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271 Cards in this Set
- Front
- Back
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What is Intramembranous Ossification?:
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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 |
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What is Endochondral Ossification?
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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 |
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What is the difference between Traumatic and Pathologic Fractures?
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Answer: Traumatic: When a normal bone fractures under abnormal force
Pathological: When an abnormal bone fractures under normal force |
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What is Osteochondrosis (or osteochondritis)?
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Answer:
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 |
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Name 4 ways to introduce infection (ie: cause osteitis and osteomyelitis).
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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 |
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Describe Degenerative Joint Disease (looking for key words!)
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AKA: Osteoarthritis, osteoarthrosis, degenerative arthritis, arthropathy
Answer: 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 |
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7. What are the 2 circumstances in which DJD occurs?
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Answer:
1) Joints with normal cartilage placed under abnormal stress 2) Joints with abnormal cartilage placed under normal stress |
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Synovial Fluid
Monocyte : Neutrophil Ratio |
9 : 1
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DJD is a
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PROGRESSIVE disease of synovial joints
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DJD begins as
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Irreversible Degeneration of Articular Cartliage
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DJD May be accompanied by (3)
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CHANGES IN SOFT TISSUE
FORMATION OF OSTEOPHYTES SCLEROSIS OF SUBCHONDRAL BONE (modeling) |
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DJD May OR May Not be associated with
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Clinical Signs
Swelling Pain Lameness |
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The Cause of DJD is
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not fully understood
likely represents a common set of lesions associated with a variety of disease processes |
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DJD Initiation might be (4)
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Degeneration of Articular Cartilage
Inflamamation of the Joint Capsule Inflammation of Synovium Increased Stiffness of Subchondral Bone |
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DJD will ALWAYS include
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Degeneration of Articular Cartilage
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DJD can occur in Joints With (2)
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Normal Cartilage following Abnormal Stresses
Abnormal Cartilage following Nomral Stresses |
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Early Stages of DJD are recognized as
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Chondromalacia
Dull or rough apperarance Yellow Brown Discolouration |
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Later Stages of DJD are characterized by
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Fibrillation and Focal Erosions of Articular Cartilage
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Continued use of a Joint with DJD results in
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Eburnationa and Changes in Subchondral Bone
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The Articular Cartilage of a Joint with DJD
Releases _________________ Which _________________ And may be accompanied by (2) |
Break Down Products
Which Exacerbates inflammation of the Synovium And may be accompanied by `` `` Villus Hyperplasia `` `` Osteophyte Production |
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Osteochondrosis is a
Disorder of (2) in |
Physes
Articular Cartilage of Endochondral Bones in Growing Animals |
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Osteochondrosis is defined as....
Resulting in .... |
Focal or Multifocal
Failure (or delay) of Endochondrial Ossification Resulting in Localized Thickening of Hyaline Cartilage |
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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 |
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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 |
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Osteochondritis Dessicans (OCD)
arises from .... via.... |
Osteochondrosis of Articular Cartilage
Clefts develop `` `` within foci of thickended cartilage or `` `` between thickended cartilage and underlying bone Creating `` flaps or `` free fragmentss of cartilage ie a Dissecting Lesion |
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What are
Joint Mice What can happend to them |
Fragments of Free Cartilage
in an OCD joint Which can `` `` Ossify |
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Brain Edema (4)
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Cytotoxic
`` `` increase intracellular fluid `` `` eg polioencephalomalacia rumminants Vasogenic `` `` increased vascular permeability `` `` eg any dz producing vasculitis or increased permeability Hydrostatic `` `` increased CSF Pressure `` `` eg hydrocephalus Hypo-Osmotic `` `` low plasma osmolarity relative to brain `` `` eg sodium salt poisoning |
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Cerebellar Hypoplasia
Et (2) |
Viral infection while precursor cells are undergoing Mitotic Division
Kittens `` `` feline parvovirus infection Calves `` `` BVDV |
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Meningeoencephalocoele
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Brain forms but no closuere on dorsal surface
`` tf meningies and or brain bulge out |
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Spina Bifida
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Lumbar Spine
Skin Lesion continuous with spinal cord |
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Hydranencephaly
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Formation of fulid filled spaces
`` `` within brain `` `` as a result of NECROSIS |
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Hydrocephalus
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Abnormal collection of fluid within Cranial Cavity
`` `` usually in Ventricular System `` `` results in pressure necrosis |
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Abiotrophy
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Brain formed normally
`` `` suffered premature degeneration `` `` usually death of Purkinji CELLS |
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Infectious Agents May Reach Brian via (4)
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Direct Extension
`` `` Osteomyelitis of Cranium Via Fused Dura Mater `` `` penetration of duramater `` `` `` Otitis Media / Interna `` `` `` rostral cranium via Cribiform Plate Hematogenous `` `` 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 |
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Suppurative CNS infections almost always caused by...
