset of severe dyspnea, tachypnea
Pathogenesis
o Activation of pulmonary macrophages ->
o Cytokine Release
->
o Stimulation of neutrophils – release enzymes + free radicals ->
o Damage to endothelium and alveolar epithelium ->
o Severe Edema
42
Atelectasis
• Collapse or incomplete expansion of alveoli
Congenital:
• Failure of lungs to expand at birth
Acquired
• Restrictive - pressure on lungs - > fibrosis
• Obstructive - collapse distal to obstruction due to resorbed fluid
43
Emphysema
* Emphysema- air trapped in alveoli or interstitium
* Reduced ventilation -> ventilation/perfusion mismatch
* Expiratory dyspnea
* Hypoxia and hypercapnia
44
Pulmonary Hypertension
• Increased pulmonary vascular resistance
Causes
• Vasoconstriction
• Vascular obstruction
• Vascular volume overload
Usually secondary to other dz
• Cardiac dz, lung dz, thromboembolism, hypervolemia
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Cellular Changes in Pneumonia
Fibrin
o Sign of acute severe injury
Neutrophils
o Predominate with most bacterial infections
Macrophages
o Alveolar macrophages come quickly
o More macrophages with chronicity
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Alveolar septal response to Pneumonia
Acute
o Edema and leukocytes in the interstitium
Chronic
o Squamousmetaplasia
o Fibrosis
o Non-suppurative inflammation
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Transient Vs Chronic Injury in pneumonia
Transient Injury
• Complete repair in <1wk
Chronic Injury
• Fibrosis (restricts alveoli)
48
Classification of pneumonia
Etiology
o bacterial, viral, parasitic, toxic
Type of inflammation
o Suppurative
o Fibrinous
o granulomatous
```
Distribution
o Cranioventral -
o Lobar
o Diffuse
o multifocal
```
Morphologic type
o Broncho
o Interstitial
o bronchointerstitial
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Distribution of Pneumonia
* Multifocal - granulomatous
* Lobular (ruminants)
* Lobar – usually cranioventral
* Dorsocaudal - parasitic
* Diffuse
50
Bronchopneumonia; facts, Resp signs, Systemic signs
* Most common pneumonia
* Origination of inflamm @ bronchiolar-alveolar junction
* Aerongenous
* Bacterial
* Cranioventral
```
Respiratory Signs
o Productive cough
o Tachypnea
o Dyspnea
o Wheeze
o Exercise intolerance
```
```
Systemic Signs
o Lethargy
o Anorexia
o Fever
o Weight loss
o Rough coat
```
51
Suppurative Bronchopenumonia
o Obstructive due to exudates
o Often bilateral, cranioventral (lobar), or lobular
o Acutely lungs are swollen and consolidated
o Over time exudates resolve, lung often atelectatic
52
Fibrinosuppurative Bronchopneumonia; basics, histo
```
o more severe than suppurative
o lobar pattern
o Protypical example: Shipping fever
o Can be caused by aspiration
o Hemorrhage, fibrin, necrosis
o Complete resolution is uncommon
```
Histo
• Acute - massive fibrin + neutrophils in airspaces
• Chronic- Fibrosis of severely damaged tissues = permanent changes
53
Interstitial Pneumonia; histo, entry & two types of damage
Histo
• diffuse to patchy damage to alveolar septa
• Type II pneumocyte hyperplasia
Entry
o Aerogenous – inhalation of toxic gases
o Hematogenous – spread via the blood (most common)
Primary epithelial damage
o Toxic gasses, local generation of toxic compounds by metabolism in clara cells
o Damage secondary to viral infections
Primary endothelial damage
o Septicemia, DIC, migrating parasite larvae, endotheliotropic viruses, immune complex disease
54
Acute Bovine Pulmonary Edema & Emphysema (fog fever); pathogenesis, symptoms, histo
o Example of interstitial pneumonia
Pathogenesis
• Cow used to poor forage moved to lush pasture (high in L-tryptophan) ->
• L-tryptophan converted to 3-methylindole in rumen ->
• 3-MI absorbed into circulation ->
• Metabolized to toxic intermediate by Clara cells (toxic to pneumocytes and endothelium) ->
• Necrosis ->
• Acute edema and interstitial emphysema
Symptoms
• Severe dyspnea, froth from mouth, mouth breathing, extended neck
• NO FEVER
Histo
• Edema, emphysema, Type II pneumocyte hyperplasia
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Chronic Interstitial Pneumonia; histo, gross lesions, causes
Histo Lesions
• alveolar fibrosis
• Macrophages, lymphocytes, plasma cells in interstitium
Gross Lesions
o Lungs don’t collapse
o rib impressions on surface of lungs
Causes
o Viral (mostly)
o Mycoplasma
56
Embolic Pneumonia
* Septic emboli lodge in lungs
* Bacteria trapped in vessels -> infections spreads into interstitium
* random multifocal distribution
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Granulomatous Pneumonia; causes
* Well circumscribed, variably sized, firm nodules
* May be mineralized
* Random distribution
* Usually chronic
* aerogenous or hematogenous
Causes
o Fungi, bacteria, foreign material, migrating parasites
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Neoplasia of the lungs
* Primary = uncommon
* Metastatic from other place common
* Ex: Feline lung-digit syndrome
59
Feline Lung Digit Syndrome
- primary pulmonary tumor (carcinoma or adenocarcinoma)
- commonly metastasize to digits
- mass on digits in cats indicative of pulmonary neoplasia
60
Delete me
Delete me
61
Reserve Capacity of the kidney
* Can lose 66% of nephrons and have normal function
* loss of ~70% of nephrons = Isosthenuria
* loss of 70-75% of nephrons = Azotemia
* Further nephron loss = Renal Failure and Uremia
62
Function of the glomerulus
* Filtration barrier between blood and urinary space
| * Restricts cells & proteins
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Function of Proximal convoluted tubules
* Protein resorption (few that made it thru glomerulus)
* Resorption of 65% H2O, amino acids, glucose, Na, K, Cl
* High metabolism
= sensitive to hypoxia & toxins
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Function of Loop of Henle
* Resorption of 20% H2O, Na, Cl
| * Maintains concentration gradient in medulla
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Function of Distal Convoluted Tubule
* Resorption of water due to ADH
* Resorption of Na and excretion of K due to ALD
* Save the Na pee the potassium
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Function of Collecting Duct
Resorption of H2O due to ADH
67
Blood Flow in the nephron
o nephrons required to maintain conc. gradient of interstitium
o conc. gradient in interstitium required for functional nephron
68
4 Nephron Endocrine Functions
```
Produces renin (RAS)
o increases blood vol
```
Erythropoietin production
o In response to hypoxia
o Stimulates RBC production
Activates Vit D
o Helps Ca absorbtion
Degradation of PTH
o Ca homeostasis
69
How does renin increase blood volume?
o Decreased renal profusion (dehydration, hemorrhage, heart failure, etc) ->
o production of renin ->
o converts angiotensinogen into angiotensin I ->
o Ang I into Ang II by ACE produced by lungs ->
o Ang II vasoconstricts arterioles AND
o Ang II goes to pituitary to stimulate ADH production ->
o ADH causes resorption of water in distal tubules AND
o Ang II works on adrenal gland to produce ALD AND
o Ang II constricts efferent arterioles to insure time to filter blood
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Azotemia
o Elevated BUN/creatinine
o Consequence of reduced GFR
Pre-renal
• Decreased renal profusion
• Azotemia but maintaining conc ability
Renal
• When >75% of nephrons are non-functional
• Azotemia w/ loss of ability to concentrate urine (isosthenuria)
Post Renal
• Obstruction of outflow of urine
71
Uremia
o Clinical syndrome due to renal failure
o Functional reserve of kidney lost
o Acute kidney injury or chronic renal failure
o Many multisystemic symptoms
72
Signs of Kidney Disfunction
* Azotemia
* Uremia
* change in urine quantity
* change in urine conc.
