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004 - Systemic Pathology > BONE-06 > Flashcards

BONE-06 Flashcards

1
Q

(READ Before this Slide)

last slide on page 10

(Alteraions in myofiber side: Atrophy)

  1. Reduction in size - reduced fiber diameter of cross sectional area
  2. Causes? (3 of them)
  3. see more gross lesions or histological?
  4. how fast is process?
  5. different from hypoplasia how?
A
  1. denervation, disuse, cachexia
  2. gross
  3. rapid
  4. hypoplasia mean incomplete development
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2
Q

(Alteration in myofiber size: Hypertrophy)

  1. increase in muscle fiber diameter or cross-sectional area by what?
  2. physiologic hypertrophy considered normal - due to what?
  3. compensatory hypertrophy is nonspecific and occurs secondary to what two things?
A
  1. addition of myofilaments
  2. exercise conditioning
  3. decrease number of functional myofibers

or

interference with normal metabolic processes

(pic - monkey has been given anabolic steroid)

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3
Q

(Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(A. Circulatory)

(Downer Syndrome)

  1. muscle ischemia due to what?
  2. good condition - what animal most commoly?
  3. Pressure within muscles exceeds what?
  4. acute looks how?

chronic?

A
  1. external pressure
  2. cows
  3. venous and arterial pressure
  4. muscles dark and hemorrhagic

pale

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4
Q

(Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(B. Nurtritional)

  1. principal deficincies are what?
  2. resuilt in loss of antioxidant defense

Hi oxygen requirement and high contractile activity make striated muscle sensitive to what?

  1. Selective, segmental degereneration of what?

what remain intact

A
  1. selenium and vitamin E
  2. oxidative injury
  3. contractile components

basal lamina and satellite cells

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5
Q

(Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(Nutritional Myopathy)

  1. Vitamin E/selenium-containing enzymes are physiologic antagonists to what?
  2. In absence of protection, cellular membranes modified by what?

altering ability to do what?

  1. Mitochondrial calcium overload leads to what two things?
A
  1. free radicals
  2. free radicals

maintain ion gradients

  1. calcium-induced hypercontraction of myofibrils & degeneration of myofibers
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6
Q

(Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(Nutritional Myopathy)

  1. occurs in what primarily?
  2. usually what age?
  3. Clinical signs may be precipitated by what?
A
  1. pigs and herbivores
  2. _young (_can occur in utero)

(Neonatal animals rely on stores of selenium accumulated during gestation)

  1. physical activity

(Stiffness, dyspnea (heart failure), shuffling gait, recumbency)

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7
Q

(Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(Nutritional Myopathy)

(Lesions)

  1. affected muscle looks like what?
  2. marked what of muscle?
  3. Pale, irregularly opaque, yellow to creamy white
  4. usually what muscles affected?
  5. what muscles in young?
  6. uni or bilateral?
  7. may develop myoglobinuria
A
  1. pale (white muscle disease)
  2. mineralization
  3. thigh and shoulder
  4. tongue and neck
  5. bilateral
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8
Q

(Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(Nutritional Myopathy)

A
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9
Q

(Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(Nutritional Myopathy)

A
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10
Q

(Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(Nutritional Myopathy)

(Pigs)

  1. Spontaneous disease where intensive pig rearing practiced
  2. what more common - skeletal lesions or hepatic necrosis (hepatosis dietetica) and mycardial necrosis and hemorrhage (mulberry heart diesease)
  3. most common when?
  4. injections of what can cause?
  5. gross lesions?
  6. mortality?
A
  1. latter
  2. 6-20 weeks
  3. iron (catalyst for lipid peroxidation of cell membranes)
  4. difficult to detect (pale muscles)
  5. can be high
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11
Q

Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(C. Toxic)

  1. phytotoxins, chemical toxins, pharmacological toxins

2. may be difficult to distinguish from what?

  1. segmental or diffuse skeletal muslce or myocardial lesions?

4. Act by destroying vit E or selenium?

inhibited by addition of these nutrients?

  1. more or less lethal that nutritional deficiencies (persistent or generalized toxic influence)
  2. unremarkable and nonspecific lesions; less often associated with what?
A

2. nutritional myopathies

  1. segmental
  2. no

no

  1. generally more
  2. mineralizeation of tissues
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12
Q

Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(C. Toxic Myopathies)

(Monensin Toxicity)

  1. what is it?
  2. used for what in ruminants?
  3. what in birds and animals?
  4. very toxic to monogastrics or at high doses for ruminants
  5. order or toxicity?
A
  1. antibiotic fermentation product (Streptomyces cinnamonensis)
  2. grwoth promotion (added as premix)
  3. coccidiostat
  4. Horses>dogs/pigs>sheep/goats>cattle>poultry
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13
Q

Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(C. Toxic Myopathies)

(Monensin Toxicity)

  1. monensin is an ionophore that does what on molecular level?
  2. Results in what?
  3. what may account for the low level of calcification of the muscle fragments?
A
  1. distorts membrane transport of sodium and potassium
  2. calcium overload –> death of skeletal/cardiac muscle
  3. Early mitochondrial destruction
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14
Q

Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(C. Toxic Myopathies)

(Monensin Toxicity)

(Clinical Signs)

Lethargy
•Stiffness
•Muscular weakness
•Recumbency
•Horses may exhibit colic symptoms

(Postmortem LEsions)

  1. ill-define pale streaks in myocardium and skeletal muscle
  2. is minearlization of muscle a feature?
  3. see what in chronic?
A
  1. not a major one
  2. atrophy of skeletal muscles
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15
Q

Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(D. Exertional Myopathies)

  1. Intensive or exhaustive activity of major muscle masses
  2. Glycolytic fibers vs. the type 1 oxidative fibers

what gets rapidly/abberantly used?

leading to what?