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Bacteria
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Non-suppurative CNS infections usually caused by...
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Viruses
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Meningitis practically refers to
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Inflammation of
`` `` Arachnoid Space and `` `` Pia Mater Often `` `` E. coli `` `` Strep. suis |
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Brain Abscess
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Suppurative Inflammation
Slow Growth `` `` tf large size before clinical signs `` `` Pressure Atrophy and Necrosis |
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Thrombotic Meningoencephalitis
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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 |
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Literiosis
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Suppurative Inflammation
Listeria monocytogenes Oral Mucosa > Trigeminal etc > Axonal Flow > Ganglia `` `` localized usually Pons and Medulla `` `` unilateral `` `` minimal vascular cuffing |
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Non-suppurative Inflammation
Characteristics |
No Gross Lesions
Just say no to Neutrophils Perivascular Cuffing `` `` Lymphocytes `` `` location usually specific to dz Almost always viral |
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Rabies
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Non-suppurative Inflammation
Entry via wounds > Replicates in Muscle Tissue > migrates to nerves Axonal Flow > Spinal Cord > Brain > Salivary Gland `` `` sheds late in dz Gross `` `` no lesions Histo `` `` Negri Bodies in Neurons `` `` `` usually... |
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Canine Distemper
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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 |
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...opathy
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Degenerative Dz
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Cervical Stenotic Myelopathy
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Malacic Dz of Spinal Cord
`` `` via external compression `` `` wobbler syndrome `` `` large fast growing dogs and horses (TB / QTR) `` `` joint instability |
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Intervertebral Disc Degeneration
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Intervertebral Disc Malacic Dz of Spinal Cord
`` `` via external compression `` `` herniation is dorsal `` `` mainly thoraco-lumbar `` `` Anulosis Fibrosis bulges / ruptures `` `` `` +/- Pulposis Nuclosis |
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Malacia
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Softening
Used to Describe `` Gross appearance of Necrosis in CNS |
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Thiamine Deficiency in Carnivores
Results in ... Via... And Looks like... |
Polioencephalomalacia
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 |
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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 |
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Cerebral Cortical Necrosis of Ruminants
aka... Signs... Lesions... 2 Ways... Cool Dx |
Polioencephalomalacia of Ruminants
Depressed stupor > Headpressing (intra cranial pr) > blindness > death Lesions `` `` 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 or 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 |
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Lead Poisoning
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Polioenchephalomalacia
No gross lesions in CNS Multisystemic interference with many enzyme systems CNS highly susceptable to energy deficits `` `` Laminar Necrosis of Neurons `` `` +/- cytoxic edema |
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Sodium Salt Poisoning
How, What, Characteristic Histo |
Polioencephalomalacia
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... but Organic colloids move out of brain slowly `` `` tf water moves into brain Voila `` `` Brain Edema `` `` Pressure Necrosis `` `` `` Appears as `` `` `` `` Laminar Necrosis of Grey Matter Histo `` `` Eosinophil Accumulation in Meningies `` `` Typical Marker |
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TSE
Name 4 How do they work? |
Tranmissible Spongiform Encephalopathies
Scrapie 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 ↓ |
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Why can you smack most animals on the head with little effect
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Low ratio of
`` `` Brain Mass : Skull Sinus Mass tf Resistance of CNS to Traumatic Accidents |
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Concussion
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Traumatic Accident
Increase Cranial Pressure Usually no Gross Lesions Axonal Damage `` `` usually reversible |
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Contusion
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Traumatic Accident
Increase Cranial Pressure Focal Injury `` `` hemorrhage `` `` tear or break in parenchyma |
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Coup-contrecoup Lesion
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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 |
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Cerebrovascular Accidents
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Not common compared to Humans
Dogs `` infarcts (aka stroke) `` local thrombus formation Horses `` infarcts via strongyle larvae emboli |
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Ischemic Myelopathy
aka |
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 M |