* Proteinuria
* Hematuria
* Glucosuria
* Urinary Casts
* Changes in production of erythropoietin, calcitrol, renin
73
Requirements to conc urine & chsnges in urine due to kidney dysfunction
Requirements to conc urine
• Functional interstitium
• ADH responsive epithelial cells in distal nephron
• ADH
o Polyuria
Isosthenuria: osmolarity of urine = plasma
• w/ Azotemia: likely renal failure
• No azotemia: may be appropriate or renal dz because conc. ability lost before azotemia shows
74
Proteinuria
Pre-renal
• Hemoglobinuria, myoglobinuria, bilirubinuria, ketonuria
```
Renal
• Glomerular
• increased permeability (very high)
• Tubular
• inability to resorb proteins (typically low)
```
Post Renal
• Most common
• Lower urogenital tract dz
75
Calcitrol & Renal Failure
o active Vit D3
o Produced via 1α-hydroxylase in renal tubular cells
o Promotes absorption of Ca from gut
o Chronic renal failure (CRF) can be associated with hypocalcemia
76
Erythropoietin & Renal Failure
o Produced by kidney in response to hypoxia
o Stimulates RBC production
o Chronic renal failure (CRF) can be associated with non-regenerative anemia
77
Renin & Renal Failure
o Chronic renal failure (CRF) -> increased renin ->
o Increased blood vol. ->
o Hypertension
78
Renal Dz Vs Renal Failure Vs End Stage Kidney
Renal Dz
o Lesions in kidney
Renal Failure
o Clinical syndrome due to decreased renal function
End stage
o Chronic, irreversible, progressive dz that results in common pathologic state
o Comparable to cirrhosis of liver
79
Kidney Response to Injury
o New nephrons not formed following renal maturation
o Nephron function is all or nothing
o Damage to one component = decreased function of other components
80
Glomerular Response to Injury
Acute
• Proliferation or necrosis of cells
• Rupture or thickening of basement membrane
• Infiltration of inflammatory cells
Chronic
• Atrophy and fibrosis of glomerular tuft
81
Tubule Response to Injury
* Epithelial cells: Degeneration, necrosis, atrophy
| * Epithlium can regenerate if basement membrane is intact!
82
Interstitial Response to Injury
Acute:
• edema,
• hemorrhage,
• inflammation
Chronic:
• inflammation,
• fibrosis
83
Pre-renal disorders (Circulatory); USG, causes
Underperfusion
• Decreased GFR = azotemia w/ concentrated urine
• Activation of RAS
• If severe and prolonged -> Ischemic necrosis
Hyperemia / Congestion
• Acute septicemia
Hemorrhage
• Renal cortical or large
Infarction
• Vascular occlusion (wedge)
• Necrosis + hemorrhage -> fibrosis
Cortical necrosis
• DIC secondary to septicemia, endotoxemia
Medullary necrosis
• due to NSAIDs
84
How do NSAIDs cause medullary necrosis
* NSAIDs ->
* decreased prostaglandins ->
* vasoconstriction ->
* local ischemia ->
* necrosis
85
Pre-renal disorders (ADH disturbance)
o Diabetes insipidus
Neurogenic
• Pituitary gland does not produce ADH
• No ADH -> decreased urine concentration -> PU/PD
• Kidneys are normal
Nephrogenic
• ADH produced normally
• Kidney’s can’t respond -> decreased urine concentration
86
Pre-renal disorders (ALD disturbance)
Deficiency
• Adrenocortical insufficiency
• Excessive loss of Na & retention of K
• Elevated K -> bradycardia
Excess
• Excessive RAS activation
• congestive heart failure
87
4 Signs of Glomerular Dz
o Proteinuria
• Most important loss of Albumin
• Protein loss > resporptive capacity of PCT -> Proteinuria
• No azotemia & No change in GFR
o Hypoalbumenia
o Edema
• Decreased oncotic P -> activation of RAS -> fluid retention
o Hyperlipidemia
• Hypoalbuminemia -> increased synthesis of lipoproteins
88
Glomerular Nephritis basic & early stages Vs progressive
o “Inflammation” of the glomerular tuft
o common cause of renal failure in dogs
o usually cannot identify Ag involved
Early stages
• Urine concentrating ability is still intact
Progressive
• Loss of entire nephron -> renal failure/uremia/etc
89
Classification of Glomerular Nephritis
Membranous
• thickening of capillary basement membranes
Proliferative
• increased cellularity of glomerular tuft
Membranoproliferative
• Both
90
Pathogenesis of Glomerular Nephritis
* Endogenous or exogenous Ag Binds Ab ->
* Ag/ab complex circulates and lodges in glomerular capillaries ->
* Fix complement -> inflammation + bioactive mediators
91
Gross & Histological Lesions of Glomerular Nephritis
```
Gross Lesions
• Often none!
• Glomeruli may be prominent (red dots)
• Chronic
• Renal fibrosis = shrunken, granular, pale grey dots
```
```
Histo Lesions
• Cellular proliferation
• Thickening of the basement membrane
• Abnormally porous
• Glomerulosclerosis
```
92
Amyloidosis
o Less common than glomerular nephritis
o Amyloid may be deposited in other sites
o Mostly dogs, sometimes cows
o Present w/ CRF
o Always chronic, progressive and irreversible
o Breed dispositions: shar pei, Asian cats
93
Amyloidosis: Gross & Histological Lesions
```
Gross Lesions
• Acute:
o none
• Chronic:
o capsular surface irregular & mottled
o iodine makes glomeruli black & prominent
```
Histology
• Amorphous eosinophilic material w/in glomeruli
• Congo red stain = apple green
• Advanced cases: extensive fibrosis
• Surviving tubules contain abundant protein casts
94
Amyloid; where is it deposited, 2 forms
* Insoluble fibrillary protein that is resistant to proteolysis
* Deposited in mesangium between endothelium and basement membrane
Forms:
• Reactive
• Idiopathic
95
Renal Tubule dysfunction; symptoms, causes
o Impaired urine concentrating ability -> Isosthenuria, PU/PD
Pre-renal
• Diabetes Insipidus
• Adrenocortical
Renal
• Loss of sufficient nephrons
96
Uremia & causes
* clinical syndrome associated with fluid, electrolyte, hormone imbalances, and metabolic abnormalities due to renal failure
* FATAL if not corrected
Causes
• Electrolyte/fluid imbalance
• Uremic toxins
97
Uremia Pathophysiologies
* Dehydration
* Edema
* Metabolic acidosis
* Non-regenerative anemia
* Vomiting
* Ulcerative/necrotic stomatitis
* Malaise, lethargy
* Weight loss
* Electrolyte Issues
98
Changes in K, P, Ca due to Uremia in dogs, cats, cows, horses
Potassium and blood pH
• Dogs, cats, horses:
• Hyperkalemia and acidosis: oliguric or anuric (AKI)
• Hypokalemic: polyuric (CRF)
• Cattle:
• Hypokalemic: alkalosis, decreased intake, increased salivary excretion
• Alkalosis + hypochloremia: Sequestration in atonic abomasum
```
Phosphorous
• Dogs, cats, horses:
• Hyperphosphatemia
• Decreased renal clearance
• Cattle:
• +/- hyperphosphatemia
• Salivary secretion
```
```
Calcium
• difficult to predict!
