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Systemic Pathology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

2 Types of Bone Formation

A

Endochondral
• bone formation on a cartilage template
• Ex: growth plate or fracture repair

Intramembranous
• formation from a loose fibrous framework

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2
Q

Requirements for complete repair of bone

A
  • Limited motion
  • Adequate vascularity
  • Sterility
  • Apposition
  • Adequate host nutritional status
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3
Q

Secondary Lesions in Bone

A
  • “reactive” new bone (infection, neoplasia)
  • microfractures, compression fractures (physes)
  • hemorrhages (physes)
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4
Q

3 Techniques for Examination of Bone

A

Imaging
• radiography & MRI

Biopsy
• avoid reactive new bone
• sample multiple sites
• Best practice: submit radiograph with biopsy
• diagram lesion to show biopsy site(s)

• Amputation: consider submission of entire limb
• Very thin sample
• demineralization is required to section bone
• prolongs turn-around time

Necropsy

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5
Q

Basics of Secondary Bone Healing

A

o Transforms unstable fracture into rigid bone
o no rigid fixation -> motion stimulates callus (granulation tissue) -> stabilizes & provides extraosseus blood supply
o inflammation -> repair -> remodeling

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6
Q

Inflammatory Phase of 2nd Bone Healing

A

Tissue damage & hemorrhage
• clot formation 

• disruption of blood supply 

• ischemic necrosis of bone

Inflammation 

• Increase vascular permeability 

• emigration of phagocytes 

• new blood supply (extraosseous) 


Granulation tissue
• Fibroblasts
• Neovascularization

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7
Q

Repair Phase of 2nd Bone Healing

A

Pluripotent mesenchymal cells unite fracture fragments
• Osteoblasts, chondroblasts, fibroblasts
• Increased O2 due to blood supply

Cells & matrix form callus
• Periosteal & endosteal
• Excessive motion = problem -> decrease O2 & increase callus size

Increased osteogenesis
• Cartilage & necrotic bone replace w/ new bone = endochondral ossification

Hard callus
• Strong enough for support but not max strength

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8
Q

Remodeling Phase of 2nd Bone Healing

A

Osteoclastic resorption
• Replaces woven bone w/ cortical bone

Re-establish normal blood supply
• Resorption of endosteal callus
• Resorption of periosteal callus & loss of extraosseus blood supply

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9
Q

Primary Bone Healing; requirements, 2 subtypes

A

o no callus formation

Requirements
• Adequate blood supply

• Rigid immobilization
(most important)
• Excellent reduction and anatomic alignment

Subtypes
• Contact
• Gap

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10
Q

Osteomyelitis; what is it? clinical signs?

A

o Inflammation of the bone
o Usually caused by infection

Clinical Symptoms
•	Lameness
•	Paresis
•	Draining tracts
•	Fever
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11
Q

Osteomyelitis; tissue response, sequestrum

A

Tissue Response
• Necrosis of bone (osteolysis) & inflammatory exudate
• Removal of dead bone (resoprtion)
• Production of new bone (regeneration)

Sequestrum
•	Necrotic bone = no blood supply
•	Surrounded by exudate & involucrum
•	Resorption can’t occur
•	May drain via tracts and dissolve (if small)
•	Surgical removal usually required
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12
Q

Osteomyelitis Sequestra in horses

A
  • Non-healing draining lesion
  • May drain distant to primary site
  • Usually no lameness

Treat
• Surgical excision
• Antibiotics usually don’t work due to decreased blood supply

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13
Q

Causes of Osteomyelitis

A
  • Trauma
  • Direct extension from infected site

Hematogenous
• Often multifocal
• Bacteremia

Specific Organisms
• Aerobic or anaerobic bacteria
• Fungi

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14
Q

Vertebral Osteomyelitis

A

o Causes posterior paresis in pigs

Paresis due to:
• Pathologic fracture
• Myelomalacia
• myelitis

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15
Q

Nutritional Bone Dz; Common lesions & nutritional components

A

Common Lesions
• Osteopenia (bone loss)
• Bone deformities
• Pathologic fractures

Common Nutritional Components
•	Common in exotics
•	Fad diets
•	Economic stress
•	Mixing errors
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16
Q

Basics of Metabolic Bone Dz

A

o Failure of bone production, mineralization, and/or maintenance
o Osteodystrophy = defective bone formation
o Occurs in young during formation or adults during remodeling
o Forms of metabolic bone Dz overlap
o Nutritional deficiencies are often cause but ratio more important than overall level

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17
Q

Forms of Metabolic Bone Dz

A

Osteomalacia
• decreased mineralization of osteoid in adults

Osteoporosis
• decreased amount of normal bone

Rickets
• Decresed mineralization of osteoid & cartilage during growth

Fibrous osteodystrophy
• Osteoporosis or osteomalacia + intertrabecular fibrosis
• Due to increased PTH

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18
Q

Osteoporosis; basics, causes, examples of causes

A
  • pathologic reduction in bone mass 

(adults)
  • cortical bone is reduced in thickness & increased in porosity 

  • potentially reversible 

  • localized or generalized 


causes:
• excessive rate of bone removal
• subnormal production of new bone

Examples
• Disuse
• Starvation
• Ca deficiency

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19
Q

Osteomalacia; pathogenesis, lesions, compensation, causes, clinical signs

A

• defective mineralization of osteoid (adults)

pathogenesis:
• part of the normal remodeling process, aged, well-mineralized bone is removed ->
• replaced by osteoid that is inadequately mineralized. 


lesions
• unmineralized osteoid matrix + active resorption

Compensation:
• excessive deposition of osteoid matrix at places where the mechanical forces are strongest.

