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271 Cards in this Set

  • Front
  • Back
What is Intramembranous Ossification?:
Answer: “do novo formation of bone in the mesenchyme”

1) Begins with condensation (↑ density) of mesenchymal cells
2) Some differentiate into osetoblasts & begin to form osteiod, which is quickly mineralized into woven bone
3) The spicules of woven bone ↑ in size and coalesce to form a continuous piece of bone

Ex: Skull, maxilla, portions of the mandible & membrane bones
What is Endochondral Ossification?
Answer: “replacement of cartilage with bone”

1) Condensation of mesenchymal cells
2) Differentiation in to chondroblasts that form a cartilaginous model of anlage.
3) All mesenchymal cells in that model will differentiate into chondroblasts and mature chondrocytes
4) W/O blood supply, cartilaginous model degenerates and calcifies
5) Further developed by neovascularization, repopulation with stem cells, and production of woven bone

Ex: Tubluar bones, vertebrae, pelvic bones, bones at base of skull
What is the difference between Traumatic and Pathologic Fractures?
Answer: Traumatic: When a normal bone fractures under abnormal force

Pathological: When an abnormal bone fractures under normal force
What is Osteochondrosis (or osteochondritis)?
Defn: Focal or multifocal failure (or delay) of endochondral ossification resulting in localized thickening of hyaline cartilage.

- May occur at physeal or articular areas
- Pain or lameness may occur b/c not as stable as bone subject to injury
Ex: Gerneralize osteochondrosis in swine, UAP in dogs, epiphysitis in horses
Name 4 ways to introduce infection (ie: cause osteitis and osteomyelitis).
Answer: Commonly via Bacteria (also fungi, protozoa, and viruses)
1. Direct introduction during a traumatic event

2. By extension from a soft tissue (Otitis media, peritonitis)

3. Extension from a bacterial arthritis

4. hemoatogenously
Describe Degenerative Joint Disease (looking for key words!)
AKA: Osteoarthritis, osteoarthrosis, degenerative arthritis, arthropathy

Defn: Progressive disease of synovial joints which begins as irreversible
degeneration of the articular cartilage and maybe accompanies by:
- changes in the soft tissue
- formation of osteophytes
- sclerosis of subcondral bone
And may of may not be associated with clinical signs.

• include all underlined words!
• Cannot cure 
7. What are the 2 circumstances in which DJD occurs?
1) Joints with normal cartilage placed under abnormal stress
2) Joints with abnormal cartilage placed under normal stress
Synovial Fluid

Monocyte : Neutrophil Ratio
9 : 1
DJD is a
PROGRESSIVE disease of synovial joints
DJD begins as
Irreversible Degeneration of Articular Cartliage
DJD May be accompanied by (3)


DJD May OR May Not be associated with
Clinical Signs



The Cause of DJD is
not fully understood

likely represents a common set of lesions associated with a variety of disease processes
DJD Initiation might be (4)
Degeneration of Articular Cartilage

Inflamamation of the Joint Capsule

Inflammation of Synovium

Increased Stiffness of Subchondral Bone
DJD will ALWAYS include
Degeneration of Articular Cartilage
DJD can occur in Joints With (2)
Normal Cartilage following Abnormal Stresses

Abnormal Cartilage following Nomral Stresses
Early Stages of DJD are recognized as

Dull or rough apperarance

Yellow Brown Discolouration
Later Stages of DJD are characterized by
Fibrillation and Focal Erosions of Articular Cartilage
Continued use of a Joint with DJD results in
Eburnationa and Changes in Subchondral Bone
The Articular Cartilage of a Joint with DJD

Releases _________________

Which _________________

And may be accompanied by (2)
Break Down Products


Exacerbates inflammation of the Synovium

And may be accompanied by
`` `` Villus Hyperplasia
`` `` Osteophyte Production
Osteochondrosis is a

Disorder of (2) in

Articular Cartilage of Endochondral Bones


Growing Animals
Osteochondrosis is defined as....

Resulting in ....
Focal or Multifocal

Failure (or delay) of Endochondrial Ossification

Resulting in

Localized Thickening of Hyaline Cartilage
The Focus of Retained Cartilage in Osteochondrosis is

and results in
Not as stable as bone

tf may be subject to injury
`` `` Leading to Pain and Lameness

Focal Disruption of Longitudinal Bone Growth
In Osteochondrosis

Focal Disruption of Endochondrial Ossification and Longitudinal Bone Growth

Has the potential to....

And May lead to....

Which Predisposes Joint to....
Alter the shape of an articular surface

Which may lead to
`` `` Angular Limb Deformities
`` `` Abnormal Articulation

Predisposing to DJD
Osteochondritis Dessicans (OCD)

arises from ....

Osteochondrosis of Articular Cartilage

Clefts develop
`` `` within foci of thickended cartilage or
`` `` between thickended cartilage and underlying bone

`` flaps or
`` free fragmentss of cartilage

ie a Dissecting Lesion
What are

Joint Mice

What can happend to them
Fragments of Free Cartilage

in an OCD joint

Which can
`` `` Ossify
Brain Edema (4)
`` `` increase intracellular fluid
`` `` eg polioencephalomalacia rumminants

`` `` increased vascular permeability
`` `` eg any dz producing vasculitis or increased permeability
`` `` increased CSF Pressure
`` `` eg hydrocephalus

`` `` low plasma osmolarity relative to brain
`` `` eg sodium salt poisoning
Cerebellar Hypoplasia

Et (2)
Viral infection while precursor cells are undergoing Mitotic Division

`` `` feline parvovirus infection

`` `` BVDV
Brain forms but no closuere on dorsal surface
`` tf meningies and or brain bulge out
Spina Bifida
Lumbar Spine

Skin Lesion continuous with spinal cord
Formation of fulid filled spaces
`` `` within brain
`` `` as a result of NECROSIS
Abnormal collection of fluid within Cranial Cavity
`` `` usually in Ventricular System
`` `` results in pressure necrosis
Brain formed normally
`` `` suffered premature degeneration
`` `` usually death of Purkinji CELLS
Infectious Agents May Reach Brian via (4)
Direct Extension
`` `` Osteomyelitis of Cranium Via Fused Dura Mater
`` `` penetration of duramater
`` `` `` Otitis Media / Interna
`` `` `` rostral cranium via Cribiform Plate

`` `` most common
`` `` capillaries of meningies or brain
`` `` `` esp capillary bed of Pituitary

Leukocytes Enter Brain
`` `` Macrophages and T Cells introduce Intracellular Parasites
`` `` `` ie Blastomycosis

Retrograde Axonal Flow
`` `` rabies
`` `` listeriosis
Suppurative CNS infections almost always caused by...
Non-suppurative CNS infections usually caused by...
Meningitis practically refers to
Inflammation of
`` `` Arachnoid Space and
`` `` Pia Mater

`` `` E. coli
`` `` Strep. suis
Brain Abscess
Suppurative Inflammation

Slow Growth
`` `` tf large size before clinical signs
`` `` Pressure Atrophy and Necrosis
Thrombotic Meningoencephalitis
Suppurative Inflammation

Histophilus somni a good bet

Bacteremia > Vasculitis > Thrombi and Hemorrhage > Infarct
`` `` local to site of injury
`` `` vessels btwn grey and white matter

Small lesions but dramatic impact bc rapid growth
Suppurative Inflammation

Listeria monocytogenes

Oral Mucosa > Trigeminal etc > Axonal Flow > Ganglia
`` `` localized usually Pons and Medulla
`` `` unilateral
`` `` minimal vascular cuffing
Non-suppurative Inflammation

No Gross Lesions

Just say no to Neutrophils

Perivascular Cuffing
`` `` Lymphocytes
`` `` location usually specific to dz

Almost always viral
Non-suppurative Inflammation

Entry via wounds
> Replicates in Muscle Tissue > migrates to nerves

Axonal Flow > Spinal Cord > Brain > Salivary Gland
`` `` sheds late in dz

`` `` no lesions

`` `` Negri Bodies in Neurons
`` `` `` usually...
Canine Distemper
Non-suppurative Inflammation

Usually Respiratory > Replication Resp Tract / Lymph Nodes

Migration via Leukocytes to CNS
`` `` tf CNS involvement late in dz
`` `` Oligodendricytes injured
`` `` `` tf Degeneration of Myelin
`` `` `` `` tf variable clinical signs
`` `` `` `` mainly Cerebellum Afferents

Perivascular Cuffing
`` `` lymphocytes

May be inclusion bodies in Astrocytes
Degenerative Dz
Cervical Stenotic Myelopathy
Malacic Dz of Spinal Cord
`` `` via external compression

`` `` wobbler syndrome
`` `` large fast growing dogs and horses (TB / QTR)
`` `` joint instability
Intervertebral Disc Degeneration
Intervertebral Disc Malacic Dz of Spinal Cord
`` `` via external compression

`` `` herniation is dorsal
`` `` mainly thoraco-lumbar
`` `` Anulosis Fibrosis bulges / ruptures
`` `` `` +/- Pulposis Nuclosis

Used to Describe
`` Gross appearance of Necrosis in CNS
Thiamine Deficiency in Carnivores

Results in ...


And Looks like...