• Dogs, cats, cattle:
• Usually low normal to mild hypocalcemia in CRF
• Secondary hyperparathyroidism
• Horses:
• Often hypercalcemic
• Normally have high renal excretion
```
99
Gross Lesions of Uremia
o Ulcerative and hemorrhagic gastritis
o Gastric mucosal mineralization
o Subpleural intercostal mineralization
o Chronic renal lesions + Renal mineralization
100
Renal Secondary Hyperparathyroidism; basics & pathogenesis
o Sequel to chronic renal failure
```
Pathogenesis
• CRF ->
• Increased phos retention + decreased Ca absorption ->
• Hyperphosphatemia and hypocalcemia ->
• PTH secretion ->
• Ca resorption from bone
```
101
Renal Secondary Hyperparathyroidism; lesions
Renal fibrous osteodystrophy
• Increased PTH -> demineralization of bone -> replacement with fibrous connective tissue
• Dogs: Rubber jaw
Soft tissue mineralization
• Dystrophic & metastatic
• Common in stomach, lungs, pleura, kidneys
102
Acute Kidney Disease; presentation & general causes
Presentation
• Sudden loss in nephron function
• Failure of excretory, hemodynamic and filtration functions
• Potentially reversible if diagnosed and treated early
```
Causes
o Inadequate renal perfusion
o Urinary obstruction
o Massive renal infection
o Massive/multiple renal infarctions
o Acute tubular necrosis
```
103
Acute Tubular necrosis; basics & pathogenesis
* Most common cause of Acute kidney injury
* Ischemic or toxic damage
* NOT inflammatory
Pathogenesis
• Sudden death of tubular epithelial cells ->
• Shedding casts into tubular lumen ->
• dead cells cause Intratubular obstruction ->
• filtrate leaks back into kidney ->
• Damage to tubules causes increase in Renin ->
• Excessive vasoconstriction & GFR
104
Causes of Acute Tubular necrosis in horses, cattle, dogs, cats, all species
Horses
o Aminoglycoside antibiotics
o Rhabdomyolysis
o NSAIDs
```
Cattle
o Heavy metals
o Plants Oak leaf poisoning
o Hemo/myoglobinuria
o Leptospirosis
```
```
Dogs
o Grapes,
o NSAIDs,
o aminoglycosides,
o chemo therapteutics,
o antifungals
o Leptospirosis
```
Cats
o Lilies
o NSAIDs
All Species!
o Ethylene glycol!!
105
Acute Tubular necrosis gross lesions & histo
Gross Lesions
• minimal renal swelling
Histology
• PCT most susceptible to ischemic and toxic insults
• Tubular epithelial degeneration and necrosis
• Sloughing of cellular tubular into lumina
• Interstitial edema
106
Chronic Renal Failure basics & first function lost
* An irreversible and progressive disease
* First function lost is concentration ability -> PU/PD
* Poor long term prognosis, but many patients with CRF often survive months to years
* Can progress to end stage kidney
107
Chronic Renal Failure: Gross & Histo Lesions
Gross:
o Shrunken, firm, vaguely nodular kidney
o Loss of parenchyma + replacement by fibrosis
Histo:
o Interstitial fibrosis
o Sclerotic glomeruli
o Mononuclear tubulointerstitial inflammation
o Thin, dilated tubules with attenuated epithelium
108
Causes of Chronic Renal Failure
* Inciting cause is not evident
* Any portion of nephron targeted
* Congenital
* Chronic pyelonephritis
* Ischemia
* Glomerularnephitis
* Amyloidosis
* Acute kidney injury w/ a lot of damage
109
Acute Kidney Injury Vs Chronic Renal Failure: frequency of urination, clinical symptoms, lab findings, imaging findings
Frequency of Urination
o AKI: Oliguric/Anuric
o CRF: Polyuric
Clinical findings
o AKI: symptoms of underlying cause
o CRF: Thin, rough hair coat, pale
Lab findings
o AKI: Hyperkalemia, hyperphosphatemia
o CRF: Hypokalemia, hyperphosphatemia, anemia, hyperparathyroidism
Gross/imaging findings
o AKI: kidneys normal to enlarged
o CRF: kidneys small
110
Interstitial Nephritis: basics & 2 forms
* inflammation in the interstitium
* Often mild and incidental
* Usually associated with some degree of fibrosis (if chronic)
Suppurative
• usually bacterial and hematogenously spread
Nonsuppurative:
• lymphoplasmacytic or granulomatous
111
Causes of Suppurative Interstitial Nephritis
```
o Leptospirosis
o White spotted kidney
o MCF
o FIP
o Infectious canine hepatitis
o Systemic granulomatous disease
```
112
Pyelonephritis: basics and what does a UA look like
* Inflammation centered on renal pelvis
* Ascending infection
* Often Bilateral & Females
* Animals usually sick/painful
* progress to renal failure
UA:
• casts, hematuria, proteinuria, bacteruria,
pyuria
113
Progressive Renal Nephropathies in dogs
* Dysplasias of several breeds
* unknown inheritance pattern
* Persistent PU/PD, progressing to CRF
* Severe bilateral renal fibrosis in young dogs
114
Interstitial Amyloidosis
* amyloid in interstitium of lungs
* Cats w/ CRF
* Cause unknown
* +/- glomerular amyloidosis
* takes up congo red stain
115
Granulomatous Nephritis
* Systemic granulomatous disease
| * Classic example: FIP
116
Papillary Necrosis
• Caused by NSAIDs
117
Renal Neoplasias
o Primary renal neoplasia
• uncommon
Epithelial:
• Renal adenoma/adenocarcinoma or transitional cell carcinoma
Mesenchymal:
• Rare
o Multicentric
• Lymphoma (cats, cattle, chicken)
o Metastatic
• More common
o Embryonic
• Nephroblastoma (pigs & dogs)
118
Developmental Anomalies of kidneys
o Aplasia, hypoplasia, dysplasia
o Ectopic kidneys
o Fused kidneys
o Polycystic kidneys (cats)
119
Renal Parasites
Dogs
• Dioctophyma Renale
Pigs
• Stephanurus dentatus
120
Signs of Post renal dysfunction
```
o Incontinence
o Anuria
o Pollakiuria
o Dysuria
o Stranguria
o UTI
```
121
UTI
* Inflammatory
* Common in Dogs & cats
* Can be subclinical
* Can extend to genital structures.