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Neoplasia of CNS
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Primary Tumors may arise from any CNS Cell
Rapid Space Occupation > Compression > Necrosis |
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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 |
Andenohypophysis
`` pars distalis `` pars tuberalis `` pars intermedia Neurohypophysis `` median eminence `` infunidbular stalk `` pars nervosa (infundibular process) Adrenal Cortex Adrenal Medulla Follicular Cells of Thyroid Parafollicular Cells of Thyroid Parathyroid Carotic Body Aortic Body |
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Neurohypophysis
2 Hormones |
ADH
Oxytocin |
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ADH
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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 |
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Oxytocin
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Stimulates myometrial contractions during parturition
Stimulates Milk Letdown in response to suckling |
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Diabetes Insipidus (DI)
What How Types |
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 |
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Primary Central DI
Types 2 |
Idiopathic
`` most common Congenital `` rare |
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Secondary Central DI
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Aquired
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 |
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Pars Distalis
Where is it Name 8 Hormones |
Adenohypophysis
TSH ACTH GH FSH LH PRL `` Prolactin MSH `` Melanocyte Stimulating Hormone |
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TSH
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Thyroid Stimulating Hormone
Promotes `` `` Growth of Thyroid Gland `` `` Production and Secretion of Thyroid Hormones `` `` `` Primarily T4 (Thyroxine) |
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ACTH
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Adrenocorticotropic Hormone
Promotes `` `` Growth of Adrenal Cortex `` `` Production and Secretion of `` `` `` Corticosteroids |
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GH
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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 |
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Pars Intermedia
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Adenohypophysis
Well developed in vet spp `` `` in some spp produces MSH `` `` site of ACTH synthesis and secretion in dogs |
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Pars Tuberalis
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Adenohpohysis
Function unknown Provides scaffold for capillaries of `` `` Hypophyseal Portal System |
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Hypophyseal Portal System
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Located in Pars Tuberalis of Adenohypopysis
Transports Releasing Hormones (factors) `` `` produced in Hypothalamus to `` `` cells in Adenohypophysis |
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Pituitary Cysts
Where How Signs |
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 `` `` |
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Panhypopituitarism
aka Mechanism Signs |
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 |
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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 Craniopharyngiomas |
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Pituitary Pars Intermedia Dysfunction
akas Spp What 10 Clinical Signs |
Pituitary Dependent Hyperadrenocorticism or Cushings Dz
Old Horses Hirstutism - Hypertrichosis PU PD Hyperglycemia Glucosuria Generalized Hyperhidrosis Intermittent Pyrexia Polyphagia Myasthenia Somnolence |
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PDH in Dogs
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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 Note: `` `` PDH used because adenoma not detected in all cases |
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Macroadenoma
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Pituitary Tumor > 1 cm
15 - 20% of dogs with PDH |
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Microadenoma
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Pituitary Tumor < 1 cm
40 - 45% of dogs with PDH Note cannot detect tumors < 3 mm with CT or MRI |
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Acromegaly
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Enlargement of
`` skull `` mandible `` paws `` and other organs `` `` tf there is hope for Rob Rare `` cats, dogs, sheep GH Secreting Adenoma |
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Endocrinologically Inactive Adenomas
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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 |
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Craniopharyngiomas
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Benign Tumors
`` `` arise from remnants of Rathke's Pouch `` `` `` OUTSIDE of Sella Turica Often in Young Clinical Dz via Compression |
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Adrenal Cortex
Structure 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 Medulla `` `` Catecholamines |
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Mineralocoricoid Hormones
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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 |
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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 `` `` `` `` HEPATIC GLYCOGENESIS `` `` `` `` augmenting lipolysis `` `` `` impairing `` `` `` `` Peripheral Tissue Glucose Uptake Glucocorticoid Hormones `` Inhibit `` `` Inflammatory, Allergic and Immunologicla responses `` Alter `` `` contective tissue response to injury `` Impede `` `` cartilage production |