  1. coagulation of what?
  2. diffusion of what?
  3. water lost to what?

leading to what?

  1. Myoglobinemia, myoglobinuria, and metabolic acidosis
A
  1. glycogen

local heat and lactic acid

  1. contractile proteins
  2. lactate and heat
  3. interstitium

increased pressure/ischemia

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16
Q

Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(D. Exertional Myopathies)

  1. aka what?
  2. Two general syndromes recognized clinically in Horses

what are they?

A
  1. exertinoal rhabdomyolysis (necrosis), chronic intermittent rhabdomyolysis; Monday morning disease; tying up
  2. sporadic exertional rhabdomyolysis

recurrent exertional rhabdomyolysis

17
Q

Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(D. Exertional Myopathies)

(a. Sporadic Exertional Rhabdomyolysis)
1. occurs following exercise in horses with previous history of what?

(Lesions)

  1. most obvious where?
  2. muscles look how?
A
  1. satisfactory performance :)A)
  2. gluteal and lumbar regions (often widespread though)
  3. moist, swollen, dark; may have streaks of pallor
18
Q

Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(D. Exertional Myopathies)

(a. Sporadic Exertional Rhabdomyolysis - cont)

(Lesions)

  1. how do kidneys look?
  2. severe damgage to what of kidney by what?
  3. Oliguria, anuria, renal failure, death
  4. Exercise exceeds horse’s underlying state of training
  5. how long for repair?
  6. Outcome depends on nature and duration of initiating exercise and severity of clinical signs
A
  1. swollen with brown cortex and brown-red streaks in medulla
  2. PCT by myoglobin or renal ischemia

(what kills them is renal lesion)

  1. 4-8 weeks
19
Q

Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(D. Exertional Myopathies)

(a. Sporadic Exertional Rhabdomyolysis - cont)

(Etiology)

  1. what viruses have been implicated?
  2. Mild muscle stiffness with concurrent viral infections is likely the result of the release of what?
  3. More severe rhabdomyolysis may be due to exertion during a concurrent systemic infection and/or viral replication in muscle tissue
A
  1. EHV-1 and Equine influenza
  2. endogenous pyrogens
20
Q

Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(D. Exertional Myopathies)

(b. Recurrent Exertional Rhabdomyolysis)
1. recurrent episodes, even with light exercise
2. how long for recovery?
3. reported in what?
4. no gross lesions
5. inherited as what?

A
  1. its rapid
  2. many breeds
  3. autosomal dominant with variable expression in thoroughbred
21
Q

Diseases of Muscle)

(1. Degenerative Diseases of Muscle)

(D. Exertional Myopathies)

(b. Recurrent Exertional Rhabdomyolysis)

(Pathogenesis)

1-2. What are the two possibilites?

A
  1. Alteration in muscle cell calcium regulation

and

Disorder in carbohydrate storage and utilization (polysaccharide storage myopathy [PSSM])

read the details

22
Q

(Inflammatory Myopathies)

(Inflammation of Muscle)

  1. Other myopathies may be accompanied by inflammation
  2. True myositis occurs only when?
  3. causes?
A
  1. Inflammatory cells are directly responsible for initiating and maintaining myofiber injury and

nflammation is directed at the myofibers and not at the stroma

  1. bacterial, viral, parasitic, immune-mediated
23
Q

(Inflammatory Myopathies)

(Bacterial Myositis: Gas Gangrene)

  1. Muscles highly susceptible to bacteria of what genus?
  2. Organisms are highly toxigenic, causing what?
  3. exist in envrinoment as what?
  4. what is result of systemic intoxication?
  5. Germination of spores requires what?
A
  1. colstridium (anaerobic, gram +)
  2. extensive necrosis, gas formation
  3. resistant spores
  4. death
  5. precise local conditions (deep penetrating wounds)
24
Q

Inflammatory Myopathies)

(Bacterial Myositis: Gas Gangrene)

  1. Resulting lesions called what?
  2. pathologic clostridia found where?
  3. Any contamination of what likely to introduce these pathogens?
  4. Most such wounds heal routinely, however (conditions must be perfect for development of gas gangrene)
A
  1. gas gangrene
  2. soil and feces
  3. open wound
25
Q

Inflammatory Myopathies)

(Bacterial Myositis: Gas Gangrene)

  1. usually mixed infections
  2. what are 4 most important organisms?
  3. Each of these organisms also cause a specific disease in pure infections that is NOT associated with surface wounding
A
  1. C. septicum, C. perfingens, C. novyi, C. Chauvoei
26
Q

Inflammatory Myopathies)

(Bacterial Myositis: Gas Gangrene)

  1. what animals are highly suscuepible?
  2. Castration, shearing, penetrating stake wounds, parturition, and inoculation sites
A
  1. ruminants, horses, and swine

(carnivores rarely affected)

27
Q

Inflammatory Myopathies)

(Bacterial Myositis: Gas Gangrene)

28
Q

Inflammatory Myopathies)

(Myositis: Blackleg)

  1. Gangrenous myositis of ruminants caused by what?
  2. Characterized by activation of what in muscle?
  3. common in what animals?
  4. age in cattle?
  5. animals in good condition
A
  1. C. chauvoei
  2. latent spores
  3. cattle and sheep, rare in other domestic
  4. 9 months - 2 years
29
Q

Inflammatory Myopathies)

(Myositis: Blackleg)

  1. Pastured animals; summer
  2. Spores found in many tissues of normal animals
  3. Latent spores germinate when what occurs?
A
  1. local event creates muscle damage or low oxygen tension
30
Q

Inflammatory Myopathies)

(Myositis: Blackleg)

31
Q

Inflammatory Myopathies)

(Myositis: Blackleg)

004 - Systemic Pathology (24 decks)

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