* Can result in septicemia
* Bacteria: fecal in origin
* Horses: Foaling injury or urogenital conformation
122
Cystitis; two causes
Caused by toxin
(few)
Caused by bacteria (most)
123
Chronic cystitis
* Mucosal hyperplasia
* Nodular lymphoplasmacytic infiltrate
* Chronic inflammation or irritation
* Mycotic cystitis may occur
124
Urolithiasis; basics & risk factors
* Oversaturation of urine substances -> precipitation and growth
* May lodge in urinary tract -> Life threatening!
* Common sites of obstruction dependent on
species
* Males predisposed
```
Risk Factors
• UTI
• urine stasis
• urine pH
• hereditary
```
125
Feline Urologic Syndrome (FUS) or Lower Urinary Tract Disease (FLUTD): clinical signs & presentation
• Multifactorial disease
Clinical signs
• Dysuria, hematuria, crystalluria, inappropriate urination, urethral obstruction
Clinical presentation
• Obstructed
• Unobstructed- recurrence possible
126
Ruptured Bladder
* Foals (during birth), Steer, goats
| * Measure abdominal Cr/K vs serum Cr/K
127
Neoplasia of Lower Urinary Tract: basic & symptoms
* Transitional Cell Carcinoma
* Most common near trigone
* In cattle, may be associated with Braken Fern
Symptoms
• Dysuria, hematuria, obstruction
128
3 Developmental Abnormalities of lower urinary tract
Patent urachus
Persistent urachal remnant
• May predispose to cystitis
Ectopic ureters
• Ureters open directly into the urethra
• incontinence
129
Bacterial cystitis: risk factors, symptoms, lesions
* Lower urinary tract = sterile
* Ascending infection
```
Risk Factors
o Retention of urine
o Trauma
o Glucosuria -> Emphysematous cystitis
o Obstruction
```
Symptoms
o Dysuria & pollakiuria
o Urine: Cloudy, odiferous, red-tinged
o Pyuria, hematuria, bacteruria
Lesions
o Thickened bladder wall w/ Edema & inflammatory infiltrates
130
Define: systole, diastole, pre-load, after load
Systole:
o ventricular contraction
o “pumping”
Diastole
o the period of ventricular relaxation
o “filling”
Preload
o The quantity of blood returning to the heart during diastole
o Diastolic wall stress
o Related to venous pressure
Afterload
o Impedance to ventricular emptying
o Systolic wall stress
o Related to systemic blood pressure
131
Define: cardiac output & stroke volume
Cardiac Output
o Stroke volume x heart rate OR
o Blood pressure / systemic Vascular Resistance
Stroke Volume
o Increases when myocardial contractility & preload are increased
o Decreases when afterload is increased
132
Renin-angiotensin system
o Activated in response to low Cardiac output
o Goal: Increasing blood volume
by maintaining systemic blood pressure
o Renal failure -> systemic hypertension & hypervolemia
133
Forward Vs Backward Heart Failure
Forward:
o Poor Cardiac output
Backward:
o Back up into venous circulation (Congestive heart failure
134
Acute L Ventricular Failure; forward, backward, causes
Forward Failure
o Decreased CO -> Decreased Systemic BP -> Increased Sympathetic Tone ->
o Shunting of blood from skin, GI tract, and kidneys to brain and heart
o Pale mucous membranes
o Oliguria
Backward Failure
o Decreased CO -> Backup into left atrium -> lungs ->
Pulmonary congestion and edema
```
Causes
o Large ventricular septal defects
o Infarction of left ventricle
o Bacterial endocarditis
o Acute myocarditis
o Conduction failure
```
135
Acute R Ventricular Failure; forward, backward, causes
Forward Failure
o Decreased CO -> Decreased pulmonary BP -> Increased Sympathetic Tone ->
o Shunting of blood from skin, GI tract, and kidneys to brain and heart
o Pale mucous membranes
o Oliguria
Backward Failure
o Decreased CO -> Backup into R atrium -> systemic ->
o Systemic congestion of liver
Causes
o Pulmonary thromboemboli
o Acute myocarditis
o Infarction of right ventricle
136
Acute biventricular failure
• Right ventricle is a weaker muscle -> signs primarily of right heart failure first
Causes
o Acute, severe, bilateral myocarditis
o Cardiac tamponade
137
3 forms of Chronic Heart Failure
• Failure of Adaptive mechanisms -> Decompensated -> decreased Cardiac output
Left sided CHF
o Back up/congestion in lungs
Right sided CHF
o Back up/congestion in systemic circulation (liver)
138
Physical signs of congestive heart failure L Vs R
```
Left (Respiratory symptoms)
o Rales (alveolar edema)
o Frothy, pink expectorant
o Shortness of breath, tachypnea
o Dyspnea
o Cough
```
```
Right (systemic venous congestion)
o Generalized venous engorgement (jugular pulse)
o Hepatomegaly
o Ascites
o Pleural effusion (cats L & R)
o Pericardial effusion (cats L & R)
o Dependent peripheral edema
o Weight gain (retained fluid)
```
139
3 Heart Adaptations to injury
Cardiac Dilation
o Frank-Starling Phenomenon
• as a myocyte stretches, the contractile force is increased
o W/ excessive stretch, contractile strength is decreased
o Seen in decompensated heart failure
o Triggers hypertrophy
Cardiac Hypertrophy
o To relieve stress on wall, cells grow large = “stronger”
o Pressure overload = concentric hypertrophy
o Volume overload = eccentric hypertrophy
Activation of Neuro-hormonal Mechanisms
140
Activation of Neuro-hormonal Mechanisms in response to heart injury
o Increased HR, stronger contractions, vasoconstriction
AND
o Decreased cardiac output ->
o Activation of renin-angiotensin system ->
o Vasoconstriction
o Increased ADH -> water retention
o Increased aldosterone -> Na & water retension
o All can lead to cardiac edema
141
2 Mechanisms behind Cardiac Edema
Backwards failure
• increased systemic/pulmonary venous pressure ->
• hemodynamic edema
Forward failure
• activation of RAS -> water retention -> hypervolemia -> edema
142
Treatment of Cardiac Failure
o Goals
= Improve CO
Forward failure
• Increase stroke vol -> Increase CO
• Decrease afterload -> increase CO
• Arteriodilators, diuretics, ACE inhibitors, beta blockers
Backward Failure
• Decrease/normalize preload -> decrease congestion
• Venodilators, diuretics, ACE inhibitors, cardiac conduction modulators
143
Cor Pulmonale
o Heart dz secondary to lung or pulmonary vessel dz
Acute
• Usually secondary to thrombus/embolus in pulmonary artery or its large branches
Chronic
• Usually secondary to chronic hypoxia and/or pulmonary hypertension
• Ex: brisket & heartworm Dz
144
Chronic Cor Pulmonale: Brisket Dz
* Cattle pastured >6000 ft
* Low O2 -> chronic hypoxia
->
* Chronic pulmonary hypertension ->
* R ventricular backwards failure -> peripheral edema
145
Chronic Cor Pulmonale: Heartworm Dz
• Adult Dirofilaria immitis live in pulmonary arteries ->
• pulmonary hypertension
&
• Worms cause damage to vessels -> pulmonary hypertension
&
• Migration of worms can predispose to pneumonia -> chronic hypoxia -> pulmonary hypertension
146
Basics of Aortic Valve Dz
o Stenotic, regurgitant, or both
Aortic stenosis