Causes
• Vit D deficiency
• Phosphorus deficiency

Clinical Signs
• Soft bones
• Pathologic fractures
• Deformities

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20
Q

Rickets; causes, clinical signs

A
  • Juvenile form of osteomalacia
  • Inadequate mineralization of osteoid & cartilage

Causes
• Vit D deficiency
• Phosphorus deficiency

Clinical Signs
• Lameness
• Enlarged metaphyses
• Pathologic fractures

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21
Q

Rickets pathogenesis

A
  • Failure of mineralization of cartilage 
->
  • Failure of degeneration of chondrocyte columns 
->
  • Formation of osteoid 
->
  • Overgrowth of fibrous tissue in the metaphysis ->
  • Deformities in the shape & structure of bone ->
  • enlargement of joints of limbs ->
  • microfractures, microhemorrhage, repair, etc
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22
Q

Fibrous Osteodystrophy; pathogenesis & clinical signs

A

Pathogenesis
• Hyperparathyroidism (increased PTH) ->
• Increase osteocalstic resorption of bone ->
• Osteoporosis or osteomalacia ->
• Excessive fibrous CT btwn remaining trabeculae

Clinical Signs
• Lameness
• Pathologic fractures
• Rubber jaw, enlarged head

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23
Q

Two Causes/paths of Secondary Hyperparathyroidism

A 
Dietary imbalance in Ca/P
•	Hyperphosphatemia ->
•	Hypocalcemia –>
•	Increased PTH ->
•	Fibrous osteodystrophy
Chronic Renal Dz
•	Decreased ability to excrete phosphate ->
•	Hyperphosphatemia ->
•	Decreased ability to resorb Ca ->
•	Functional hypocalcemia ->
•	Decreased ability to hydroxylate Vit D ->
•	Decreased ability to catabolize PTH ->
•	Fibrous osteodystrophy
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24
Q

Primary Vs Psuedo Hyperparathyroidism

A

Primary
• Uncommon
• Caused by functional PTH tumors
• Clinical signs due to hypercalcemia

Signs
o PU/PD, vomit, weakness, metastatic calcification
o Fractures +/- facial hyperostosis

Pseudohyperparathyroidism
• common
• paraneoplastic syndrome

• hypercalcemia induced by “pth-like” factor
• mild bone atrophy
• clinical signs are due to hypercalcemia

Tumors
o	lymphoma (dogs), 
o	adenocarcinoma of anal sacs (dogs)
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25
Q

Chondrodysplasia; basics & example

A
  • Defective cartilage formation
  • inherited 

  • unequal 
growth across physis
  • endochondral ossification 

  • irregular, haphazard columns of chondrocytes 

  • EX: snorter calves (short & smushed face)
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26
Q

Angular Limb Deformities; basics & common types in horses, llamas, dogs

A
  • Medial or lateral deviation of distal limb
  • Unequal growth across physis
  • Treat w/ osteoectomy

Foal:
• carpus valgus - incomplete ossification of carpal and tarsal bones

Llamas:
• Deviation typically centered on distal radius & ulna

Dogs:
• radius curvus - premature closure of the physis at the distal ulna

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27
Q

6 Bone Tumors

A

Osteosarcoma
• Common & important

Other primary neoplasias
• Fibrosarcoma
• hemangiosarcoma

Metasttic tumors

Chondrosarcoma
• 2nd most common

benign tumors of bone
• uncommon

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28
Q

Osteosarcoma Basics

A
  • mesenchymal tumor
  • produces osteoid and/or bone

  • > 80% of primary bone tumors in dogs & cats
  • common in large heavy dogs
  • Dogs (7.5 yr), Cats: (10.5 yr)
  • Metaphysis of long bone (usually forelimb in dogs)
  • Presents w/ lameness +/- swelling
  • Radiographs to diagnose
  • Dogs > cats > horses/cows
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29
Q

Osteosarcoma Behavior & Survival

A

Behavior
• Aggressive local invasion (osteolytic)
• destroys cortical bone
• rarely crosses joints
• undermines the periosteum and stimulates reactive new bone
• Micrometastasis
• Early pulmonary metastasis

Survival
• w/ surgery & chemo > w/ surgery > w/o surgery

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30
Q

Osteosarcoma in the Axial Skeleton

A
  • Uncommon
  • Most common site is maxilla
  • May have longer survival rate than appendicular
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31
Q

Secondary Bone Tumors; symptoms & 3 mechanisms

A

Symptoms
• pain - pathologic fracture
• +/- hypercalcemia
• osteolysis +/- new bone formation

3 mechanisms
• Bone marrow - plasma cell myeloma vertebral lesions
• Local invasion - Oral SCCa -> mandible Nasal adenoCA -> skull
• Metastasis - K9 prostatic and transitional cell Ca

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32
Q

Chondrosarcoma; basics & behavior

A
  • Malignant mesenchymal tumor that produces cartilage
  • Dogs & sheep

Behavior
• flat bones = ribs, nasal cavity, skull
• most arise in medullary cavity

• may destroy existing bone (osteolysis)

• develop slower, metastasizes later, can get very large w/o signs, better prognosis

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33
Q

Intervertebral Disks

A 
Nucleus Pulposus
•	Center of disc
•	gelatinous, avascular
•	85% water 
•	shock absorber 
Annulus Fibrosus
•	thick, fibrous membrane
•	thickest ventrally
•	outer fibers blend with dorsal & ventral spinal ligaments 
•	provide strength
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34
Q

Intercapital Ligaments

A

o collagenous cord head of rib -> dorsal aspect of disc -> head of oppposite rib.
o stabilize ribs
o adds strength to annulus fibrosus
o No intercapital ligament for first pair or last two pairs of ribs.
o ligament for 11th pair of ribs is smaller

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35
Q

Pathogenesis of IVDD

A
  • loss of H20 and proteoglycans in nucleus pulposus ->
  • reduced cellularity
->
  • increased collagen = decreased compressibility
->
  • loss of distinction between annulus fibrosus & nucleus pulposus ->
  • central portion of nucleus -> fibrocartilage ->
  • chondrometaplasia +/- mineralization ->
  • weakened annulus ->
  • dorsal herniation of altered nucleus pulposus ->
  • degeneration & rupture of annulus fibrosus ->
  • extrusion of disk material into spinal canal ->
  • compression of spinal cord
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36
Q

Chondrodystrophic Breeds Vs Non in IVDD

A 
Chondrodystrophic 
•	EX: Dachshund
•	Accelerated process
•	Chondroid metaplasia w/in 1st year of life
•	Calcification of disc is common

