Pathology Exam Flashcards


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created 2 months ago by Nicholas_Bacon
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From Heart Pathology to Nervous System Pathology
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1

What are the three layers of the heart?

  1. Pericardium (epicardium)
  2. Myocardium (heart muscle)
  3. Endocardium (includes valves)
2

Where is the visceral pericardium?

Right against the heart on the outside. Also called the epicardium.

3

What are Purkinje cells?

Modified cardiomyocytes that function in conduction.

4

What type of muscle is the myocardium?

Involuntary striated muscle. Arranged in sarcomeres. Branched fibers connect via intercalated discs. Contain increased mitochondria.

5

How much bigger is the left ventricular myocardium compared to the right myocardium?

2-4 times thicker.

6

What is the endocardium?

Inner lining and the valves.

  • Equivalent to tunica intima of BV.
  • Endothelial cells on the inner most surface.
  • Close contact with blood, important in hemostasis.
7

What are the four cardiac valves?

  1. Right atrio-ventricular (tricuspid)
  2. Pulmonary
  3. Left atrio-ventricular (mitral)
  4. Aortic
8

How do the valves of the heart look normally?

Thin, translucent and shiny. Valves should be smooth and shinny.

9

What are the AV valves attached to and what does it look like?

Attached to papillary muscle via the chordae tendinae. Cordae should be long, slender, smooth and shinny.

10

What are differentials for an enlarged cardiac silhouette?

  • Cardiomegaly
  • Tumor
  • Pericardial effusions - hydropericardium, hemopericardium, pericarditis
11

What are the compensatory mechanisms of the cardiac system?

  • Activation of neurohumoral mechanisms
  • Cardiac dilation
  • Cardiac hypertrophy
12

What are the neurohumoral mechanisms of the cardiac system?

Depression in cardiac output.

  • Get release of NE which increases HR and contractility and vasoconstriction
  • Redistribution and decreased renal blood flow. Causes increased renin, angiotensin and aldosterone. This increase Na, water reabsorption and aldosterone with vasoconstriction.
  • Increase in ADH, increase of retention of water and increased blood volume.
13

Are cardiac hypertrophy and dilation helpful?

Yes but only as a short-term fix. If you push it too far, you get decompression.

14

What is Cardiac Dilation?

  • Myocardial fibers stretch leading to increase contractile force, increased stroke volume and increased cardiac output.
  • Increased contractile force has a limit. Increased stretch causes decreased tension.
  • Acute volume overload leads to dilation.
  • Chronic volume overload causes eccentric ventricular hypertrophy.
15

What is cardiac hypertrophy?

Increase in heart mass due to increased cell size. There is primary and secondary.

16

What is the difference between primary and secondary hypertrophy?

  • Primary disease of the myocardium (genetic or idiopathic)
  • Secondary cardiac hypertrophy due to sustained increase in cardiac workload. Volume overload, pressure overload. Due to trophic signals.
17

Other than primary and secondary, how can cardiac hypertrophy be classified?

  • Eccentric - increased ventricular preload (volume overload)
  • Concentric - increased ventricular afterload (pressure overload)
18

How does eccentric cardiac hypertrophy present?

Thin ventricular wall and distended ventricle.

19

How does a concentric cardiac hypertrophy present?

Thick ventricular wall and reduced ventricular chamber.

20

What gross changes would you see with right, left and bi-ventricular cardiac hypertrophy?

  • Right - broad base
  • Left - increased length
  • Bi-ventricular - globose (rounded)
21

What are the cellular stages in cardiac hypertrophy?

  1. Initiation: increase cell size (sarcomeres/mitochondria)
  2. Compensation: stable hyperfunction (no clinical signs)
  3. Deterioration: degeneration of hypertrophied cardiomyocytes (loss of ventricular contraction
22

What the possible sequelae of heart disease?

  • No clinical disease with lesions at necropsy
  • Clinically detectable but no heart failure
  • Or uncompensated can lead to heart failure of two types; acute forward heart failure
  • Congestive hear failure
23

What is the difference between backwards and forwards heart failure?

  • Backwards: inability to empty the venous reservoirs
  • Forwards Decreased blood outflow via the great vessels

Both can occur together in the end stages of heart failure.

24

What categorizes congestive heart failure?

  • Ascites
  • Pleural effusion
  • Pulmonary edema
25

What characterizes low output heart failure?

  • Syncope
  • Lethargy
  • Hypotension
26

What are the pathophysiological mechanisms of cardiac dysfunction and failure?

  • Disturbances in impulse formation and conduction
  • Depressed myocardial contractile strength
  • Impeded blood flow
  • Regurgitant blood flow
  • Abnormal pattern of blood flow
  • Restricted atrial/ventricular filling
27

What causes congestive heart failure and what does it result in?

  • Occurs when diastolic filling pressures result in decreased venous return.
  • Results in increased hydrostatic pressure, edema and congestion.
  • Can occur at the end stage of many chronic diseases or acutely when in shock
  • Can be right-sided, left sided or bilateral.
28

What are the steps of right sided heart failure?

  1. Systemic venous congestion
  2. Generalized edema. Chronic passive hepatic congestion.
  3. Leads to nutmeg liver
29

What are the steps of left sided heart failure?

  1. Pulmonary venous congestion
  2. Pulmonary edema and intra-alveolar macrophages
  3. RBCs phagocytosed by alveolar macrophages
  4. Iron in alveolar macrophages
  5. Heart failure cells
30

What are the main shunts in fetal circulation?

  • Ductus venosus
  • Foramen ovale
  • Ductus arteriosus
31

What happens to fetal circulatory shunts?

At birth, the shunts, and umbilical vessels not needed and become occluded functionally and then structurally.

32

What can cause congenital heart defects?

  • Genetic
  • Maternal viral infections
  • Nutritional deficiencies; vitamin A, pantothenic acid, riboflavin, folate
  • Drugs: thalidomide, ethanol, salicylates
  • Other teratogens: radiation, fetal hypoxia
  • Multifactorial: genetic/environmental factors
33

What are 7 common congenital heart defects?

  • Patent ductus arteriosus (PDA)
  • Atrial septal defect (ASD)
  • Valvular dysplasia
  • aortic and pulmonic stenosis
  • Teratology of fallot
  • Persistent right aortic arch, ectopia cordis
34

What common congenital heart defects cause left to right shunting of blood and also volume overload?

  • Patent ductus arteriosus (PDA)
  • Atrial septal defect (ASD)
  • Ventricular septal defect (VSD)
35

What common congenital heart defects causes right to left shunting of blood?

  • Teratology of Fallot
36

What common congenital heart disease causes pressure overload?

Aortic and Pulmonic Stenosis

37

What is a Patent Ductus Arteriosus?

Ductus arteriosus connects pulmonary artery to the aorta in the fetus. Closes after birth. Functionally within hours and can take weeks after birth to close structurally. Forms ligamentum arteriosum. Failure to close leads to PDA.

38

What are some dog breeds predisposed to PDA?

3:1 female to male ratio

  • Yorkshire terriers
  • Shetland sheepdogs
  • Chihuahua
  • Poodle
  • Maltese
  • Pomeranian
  • Newfoundlands
39

What are the hemodynamics of PDA?

  • Blood shunts L to R via PDA
  • Increased blood flow to the lung
  • Increased venous return to the LA + LV
  • Volume overload LV
  • LV eccentric hypertrophy
40

What would you see clinically with a PDA?

  • Continuous murmur
  • Bounding femoral pulses
  • +/- arrythmia
  • Left congestive heart failure
41

What occurs in rare cases of a PDA?

  • Increased blood flow to the lungs leads to pulmonary hypertension
  • Causes pressure overload RV
  • RV concentric hypertrophy

Can also get a hunt reversal. Can cause: cyanosis, lethargy, exercise intolerance, collapse and erythrocytosis.

42

What is a Patent foramen ovale and what does it result in?

Not a true ASD, a flap covers the foramen ovale.

  • If LA pressure > RA pressure it remains closed
  • If RA pressure > LA pressure it can open
43

What is an interartrial communication (atrial septal defect)?

  • Fixed opening.
  • Failure of complete development of the interatrial septum.
44

What are the hemodynamics of an atrial septal defect?

Only happens if defect is quite large.

  • Blood shunt from LA to RA
  • Increased blood volume in the right ventricle
  • Volume overload of RV
  • RV eccentric hypertrophy
45

What is a Ventricular Septal Defect?

Communication between the RV and LV. Occurs in all species - common, especially horses and cattle.

Embryonically a muscular septum grows upward to meet the membranous septum as it grows down.

  1. High VSD - defect in the membranous portion
  2. Low VSD - defect in the muscular portion
46

What are the hemodynamics of a Ventricular Septal Defect?

  • Blood shunt from LV to RV
  • Increase blood volume in the right ventricle
  • Equalization of pressure across the ventricles
  • LV hypertrophy/RV hypertrophy
47

What is valvular dysplasia?

Can be difficult to appreciate. Most common in dogs/cats.

  • Short, tick, misshapen leaflets
  • Rolled edges
  • Absent or short cordae tendinae
  • Fusion of leaflets or the chordae to the ventricular wall
  • Thick or atrophic papillary muscles
48

What does valvular dysplasia normally result in?

Typically causes valvular insufficiency - regurgitation though the valve.

Or can cause stenosis of the valve. Rare.

49

What are the hemodynamics of valvular dysplasia?

  • Dysplastic valve is insufficient
  • Regurgitant blood flow during systole
  • Volume overload of atrium and ventricle
  • Atrial dilation. Eccentric ventricular hypertrophy.
50

What is a pulmonic stenosis?

A stenosis is a narrowing of the valve orifice. Constriction bond of fibrous or muscular tissue or fusion of the valve leaflets. Depending on the location, pulmonic stenosis is classified as: valvular, subvalvular or supravalvular. Valvular is most common.

51

What are the hemodynamics of a Pulmonic Stenosis?

  • Stenotic valve restricts outflow
  • Pressure overload of RV
  • RV concentric hypertrophy
  • Right heart failure
52

What is a Subaortic Stenosis (SAS)?

  • Narrowing of the aortic valve orifice
  • The stenotic site is typically formed by a constricting band of fibrous or muscular tissue
  • Post-stenotic dilation is frequently found in the aorta
53

What are the hemodynamics of a Subaortic Stenosis (SAS)?

  • Stenotic valve restricts outflow.
  • Pressure overload of LV
  • LV concentric hypertrophy
  • If severe: 1. arrhythmias and sudden cardiac death 2. congestive heart failure
54

What lesions are normally found in a Subaortic Stenosis?

  • Post-stenotic dilation is often found in the aorta distal to stenosis
  • Jet lesions - endocardial fibrosis. Indicate damage to the intima due to turbulent blood flow.
55

What are the defects noted in Tetralogy of Fallot?

  1. Ventricular septal defect
  2. Overriding aorta
  3. Pulmonic stenosis
  4. Right ventricular hypertrophy (RVH)
56

What are the hemodynamics of Tetralogy of Fallot?

  • Stenotic valve restricts outflow
  • Pressure overload of RV
  • RV concentric hypertrophy
  • R to L shunt through VSD
  • Cyanosis
57

What tends to happen to those with Tetralogy of Fallot?

Affected animals tend to die as a result of severe hypoxia and hyperviscosity syndrome rather than heart failure.

58

What is a persistent right aortic arch?

  • Aorta incorrectly formed from the 4th right aortic arch rather than from the left 4th aortic arch in embryo.
  • Trachea and esophagus enclosed by; right aortic arch, pulmonary artery, ligamentum arteriosum. Causes localized esophageal constriction.
  • Esophageal constriction results in dysphagia, reurgitation and megaesophagus
  • No cardiac signs
59

What is an ectopic cordis?

It is when the heart is in an abnormal location.

60

What are the abnormal locations of the heart in an ectopic cordis?

  • Extrathoracic
  • Intraabdominal
  • Pre-sternal
61

What can cause notable pericardial sac enlargement (distension of the pericardial sac)?

  • Excess fluid
  • Non-fatal progressive pericardial hemorrhage
  • Exudate in pericarditis
  • An enlarged heart
62

What is the difference between a pericardial effusion formed from transudate, blood and exudate?

  • Transudate - hydropericardium (clear fluid, low cellularity and low protein)
  • Blood - hemopericardium (red fluid, RBCs and protein)
  • Exudate - pericarditis (turbid fluid, high cellularity and high protein
63

What is a pericardiocentesis used for?

  • Therapeutic reasons
  • Diagnostic testing
64

What is the pathogenesis of a transudate in the pericardial sac?

Pericardial surfaces remain smooth and glistening

  • Increased hydrostatic pressure: right heart failure
  • Decreased colloidal osmotic pressure (hypoproteinemia): starvation, protein losing enteropathy/nephropathy
  • Increased vascular permeability: sepsis, DIC, mulberry heart disease
  • Decreased lymphatic drainage - due to a heart based tumor
65

What is a hemopericardium?

Accumulation of blood in the pericardial sac

66

What causes a hemopericardium?

By atrial or aortic rupture:

  • Rupture of atrial hemangiosarcoma
  • Chronic valvular regurgitation and atrial dilation and rupture
  • Iatrogenic
  • Aortic rupture

Acute hemorrhage can cause cardiac tamponade, if severe can cause sudden death

67

What leads to a cardiac tamponade?

If intrapericardial pressure > intracardial pressure then compression of heart may prevent diastolic filling = cardiac tamponade.

68

What characterizes inflammation of the pericardium (pericarditis)?

  • Usually diffusive
  • Suppurative
  • Fibrinous
69

How would pericarditis present in a Cow?

  • Brisket edema and bottle jaw
  • Jugular vein distension
  • Murmur
  • Decreased GI motility and scant feces
  • Distended pericardium on US
  • Pericardiocentesis - fetid yellow fluid
70

What is traumatic reticuloperitonitis?

  • Metal objects from reticulum penetrates the reticular wall, diaphragm and pericardium
  • Pericardial sac filled with fibrinosuppurative exudate
71

What is Glasser's Disease?

  • Glaesserella (Haemophilus) parasuis
  • Causes fibrinous polyserositis: peritionitis, pleuritis, pericarditis, arthritis, meningitis
72

What are the differentials for Glassers disease?

  • Streptooccus suis
  • Mycoplasma hyohinis
  • Actinobacillus
73

What occurs with chronicity of pericarditis?

  • Organization of exudate leads to fibrosis and adhesions (organizing fibrinous pericarditis)
  • Heart is encased in fibrous tissue
  • Obliterates the pericardial space
  • Limits diastole expansion, can lead to right heart failure
74

What is acquired localized endocardial fibrosis?

  • Jet lesions
  • Abnormal blood turbulence in the atria or ventricles
  • Turbulence can result in mechanical injury damaging the endocardium
  • Most commonly seen in the atria in association with valvular insufficiences
75

What are the gross findings of Acquired localized endocardial fibrosis?

The endocardium appears focally thickened with a rough or corrugated surface.

76

What is acquired diffuse endocardial fibrosis and why is it relevant?

  • Occurs secondary to prolonged cardiac dilation
  • Grossly: the endocardium appears diffusely thickened with a rough or corrugated surface.
  • Clinical relevance: can impair and reduce stroke volume which can lead to congestive heart failure.
77

What is endocardial mineralization?

Abnormal deposition of calcium or mineral in the endocardium and arteries. Metastatic or dystrophic mineralization. The endocardium is roughened with pale yellow/white gritty plaques

78

What are the differentials for endocardial mineralization?

  • Hypervitaminosis D; iatrogenic, cholecalciferol rodenticides, toxic plants
  • Cachectic disease; Johne's disease, tuberculosis
  • Renal failure (uremia)
  • Paraneoplastic syndrome
79

What is a valvular cyst and is it important?

  • Particularly common in calves
  • There is no clinical significance, incidental findings
  • Cysts may rupture and disappear
80

What is the difference between a valvular hemocyst and a valvular lymphocyst?

  • Hematocyst - when the content is blood
  • Lymphocyst - when the content is clear fluid
81

What is Myxomatous Valvular Degeneration?

Degenerative heart valve disease = endocardiosis.

  • Common in dogs
  • Increased incidence with age (75% are 16yr)
  • Toy and small-med breeds
  • Mitral valve (80%)
  • Mitral and tricuspid (15%)
  • Tricuspid only (5%)
  • May or may not cause valvular dysfunction and clinical signs
82

What characterizes Myxomatous Valvular Degeneration?