• stenosis of valve = smaller opening -> increase L ventricular P -> concentric L ventricular hypertrophy
Aortic Insufficiency
• Leaky valve -> blood leaks back into LV -> heart must increase Vol of blood pumped -> L ventricular dilation & eccentric hypertrophy
147
Endocardiosis: basics, groos, & histo
* Chronic degenerative valvular dz
* Older animals, Dogs, (small breeds)
* Murmur
* Does NOT always cause Cardiac Failure
* Left A-V (mitral) most common
Gross
• Thick, smooth, white, opaque nodules
Histo
• Myxomatous degeneration
148
Pathophysiology of endocardiosis
* Abnormal valve ->
* Regurgitation ->
* left atrial dilation + left ventricular dilation ->
* eccentric hypertrophy
->
* decrease COutput ->
* increased Renin ->
* increased blood volume ->
* increased preload
149
Valvular endocarditis: basics & gross/histo lesions
* Infection/ inflammation of endocardium lining the valves
* No age or species predilection
* Dogs: Mitral is most common
* Ruminants: Tricuspid most common
* Murmurs are common
* Does NOT always cause cardiac failure
* Undulant fever
Gross
• Rough, yellow, grey, red, friable
Histo
• Fibrin, bacteria, leukocytes
150
Pathophysiology of Valvular endocarditis
* Bacteremia + endothelial injury/turbulence/hypercoagulability ->
* Bacterial adherence to valve ->
* Proliferative/inflammatory lesion ->
* Septicemia, thromboembolism, glomerulonephritis, valvular fibrosis, myocardial abscessation
151
Dilated Cardiomyopathy
* Congestive heart failure is often the first sign
* All 4 chambers are enlarged, Thin, flabby
* Dobermans and Boxers
* Probably genetic
152
Hypertrophic Cardiomyopathy & what are the results
* Most common in cats
* Ventricular Hypertrophy without dilation
* Genetic in Maine Coon
Results
o Decreased ventricular vol & resistance to filling = reduced preload
o Obstruction to outflow = increased afterload
o Myocardial necrosis = decreased contractility
o Atrial thrombosis = reduced preload
153
Restrictive Cardiomyopathy
* Less common
* Mostly in cats
* Decreased diastolic vol due to fibrosis
154
Secondary Cardiomyopathy causes in cats; Nutritional causes in other animals, gross/histo lesions
* Systemic dz
* Can be from hyperthyroidism in cats, toxins, or injury
Mostly nutritional cause
• Vit E/selenium deficiency -> dz in cows & pigs
• Taurine deficiency -> dilated cardiomyopathy in cats
• Grain free -> dilated cardiomyopathy in dogs
Gross
• Pale streaks, fibrosis/minerlization
Histo
• Cellular degeneration/necrosis, Fatty change, Fibrosis, mineralization
155
Hydropericardium
• Clear to straw colored, watery, fluid
```
Causes
• Any causes of
generalized edema
• Toxemias
• Anemia (esp in pig)
• Neoplasms
• Idiopathic
```
156
Hemopericardium
• Blood
```
Causes
• Rupture of hemangiosarcoma
• Rupture aorta
• Ruptured myocardium
• Iatrogenic
```
157
Pericarditis basics, gross, & route
* Inflammation w/in pericardium
* serous, fibrinous, purulent exudate
```
Route
• Hematogenous
• Extension from myocarditis
• Extension from lymphatics
• Traumatic penetration
```
158
Traumatic Pericarditis
• Reticulopericarditis =
“Hardware Disease”
Pathophysiology
• Cattle swallows wire/nail/sharp object ->
• normal ruminal/reticular contractions ->
• penetration of object through diaphragm & pericardium ->
• direct implantation of bacteria
Can cause
o Fibrinopurulent pericarditis
o Restrictive/constrictive pericarditis
o Congestive heart failure
159
Cardiac Compression; acute & chronic causes & result
• Rise in intrapericardial pressure -> compression of great veins, atria, & ventricles
(R side first)
Acute Causes
• cardiac tamponade
• Hemorrhage
• Acute heart failure
Chronic
Causes
• Effusions, constrictive pericarditis, tumors
Result
• congestive heart failure (right sided)
160
Congenital Cardiac Dz: signalment & concequences
```
Young animals w/
• Cardiac murmur
• Polycythemia
• Cyanosis
• Congestive heart failure
```
Consequence
• Shunting of blood
• Obstruction of blood flow
161
Treatment of Cardiac Failure: increase SV, Decrease Afterload, decrease Preload
Increase SV
• (+) ionotropes
• cardiac conduction modulators
```
Decrease Afterload
• arteriodilators
• ACE inhibitors
• beta blockers
• diuretics
```
Decrease Preload
• venodilators
• ACE inhibitors
• diuretics
162
4 Congenital Cardiac Defects
Congenital shunts
• L to R or R to L
Pulmonic Stenosis
• Constriction of pulmonary artery or valve
Aortic Stenosis
• Constriction of endocardium just below aorta
Persistent R Aortic Arch
• Ligamentum arteriosum forms a band over the esophagus -> megaesophagus
163
L to R Congenital Shunt
o Oxygenated blood from L side goes through the lungs a second time
o No cyanosis
o Due to ventricular septal defect OR
Patent ductus arteriosus (PDA)
• Small patency
• SVR > pulmonary vascular resistance
164
R to L Congenital Shunt
o Poorly oxygenated blood from the R heart bypasses the lungs
o CYANOSIS
```
Tetralogy of fallot
• Ventricular Septal Defect
• Subpulmonic Stenosis
• Overriding (Dextraposed) Aorta
• Right Ventricular Hypertrophy
```
Patent ductus arteriosus (PDA)
• Large & chronic
• Pulmonary arterial hypertension->
• increased pulmonary vascular resistance > systemic vascular resistance -> right ventricular hypertrophy -> right to left shunt
165
Endocardiosis V Endocarditis
```
Endocardiosis
• Dogs
• Older
• Afrebrile
• Murmur
• Smooth, white, nodular
expansions of the valve
• Myxomatous degeneration
```
```
Endocarditis
• Any species
• All ages
• Undulant fever
• Murmur
• Rough, friable, tan/grey/red aggregates on the valve
• Inflammation, fibrin, necrosis
```
166
Arteriosclerosis
* not common in vet med
| * affects primates & birds due to old age & inappropriate diet
167
Arteritis
* Feature of many infectious and immune-mediated diseases
* Viral, Bacterial, Mycotic, Parasitic, Immune mediated
* Ex: Verminous Arteritis
168
Verminous Arteritis
• Horses
Pathophysiology
o Larvae migrate through colonic wall into mesenteric arterioles to root of the cranial mesenteric artery
->
o Damage to arteries ->
o inflammation (arteritis), dilation (aneurysm), thrombosis ->
o downstream ischemia/infarcts in gut
169
Arterial Rupture
• Due to trauma, abnormality, or spontaneous
Horses
o Aortic rupture
o Carotid artery rupture secondary to guttural pouch infection
Turkeys
o Aortic rupture
170
Arterial Occlusion
Thrombosis
o damage to vessel wall -> local clotting
Thromboembolism
o formation of thrombus -> embolizes -> flows downstream -> obstruction
171
Aneurysms
* dilation due to abnormal blood flow
* Usually arterial
* Caused by congenital anomaly, trauma, arteritis, etc
172
Venous Dz
* Portocaval shunts
* Phlebitis (inflammation)
* Venous thrombosis
173
Primary Cardiac Tumors
Hemangiomas
• Benign neoplasms of the skin of dogs
Hemangiosarcomas
• Spleen and right atrium in dogs
• Highly metastatic!