Non- Chondrodystrophic
• Degeneration later in life
• Mineralization is uncommon
• Only partial rupuyre of annulus w/ dorsal bulge of disc

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37
Q

Common Sites Herniated Disks

A
  • T11 – L3 (mostly)
  • Cervical
  • Where there is not intercapital ligaments
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38
Q

Classification of Herniated Disks

A

Type I
• Most common
• Complete prolapse of disc +/- explosion (extrusion)
• Unilateral signs

Type II
• Partial rupture/buldging (protrusion)
• More usual in non-chondrodystrophic breeds

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39
Q

IVDD; Symptoms, Diagnosis, Treatment

A

Symptoms
• Ischemic myelopathy = neuro signs
• Pain (most common)

Diagnosis
• Signalment, history, neuro exam
• Imaging: rads, myelogram, MRI


Treatment
• Corticosteroids + confinement
• Surgery: dorsal laminectomy or hemilaminectomy

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40
Q

Cervical vertebral malformation-malarticulation; Basics & Causes

A

o Cervical spinal atrophy due to stenosis of vertebral column
o Wobblers
o Static or dynamic (happens w/ movement)

Causes
•	Congenital
•	Developmental
•	Osteoarthritis
•	Nutritional
•	Combo
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41
Q

Wobblers in Horses; clinical signs & Lesions

A

• Myelomalacia = focal compression of spinal cord

Clinical signs 
•	ataxia “wobbles” 
•	general proprioceptive deficits

•	more apparent in the hind limb 
•	before 3YO
•	thoroughbreds

Lesions
• Stenosis
• Vertebral column subluxation
• Secondary osteoarthritis

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42
Q

Wobblers in Dogs; True malformation Vs Secondary Change

A
  • Cervical spondylomyelopathy
  • Static or dynamic

True malformation
• Stenotic lesion
• Rounding of Cranioventral vertebrae
• EX: young great danes

Secondary Change
•	Disk associated
•	Middle age/old Dobermans
•	Thickening of dorsal annulus fibrosus ->
•	Ventral compression of cord
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43
Q

Spondylosis; basics, signs in dogs Vs cows & sheep

A

o Proliferative spurs of bones (osteophytes)
o Develop at ventral & lateral aspects of vertebral bodies
o Bridge to adjacent vertebrae

Dogs
• Common in old dogs
• Often asymptomatic
• May have stiffness, decreased motion, pain
• If severe AND extending dorsolaterally -> impinge nerve roots

Cows & Sheep
•	Bulls & rams
•	Breeding males
•	Slowly progressive
•	Usually subclinical
•	Clinical signs following bridging fracture: stiff, reluctance to mount, CNS signs
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44
Q

Vertebral Osteomyelitis; basics, symptoms

A

o Hematogenous
o Bacterial caused
o Localized in epiphysis

Symptoms
• Paresis/paralysis
• Spinal cord compression
• Myelitis

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45
Q

Diskospondylitis

A

o Infection of intervertebral disc w/ osteomyelitis of contiguous vertebrae
o Hematogenous
o Bacterial caused

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46
Q

Articular Cartilage Response to Injury; superficial, deep, progressive

A

o Limited regeneration
o Damage can’t be seen on rads but healing may be

Superficial
• No healing
• No worsening

Deep
• May heal w/ fibrovascular tissue -> fibrocartilage

Progressive Damage
• Loss of proteoglycans + tearing of collagen fibers ->
• Fibrillation (dull, rough, yellow brown cartilage) ->
• Exposure of subchondral bone ->
• Eburnation (dense, polished, ivory like)

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47
Q

Repair Cartilage in Place of Articular Cartilage

A 
o	fibrous (fibrocartilage) 
o	hypercellular 
o	Type I collagen predominates 

o	diminished glycosaminoglycans 
o	inferior substitute
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48
Q

Synovial Membrane Response to Injury; acute, chronic, what is pannus

A

Acute
o hypertrophy & hyperplasia of synovial cells -> proliferative synovitis
o may have villous hypertrophy

Chronic
•	Granulation tissue arises at synovial membrane -> articular surface = pannus
•	May dmage underlying cartilage
•	May progress to ankylosis
•	Produces catabolic factors

Pannus:
• cloth like
• invasive granulation tissue
• releases collagenolytic enzymes

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49
Q

Periarticular (perichondral) Bone Response to Injury

A

o Cartilagenous nodules ->
o Converted to bone via endochondral ossification =
o Periarticular osteophytes

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50
Q

Synovial Fluid Response to Injury

A 
o	Increased quantity of fluid
o	Inflammatory cells
o	Fibrin & immunoglobulin 
o	Synovial cells
o	Change in viscosity
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51
Q

Osteoarthritis; basics & pathogenesis

A

o Progressive deterioration & loss of articular cartilage
o Eventually leads to eburnation & osteophytes

Pathogenesis
• Decreased matrix macromolecules ->
• Increased metalloenzymes ->
• Degredation of proteoglycans & collagen ->
• Changes in mechanical properties of cartilage ->
• More damge -> more destruction (cycle)

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52
Q

Osteoarthritis; Treatment & Causes

A 
Treatment
•	Weight control
•	Anti-inflammatory & pain management
•	Exercise
•	Chondroprotective agent
Causes
•	Trauma to articular cartilage
•	Abnormalities in conformation
•	Joint instability
•	Joint incongruence
•	Lubrication failure
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53
Q

Osteochondrosis; basics & pathogenesis

A

o Dyschondroplasia
o focal or multifocal areas of failure of endochondral ossification in epiphyseal
(and/or physeal) growth cartilage
o young, rapidly growing animals
o multiple joints usually affected
o particular joints characteristic for particular species

Pathogenesis
• hypertrophic zone of cartilage cells focally retained & calcification of matrix FAILS
->
• Capillaries do not invade abnormal matrix ->
• no endochondral ossification ->
• focus of retained, thickened cartilage ->
• Site of weakness

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54
Q

Osteochondrosis; lesions, symptoms

A

Lesions
Thickening of cartilage in epiphysis
• limits nutrient diffusion = necrosis of deeper layer

