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Final- Muscle Flashcards

1
Q

You are called out to a farm to investigate a sad scene…..

Clinical signs

Around 30% of 2 month old lambs in a mob of 40

Lying on their chest, roll on to their side

Weak, stiff

Die within a few days

What can we do to figure out what the pathological process was that resulted in these signs??

A

You are going to do a euthanize and necropsy an acute disease. You don’t want to wait for a natural death because you can get secondary infections etc that will hide the primary pathological process.

You are going to examine muscle bellies.

What is abnormal? There are muscles that are paleish white, swollen, firm, and dry to the touch(not shiny).

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2
Q

What is an addition pathological process for Skeletal Muscle?

A

Biochemical

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3
Q

What pathological process is responsible for this apperance(same as the sheep case)?

A

Degeneration/necrosis- results in a pale color because more water is coming into the muscle

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4
Q

What makes muscles pale other than degeneration/necrosis?

A

Fig. 15-9 Pathologic changes resulting in pale skeletal muscle.

A, Pale streaks, necrosis and mineralization, degenerative myopathy, canine X-linked muscular dystrophy, diaphragm (left side), dog.
B, Localized pallor, necrosis, injection site of an irritant substance, semitendinosus muscle, cow. The irritant was injected just under the perimysium and caused necrosis and disruption of the myofibers. Some irritant seeped down between the fascicles to cause necrosis, but the fascicles of myofibers are still in place.
C, Overall pale muscle with pale streaks from collagen and fat infiltration, denervation atrophy, equine motor neuron disease, horse. Equine motor neuron disease muscle (right) compared with normal muscle (left). Yellow tint; FAT WHERE YOU HAVE LOST SKELETAL MUSCLE, GREASY AND YELLOW
D, Enlargement and pallor, steatosis, longissimus muscles, neonatal calf. The majority of the muscles have been replaced by fat.

calicification can also do this

Fibrious connective tissue

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5
Q

Gross morphological diagnosis =

A

BEST ONE: skeletal muscle degeneration and necrosis

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6
Q

What is abnormal about this image?

A

Sacroplasm/cytoplasm is vacuolated, condensed, loss of cross striations

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7
Q

Things myofibers do when they are hurt:

A

They die:

  • Vacuolation of sarcoplasm
  • Condensation of sarcoplasm (looks hyper-eosinophilic, and lose striations)
  • Nuclear pyknosis
  • Calcification(dystropic)

They regenerate:

  • Internalization of nuclei
  • Macrophages infiltrate
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8
Q

What types of causes incite this pattern of degeneration and necrosis?

A

Pathology report: polyphasic skeletal muscle degeneration and necrosis( myocytes are in different stages of injury and regeneration vs in others where the myocytes are all in the same stage- monophasic)

This means that there is an ONGOING PROBLEM!

Causes of polyphasic lesions:

Ongoing insults

Nutritional deficiency – vitamin E/Se

Ongoing toxicities

Genetic defects in myocyte

structural/metabolic elements

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9
Q

How does nutritional deficiency cause this mess?

A

Pathogenesis: vitamin E/Se deficiency is needed for enzymes like glutathione peroxidase/reductase causeslack of ability to scavenge free radicals. This causes oxidative damage (lipoperoxidation of cell membranes) –> myocyte injury

Free Radicals cause necrosis

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10
Q

What would the path report say about this and what was the cause?

A

Monensin toxicity in a horse

path report- actue MONOPHASIC skeletal muscle degeneration and necrosis

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11
Q

Causes of monophasic lesions

A

Causes of Monophasic Lesions:

A single insult

Trauma (will be focal at the site of trauma)

Exertion, capture

Toxin – ionophores, plants

(coffee senna)

HORSES ARE REALLY SENSTIVE—–USUALLY FROM EATING A RUMINANT RATION

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12
Q

Edx

A

Monesin Toxicity

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13
Q

Our lambs with polyphasic muscle degeneration and necrosis…..

Follow up

A

You rule out access to toxic plants

Further research – they are from a Se deficient area

You arrange dietary vitamin E/Se supplementation

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14
Q

White Muscle Disease

A

Or Nutritional myopathy

Caused by Vitamin E / Se deficiency

See lesions in the most active muscles- because that is where the most free radicals are

Can see lesions in the heart with this condition and other metabolic/toxic myopathies of skeletal muscle

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15
Q

Mdx?