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Sex Steroids (3)
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Progesterones
Estrogens Androgens Low quantities Purpose Unknown |
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3 Elements of Cortisol Synthesis and Release Regulation
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Negative Feedback Loop via
Hypothalamus Adenohypophysis Adrenal Cortex |
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Name and Sketch
3 Mechanisms Each of Hyperadrenocorticism Hypoadrenocorticism |
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 |
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7 Lesions of the Adrenal Cortex
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Hypoplasia
Accessory Adrenal Cortical Tissue Hyperplasia Nodular Hyperplasia Idiopathic Adrenal Cortical Atropy and Adrenal Insufficiency Cortical Adenomas Cortical Carcinomas Cortical Atrophy |
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Adrenal Cortical Hypoplasia
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Rare
Associated with abnormal dev of pituitary gland |
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Accessory Adrenal Cortical Tissue
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Common Finding
Normal Cortical Tissue found in `` `` medulla `` `` capsule `` `` periadrenal fat `` `` perirenal fat `` `` near testes |
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Adrenal Cortical Hyperplasia
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Diffuse Cortical Hyperplasia
`` uniform bilateral enlargement of adrenal coritces Response to `` ACTH secreting ademoma of pituitary `` chronic stressful event |
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Nodular Adrenal Cortical Hyperplasia
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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 |
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Idiopathic Adrenal Cortical Atrophy and Adrenal insufficiency
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Common cause of hypodrenocorticism in dogs
Immune Mediated? `` involve infiltration of `` `` lymphcytes `` `` plasma cells |
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Adrenal Cortical Adenomas
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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 |
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Adrenal Cortical Carcinomas
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Rare
`` cattle and older dogs Bilateral `` 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 |
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Hyperadrenocorticism
3 Mechanisms |
ACTH Secretion via Pituitary Neoplasm
Glucocorticoid Secretion via Functional Adrenal Neoplasm Excessive Administration of `` `` Glucocorticoids (usually) `` `` ACTH |
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Hyperadrenocorticism
Clinical Signs Dogs |
PU / PD
Polyphagia Abdominal Enlargement Obesity Excersise Intolerance Muscle Weakness Lethargy HEpatomegaly Osteoporosis Alopecia / Failure to regrow Pruritis Thin Skin Pyoderma or dermatitis `` immunosuppression Hyperpigmentation |
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Hypoadrenocorticism
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 Anorexia Vomiting Weakness Weight loss Dehydration Diarrhea Shivering / hypothermia PU +/- PD |
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Adrenal Associated Endorinopathy (AAE)
Species Mechanism Clinical Signs |
Ferrets
`` `` 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 |
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Catecholamine Hormones
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Adrenal Medulla
`` Epinephrine `` Norepinephrine Sympathomimetic |
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Epinepherine
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Released in response to
`` hypoglycemia `` stress Inotropic Chronotropic Promotes Glycgenolysis |
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Norepinephrine
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Released in Response to
`` Hypotension `` stress Powerful Vasopressor |
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Pheochromocytomas
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Neoplasms of coloured cells of Adrenal Medulla
`` most common neoplasm of AM `` common in `` `` cattle and dogs Benign `` Large and may compress surrounding soft tissue `` `` impede ureters Malignant `` invade surrounding tissue `` `` caudal vena cava `` `` aorta `` metastisize Non Functional `` majority Functional `` rare `` tachcardia `` caredia hypertrophy `` edema `` hypertension `` `` thickended vessel walls |
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Thyroid Hormone Feedback Loop
3 Structures 3 Hormones |
Hypothalamus
`` TRH Adenohypophysis `` 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 |
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Accessory Thyroid Tissue
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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 |
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Thyroglossal Duct Cysts
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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 |
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Idiopathic Follicular Atrophy
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Progressive loss of Follicular Epi
`` `` replacement with `` `` `` adipose and CT Accounts for 1/2 cases of `` `` Acquired Hypothyroidism in Dogs |
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Lymphocytic Thyroiditis