Osteochondritis dissecans =
• cartilage sparation -> flap stimulates inflammation -> inflammation inhibits fibrocartilage

Subchondral Cysts
• Cartilage damage weakens underlying bone -> cyst formation
• mostly in HORSES
• Radiograph: focal area of radiolucency in the epiphysis

Symptoms
• Lameness / pain
• Can progress to chronic osteoarthritis

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55
Q

Neonatal Septicemia & Polyarthritis; baics, route, symptoms

A
  • Serofibrinous joint fluid
  • High number neutrophils on cytology
  • Can progress to destruction of cartilage
  • Usually irreversible damage
  • Hematogenous Route

Symptoms
• Swollen, hot, painful joints
• Febrile

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56
Q

Non-Infectious Arthritis (Erosive/Deforming)

A
  • Ex: Rheumatoid
  • Dogs most common
  • Immune mediated destruction & ankylosis of joints
  • Soft tissue swelling -> erosion -> destruction of cartilage & bone

Diagnosing Rheumatoid
• Rheumatoid factor is auto-Ab against FC portion of IgG

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57
Q

Systemic Lupus Erythematosus; basics, symptoms, diagnosis

A
  • Non-erosive non-deforming non-infectious arthritis
  • Multisystemic auto-immuned Dz
  • Circulating immune complexes and/or Abs against blood cells

Symptoms
o No single clinical sign
o IMHA, thrombocytopenia, leukopenia, glomerulonephritis
o polymyositis, polyarthritis, polyarthralgia, dermatitis
o shifting leg lameness, recurrent fever
o minimal villous hypertrophy, no destructive pannus
o NO irreversible damage to cartilage


Diagnosis
o ANA – Ab to DNA or nucleoproteins
o Not very sensitive

58
Q

Immune Complex Deposition in joints; basics, 2 causes, symptoms

A

• Non-erosive non-deforming non-infectious arthritis

Drug Hypersensitivity
o Deposition of drug-Ab complexes (antibiotics)

Secondary to infectious dz
o Antigenemia or bacteremia
o Circulating immune complexes
o Reactive polyarthritis

Symptoms
•	fever

•	glomerulonephritis 
•	anemia
•	thrombocytopenia 
•	lymphadenopathy 
•	polyarthritis (non-erosive)
59
Q

Reactive Polyarthritis, symptoms, rads, arthrocentesis, treatment

A

• Reaction to drug or infection

Symptoms
• Polyarticular lameness
• Fever
• No antibiotic response

Radiographs
• Lack of bony change

Arthrocentesis
• Sterile
• Increased neutrophils

Treatment
• Remove drug
• Resolve infection

60
Q

How is the endocrine system regulated

A

o Negative feedback is primary control mechanism
o Hierarchical levels of regulation
o Cross communication btwn endocrine organs

61
Q

Primary Vs Secondary Endocrine Dz

A

Primary Disease
• originates w/in the endocrine gland

Secondary Disease:
• originates outside of the gland
• inflammation in one organ can cause damage to a neighboring endocrine gland

62
Q

Disease due to excess hormone activity (4 categories)

A

Primary:
• usually due to functional neoplasia of endocrine tissue (with unregulated hypersecretion of hormone)

Secondary:
• Excess stimulation of the gland
• Inadequate inhibition (loss of negative feedback) on the gland
• Inadequate degradation/excretion of the hormone

Iatrogenic:
• exogenous source of a hormone (steroid therapy)

Non-endocrine neoplasia (paraneoplastic syndrome):
• some neoplasias secrete hormone homologs with hormonal activity

63
Q

Disease due to inadequate hormone activity (3 categories)

A

Primary:
• usually auto-immune damage to the gland

Secondary:
• Inadequate stimulation
• Inadequate nutrition necessary for hormonal production
• decreased target cell receptors/response
• increased degradation/excretion of the hormone

Iatrogenic:
• surgical or medical destruction or inhibition of the gland

64
Q

Atrophy Vs Hypoplasia

A

Atrophy
o After development
o Caused by chronic inflammatory or chemical destruction (irreversible) and lack of hormonal stimulation (reversible)

Hypoplasia
o Before organ maturity
o Caused by inadequate organ development (irreversible)

65
Q

Neoplasia of Endocrine; basics, 4 types

A
  • irreversible unregulated proliferation of abnormal cells
  • may or may not be functional

adenoma:
o benign

microadenoma
o NOT grossly visible

macroadenoma
o grossly visible mass

adenocarcinoma
o malignant

66
Q

Diseases of the Adenohypophysis of the pituitary

A

Hypopituitarism:
• deficient pituitary hormonal activity

Hyperpituitarism:
• excess pituitary hormonal activity

67
Q

Hypopituitarism; causes, pathogenesis, clinical signs

A

Causes
o Non-functional neoplasms can leading to deficient production of hormones (adenoma most common)
o Inflammation/infection (Pituitary abscess ruminants)
o Pituitary cysts (cause dwarfism)

Pathogenesis
o Mass effect or destruction of tissue
o Loss of functional pituitary & compression of adjacent structures

Clinical Signs
o Peripheral endocrine gland atrophy due to lack of hormonal stimulation
o Reduced antidiuretic hormone (ADH) production and secretion
o Blindness (compression upon the optic chiasm)
o +/- CNS signs

68
Q

Hyperpituitarism; usual cause, example diseases

A
  • Often caused by neoplasia
  • Pituitary pars intermedia dysfunction (Equine)
  • Pituitary-origin canine Cushing’s syndrome
69
Q

Pituitary pars intermedia dysfunction; species & pathogenesis

A

o Affects 81% of horses > 15YO

Pathogenesis
• Gradually decreased hypothalamic dopamine ->
• reduced inhibition of some hypothalamic hormone production ->
• hyperstimulation ->
• functional pituitary adenoma of the pars intermedia (slow growing macroadenoma)

70
Q

Pituitary pars intermedia dysfunction Clinical Signs

A

• Due to compression of hypothalamus

4H’s
• hairy, hyperhidrosis, hungry, heavy

Hirsutism
• Hypertrichosis (hairy) due to lack of seasonal shedding cycles

Hyperhidrosis
• excessive sweating due to hirsutism and loss of body temperature control