Nodular thickening of the valve with a smooth, shiny surface.

83

What occurs if Myxomatous Valvular Degeneration is mild or severe?

If mild: typically no clinical signs

If severe:

  • Mitral valvular insufficiency
  • LV eccentric hypertrophy
  • Left atrial dilation
  • Jet lesions
  • Left congestive heart failure
  • Left atrial dilation
84

What occurs if you have rupture of the chordae tendinae?

You often get sudden collapse and death.

85

What is endocarditis?

Most frequently caused by bacteria and to a much lesser extent, fungi or parasites.

According to location, can be classified as: valvular endocarditis, mural endocarditis

86

What are the gross appearance of endocarditis?

  • Vegetative: cauliflower-like mass exudate and fibrin attached to a heart valve or endocardium
  • Ulcerative: when the endocardium is denuded
87

What are the clinical signs of endocarditis?

  • Pyrexia
  • Lameness
  • Murmurs
88

What are common isolates from Vegetative Valvular Endocarditis in cattle, in pigs an in horses?

Cattle - Trueperella pyogenes. Most often affects the right caval thrombosis

Pigs - Streptococcus suis, Erysipelothrix phrusiopathiae

Horses - Streptococcus equi, ACtinobacillus equuli

89

What are common isolates from vegetative valvular endocarditis in dogs and cats?

Dogs - Staphylococcus aureus, Streptococcus spp, Bartonella

Cats - Bartonella, Streptococcus

90

What is a common sequelae of vegetative valvular endocarditis?

  • Thromboembolism: mitral or aortic endocarditis leads to renal infarcts. Tricuspid and pulmonic endocarditis lead to embolic pneumonia or, less commonly, pulmonic infarcts
  • Congestive heart failure because of valvular dsfunction
91

What is the normal structure of myocardium?

  • Has striations (sarcomeres)
  • Cardiomyocytes are branched and join each other through the intercalated disks
  • Cardiomyocytes are susceptible to damage from hypoxia, free radicals, viruses, bacteria, toxins, etc
92

What does myocardial degeneration present as?

Loss of striations, hypereosinophilia, swelling, dissolution of sarcoplasm and myofibrils, and nuclear condensation

If severe, myocardial necrosis may be seen grossly as pallor

93

How does cell necrosis and calcification occur in myocytes?

In many degenerative diseases mineral is sequestered in the sarcoplasm/organelles of the cardiomyocytes. Causes myocardial calcification or mineralization

94

How do myocytes repair after necrosis?

  • Necrosis elicits an immune response
  • Macrophages and neutrophils infiltrate and start phagocytizing necrotic debris
  • Cardiac muscle has almost no ability to repair
  • Necrotic tissue is replaced by CT (fibroblast)
  • Results in myocardial fibrosis (scarring)
95

What can cause cardiomyocyte necrosis?

  • Ischemic
  • Toxic
  • Nutritional
  • Neurogenic
96

What is a heart attack?

  • Myocardial infarct.
  • Very common in humans; atherosclerosis means heart attack
  • Rare in animals
97

What are some examples of cardiotoxins?

  • Ionophores: monensin
  • Antineoplastic meds: cyclophosphamide, doxorubicin
  • Doxycycline (calve)
  • Toxic plants: gossypol, white snakeroot, Nerium oleander, Cassia occidentalis
  • Cantharidin (blister beetle)
98

What is a nutritional myopathy?

  • Affects farm animals
  • Often manifests as sudden death; occurs mostly in rapidly growing animals, exacerbated by exercise or stress
  • Can affect fetuses and cause abortion
  • For unknown reasons, sometime WMD affects only skeletal muscle, or cardiac muscle, and sometimes both.
  • Responds well to treatment, but only at the early stages of the disease
99

What is the pathogenesis of a nutritional myopathy (white muscle disease)?

  • Free radicals are pronounced during normal cardiac metabolism
  • Selenium and vitamin E deficiency
  • Decreased scavenging of free radicals
  • Peroxidation of cell membranes
  • Cardiac and skeletal muscle necrosis and mineralization
100

Where does nutritional myopathy effect in calves and lambs?

  • Affects LV in calves
  • Affects RV in lambs
101

What is neurogenic myocardial necrosis (brain heart syndrome)?

  • Brain trauma can cause myocardial necrosis
  • Possibly due to release of catecholamines
  • Catecholamine release from a pheochromocytoma causes the same lesions.
102

What are the different forms of myocarditis?

  • Suppurative (bacteria)
  • Lymphocytic (virus)
  • Eosinophilic (allergies/parasites)
  • Hemorrhagic (nasty bacteria)
  • Granulomatous (hard to clear)
103

What is Parvoviral myocarditis?

Canine Parvovirus (CPV-2).

Canine parvovirus causes enteritis. Rarely causes myocarditis in newborn pups.

104

What does Histophilus somni cause?

  • Thrombotic meningoencephalitis (TME)
  • Bronchopneumonia
  • Myocarditis - feedlots especially
  • Arthritis
  • Reproductive problems
105

What does myocarditis by Histophilus somni infection cause?

  • Vasculitis with infarction of the myocardium
  • OFten involves the papillary muscles
  • Can also cause multifocal myocardial abscesses
  • Can cause acute death or chronic progressive heart failure
106

What can Trueperella pyogenes?

  • Can cause infection and inflammation in many organs
  • In some cases blood dissemination leads to heart abscesses or endocarditis
107

What is a cardiomyopathy?

Refers to a primary myocardial abnormality that results in cardiac hypertrophy and/or electrical disturbances and may result in congestive heart failure or sudden unexpected death

Genetic or idiopathic in origin. Mutations in genes coding for contractile proteins, cytoskeletal proteins, mitochondrial enzymes.

108

What are the four main forms of cardiomyopathy?

  1. Hypertrophic cardiomyopathy (HCM)
  2. Dilated cardiomyopathy (DCM)
  3. Restrictive cardiomyopathy (RCM)
  4. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
109

What are the clinical signs of hypertrophic cardiomyopathy?

  • Lethargy, discomfort/hiding, dyspnea, tachypnea, acute paralysis of the hindlimbs
  • Often no overt signs, but detection of murmur
  • Occasionally causes sudden death. Anesthetic death.
110

How do the gross findings present in Hypertrophic Cardiomopathy?

  • Increased heart mass
  • Concentric hypertrophic
  • Symmetric or Asymmetric: LV, IVS, +/- RV
  • Left atrial dilation
  • Stiff fibers
  • Impaired ability to accept diastolic flow from the left atrium
  • Relatively normal systole until the end-stage
111

What are some less common gross findings of HCM (hypertrophic cardiomyopathy)?

  • Ventricular fibrosis
  • Atrial thrombosis (10-20% caudal aortic thrombi)
112

What is "Secondary hypertrophic cardiomyopathy"?

Non-genetic in origin

Hyperthyroidism in cats. Concentric biventricular hypertrophy is a compensatory change.

113

What is dilated cardiomyopathy?

  • Most common form of canine cardiomyopathy. Most common in large breed dogs.
  • Clinical signs include: dyspnea, depression, weight loss, syncope, murmur, arrhythmia, abdominal distension
114

What are the gross findings of dilated cardiomyopathy?

  • Increased heart mass
  • Biventricular eccentric hypertrophy and atrial dilation
  • Thin flabby walls
  • Attenuated papillary muscles
115

What is DCM characterized by and the histological changes?

Characterized by: progressive cardiac dilation, decreased contractile force, systolic dysfunction

Histology: Subtle changes, wavy attenuation of cardiomyocytes, degeneration and fibrosis

116

What is secondary dilated cardiomyopathy?

Taurine deficiency. Eccentric hypertrophy resembling DCM occurs in cats, farmed foxes and some breeds of dogs.

Recently increased incidence of dilated cardiomyopathy in dogs breeds not genetically prone to this disease. Correlation with BEG pet foods. Several brands and diets implicated.

117

What is restrictive cardiomyopathy?

  • Primarily in cats
  • Often used as a functional term rather than disease entity.
  • Diagnosed based on echocardiography
  • Characterized by left ventricular stiffness that impairs ventricular filling, impairs diastolic function
  • Ventricular thickness is typically normal
  • Systolic function is usually normal
  • One (left) or both atria are enlarged
  • Murmurs and dysrhythmias are common.
  • Left congestive heart failure often occurs
  • Few cats survive for more than 1 year after diagnosis
118

What are the gross findings of restrictive cardiomyopathy?

  • LY fibrosis
  • Endocardial
  • Myocardial
  • Atrial enlargement
  • +/- mural thrombi
  • Some cases may represent end-stage HCM or infarction from HCM
119

What is Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?

  • Primarily in Boxer dogs. Striatin gene mutations.
  • Less often in other dog breeds and in cats
  • May see: ventricular arrhythmias, syncope, heart failure, sudden death.
120

What are the gross findings and histology for ARVC?

Arrhythmogenic Right Ventricular Cardiomyopathy.

Gross findings: +/- eccentric hypertrophy of the right ventricle

Histology: replacement of RV (+/-LV) cardiomyocytes by adipose or fibroadipose tissue

121

What is an Excessive moderator band?

  • They are false tendons
  • CT bands span between the IVS and LV free wall
  • Minimal heart enlargement
  • Incidental or a rare cause of LHF
122

What is a congenital endocardial fibroelastosis?

  • Hereditory disease in Burmese cats
  • Diffuse endocardial fibrosis
  • LV eccentric hypertrophy
  • Histology: Abnormal deposits of collagen and elastic fibers in the endocardium
123

What are the 6 things that for the vascular system?

  • Arteries
  • Arterioles
  • Capillaries
  • Venule
  • Veins
  • Lymphatic vessels
124

What are the three layers of any tubes in the vascular system?

  • Tunica media
  • Tunica intima
  • Tunica adventitia
125

What are the conditions characterized by hardening of the arterial wall with loss of elasticity +/- reduced vascular lumen?

  • Arteriosclerosis
  • Atherosclerosis
  • Arterial (medial) hypertrophy
  • Aneurysms
  • Fibrinoid necrosis
  • Vasculitis
126

What is arteriosclerosis?

  • Degenerative change that results in hardening of the artery
  • Mainly found in elastic arteries (aorta)
  • Arterial branching sites are commonly affected, turbulance may play a role. Typically no clinical significance
127

What are the gross and histological findings with arteriosclerosis?

Grossly: intima has raised corrugated white plaques +/- mineralization

Histological: Fibrosis in the intima, smooth muscle hypertrophy in the media

128

What is atherosclerosis?

  • Refers to the formation of cholesterol plaques in the intima and media of arteries
  • Large elastic arteries and medium arteries
  • Common in humans: coronary artery is heart attack, carotid/cerebral arteries is stroke)
  • Rare in animals
129

What can cause atherosclerosis in dogs?

  • Hyprhtyroidism
  • Diabetes mellitus
  • Hyperlipoproteinemia
130

What are the gross lesions and histology that occur in atherosclerosis?

  • Prominent thick yellow - white arteries
  • Histology: plaques in the intima and media, composed of foamy lipid-laden macrophages, cholesterol clefts, fibroblast and smooth muscle proliferation
131

What is medial hypertrophy?

  • Occurs in muscular arteries
  • Characterized by hypertrophy of the smooth muscle (medial hypertrophy)
  • Can result in loss of elasticity and occlusion of the arterial lumen
  • Often caused by systemic hypertensions or increased volume flow
132

What is the progression of medial hypertrophy?

  • High altitude
  • Chronic alveolar hypoxia
  • Pulmonary arterial constriction
  • Medial hypertrophy
  • Increased vascular resistance
  • RV hypertrophy
  • RHF - cor pulmonale
133

What is an aneurysm?

Refers to localized weakening and dilation of blood vessels. Particularly elastic arteries and to a lesser extent veins.

Aneurysms are prone to rupture and cause hemothorax, hemoabdomen, hemopericardium, etc.

134

What are the two main anatomic types of aneurysms?

  • Saccular aneurysms: spherical dilation of the blood vessel resembling balloon willed with blood
  • Dissecting aneurysms: a tear of the intima allows blood to enter into the potential space between the intima and media, progressively dissecting the wall of the vessel
135

What are the most common causes of aneurysms in horses, dogs and pigs?

  • Horses - strongylus vulgaris. Cranial mesenteric artery and aorta
  • Dogs - Spirocerca lupi in the aorta
  • Mares and pigs - Copper deficiency, uterine artery
  • Trauma
136

What is fibrinoid necrosis?

Refers to the vascular necrosis with the microscopic deposition of acidophilic proteinaceous material in the walls of the arteries and platelets.

137

What is fibrinoid necrosis associated with?

  • Viral infections: CSF, PCV-2, MCF
  • Toxic conditions: uremia, mercury poisoning
  • Bacterial toxins: enterotoxemia, edema disease of swine
  • Nutritional deficiencies: Mulberry heart disease
  • Immune mediated vasculitis: systemic lupus erythematosus. Purpura hemorrhagical in horses: Streptococcus equi
138

What is Mulberry heart disease?

Vitamin E/Selenium deficiency leads to decreased scavenging of free radicals leads to fibrinoid necrosis and thrombosis of small vessels leads to hemorrhage and necrosis in the heart

139

What is vasculitis?

Refers to inflammation of the blood vessels.

140

What are common causes of vasculitis:

  • Systemic infections (virus, bacteria, fungi) or toxins
  • Hypersensitivity reaction/autoimmune reactions Ag-Ab complex deposition
  • Adverse drug reactions
141

What are the consequences of vasculitis?

  • Hemorrhage
  • Edema
  • Thrombosis (leads to DIC)
  • Infarcts
142

What is arteritis caused by?

  • Strongylus vulgaris - verminous arteries
  • Dirofilaria immitis - heartworm disease
143

What is Strongylus vulgaris and what does it cause?

  • Causes arteritis in the Verminous artery
  • Larvae (L4) migrate in the wall of the aorta and mesenteric artery. Damaged the wall of the vessel inducing inflammation
  • Adult worm lives in the small intestine
144

What is Dirofilaria immitis and what does it cause?

  • Parasite of dogs that causes arteritis or heart worm disease
  • Adult worms in the pulmonary arteries
  • Infections are often asymptomatic, detected on routine blood testing
  • Occasionally infects cats, wild felids and canids, ferrets, etc.
  • Often produce no or few microfilariae. Can be difficult to diagnose on routine testing.
145

What is the progression of Dirofilaria immitis?

  • Adults in lumen of Pulmonary arteries
  • Proliferative endoarteritis and arteriosclerosis
  • Pulmonary hypertension
  • Right heart failure
146

What are the clinical signs of heart disease?

Cough, exercise intolerance, dyspnea, ascites

147

What is phlebitis?

  • Refers to inflammation of the veins
  • Inflamed veins often become thrombosed leads to thrombophlebitis
148

What are the most common forms of thrombophlebitis in vet practice?

  • Iatrogenic jugular thromboplebitis in all species, a potential complication of venipuncture
  • Femoral thrombophlebitis, prolonged prostration in large animals can result in inflammation and thrombosis of femoral veins.
  • Vena caval thrombosis in cattle
  • Omphalophlebitis
149

What is omphalophlebitis?

  • Inflammation of the umbilical vein
  • Particularly common in farm animals
  • Ascending infection after birth, opportunistic bacteria (E. coli).
  • Sepsis may result
150

What are the most common primary cardiovascular tumors seen in domestic animals?

  • Hemangiosarcoma/hemangioma
  • Rhabomyoma/Rhabdomyosarcoma
  • Heart base tumor: aortic body chemodectoma, carotid body chemodectoma
  • Mesothelioma
151

What is the most common secondary cardiovascular tumor in domestic animals?

  • Lymphoma
152

What is a hemangioma?

  • Benign tumor of endothelial cells
  • Common in dogs
  • Less often in cats, horses and ruminants
  • Can arise in any tissue
  • Most common in the skin
153

What is a hemangiosarcoma?

  • Malignant tumor of endothelial cells.
  • Hemangiosarcoma is an important canine malignancy. Less common in cats, cattle, horses, etc.
  • Hemangiosarcoma most commonly arises in the right atrium and the spleen
  • Other common sites include the liver and lungs, and can occur to any site.
  • Masses are often dark red in colour and can be single or multiple
  • Bloody on section
154

What are the consequences of a cardiac hemangiosarcoma?