Hemangiopericytomas
Rhabdomyomas and rhabdomyosarcomas
• Rare
174
Metastatic & Heart Base Tumors
Metastatic
• Lymphoma
Heart Base
• Aortic body tumors
• Ectopic thyroid/parathyroid
175
Words for White & Grey Matter of Brain
o Leuko – white
| o Polio - grey
176
Lesion Localization Supratentorial V Infratentorial
Supratentorial
• Focal lesion will affect contralateral side
• Signs of dysfunction: Behavior, Initiation of Movement, Seizures
Infratentorial
• Brainstem & cerebellum
• Focal lesion will affect ipsilateral side
• Signs of Dysfunction: Wakefulness, Breathing, Vestibular System
177
Upper Motor Neuron Dz Vs Lower Motor Neuron Dz
Upper Motor Neuron Dz
• Paresis (weakness)
• Hyperreflexia/clonus = lack of inhibition of myotactic reflexes
• Spasticity/hypertonia = lack of inhibition of lower motor neurons
```
Lower Motor Neuron Dz
• Hypotonia/flaccidity
• Hyporeflexia/areflexia
• Paresis/paralysis
• Muscle atrophy
```
178
Lesion Localization in Spinal Cord
C1-C4 (cervical)
• UMN signs to all 4 limbs
C5-T2 (cervicothoracic)
• LMN to front limbs
• UMN to hind limbs
T3-L3 (Thoracolumbar)
• UMN signs in hindlimbs
L4-S2 (lumbosacral)
• LMN signs to hindlimbs, perineum, pelvic viscera
S3-C
• Controls tail
179
CNS Response to Injury
* Limited regeneration
* Damage to cell body = loss of nerve & axon
* Damage to axon = necrosis of axon distal to injury (Wallerian degeneration)
180
Wallerian Degeneration on Histo
* Swollen hypereosinophilic axons = spheroids
* Swollen myelin sheaths = vacuoles in white matter
* Microglia phagocytose degenerate axon = Gitter Cell
* Gitter cell + swollen myelin sheath= digestion chamber
181
Space Occupying Lesions in CNS
* CNS encased in bone
* Little swelling = compression
* “Benign” hemorrhage or edema = profound CNS signs/damage
182
CNS & Susceptibility to Injury
* pathogens that would not necessarily cause disease in other tissues cause severe CNS disease
* Neurons > oligodendroglia > astrocytes > microglia > endothelium
Neurons
• most susceptible
• Minimal energy Stores
• High oxygen needs
183
Portals of Injury for Infectious Dz of the brain
* Direct extension (stab, ear)
* Hematogenous
* Leukocyte migration
* Retrograde axonal migration
184
Abscesses in Brain; histo & clinical signs
• Uncommon
Histo:
• Neutrophils and macrophages, necrosis, gliosis at periphery
Clinical signs:
• Dependent on location
• Tissue damage + space occupying lesion
185
Suppurative meningitis/meningioencephalitis; who does it affect, portal, common bacteria, clinical signs, gross & histo lesions
• Common in young food animals
Portal
• Usually septicemia
Common organisms:
• E coli, Salmonella sp, Streptococcus sp
```
Clinical signs
• Usually ill- fever, anorexia
• Depression
• Cranial nerve deficits
• Seizures/coma
```
Gross:
• Pale yellow, cloudy meninges
• +/- hemorrhage
Histo:
• Neutrophils +/- bacteria
186
Listeria Monocytogenes; basics & associated syndromes
* Gram (+) bacteria
* ruminants
* source is poorly cured silage
Syndromes
• Abortion
• Encephalitis
• Septicemia
187
Listeria Monocytogenes; portal, histo, clinical signs
Portal:
• Invasion of sensory and motor nerves in oral cavity ->
• Retrograde + anterograde extension up trigeminal nerve (CN5) ->
• trigeminal ganglion ->
• brainstem (pons)
Histo
• Suppurative inflammation (microabscesses)
```
Clinical Signs
• Dullness
• Circling
• CN deficits
• Fever
```
188
Thrombotic Meningoencephalitis; who does it affect, organism involved, portal, gross & histo, clinical signs
• usually feedlot cattle
Organism
• Histophilus somni, gram (–) bacteria
Portal
• Hematogenous
Gross
• Random multifocal hemorrhage
Histo
• Vasculitis with thrombosis
• Secondary suppurative inflammation, necrosis
Clinical Signs
• Fever, anorexia, depression
• Variable neurologic signs
• Ataxia, circling, head pressing, blindness, death
189
Distemper Virus (morbilivirus); Basics, Initial signs, Pathogen/phys,
* Vaccines = severely reduced incidence
* Wildlife reservoirs
Initial signs:
• conjuncitivis, rhinitis, diarrhea
```
Pathogen/phys
• Aerosolization between animal ->
• local, then systemic lymph ->
• leukocytes ->
• brain ->
• Oligodendrocytes ->
• demyelination ->
• encephalomyelitis
```
190
Distemper Virus (morbilivirus); Histo & Associated Lesions
```
Histo
• Random multifocal
• Nonsuppurative perivascular cuffs
• Vacuolation of the white matter
• Cytoplasmic and intranuclear inclusions
```
Associated Lesions
• Hard foot pads
• Enamel hypoplasia
191
Distemper Virus (morbilivirus); 2 Clinical Syndromes
• 50-70% subclinical
“Classic” encephalitis (acute)
• Unvaccinated puppies
• Early - Fever, conjunctivitis, respiratory signs, V/D, death
• Neurologic signs - seizures, myoclonus, “Chewing gum fits”
“Old Dog” encephalitis (chronic)
• Slowly progressive
• Less seizures, myoclonus
• Circling, compulsive walking, blindness, paralysis
192
Rabies Virus (Lyssavirus); exposure, portal, histo, incubation period, 3 main clinical manifestations
Exposure
• Bite wounds
Portal
• Retrograde axonal transmission
Histo
• Nonsuppurative encephalitis
• Negri bodies: intracytoplasmic inclusion bodies
• Use fresh brain
Incubation Period
• 1-8wks
3 Main Clinical Manifestations
• Prodromal ->
• Furious/excitatory ->
• Dumb/Paralytic
193
West Nile Virus (Flavivirus); basics, gross, histo, clinical signs
* Infects Birds, horses, people
* Transmission by mosquitos
* Viremia -> hematogenous spread to CNS
Gross
• Multifocal petechiae, esp gray matter of brainstem and spinal cord
Histo
• Non-suppurative polioencephalomyelitis
Clinical Signs
• Fever, depression,
• Ataxia
• Paresis- paralysis
194
Differential Diagnosis for horses w/ Acute nonsuppurative meningoencephalomyelitis
* West Nile Virus
* Eastern Equine Encephalitis,
* WEE, VEE
* Equine Herpesvirus
* Rabies Virus
* Equine Protozoal Myelitis
195
Fungal Dz of the CNS; basics, common Dzs, Portal
* Granulomatous Inflammation
* Often part of systemic infection
* Often forms a mass-like lesion
```
Common Fungal Dz
• Cryptococcus felis/neoformans
• Blastomycosis dermatitidis
• Histoplasma capsulatum
• Coccidiodes immitus
```
Portal
• Inhaled-> lungs -> hematogenous -> CNS
• Direct nasal extension
196