Polyuria/polydipsia
• due to reduced antidiuretic hormone secretion

Somnolence
• Sleepiness due to loss of hypothalamic control of sleep patterns

Polyphagia
• overeating due to damage to the hypothalamic appetite center

Laminitis
• Idiopathic

71
Q

Pituitary-origin canine Cushing’s syndrome Primary & Secondary Lesions

A

Primary Lesion
• ACTH-secreting pars distalis adenoma (most common)
• Microadenoma more common than macro

Secondary Lesion
• Bilateral adrenocortical hyperplasia

72
Q

Diseases of Neurohypophysis of the pituitary

A

diabetes insipidus

  • Neurogenic
  • Nephrogenic
73
Q

Diabetes Insipidus Neurogenic; Pathogenesis & Clinical Signs

A

Pathogenesis
• Neoplasia, Inflammation/Infection, or Pituitary Cysts ->
• destruction of neurohypophysis or hypothalamus ->
• loss of ADH synthesis OR loss of ADH transport/release

Clinical Signs
• Polydipsia & Polyuria

74
Q

Hyperadrenocorticism Clinical Signs

A

• All forms have same clinical signs but different underlying causes

Clinical Signs
•	Prolonged elevated cortisol -> excessive/chronic stress response
•	Polyphagia 
•	Hepatomegaly due to excessive glycogen storage
•	Skin changes
•	Muscle wasting & weakness and lethargy 
•	Pendulous abdomen
•	Immunosuppression 
•	Hypertension 
•	hypercoagulability 
•	Hyperlipemia / Hypercholesterolemia 
•	PU/PD
•	Hyperglycemia (variable)
75
Q

Pituitary-dependent hyperadrenocorticism; primary & secondary lesions, pathogenesis

A

• Most common form of canine hyperadrenocorticism

Primary lesion:
o Functional pituitary adenoma

Secondary endocrine lesion:
o Bilateral adrenocortical hypertrophy

Pathogenesis of secondary lesions:
o	Functional pituitary adenoma ->
o	unregulated hypersecretion of ACTH ->
o	bilateral hyperplasia of zona fasciculata ->
o	hypersecretion of cortisol
76
Q

Adrenal-based hyperadrenocorticism; primary & secondary lesions, pathogenesis

A

Primary lesion:
o Functional adrenal cortical neoplasm: usually adenoma, rarely carcinoma

Secondary lesion:
o Contralateral adrenocortical atrophy

Pathogenesis of secondary lesions:
o Functional adrenal cortical neoplasm ->
o unregulated hypersecretion of cortisol ->
o suppression of pituitary ACTH secretion ->
o contralateral adrenocortical atrophy

77
Q

Iatrogenic Hyperadrenocorticism; primary & secondary lesions, pathogenesis

A

• very common

Primary cause:
o Excessive use of exogenous corticosteroids

Secondary lesion:
o Bilateral adrenal cortical atrophy

Pathogenesis of secondary lesions:
o Prolonged excessive exogenous corticosteroid administration ->
o (-) feedback on the hypothalamic-pituitary-adrenal axis ->
o suppressing pituitary ACTH secretion ->
o affects both adrenals.

78
Q

Hyperadrenocorticism in ferrets (adrenal associated endocrinopathy); signalment, primary lesions, pathophysiology, clinical signs

A

Signalment:
o Females > males
o Adults, usually fixed

Primary Lesion:
o Unilateral adrenocortical adenoma/adenocarcinoma
o Bilateral hyperplasia

Pathophysiology:
o Increased production of adrenocortical estrogenic steroids ->
o hyperestrogenism

Clinical signs:
o bilaterally symmetric alopecia
o Vulvar enlargement (common)
o Pyometra/endometrial hyperplasia (common)
o Anemia/thrombocytopenia (common) due to bone marrow suppression
o Polyuria/polydipsia (uncommon)

79
Q

Typical Addison’s Disease; primary lesion & two precursors to pathophysiology

A

Primary Lesion
o Adrenal cortical atrophy/necrosis

Pathophysiology
o Idiopathic
o Iatrogenic

80
Q

Iatrogenic Pathophysiologies of Typical Addison’s

A

Adrenalectomy ->
• rapid loss of 50% of total functional adrenal cortex ->
• transient Addison’s disease ->
• contralateral gland develops compensatory hyperplasia.

Cytoxic drug overdose ->
• rapid & selective destruction of adrenal cortex ->
• bilateral loss of functional cortex. ->
• Irreversible if sufficient loss.

Receptor inhibition therapy (e.g. Trilostane) for Cushing’s

81
Q

Reduced Functional Mass of Zona Glomerulosa Vs Zona Fasciculata

A

Zona Glomerulosa
• Decreased K+ excretion = Hyperkalemia
• Decreased Na retention = hyponatremia

Zona Fasciculata
• Deficient cortisol
• Vomiting, diarrhea, anorexia, weight loss

82
Q

Clinical Signs of Typical Addison’s

A

Can be episodic & variable
o GI signs
o Muscle weakness, arrhythmias, bradycardia
o PU/PD
o Hypotension, renal insufficiency/failure
o hypoglycemia
o No response to exogenous ACTH

83
Q

Atypical Addison’s Disease; primary lesion, pathophysiology, clinical signs

A

Primary lesion:
o Atrophy of the adrenal zona fasciculata, ONLY

Pathophysiology
o Reduced functional mass of zona fasciculata ->
o deficient cortisol but NOT deficient aldosterone ->
o signs related to low cortisol.

Clincal Signs
o GI signs
o PU/PD
o Hypoglycemia

84
Q

Atypical Addison’s Disease;; 3 Pathogenesis

A

Iatrogenic:
• Long-term usage of corticosteroids ->
• inhibition of CRH & ACTH release ->
• reversible atrophy of the zona fasciculata.