  • Can cause cardiomegaly, congestive heat failure, hemopericardium, +/- cardiac tamponade
  • Readily metastasizes to the lungs, liver, brain, spleen.
155

What is a Rhabdomyoma and a Rhabdomyosarcoma?

  • Rhabdomyoma - Benign tumor of skeletal muscle
  • Rhabdomyosarcoma - malignant tumor of skeletal muscle

Cardiac rhabdomyoma has been described in pigs, cattle, sheep. Often found incidentally at slaughter.

May be congenital. Appears as a white solid mass within the myocardium

156

What is a chemodectoma (paraganglioma)?

Tumor of the chemoreceptors, aortic body tumor.

  • Usually benign
  • Typically non-functional
  • Aortic body tumors form single or multiple masses neat the base of the heart within the pericardial sac.
  • Hence a space-occupying mass.
  • Brachycephalic breeds are redisposed and may have concurrent aortic tumors occur in the neck
157

What is a chemodectoma?

Aortic body tumor. Grey-white nodular mass surrounding the great arteries at the heart base.

158

What are the differentials for a chemodectoma?

Include other neoplasms that may cause a heart base mass:

  • Ectopic thyroid carcinoma
  • Mesothelioma
159

What is a mesothelioma?

  • May arise form the pericardium
  • Diffuse pericardial involvement is more common than discrete mass, causes pericardial effusion, which can lead to cardiac tamponade.
  • May have concurrent pleural and/or peritoneal involvement and effusions
  • Can be difficult to diagnose.
160

What is lymphoma?

The heart is often involved with lymphoma in cattle (enzootic bovine leukosis - bovine leukemia virus)

161

What is the function of the kidney?

To maintain a constant extracellular environment.

162

How does the kidney maintain a constant extracellular environment?

  1. Regulation of water and electrolytes - filtration and reabsorption
  2. Excretion of metabolic waste products
  3. Elimination of foreign substances

Produces a large volume of protein-free glomerular filtrate. Selectively permeable filtration barrier. Selective reabsorption of constituents needed by the body

163

What is the nephron?

The functional unit of the kidney

164

What is the nephron composed of?

  • Renal corpuscle
  • Renal tubules
165

What is the renal corpuscle composed of?

  1. Glomerulus
  2. Its surrounding Bowmans capsule
  3. The space between them is the uriniferous space.
166

What are the renal tubules composed of?

  1. Proximal tubule
  2. Loop of Henle
  3. Distal tubules
167

What is a uriniferous tubule composed of?

Of a nephron and its collecting duct.

168

What is the glomerulus?

A complex, convoluted tuft of fenestrated endothelial-lined capillaries held together by the mesangium. The glomerular capillaries interdigitate with the visceral lining of Bowman's space.

169

What is glomerular filtration barrier composed of?

  1. Fenestrated endothelium of the glomerular capillaries
  2. The glomerular basement membrane (GBM) of basal lamina
  3. Pedicles of podocytes (visceral epithelial cells)
170

What are some general characteristics of the Glomerular filtration barrier?

  • Main function is to filter plasma to maintain ionic and osmotic homeostasis in the blood
  • The glomerular filtration barrier is size-selective. It is normally impermeable to large macromolecules such as proteins.
  • Small and medium-sized solutes pass through the filtrate are reabsorbed in the tubules and returned to the plasma.
171

How does the glomerular filtration barrier normally function?

  • The glomerular filtrate does not contain large macromolecules (protein)
  • The glomerular filtrate DOES contain ions (K, Na) and sugars (glucose)
  • Some components of the glomerular filtrate are reabsorbed to maintain homeostasis
  • These components are reabsorbed in the renal tubules
172

What is the proximal convoluted tubule?

Is metabolically very active because of its important function in reabsorbing much of the glomerular filtrate. 65% of sodium and water present in the glomerular filtrate

173

What is the loop of Henle?

  • The gradient of hypertonicity in the loops of Henle that extend into the medulla is important for water reabsorption.
174

What is the distal convoluted tubule?

Ion transport - especially Aldosterone mediated Na/K levels. Macula densa cells respond to changes in the sodium chloride levels in the distal tubule of the nephron.

175

What are the collecting ducts?

Controlled reabsorption of water

176

What is the only hypertonic tissue in the body?

The renal medulla is the only one.

  • The vasa recta, containing mainly blood which has been filtered through the glomeruli, play a prominent role in maintaining the high osmolarity of the medullary interstitial.
  • The solute concentration of the medulla is about one half due to sodium, and one half due to urea.
  • The loops of Henle dip into the medulla, the hypertonicity of the surrounding medullary intersititium is important for water resorption.
177

What is the benefit of a very close apposition between tubular and vascular components of the kidney?

Very little intervening space. Allows for easy exchange of materials between the glomerular filtrate and blood

178

What is the order of the urinary system?

  • Nephrons
  • Collecting ducts
  • Renal calyves/renal pelvis
  • Ureter
  • Urinary bladder
  • Urethra
179

How does the blood flow through the kidney?

  • Flow to juxtamedullary nephrons is maintained more effectively than is flow to outer cortical nephrons.
  • May be directed from outer cortex to inner cortex under certain conditions.
  • Helps to better conserve water and help maintain the circulating blood volume.
180

What parts of the kidney are most susceptible to acute and low-grade prolonged ischemia?

  • Cortex most susceptible to acute ischemia
  • Medulla is more susceptible to low-grade prolonged ischemia and to infection
181

What is renal disease?

Any deviation from normal renal structure or function, without implying clinical significance.

182

What is renal failure?

Inability of the kidney to maintain normal function, and consequent loss of homeostasis. Renal failure requires a loss of 75% of renal function.

183

What is Urea and Creatinine?

Metabolic waste products that are excreted in the urine at a relatively constant rate. Abnormal retention in the blood implies reduced glomerular filtration rate

184

When can a reduced GFR be seen?

  1. Prerenal disease (decreased renal perfusion)
  2. Renal disease (acute kidney injury or chronic renal failure)
  3. Post-renal disease (urinary tract obstruction
185

What is azotemia?

Biochemical abnormality

Refers to blood elevation of urea and creatinine.

Mostly due to decreased glomerular filtration rate

186

What is uremia?

  • Clinical condition
  • Results in azotemia build up in the body and become associated with a constellation of clinical signs
  • Extrarenal lesions may be seen
  • Uremic animals are always azotemic, but azotemic animals are not necessarily uremic.
187

What is prerenal azotemia?

Renal hypoperfusion leading to decreased GFR

Dehydration (most frequent), heart failure, hypovolemia, shock

188

What is renal azotemia?

Renal disease - reduced GFR- failure to filter or excrete metabolic waste products.

  • acute kidney injury, chronic renal failure
  • Nephritis, nephrosis, amyloidosis, end-stage kidney disease
189

What is postrenal azotemia?

  • Urinary tract obstruction - inability to excrete urine - reduced GFR
  • Ureteral or urethral calculus, urethral or ureteral obstruction by a bladder tumor, rupture of the urinary bladder, etc.
  • Urinary tract obstruction leads to hyperkalemia - cardiovascular depression
190

What are the extra-renal lesions that can be seen in uremia?

  • Uremic stomatitis/glossitis
  • Uremic gastritis and colitis
  • Endocarditis/mucocarditis
  • Tissue mineralization
  • Pulmonary edema
  • Visceral gout in birds
  • Other biochemical, functional and morphological changes
191

What is uremic stomatitis?

Urea in saliva. Oral bacteria produce urease, which transforms urea in to ammonia, ammonia irritates the oral epithelium. Ulceration of the mucosa with adhered brown, foul-smelling, mucoid material

192

What is uremic gastritis?

  • Mucosal mineralization
  • Degeneration of arterioles in mucosa or submucosa with resultant infarction
193

What is uremic endocarditis/mucocarditis?

  • Finely granular, rough plaques due to subendothelial degeneration
194

What is Uremic tissue mineralization?

  • Mainly seen in dogs
  • Can be seen in the pleura, pericardium, stomach, kidney, arteries and lung
  • Finely granular, white plaques. Most commonly seen grossly in the costal pleura
  • Due to a combination of metastatic mineralization and dystrophic mineralization
195

What is uremic pneumonopathy (pulmonary edema)?

Uremic damage to air-blood barrier.

Plus or minus: mineralization of vascular basement membrane, heart failure, hypoproteinemia, plasma fluid leaks into alveoli leads to pulmonary edema

196

What is visceral gout in birds?

  • Urate deposits (chalky material) on the surface of visceral organs, such as the epicardium and liver
  • Main underlying problems: dehydration and/or renal failure
197

What other biochemical, functional and morphological changes can occur during renal failure?

  • Acidosis
  • Anemia
  • Heart failure
  • Hypertension
  • Dehydration
  • Edema and ascites
  • Depression
  • Fibrous osteopathy
  • Thrombosis
198

What are the 8 developmental abnormalities and familial renal diseases?

  1. Renal aplasia
  2. Renal hypoplasia
  3. Renal dysplasia
  4. Renal cysts and Polycystic kidney disease (PKD)
  5. Familial renal disease (progressive juvenile nephropathy)
  6. Ectopic kidneys
  7. Ectopic ureters
  8. Patent urachus
199

What is renal aplasia?

One or both kidneys fail to develop. Rare

May be associated with other congenital developmental abnormalities. Cardiac defects, dysraphism, abnormal developmental of gonads

May be unilateral or bilateral? Unilateral is often an incidental finding accompanied by hypertrophy of the contralateral kidney. Bilateral is not compatible with life.

200

What is renal hypoplasia?

You know. Rare. Unilateral and bilateral.

Grossly can be difficult to differentiate from renal dysplasia and renal fibrosis. But, with renal hypoplasia the ratio of cortex to medulla is usually normal. Bilateral renal hypoplasia usually progresses into renal failure.

201

What are some general characteristics of a renal cyst?

All species, especially pigs and calves.

Can be unilateral or bilateral. May be few or many cysts, in cortex and/or medulla. Variable size.

Often fluid-filled and lined by attenuated epithelium.

May results from: tubular epithelial basement membrane diverticula or tubular epithelial disordered growth with cystic hyperplasia.

202

What is PKD?

Polycystic kidney disease. Persian cats and Bull Terrier dogs. Both forms can be associated with biliary and pancreatic cysts.

203

What are the two forms of PKD?

  • Recessive form: Rapidly progressive. Massive nephromegaly diagnosed in infancy. Cysts are small and involve the cortex and medulla. Hepatic fibrosis is also a consistent finding.
  • Dominant form: slowly progressive,. Can lead to death from renal failure in late adulthood. Cysts can be up to 3-4cm, gradual increase in size. Cysts replace entire renal parenchyma.
204

What is an ectopic kidney?

  • Ectopic kidneys - normal kidneys in abnormal locations, Usually in pelvic or inguinal region
  • Most commonly seen in pigs and dogs
  • May unilateral or bilateral
  • Ectopic kidneys have normal function but are prone to ureteral obstruction and subsequent hydronephrosis.
205

What are ectopic ureters?

Termination of one or both ureters at a site other than the trigone of the urinary bladder. Most often terminates in the urethra.
Rare. But the second most common cause of primary urinary incontinence in dogs.

206

What might an ectopic ureter predispose you to?

To vesicouretral reflux. Predisposing factor for development of pyelonephritis.

207

What is a patent urachus?

  • Urachus: normal fetal communication between the urinary bladder and the umbilicus. Normally the urachus closes at birth.
  • Patent if it sticks around after birth. Also considered a patent urachus if it reopens after birth.
208

What is the main issue of a patent urachus?

Bacterial urinary tract infections.

209

What are the two postmortem changes noted in the liver?

  1. Autolysis
  2. Pseudomelanosis
210

What are the 4 antemortem lesions observed in the urinary tract?

  1. Hyperemia and congestion
  2. Lipofuscinosis
  3. Hemoglobin
  4. Myoglobin
211

What is autolysis?

Common finding at necropsy. Kidneys are soft, friable and pale.

Kidneys pay become "pulpy" in appearance

212

What is pseudomelanosis?

  • Dark discolouration in autolyzed tissues
  • Bacteria - hydrogen sulfide - reacts with iron in hemoglobin - forms black FeS pgiment
213

What is hyperemia and congestion?

  • Bright or dark red kidneys
  • Can be physiological or pathological: hyperemia of inflammation, passive congestion, hypostatic congestion
214

What is lipofuscinosis?

  • Diffusely dark brown kidneys
  • Lipofuscin - aging pigment
  • Accumulates in tubular epithelial cells over time to regular turnover of cells
  • An incidental finding seen in adult cattle.
215

What is hemoglobinuria?

Caused by accumulation of hemoglobin. Dark red to black kidneys. Seen due to intravascular hemolysis

216

What is myoglobinuria?

Caused by accumulation of myoglobin. Dark red or black kidneys. Seen in severe rhabdomyolsis (skeletal muscle damage). Capture myopathy, etc.

217

What is the process of hemoglobinuric nephrosis?

IV hemolysis-anemia-hypoxia-hypoxic tubular necrosis

hemoglobinemia-hemogloinuria-hemoglobin casts-tubular obstruction and dilation-constricts peritubular capillaries and veins-worsens hypoxia-exacerbates hypoxic tubular necrosis

Intracellular hemoglobin dissociates into heme and globin. Ferrihaemate has a direct nephrotoxic effect which potentiates acute tubular necrosis-hypoxic and toxic tubular necrosis

218

How would you differentiate between hemoglobin and myoglobin?

  • Hemoglobin: IV hemolysis - RBCs in circulation rupture - free hemoglobin + decreased RBC #s - anemia = hemoglobinuric nephrosis + pink plasma
  • Myoglobin: Severe rhabdomyolysis - free myoglobin + muscle enzymes released into circulation - increased CK + myoglobinuric nephrosis + clear plasma
219

What are the characteristics of a renal hemorrhage?

Common, often overlooked at post mortem. Remove renal capsule to examine renal parenchyma.

Petechial or ecchymotic. Glomeruli are often preferentially involved.

Looks like a turkey egg.

220

What are the general characteristics of a renal infarct?

  • Kidneys have end arteries or terminal arteries, an artery that is the only supply of blood to a portion of tissue. Very little collateral blood supply
  • Renal infarcts are typically triangular shaped due to thrombosis/thromboembolism of renal vessels
  • Size of infarct depends on size of affected vessels
221

What is the difference between a interlobar artery obstruction and a interlobular artery obstruction?

Interlobar artery obstruction: Cortex + medulla affected

Interlobular artery obstruction: Cortex only infarcted

222

How do acute and chronic renal infarcts present?

  • Acute. Red. Swollen and dark red due to hemorrhage. Infarction of blood vessels in affected wedges
  • Chronic. Pale. Red cell lysis and removal (2-4 days) Parenchymal loss. Healing by fibrosis (Weeks to months). The fibrosis contracts the lesion resulting in cortical depression. May be surrounded by a thin rim of hyperemia.
223

What is the progression of renal infarcts?

  1. Acute renal infarcts - swollen and red (slight buldge)
  2. Subacute renal infarcts - pale center, hyperemic rim
  3. Chronic renal infarcts - pale and depressed
224

What is the most common cause of renal infarcts?

Valvular endocarditis in the left side of the heart. Mitral valves, aortic valve. Most commonly seen in: cattle and pigs.

225

What is diffuse renal cortical necrosis?

Widespread renal vascular thrombosis.

Occurs with: endotoxemia/septicemia, DIC, can also by caused by severe hypoperfusion (hypovolemic, cardiogenic, septic)

Grossly: results in a mosaic pattern of necrosis. Reflects the functional heterogeneity of the organ.

226

What is renal medullar (papillary) necrosis?

  • Caused by low-grade, prolonged ischemia/ hypoperfusion
  • Treatment with anti-inflammatory and analgesic drugs.
  • NSAIDs, phenacetin, aspirin. Inhibits the synthesis of PGEs in the renal medulla - decrease blood perfusion to papillary interstitium. Dehydration is an important compounding factor.
  • Secondary to other renal lesions that decrease medullar vascular perfusion. Medullary amyloidosis (cats), pyelitis, pelvic calculi. Occlude or compress medullary blood vessels.
227

What is hydronephrosis?