A

Heart from a calf with White Muscle Disease (nutritional myopathy from vitamin E/Se deficiency).
MDx: Cardiac myonecrosis.

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16
Q

Where else are you going to see white muscle disease?

A
  • heart
  • muscles of mastication
  • tongue(espesically in suckling animals)
  • diaphram
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17
Q

Single or multiple episodes

General signs of pain, anxiety, cramping most prominent after exercise

Multiple muscle groups look like this

In a horse

A

Exerional rhabdomyloysis(Tying up, azoteria)- necrosis/ lysis of skeletal muscle

ionic events of contraction can produce an adverse enviornment when extreme

may have an underlying metabolic conidtions which predispose such as polysaccharide storage disease

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18
Q

What types of causes typically incite this pattern of necrosis?

A

Acute Toxicity or Exertion

but NOT trauma because it’s mutifocal

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19
Q
A

“Exertional rhabdomyolysis” (Tying up, azoturia) – necrosis/lysis of skeletal muscle

During periods of exertion

Ionic events of contraction can produce an adverse environment when extreme

May have underlying metabolic conditions which predispose, such as polysaccharide storage disease

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20
Q

What other species is seen with foci of skeletal muscle necrosis?

A

Foci of skeletal muscle necrosis common in sled dogs, also observe in racing greyhounds

Exertional? Vit E/Se deficiency involvement? Underlying myocyte metabolism issue? lactosis, lesions in the heart, myglobin injures the kidneys

Sled dog myopathy – lethal, generalized lesions involving non-locomotory muscles

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21
Q

“Azoturia”

A

“Azoturia” = excess nitrogen in urine
This muscle is from a 1 year old deer with capture myopathy.
Why is the kidney and urine abnormal??

red urine from myoglobin from severe muscle necrosis

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22
Q

Capture myopathy

A

Zoo and wild birds

Exertion, stress during capture/handling/transport

• Anaerobic glycolysis —->hyperthermia, metabolic acidosis

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23
Q
A

“Malignant hyperthermia” – another example of a metabolic condition predisposing to necrosis

IN PIGS

muscle bellies are pale and dry

Pathogenesis: inherited defect in skeletal muscle ryanodine receptor==> excessive Ca release and contraction when stimulated —–>heat production and myocyte necrosis

stress can set off the receptor

MDx: focal muscle degeneration and necrosis

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24
Q

Are the pale streaks in this muscle due to degeneration and necrosis?

A. Yes B. No

A

NO because it’s fat!!!