Neurons in Grey Matter have high energy requirements
`` `` thiamine is popular cofactor for many energy pathways
`` `` `` biochemistry is indeed beautiful

Result is Bilateral Necrosis of Grey Matter of
`` `` Pons and Medulla
`` `` aka Chastek Paralysis
Why is a steady diet of Inland Fish bad for your favorite

Sled Dogs and Mink
Inland fish are high in
`` `` Thiaminase

tf energy mediated Polioenchphalomalacia
Cerebral Cortical Necrosis of Ruminants




2 Ways...

Cool Dx
Polioencephalomalacia of Ruminants

Depressed stupor > Headpressing (intra cranial pr) > blindness > death

`` `` Wet Brain
`` `` Flattened Sulci
`` `` subltle yellowing
`` `` herniation
`` `` `` cerebellar coning

Idiopahtic likely related to thiamine
`` `` ie energy metabolism
`` `` via bacterial thiaminase?
`` `` sometimes juvenilles respond to thiamine therapy


High Sulpher Diets
`` `` via prarie water
`` `` drought resistant forage
`` `` interference with energy metabolism

Either way putting the whammy on energy production
`` `` results in cytotoxic edema
`` `` tf degeneration of myelin
`` `` `` tf Laminar Necrosis via
`` `` `` `` layers of vaculation and macrophages
`` `` `` `` `` two layers = Bifringince

Fluorescence via Woods Lamp
`` `` via bifringence
`` `` 2 - 3 days into dz
Lead Poisoning

No gross lesions in CNS

Multisystemic interference with many enzyme systems

CNS highly susceptable to energy deficits
`` `` Laminar Necrosis of Neurons
`` `` +/- cytoxic edema
Sodium Salt Poisoning

How, What, Characteristic Histo

Pigs and Chickens, Rarely Ruminants

Osmotic Imbalance
`` `` plasma vs brain

High Salt intake and Water Deprivation

Hypernaturemia > ↑ plasma osmolarity > water out of brain and Na / Cl (rapid) and organic colloids (slow) in

Now add water and...

Animal Drinks > ↓ plasma osmolarity > water and Na / Cl move out right quick...


Organic colloids move out of brain slowly
`` `` tf water moves into brain

`` `` Brain Edema
`` `` Pressure Necrosis
`` `` `` Appears as
`` `` `` `` Laminar Necrosis of Grey Matter

`` `` Eosinophil Accumulation in Meningies
`` `` Typical Marker

Name 4

How do they work?
Tranmissible Spongiform Encephalopathies


Bovine Spongiform Encephalopathy

Chronic Wasting Disease

Trnsmissible Mink Encephalopathy

Prion Protiens are particulary rich in Nervous Tissue

Misfolding can result in altered conformation
`` `` ↑ amount of beta pleats
`` `` induces other prion proteins to misfold into same confromation

Altered conformation extremely resistant to proteases
`` `` tf accumulation in cells
`` `` tf cell death

Accumalation starts in Obex of Brain
`` `` chronic
`` `` progressive
`` `` universally fatal
`` `` No Inflammation
`` `` vaculated cells
Why can you smack most animals on the head with little effect
Low ratio of
`` `` Brain Mass : Skull Sinus Mass


Resistance of CNS to Traumatic Accidents
Traumatic Accident

Increase Cranial Pressure

Usually no Gross Lesions

Axonal Damage
`` `` usually reversible
Traumatic Accident

Increase Cranial Pressure

Focal Injury
`` `` hemorrhage
`` `` tear or break in parenchyma
Coup-contrecoup Lesion
Traumatic Accident

Blow to cranium > moving cranium hits brain
`` `` brain owie #1

Brain starts in motion > cranium stops > brain collides with opposite side of cranium
`` `` brain owie #2

Owie #2 is directly across from Owie 1
Cerebrovascular Accidents
Not common compared to Humans

`` infarcts (aka stroke)
`` local thrombus formation

`` infarcts via strongyle larvae emboli
Ischemic Myelopathy

Vascular Accident

Fibrocartilaginous Embolic Myelopathy

Acute Clinical Onset
`` `` Excersise
`` `` Traumatic Sudden Movement

Intervetebral Disk Degeneration > Pulpus Nucleosus expressed under pressure
> enters blood vessels > Infarct +/- Hemorrhage > Necrosis

May see fibrocartilagenous material in blood vessels

Neoplasia of CNS
Primary Tumors may arise from any CNS Cell

Rapid Space Occupation > Compression > Necrosis
Name 9 Endocrine Sites

that should be smiling sunnily at you from the pastoral recesses of your mind while doing the Endocrine Portion of Midterm
`` pars distalis
`` pars tuberalis
`` pars intermedia

`` median eminence
`` infunidbular stalk
`` pars nervosa (infundibular process)

Adrenal Cortex

Adrenal Medulla

Follicular Cells of Thyroid

Parafollicular Cells of Thyroid


Carotic Body

Aortic Body

2 Hormones

aka Vasopressin
`` `` formed in hypothalamus
`` `` stored in neurohypophysis

ADH release stimualed by
`` `` mainly increasing blood osmolality
`` `` decreasing blood pressure
`` `` decreasing ECF volume

Increases tubular absorption of water
Stimulates myometrial contractions during parturition

Stimulates Milk Letdown in response to suckling
Diabetes Insipidus (DI)



PU / PD via
`` `` excessive urine production > plasma hyperosmolality > thirst

A form of Diabetes (siphon) caused by
`` `` defective systnesis of ADH
`` `` `` Central DI
`` `` defective secretion of ADH
`` `` `` Central DI
`` `` non responsiveness of renal tubules to ADH
`` `` `` nephrogenic DI
Primary Central DI

Types 2
`` most common

`` rare
Secondary Central DI

Usually via Space Occupying Lesion in Pituitary
`` `` primary pituitary neoplasm
`` `` meningioma
`` `` craniopharyngioma
`` `` abscess
`` `` granuloma
`` `` cyst

also via
`` `` traumatic injury
`` `` `` hemorrhage and scarring of Neurohypophysis
`` `` `` may last days, weeks or indefinitely
Pars Distalis

Where is it

Name 8 Hormones






`` Prolactin

`` Melanocyte Stimulating Hormone
Thyroid Stimulating Hormone

`` `` Growth of Thyroid Gland
`` `` Production and Secretion of Thyroid Hormones
`` `` `` Primarily T4 (Thyroxine)
Adrenocorticotropic Hormone

`` `` Growth of Adrenal Cortex
`` `` Production and Secretion of
`` `` `` Corticosteroids
Growth Hormone (somatotropin)

Episodic Secretion via
`` `` sleep-wake cycle
`` `` physical activity
`` `` nutritional status
`` `` pregnancy
`` `` `` tf the only hope for a vet student is to get pregnant

Controls rate of skeletal and visceral growth

Affects Protein, CHO, Lipid Metabo

Directly Promotes Lipolysis

Indirectly promotes cellular replication and growth via
`` `` stimulating production of Somatomedins (growth factors)
`` `` `` by Liver and other tissues
Pars Intermedia

Well developed in vet spp
`` `` in some spp produces MSH
`` `` site of ACTH synthesis and secretion in dogs
Pars Tuberalis

Function unknown

Provides scaffold for capillaries of
`` `` Hypophyseal Portal System
Hypophyseal Portal System
Located in Pars Tuberalis of Adenohypopysis

Transports Releasing Hormones (factors)
`` `` produced in Hypothalamus
`` `` cells in Adenohypophysis
Pituitary Cysts



Develop within remnants of Rathke's Pouch
`` `` origin of Adenohyphysis

Dz via
`` `` compress surrounding tissue
`` `` interfere with local blood supply
`` `` inflammation via leakage

Clinical Signs
`` `` mainly DI
`` `` visual deficts (optic chiasm)
`` `` rarely hypofunction of adenohypophysis
`` ``



Pituitary Dwarfism

Oral Ectoderm of Rathke's Pouche
`` `` Fails to Differentiate
`` `` `` various hormone producing cells of adenohypophysis absent
`` `` tf Hypofuntion of Adenohypophysis
`` `` `` tf Secondary Hypofunction of
`` `` `` `` Thyroid Gland
`` `` `` `` Adrenal Corticies

Autosomal Ressisve in German Shepards
`` `` also other breeds

Clincial Signs
`` `` normal birth > 2 months
`` `` slow growth > 1/2 size
`` `` retain puppy coat
`` `` `` no guard hairs
`` `` bilateral alopecia
`` `` thin hyperpigmented skin
`` `` Permenant Dentition
`` `` `` delayed or absent
`` `` delayed physial closure
Name 5 Neoplasms of Adenohypophysis

3 Functional

2 Non Functional
Adenomas of Pars Intermedia

ACTH Secreting Adenomas or Adenocarcinomas

GH Secreting Ademona

Endorinologically INactive Adenomas

Pituitary Pars Intermedia Dysfunction




10 Clinical Signs
Pituitary Dependent Hyperadrenocorticism or Cushings Dz

Old Horses

Hirstutism - Hypertrichosis





Generalized Hyperhidrosis

Intermittent Pyrexia



PDH in Dogs
Pituitary Dependent Hyperadrenocorticism
`` `` aka Cushings

85% of Dz is from ACTH Secreting
`` `` Adenomas
`` `` Adenocarcinomas
`` `` 85% Pars Distalis
`` `` 15% Pars Intermedia

Excessive ACTH >
`` `` bilateral cortical hyperplasia
`` `` > excess cortisol

50/50 Benign or Malignant

Boston Terriers and Dachshunds

`` `` PDH used because adenoma not detected in all cases
Pituitary Tumor > 1 cm

15 - 20% of dogs with PDH
Pituitary Tumor < 1 cm

40 - 45% of dogs with PDH

Note cannot detect tumors < 3 mm with CT or MRI
Enlargement of
`` skull
`` mandible
`` paws
`` and other organs
`` `` tf there is hope for Rob