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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 |
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Goiter ala Dr. Allen
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Descriptive Term
Non Neoplastic AND Non Inflammatory Enlargement of Thyroid Gland to at least 2 X |
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Thyroid Gland Hyperplasia
Mechanism 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 |
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Collid Goiter
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Enlargement of Thyroid via
`` `` Markedly Distended Follicles `` `` Thought to be involutional (resolution) phase of `` `` `` Hyperplastic Goiter |
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Thyroid Gland Adenomas
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aka Follicular Cell Adenoma
`` Benign neoplasms of follicular cells Older Animals `` esp Non functional in Horse Expansile Pale Mass Functional = Hyperthyroidism `` `` common cats |
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Thyroid Gland Carcinomas
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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 |
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3 Conditions of Thyroid Gland
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Hyperthyroidism
Acquired Hypothyroidism Congenital Hypothyroidism |
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Hyperthyroidism
Cats vs Dogs Clinical |
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 |
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Acquired Hypothyroidism
Species 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 Anemia `` mild non regenerative Hpercholesterolemia |
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Hyperthyroidism
Cats Clinical |
Weight Loss
Polyphagia Vomiting PU /PD Hyperactivity or Restlessness Decreased Appetite Diarrhea Enlargement of Thyroid gland Thin Heart Murmur Tachycardia abnormal Heart Sounds `` gallop rhythm Hyperkinesis |
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Congenital Hypothyroidism
Spp 3 Mechanisms |
Rare except Horses NW of NA
Thyroid Gland Aplasia Thyroid Gland dysplasia Dyshormonogenesis `` 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 |
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Congenital Hypothyroidism Horses
Clincal |
Long to Normal Gestation
High incidence of Dystocia Dysmature Poorly developed Bones Soft Silky Hair Coat Soft Pliable Ears Mandibular Prognathism `` apalastic maxilla Flexed Legs `` ruptured extensor tendons |
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Parafollicular Cells
Hormone Purpose Lesions |
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 Hyperplasia `` response to chronic hypercalcemia Neoplasia `` 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 |
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Parathyroid Gland
Function |
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 |
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Atrophy of Parathyroid Glands
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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 |
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Diffuse Parathyroid Hyperplasia
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Typically accompanied by hypertrophy of
`` `` Chief Cells Uniform enlargement `` via `` `` long term dietary Ca insufficiency `` `` chronic renal failure |
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Parathyroid Adenomas
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Occasionally old Dogs
Discrete Mass in a single parthyroid gland If Functional `` primary hyperparathyroidism |
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Primary Hyperparthyroidism
What How Who Clinical - 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 |
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Secondary Hyperparathyroidism
What 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 Nutritional `` growing animals with diet `` `` deficient Ca `` `` excess phosphorous `` `` ie pigs all grain `` `` ie horses creal hay, grain, bran `` `` ie cats dogs all meat Renal `` chronic severe renal dz `` `` older dogs and cats `` `` complex pathogenesis `` `` `` aka renal osteodystrophy |
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Hypoparathyroidism
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Uncommon
`` ie thyroid surgery in cats Deficient PTH via `` reduced secretion by parathyroids |
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Chemoreceptor Organs
2 Dz Nomenclature |
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 Neoplasia `` benign or malignant `` `` Chemodectoma of `` `` `` carotid or aortic body |
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Aortic Body Chemodectoma
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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 |
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Carotid Body Chemdectoma
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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 |
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Aneurysm –
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a sac formed by the local dilatation of the wall of an a., v., or heart
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Arteriosclerosis –
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grp of dzs in humans characterized by thickening and loss of elasticity of the arterial walls; of no importance to ans
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Atherosclerosis –
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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
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Arteritis –
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(I) of an a.