Abnormal and permanent dilation of the renal pelvis, with progressive loss of renal parenchyma. Can be unilateral or bilateral.

Caused by increased pressure in the kidney due to partial or complete urine outflow obstruction. The urine outflow obstruction can be anywhere from the renal pelvis to the urethra.

Hydroureter (dilation of the ureter) is also often seen with hydronephrosis.

228

What can glomerular lesions cause?

  • Interference with glomerular blood flow (decreased formation of filtrate and peritubular blood flow)
  • Altered glomerular permeability (leakage or proteins into uriniferous space leads to proteinuria)
229

What are the four things that proteinuria can lead to?

  • Hypoproteinemia
  • Hyperlipoproteinemia/hypercholesterolemia
  • Hypercoagulability
  • Immunosupression
230

How does proteinuria lead to hypoproteinemia?

Protein loss in urine leads to hypoproteinemia leads to decreased intravascular oncotic pressure leads to generalized edema and cavitary effusions.

231

How does proteinuria lead to Hyperlipoproteinemia/hypercholesterolemia?

Hypoproteinemia leads to generalized increase in protein production by the liver leads to increased lipoproteins leads to hyperlipoproteinemia and hypercholesterolemia

232

How does proteinuria lead to hypercoagulability?

Antithrombin III loss in urine leads to decreased anticoagulants in blood lead to hypercoagulability

233

What are the nephrotic symptoms that proteinuria can lead to?

  1. Hypoalbuminemia
  2. Proteinuria
  3. Hyperlipidemia
  4. Fluid accumulation in interstitial spaces and/or body cavity. Edema and cavitary effusions

Effected animals frequently have markedly abnormal urine protein: creatinine (UP:UC) ratios because of urinary loss of large amounts or protein.

234

What is embolic nephritis?

Also called suppurative glomerulitis. Caused by bacteremia. Bacteria in blood stream leads to bacteria thromboemboli in glomerular capillaries and intersitial capillaries lead to suppurative glomerulitis. If the animal survives, focal lesions may progress to form renal abscesses.

235

What are the two main immune-mediated mechanisms of Glomerulonephritis (GN)?

  1. Glomerular deposition of antigen-antibody complexes
  2. Autoantibodies directed against the glomerular basement membrane (GBM)
236

How does Glomerular deposition of antigen-antibody complexes lead to glomerulonephritis (GN)?

  • Persistent antigenemia leads to Ag-Ab complexes, deposition of complexes in glomerular basement membrane, complement fixation on GBMs, leukocyte infiltration
  • Deposition of the antigen-antibody complex is irregular, resulting in "lumpy-bumpy" thickening of the GBMs.
  • Persistent antigens can be viral, bacterial, parasitic, or other. Often idiopathic
237

How do autoantibodies directed against the GBM lead to glomerulonephritis?

  • Autoantibodies directed against the GBM, complement fixation on GBMs, leukocyte infiltration
  • Rate in domestic animals
  • Uniform linear thickening of GBMs. Antibodies are individualized in the blood, distribute more evenly in GBM, linear thickening of GBM.
238

How is GN definitively diagnosed?

  • Immunofluorescence
  • Transmission electron microscopy (TEM)
239

What lesions are visible with GN, but acutely and chronically?

  • Acute: subtle lesions - kidneys appear swollen and pale
  • Chronic: Kidneys shrunken and granular. Gross lesions overlap with chronic interstitial nephritis.
  • Worsening glomerular lesions leads to end stage kidney.
240

What is renal amyloidosis?

Heterogeneous group of disease caused by deposition of amyloid tissues.

Kidney is the organ most commonly affected by amyoidosis: glomeruli (usually), medulla (Cats).

241

What is primary amyloidosis?

Deposition of amyloid lead to glomeruli. Derived from immunoglobulin light chains produced by abnormal plasma cells.

Rare in domestic animals

242

What is secondary (reactive amyloidosis)?

Deposition of a portion of serum amyloid A, leads to glomeruli. Associated with chronic antigenic stimulation.

Most common form in domestic animals

243

What is familial amyloidosis?

Deposition of amyloid fibrils, medullar interstitium.

Associated with production of abnormal proteins which deposits in tissues as amyloid fibrils.

244

What are the two breeds associated with Renal amyloidosis?

  • Chinese Shar Pei dogs
  • Abyssinian cats
245

What are the gross lesions of renal amyloidosis?

  • Kidneys are enlarged, pale, tan to yellow, and may have a waxy texture
  • The kidneys have a granular surface
  • Amyloid stains black when Lugol's iodine is applied to fresh tissue.
246

What are the microscopic lesions of renal amyloidosis?

  • Deposits of pink amorphous material in the glomeruli or in the medullar interstitium
  • Apple-green birefringence when stained with the special stain Congo red and viewed under polarized light
247

What is acute renal cortical tubular necrosis and what are the two types?

Very susceptible to ischemic or toxic damage.

  1. Ischemic tubular necrosis
  2. Nephrotoxic tubular necrosis
248

What does ischemic tubular necrosis follow?

  • Follows a period of hypotension (shock) or severe acute anemia.
  • Endogenous compounds may exacerbate the tubular necrosis
  • May affet the tubular basement membranes
249

What are the gross lesions and microscopic lesion of ischemic tubular necrosis?

  • Gross lesions: Swollen kidney, possible colour change
  • Microscopic lesions: patchy tubular necrosis
250

What happens to the tubular basement membrane during nephrotoxic tubular necrosis?

Typically preserved. Potential for repair is good if the animal survives the acute stage of the disease.

Ex": ethylene glycol - oxalate crytalluria

251

What is the disease process of acute tubular necrosis?

  1. Ischemic or toxic both cause acute necrosis characterized by cellular swelling, pyknosis, karyorrhexis and karyolysis.
  2. Subsequent to nephrotoxic necrosis, there is sloughing of necrotic epithelium into the tubular lamina. The basement membranes remain intact and act as a scaffold for tubular epithelial regeneration to occur.
  3. Ischemia may result in tubularrhexis. Necrotic epithelial cells slough into the tubular lumen, the basement membrane is disrupted, macrophages infiltrate and fibroblasts proliferate.
  4. Fibrosis with tubular atrophy results.
252

What is crystaluria?

Crystal precipitates. Seen in some types of nephrosis. Oxalates, urates, sulfa toxicity, melamines.

Dehydration facilitates deposition of some crystals in renal tubules

253

What is interstitial nephritis?

  • Damage to the tubules and/or interstitium results in local inflammation. Tubules and interstitium are intimately associated, so damage to one affects the other.
  • Results in impaired resorption and concentration of glomerular filtrate and/or impaired excretion of metabolic products.
  • Can be multifocal or diffuse.
254

What is multifocal interstitial nephritis?

  • Common incidental findings.
  • Often seen grossly: few to many small while foci or streaks
  • Microscopically: aggregates of lymphocytes and plasma calls in the renal interstitium
  • Can progress to interstitial fibrosis
  • Presumed to be foci of previous infection and inflammation (white spotted kidney)
255

What is diffuse interstitial nephritis?

  • Uncommon
  • Diffuse tubulinterstitial disease
  • Best illustrated by Lepto. Evades host immune systme while still inciting inflammation - diffuse interstitial nephritis
256

What is the difference between acute and chronic cases of diffuse interstitial nephritis?

  • Acute case: kidneys are diffusely swollen and mottled appearance
  • Chronic cases: kidney shrunk, pale and firm, and the capsule is firmly adherent to the cortex. Can progress to chronic renal failure and "end-stage kidneys.
257

What is pyelitis and pyelonephritis?

  • Pyelitis - inflammation of the renal pelvis
  • Pyelonephritis - inflammation of the renal pelvis and renal parenchyma.

Most often is purulent in nature

258

What is the pathogenesis of pyelonephritis?

  • Cystitis - ascending bacterial infetion-bacteria ascend ureters-bacteria and inflammation infiltrate and damage the renal pelvis-renal CDs and tubules-renal parenchyma-pyelonephritis
  • Not necessarily symmetrical between the two ureters of kidneys
  • Females > males
  • Predisposed by vescioureteral reflux
259

What is vesicoureteral reflux (VUR)?

  • Retrograde flow of urine form the bladder up the ureters during urination
  • May carry bacteria all the way up to the kidneys
  • Normally prevented by the oblique insertion of the ureters into the bladder wall = a functional vesicoureteral valve.
260

What is VUR common in?

Vesicoureteral reflux (VUR).

  • Shorter intravesical length or the ureters
  • Less oblique entry through the bladder wall
  • May resolve. If does not resolve, may be due to a congenital defect.
261

What can predispose you to a VUR?

Vesicoureteral reflux.

  • Cystitis, ureteritis-loss of muscle tone-altered ureteral peristaltic waves-decreased integrity of vesicouretheral valve
  • Failure of the bladder to empty properly can also cause VUR. Urethral blockage, bladder muscle failure, damage to the nerves that cause bladder emptying
262

What is the most susceptible part of the kidney to infection?

Medulla

  • First region of the kidney exposed to ascending infection
  • Relatively poor vascularity, relative hypoxia-decreased inflammatory response and decreased activity of leukocytes.
  • Hypertonic environment-decreased activity of leukocytes
  • Concentration of various metabolic waste products-interferes with inflammatory process.
263

What are the most common bacterial isolates from pyelonephritis in cattle, pigs, dogs and cats?

Cattle:

  • Corynebacterium renale
  • Escherichia coli
  • Trueperella pyogenes
  • Staphylococcus

Pigs:

  • Actinobaculum suis
  • E. coli
  • Trueperella pyogenes
  • Staphylococcus

Dogs and cats:

  • E. coli
  • Proteus spp.
  • Enterbacter spp.
  • Pseudomonas aeruginosa
264

What are the gross lesions seen in acute and chronic pyelonephritis?

  • Acute: mucopurulent exudate in pelvis, necrosis of renal papilla +/- extension up into cortex
  • Chronic: marked renal scarring and fibrosis, check for evidence or ureteritis and cystitis
265

What are the microscopic lesions of acute and chronic pyelonephritis?

Acute:

  • Suppurative inflammation in renal pelvis
  • Necrosis and exfoliation of epithelium with neutrophils and bacteria into renal tubular lumina

Chronic:

  • Interstitial fibrosis with loss of tubules and chronic residual lymphoplasmacytic inflammation, often with irregular widening of the renal pelvis.
266

What is the self-perpetuating process of chronic renal failure?

  • Compensatory capillary hypertension in surviving glomeruli and hyperfiltration by those glomeruli - glomerulosclerosis
  • Compensatory hyperfunction by surviving tubules-tubular injury
  • Altered renal metabolism from inflammation injuries surviving nephrons - tubular injury
  • Tubular injury - tubulointerstitial inflammation and fibrosis
  • Interstitial fibrosis - interferences with blood perfusion
267

What is an end-stage kidney?

  • When severe, chronic inflammation and fibrosis obscure the type of primary insult
  • Predominant gross lesion = renal fibrosis
268

What are 5 things that can leads to end-stage kidney?

  • Interstitial nephritis
  • Pyelonephritis
  • Glomerulonephritis
  • Granulomatous nephritis
  • Massive infarction
269

What is granulomatous nephritis?

  • Usually occurs with multisystemic granulomatous diseases such as feline infectious peritonitis (FIP)
  • Granulomatous inflammation may result in gross nodules or be microscopic
  • Occasionally, lesions can be difficult to differentiate from tumors.
270

What are 2 parasitic diseases that affect the kidney?

Dictophyma renale (dog, mink, cats)

Stephanurus dentatus (pigs)

271

What are the characteristics of Dioctophyma renale?

  • Effects dog, mink, cats
  • Giant kidney worm
  • Largest parasitic nematode (1m long)
  • Resides in the renal pelvis-hydronephrosis-destroys the renal parenchyma-renal capsule
  • Right kidney most commonly effected
  • Clinical signs: hemoturia, pollakiuria, weight loss, renal/abdominal pain
  • Urinalysis: proteinuria, hematuria, pyuria.
272

What is Stephanurus dentatus?

  • Parasite of pigs
  • Widely distributed in tropical and subtropical countries
  • Encysts in perirenal dat and adjacent tissues = perirenal cysts. The cysts communicate with the renal pelvis
273

What is urolithiasis?

  • Formation of solid or semi-solid concretions=urinary calculi=stones=uroliths
  • Composed of a wide variety of materials, often mixed with protein matrix
  • Vary in size, shape and consistency. From sand-like to large stones
274

What are uroliths composed of?

  1. Minerals - 90-98% of stone composition
  2. Organic matrix - 2-10% of stone composition

The organic matric often acts as a nidus for the formation and aggregation of crystal/mineral materials

275

What is Ruminant urolithiasis primarily considered?

Nutritional disease

  • Imbalance of minerals in diet and/or diet alters urine pH, both of which can favor formation of some types of uroliths
  • Diets high in phosphate-struvite uroliths
  • High level of silica in native pastures grazed by cattle-silica uroliths
  • Ruminant consuming high-oxalate plants-calcium oxalate uroliths
  • Ruminants on clover-dominant pastures-calcium carbonate uroliths
276

What can cause a struvite crystal in dogs and cats?

Bladder infection. Urease-positive bacteria-increase free ammonium ions and raises the urine pH-favor formation of struvite crystals. Neutralize to alkaline pH favors the formation of struvite crystals by: alkaline ph - increase of phosphate ions. Alkaline ph - decrease solubility of struvite

277

What is urolithiasis?

  • In dogs and cats, calcium oxalate calculi tend to form in acidic urine. Therefore are not usually associated with UTI
  • Factors involved in their occurrence are poorly understood. Dietary mineral content, genetics/metabolism influences on blood/urine.
  • In some cases they occur with hypercalcemia-hypercalciuria
278

What are the two most common types of uroliths in dogs and cats?

  1. Struvite (form in alkaline urine)
  2. Calcium oxalate (usually in acidic urine)
279

What are the possible consequences of urolith formation?

  • None (passed in urine)
  • Hydronephrosis, due to partial or complete obstruction of urine outflow.
  • Complete ureteral obstruction, pressure necrosis of ureter- ureteral rupture - uroabdomen
  • Chronic cystitis form from irritation by the uroliths and/or urine stasis due to partial urinary outflow obstruction
  • Complete urethral obstruction. Bladder distension and rupture-uroabdomen.
280

What does a urinary bladder rupture lead to?

Uroabdomen

281

What is urolithiasis?

Urethral obstruction. Common in males, longer and narrower urethra.

Tends to occur in particular anatomic sites among the urethra

Anatomic sites of predisposition for obstruction vary with species.

282

Where does a urethral obstruction tend to happen in Bulls, rams, dogs and tom cats?

  • Bulls: Ischial arch (pelvic brim) or sigmoid flexure
  • Rams: urethral process
  • Dogs: behind the os penis
  • Tom cats: anywhere along the urethra.
283

What is a urethral plug?

  • Common condition of male cats.
  • Characterized by obstruction of the urethra by a urethral plug. Typically mix of protein, cellular debris, and struvites Protein matrix = rubber-like
284

What is the pathogenesis of the urethral plug?

  • Bladder infection by virus
  • Alkaline urine pH
  • Inhibition of ureteral growth by early castration
  • Diet high in magnesium and phosphate
  • Cold winter months: decrease fluid consumption and less frequent urination
285

What is FLUTD?

Feline lower urinary tract disease.

Caused b either urethral plugs OR urethral calculi may be the cause of FLUTD

286

What do urethral plugs look like grossly?

  • Causes urinary outflow obstruction
  • Urinary bladder is distended, hemorrhagic and inflamed "plum bladder"
287

What is cystitis?

Due to bacterial infections, formations and accumulation of uroliths, or exposure to toxic compounds (uncommon).

Normal animal urine has natural antibacterial activity: low pH, high osmolarity, normal voiding of urine

Higher incidence of cystitis in females. Shorter and wider urethra. Bacteria involved are similar to those causing pyelonephritis

288

What are the toxic compounds that cause cystitis due to toxic compounds in a horse, cattle, dogs and cats.

  • Horses: ingestion of blister beetle: hemorrhagic cystitis
  • Cattle: ingestion of bracken fern: hemorrhagic to proliferative cystitis
  • Dogs & cats: treatment with cyclophosphamide: sterile hemorrhagic cystitis
289

Characteristics of acute cystitis?