`` cats, dogs, sheep

GH Secreting Adenoma
Endocrinologically Inactive Adenomas
Neoplasms of Adenohypophysis

Most common in Dogs and Cats

May attain considerable size before clincal signs via
`` `` compressing portions of
`` `` `` pituitary
`` `` `` overlying brain

Clincal Signs
`` dimminshed edocrine function
`` `` thyroid
`` `` adrenal cortex etc
`` DI
`` Any CNS Disorder
`` `` ie blindness
Benign Tumors
`` `` arise from remnants of Rathke's Pouch
`` `` `` OUTSIDE of Sella Turica

Often in Young

Clinical Dz via Compression
Adrenal Cortex


Hormone Classes (3)
Cortex from Mesoderm

Medulla from Neural Crest Ectoderm

Cortex : Medulla : Cortex
`` `` 1:1:1

Cortex - Outer to Inner
`` `` Zona Glomerulosa
`` `` `` Mineralocorticoids
`` `` Zona Fasiculata
`` `` `` Glucocorticoids
`` `` Zona Reticularis
`` `` `` Sex Steroids

`` `` Catecholamines
Mineralocoricoid Hormones
Regulation of Electrolyte and Water Balance

Aldosterone of Renin - Aldosterone - Angiotensin System (RAAS)
`` hypotension or reduced ECF > Renin release from Juxtaglomerular Apparatus
> Renin cleaves Angiotensinogen > Angiotensin I
> ACE converts Angiotensin I to II in lungs
`` Actions of Angiotensin II
`` `` vasoconstriction
`` `` release of Aldosterone

Action of Aldosterone
`` acts on kidney DT Cells as well as epi cells of
`` `` sweat glands
`` `` salivary glands
`` `` GI tract
`` conservation of
`` `` Na, Cl, Bicarb
`` secretion of
`` `` K, H+
> Retention of Water
Glucocorticoid Hormones

Hormone of Interest

General Actions
Cortisol aka Hydrocortisone

Glucocorticoid Hormones Regulate
`` `` CHO, protein and lipid metabo
`` `` maintain fasting blood glucose via
`` `` `` promoting
`` `` `` `` gluconeogenesis
`` `` `` `` augmenting lipolysis
`` `` `` impairing
`` `` `` `` Peripheral Tissue Glucose Uptake

Glucocorticoid Hormones
`` Inhibit
`` `` Inflammatory, Allergic and Immunologicla responses
`` Alter
`` `` contective tissue response to injury
`` Impede
`` `` cartilage production
Sex Steroids (3)



Low quantities Purpose Unknown
3 Elements of Cortisol Synthesis and Release Regulation
Negative Feedback Loop via



Adrenal Cortex
Name and Sketch

3 Mechanisms Each of


Functional Pituitary Tumor

Fuctional Adrenocortical Tumor

Chronic Iatrogenic Corticosteroids

Deficent ACTH Secretion

Adrenocorical Atrophy

Sudden Cessation of Chronic Iatrogenic Corticosteroids

Now draw em out - Go ON you know you want to
`` `` see pg 11 of handout
7 Lesions of the Adrenal Cortex

Accessory Adrenal Cortical Tissue


Nodular Hyperplasia

Idiopathic Adrenal Cortical Atropy and Adrenal Insufficiency

Cortical Adenomas

Cortical Carcinomas

Cortical Atrophy
Adrenal Cortical Hypoplasia

Associated with abnormal dev of pituitary gland
Accessory Adrenal Cortical Tissue
Common Finding

Normal Cortical Tissue found in
`` `` medulla
`` `` capsule
`` `` periadrenal fat
`` `` perirenal fat
`` `` near testes
Adrenal Cortical Hyperplasia
Diffuse Cortical Hyperplasia
`` uniform bilateral enlargement of adrenal coritces

Response to
`` ACTH secreting ademoma of pituitary
`` chronic stressful event
Nodular Adrenal Cortical Hyperplasia
Bad Term

Common Older Animals

Spherical masses in
`` medulla
`` cortex
`` capsule

Expansile with compression of surrounding tissue

Would be more accurately decsribed as Adenomas
`` `` because no stimulus for change identified
Idiopathic Adrenal Cortical Atrophy and Adrenal insufficiency
Common cause of hypodrenocorticism in dogs

Immune Mediated?
`` involve infiltration of
`` `` lymphcytes
`` `` plasma cells
Adrenal Cortical Adenomas
Fequently in Older Dogs
`` rarely other spp

Signle well demarcated mass in ONE adrenal gland

Usually non functional
`` if functional
`` `` hyperadrenalcorticism
`` `` bilateral atrophy of otherwise healthy cortices
Adrenal Cortical Carcinomas
`` cattle and older dogs

`` often invade surrounding tissue

May obliterate adrenals and erode into cauda vena cava or aorta
`` `` thrombosis +/- intra abdominal hemorrhage

May Metastasize

Usually non functional
`` if functional
`` `` hyperadrenalcorticism
`` `` bilateral atrophy of otherwise healthy cortices

3 Mechanisms
ACTH Secretion via Pituitary Neoplasm

Glucocorticoid Secretion via Functional Adrenal Neoplasm

Excessive Administration of
`` `` Glucocorticoids (usually)
`` `` ACTH

Clinical Signs Dogs


Abdominal Enlargement


Excersise Intolerance

Muscle Weakness




Alopecia / Failure to regrow


Thin Skin

Pyoderma or dermatitis
`` immunosuppression


3 Mechanisms

9 Clinical Signs
Deficient ACTH Secretion via
`` `` ptiuitary dz

Deficient Adrenocortical Hormone secretin via
`` `` adrenocortical atrophy

Sudden cessation of prolonged exogenous glucocorticoid administration

Clinical Signs
`` Note if primary dz
`` `` both mineralocorticoids and glucocorticoids are deficient
`` if Secondary Dz (loss of ACTH)
`` `` only glucocorticoids deficient

Deression or lethargy




Weight loss



Shivering / hypothermia

PU +/- PD
Adrenal Associated Endorinopathy (AAE)



Clinical Signs
`` `` middle age and older

Proliferative Lesions
`` usually unilateral on left side
`` `` nodular cortical hyperplasia
`` `` adenoma
`` `` carcinoma
`` Secrete Excessive Estrogenic Hormones
`` rarely secrecte excessive glucocorticoids
`` Eitiology unknown

Clinical Signs
`` Symmetrical Alopecia starting at base of tail
`` pruritis
`` Enlarged Vulva spayed females
`` males have difficulty urinating
`` `` urethral hypoplasia
`` `` prostatic dz
`` `` musky odor
Catecholamine Hormones
Adrenal Medulla
`` Epinephrine
`` Norepinephrine

Released in response to
`` hypoglycemia
`` stress



Promotes Glycgenolysis
Released in Response to
`` Hypotension
`` stress

Powerful Vasopressor
Neoplasms of coloured cells of Adrenal Medulla
`` most common neoplasm of AM
`` common in
`` `` cattle and dogs

`` Large and may compress surrounding soft tissue
`` `` impede ureters

`` invade surrounding tissue
`` `` caudal vena cava
`` `` aorta
`` metastisize

Non Functional
`` majority

`` rare
`` tachcardia
`` caredia hypertrophy
`` edema
`` hypertension
`` `` thickended vessel walls
Thyroid Hormone Feedback Loop

3 Structures

3 Hormones
`` TRH

`` TSH

Thyroid Gland
`` T4 > T3
`` 10 : 1

Note T4 converted to T3
`` liver
`` kidney
`` CNS

T3 is active hormone
`` differentiation during development
`` increases BMR of ALL cells
Accessory Thyroid Tissue
Common esp Dog

Embryonic development close to aortic sac
`` tf accessory tissue from base of tongue to diaphragm
`` `` base of heart most common

Fully functional and capable of neoplasm
Thyroglossal Duct Cysts
Most Frequent Dogs and Pigs

Remnants of Embryonic thyroglossal duct

Fluctuant Swellings in
`` `` ventral neck
`` `` may from fistulaous tract to skin

Thyroid Follicular Epithelium may undergo neoplastic transformation
Idiopathic Follicular Atrophy
Progressive loss of Follicular Epi
`` `` replacement with
`` `` `` adipose and CT

Accounts for 1/2 cases of
`` `` Acquired Hypothyroidism in Dogs
Lymphocytic Thyroiditis
Progressive imflammatory dz dogs

Thyroid Gland Infiltrated
`` `` lymphocytes
`` `` plasma cells
`` `` macrophages

Accounts for the other 1/2 cases of
`` `` Acquired Hypothyroidism in Dogs

Immune Mediated ala
`` `` Hashimoto's Dz humans
Goiter ala Dr. Allen
Descriptive Term

Non Neoplastic AND Non Inflammatory

Enlargement of Thyroid Gland to at least 2 X
Thyroid Gland Hyperplasia


4 Causes
aka Hyperplastic Goiter

Hypertrophy AND Hyperplasia of
`` `` follicular Cells

Failure of sufficient Production and Secretion of T4
`` `` tf increased secretion of TSH

Iodine Deficiency

Iodine Excess

Gotrogenic Substances

Defects in biosythetic Enzymes
Collid Goiter
Enlargement of Thyroid via
`` `` Markedly Distended Follicles
`` `` Thought to be involutional (resolution) phase of
`` `` `` Hyperplastic Goiter
Thyroid Gland Adenomas
aka Follicular Cell Adenoma
`` Benign neoplasms of follicular cells