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25
Does this calf have skeletal muscle degeneration and necrosis? A. Yes B. No
B- THIS IS NORMAL IS A YOUNG ANIMAL- it will feel soft
26
Another farm call... 34 of 120 yearlings are dead.
hemorage- bright red! necrosis- skeletal muscle- VERY DRY
27
What is abnormal about this and what pathological process is responsible?
Muscles are dark red, swollen, softened/friable, palpable crepitus degeneration/necrosis, inflammation/repair, and circulatory disorder edema!
28
What would be on the path report and what would we do to confirm the etiology of this condition?
Pathology report: Morph Dx - Acute necrotic and hemorrhagic myositis(primary process is inflammation) Comments - Gram positive bacilli identified, consistent with Clostridium chauvoei infection Disease Dx - “Black leg” to confirm etiology- culture the muscle
29
If this is just a bacterial infection of muscle(Black leg), why did it kill so many cattle?? And why are we seeing these other lesions?
Pathogenesis: Ingestion of spores leads to dissemination to muscle via blood leads to latency leads to tissue hypoxia/acidosis leads to bacterial proliferation leads to production of exotoxins leads to myonecrosis and systemic endothelial damage **leads to death from septicemic shock** YOU ALSO SEE EPICARDIAL PETECHIAL HEMMORRAGE AND SEROUS PLEURAL EFFUSION
30
What triggers outbreaks of Black Leg?
Parturition Handling - IM meds/vax, marking, shearing, etc Trauma during confinement Soil disturbance You just have to vaccinate!
31
Types of causes inciting myositis
_Necrotic/hemorrhage–_Clostridium chauvoei, C. septicum _Suppurative–_pyogenic bacteria _Lymphocytic–_immune-mediated; NO GROSS CHANGE IN THE TISSUE; microscopic dx _Eosinophilic–_active protozoal/ parasitic infections, immune- mediated Granulomatous
32
Suppurative myositis in a horse with Pigeon fever caused by Corynebacterium pseudotuberculosis
33
Eosinophilic myositis in a cow weird coloration(lavender, gray-green)---- typical of eosinophils pathogenesis: parasites- tapeworms, sacrocysts
34
MDx: Focal suppurative myositis
35
MDx: Diffuse eosinophilic myositis Major Causes: parasites and immune mediated Eosinophilic myositis in a dog with “Masticatory myositis” (immune-mediated), active phase
36
Masticatory myositis
37
What happens in the end stage of Masticatory myositis”
MDx: chronic eosinophilic myositis & Muscle atrophy atrophy of the temporalis muscle
38
Exophthalmus due to “Extraocular polymyositis”. Histological MDx: eosinophilic myositis of extraocular muscles. autoimmune pathogenesis
39
Intralesional protozoa in small animal – toxoplasma vs neospora eosinophilic
40
Eosinophilic myositis in a cow with Sarcocystis spp. infection
41
Sheep esophagus infected with sarcocystis gigantica Some spp. of Sarcocyst you can see grossly. **Often do not have eosinophilic response.**
42
Cysticercus ovis in skeletal muscle of a sheep. MDx: skeletal muscle parasitic cysts. +/-eosinophilic/granulomatous myositis
43
ANOTHER farm call!! .... “downer cow”, can’t send to slaughter, want to make sure no diseases that will affect other animals. What can we do to determine the pathological process responsible for this presentation? What is morphologically abnormal/ what is the MDx?
There are discrete areas of muscle pallor bordered by reddened zones in the pectoral muscle of a cow. MDx: skeletal muscle degenration and necrosis or infart infart- geometric lesion with well demarkcated borders; also the cow was down, so he was lying on it
44
pathogenesis of this?
Leg Pathogenesis: recumbency leads to increased intramuscular pressure leads to poor perfusion leads to ischemia leads to **_infarction_** **Can see a similar lesion post- anesthesia of large animals.** pale, dry- arterial congested like this one- venous
45
Melon headed whale, stranded at Brunswick heads (Gold Coast, QLD), May 2014.
Path report MDx: Focal monophasic myonecrosis. Pathology report comment: Due to infarct given history of beaching? Trauma during transport to Sea World? Capture myopathy? Vs. primary cause of beaching? Infart due to beaching due to encephalsis
46
**“Compartment Syndrome”** Pathogenesis: rapid muscle growth-----\> period of increased circulation (exertional) ---\> muscle swelling confined by facia ----\>impedes blood supply----\> ischemia ---\>infarction Supermarket chicken breast- chickens bred to put on a lot of breast muscle very fast.
47
MDx: Intramuscular hemorrhage Cause: trauma (esp penetrating wounds, fractures)
48
MDx: Intramuscular hemorrhage cause: trauma( esp penetrating wounds, fractures)
49
Is hemorrage a common lesion in muscle?
NO! If it is there, you should be thinking TRAUMA!
50
Your next consult is a rabbit... Or a pig... Or a puppy, take your pick... Since birth cannot stand, limbs abducted, flattened chest, alert and otherwise normal.
Morph Dx – Myocyte hypoplasia Disease Dx - “Splay Leg” or “Swimmer Syndrome"
51
What is morphologically abnormal? What pathological processes could account for this appearance? How could this be caused?