Cryptococcocus neoformans; basics, portal, gross/histo lesions
* Primarily infects cats
* Thick mucopolysaccharide coat protects from immune response
Portal
o Direct extension from nasal infection
o hematogenous secondary to pulmonary infection
Gross
o “Cysts in the brain”
Histo
o Many organisms
o +/- inflammation
197
Toxoplasma gondii; basics, pathogenesis, gross, histology, clinical signs
* Results in disseminated dz, CNS infection, or abortion
* definitive host (full life-cycle) = cats
* Immunocompromised hosts
```
Pathogenesis in intermediate hosts
o Hematogenous to CNS->
o infects endothelial cells + leukocyte trafficking ->
o Form cysts in brain ->
o tachyzoites rupture out ->
o necrosis and inflammation
```
Gross
o none to small foci of malacia/hemorrhage
Histology
o necrosis, gliosis, protozoal organisms
Clinical signs
o Seizures, paresis, weakness, depression, circling, blindness, ataxia
198
Neospora cranium
* Similar to toxoplasma
* Definitive host = dogs
* CNS dz in dogs
* Abortion in cows
* Diagnostic: IHC, PCR
199
Two Types of Parasitic CNS Diseases
Migration in aberrant host
• EX: Larvae of Baylisascaris procyonis (round worm of raccoons) -> CNS disease in dogs (and humans)
Normal host w/ aberrant migration
200
Prions - Transmissible Spongiform Encephalopathies; High efficacy transmission V Low efficacy
• Very long incubation period (only seen in adults)
High Efficiency Transmission
• Animal to animal spread common (ingestion at birth)
• Ex: CWD, Scrapie
Low Efficiency Transmission
• No animal to animal transmission
• Ex: BSE - transmitted by contaminated feedstuffs
201
Prions - Transmissible Spongiform Encephalopathies; pathogenesis, histo, clinical signs in sheep deer cattle
Pathogenesis
• Ingestion ->
• proliferates in lymphoid tissue ->
• splanchic nerves & retrograde axonal transport ->
• spinal cord and brain ->
• gradual accumulation of abnormal prion protein in astroglia and neurons
```
Histo
• Vacuolar degeneration of neurons
• Neuronal loss
• Astrogliosis
• NO inflammation
```
```
Clinical Signs
Sheep
o Scrapie
o Severe pruritis = wool loss, weight loss, incoordination
o Genetic resistance/susceptibility
```
Elk and Deer
o Chronic Wasting Disease
Cattle
o BSE/ “Mad cow disease”
o Hyperexcitability, incoordination, aggressiveness
202
Granulomatous meningoencephalitis; who gets it, gross, histo
• Typically young, small breed dogs
Gross
o Focal - presents as mass lesion
o Disseminated - typically progressive, multifocal signs
Histology
o Angiocentric to coalescing
o Macrophages and lymphocytes (nonsuppurative)
o Commonly in brainstem and midbrain
203
Necrotizing Encephalitides; two types, who gets it, clinical signs, gross, histo
* necrotizing meningoencephalitis,
* necrotizing leukoencephalitis
* young small breed dogs
* overlapping neuropathology
Clinical signs
o Multifocal & variable
o seizures, depression, circling, vestibular-cerebellar, visual deficits, death
o Rapidly fatal
Gross
o Necrotizing lesions & Cavitation
o NME- cerebral cortices and meninges
o NLE- periventricular white matter, brainstem
Histology
o Necrosis + non-suppurative inflammation
204
MUE
o meningoencephalitis of unknown origin
o used when animal is still alive
o refers to:
* necrotizing meningoencephalitis,
* necrotizing leukoencephalitis
* Granulomatous meningoencephalitis
205
Thiamine Deficiency in Ruminants; basics, gross, histo, clinical signs
o B1 via microbes in rumen
o Changes in ruminal flora due to acidodis = thiaminase producing bacteria
o Thiaminase containing plants (Bracken fern, horsetail)
o Ingestion of sulfur (corn, sugar cane)
o results in polioencephalomalacia
Gross
• Necrosis cerebral hemispheres (if severe)
• Autoflourescence
Histo
• Laminar cortical necrosis
Clinical Signs
• ataxia, cortical blindness, seizures, death
206
Thiamine Deficiency in Carnivores; basics, gross, histo, clinical signs
```
o need B1 in diet
o Fish containing thiaminases
o Decreased thiamine intake
o Excessive heating of foods
o Preservation of meat with sulfites
o Upper GI disease causing decreased absorption
o results in polioencephalomalacia
```
Clinical Signs
• Depression, anorexia, neck ventroflexion, ataxia, paresis, seizures
Gross
• Malacia- Caudal colliculi, bilaterally symmetric
Histo
• Neuronal necrosis
• Neuropil vacuolation/gliosis
207
DfDx for Polioencephalomalacia in ruminants
* Changes in ruminal flora
* Thiaminase containing plants
* Sulfur toxicity
* Lead toxicity
* Water deprivation/Salt toxicity
208
Clostridium perfringens type D Enterotoxemia; basics, pathogenesis, clinical signs, gross, histo
* Pulpy kidney disease or overeating disease
* GI tract bacteria produce TOXIN
= Neurologic disease
* Sheep >>> goats > cattle
```
Pathogenesis
o Change in feed ->
o Intestinal overgrowth of C. perfringens type D ->
o production of EPSILON TOXIN ->
o damages endothelium ->
o edema and ischemic necrosis
```
Clinical Signs
o Death
Gross
o Bilaterally symmetric (leuko) encephalomalacia
o Autolysis (Pulpy kidney)
Histology
o Vascular degeneration and necrosis
o Edema
o Secondary necrosis
209
Nigropallidal Encephalomalacia in Horses ; cause, gross, histo, clinical signs
• Caused by yellow starthistle or Russian knapweed
Gross
o Globus pallidus/substantia nigra
o Malacia
Histo
o Neuronal necrosis
o Neuropil vacuolation
Clinical Signs
o Acute presentation after chronic grazing
o Persistent chewing movement and difficulty prehending food/swallowing
o Death due to progressive starvation/emaciation
o Depression, somnolence
210
Leukoencephalomalacia in Horses; cause, gross, histo, clinical signs
• “moldy corn poisoning” = mycotoxin
Gross
o Malacia in the white matter of the cerebrum
Histo
o Necrosis & vacuolation
Clinical Signs
o Depression, head pressing, aimless wandering, blindness, seizures
211
Concussion V Contusion
Concussion:
o temporary loss of consciousness following head trauma
o diffuse change w/ no detectable lesions
Contusion
o Focal brain injury - hemorrhage
o Coup and contrecoup lesions
212
Acute Brain Swelling & Infarcts
Acute brain swelling
o Not cerebral edema
o unregulated vasodilatation following trauma
Infarcts
o Thrombosis or embolism in the cerebrospinal arterioles.
