Endocrine Exam 2

Front 1

Discuss the interactions of energy sources with the TCA cycle in cattle.

Back 1

Volatile fatty acids produced from fermentation are Acetate (70%), Propionate (20%), and Butyrate (10%).
Propionate is converted to oxaloacetate, which is then either converted to glucose or enters the TCA cycle.
Acetate and Butyric acid are converted to acetyl coA. If oxaloacetate is present, this also enters the TCA cycle; if not, it is converted to ketone bodies.

Front 2

Discuss the causes of a negative energy balance in cattle.

Back 2

1. High milk production
2. Reduced rumen volume
3. Decreased appetite due to increased estrogen levels
4. Switch to high grain/silage diet at freshening
5. Inadequately balanced ration
6. Excessive butyrate in silage
7. Decreased intake due to disease-eg. mastitis, metritis, DA.
8. Starvation

Front 3

Understand the response to negative energy balance in cattle.

Back 3

1. Hormonal response to negative energy balance=decreased insulin production and increased production of all "anti-insulin" hormones, causing peripheral insulin resistance.
2. After glycogen is depleted, fat stores are mobilized. Glycerol can be used to produce glucose, but fatty acids cannot. Beta oxidation of fatty acids produces Non-esterified fatty acids(NEFAs), which convert to Acetyl coA. Without oxaloacetate from the production of proprionate, Acetyl coA cannot enter the TCA cycle, and is converted into ketone bodies. Ketosis ensues.

Front 4

Be able to discuss the diagnosis and rational therapy of ketosis in individual cattle.

Back 4

Diagnosis: Detection of moderate to large levels of ketones on urine dipstick is the most common method of diagnosis.
Treatment: Establish positive energy balance, transfaunate if needed, propylene glycol (converted to glucose, 150-200 mL PO BID max), IV dextrose administration (CRI is best, but BID bolus can be done on the farm), glucocorticoids (activates hormone sensitive lipase, only use if BCS 3 or less).

Front 5

Discuss cattle herd management to prevent ketosis.

Back 5

1. Maintain BCS of 3.5-underconditioning leads to negative energy balance, over conditioning leads to fatty liver disease.
2. Monitor blood NEFA concentrations or blood B-hydroxybutyrate levels
3. Transition diet for cows in the last 3-5 weeks of pregnancy, and first 4 weeks of lactation. Allows time for rumen flora to adjust to higher calorie/concentrate lactation diet.

Front 6

What causes protein energy malnutrition in ruminants?

Back 6

1. Primary cause is lack of feed/poor quality feed; unable to meet metabolic needs-most common in late fall and winter when soluble fiber content of hay is decreased; more common with round bales.
2. Pregnancy-decreased rumen capacity. Fetal growth unaffected b/c maternal lipid and protein mobilization.

Front 7

Understand the difference between bovine ketosis and pregnancy toxemia (fatty liver).

Back 7

Ketosis->production of ketone bodies in response to negative energy balance.
Pregnancy toxemia->mobilization of fats due to negative energy balance overwhelm the liver.
Risk factors are similar for both, except that fatty liver occurs more frequently in cattle with a BCS >4

Front 8

Discuss the pathophysiology of fatty liver disease of cattle.

Back 8

1. Negative energy balance state triggers fatty acid release from adipose tissue.
2. Liver can use triglycerides for ketone formation, the TCA cycle, or VLDL production(not very responsive in cattle); but all of these process are rate limiting.
3. When TG release is excessive (fat animals!), these processes are overwhelmed, and excess TG's are stored in hepatic cells, causing damage.

Front 9

How is fatty liver disease diagnosed in the individual cow?

Back 9

Clues: BCS >4, massive weight loss during illness, remains ADR inspite of treatment.
Diagnosis: Liver biopsy-if >34% fat, will float in formalin. Can do histopath/cytology, but typically takes to long or is expensive if rush results.

Front 10

Treatment and management of fatty liver disease in the individual cow, and the herd.

Back 10

Individual: Establish positive energy balance, transfaunate, B12 supplements. Similar to ketosis, but must treat longer and prognosis is poor.
Herd: Maintain BCS of 3.5 at the time of calving.