Idiopathic:
• May progress to typical (full) Addison’s disease
• irreversible

Pituitary insufficiency
• congenital panhypopituitarism (rare)

85
Q

2 Types Hyperplasia of the adrenal cortex

A

Nodular cortical hyperplasia (unilateral or bilateral):
• Usually z. glomerulosa or z. fasciculata
• Very common in adult animals
• clinically insignificant.
• Looks normal grossly

Diffuse and bilateral cortical hyperplasia:
• Usually due to hypersecretion of ACTH by a functional pituitary neoplasm

86
Q

2 Neoplasia of Adrenal Cortex

A

Adrenal cortical adenoma
• Usually functional causing hyperadrenocorticism
• Can look like nodular cortical hyperplasia
• Should be encapsulated
• Will commonly be larger than nodular hyperplasia

Adrenal cortical carcinoma
• May be functional in dogs, but usually not
• Locally invasive
• Can invade caudal vena cava causing hemoabdomen
• May be bilateral
• Can metastasize

87
Q

Neoplasia of Adrenal Medulla, basics & clinical signs

A

• Pheochromocytoma
most common
• cattle and dogs (commonly malignant in dogs)
• can look like adrenal cortical neoplasms
• usually unilateral areas of necrosis
• often invasive & metastatic
• most are nonfunctional
• can have sporadic release of (nor)epinephrine:

Clinical Signs (of functional)
• paroxysmal (episodic) hypertension & tachycardia
• periodic panting, tachypnea, and collapse +/- GI signs
• ventricular hypertrophy

88
Q

Diabetes Mellitus clinical signs & pathophysiology

A 
Clinical Signs
•	Persistent hyperglycemia postprandial & fasting
•	PU/PD
•	Polyphagia w/ weight loss
•	Cystitis
•	Bilateral cateracts
Pathophysiology
•	Low insulin secretion or activity ->
•	Decreased cellular glucose uptake ->
•	Persistent hyperglycemia ->
•	Glucagon secretion ->
•	Paradoxical mobilization of energy sources ->
•	Hepatic lipidosis & weight loss
89
Q

What happens if Diabetes Mellitus is left untreated

A
  • Ketoacidosis & ketonuria ->
  • Osmotic polyuria ->
  • Shock & acidosis ->
  • Osmotic cellular dehydration ->
  • Diabetic coma
90
Q

Primary Diabetes Mellitus (Type I); basics, lesions, pathogenesis

A

o Defect in insulin system
o Insulin dependent
o Most common form in dogs

Primary Lesions
• Autoimmune isletitis
• Congenital deficiency

Pathogenesis
•	Damage to Beta cells ->
•	Deficient insulin levels
OR
•	Congenital deficiency of beta cells & islets ->
•	Deficient insulin levels
91
Q

Primary Diabetes Mellitus (Type II); basics, lesions, pathogenesis

A

o Non-insulin dependent
o Most common form in cats

Lesions
• Not always present
• Can have islet (beta cell) vacuolation & amyloidosis

Pathogenesis
• Chronic glucose/lipid toxicity (obesity) ->
• Insulin resistance ->
• Deficient insulin activity ->
• Pre-diabetes & increased insulin demand ->
• Mild dysregulation of blood glucose ->
• Beta cell exhaustion ->
• Deficient insulin secretion & resistance

92
Q

Secondary diabetes Mellitus; basics, two causes

A

• Defect in other system that affects insulin

Secondary loss of beta cells due to
o Infiltrative neoplasia into islets
o Chronic relapsing pancreatitis

Secondary inhibition of insulin activity due to
o Insulin receptor antagonism by hormones
o Hypercortisolism
o Acromegaly & growth hormone

93
Q

Excess Insulin; species, causes, clinical signs

A

• Ferrets > dogs&raquo_space;> cats

Cause
• Functional pancreatic beta cell neoplasm
• Ferrets: Beta cell adenoma (insulinoma)
• Dogs: beta cell carcinoma (malignant insulinoma)

Clinical Signs
• Episodic hypoglycemia due to sporadic insulin release
• Weakness & lethargy
• Collapse, seizures, obtunded

94
Q

Typical Addison’s Disease; deficiencies and results thereof

A 
Deficient cortisol
•	Leukocytosis
•	Neutrophelia
•	Eosinophilia
•	Hypocholesterolemia
•	Hyponatremia

Deficient ALD
• Hyponatremia
• Hyperkalemia

95
Q

Pituitary Pars Intermedia Dysfunction (PPID); basics, species, clinical signs

A

• Hypothalamus dysfunction of equine

Clinical Signs
•	3 Hs
•	hirsutism (hairy)
•	hyperhidrosis (sweaty)
•	polyphagia (hungry)
•	somnolence (sleepy)
96
Q

Thyroid Basic Structure & Function

A

Follicular cells
• produce T3 & T4

Parafollicular cells (C cells)
• produce calcitonin
• prevent hypercalcemia
• increase renal clearance of Ca & P

T3
• increases metabolic rate

TSH
• Stimulates follicular cell hyperplasia
• Thyroid hormone production requires iodine

97
Q

Hypothyroidism in Dogs; age, gross/histo lesions & clinical signs

A

• Middle aged

Grossly
• Small atrophied thyroid

Histo
• Lymphocytic thyroiditis – autoimmune (most common)
OR
• Idiopathic follicular atrophy

Clinical signs
•	Fat
•	Five
•	Flaky
•	Furless
•	Weight gain w/o polyphagia
•	Nonregenerative anemia
•	Lethargy & weakness
•   
   Hyperlipidemia/cholesterolemia
•	Neuromuscular symptoms
98
Q

Hypothyroidism in Grazers; age, lesions & causes

A

• Fetuses or neonates = congenital

Grossly
• Large thyroid = goiter
• Diffuse follicular hyperplasia

Causes
• Iodine deficiency
• Iodine toxicity inhibits hormone synthesis
• Goitrogenis plants inhibit hormone synthesis

99
Q

Hyperthryroidism; species, lesions, clinical signs

A

• Common in cats

Primary Lesions
• Nodular/multinodular hyperplasia of thyroid
• Large thyroid

Clinical Signs
• Weight loss w/ polyphagia
• Hyperactivity
• Tachycardia/arrrhytmias

100
Q

Neoplasias of the thyroid

A

Thyroid follicular adenoma
o Unilateral w/ contralateral atrophy
o Causes hyperthyroidism