Older Animals
`` esp Non functional in Horse

Expansile Pale Mass

Functional = Hyperthyroidism
`` `` common cats
Thyroid Gland Carcinomas
aka Follicular Cell Carcinomas

Malignant Neoplasms of Follicular Cells

Uncommon Vet Spp
`` but more common than canine thyroid adenoma

+/- Functional

Rapid Invasion and Metastisis
`` from any thyroid epi
3 Conditions of Thyroid Gland

Acquired Hypothyroidism

Congenital Hypothyroidism

Cats vs Dogs

aka Thryroidtoxicosis

Multisystemic Dz via high T3 / T4
`` `` common cats
`` `` `` one or more Functional Thyroid adenomas
`` `` `` `` 70% bilat
`` `` uncommon dogs
`` `` `` iatrogenic
`` `` `` fucntional thyroid carcinomas
`` `` rare other spp

Slowly Progressive
`` clinical signs related to increased BMR
`` `` highly variabel
`` cats = cardiomyopathy
`` `` usually hypertrophic
`` `` rarely dilative
Acquired Hypothyroidism


Clinical Signs
Multisystemic Dz via deficiency of T4 / T3

Occurs in Dogs (0.2%)
`` Goldies and Dobermans
`` usually primary lesion of thyroid gland

Overdiagnosed in Horses

Extremely Rare other spp

Clinical - related to decreased BMR

Lethargy / Mental Dullness

Weight Gain

Skin Dz
`` excessive shedding
`` symmetrical alopecia of trunk
`` dry hair
`` seborrhea
`` pyodrma

Cold intolerance

`` mild non regenerative



Weight Loss




Hyperactivity or Restlessness

Decreased Appetite


Enlargement of Thyroid gland


Heart Murmur


abnormal Heart Sounds
`` gallop rhythm

Congenital Hypothyroidism


3 Mechanisms
Rare except Horses NW of NA

Thyroid Gland Aplasia

Thyroid Gland dysplasia

`` genetic (biochemical) defect
`` iodine deficient dam
`` teratogen
`` `` ie Excess Iodine

Aresseted Physical and Mental Development
`` aka Cretinism
`` present at birth in precosial spp
`` weeks to months atricial spp
`` `` fetal bones
`` `` `` no epiphysis
Congenital Hypothyroidism Horses

Long to Normal Gestation

High incidence of Dystocia


Poorly developed Bones

Soft Silky Hair Coat

Soft Pliable Ears

Mandibular Prognathism
`` apalastic maxilla

Flexed Legs
`` ruptured extensor tendons
Parafollicular Cells



aka C (clear) Cells

2nd population of endocrine cells in thyroid gland
`` small clusters between follicles
`` individuals in follicular epi

Synthesize and Secrete Calcitonin
`` in response to hypercalcemia
`` lowers plasma Calcium and phosphate levels via
`` `` decreasing calcium absorption in SI
`` `` increasing calcium secretion in kidney
`` `` inhibits bone resorption
`` `` `` antagonistic to Parathyroid Hormone

`` response to chronic hypercalcemia

`` associated high Ca diet and Parafollicular Cell Hyperplasia
`` occasionally
`` `` old bulls
`` `` `` associated with Pheochromocytomas
`` `` old horses
`` aka Ultimobranchial Tumors

Parafollicular Cell Adenomas
`` < 3 cm and discrete

Parafollicular Cell Carcinomas
`` large and replace thyroid lobe(s)
`` Metastasize to
`` `` regional lymph nodes
`` `` lungs
Parathyroid Gland

Synthesis and Secretion of Parathyroid Hormone (PTH)
`` response to hypocalcemia

PTH Elevates Blood Ca via
`` promoting release of Ca from bone via
`` `` activating osteoclasts
`` `` inhibiting osteoblasts
`` `` promotes renal
`` `` `` Ca absorption
`` `` `` phosphate secretion
`` `` indirectly via Vit D increases SI absorption of Ca
Atrophy of Parathyroid Glands
Occurs with Pseudohyperparathyroidism
`` much better known as
`` `` Humoral Hypercalcemia of Malignancy (HMM)

Occurs when Chronic Hypercalcemia is induced by action of
`` PTH Related Protein (PTHrP)
`` `` secreted by malignant neoplasms
`` `` manifistation of a Paraneoplastic Syndrome
Diffuse Parathyroid Hyperplasia
Typically accompanied by hypertrophy of
`` `` Chief Cells

Uniform enlargement
`` via
`` `` long term dietary Ca insufficiency
`` `` chronic renal failure
Parathyroid Adenomas
Occasionally old Dogs

Discrete Mass in a single parthyroid gland

If Functional
`` primary hyperparathyroidism
Primary Hyperparthyroidism




- 3 organs
Excessive PTH via
`` parathyroid
`` `` adenoma
`` `` carcinoma

Rare Vet spp

Clinical - Mild, Insidious, Nonspecific
`` Renal
`` gastrointestinal
`` Neuromuscular

`` Hypercalcemia
`` PU / PD
`` Listlessness
`` Incontinence
`` Weakness
`` Exercise Intolerance
`` Inappetance
Secondary Hyperparathyroidism


2 Causes
Stimulus for low blood calcium
`` `` Produces Compensatory increase synthesis and production of PTH
`` `` > normocalcemia or rarely mild hypercalcemia
`` `` `` but at expense of bones

`` growing animals with diet
`` `` deficient Ca
`` `` excess phosphorous
`` `` ie pigs all grain
`` `` ie horses creal hay, grain, bran
`` `` ie cats dogs all meat

`` chronic severe renal dz
`` `` older dogs and cats
`` `` complex pathogenesis
`` `` `` aka renal osteodystrophy
`` ie thyroid surgery in cats

Deficient PTH via
`` reduced secretion by parathyroids
Chemoreceptor Organs



Arotic and Carotid Bodies

Chemoreceptosrs that Sense
`` `` pO2,
`` `` pH,
`` `` pCO2
`` involved in regulation of
`` `` cardiovascular function
`` `` respiration

Direct Neural input to
`` vasomotor centres
`` respiratory centers

Endocrine Function via
`` release of Catecholamines

`` benign or malignant
`` `` Chemodectoma of
`` `` `` carotid or aortic body
Aortic Body Chemodectoma
Single Masses or Multiple Nodules
`` within pericardial sac
`` near base of heart

Cardiac Tamponade via
`` bleeding into pericardial Sac
Compression or invasion of
`` `` Atria
`` `` Great Vessels
`` `` Trachea

Metasitisis to other organs is rare
Carotid Body Chemdectoma
Usually Single Slow Growing masses in Neck near Head

Dz via
`` compressin or invading
`` `` carotid artery
`` `` jugular vein
`` `` lymphatics
`` `` cranial nerves
`` metastasis to other organs
Aneurysm –
a sac formed by the local dilatation of the wall of an a., v., or heart
Arteriosclerosis –
grp of dzs in humans characterized by thickening and loss of elasticity of the arterial walls; of no importance to ans
Atherosclerosis –
a common form of arteriosclerosis in humans in w/c yellowing deposits of plaque (atheromas) containing cholesterol, other lipoid material, and lipophages are formed w/I the intima of lrg and sm a.s
Arteritis –
(I) of an a.
Cardiac tamponade –
compression of the heart due to collection of fluid or blood w/i the pericardial sac; causes interference w/ heart action and subsequent sudden death or congestive heart failure. The heart shadow is enlarged , the heart sounds on auscultation are muffled
Cardiomyopathy –
a general diagnostic term designating myocardial dz of u/k cause
Cor pulmonale –
right ventricular HF due to pulmonary hypertension 2° to dz of bvs of lung; usually chronic and due to COPD or heartworm dz. Clinical signs are those of congestive HF
Disseminated Intravascular Coagulation (DIC) –
characterized by widespread formation of microvascular thrombi, most commonly seen as as result of septicemia/endotoxemia, viral or immunologic injury to endlm, protein losing nephropathy, uremia, disseminated metastatic neoplasia, etc; widespread coagulation also stimulates fibrinolysis; thrombosis and fibrinolysis together consume clotting factors
Endocardium –
endl lining mb of cavities of heart and CT bed on w/c it lies
Endocarditis –
exudative and proliferative (I)y alterations of endocardium, characterized by presence of vegetations on the surface of the endocardium or in the endocardium itself, and most commonly involving a heart valve, but also affecting the inner lining of the cardiac chambers or the endocardium elsewhere. Lesions on valves may interfere w/ ejection of blood from heart by causing insufficiency or stenosis of the valves. Murmurs assoc/d w/ heart sounds are the major manifestation and if interference w/ blood flow is sufficiently severe congestive HF ds. The further hazard w/ endocarditis, esp if bacterial in origin, is that of septic emboli in the lungs or other organs.
Endocardiosis –
common cause of cardiac dz in dog. Characterized by chronic fibrosis and nodular thickening of the free edges of the AV valves. In the worst cases the valve cusps are distorted converting a minor leak into massive incompetence. Leads to congestive HF. No specific cause.
Epicardium –
the inner layer of the serous pericardium, w/c is in contact w/ heart
Hemangioma –
a benign tumor made up of newly formed bvs, clustered together. In ans occur mostly on skin and in spleen. In birds, may be caused by leucosis virus.
Hemangiosarcoma –
a malignant tumor of endl cells characterized by extensive metastasis, being cavitatious, and bleeding profusely if cut. Occurs in spleen, liver, skin, RA, and m. It can cause severe (H)ic anemia by bleeding internally. Common is GS dogs. AKA angiosarcoma.
Hematoma –
a localized collection of extravasated blood, usually clotted, in an organ, space or tissue. Contusions (bruises) are familiar forms of hematoma that are seldom serious. Hematomas can occur almost anywhere in the body; they are almost always present w/ a fracture and are esp serious when located w/i skull, where they may produce local P on brain. In minor injuries the blood is absorbed unless infection ds.
Hemopericardium –
an effusion of blood in the pericardial cavity, caused by rupture of the atrium, perforation of the ventricle or rupture of a coronary a. It is usually manifested by a very sudden death.
Hydropericardium –
an excess of transudate in the pericardial cavity. The cardiac shadow is enlarged and distorted on radiography; its size encroaches on the area over w/c lung sounds can nly be heard
Lymphangitis –
(I) of a lymphatic vessel. It is a common finding in dzs of ans, and is of partic nbce in horses b/c of the need to differentiate causes from Glanders, and in cows b/c of importance of this lesion in bovine tuberculosis
Lymphadenitis –
(I) of LNs; a common incidental finding in dzs of ans. It is also a principal presenting sign in some others, esp strangles in horses, cervical abscess of pigs, bovine tb, gaseous lymphadenitis in sheep and goats, and lymphosarcoma in dogs and cats.
Myocardium –
the middle and thickest layer of the heart wall, composed of cardiac m
Myocarditis –
(I) of the muscular walls of the heart (the myocardium). The condition may result from bacterial or viral infections or it may be a toxic (I) caused by drugs or toxins from infectious agents.
Omphalophlebitis –
(I) of the umbilical veins
Pericardium –
the fibroserous sac enclosing the heart and the roots of the great vessels, composed of external (fibrous) and internal (serous) layers.
Pericarditis –
(I) of the pericardium. Initially there is an audible friction rub on auscultation. Later as fluid accumulates there is muffling and s/tms washing machine sound on auscultation. Congestive HF ds terminally. Classified according to exudates prod/d as fibrinous, fibrinohemorrhagic, hemorrhagic, purulent.
Phlebitis –
(I) of a vein. Not serious when the (I) is located in a superficial vein since these veins are numerous enuf to permit the flow of blood to be rechanneled, so that the (I)d vein is bypassed. When a deep vein is involved it is potentially more dangerous. It can also have serious consequences if it leads to cerebral abscesses. Common causes in ans are omphalophlebitis and injection phlebitis caused by inadvertent injection of irritant substances or the prolonged use of IV catheters. The vein is swollen and painful and the blood flow is obstructed.
Vasculitis –
(I) of a vessel; common causes include allergic, immune-mediated.
Cardiac myocytes are
post mitotic  no fxnal capability to regenerate
-this is diff from other myocytes in the body
-they can only replace themselves in very young ans
-if necrosis of myocytes occurs  fibrosis
-they have a limited spectrum of response to injury
Responses of heart to ↑ workload