  • May see mucosal hemorrhage and ulceration
  • May see hemorrhagic to fibrinosuppurative exudate
290

Characteristics of chronic cystitis?

  • Often results in mucous metaplasia of the transitional epithelium - mucous production
  • Often see formation of lymphoid follicles. If visible, follicular cystitis
  • Chronic inflammation can result in formation of inflammatory polyps
291

What does chronic cystitis often result in?

Often results in mucous metaplasia of the transitional epithelium - mucous production

292

What is follicular cystitis?

Think of nodular lymphoid hyperplasia as the body attempt at making tiny local lymph nodes in areas of chronic inflammation

293

What are urinary inflammatory polyps?

Chronic inflammation can result in formation of inflammatory polyps.

294

What is emphysematous cystitis?

  • Develops in some dogs and cats with diabetes mellitus
  • Thought to be caused by fermentation of excess sugar in the urine by glucose-fermenting bacteria
  • Emphysema (gas bubbles) in urinary bladder wall due to bacterial fermentation of glucose in urine
295

What is feline idiopathic cystitis?

  • Common condition in cats
  • MOST COMMON CAUSE of FLUTD
  • Most common in middle-aged, overweight, indoor, male cats
  • Diagnosis of exclusion. Made by ruling out over causes of UTI.
296

What is feline idiopathic cystitis characterized by?

  • Dysuria (painful urination)
  • Hemoturia (blood in urine)
  • Pollakiuria (abnormally frequent urination)
297

Are tumors of the urinary tract common?

They are quite rare. Bladder tumors>renal tumors.

Dogs>cats>other species

298

What are the 5 primary epithelial tumors of the urinary system?

  1. Renal adenoma
  2. Renal adenocarcinoma
  3. Nephroblastoma (embryonal nephroma)
  4. Transitional cell papilloma
  5. Transitional cell carcinoma
299

What are primary mesenchymal tumors?

  • Fibroma/fibrosarcoma, leiomyoma/leiomyosarcoma, hemangioma/hemangiosarcoma
  • Are rare in domestic animals
  • Can be seen with bracken fern poisoning in cattle
300

What are secondary mesenchymal tumors?

Lymphosarcoma (common multicentric/multisystemic disease)

301

How do renal adenomas present?

Rarely. Appears as small solitary cortical mass. Solid or a little papillated.

302

What are renal carcinomas?

  • More common than adenomas
  • Large compressive mass
  • Microscopic features: neoplastic epithelial cells arranged in tubules or papillary arrangements
303

What is a nephroblastoma (embryonal nephroma)?

  • Very common tumor in young pigs and chickens, uncommon in other species
  • Seen mostly as an incidental finding at slaughter
  • Large solitary mass or multiple masses
  • Microscopic features: fetal glomeruli, tubules, and mesenchymal components
  • Can be behaviourally benign or malignant
304

What is a transitional cell papilloma?

  • Rare, except in cattle grazing bracken fern
  • Inflammatory polyps are more common
  • Can be found in the mucous of the renal pelvis, ureter or urinary bladder.
305

What is a transitional cell carcinoma (TCC)?

  • Most commonly diagnosed tumor in the urinary bladder of domestic animals
  • Most ommonly found in the trigon of the bladder
  • Are usually solitary masses, but multiple masses can be seen.
  • Gross appearance: papillary masses or non-papillary/flt plauqes or masses
  • Frequently metastasizes to regional lymph nodes and lungs
306

What can Bracken fern poisoning result in?

  • Enzootic hematuria
  • Urinary bladder neoplasia: transitional cell papilloma, transitional cell carcinoma, sarcoma
307

How would you differentiate between bilateral renal lymphosarcoma and FIP?

Interpret the renal lesions within the full clinical picture.

Look for other lesions within the cat to help suport differentials.

308

What are the pancreas structure?

  • Endocrine pancreas - islets - insulin and glucagon. Hormones released into blood stream
  • Exocrine pancreas - acinar cells - digestive and electrolytes Digestive enzymes. Enzymes for digestion of lipids, proteins and carbohydrates
309

What is the pancreatic blood supply?

  • Capillaries radiate out from islet sinusoids.
  • Islet hormones - trophic or inhibitory effects on acinar cells.
310

What are enzymes stored as in the pancreas?

  • Stored and released as proenzymes
  • Proenzymes are activated in the gut
  • If activated within the pancreas ca cause acute necrotic necrosis
311

What is ectopic pancreatic tissue?

Incidental finding in dogs. Gross pathology: small nodules in the submucosa or muscularis of the stomach, intestine, and/or ballbaldder, in the parenchyma of the liver and spleen and/or in the mesentery.

312

What is exocrine pancreatic hypoplasia?

Sporadic in calves, rare in other animals. Results in exocrine pancreatic insufficiency (EPI). Clinical syndrome: deficiency of pancreatic enzymes, maldigestion, poor weight gains/weight loss

Islets are normal but acinar cells are small and basophillic.

313

What does exocrine pancreatic hypoplasia appear similar to?

Juvenile pancreatic atrophy in dogs.

Inflammation and lipofuscin accumulation are not seen in cases of pancreatic hypoplasia.

314

What are pancreatic duct abnormalities?

  • Literally anything where the ducts aren't attached normally/
315

What is exocrine pancreatic atrophy (juvenile pancreatic atrophy)?

  • Autoimmune pancreatitis
  • German Shepherds
  • Autosomal recessive inheritance
  • Causes exocrine pancreatic tissue loss - exocrine pancreatic insufficiency (EPI): maldigestion, weight loss, nutritional deficiencies.
316

What are the gross and microscopic findings for exocrine pancreatic atrophy?

Gross: very small pancreas

Microscopic: lymphocytic inflammation, lipofuscin, possible fibrosis and fatty infiltration. islets are usually normal

317

What are other causes of pancreatic atrophy?

  • Starvation
  • Loss of body condition due to chronic disease
  • Vitamin or mineral deficiency
  • Duct obstruction
318

What is the most important disease in the exocrine lecture?

Acute pancreatic necrosis

319

What is acute pancreatic necrosis?

Most common in dogs, also seen in cats. Miniature Schnauzers are more often affected. Genetic form in humans

Clinical signs: vomiting, diarrhea, anorexia, abdominal pain, pay progress to shock and death

320

What are predispositions to acute pancreatic necrosis?

Female gender, high fat diet, obesity, hyperlipidemia, hypothyroidism, hypercalcemia, uremia, abdominal trauma.

321

What are the mechanisms that lead to acute pancreatic necrosis?

Starts with pancreatic acinar cell injury. Occurs via three mechanisms.

  1. Pancreatic duct obstruction
  2. Direct injury to exocrine pancreatic acinar cells
  3. Disturbances to enzyme trafficking within acinar cells.
  4. Unknown mechanism - episodes after a high fat meal by a dog
322

What is the pathogenesis of acute pancreatic necrosis?

  • Initiating mechanism, exocrine pancreatic acinar ce injury, disruption of cells membranes
  • Extracellular calcium enters the damaged cells, increased intracellular calcium activates trypsin within the acinar cells
  • Trypsin activates elastase and phospholipase, autodiestion of the pancreas, peripancreatic adipocytes and local vasculature leads to release of inflammatory mediators and initiation of clotting cascade
  • Pancreatic and peripancreatic hemorrhage, edem, thrombosis and inflammation
  • Can lead to shock, DIC and death.
323

What does the autodigestion of the pancreas also affect?

The pancreatic islets.

Damaged islets release glucagon, glucagon stimulates thyroid C cells to release calcitonin. , hypocalcemia.

324

What is chronic relapsing pancreatitis?

Recurrent bouts of pancreatic necrosis necrosis and inflammation can occur.

Can eventually destroy the pancreas. Exocrine pancreatic insifficiency. Diabetes mellitus.

325

What are the gross pathology of acute pancreatic necrosis?

  • Pancreatic edema and hemorrhage
  • Perpancreatic edema
  • Peripancreatic enzymatic fat necrosis, local petionitis
326

What lesion in other organs may be seen in acute pancreatic necrosis?

  • Multifocal hepatic necrosis
  • Pulmonary edema or interstitial pneumonia
  • Myocardial necrosis
  • Renal failure
327

What are the findings in chronic pancreatic lesions?

Multifocal pancreatic lesions.

A modest degress of regeneration can occur

Extensive fibrosis

Ductular hyperplasia

328

What are the differences between cats, dogs and horses in terms of acute pancreatic necrosis?

  • Cats: acute pancreatic necrosis, suppurative pancreatitis
  • Dogs: acute pancreatic necrosis, can have prominent hemorrhage and a worse prognosis, can have a hormarrhagic form with peritubular fibrosis
  • Horses: strongyle larval migration - necrosis and inflammation
329

What is chronic interstitial pancreatitis?

cats>horses>other species

Predisposing factors: duct malformations, parasites, high duodenal pressure, cholangitis

Usually not associated with long-term adverse effect. May lead to exocrine pancreatic insufficiency (EPI) in some cats.

330

What are the gross and microscopic findings in chronic interstitial pancreatitis?

Gross - pancreas is shrunken and nodular as a result of chronic interstitial fibrosis and exocrine pancreatic nodular hyperplasia

Microscopic - small remaining acini separated by bridging fibrosis and lymphoplasmacytic interstitial inflammation.

331

When is chronic interstitial pancreatitis seen in cats, dogs and horses?

  • Cats: seen with cholangitis due to fusion of bile duct with pancreatic duct.
  • Dogs: long term outcome of pancreatic necrosis or repeated, mild pancreatitis
  • Horses: parasite migration, ascending bacterial infection, extension from chronic eosinophilic gastroenteritis, or cholangitis
332

What is an exocrine pancreatic nodular hyperplasia?

  • Common incidental finding of aged dogs, cats and cattle
  • May be regenerative attempt in cats following pancreatitis.
  • Ofetn seen with chronic interstitial pancreatitis in cats.
  • Gross findings: multiple smooth firm pale nodules
333

What histological findings will you see in exocrine pancreatic nodular hyperplasia?

Uncapsulatednodules of acinar cells that have variable numbers of zymogen granules and possibly contain vacuoles. Nodular don't compress adjacent tissue and do not ontain pancreatic islets.

334

What is an exocrine pancreatic adenoma?

  • Very rare
  • Occasionally observed in cats
  • Gross: Resembles nodular hyperplasia, but exists as a single large nodule
  • Histology: acinar cells usually in a tubular arrangement with cystic spaces, surrounded by a thin fibrous capsule ad compresses adjacent parenchyma.
335

What is an exocrine pancreatic carcinoma?

  • Rare aggressive tumor of dogs and cats
  • May be accompanied by multifocal necrotizing panniculitis
  • Rarely, cats can develop a paraneoplasic syndrome characterized by alopeCia of the ventrum, legs and face.
  • Gross - single or multiple gray-to-yellow or gritty nodules with adhesions and local invasions. May seed peritoneal cavity and or metastasize to regional lymph nodes COMMONLY INVADES DUODENUM AND MAY CAUSE INTESTINAL OBSTRUCTION
336

What are the histological findings of exocrine pancreatic carcinoma?

Neoplasm with neoplasic exocrine pancreatic acinar cells arranged in tubules, acini, or solid lobules, often supported by abundant amounts of dense fibrous tissue

337

What are endocrine glands?

  • Secrete hormones into blood stream which affects a wide variety of distant target tissues to maintain homeostasis
  • Contrast with exocrine glands
  • Disorders are manifest by derangement of target organ function
338

What are the different forms of hyperactivity?

  1. Primary hyperfunction
  2. Secondary hyperfunction
  3. Hyperactivity secondary to diseases of other organs
  4. Hypersecretion of hormones or hormone-like substances by non-endocrine tumors
  5. Iatrogenic syndromes of hormone excess
339

What are the endocrine hypoactivity diseases?

  1. Primary hypofunction
  2. Secondary hypofunction
  3. Endocrine dysfunction due to failure of target tissue to respond to hormone
340

What does the neurohypophysis do and what is apart of?

Pars nervosa of the pituitary. Hormones from hypothalamus go to the pars nervosa by axonal process and terminate on fenestrated capillaries, released to general circulation

341

What is the adenohypophysis?

The pars intermedia and the pars distalis of the pituitary gland.

342

What is adenohypophyseal aplasia/hypoplasia in cattle?

  • Genetic defect in Guernseys and Jerseys
  • Hypoplasia of target organs
  • Gestation is prolonged
  • Fetal development stops at 7 months
343

What is adenohypophyseal aplasia/hypoplasia in sheep?

Ewe ingest Veratrum calfornicum (cyclopamine).

  • Hypoplasia of target organs
  • Gestation is prolonged
  • Fetus will continue to grow + cyclopamine
344

What is the mechanism of prolonged gestation?

  • Small or absent pituitary
  • Decreased ACTH
  • Hypoplasia of the adrenal cortex
  • Decreased glucocorticoid secretion
  • Decreased estrogen produced by placenta
  • Decreased prostglandins produced by uterus.
  • Parturition isn't initiated, gestation is prolonged
345

What is a pituitary cyst?

Failure of differentiation of oropharyngeal ectoderm of Rathke's pouch. Progressively enlarging cyst in the sella turcica - complete or partial absence of adenohypophysis and compression of neurohypophysis

May lead to pituitary dwarfism/juvenile panhypoepituitarism

346

What is pituitary dwarfism?

Juvenile panhypopituitarism.

  • Failure to grow, also can develop secondary atrophy f thyroid glands (decrease THS), adrenal cortices (decrease ACTH), gonads.
  • Compression of the pars nervose may lead to decrease ADH, causing water loss through urine
347

What are the two inflammatory diseases of the pituitary?

  1. Abscesses
  2. Infiltration of mononuclear inflammatory cells
348

What are some characteristics of pituitary abscesses?

  • Sporadically in ruminants and swine
  • Caused by bacteria or mycotic agents
  • Neurological signs due to local extension of the inflammation
349

When does infiltration of the pituitary by mononuclear inflammatory cells?

In some viral and protozoan disease as part of encephalitis or meningitis.

350

What are the different types of proliferative lesions of the pituitary?

  • functional - increased secretions of specific trophic hormone that stimulates a target organ
  • Nonfunctional - no hormone production but destructive to adjacent structures
  • Adenomas - distinguishable from nodular hyperplasia by their size and presence of capsule and compression of the adjacent tissue
  • Carcinoma - invasive
  • Craniopharyngiomas - occur in young animals, with space-occupying/compressive effects
351

How do functional Ademomas of the pars distalis present?

  • ACTH-secreting adenoma
  • Usually in dogs, often small tumors
  • Excess GC production from adrenals - Cushings Dz
352

How do nonfunctional adenomas of the pars distalis normally present?

Usually become large before causing clinical signs

353

What is a Somatotroph Adenoma?

Secretes growth hormone/somatotropin.

These tumors cause gigantism in the young and acromgealy in adults

Feline acromegaly is associated with insulin resistant diabetes mellitus

Adenoms of Lactotrophs, Gonadotrophs and Thyrotrophs. Excess prolactin, secretion, reported in non-pregnant, lactating goats, some strains of laboratory mice, pet rats

354

What is the clinical disease of focus for an adenoma of the pars intermedia?

Pituitary pars intermedia dysfunction.

  • In dogs can be active or inactive
  • In horses, often large and compress neurohypophysis and hypothalamus. Pituitary pars intermedia dysfunction, PPID. Hirsutism, hyperglycemia, polyphagia, muscle atrophy/weakness, laminitis, intermittent hyerppyrexia, hyperhidrosis and PU/PD
355

What is the pathogenesis of Pituitary pars intermedia dysfunction?

  • Melanotrope secretion of proopiomelanocortin (POMC) is normally inhibited by dopamine from hypothalamus.
  • Constant loss of dopamine secreting cells - proliferation of melanotropes and increased POMC
  • Varying amounts of ACTH, corticotropin-like intermediate lobe protein (CLIP), melanocyte stimulating hormone (MSH), beta-endorphin + mass effects/pressure on hypothalamus
356

What is a pituitary carcinoma?

Most are inactive. Leads to panhypopituitarism, diabetes insipidus

CNS dysfunction +/- metastasis.

Metastatic tumors to this site are uncommon, consequences would be similar to primary carcinoma.