Follicular carcinoma
o Usually not function
o Dogs > cats

101
Q

Function & cells of the parathyroid gland

A

Chief cells
• Produce PTH
• Prevent hypocalcemia

102
Q

Hypoparathyroidism; species, causes, clinical signs

A

• Dogs

Causes
•	Parathyroiditis
•	Neoplasia
•	Thyroidectomy
•	Atrophy due to high Ca diet & sudden removal of Ca

Clinical Signs
• Persistent hypocalcemia
• Muscle spasms and weakness

103
Q

Main Clinical Finding of Hyperparathyroidism

A
  • Fibrous osteodystrophy

* Osteoporosis or Osteomalacia PLUS Intertrabecular Fibrosis

104
Q

Four types of Hyperparathyroidism; causes & relation to Ca

A

Primary
• Associated w/ hypercalcemia
• Unregulated PTH -> hypercalcemia
• Caused by functional chief cell neoplasia

Psuedo
• Associated w/ hypercalcemia
• Caused by non chief cell neoplasia (paraneoplastic)

Renal Secondary
•	Associated w/ normal to hypocalcemia
•	Chronic renal failure ->
•	inability to activate vit D ->
•	chronic increase in PTH ->
•	Bilateral chief cell hyperplasia 
Nutritional Secondary
•	Associated w/ normal to hypocalcemia
•	Improper Ca/P ratio +/- vit D deficiency ->
•	Chronic increase in PTH ->
•	Bilateral chief cell hyperplasia
105
Q

Clinical signs of primary & pseudo Hyperparathyroidism

A
  • Mild/absent signs
  • Bradycardia
  • PU/PD
  • Urinary calculi
  • Metastatic mineralization
106
Q

Define: erythema, indurated, lichenification, uticaria, macule

A

Erythema
o Redness of the skin due to capillary congestion

Indurated
o Hardened

Lichenification
o Thickening of skin

Uticaria
o Transient hives

Macule
o circumscribed spot of normal skin thickness but with altered color

107
Q

Diagnosis of Dermatologic Conditions

A

Most important symptoms for diagnosis
• Pruritis
• Symmetry (endocrine)

Diagnostic Methods
•	Skin scrape
•	Culture
•	Cytology
•	Intradermal skin test
•	Serology for IgE
•	Biopsy & histo (*)
108
Q

Submitting a biopsy for derm issues

A
  • signalment, complete dermatologic history and physical exam findings
  • Fix specimens in 10% buffered formalin.
  • use dermatopathologist in difficult cases.
  • Send Photos!
109
Q

Microscopic Changes on histo that help diagnose derm issues

A
  • Pattern of cellular infiltrate
  • Predominant cell type
  • ID of a causative agent
110
Q

Perivascular Inflammation; where is it, causes

A

o In the superficial dermis

Causes
• Allergies
• ectoparasites

111
Q

Interface dermatitis; what is it, causes

A

o dermoepidermal junction obscured by cellular infiltrate and/or hydropic degeneration of basal epidermal cells

causes
• lupus erythematosus
• drug eruption

112
Q

Vasculitis (of skin); what is it, causes

A

o multifocal hemorrhage and/or ulceration

Causes
• Immune complex deposition
• Sepsis

113
Q

Folliculitis / Perifolliculitis; causes of primary vs secondary & furunculosis

A

o Often has pustules

Primary
• Dermatophytes (ring worm)
• Demodex canis mites

Secondary
•	Bacterial infection secondary to underlying condition
•	Allergy
•	Endocrinopathies
•	Trauma
•	Ectoparasites

Furunculosis
• hair follicle rupture which incites pyogranulomatous or granulomatous reaction

114
Q

Nodular or diffuse dermatitis; what is it, causes

A

o Often pyo/granulomatous

Causes
• Infectious organisms: bacteria, fungi
• Foreign body: necrotic fat, suture, etc

115
Q

Intraepidermal vesicles & pustules; what is it, causes

A

o Between layers of epidermis

Causes
o	pemphigus foliaceus 
o	viral vesicular diseases 
o	pemphigus vulgaris – DEEP intraepidermal 
o	impetigo
116
Q

Impetigo

A
  • puppy pyoderma
  • Superficial pustular dermatitis
  • Most commonly coagulase-positive Staphylococcus

  • Kittens – Pasteurella multocida
117
Q

Subepidermal Vesicular Dz; where is it, causes

A

o Deep to epidermis

o Ex: bullous pemphigoid

118
Q

Mechanisms of Alopecia

A

o Destruction of normal hair shaft
o Failure of cyclical hair growth (endocrine)
o Toxic or metabolic disturbances

119
Q

Acanthosis; basics, gross & microscopic lesions

A

o Epidermal Hyperplasia
o Common non specific response to chronic injury

Gross Lesion
• Lichenification – thick & deep fissured skin

Microscopic Lesions
• Increased ancanthocyte layer

120
Q

Secondary Seborrhea

A

o Scaling secondary to underlying dz
o Common
o May be accompanied by greasiness & foul odor
o Reaction to chronic process
o Hypothyroid, low humidity, ectoparasites, etc

121
Q

Primary Seborrhea; basics & two forms

A

o Increased scale formation
o Primary defect in epidermal turnover
o Often breed specific & idiopathic (spaniels, hounds)

Seborrhea sica
• Dry skin w/ scaling

Seborrhea oleosa
• Greasy skin w/ scaling

122
Q

Parakeratosis; basics, cause, histologic description

A

o dry, scaly skin
o zinc deficiency,

Histologic Diagnosis
• thickened stratum corneum; partially keratinized, still contain nuclei

123
Q

Hyperpigmentation (melanosis); two forms

A

o Increased activity of melanocytes

Localized
• Chronic irritation
• Inflammation

Generalized
• Systemic stimulus such as hormones

124
Q

Hypopigmentation; two forms

A

Congenital
• Albinism (tyrosine deficiency)