Front 11

Milk fever: what factors can influence ionized calcium levels in the blood?

Back 11

1. Decreased rumen motility/absorption: must be normal for Vit D to have full affect in GI absorption.
2. High milk production-some individuals are not capable of mobilizing calcium in the face of high loss.
3. Dietary balance of Ca/Mg/Phos-especially important in prepartum diet. May influence the parathyroid's ability to respond to increase Ca needs postpartum.
4. Blood pH-Acidic blood pH pushes calcium to the ionized form!

Front 12

Pertinent clinical signs of milk fever.

Back 12

Downer cow
Kink in neck
Reduced muscle tone-especially in the jaw

Front 13

Treatment of individual cattle with milk fever, and management of milk fever in a herd.

Back 13

Individual: Ca borogluconate slowly IV. If response not rapid, give another 1/2 dose SQ. Monitor for arrhythmias while administering.
Herd: Give calcium gel at parturition, avoid overfeeding calcium, over conditioning, and stress. Supplement diet with magnesium. Oral or inj. Vit D prior to calving. Add ammonium chloride to diet a few weeks before parturition to shift DCAD towards acidity.

Front 14

Pertinent clinical signs of hypomagnesemia in cattle.

Back 14

Hyperesthesia
Incoordination
Extensor rigidity
Muscle tremors
Opisthotonus
Bellowing
Increased TPR
Loud heart sounds

Front 15

Treatment of individual cattle with hypomagnesemia, and management of hypomagnesemia in a herd.

Back 15

Individual: Ca borogluconate
Herd: Feed proper Ca/Mg/Phos ratios in diet.

Front 16

Which serum enzyme is best for monitoring severity of acute muscle damage and response to therapy in horses? Which serum enzyme is best for documenting damage after recovery?

Back 16

CK-because of it's rapid peak and decay, CK is used to assess acute/ongoing muscle damage, and response to therapy.
AST-because of longer peak and decay time, AST is used to document previous damage during recovery.

Front 17

What are the causes of muscle atrophy in horses? Hypertrophy?

Back 17

Atrophy-denervation, disuse, cachexia, post-circulatory disturbances, extensive myolysis.
Hypertrophy-training, compensation for fiber loss elsewhere, in response to other muscle disorders.

Front 18

What things would cause a mild (<1000) increase in serum CK activity in horses?

Back 18

Exercise and transport can cause mild elevations in CK

Front 19

What are the most common clinical signs of rhabdomyolysis in horses?

Back 19

Cramping/stiff gait-worse in the hind limbs
Reluctance or inability to move
Muscles are firm and painful on palpation
Anxiousness, sweating, tachycardia, and tachypnea-2ndary to pain
Microscopic or gross myoglobinuria

Front 20

What are the three major goals in treating rhabdomyolysis in horses?

Back 20

Limit further muscle damage
Restore fluid and electrolyte balance
Supportive and symptomatic care

Front 21

What are three types of drugs that can be used to limit further muscle damage associated with rhabdomyolysis in horses?

Back 21

Anti-inflammatories: NSAIDs, DMSO or corticosteroids
Dantrolene sodium-slows Ca release from sarcoplasmic reticulum
Methocarbamol-muscle relaxant

Front 22

What is the most important treatment component for horses with potential renal failure from exertional rhabdomyolysis?

Back 22

Aggressive diuresis until myoglobinuria is gone and BUN/Crea are normal.

Front 23

What anesthetic/surgery factors predispose a horse to rhabdomyolysis?

Back 23

Heavily muscled or heavy body weight horses
Long anesthesia time
Difficulty maintaining blood pressure
Amount of padding provided during surgery

Front 24

Which type of genetic recurrent rhabdomyolysis occurs in quarter horses? Thoroughbreds? What is the diagnostic test of choice for either of these?

Back 24

Quarter Horse: Polysaccharide storage myopathy
Thoroughbreds: Recurrent exertional rhabdomyolysis
Muscle biopsy may be used to diagnose both.

Front 25

What is the proposed pattern of inheritance of these disorders?