357

What is the hypophyseal form of diabetes insipidus?

Any lesion that interferes with ADH synthesis/secretion

  • In the presence of ADH, the CD in kidney are permeable, allowing water to be reabsorbed, small amount of concentrated urine is produced
  • In the absence of ADH, the CD are impermeable to water, large amount of dilute urine is produced
358

What is the nephrogenic form of diabetes insipidus?

  • Hereditary defects in the ADH receptor or occasionally in the water channel
  • CD cells fail to respond to normal or elevated circulating ADH
  • Both forms - PU/PD and urine of low osmolality
  • Exogenous ADH - increase in urine osmolality and decrease volume in hypophyseal DI
359

What is the structure and function of the adrenal gland?

  • Outer cortex makes corticosteroids
  • Inner medulla makes catecholamines
360

What are the different zones of the adrenal gland?

  • Capsule
  • Zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
  • Adrenal medulla
361

What does the zona glomerulosa?

Aldosterone (mineralcorticoid)

  • Retain sodium, chloride and water
  • Lose K
  • Not controlled by ACTH
362

What does the zona fasciculata produce?

Cortisol (GC).

  • Causes hyperglycemia via gluconeogenesis and insulin resistance
  • Protein catabolism and lipolysis
  • Suppress inflammation, healing and immune response
  • Controlled by ACTH
363

What does the zona reticularis produce?

Androgens (sex steroids, testosterone)

  • Also controlled by ACTH
  • Not covered
364

What causes inflammation of the adrenal gland (adrenalitis)?

  1. Viruses - herpes causes necrosis with inclusion bodies
  2. Bacteria - gram- and mycobacteria
  3. Fungi - dimorphic fungi
  4. Parasites - toxoplasma
  5. Immune mediated - inflammation destroys all layers of adrenal cortex
365

What is Waterhouse-Friderichsen Syndrome?

Inflammation doesn't usually lead to reduced hormone level BUT sepsis, thrombosis and necrosis with loss loss of function.

Important in septic neonates, can occur in adults too

366

What can cause atrophy and degeneration of the adrenal cortex?

  • Can result from longstanding immune-mediated inflammation. Destruction of all three layers. GC and MC will be low
  • Can result from loss of ACTH from the pituitary if the pituitary has a destructive lesion. Atrophy of zona reticularis and fasciculata, but glomerulosa remains GCs will be low, but MC still secreted.
367

What happens with diffuse hyperplasia?

  • Increased ACTH
  • Cortex uniformly enlarged
  • Excess GC
  • Cushings
368

What is nodular pituitary hyperplasia and how does it present?

  • Seen in old horses, dogs and cats
  • Often multiple, bilateral and yellow
  • Hyperplasias secondary to ACTH is usually functional. Nodular hyperplasia is often incidental but can be functional
369

What is a adrenal cortical adenoma and what would you normally find it in?

  • Especially in old dogs. Adenomas are usually larger, encapsulated and compressive compared to nodular hyperplasia
  • Usually Z.F. in dogs
370

What is a adrenal cortical carcinoma and what would you normally find it in?

  • Old dogs, cattle
  • Often bilateral and may invade vena cava, with metastases
371

What are the different forms of hyperadrenocorticism?

  1. Secondary hyperadrenocorticism (most cases, 80%): pituitary dependent or idiopathic
  2. Primary hyperadrenocorticism (10-15%): functional cortical neoplasm esp adenoma, pituitary independent
  3. Istrogenic hyperadrenocorticism (5-10%): overmedication
372

What are the clinical signs seen with hyperadrenocorticism?

Due to the effects of cortisol

  • PU/PD - increased GFR and interference with ADH
  • Polyphagia - direct affect on satiety center
  • Hepatomegaly - steroid hepatopathy
  • Pendulous abdomen - muscle atrophy/weakness from protein catabolism and hepatomegaly
  • Skin lesions - dermal atrophy, bilateral symmetric alopecia, delayed wound healing
  • Calcinosis cutis - esp skin, +/- lung
  • Increased susceptibility to bacterial infections due to immunosuppression
373

How would you test for Hyperadrenocorticism?

Low dose dexamethasone test

  • Measure baseline control
  • Administer dexamethasone and attempt to trigger negative feedback loop and inhibit ACTH secretion
  • In normal dogs, ACTH will be suppressed, and cortisol levels will decrease
  • In cushinoid dogs, ACTH are unchanged and cortisol levels wil reamin high.

High dose dexamthasone test

  • Cortisol will drop in normal dogs and in most dogs with secondary hyperadrenocorticism
  • Cortisol levels will remain high in dogs with primary hyperadrenocorticism
  • ACTH is already low in these dogs, it ant be suppressed further
374

What is primary or typical Addisons disease?

Destruction of all three cortical layers of the pituitary.

Decreased GC AND MC.

375

What secondary or atypical addisons?

  • Pituitary problem leads to decreased ACTH
  • Inner 2 layers of cortex atrophy
  • Decreased GC
  • Zona glomerulosa remains, MC secreted as needed
376

What are the two forms of Primary Hypoadrenocorticism?

  • Bilateral idiopathic adrenal cortical atrophy, esp young to middle-aged female dogs, autoimmune/hereditary. Standard poodle, Portuguese Waterdog and Bearded Collie. Destruction of all 3 layers leads to deficient production of all cortical hormones
  • Bilateral destruction of adrenal glands due to inflammation, infarction, hemorrhage, tumors
377

What is characteristics of Primary hypoadrenocorticism?

Bilateral atrophy of all three cortical layers. Resulted in pituitary gland corticotroph hyperplasia

378

What are the clinical signs of Primary hypodarenocorticism (addisons)

  • Hypoatremia and hyperkalemia - hallmark of Addison
  • Lethargy, stress intolerance, bradycardia, anorexia, vomiting and diarrhea leading to dehydration/emaciation
  • Possible acute circulatory failure, ie cardiogenic/hypovolemic shock
  • +/- hypoglycemia, hemoconcentration and low plasma cortisol
  • Electrolyte abnormalities and bradycardia in primary Addisons is due to deficiency of Aldosterone (MC), due to atrophies zona glomerulosa
379

What does secondary (atypical) hypoadrenocorticism result in?

  • ACTH deficiency results in trophic atrophy of inner 2 zones
  • Destructive pituitary lesions damaged corticotrophs leading to reduced ACTH
  • Iatrogenic: following sudden withdrawal of GC after prlonged usage
380

What is the structure and function of the adrenal medulla?

  • Catecholamines derived from tyrosine - NE to epinephrine
  • Triggered by fright/stress: fight or flight
381

What proliferative lesions occur in the adrenal medulla?

  • Adrenal medullary hyperplasia - adrenal medullar hyperplasia, diffuse or nodular, older bulls, mares, mice
  • Pheochromocytoma - mainly in dogs and cattle, tumor is often large and encapsulated - may invade the vena cava and metastasize. Sometimes functional - tachycardia, typertension and cardiac hypertrophy, panting, collapse
382

What is the function of the Thyroid follicular cells?

  • Follicular activity controlled by stimulating hormone (TSH) from pituitary
  • Follicular cells make T4 and T3 depends on availability of iodine. Negative feedback: high thyroid hormones cause lower TSH.
  • Regulate growth/metabolic activity - increase BMR
383

Developmental anomalies of the thyroid?

  1. Ectopic thyroid - can occur near the base of the heart, can become malignant, forming a heart-based tumor in dogs
  2. Thyroglossal duct cysts - can also be site of tumor formation
384

What is lymphocytic (immune-mediated) thyroiditis?

  • Esp dogs, can cause hypothyroidism
  • Due to autoantibodies to thyroglobulin and other colloid antigens
  • Multifocal to diffuse infiltrate of lymphocytes, plasma cells and macrophages - later fibrosis
385

What is idiopathic follicular atrophy?

  • Follicular thyroid replaced with adipocytes.
  • Likely end-stage immune-mediated thyroiditis
386

What are the proliferative lesions of the thyroid?

  1. Diffuse follicular hyperplasia (goiter)
  2. Nodular follicular hyperplasia
  3. Follicular adenoma
  4. Follicular carcinoma
387

What characterizes diffuse follicular hyperplasia and what are the four major mechanisms?

Non-neoplastic, noninflammatory enlargement due to increased TSH secretion. Results from inadequate T4 and T3

  1. Iodine deficient diet
  2. Goitrogenic compounds interfering with hormone synthesis
  3. Excess dietary iodine
  4. Genetic enzyme defects in hormone synthesis
388

What is diffuse follicular hyperplasia and what does it lead to?

  • Low T3/T4 leads to high TSH, which leads to follicular hyperplasia and marked enlargement
  • Large, deep red thyroids, myxedema, less hair, small size
389

What is colloid goiter?

  • Despite large size, is actually atrophy
  • Represents involuntary phase of hyperplastic goiter
  • If iodine is provided, rising T3 and T4 will shut down TSH synthesis.
  • Gland becomes pale. Follicular cells become flattened, surround colloid-filled follciles
390

What is multifocal nodular hyperplasia?

  • Idiopathic
  • Usually incidental finding in old animals, except cats where it may be functional
  • Thyroids moderately enlarged with multiple, irregular, non-encapsulated nodules
391

What is a follicular cell adenoma?

  • May be functional; cats> dogs and horses
  • Adenomas usually single, encapsulated nodular or cystic masses
  • Surrounding thyroid tissue may be atrophied if mass is functional
392

What is follicular cell carcinoma?

  • More common in dogs (usually non-functional)
  • Typically multi-nodular, invade local tissue and often metastasize early to the lungs
  • May arise from accessory thyroids
393

What is the clinical presentation of hypothyroidism?

Usually dogs: beagles, golden and labs, dobermans. Rare in cats.

Due to lymphocytic thyroiditis and/or follicular collapse: loss of TSH usually is NOT the cause. Autoantibodies may be detectable

75% of gland must be lost before hypothyroidism occurs

394

What are the clinical signs and lesions seen with hypothyroidism?

  • Decreased metabolic rate: lethargy, increased weight
  • Skin lesions - bilateral symmetric alopecia, hyperpigmentation +/- myxedema
  • Hypercholesterolemia - atherosclerosis
  • Lab tests reveal low T3/T4, high cholesterol, TSH is usually increased
395

What are some characteristics of hyperthyroidism?

  • Hyperthyroidism and diabetes mellitus are the most common endocrine disease of cats
  • Elevated T3/T4, TSH usually low
  • Usually aged cats with nodular hyperplasia or functional adenomas. Gland enlargement may be palpable long before clinical signs
396

What are the clinical signs and lesions of hyperthyroidism?

  • PU/PD, increased activity and weight loss in spite of polyphagia
  • May see cervical swelling, coughing and dyspnea
  • Cardiac left ventricular hypertrophy
  • Lab test: serum total T4 is screening test of choice for hyperthyroidism
397

What are the structure and function of Thyroid C (parafollicular) cells?

  • Secrete calcitonin
  • If Ca gets too high, calcitonin lowers Ca levels
398

What is calcitonin released from and how does it lower Ca levels?

Tyroid C (parafollicular) cells

  1. Inhibiting bone reabsorption
  2. Promoting Ca less in urine
399

What proliferative lesions can be seen in Thyroid C (parafollicular) cells?

  • Hyperplasia, adenoma, carcinoma
  • All three seen in aged bulls
  • Possible excessive dietary Ca for bulls on cow diet = prolonged stimulation of C cells
400

What are the single type of secretory cells in parathyroid glands?

Chief cells: parathyroid hormone, leads to increased Ca.

Morphology, # and location varies with species

401

What are some characteristics of PTH?

  • Minute-to-minute, fine regulation of Ca
  • PTH level controlled by direct feedback system based on CA/Ph
  • Causes increased Ca levels
402

How does PTH increase calcium levels?

  1. Increase intestinal absorption of Ca (via vit D)
  2. Increased bone reabsorption of Ca
  3. Increased renal reabsorption of Ca
403

What are two examples of developmental anomalies and inflammation associated with the parathyroid glands?

Parathyroid cysts - usually incidenta;

Lymphocytic parathyroiditis. Rare in dogs, believed to be autoimmune. Causes hypoparathyroidism

404

What are the causes of Parathyroid hyperplasia?

Results of low blood calcium, seen in secondary hyperparathyroidism.

  1. Diet: decreased calcium, or decrease vitamin D, or increase in phosphorus
  2. Renal disease: failure to excrete phosphorus leads to hyperphosphatemia and hypocalcemia. Failure to activate enough vit D3, leads to hypocalcemia
405

What are some proliferative lesions of the parathyroid glands?

Parathyroid adenoma. Aged animals, usually dogs and some rat strains. Often functional (primary hyperparathyroidism). Encapsulated, sharply demarcated.

Parathyroid carcinoma. Rare, often functional (primary hyperparathyroidism)

406

What is the clinical disease focus of the parathyroid?

Hypoparathyroidism.

Adult dogs rare. Particularly in smaller breeds.

407

What causes Hypoparathyroidism?

Insufficient PTH secretion due to:

  • Lymphocytic parathroiditis (most common)
  • Destruction of the parathyroids by neoplasms
  • Accidental removal during thyroid surgery
  • Long-term hypercalcemia from calcinogenic plants or humoral hypercalemia of malignancy. Will cause low PTH due to high calcium, symptoms depend on Ca levels.
408

What are the signs and lesions of hypoparathyroidism?

Reduced osteoclastic bone reabsorption (due to low PTH).

Increased neuromuscular excitability and tetany (due to low Ca). Restlessness, nervous, ataxic, weak, tremors progressing to seizures.

409

What is Parturient Paresis (milk fever)?

Form of hypoparathyroidism.

  • Onset of lactation, sudden Ca loss in milk, slow Ca release from skeleton, hypocalcemia, hypophosphoatemia, paresis leading to recombency, death
  • Cows fed a high Ca diet bfeore parturition, increased calcitonin secretion and inactive parathyroids.
  • Similar contidion in the bitch, mare and ewe.
410

What are the different types of hyperparathyroidism?

  • Primary hyperthyroidism - proliferative lesions lead to excess PTH
  • Secondary hyperparathyroidism - other disease lead to excess PTH
  • Pseudohyperparathyroidism - non-endocrine tumors secrete PTH-mimicking substances
411

What causes primary hyperparathyroidism and what does it lead to?

  • Due to functional parathyroid adenoma or carcinoma
  • Produce excess PTH in spite or high Ca (negative feedbac doesn't work)
  • See hypercalcemia, PU/PD, weakening of bones (fibrous estodystrophy)
412

What are the two different forms of secondary hyperparathyroidism?

  • Secondary to nutritional imbalances
  • Secondary to renal disease
413

What are some characteristics of Secondary hyperparathyroidism secondary to nutritional imbalances?

  • Horses, goats, cats, dogs, nonprimates, birds and reptiles
  • In response to excess dietary Phos and low vita D3
  • Horses on high-grain on all-meat diets
414

What are some characteristics of Secondary hyperparathyroidism secondary to renal disease?

Normally in small animals

  • Response to hypocalcemia resulting from:
  • hyperphosphatemia due to decrease GFR
  • Impaired activation of vit D3
415

What is the outcome of secondary hyperparathyroidism (both kinds)?

  1. Hyperthrophy and hyperplasia of parathyroid (Chief) cells, get bilateral enlargement (hyperplasia) or parathyroids
  2. Excess PTH - generalized fibrous osteodystrophy
416

What is the fibrous osteodystrophy?

Osteoclastic bone reabsorption causes bone loss, which is replaced with fibrous CT.

Bones become soft and rubbery, maxilla can become swollen.

417

What is pseudohyperparathyroidism (humoral hypercalcemia of malignancy/HHM)?

  • Types of paraneoplastic syndrome
  • Tumor secretes 'humoral' factors (PTHrP) which bind to PTH receptors leading to hypercalcemia/hypophosphotemia
  • Seen with apocrine gland adenocarcinoma of anal sac and lymphoma.
418

What different cells are within the pancreatic islet and what do they release?

  • Alpha cells - glucagon
  • Beta cells - insulin
419

How is the regulation of blood glucose done?

Insulin

  • Anabolic (builds/stores stuff)
  • Insulin lowers blood sugar

Glucagon

  • Catabolic (breakdown/liberates stuff)
  • Glucagon increases blood sugar (released from gylcogen)
420

What are the developmental anomalies and miscellaneous lesions of the pancreas?