-fxn of heart is to pump blood
-heart has to respond quickly to ↑ demand for blood
-can ↑ it’s physiological output by 3-5X

-heart rate
-more strokes/min
-at some point this is no longer effective to ↑ CO b/c no time for ventricular filling  can result in ventric fibrillation (therefore it is limited)
-quick response

-stroke volume
-heart has to dilate to do this (↑ size of ventricle)
-you eventually reach a point where it can be stretched no further  happens suddenly  can no longer move blood efficiently ande muscular force drops off therefore this is limited too
-quick response

-dilation and m. hypertrophy (ht)
-↑ amt of m in heart (↑ size of fibres)
-remember these are post-mitotic so can’t have hyperplasia (hp)
-ht is a physiological phenomena
-dilatation can occur rapidly
-need 3 things for ht:
a) time (therefore if seen, you know it’s chronic)
b) healthy myocardium
c) good vasculature to heart
-ht is helpful only to a certain point; get problems when:
a) m. of heart may ↑ in size, but ventricular cavity/opening may not
b) size of cells ↑, but M don’t ↑ proportionally so cells lack en mechs to
keep them running efficiently
c) no new blood vessels added w/ ht; about 1:1 cap to myocytes; therefore
blood supply not adequate b/c of ↑ diffusion distance

*there are limitations to each of the above responses (hr, sv, dilatation and ht)
-high alt. dz 
low to high movement; some cattle will die w/I 24h;
these will have very dilated hearts b/c PCV has ↑ so much and heart is having to pump a lrgr vol of blood
-if see T shape it’s L side of heart; pap m are on R side??? Db check
Heart Failure:
the potential end-point for all forms of serious heart (h) dz

-“inability of the pumping K of the h to meet metabolic demands of the body”

-“when the h can’t maintain an output adequate for the metabolic needs of the tissues and organs of the body”

-ans get along fine until there’s ↑ demand on the h; ie: exercise intolerance
Heart failure occurs because: 2
1) there is ↓ ability of h to contract and move blood
2) there is an inability to fill the cardiac chambers w/ blood
↓ ability of h to contract and move blood
-impaired ability of the myocardium to contract (pump failure)
-a/t that interferes w/ h fxn (any damage to myocardium):
-necrosis/degen/n is a common cause
-C. chauvoei  blackleg  causes myocardial damage w/c calves can die of
-lymphosarcoma  lymphoid tissue infiltrates h HF is ultimate cause of death in this case too
-dilatation of h; can’t create enuf strength to pump
-vasculature of h is inadeq  uncommon in ans
P overload
-having to work against an abn P gradient
-ie: vessel that h is trying to push blood thru is abnly sm
-usually seen w/ vascular stenosis in ans
-in Newfie breed  see congenital stenosis of aortic valve  d ht of
L. h
-other breeds of dogs and pigs get stenosis of pulm. a.  would
result in ↑ R side
-if get too much R in tissues can see this too (usually occurs in lungs b/c of too much P possibly b/c of R from fibrosis from chronic pneumonia; ↑ P could also be due to pleural cavity filled w/ fluid; lungs don’t expand well in these cases)
volume overload
-h can’t keep up w/ vol returning to it
-an doesn’t have too much blood overall, just too much in the wrong place
-s/tms ans have too viscous of blood (polycythemia) b/c of ie: high altitude
or other cond/ns
Inability to fill the cardiac chambers w/ blood
-most common reason  s/t outside compressing h that intereferes w/ dilation, therefore can’t fill; ie: fibrinous pericarditis or cardiac tamponade (H into pericardial sac)
-R is side that is affected more so by P so it’s affected more by this than L side
failure of one side of h
inevitably affects other side

-can’t have a prob on one side w/o having a prob on the other
-if prob on one side goes on for long enuf, you’ll see effects on opposite side

(need to insert diagram in here)
venous pump arterial

-should be balanced amt of blood

venous failing pump  arterial

-hypoxia -ischemia
-↑ hydrostatic P -hypoxia
-anoxia -forward
-backwards effects effects
-damming back
-get edema

-effects are seen more on the venous side

* ↑ R in periphery doesn’t generally affect L side of h
Physiologic responses to a failing h

by the h
-by ↑ vol moved (dilatation)  short term
-↑ HR  short term
-ht  long term
Physiologic responses to a failing h

by peripheral circ/n
-HF sensed as hypoxia so peripheral circ/n responds by diverting blood to nb centers  vasoconstriction so periphery is poorly nourished
-helpful in short term
-↑R  redistribution of blood
Physiologic responses to a failing h

by the kidneys
-kidneys sense HF b/c of relative hypoxia
-activate rennin-angiotensin system  retention of Na+/H2O
-good thing if hypoxia was due to blood loss, but if problem is pumping it’s bad b/c creates more volume to pump, therefore diuretics commonly used so blood vol doesn’t ↑
Physiologic responses to a failing h

by the bone marrow
-also senses hypoxia so ↑ erythropoesis (helpful in short term, but not long term)  may make blood more viscous and harder to pump therefore exacerbating problem in long term
Left Sided HF (The major effect is
backwards, ie: on the lungs)

-get accum/n of venous blood in lungs
-get ↑ hydrostatic P in lungs and relative hypoxia  pulmonary edema and congestion
-lungs will be wet, heavy, fail to collapse, dark red
-will see froth in trachea  tells you there is pulmonary edema
-histologically see lots of cells in alveolar space (RBCs leaking in b/c of hypoxia  RBCs picked up by macs w/c process them  hemosiderin accumulates  HF cells (can even be found in tracheal foam w/ TTW)
-Mason’s trichrome stain  stains fibrous tissue  get fibrosis of alveolar wall  not good in lungs b/c get alveolar cap block and fibrosis intereferes w/ gas exchange
-don’t see many peripheral effects; probably see relative hypoxia, but we don’t really recognize this in ans
Right Sided HF (the major effect is
backwards, ie: on the peripheral and visceral circ/n)

-majority of changes are on venous side
-see severe passive congestion of liver, kidneys and edema (b/c of hypoxia and ↑ hydrostatic P) in dependent areas (nutmeg liver in lrg ans)  can get fibrosis
-much more likely to see results related to kidney (Na/H2O retention); not common w/ LS HF
-where edema collects is spp dependent
-in cattle, don’t see edema in legs, usually seen in brisket and under jaw
-in horses, see edema in legs and along ventral midline
-in dogs, see ascites
-in cats, accumulate fluid in chest, can have ascites as well
-in all spp there is hepatic congestion
-also get cyanosis w/ RS HF
Remember that, w/ time, failure of one side of heart
inevitably affects the other side
-can’t dx HF by looking at h, need to see the other signs in body
Cardiac anomalies (many of these, especially in dogs, are