Aquired
• Localized
• Permanent loss of melanocytes

125
Q

Surface Vs Superficial Vs Deep Pyoderma

A

Surface pyoderma
• Skin fold dermatitis

Superficial pyoderma
•	Short duration
•	Does not cause lymphadenopathy
•	Good prognosis
•	Ex: puppy impetigo
Deep pyoderma
•	Serious deep skin infection
•	Invades dermis +/- subcutis
•	Often chronic
•	May cause scarring
•	Often regional lymphadenomegaly
•	Usually secondary to underlying dz
126
Q

Basics of skin fungal infections

A

o Often sporadic
o Associated w/ local debilitation or immunodeficiency
o Distinct geographic zones
o Usually not contagious

127
Q

Deep Skin Mycoses; two forms

A 
Cutaneous/subcutaneous
•	Traumatic implantation
•	nodular/diffuse dermatitis
•	granulomatous or pyogranulomatous
•	may require special stain
•	Ex: sporothricosis

Systemic infection spread to skin
• exist in soil or vegetation
• sporadic dz
• primary or opportunistic pathogens

128
Q

Superficial Fungal Infections of Skin

A
  • exception to many of the “rules“ 

  • caused by several fungi that invade and destroy keratin
  • tissue response may be mild 

  • often w/ secondary bacterial infection 

  • can see severe folliculitis & furunculosis
129
Q

Malassezia; asics, clinical signs, diagnosis

A
  • Commensal yeast isolated form ear & skin of healthy dogs
  • Unipolar budding yeast (peanut shape on stained slides).
  • Alterations in host defenses allows infection

Clinical Signs
• pruritus – often intense 

• odor – “rancid fat” 

• erythema - papules & macules 

• generalized or localized 

• scaling, crusting, ALOPECIA, greasy skin 

• secondary lesions = lichenification & hyperpigmentation 


Diagnosis
• Skin scrape or “scotch tape” impression
• Response to meds

130
Q

Visible Skin Parasites

A
  • Ticks, lice, flies, fleas
  • Mild lesions
  • Pruritis
  • Flea saliva is allergen
131
Q

4 Skin Mites

A

Cheyletiella
• Walking dandruff
• Mites walking on fur

Psoroptes
• Superficial

Sarcoptes
• Burrow in epidermis
• Very hard to find on scrape
• Very pruritic

Demodex canis
• Normal fauna in hair follicles of dogs
• Transmitted to pups at birth
• Can cause demodicosis

132
Q

Localized Vs Generalized Demodicosis

A 
Localized
•	Common in young dogs
•	small, circumscribed, erythematous, scaly, area of alopecia
•	non-pruritic OR pruritic 
•	on face or forelimbs 
•	resolves spontaneously

Generalized
• Severe disease
• Life-threatening secondary pyoderma
• Usually underlying cause
• Juvenile onset - Treat w/ Amitraz or Ivermectin
• Adult Onset - Poor prognosis in dogs >2yo

133
Q

Diagnosis of Demodicosis

A

o Deep skin scraping reveals MANY mites

o Always rule out in any pyoderma case

134
Q

Equine Cutaneous Habronemiasis (Summer Sores); basics & diagnosis

A
  • deposition of larvae of Habronema sp. or Draschia sp. into skin wounds or moist areas of the body (by flies)
  • rapidly growing, reddish brown granulation tissue
  • numerous yellow granules can be expressed
  • often pruritic
  • medial canthus of the eye & prepuce / penis

Diagnosis
o Biopsy reveals granulomatous & eosinophilc inflammation +/- parasite larvae

135
Q

Endocrine Dz of Skin; basics & clinical signs

A

o Most common in dogs
o Alopecia = primary change
o Too much or too little hormone

Clinical Signs
•	Bilaterally symmetric 
•	Non-inflammatory

•	Non-pruritic
•	Gradual onset 
•	Chronic 
•	Usually truncal

•	Hair is easily removed
•	Often a secondary seborrhea

•	Can have bilaterally symmetrical hyperpigmentation
136
Q

Urticaria

A
  • Hives
  • Type I hypersensitivity
  • Dermal edema due to histamine mediated increase in vascular permeability
  • Variably pruritic
137
Q

Atopy; basics, lesions, diagnosis

A
  • Common
  • Genetic
  • Pruritic
  • Inhaled Ags
  • Type I
  • 9mo-3yo
  • face rubbers & foot lickers
Lesions
•	Self trauma
•	Secondary pyoderma
•	Secondary seborrhea
•	Acanthosis

Diagnosis
• Intradermal skin test (gold standard)
• Serum IgE

138
Q

Allergy Testing; baiscs, two tests

A
  • Short shelf life
  • Use if owner wants to pursue immunotherapy

Skin
• Measures cell bound allergen specific IgE

Serum
• Measures circulating allergen specific IgE

139
Q

Flea Bite Hypersensitivity; basics & distribution

A
  • most common hypersensitivity skin disorder in dogs & cats
  • Type I and IV involved

  • pruritic, papular and crusting dermatitis
  • may be seasonal
Classic distribution 
•	Looks like dog is wearing pants
•	dorsal lumbosacral
•	caudomedial thighs
•	ventral abdomen
•	flanks and neck
140
Q

Food Allergy

A
  • Pruritis: non-seasonal, +/- responsive to glucocorticoids
  • 70% have no history of dietary change
  • good prognosis
IF you can identify and eliminate allergen

elimination diet
• ~10wks (3 wks not long enough)
• novel protein or hydrolysate
• then re-introduce diet and look for recurrence

141
Q

Contact Hypersensitivity

A
  • uncommon
  • variably pruritic
gross lesion = papules & macules
  • sparsely haired skin in areas of contact
  • Type IV hypersensitivity
  • Diagnose w/patch test
142
Q

Pemphigus; basics, pathogenesis, how to differentiate types

A
  • Group of uncommon autoimmune diseases
  • Fragile vesicles, bullae & pustules -> erosions and ulcers

Pathogenesis
• Auto Abs directed against desmosomes ->
• Disrupt keratin adhesion (acantholysis) ->
• Vesicles or bullae ->
• Inflammation ->
• Pustules

Differentiate Pemphigus Dz
• Severity
• Lesion distribution
• Site of acantholysis

Systemic Pathology (2 decks)

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