  • Hypoplasia or aplasia: causes diabetes mellitus (DM) in young dogs
  • Idiopathic pancreatic atrophy: entire pancreas is very small, ay cause DM in some animals
  • Islet of amyloidosis: occurs in cats, amyloid is deposited in islets and may contribute to DM
  • Vacuolar degeneration of beta cells: chronic stimulation from hyperglycemia leads to degeneration. Beta cells work harder, eventually worn out and degenerate, leads to diabetes mellitus
421

What are three inflammatory diseases of the pancreatic islets?

  • Acute pancreatic necrosis leads to destruction of islets
  • Chronic relapsing pancreatitis causes loss of exocrine and endocrine pancreatic tissue with replacement of fibrosis
  • Immune mediated lymphoplasmacytic isletitis occurs in occasionally in dogs
422

Are tumors common in the pancreas and what hormone normally dominates?

- rare, malignant variety are more common.

- insulinoma, insulin is normally dominant.

423

What are some characteristics of Beta Cell Neoplasms (pancreas)?

  • Often functional, producing excess insulin (insulinomas)
  • Adenomas are encapsulated, in contrast to carcinomas (larger/locally invasive/may metastasize)
  • In functional, severe hypogylcemia, weakness, fatigue, CNS signs
  • Dx - high serum insulin, low blood glucose and one or more nodules in the pancreas, IMMUNOHISTOCHEMISTRY to confirm proliferation of insulin-producing cells
424

What are the two proliferative lesions of the pancreatic islets?

  1. Beta cell neoplasms (insulomas)
  2. Non-beta cell neoplasms: glucogonomas
425

What are some characteristics of non-beta cell neoplasms: glucagonomas?

  • Rare (dogs)
  • Excess glucagon leads to hyperglycemia, secondary diabetes mellitus, +/- superficial necrolytic dermatitis (rare)
426

What are the two types of diabetes mellitus?

  • Type I
  • Type II
427

What is type I diabetes mellitus?

  • Destruction of beta cells - complete less of insulin secretions
  • Insulin-dependent from time of Dx
  • Humans and cattle
  • Canine DM is similar to type I DM
428

What is type II diabetes mellitus?

  • Insulin resistance (insulin present, tissues not responding, IAPP contributes
  • Over time can develop into insulin-dependent DM (exhausted beta cells degenerate, low insulin)
  • Humans and cats, obesity
  • Cats are often insulin dependent by the time they are diagnosed
429

What is secondary diabetes mellitus?

Other hormones antagonize insulin in peripheral tissues.

  • Glucagon (glucagonoma)
  • Progesterone (diestrus/pseudopregnancy)
  • Growth hormone (pars distalis/somatotroph adenoma)
  • Glucocorticoids** (adrenocortical tumor, Cushings, iatrogenic)
430

What are some facts of diabetes mellitus in dogs?

  • Common endocrinopathy of dogs (1:200), females>males
  • Most clinically like type I diabetes
  • Associated with the following: destruction of islets, insulin antagonism, aplasia/hypoplasia of pancreatic islets, immune destruction of beta cells (rare)
431

How does diabetes mellitus present in cats?

(see type II DM in notes)

  • Relatively uncommon, most cases resemble type II diabetes

Associated with:

  • IAPP secretion: promotes insulin resistance in tissues, inhibits insulin secretion. Can lead to amyloidosis
  • Vacuolar degeneration of beta cells (overstimulation/exhaustion) because fo insulin resistance
432

What are the clinical signs and lesions associated with diabetes mellitus?

  • Hyperglycemia and glyosuria - decreased insulin or insulin resistance
  • PD/PU - glucosuria - osmotic diuresis with compensatory PD
  • Polyphagia - affect on satiety center
  • Loss of weight - glucosuria and generalized catabolism
  • Weakness - decrease tissue/muscle glucose, protein catabolism +/- polyneuropathy
  • Hepatic lipidosis - increased lipolysis in adipose tissue - excess fatty acids to liver
  • Bilateral cataracts - excess glucose leads to altered metabolism in the lens: increased sorbitol and glutathion depletion
  • Recurrent infections - decrease leukocyte kinetics and increase glucose substrate
  • Vascular damage - glomerulosclerosis and retinopathy
  • Neuopathies - peripheral demyelinating neuropathies
433

What is the structure and function of chemoreceptor organs?

  • Tissue in aortic body (heart based tumors)
  • Also called nonchromaffin paraganglia - esp aortic and carotid body
  • Chemoreceptor that sense change in pH (CO2/O2)
  • Brachycephalic breeds at risk
434

What are some characteristics of aortic body adenoma/carcinomas?

  • More common than carotid body tumors
  • Rarely functional - usually heart failure due to space-occupying nature
  • "heart-base tumor"
435

What is key about CNS pathology?

  1. Generally, any lesion in the CNS is potentially significant
  2. In several disease of the CNS, most viral infections, the nervous tissue exhibits no gross lesions. Exudate and degenerated tissue=pale. Insufficient time for extensive lesions.
  3. Limited room for expansions. Significance of edema and space-occupying lesions
  4. Limited capacity for regeneration. Neurons cannot regenerate. Axons in CNS have limited regeneration. Axons in PNS exhibit more robust regeneration.
  5. Capacity for fibrosis is limited. Astroglial scars "wall off" lesions.
  6. The BBB. Protects against infections and toxins. Blocks some drugs and antibodies
436

What is the prefix for brain infection and spinal cord infection?

encephalo-

myelo-

Grey matter on the outside. White matter on the inside

437

What is the prefix for grey matter and for white matter?

  • Grey matter - polio
  • White matter - leuko
438

What is malacia?

  • Gross descriptive term "softening"
  • Necrosis in the CNS
  • Nonspecific. Cause or effect of inflammation.
  • Infarction, intoxication, nutritional deficiency, etc.
439

How is malacia a clue to etiology?

  • Distribution is a clue to etiology?
  • Either metabolic or toxic.
440

When is malacia more likely caused by an infection?

If random then it is more likely infection

Other causes: trauma, vascular accidents (infarction, thrombosis), neoplasias

441

What are the cellular responses to neuronal cell injury?

Acute neuronal necrosis (metabolic arrest change, ischemic neuronal necrosis): acute cell death, neuron equivalent of coagulation necrosis

Nonspecific - many possible causes.

  • Anything interfering with high metabolic demand for oxygen or glucose, hypoxia, ischemia, hypoglycemia
  • Some toxins
  • Thiamine deficiency
  • Salt poisoning
  • Trauma
442

What are the vulnerability to hypoxia or hypoglycemia in the different neurons and areas of the brain.

Neurons** cerebral cortex (5-6min), purkinje cells, cerebellum (6-8min), basal ganglia (10min), brain stem (15min)

Oligodendrocytes

Astrocytes

Microglia and blood vessels

443

What does axonal injury look like?

  • Swelling, spheroid formation
  • Focal accumulation of neurofilaments, mitochondria, and other organelles causes by a disruption in axonal transort
444

What are the astrocyte responses to injury?

  1. Swelling (hydropic degeneration)
  2. Astrogliosis (proliferation)
  3. Hypertrophy (gemistocytes)
445

What occurs when oligodendrocytes are injured?

You get a loss of myelin. White matter>grey matter.

Formation and turnover of myelin. Interfasicular and perineuronal

  1. Injury=demyelination
  2. Proliferation
446

What are some characteristics of microgial cells?

  • Resident population of macrophages in the CNS.
  • Proliferation of glial cells=gliosis
  • Common response to viral infections (but occur in many diseases)
447

What are gitter cells?

  • Activated microglia (or blood monocytes) with foamy cytoplasm
  • Phagocytic (myelin, cell membranes)
  • Common in clean-up of necrosis
448

How do axons and myelin sheaths respond to injury?

Axons can survive without myelin. Decreased conductance, degenerate over time.

Myelin quickly breaks down if axon is lost.

449

What is the difference between primary and secondary demyelination?

Primary is injury to:

  • oligodendrocytes (CNS)
  • Schwann cells (PNS)
  • Myelin

Secondary follows injury to axons. Also called " Wallerian Degeneration"

450

What are categories of primary demyelination?

  1. Abnormal myelin formation - inherited enzyme defects and leukodystrophies
  2. Impairment of myelin synthesis/maintenance
  3. Loss of myelin secondary to cytotoxic edema
  4. Direct damage to myelin
  5. Immune-mediated destruction; coonhound paralysis, canine distemper virus
451

What is secondary demyelination?

Wallerian degeneration. Axons require axoplasmic flow of cytoplasmic materials for survival. When an axon is destroyed, it degenerates DISTALLY. Myelin breakdown quickly follows axon degeneration.

There are similarities and differences between secondary demyelination in PNS and CNS

452

What are the steps of Wallerian degeneration in the PNS?

  1. Degeneration/fragmentation
  2. Debris removal
  3. Axon regeneration
  4. Remyelination

Functional repair is possible under correct circumstances

453

What are the factors that influence a functional repair of axonal damage in the PNS?

  1. Viable neuron cell body
  2. Narrow gap
  3. Pathway for repair: column of Schwann cells and endoneurial tube
454

What are impediments to functional repair of axonal damage in the PNS?

  1. Any functional or physical obstruction, especially fibrosis
  2. Distance, regenerating axons become "tangled" in accumulating collagen fibers.

Outcome: amputation neuroma

455

Why is Wallerian degeneration in the CNS more limited?

  1. Less efficient phagocytosis, oligos<Schwann cells, microglial cell activation needed
  2. Limited remyelination, oligos have reduced capacity
  3. Minimal axonal regeneration, less than 1mm, myelin breakdown products are inhibitory. ECM is also inhibitory.
456

What can cause focal ischemic encephalopathy?

Localized

  • Thrombosis/embolism
  • Hemorrhage
  • Inflammation
  • Neoplasia

Often acute, may progress. Neurologic signs depend on site affected

457

What can cause global ischemic encephalopathy?

Hypoxia of whole brain

  • Hypotension/shock
  • Cardiac insufficiency
  • Anesthetic complications
  • Premature placental separation, dystocia, umbilical torsion
458

What characterizes vasogenic cerebral edema?

  • Caused by trauma, inflammation, hypertension
  • Endothelial damage and breakdown of BBB
  • Increased vascular permeability
  • Extracellular fluid accumulation
  • Edema resulting from increased vascular permeability
459

What characterizes cytotoxic cerebral edema?

Direct or indirect injury to cells. Edema resulting from damage to cells that disrupts mechanisms of cellular fluid control

  • Interference with mechanisms that control cell volume.
  • Intracellular fluid accumulation
  • Equivalent to hydropic change
  • May be reversible
  • Outcomes include primary demyelination
  • Hepatic encephalopathy in goat
460

What occurs when the brain was swollen?

  1. Cerebellar herniation/flattening of medulla
  2. Flattening of gyri, shallow sulci
461

What is hydroencephalus?

  • Abnormal accumulation of CSF in the cranial cavity
  • Usually under increased pressure
  • Congenital or acquired
  • Internal or communicating
462

Where is CSF made?

Choroid plexus

463

What is the order that CSF travels through the CNS?

  • Choroid plexus
  • Lateral ventricles
  • interventricular foramen
  • third ventricle
  • mesencephalic aqueduct
  • fourth ventricle
  • lateral aperatures
  • subarachnoid space
  • resorbed through arachnoid villi or drained via venous or lymphatic system
464

What does a big, domed head shortly after birth mean?

congenital hydroencephalus

465

What are some characteristics of congenital hydroencephalus?

  • Dogs, calves and pigs
  • Can be severe
  • Etiopathogenesis often unknown - malformation of mesencephalic aqueduct, ependymal cell cilial dysfunction, viral infection
  • Cranial malformation in some cases, doming of skull
  • Can lead to dystocias
466

What are some characteristics of acquired hydroencephalus?

  • Less severe
  • Lacks cranial doming
  • Can occur in older dogs
  • Many causes: neoplasia, inflammation, CSF overproduction
467

When does hydroencephalus present unilaterally vs bilaterally?

Bilaterally if the mesencephalic aqueduct is blocked.

Unilateral if lateral ventricle is blocked

468

What are some characteristics of Hydranencephaly?

  • Cavitary defects in brain tissue
  • Form in cerebral hemispheres in areas normally occupied by white matter
  • In utero infections. Necrosis of groups of neuroblasts during development, failure of normal neuronal migration/failure of tissue formation
469

What is the milder form of hydranencephaly?

Porencephaly. In utero infection at critical periods.

  • BVDV- calves
  • Border disease virus- lambs
  • Bluetongue virus- calves and lambs
  • Feline parvovirus- kittens
470

How is hydrocephalus and hydranencephaly told apart?

Hydrocephalus

  • VENTRICLES enlarged
  • Smooth inner surface
  • Often bilaterally symmetrical
  • Excess CSF

Hydranencephalus

  • CAVITIES in WHITE matter
  • Irregular surface, asymmetrical
  • Bands of white matter
  • Ventricles not directly involved
  • Due to destruction of NEUROBLAST in utero
471

What is cerebellar aplasia/hypoplasia?

  • One of the most common congenital NS defects in domestic animals
  • All species
  • Destruction of actively mitotic germinative cells. Especially external granular layer
  • In utero infections
  • Parvoviruses
  • Pestiviruses
  • Evidence supports a genetic cause as well
472

What is a concussion?

  • Transient loss of consciousness and reflexes after sudden head trauma
  • Multiple episodes - degenerative changes
  • Less common in animals than humans
473

What is a contusion?

  • Shearing and displacement forces of greater magnitude than a concussion.
  • Hemorrhage
  • Coup vs contrecoup
474

What is worse a concussion or a contusion?

A contusion is worse.

475

What is the difference between coup and contrecoup?

Contrecoup: hemorrhage on surface of the brain opposite to the point of impact

  1. Head freely moveable
  2. Rapid acceleration/decceleration
  3. Brain lags behind
  4. Brain strikes cranial cavity at point of impact=coup
  5. Vessels stretch and tear on opposite point of impact=contrecoup
476

What is an Intervertebral Disk Disease?

Dorsal herniation. It is a compressive injury to spinal cord.

  • Nucleus pulposis is a shock absorber
  • Chondroid metaplasia occurs in the nucleus pulposis.
477

What is Hansen Type 1: chondrodystrophic?

  • Rapidly progressive, younger age.
  • Chondroid metaplasia with acute herniation.
  • Nucleus pulposis has explosively herniated into the spinal canal
478

What is Hansen Type 2: non-chondrodystrophic?

  • Slowly progressive
  • Aging change: fibrous metaplasia of disk
  • Annulus fibrosis + dorsal longitudinal ligament have slowly protruded into the canal
479

What does the outcome of Intervertebral Disk Disease depend on?

  1. Amount of space between cord and vertebrae
  2. Rate at which compression occurs

(Type 1=more rapid, less compensation time)

Direct compression and/or ischemia due to blood vessel compression - focal MALACIA - secondary demyelination

480

What is Cervical Stenotic Myelopathy (Woddler Syndrome)?

Multifactorial: hereditary predisposition, fast growth rate, nutritional factors. Narrowing of cervical spinal canal.

481

What are the two forms of Cervical Stenotic Myelopathy (Wobblers Syndrome)?

  1. Cervical vertebral instability - dynamic narrowing of the cervical spinal canal during flexion. Often C3-C5.
  2. Cervical vertebral static stenosis - narrowing of the spinal canal due to formation of new bone. Grossly: see osteochondrosis of articular facets, thickened ligamentum flavium or dorsal lamina, osteophyte/new bone formation that narrows spinal cord. C5-C6, C6-C7. Large breed dogs.
482

What is equine laryngeal hemiplasia?

Equine recurrent laryngeal paralysis. "Roarer syndrome".

Etiology unknow, but associated with long necks: mechanical factors suspected.

Secondary demyelination of left (usually) recurrent laryngeal nerve. Denervation atrophy of CAD muscle. Failure to ABDUCT arytenoid cartilage. Inspiratory strider (noise)

483

What are the disease-causing agents that "hijack" the retrograde axonal transport system to enter the CNS?

  • Prions
  • Rabies virus
  • Herpesvirus
  • Listeria monocytogenes
  • Tetanus toxin
484

What are the diseases caused by Transmissible Spongiform Encephalopathies (TSEs)?