213
Cerebral edema; 4 types, gross lesions
• Causes loss of blood brain barrier
Vasogenic Edema
o leaky vessels
o Fluid w/in extravascular/extracellular space
Cytotoxic Edema
o intracellular edema
Hydrostatic Edema
o increased CSF pressure
o Fluid w/in periventricular space (whitematter)
Hypo-osmotic edema
o Over consumption of water, loss of sodium
o Fluid w/in extracellular and intracellular spaces
Gross
o Flattening of the sulci and gyri
o Transtentorial herniation of the cerebrum
o Herniation of the cerebellum through foramen magnum
214
Cerebellar Hypoplasia; gross, histo, clinical signs
* Usually secondary to in utero viral infections
* Panleukopenia (parvovirus) in cats
or BVD in cattle
Gross
o Small cerebellum
Histo
o Loss of external granular layer
Clinical Signs
o Often aborted
o Vestibular signs
215
Cerebellar Abiotrophy
* Similar to hypoplasia, but loss of Purkinje cells occurs AFTER birth
* Rare
Clinical signs
o after about 4 months of age
o progressive
o Ataxia, vestibular dysfunction
216
Hydrocephalus
• fluid within ventricular system
Congenital
o Genetic disorders
o Inflammation with in utero infections
Acquired
o After birth: inflammation, neoplasia
217
Hepatic encephalopathy
* Liver failure or PSS
* Toxins absorbed by GI tract
* Alteration in transmembrane movement of amino acids, water and electrolytes
* Inhibit action potentials in neurons
```
Clinical Signs
o Most severe after eating
o Depression
o Vomiting
o Head Pressing
o Seizures
```
218
Lyposomal Storage Dz
* Disruption of lysosomal degradation
* Genetic or toxic
* Accumulation of products -> cellular dysfunction & death
Histo
o Swollen neurons
219
CNS Neoplasia
Meningioma
o Most common
o Arises from meninges
Astrocytoma, Oligodendroglioma
o Difficult to distinguish grossly
o Aggressiveness varies
Ependymoma
o Cells lining ventricles
o Causes secondary hydrocephalus
Metastatic Tumors
o Hematogenous or direct extension
220
Equine Protozoal Myelitis; cause, gross, histo, clinical signs
Cause
o Sarcocystis neurona from oppossum feces
Gross
o Multifocal, random necrosis/hemorrhage
```
Histo
o Gray and white matter (random)
o Necrosis and hemorrhage
o Mixed inflammation
o Gliosis
o parasitic cysts
```
Clinical Signs
o Ataxia
o Muscle atrophy
o Urinary incontinence
221
Spinal Fractures & Trauma
* May cause shearing
* May cause hemorrhage
* May cause compression and damage
* Wallerian degeneration of axons will occur cranial and caudal to site of trauma
222
Cervical Stenotic Myelopathy; gross, histo, clinical signs
* Wobbler’s Dz
* Young large breed dogs & horses
Gross
o May see narrowed spinal canal
o Radiography is often more sensitive than necropsy
Histo
o Wallerian degeneration
Clinical Signs
o Paresis and ataxia of all 4 limbs
o Loss of conscious proprioception
Static
o narrow spinal canal
Dynamic
o spinal canal narrows depending on position of head
223
Intervertebral Disc Dz; types, gross, histo, clinical signs
* Dogs
* Degeneration of intervertebral disc
* Severity depends on amount of compression & speed it occurs
Type 1
o Degeneration of nucleus pulposus
o Rupture & extrusion of disc material
o usually acute
Type 2
o Degeneration of annulus fibrosus
o Weakening & protrusion of disc
o usually chronic
Gross
o Extrusion or protrusion of disc into spinal canal
o +/- collapse of the disc space
Histo
o Wallerian degeneration
Clinical Signs
o Pain
o Paresis
o Paralysis
224
Fibrocartilagenous Emboli (FCE); gross, histo, clinical signs
• Fibrocartilage from nucleus pulposus in vessels causes infarction in spinal cord
Gross
o Infarction
Histo
o Fibrocartilage evident in vessels
Clinical Signs
o Acute onset
o Paresis/Paralysis
225
Basics of Syringomyelia & Spinal Bifida
```
Syringomyelia
• Cyst in spinal cord filled with CSF
Spinal Bifida
• Failure of closure of spinal canal during development
```
226
Spinal Cord Neoplasias
Uncommon
• Meningiomas
• Gliomas
• Thoracolumbar spinal cord tumors
227
Acute Idiopathic Polyradiculoneuritis (Coonhound Paralysis); what is it, histo, clinical signs
• Inflammation of peripheral nerve and spinal roots
```
1-2 weeks following “exposure”
• Raccoon bites
• Vaccination
• Campylobacter
• Suspected autoimmune
```
Histo
• Degeneration & inflammation of peripheral nerves
```
Clinical signs
• Progressive paresis -> paralysis
• Bladder/bowel/tail movements normal
• Death may occur via respiratory paralysis
• May recover with supportive care
```
228
Colonic Aganglionosis (lethal whit foal syndrome)
* Foals born w/o myenteric & submucosal ganglia in colon
| * Born normal, soon die due to atony of colon and failure to pass feces
229
Peripheral Nerve Neoplasia
* Schwannoma
(schwann cells)
* Peripheral Nerve Sheath Tumor (fibroblasts)
(these are soft tissue sarcomas)
230
Clostridium Tentani (tetanus); what is it, clinical signs
* Enters nerve endings near wound -> retrograde axonal transport to CNS -> neural-neural junctions
* Prevents release of neurotransmitters by inhibitory interneurons
* Horses, cows, sheep >>> dogs & cats
```
Clinical Signs
• Muscle rigidity/stiffness
• Hyperesthesia
• Hyperreflexia
• Muscle spasticity and hypertonia
• Colic
```
231
Clostridium Tentani (tetanus) Pathogenesis
* Endospores ubiquitous in environment ->
* Wound ->
* anaerobic conditions ->
* vegetative form ->
* neurotoxins (tetanospasmin) ->
* Toxin released when bacterial dies
* Binds at NMJ ->
* Absorbed and transported via axon to spinal cord ->
* Crosses synapse to presynaptic inhibitor neuron ->
* Blocks release of inhibitor neurotransmitters ->
* Loss of inhibition -> rigidity and hyperreflexia
232
Clostridium Botulinum (botulism)
* Ingestion of feed contaminated w/ toxin
* Toxin binds receptors on presynaptic terminals of peripheral cholinergic synapses
* Toxin is taken up by the neuron and blocks release of acetylcholine
* Results in flaccid paralysis
233
Myasthenia Gravis
* blockade of signaling at neuromuscular junction ->
* Weakness and atrophy of skeletal muscles and/or esophagus
Autoimmune
• Abs to acetylcholine receptors
• Idiopathic or paraneoplastic
Congenital
• Deficiency of acetylcholine receptors