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Cardiac tamponade –
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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
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Cardiomyopathy –
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a general diagnostic term designating myocardial dz of u/k cause
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Cor pulmonale –
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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
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Disseminated Intravascular Coagulation (DIC) –
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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
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Endocardium –
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endl lining mb of cavities of heart and CT bed on w/c it lies
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Endocarditis –
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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.
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Endocardiosis –
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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.
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Epicardium –
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the inner layer of the serous pericardium, w/c is in contact w/ heart
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Hemangioma –
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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.
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Hemangiosarcoma –
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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.
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Hematoma –
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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.
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Hemopericardium –
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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.
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Hydropericardium –
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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
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Lymphangitis –
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(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
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Lymphadenitis –
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(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.
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Myocardium –
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the middle and thickest layer of the heart wall, composed of cardiac m
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Myocarditis –
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(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.
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Omphalophlebitis –
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(I) of the umbilical veins
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Pericardium –
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the fibroserous sac enclosing the heart and the roots of the great vessels, composed of external (fibrous) and internal (serous) layers.
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Pericarditis –
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(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.
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Phlebitis –
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(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.
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Vasculitis –
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(I) of a vessel; common causes include allergic, immune-mediated.
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Cardiac myocytes are
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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 |
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Responses of heart to ↑ workload
3 |
-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) |
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-high alt. dz
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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 |
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Heart Failure:
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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 |
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Heart failure occurs because: 2
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1) there is ↓ ability of h to contract and move blood
2) there is an inability to fill the cardiac chambers w/ blood |
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↓ ability of h to contract and move blood
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-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 |
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P overload
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-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) |
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volume overload
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-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 |
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Inability to fill the cardiac chambers w/ blood
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-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 |
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failure of one side of h
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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 |
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Physiologic responses to a failing h
by the h |
-by ↑ vol moved (dilatation) short term
-↑ HR short term -ht long term |
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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 |
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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 ↑ |
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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
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Left Sided HF (The major effect is
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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 |
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Right Sided HF (the major effect is
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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 |
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Remember that, w/ time, failure of one side of heart
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inevitably affects the other side
-can’t dx HF by looking at h, need to see the other signs in body |
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Cardiac anomalies (many of these, especially in dogs, are
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heritable)
-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 |
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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
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flow of blood from L to R).