  • Scrapie - sheep, goats
  • Bovine Spongiform Encephalopathy (BSE) - cattle, other species
  • Chronic Wasting Disease (CWD) - cervids
  • Transmissible Mink Encephalopathy - mink
  • Creutzfeldt-Jakob disease (CJD) - humans
  • Kuru - humans
485

What are some characteristics and signs of prion diseases?

  • Group of diseases characterized by spongiform degeneration of neurons
  • Progressive neurological signs: tremors, excitability, seizures, ataxia, proprioceptive deficits, behaviour changed, weight loss, pruritis, hair loss
  • Invariably fatal
  • Long incubation period
  • Horizontally transmissible
486

What are some characteristics of Scrapie?

  • Sheep and goats
  • Endemic worldwide except Australia, NZ
  • Prolonged incubation period
  • Invariably fatal
  • Horizontal transmission from: birthing fluids and tissues, saliva and feces.
  • Persists in the environment
  • Does not naturally infect other species
487

Where do prions reside in Scrapie?

  • Lymphoid tissues and lower GIT
  • Disseminates via lymphatic hematogenous and intraaxonal routes. Years to reach CNS.
  • Neuroinvasion: visceral sympathetic nerves, to spinal cord. Vagus nerve to medullary region of the brain stem.
488

What are some characteristics of Bovine Spongiform Encephalopathy?

  • Pathologic features similar to scrapie.
  • Cattle, 1985, Great Britain
  • 3-6 year old cattle, aggressive behaviour, hyperesthetic, falling
  • Feed-associated, meat and bone meal (MBM) from rendered products contaminated with prions.
  • Crosses species barrier. varCJD, other species.
  • 2003:: Alberta, first case BSE in Canadian cows.
489

How is TSE diagnosed?

Immunohistochemical stain: gold standard.

BSE: post mortem diagnosis only.

Scrapie can be detected antemortem

490

What is involved in BSE surveillance in Canada?

  • Criteria or testing: cattle>30 months that are dead, down, dying, or diseased OR those that are exhibiting clinical signs compatible with BSE.
  • Rapid screening tests
  • Confirmatory tests
  • ONLY brain tissue can used (unlike scrapie)
  • OBEX of brainstem
491

How does prion propagation occur?

  • Prion protein is analogue of normal protein. Induces changes in those proteins it interacts with.
  • Makes a very dense plaque resistant to proteases.
  • Need the right kind of cellular protein to be effected by it too.
492

What are the general features of viral diseases of the CNS?

  • few gross lesions
  • non-suppurative inflammation and gliosis
  • Some have predisposition/tropism for specific CNS regions
  • Some have distinct histologic lesions that aid in diagnosis, demyelination in distemper, inclusion bodies
  • Some indirectly affect CNS via vasculitis or other systemic inflammatory process
  • RECALL that in utero infections with several viruses can also cause malformations
493

What is the virus that causes rabies?

Rhabdoviridae, lyssavirus

  • highly neurotropic
  • Almost invariably fatal
  • Vaccines preventable
  • All mammals are susceptible
494

What are the lesions seen with rabies infection?

Nonsuppurative encephalomyelitis

Inclusion bodies=negri bodies

495

What are the different forms and clinical signs of rabies?

Dumb versus furious. Furious is higher virus load in brain.

Paralysis and death 4-8 days after onset of signs. This is the reason for the 10 day quarantine.

  • Dog: 75% dumb, 25% furious
  • Cats: usually furious, may have hind limb paralysis
  • Cattle: dumb, excessive vocalization
  • Horses: dumb, may present as lame or ataxic
  • Birds: not susceptible to rabies
496

What are the pathogenic steps to Rabies infection?

  1. Bite wound
  2. Local replication in muscle
  3. Invade peripheral nerves
  4. Retrograde axonal transport
  5. Neuron cell bodies (dorsal root ganglia)
  6. Spinal cord
  7. Ascends to brain via nerve fiber tracts
  8. Nonsuppurative encephalomyelitis (CLINICAL DISEASE)
  9. Spreads via anterograde axonal transport to salivary glands, corneal epithelial cells, skin
497

How is rabies diagnosed?

Gold standard (CFIA): fluorescence antibody test (FAT)

Screening test: dRIT. Reportable disease.

498

What are the viruses of canine distemper virus and what is the viral tropsim?

Paramyxoviridae, morbillivirus: measles, rinderpest, peste-des, petits ruminants, phocine distemper.

Viral tropism for: lymphoid tissues, epithelial tissues, nervous tissues

499

What is the pathogenesis of Canine Distemper Virus?

Aerosol transmission

  • Nasal mucosal macrophages
  • Leukocyte trafficking to regional lymph nodes and tonsils
  • Primary viremia
  • Lymphoid tissues
  • Replicates in lymphoid tissues or 7-9 days

Immune response dictates outcome.

  1. Neutralizing Ab - elimination OR
  2. Inadequate immune response - spread to epithelia and/or CNS
500

When does Canine Distemper Virus reach the CNS?

Reaches CNS: 1-5 weeks post infection. Key feature is demyelination.

  • Virus invades ASTROCYTES, neurons, other glial cells, and choroid plexus, ependymal cells
  • Neuronal degeneration, hypertrophy of astrocytes
  • Intracytoplasmic AND intranuclear inclusion bodies
501

What forms of demyelination do you see in Canine Distemper Virus?

Primary and secondary

502

What are some characteristics of Herpesviruses?

  • Directly neurotropic OR cause damage via vasculitis
  • Some cross species barrier
  • Many are latent in ganglia, reactivated by stress and use axonal transport
503

What are some characteristics of Equine herpesvirus 1 (4 rarely) encephalomyelitis?

  • Necrotizing vasculitis: multifocal, random hemorrhage and malacia
  • Ataxia, incontinence, etc
  • Also causes abortion, pneumonia, systemic inflammation
  • Vaccination not necessarily protective against neuro forms
504

What are some characteristics of Bovine herpesvirus (1 rarely) encephalomyelitis?

Neurotropic: necrotizing and nonsuppurative encephalitis.

505

What are some characteristics of Suid herpesvirus 1 (pseudorabies, mad itch, Aujeszky's disease)?

  • Very wide host range: pigs, dogs, cats, sheep, cattle
  • Clinical picture (non-pigs): intense cutaneous irritation. Rapid progression and high mortality rate.
  • In pigs may be mild febrile illness, respiratory disease, or encephalitis or variable severity
506

What are some characteristics of West Nile Virus?

Flaviviridae (genus Flavivirus)

  • Mosquito borne
  • Natural life cycle involves wild birds
  • Introduced to NA in 1999 - Crows in NYC
  • Horses, humans, other are dead-end hosts
  • Horses: replication limited to CNS. Neurons, microglial cells, predominantly grey mattter. May present as ataxia.
507

What are the route in infection to the CNS?

  • Often hematogenous (septicemic)
  • Local extension (traumatic, nasal, inner ear, eye)
  • Axonal transport (Listeria)
508

How is inflammation of the CNS normally characterized?

Often neutrophilic (suppurative)

May be acute, subacute, chronic

509

What is the suppurative leptomeningitis?

Lepto = pia mater + arachnoid. May progress to deeper tissue involvement.

  1. Neonatal septicemia: E. coli, Strep, Salmonella, Pasteurella, Haemophilus. Oftenmonocyte-macrophage associated
  2. Pigs > 2-3 weeks, Strept suis, Haemophilus parasuis
510

What is Infectious Thrombotic Meningoencephalitis (ITME)?

  • Young feedlot cattle
  • Etiology: Histophilus somni
  • Can be part of normal flora
  • Stress contributes to disease
  1. Bacteremia or septicemia, brain, heart, joints and others.
  2. Pneumonia
511

What are the lesions associated with Infectious Thrombotic Meningoencephalitis (ITME)?

  • Septicemia with localization in brain
  • Cerebral endothelial injury
  • Suppurative/necrotizing vasculitis AND thrombosis
  • Hemorrhage and tissue infarction
  • Necrotizing and hemorrhagic (meningo)encephalitis and vasculitis
  • Multifocal, randomly distributed regions of hemorrhage and necrosis, often visibly associated with blood vessels
  • Meninges and throughout brain parenchyma
512

What are some characteristics of Listeriosis?

  • Listeria monocytogenes
  • Grows will in cold temperatures (refrigeration)
  • pH 5-9
  • Three general syndrome: abortion/stillbirth, septicemia (young animals), encephalitis (adult ruminants)
  • Zoonotic - foodborne illness
513

What is the clinical presentation of Listeriosis?

  • Circling, unilateral paralysis of 5th or 7th cranial nerves
  • Paralysis of masticatory muscles and pharynx
  • Tongue, head tilt, head pressing
514

How does listerial encephalitis present in adult ruminants?

Cattle, sheep, goats and other ruminants

Depressed and recumbent, with multiple deficits of right cranial nerves: right ear droop, deviation of muzzle to the left, unmasticated feed in the right side of the mouth

515

What is the pathogenesis of Listeriosis?

May have no lesions OR visible malacia. Ingestion of incompletely fermented silage (pH5.5 or higher)

  • L. monocytogenes breaches oral mucosa via abrasions
  • Invades sensory and motor branches of trigeminal nerve
  • Retrograde axonal transport along cranial nerves
  • Entry and proliferation in pons, medulla, inflammation and necrosis
  • Necrotizing encephalitis
516

What are some characteristics of fungal diseases of the CNS?

  • Most opportunistic, in immunocompromised
  • Hematogenous or direct extension (nasal/sinus cribriform plate)
  • Granulomatous or pogenulomatous inflammation
517

What are some characteristics of Cryptococcosis?

  • C. neoformans, C. gattii have an affinity of CNS
  • Yeats have thick capsule, narrow-based budding
  • Occasional cases in immunocompetent hosts
518

What are some characteristics of Protozoa?

  • Some have 2-host life cycle, cause disease in intermediate and aberrant hosts
  • Definitive hosts can act as intermediate hosts and exhibit disease
  • Significant CNS lesions: random, necrotizing encaphalitis/myloencephalitis
519

What are some characteristics of Neospora caninum?

  • Fecal/oral or transplacental
  • Ruminants: fetal/neonatal encephalitis and abortion
  • Dogs: adults often subclinical but puppies infected congenitally exhibit ascending polyradoculoneuritis with paralysis, encephalitis, myositis, dermatitis and mocarditis
520

What are the protozoal CNS infectious agents?

  1. Neospora caninum
  2. Toxoplasma gondii
  3. Sarcocystic neurona
521

What are some characteristics of Toxoplasma gondii?

Feline is definitive host

  • Disease in broad range of species: dogs and cats, humans, pigs, sheep, goats and wildlife
  • Wide tissues/cell tropism with systemic necrotizing disease
  • Transplacental transmission leads to abortion
  • CNS lesions via two mechanisms: endothelial cell infection, ischemic necrosis and edema of CNS tissue, direct infection and necrosis of neurons and other CNS cells
  • Cause polyradiculoneuritis and polymyositis
522

What are some characteristics of Sarcocystis neurona?

Equine protozoal myeloencephalitis (EPM).

  • Oral route of infection - route to CNS not figured out
  • RAndom, multifocal hemorrhage and malacia
523

What is Polioencephalomalacia in ruminants?

  • Acute or chronic
  • Necrosis (MALACIA) of grey matter of cerebral cortex
  • Acute: linear pale/discoloured areas, softening. UV light highlights necrotic tissue. May have gross evidence of edema
  • Chronic: loss of tissue, laminar or linear cavitary lesions or gaps
524

What are the two causes of Polioencephalomalacia in Ruminants?

  1. Thiamine (vitamin B1) deficiency
  2. High sulfur diet or in water
525

Why does Thiamine (B1) deficiency lead to Polioencephalomalacia?

High CHO diet

  • Decreased rumen pH and moderate rumen acidosis
  • Rumen microflora imbalance
  • Proliferation of thiamine-containing bacteria AND reduction of thiamine-producing bacteria
  • Thiamine deficiency
  • Reduced cerebral glucose utilization
  • Neuronal necrosis, especially of cortical grey matter
  • Polioencephalomalacia
526

Why does high sulfur diet lead to Polioencephalomalacia?

  • Forms HS gas. Absorbed through rumen mucosa or following eructation and inhalation
  • Directly toxic to CNS: neurons of cortical grey matter most vulnerable
  • Exacerbated if: low rumen pH, hot weather, trace mineral deficiencies are present
527

What are some characteristics of lead poisoning?

  • Incidence decreasing, most common in cattle
  • Minimal CNS lesions but significant neurologic disease
  • Exposure through ingestion of flaking leaded paint, old batteries, discarded oil, etc.
  • Small animals: usually household paint, subacute to chronic
528

What are the CNS signs of lead poisoning?

  • Clinical signs: CNS GI tract
  • Acute: fragments of car batteries it reticulum, few to no lesions
  • Chronic: can progress to polioencephalitis but milder than thiamine deficiency, can involve PNS, anemia, nephropathy, other effects
  • Does NOT accumulate in the brain, blood, rumen content, liver and kidney
529

What does direct salt poisoning lead to?

Cattle (possibly other species) - rapid ingestion of large amounts of salt water.

  • Rapid intracellular dehydration cause by excess extracellular sodium
  • Inihibtion of neuronal glycolysis
  • Neuronal necrosis
  • Vomiting, diarrhea, ataxia, blindness paresis

Very acute, no obvious brain lesions

530

What does indirect salt poisoning lead to?

Pigs (possibly other species) - dehydration followed by reintroduction of water. Water deprivation:

  • gradual intracellular dehydration
  • Intracellular formation of osmotically active molecules to retain water
  • Sudden rehydration
  • Excessive cellular swelling
  • Cerebral cortical necrosis and edema
  • Eosinphilic encephalitis (pigs)
531

What is focal symmetrical encephalomalacia?

Clostridium perfringens type D. Enterotoxemia of lambs, 3-10 weeks old. Typically well-fed and in good body condition. Pulpy kidney disease, overeating disease

Overgrowth of C. perfringens type D in GIT - Epsilon toxin. Focal symmetrical encephalomalacia, affects basal ganglia, thalamus, internal capsule, cerebellum. Bilaterally symmetrical

532

What are the idiopathic inflammatory diseases of the CNS?

  • Granulomatous meningoencephalitis (GME) of dogs
  • Necrotizing encephalitis
  • Acute idiopathic polyradiculoneuritis (coonhound paralysis)
  • Neuritis of cauda equina in horses
533

What are some characteristics of Granulomatous Meningoencephalitis (GME)?

  • Young to middle aged, small breed dogs
  • Clinical: behaviour changes, circling
  • Gross: grey to red expansile areas within white matter of brain and brainstem
  • Hypothesis: delayed-type hypersensitivity of an autoimmune disease
534

What are the two types of necrotizing encaphalitis?

Two forms:

  1. Necrotizing meningoencephalitis (NME): pig, shih tzu, Maltese, malacia or cerebral hemispheres, spinal cord involvement is rare
  2. Necrotizing leukoencephalitis: yorkshire terriers, malacia of cerebral white matter
535

What are some characteristics of Acute idiopathic polyradiculoneuritis?

  • Probably auto-immune, primary demyelination of cranial and spinal nerves
  • Clinical: ascending paresis/paralysis
  • Dogs, occasionally in cats
  • No gross lesions
536

What are some characteristics of Neuritis of cauda equina in horses?

  • Inflammation of sacrococcygeal nerves
  • Perineal anesthesia, tail paralysis, urinary incontinence, fecal retention, muscle atrophy
  • Gross: thickened nerve roots, hemorrhage
537

What are some characteristics of primary tumors of the NS?

  • Rare except dogs and cats. More are age-associated.
  • Most common: meningiomas in cats and glial cell tumors in dogs
  • Can't forget brain and spinal cord are sites of metastasis
538

What are some examples of primary NS tumors?

  • Meningioma
  • Olfactory neuroblastoma
  • Glial cell tumors: astrocytoma, oligodendroglioma, mixed gliomas
  • Ependymoma
  • Choroid plexus tumors
  • Embryonal tumors
  • Peripheral nerve sheath tumors: schwannoma, neurofibroma, perineuroma, malignant peripheral nerve sheath tumors.