-variable from no effect to the anomalie being incompatible w/ life

*in fetus, lungs are not aerated b/c lungs are high density system so we don’t want to pump high P thru it

*don’t detach h from lungs until exam is done for anomalies
Defects as a result of failure of fetal cardiovascular shunts to close (the most common type of defect in domestic ans. Initially they usually involve
flow of blood from L to R).
Patent ductus arteriosis (DA)
-more common anomalie of dogs (poodles, collies, poms; inherited)
-DA is n in fetus  allows for bypass of pulm circ/n by a shunt going from the L pulmonary artery to the aorta
-should b/cm a ligament and close completely after birth
-when the newborn takes its first breath, the lungs open and pulmonary pressure decreases below that of the left heart
-because of reduced pulmonary resistance, more blood flows from the pulmonary arteries to the lungs and thus the lungs deliver more oxygenated blood to the left heart. This further increases aortic pressure so that blood no longer flows from the pulmonary artery to the aorta via the DA.
-if it remains open, blood will now shunt from L (aorta) to R (pulmonary artery) instead of from R to L as it was originally intended; creates high P in pulm a.  get pulm hypertension
-A patent ductus arteriosus allows oxygenated blood to flow down its pressure gradient from the aorta to the pulmonary arteries. Thus, some of the infant's oxygenated blood does not reach the body, and the infant becomes short of breath and cyanotic. The heart rate hastens, thereby increasing the speed with which blood is oxygenated and delivered to the body. Left untreated, the infant will likely suffer from congestive heart failure, as his heart is unable to meet the metabolic demands of his body).
-get P overload in h b/c having to pump to lungs where P is high
-more blood coming from lungs that L h has to deal w/
-see ht of Lh, s/tms Rh too
-sig of patent DA depends on size, some ans may tolerate some ° (ie: 3mm), but if > 5mm, likely to lead to HF
Atrial septal defect
- nly closes after birth to b/cm a flap (one way valve) after the 1st breath causes the P in the pulmonary circ/n to drop
-direction of movement through the foramen ovale is nly from L to R
-if flap is inadeq to cover, may see transfer of blood; this blood is coming directly into RA from LA (flow from high P to low P)
-see vol overload in R h (both atria and ventricle) so see signs of RS HF b/c blood backs up (too much in there already so not as much can return to h)
-also see pulmonary hypertension again b/c of an ↑ in P due to an ↑ in volume getting into the pulmonary circ/n
-when the P in the R h b/cms equal w/ that of the L h, no longer see shunt from L to R; if left untreated long enuf, the P of the R side can actually exceed the P of the L side and we will see a R to L shunt unoxygenated blood will then be pumped into the systemic circ/n and we’d expect to see cyanosis
-more common in cats than in dogs
-see big round hearts  is it big due to dilatation/ht? can’t say w/o opening the h
-see larger R auricle too
Ventricular septal defect
-opening n very early in life, but should be closed at birth
-doesn’t cause any problems for fetus b/c Ps are = b/w ventricles in utero
-defects are always high on septa (usually under aortic valve)
-common in calves
-effect depends on size of opening
-transfer from L to R
-many ans can compensate for this
-if large enuf to cause probs, will probably see RS ht; if an ds HF, usually see bilateral ht b/c of vol overload on L side and P overload on R
-get pulmonary hypertension
Defects as a result of failure of dt of valves or valvular openings
*stenosis is more common form of defect usually affecting outflow valves
Pulmonary artery stenosis
-occurs in several breeds of dogs (beagles, chihuauas, bulldogs; inherited)
-see ht of RV b/c of RV working harder to get past pulmonary valve
-s/tms see poststenotic dilation of pulmonary artery as a result of jetstream injury to wall
-see dilatation of RV w/ time as well if HF doesn’t kill an 1st
Aortic (sub-aortic) stenosis
- occurs in larger breeds (Newfies, GS, Boxers)
-also used to occur in Landrace pigs
-see ht of LV
-remember ht takes time, w/ time you can also see dilatation (the m has to work hard so we see ht, since there is so much R we see a damming effect w/c causes the dilatation)
-stenosis is often below valve
Valvular dysgenesis
-dysplasia of AV valves (failure of valve leaflets); usually leaky]
-not common
-in calves, s/tms see red cyst (hematocyst) on valve
-no fxnal significance b/c valves nly not vascularized
PRAA (vascular ring anomalie)
-nb in dogs
-aorta ds from 4th aa (L and R side)
-nly L arch should d and R arch should atrophy
-s/tms R arch ds and L arch may or may not atrophy
-problem involves ligamentum arteriosum (from pulmonary a to aorta)
-n: esophagus dorsal and to the R of the aorta
-if PRAA, esophagus passes thru vascular ring (aorta loops around esophagus)
-obstructs esophagus by compression
-dogs eat and vomit
-get extended esophagus on X-ray w/c ends at h base; nb for ddx (other types of megaesophagus end at different places)
-can surgically cut ligamentum arteriosum
-db walled sac
-nly contains sm amt of fluid to prevent friction
-most probs from things accumulating in this space
-fluid accumulating in space (clear, serous fluid)
-interferes w/ filling of h, particularly RS
-seen in dz assoc/d w/ generalized edema; ie: RS HF
-seen in dz assoc/d w/ vascular injury  ↑ vascular permeability
-seen in dz assoc/d w/ hypoproteinemia
-rate of accum/n more nb than volume
-if quick, can compress h
-if occurs over long period of time, h can compensate
-more dramatic than hydropericardium
-usually result of H
-in horses, get tear of aorta  bleed into pericardium  cardiac tamponade  sudden death
-in dogs, suffer tears in atrial wall  particularly in dogs w/ uremia
Cardiac tamponade
-compression of the heart due to collection of fluid or blood w/i the pericardial sac
-causes interference w/ heart action and subsequent sudden death or congestive heart failure
-quite common
-usually not a solitary lesion, expect to see other lesions w/ this
-usually result of generalized bacterial infxn (septicemia usually)


-seen w/ navel infxns
-seen w/ Pasteurella infxns (P. Mannheimia) in cattle
-seen w/ C. chauvoei (Blackleg)  does affect h as well
-most pericarditis’ are fibrinous
-when b/cm chronic may b/cm constrictive


-hardware dz (traumatic reticular pericarditis)
-probably never recover from lesions
-see constriction of R h


-intereferes w/ filling of h
Endocardium (end/m)

-when see mineralization think of 3 etiologies:
a) Vit D intoxication (usually feed mixing error)
b) uremia (can lead to tear in atrial wall in dogs)
c) Vit D analogs (s/tms occurs due to analogs in plants  not here)
-accum/n of mineral under end/m
-seen in cattle
-can occur in Johne’s dz  macs make Vit D like compound

-endocardiosis (common cause of HF in dogs; non-(I)y)

-a non-(I)y dz of end/m
-problem is most common cause of HF in older dogs
-often older dogs get along just fine  they may compensate
-will often see signs of LHF if we do see signs; (involving lungs)
-almost invariably involves LAV valves (most common) [can also be Rh too, but less common]
-degenerative change assoc/d w/ aging  we don’t understand causes
1) -accum/n of abn mucopolysaccharide material w/i valvular leaflets; get fibrosis at same time
- shape of valve changes; nly thin, flexible leaflet
- valves b/cm incompetent and leak back into atria
2) chordae tendinae also affected; nly keep leaflets from going too far back
-can b/cm thickened and contracted and tend to make valve openings insufficient
-can s/tms even tear  see acute HF when this occurs; rare