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Patent ductus arteriosis (DA)
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-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 |
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Atrial septal defect
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- 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 |
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Ventricular septal defect
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-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 |
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Defects as a result of failure of dt of valves or valvular openings
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*stenosis is more common form of defect usually affecting outflow valves
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Pulmonary artery stenosis
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-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 |
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Aortic (sub-aortic) stenosis
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- 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 |
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Valvular dysgenesis
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-dysplasia of AV valves (failure of valve leaflets); usually leaky]
-not common |
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Hematocysts
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-in calves, s/tms see red cyst (hematocyst) on valve
-no fxnal significance b/c valves nly not vascularized |
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PRAA (vascular ring anomalie)
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-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 |
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Pericardium
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-db walled sac
-nly contains sm amt of fluid to prevent friction -most probs from things accumulating in this space |
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Hydropericardium
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-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 |
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Hemopericardium
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-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 |
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Cardiac tamponade
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-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 |
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Pericarditis
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-quite common
-usually not a solitary lesion, expect to see other lesions w/ this -usually result of generalized bacterial infxn (septicemia usually) Fibrinous -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 Suppurative -hardware dz (traumatic reticular pericarditis) -probably never recover from lesions -see constriction of R h Constrictive -intereferes w/ filling of h |
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Endocardium (end/m)
Mineralization |
-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) |
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Endocarditis (Inflammatory)
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-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 |
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Valvular Endocarditis
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-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 |
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Mural Endocarditis
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-when seen on free wall
-in Blackleg, see involvement of myocardium, end/m, and epicardium |
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Myocarditis
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-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 |
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Histophilus somni myocarditis in cattle
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-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) |
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Blackleg (Clostridium chauveoi) in cattle
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-often affects h
-often dark areas -necrosis -looks dry and cooked -often fibrin on pericardium and epicardium |
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Canine parvoviral myocarditis
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-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 |
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Myocardial necrosis
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-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 |
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Nutritional myopathy (White m dz)
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-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 |
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Mulberry h dz of swine
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-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) |
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Ischemic necrosis Myocardium
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-we don’t see this often, does occur occasionally
-seen more often in humans b/c of vascular dzs |
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Cardiomyopathy
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“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) |
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Hypertrophic cardiomyopathy
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-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 |
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Dilated cardiomyopathy
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-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 |
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Restrictive Cardiomyopathy
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-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 |
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Neoplasia Heart
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-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 |
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Vessels
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-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 |
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Thrombosis (In general,
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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 circ/n |
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Saddle Thrombus (posterior aortic thrombosis in cats)
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-probably related to turbulence in h caused by cardiomyopathy
-get thrombus fr atrial wall and throws emboli to wedge in terminal aorta |
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Vena Cava (VC) Thrombosis in Cattle (Vena Caval Syndrome)
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-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 |
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Thrombosis of Cranial Mesenteric Artery from Strongylus Vulgaris
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-damaged by larvae
-pieces of material break off and cause infarction in intestine fro blocking bvs in intestines |
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DIC (Death is coming)
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-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 |
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Aneurysm
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-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) |
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Arteriosclerosis
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-not common in ans
-hardening of a. -thickening of a. wall w/ loss of elasticity and narrowing of lumen |
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Atherosclerosis
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-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 |
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Medial mineralization
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-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) |
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Vasculitis (arteritis, phlebitis, lymphangitis)
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-(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 |
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Parasitic arteritis
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-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 |
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Malignant Cattarhal Fever
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-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 |
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Feline Infectious Peritonitis (FIP)
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-(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 veins) 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. |
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Omphalophlebitis (navel ill)
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-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 |
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Lymphangitis caused by Mycobacterium paratuberculosis
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-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 |
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Hemangiosarcoma
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-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 |
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Hemangioma
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-benign tumor of bvs
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Purulent Rhinitis of Rabbits
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Pasturella multocida
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Inclusion Body rhinitis of Piglets
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Cytomeglo Virus
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Atrophic rhinitis of pigs
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Bordetella Bronchisepticus
and Paterurella Multocida |
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Strangles in Horses
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Strep equi equi
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Mycotic Rhinits Dogs
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Aspergillus
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Necrotic Laryngitis in Calves
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Calf Diphtheria
Fusobacterium necrphorum |
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Focal Necrotizing Laryngitis Cattle
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Histophilus somni
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Infectious Bovine rhinotracheitis (IBR) in Cattle
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Bovine Herpes Virus I
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Rhinotracheitis in cats
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Feline Herpes Virus
Feline Calici Virus `` also oral, ocular |
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Canine Infectious Tracheobronchitis
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Bordetella bronchiseptica
Canine parainfluenzavirus 2 Canine adenovirus 2 et al |
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Suppurative Bronchopneumonia Cattle
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Pasteurella multocida
Arcanobacterium pyogenes `` chronic suppurative Mycoplasma bovis `` dry caseous Rumen Aspiration `` gangrenous necrosis |
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Suppurative Bronchopneumonia Pigs
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Pasteruella multocida
Mycoplasma `` occasionally |
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Suppurative Bronchopneumonia Horse
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Sreptococcus spp.