Myocytes are smaller in diameter What pathological processes could account for this appearance? Degeneration/Necrosis Inflammation & Repair Circulatory Disorders **_Disorders of Growth_** Deposits & Pigmentations _Pathology report:_ Morph Dx – Myocyte hypoplasia Disease Dx - “Splay Leg” or “Swimmer Syndrome" **Pathogenesis unknown currently** Genetic predisposition Primary spinal / neuromuscular disease? Underlying infections? Overfeeding? Slippery flooring involved? You give support to the limbs, and the mycocytes will catch up over time
52
Does myocyte hyperplasia occur? Can myocytes proliferate??
Myocytes CAN NOT PROLIFERATE!!! because they are terminately proliferated muscle hypertrophy i.e. going to the gym
53
Causes of myocyte hypertrophy
Causes of myocyte hypertrophy * Exercise conditioning * Compensatory - decreased number/size functional myocytes, increased load on remaining
54
Causes of myocyte hyperplasia
Causes of myocyte hyperplasia “Double muscling” • Inactivation of the regulatory gene **myostatin** (involved in myoblast cell progression to muscle fibers) GENETIC
55
What is morphologically abnormal with this horse? Gross morphological diagnosis?
Muscles are lop-sided Regional atrophy- gross morphological dx _Causes:_ * Physiologic (Dis-use, aging) * Cachexia/malnutrition Endocrine disease – myocytes have surface receptors for hormones (hypoT, hyperA) **Denervation** – myocyte maintenance requires trophic factors generated at neuromuscular junction; _occurs quickly!_
56
What is morphologically abnormal? ( from the horse case)
The muscles from the atrophical horses would likely look like the one of the right. Fibrosis and fatty infiltration (steatosis) often develop in long- standing atrophy Notice that we can use the terms ‘atrophy’ and ‘hypertrophy’ when referring to muscle as a whole or to the diameter of a myocyte
57
What is abnormal?
Larynx from a horse clinically diagnosed with laryngeal paralysis. Note L cricoarytenoideus dorsalis muscle (due to damage to the L recurrent laryngeal nerve).
58
Which cell type do neoplasms with striated muscle differentiation (‘rhabdomyoma/sarcoma’) derive from?
Pluripotential stem cells (remember skeletal myocytes can NOT replicate even to form a neoplasm)
59
rear leg from a dog - rhabdomyosarcoma very malignant
60
Myoblast differentiation MDx: rhabdomyosarcoma
61
What do you have to use to tell if you have a rhabdomyosarcoma?
Immunohistochemistry for desmin
62
Rear leg from a dog - hemangiosarcoma from skeletal muscle
63
“Rufus”, 1 year old male Golden Retriever..... Clinical signs Exercise intolerant **Progressive generalized muscle weakness, atrophy** **Joint contractures and angular deformities** Excessive drooling, problems eating- problems with muscles of mastication What can we do to figure out what the pathological process was that resulted in these signs??
BIOPSY!
64
Rufus's histo and what would cause this?
Pathology report: Morph Dx – Polyphasic myocyte **degeneration and necrosis**, chronic, with hypertrophy, atrophy, and fibrosis _Causes of polyphasic lesions:_ Ongoing insults Nutritional deficiency – vitamin E/Se Ongoing toxicities **Genetic defects in myocyte structural/metabolic elements** **Important point: Usually not possible to discern the cause of muscle injury with histopathology – supplemental tests, clinical history usually required!**
65
What did Rufus have?
“Rufus”, 1 year old male Golden Retriever..... Follow up You research genetic myopathies of dogs and find “Muscular Dystrophy” – X-linked inherited myopathy reported in dogs and cats, especially G Retrievers – **Defects in dystrophin gene** – cytoskeletal protein You discuss with pathologist Dystrophin tested on a fresh muscle sample is very low You inform owner poor prognosis, no treatment
66
Which 3 pigments and tissue deposits are observed in skeletal muscle?
**Lipofuscin- because myocytes are so long lived** Dystrophic calcification- because there is so much Ca+ in the ER Exogenous pigments- ESPECIALLY from injections
67
MDx: polyphasic myocyte degeneration and necrosis (with dystrophic calcification) Disease: White muscle disease; cause – vit E/Se deficiency Note calcification of myofibers secondary to degeneration/necrosis.
68
What’s up with these diaphragms of 600 sheep? yellow plaques are going into the muscle
EXOGENOUS DEPOSITS Ba, Se, Au were on the spec this is a suplement for Se that was given IP instead of SQ
69
Called in to investigate several deaths of ducks at a local pond. Some surviving are very weak. What can we do to figure out what the pathological process was that resulted in these signs??
Pathology report: Morph Dx – Open. No lesions identified in over 20 sections examined. – nothing wrong with muscle or nervous system. Botulism cows chew on bones and get botulism
70
Botulism
Botulism Pathogenesis: **Decaying organic matter**--\>Clostridium botulinum thrives and elaborates exotoxin into envir.-\>\>\>ingested -------\> **toxin inhibits Ach release from nerve terminals at neuromuscular junction** ------\>progressive generalized paralysis with death by cardiorespiratory failure
71
Other “biochemical” pathological processes resulting in severe muscular clinical signs:
Neuromuscular junction disorders – Botulism, myasthenia gravis, tick paralysis Electrolyte derangements – hypokalemia (cats), hypocalcemia (cattle) Misc inherited disorders of muscle metabolism –myotonias (often involve ion channel defects – inability of fibers to relax)

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