-can see jet lesions (fibrotic scar on wall from blood shooting back into atria)
Endocarditis (Inflammatory)
-occurs across spp
-infectious process; occurs in ans w/ bacteremia
-by far the most nb dz
-causes stenosis
-interferes w/ blood flow thru valve
-material may cause a thromboembolism too
-if on LAV valve, likely to go to kidneys (renal infarcts), spleen, arthritis
-if lesion on aortic valve  go to same place as above, but also see myocardial infarcts too
Valvular Endocarditis
-LAV is most commonly affected, then aortic, then RAV, usually then pulmonary; not unusual to have multiple valves affected
-bacteria circulate and localize on h valves; probably from some other source
-s/tms related to dental dz (often in s mans)
-not easy to prod/ dz experimentally, but if you work h, tends to be easier to reproduce
-bacteria located at tips of valves  makes them sticky  get fibrin, bacteria, platelets attaching to where valves slap together
-more common on AV valves
-many bacteria can cause it, but usually spp specific
-Strep. Suis and E. rhusiopathiae  pigs
-A. pyogenes  cattle
-Opprotunistic bacteria  sm ans
Mural Endocarditis
-when seen on free wall
-in Blackleg, see involvement of myocardium, end/m, and epicardium
-not a common lesion
-if does occur, usually in assoc/n w/ other lesions (not common as a solitary lesion)
-can occur w/ extension fr. pericardium, end/m., but most come from hematogenous spread from bacteremia or endocarditis from valve
-usually supprative or necrotizing
Histophilus somni myocarditis in cattle
-this dz has changed; used to be TME  now not seen; usually h lesions now  regardless of where it is, basic problem that it’s a circulating infxn and it causes vasculitis and thrombosis at sites
-can be acute necrosis to supprative myocarditis
-localize in papillary m.s on LS  get lrg hemorrhagic areas of necrosis
-in many catlle, lesion has areas of infarction w/ areas of fibrosis w/ areas of necrosis (mixed  still in pap m tho)
Blackleg (Clostridium chauveoi) in cattle
-often affects h
-often dark areas
-looks dry and cooked
-often fibrin on pericardium and epicardium
Canine parvoviral myocarditis
-viral induced
-parvoviruses replicate in dividing cells and myocytes in h are post-mitotic
-in young pups, myocytes are still undergoing mitosis (dividing), therefore they usually die acutely w/ no intestinal lesions
-h may look a little pale and lungs are congested at PM
-get mild lymphocytic infiltration
-s/tms see intranuclear inclusion bodies
Myocardial necrosis
-may be a little (I) w/ it
-lesions slow to d; don’t see until about 18-24h (ie: myocardial infarct)
-areas then b/cm pale; if given more time areas remain pale, but d hyperemic border
-myocytes that die are not replaced
-best outcome one can hope for is fibrosis
Nutritional myopathy (White m dz)
-seen in lambs and calves
-deficiency of Vit E/ Se  antioxidants that protect m cells  w/ damage get Ca2+ moving in  uncontrolled contraction and necrosis
-tends to involve papillary m and around end/m
-both skeletal and cardiac m affected (variable as to how much of each is affected)
-not a rapid dz
-cause pale lesions b/c of mineral deposition and lack of blood flow
-see necrosis, regeneration, and fibrosis
Mulberry h dz of swine
-traditionally thought to be a Vit E/ Se deficiency  don’t know for sure, b/c it’s happening in pigs that seem to have a well nourished diet
-no involvement of skeletal m, only cardiac  acute dz in w/c pigs die
-affects rapidly growing 4-5 mo old pigs; die of acute HF
-lesion: lungs are wet w/ edema, fluid in chest and pericardial sac; often fibrin too (fibrin tells you it’s pretty severe damage of bvs)  looks like pericarditis
-see red streaking in h
-1° lesions in little vessels (necrosis or damage to little bvs  microangiopathy)
-these vessels leak and H; see acute HF  mainly on LS (therefore see effects on lungs)
Ischemic necrosis Myocardium
-we don’t see this often, does occur occasionally
-seen more often in humans b/c of vascular dzs
“generalized non-(I)y, degenerative dz of h m of uncertain etiology”
“non-(I)y myocardial dz that is not attributable to P or vol overload”

-s/t is wrong w/ cardiac m
-has more restricted definition tho  1° non-(I)y degenerative dz of myocardium
-usually don’t know cause
-commonly only seen in cat and dog (cat moreso)
Hypertrophic cardiomyopathy
-cond/n that is most common in cats
-specifically assoc/d w/ middle-aged, male cats (esp lrg breed cats like Himalayans, Persians)
-not very common in dogs, but if so, usually in lrg breed males too
-often get acute HF in these dogs
-in cats, may present w/ signs of HF, or b/c of signs related to hind legs (approx 20% have saddle thrombus  cold, painful legs)
-at PM, see enlarged h, on LS usually (LV m and intraventricular septum)
-may be symmetrical or asymmetrical involvement (ie. May be whole h, or not)
-h may be lrg, but ventricular cavity/opening is smaller
-some of these cats get atrial thrombosis (L atria)
-in older cats (some), have hyperthyroidism (usually thyroid adenoma)
-thyroid hormone may have some role in assoc/n w/ excess growth of myocytes
Dilated cardiomyopathy
-it’s most common form in dogs, does rarely occur in cats
-in dogs: usually assoc/d w/ very lrg breeds (Dobermans, St. Bernards, Great Danes)
-in cats: one form occurred b/c of dietary deficiency of Taurine  now commercial foods are supplemented w/ this
-on PM have very dilated h (As and Vs)
-dilation may be so extreme that valves are incompetent b/c valvular leaflets don’t reach each other
-occasionally see atrial/aortic thrombosis
-in Dobermans  tendency to have arrhythmias as well; may have conduction problems
Restrictive Cardiomyopathy
-only in cats
-get fibrosis under end/m for u/k reasons so Vs can’t dilate properly
-problem w/ filling
-not assoc/d w/ infxn
Neoplasia Heart
-1° neoplasia in h is rare
-2° neoplasia is not common either; 2 exceptions:
a) hemangiosarcoma in dogs
-arises from endl cells in R auricle or spleen
-metastasize widely
b) in cattle
-as part of lymphosarcoma
-tumors tend to involve h  may lead to HF
-are lined by endlm
-endlm in vessels should be continous except it’s fenestrated in the smallest vessels (arterioles, venules)
-endlm consists of metabolically active cells
-most nb action they have is to resist thrombosis
-if mild injury to endlm  ht and hyperplasia (hp)  may also get fluid and protein leakage (fibrin) into wall of vessel
-if endl cells die/ b/cm necrotic  exposes underlying collagen  induces thrombosis (platelet aggregation in particular)
-endlm is very nb  so many dzs of vessels are result of endl injury
-smooth m of vessels  can ht and b/cm hyperplastic in ans w/ hypertension
Thrombosis (In general,
thrombosis of lrg vessels leads to localized effects, while thromobosis in microvasculature (DIC) usually leads to generalized effects).

-in general  in response to endl injury/ cell death
-aided by turbulence or stasis
-in certain cond/ns  blood is hypercoaguable; ie: hyperadrenocorticism)
-can get thrombosis of lrg vessels (effect is usually local)
-can also get DIC (in tiny vessels, generalized effects)
-difference b/w thrombosis or arteries and veins
-a. thrombosis  ischemia
-if remove thrombosis  expect recovery
-v. thrombosis  ischemia and congestion/edema  fibrosis of m
-ie: downer cow gets venous thrombosis
-when thrombosis resolved  don’t get complete recovery
-where there’s poor collateral circ/n ie: kidneys
-bad place to get thrombus
-we get renal infarct  doesn’t occur in liver and lungs b/c of collateral
Saddle Thrombus (posterior aortic thrombosis in cats)
-probably related to turbulence in h caused by cardiomyopathy
-get thrombus fr atrial wall and throws emboli to wedge in terminal aorta
Vena Cava (VC) Thrombosis in Cattle (Vena Caval Syndrome)
-seen in adult cattle
-starts w/ rumenitis fr grain overload
-get liver abscess  nly doesn’t cause a problem
-s/tms they grow and impinge on VC
-if it doesn’t break thru and just causes (I) of wall and get thrombus formation in VC
 not septic, but pieces can break off
 go to h
 go thru to lungs
 usually well tolerated b/c good collateral circ/n
-more dangerous if abscess ruptures into VC
 get septic thrombosis w/c can end up in h and lungs
 when shower reaches lungs  causes abscesses throughout lungs
-if lrg abscess ruptures
 can get into lung and block many vesseld
 can lead to DEATH
-abscess in lung may also grow and pop bvs
 may swallow (rumen filled w/ blood) or she may blow it out her nose
Thrombosis of Cranial Mesenteric Artery from Strongylus Vulgaris
-damaged by larvae
-pieces of material break off and cause infarction in intestine fro blocking bvs in intestines
DIC (Death is coming)
-thrombosis of sm vessels
-can occur b/c of direct injury to vasculature (ie: viruses like bluetongue)
-can also occur b/c of s/t that directly activates clotting system (ie: endotoxin)
-get congested, edematous lungs
-get inadequate return to h so get shock
-if DIC goes on for long enuf, get bleeding b/c of consumptive coagulopathy
-local outpouching of vessel wall
-not seen often in domestic ans
-sig b/c s/tms ruptures and bleeds out immediately
-occurs in horses and tom turkeys (toms are very hypertensive)
-not common in ans
-hardening of a.
-thickening of a. wall w/ loss of elasticity and narrowing of lumen
-very common in humans
-type of arteriosclerosis
-get accum/n of lipid/fibrous material under intima of vessels  s/tms mineral there too
-these growths bulge into lumen (lipid plaque)
-sites where thrombosis can occur
-seen occasionally in dogs
Medial mineralization
-do see this in ans
-collection of minerals in media of vessels
-deposition of mineral on elastic fibres of a.
-no longer distensible/flexible
-usually nothing signif.  common in old cows
-think of uremia (dogs), Vit D tox (pigs and dogs), and analogue of Vit D (Mac prod/d or plant) (in domestic ans)
Vasculitis (arteritis, phlebitis, lymphangitis)
-(I) of a vessel
-many dzs related to (I) of a vessel
-2 main ways vessels are damaged:
a) direct injury to endlm  occurs w/ some viruses
b) result of immune-mediated dz
Parasitic arteritis
-ie: cranial mesenteric arteritis from S. vulgaris in horses
-during larval migration  under endlm in intima
-larvae spend approx 4 mo. maturing here
-cause (I), arteritis and thrombosis
-cause outpouchings (aneurysms) too
-consequence is nly n/t b/c of collateral circ/n, but s/tms end up in renal a  poor collateral circ/n  renal infarct
-s/tms even end up in brachiocephalic trunk
Malignant Cattarhal Fever
-dz of *bison, cattle
-world wide
-assoc/d w/ infxn of herpes virus from other spp (sheep here infecting other spp w/ BHV-2)
-basic lesion in MCF is arteritis
-severe and necrotizing
-in cattle  very severe necrosis of eplm of oral cavity and gut lesions  result of arteritis
-in bison  get ulcers/erosions on tongue
 d opacity of cornea
 b/c of damage to a.
-may be direct viral damage to a. and may be partially IM too
Feline Infectious Peritonitis (FIP)
-(I) of veins occurs (phlebitis)
-caused by a corona virus
-in most cats, usually mild, transient infxn
-depends on ability to mount CMI
-if good, virus cleared quickly (majority of cats)
-if impaired  d persistent viremia
 have Ag circulating for long time
 get lot’s of Ab prod/n w/c is non protective
 get Ag/Ab complexes deposited in vessels (particularly in
 results in (I)
 see a) exudation of fluid (leaky vessels)
b) (I) in peritoneum although it’s a generalized dz
wet form – some cats have major yellow fluid d in abdomen
dry form – some cats have a granulomatous response in
eyes, kidneys, liver, etc.
Omphalophlebitis (navel ill)
-another ie: of phlebitis
-direct bacterial infxn
-s/tms suppurative
-usually fibrinous
-may have material moving to liver
-usually get septicemia  arthritis/meningitis in calves
Lymphangitis caused by Mycobacterium paratuberculosis
-seen in Johne’s dz
-causes granulomatous enteritis
-causes corrugation of intestines
-lymphatics draining gut stand out
-obstructs lymphoid draining from gut
-get thin watery diarrhea
-nb in dogs
-rare in other spp
-2 sites
a) R auricle/atria
b) spleen
-very wide metastasis
-classical case  old GS who died suddenly
-benign tumor of bvs
Purulent Rhinitis of Rabbits
Pasturella multocida
Inclusion Body rhinitis of Piglets
Cytomeglo Virus
Atrophic rhinitis of pigs
Bordetella Bronchisepticus