Rhodococcus spp |
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Suppurative Bronchopneumonia Cats
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Rare
Pasteurella multocida |
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Suppurative Bronchopneumonia Dogs
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rare
Bordetella bronchispetica |
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Fibrinous bronchopneumonia Cattle
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Mannhemia haemolytica
Histophilus somni `` fibrinous or suppurative Mycoplasma mycoides `` other parts of world |
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Fibrinous bronchopneumonia Pigs
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Unusual Pattern
`` dorsal, caudo-dorsal `` occasionally cranio-ventral Actinoacillus pleuropneumoniae Actinobacillus suis |
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Interstitial Pneumonia General Agents
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Viruses
Migratory parasites Inhaled / Circulating Toxins Few Bacteremic States |
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Interstitial Pneumonia
Acute Bovine Pulmonary Emphysema and Edema |
Fall > move to lush pasture > L-tryptophan > Clara Cells in Lung > 3-Methyl-Indole
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Interstitial Pneumonia
Hypersensitivity Pneumonia Cattle |
Pig Ascarids
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Interstitial Pneumonia
Procine Respiratory and Reproducitve Syndrome PRRS |
PRRS Virus
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Interstitial Pneumonia
Many Species - Single Agent |
Canine Distemper Virus
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Broncho-Interstitial Pneumonia Cattle
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Bovine Respiratory Syncytial Virus (BRSV)
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Broncho-Interstitial Pneumonia Cats
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Clamydia
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Patterns of degeneration and necrosis (3)
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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) |
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Normal Liver function and Altered liver fx (4)
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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* |
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Differentials for enlarged yellow-brown livers: (3)
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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 |
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Xenobiotic metabolism
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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: |
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Hepatogenous or secondary photosensitization
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Example of impaired hepatic detoxification:
* chlorophyll int. bacteriaphylloerythrin (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 |
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Note: photosensitization can occur by other means: (2)
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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. |
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Protein synthesis: Liver
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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 |
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Liver Immune function: involved in systemic, local and mucosal immunity.
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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 |
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Hepatic encephalopathy
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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 |
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Bleeding tendencies: Liver
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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 |
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Hypoalbuminemia:
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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 |
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Vascular and hemodynamic changes: Liver
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chronic hepatic injury fibrosis portal hypertension ascites (EDEMA)
most commonly in dogs and cats, occasionally in sheep rarely in horses and cattle |
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Liver Dz cutaneous manifestations:
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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 |
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Entry of injurious agents to the liver can occur in 3 ways:
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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 |
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Inflammatory response to injurious agents dictated by route of entry
Hematogenous |
hepatitis
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Inflammatory response to injurious agents dictated by route of entry
Biliary |
cholangitis
Cholecystitis: inflammation of the gallbladder |
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Acute hepatitis:
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neutrophils, necrosis typically random with infectious agents
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Chronic hepatitis: characterized by
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fibrosis and mononuclear cells; persistent antigenic stimulation
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Cholangiohepatitis: both
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Hepatocytes and bile duct affected
Parasites and bacteria don’t respect the boundries of hepatocytes |
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Response of the liver to injury: Two responces
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1) Regeneration
Tremendous capacity for regeneration Requires the framework(scaffold) to still be present 2) fibrosis* |