Paterurella Multocida
Strangles in Horses
Strep equi equi
Mycotic Rhinits Dogs
Necrotic Laryngitis in Calves
Calf Diphtheria

Fusobacterium necrphorum
Focal Necrotizing Laryngitis Cattle
Histophilus somni
Infectious Bovine rhinotracheitis (IBR) in Cattle
Bovine Herpes Virus I
Rhinotracheitis in cats
Feline Herpes Virus

Feline Calici Virus
`` also oral, ocular
Canine Infectious Tracheobronchitis
Bordetella bronchiseptica

Canine parainfluenzavirus 2

Canine adenovirus 2

et al
Suppurative Bronchopneumonia Cattle
Pasteurella multocida

Arcanobacterium pyogenes
`` chronic suppurative

Mycoplasma bovis
`` dry caseous

Rumen Aspiration
`` gangrenous necrosis
Suppurative Bronchopneumonia Pigs
Pasteruella multocida

`` occasionally
Suppurative Bronchopneumonia Horse
Sreptococcus spp.

Rhodococcus spp
Suppurative Bronchopneumonia Cats

Pasteurella multocida
Suppurative Bronchopneumonia Dogs

Bordetella bronchispetica
Fibrinous bronchopneumonia Cattle
Mannhemia haemolytica

Histophilus somni
`` fibrinous or suppurative

Mycoplasma mycoides
`` other parts of world
Fibrinous bronchopneumonia Pigs
Unusual Pattern
`` dorsal, caudo-dorsal
`` occasionally cranio-ventral

Actinoacillus pleuropneumoniae

Actinobacillus suis
Interstitial Pneumonia General Agents

Migratory parasites

Inhaled / Circulating Toxins

Few Bacteremic States
Interstitial Pneumonia

Acute Bovine Pulmonary Emphysema and Edema
Fall > move to lush pasture > L-tryptophan > Clara Cells in Lung > 3-Methyl-Indole
Interstitial Pneumonia

Hypersensitivity Pneumonia Cattle
Pig Ascarids
Interstitial Pneumonia

Procine Respiratory and Reproducitve Syndrome PRRS
PRRS Virus
Interstitial Pneumonia

Many Species - Single Agent
Canine Distemper Virus
Broncho-Interstitial Pneumonia Cattle
Bovine Respiratory Syncytial Virus (BRSV)
Broncho-Interstitial Pneumonia Cats
Patterns of degeneration and necrosis (3)
a) Zonal pattern
Periportal (zone 1)
Midzonal (zone 2)
Centrilobular ~ periacinar = zone 3

b) random or multifocal: infectious agent

c) massive*
1) severe toxicity
2) acute vascular accident
3) dietetic origin ex. Hepatosis dietetica
(young pigs, def. vitamin E and/or Se)
Normal Liver function and Altered liver fx (4)
1) Bilirubin metabolism - hyperbilirubinemia
2) Bile acid metabolism - ↑ serum bile acids
3) Carbohydrate met. - steroid-induced *hepatopathy; dogs
hepatic glycogenosis
4) Lipid metabolism - hepatic lipidosis*
Differentials for enlarged yellow-brown livers: (3)
1) hepatic lipidosis
 Occurs in a number of species
 Liver appears greasy and friable

2) steroid-induced hepatopathy

3) hepatic amyloidosis: us. Secondary or reactive amyloid *
 Deposition of amyloid in liver or sometimes kidneys
 Results from  serum amyloid A secondary to chronic inflammatory process
 Gross: see diffuse yellow discoloration, friable not greasy
 Histo: atrophic hepatocytes, see amyloid with special stains
Xenobiotic metabolism
 Sometimes endogenous source
 Ie) cytochrome p450 enzymes of hepatocyte SER metabolize xenobiotics and endogenous substances for excretion in bile or urine:

a) Metabolism of xenobiotics can result in production of toxic intermediates:
 Damage can occur in a ZONAL PATTERN
 Centra-lobular region has the most activity and is affected first

b) Impaired detoxification can result in disease:
Hepatogenous or secondary photosensitization
Example of impaired hepatic detoxification:
 chlorophyll  int. bacteriaphylloerythrin (photodynamic) impaired excretion in bile  accumulates in tissues  oxidative damage  skin necrosis
 absorbed and secreted from the liver in the same matter that biliruben is ie) conjugation  secretion bile  small intestine
 if this process is impaired, it accumulates. It is a photodynamic compound so it is activated by sunlight and causes oxidative damage and necrosis
 affects pooly pigmented skin – ie) face
 alopecia occurs at first, hyperemic then ulceration
Note: photosensitization can occur by other means: (2)
Primary photosensitization
 Chemical componets of certain plants can be absorbed into tissues
 Ie) alsike clover, St. John’s wort

 congenital porphyria
 Accumulate photo reactive porphrins in skin.
Protein synthesis: Liver
 Liver synthesizes the majority of plasma proteins
 15% of proteins in the body
 Majority of plasma proteins
 Albumin:
 35-50% of protein in serum
 Affect osmolarity and fluid flux
 relatively long serum ½ life (~7-10 days);
 therefore not affected with acute liver failure but hypoalbuminemia may occur with chronic liver failure
 Many of the clotting factors produced by the liver;
 Vit K-dependent clotting factors have a relatively short ½ life (few days)
 therefore depletion can result with acute hepatic disease.
 Results in abnormal homeostasis
Liver Immune function: involved in systemic, local and mucosal immunity.
Increased risk of endotoxemia and systemic infection
 Kupffur cells line sinusoids – major factor for removing endotoxins and bacteria because the liver gets all the blood from the GI tract – This is the bodies 1st defense
 Mucosal protection – recycle IgA through the bile to protect GI and bilary system
  liver function =  risk of systemic infection and toxemia
Hepatic encephalopathy
True cause unknown
 Possible associated with  ammonia
 Liver also removes neurotransmittest so get  concentration of neurotransmitters when liver function is
 Often this is the hallmark of the disease
Bleeding tendencies: Liver
Have  clotting factors
 Liver is no longer removing fibrin degradation products
 Metabolic changes affect platelet function
 Diminished synthesis of clotting factors,
 Acute hepatic failure: DIC  hemorrhagic diathesis
Cholestasis  impaired fat absorption  ↓ fat soluble vitamin K  inactivity of factors II, VII, IX and X
severe chronic hepatic disease
 Reduced levels of albumin
 Hepatocellular damage =  protein production
 See with chronic disease because T ½ is 7-10 days
 Outcome is EDEMA because of decreased osmotic pressure within the vasculature
Vascular and hemodynamic changes: Liver
 chronic hepatic injury  fibrosis  portal hypertension ascites (EDEMA)
 most commonly in dogs and cats, occasionally in sheep rarely in horses and cattle
Liver Dz cutaneous manifestations:
 Photosensitization
 Hepatocutaneous syndrome* (superficial necrolytic dermatitis) observed in some dogs with severe hepatic disease:
 Mechanism unknown
 Associated with liver disease
 Possibly abnormalities in nutrients and required factors
 Get thickening, crusting of the face, muco-cutaneous junction, muzzle, and foot pads and contact points of the body
 Leads to necrosis and ulceration
Entry of injurious agents to the liver can occur in 3 ways:
1) hematogenous: portal v., hepatic a., umbilical v.
 Portal vein draining the GI tract
 Systemic spread – bacteria showers the liver
 Neonates – ascending infection up the umbilical vein

2) biliary
 Bile duct is open to duodenum, so get spread via ascending micro flora
 Commonly a result of parasites and bacteria

3) direct penetration
 Through body wall to the liver
 From the GI through mucosa
Inflammatory response to injurious agents dictated by route of entry

Hematogenous 
Inflammatory response to injurious agents dictated by route of entry

Biliary 
Cholecystitis: inflammation of the gallbladder
Acute hepatitis:
neutrophils, necrosis typically random with infectious agents
Chronic hepatitis: characterized by
fibrosis and mononuclear cells; persistent antigenic stimulation
Cholangiohepatitis: both
Hepatocytes and bile duct affected

Parasites and bacteria don’t respect the boundries of hepatocytes
Response of the liver to injury: Two responces
1) Regeneration
 Tremendous capacity for regeneration
 Requires the framework(scaffold) to still be present

2) fibrosis*