Back 25

PSSM-Autosomal dominant inheritance
RER-Autosomal recessive inheritance

Front 26

What is the recommended treatment for Polysaccharide storage myopathy and Recurrent exertional rhabdomyolysis?

Back 26

PSSM: Treat acute episodes with anti-inflammatories, dantrolene, fluid support, and sedation as needed. Provide consistent daily exercise. Reduce grain/carbohydrate in diet, replace with a fat source if extra calories are needed.
RER: Treat acute episodes as above. Avoid stressful triggers-stall in a quiet area, train before other horses and avoid exciting training routines, turn out if available, avoid long periods of stall rest. Remove grain from diet, replace with fat source if needed.

Front 27

What is the cause of white muscle disease?

Back 27

Selenium deficiency-free radical damage causes Ca++ influx into the mitochondria, energy stores are depleted trying to pump Ca++ back out, Ca continues to build up causing degeneration and necrosis.
Targets cardiac muscle (acute form) and skeletal muscle (subacute form)

Front 28

What is the diagnostic test of choice to confirm a selenium deficiency?

Back 28

Whole blood Selenium concentrations or blood glutathione peroxidase activity (preferred). Glutathione activity can still be tested after selenium has been given.

Front 29

How can white muscle disease be prevented?

Back 29

Analyze selenium status of soil, forage, grain, and blood levels of the horses. If less than <0.05 ppm in forage, supplement with oral Selenium and Vitamin E. May be provided through some salt block types, but not all; and horses may not ingest enough of the salt block to be properly supplemented.

Front 30

What is the underlying defect in hyperkalemic periodic paralysis (HYPP)?

Back 30

Defect in muscle membrane voltage-gated Na channel; causes channel to repeatedly open or stay open in response to increased extracellular K. Membrane becomes hypopolarized, hyperexcitable, and action potential magnitude decreases.

Front 31

What are the clinical signs of hyperkalemic periodic paralysis (HYPP)? What treatment would you recommend for an acute episode, and prevention of future episodes?

Back 31

Recurrent episodes of muscle fasciculations, weakness, and increased blood potassium. May also have prolapse of the third eyelid, sweating, and respiratory stridor/dyspnea.
Acute treatment: Dextrose, Sodium bicarbonate, and calcium gluconate.
Prevention: Acetazolamide, avoid high potassium diets, regular exercise.

Front 32

What is the mode of inheritance of hyperkalemic periodic paralysis (HYPP)? What breed and specific stallion are associated with it?

Back 32

Autosomal dominant trait with incomplete penetrance (heterozygote may or may not be affected, and to varying degrees).
Associated with Quarter Horses descended from the stallion "Impressive".

Front 33

What are the underlying mechanisms of PPID in horses? How does this differ from Cushing's disease in small animals?

Back 33

Degeneration of neurons from hypothalamus to the pars intermedia->decreased inhibition leads to pars intermedia hyperplasia->increased production of POMC->increased production of hormones from the pars distalsis (particularly ACTH->cortisol). In small animals the ACTH/cortisol overproduction results from dysfunction of the adrenal gland, pituitary, or rarely the hypothalamus itself; not the neurons connecting the hypothalamus and pituitary.

Front 34

What are the clinical signs of PPID?

Back 34

Hirsutism-Almost Pathognomonic
Muscle wasting
Chronic laminitis
PU/PD
Hyperhidrosis (sweating)
Abnormal fat deposition

Front 35

What findings on CBC and chemistry would be consistent with PPID?

Back 35

Stress responses:
-hyperglycemia
-mature neutrophilia with lymphopenia

Front 36

Name 2 tests that can be used to diagnose PPID in horses? Which is most common?

Back 36

Dexamethasone suppression test-most common
Endogenous/resting ACTH levels

Front 37

What is the treatment of choice for PPID?

Back 37

Pergolide-dopamine D2 receptor agonist; allows dopamine that is produced to remain longer and be more effective. "Prascend"-FDA approved product.

Front 38

What factors distinguish PPID from equine metabolic syndrome?

Back 38

Horses with equine metabolic syndrome will not have abnormal (high) dex suppression test results, or elevated endogenous ACTH levels.

Front 39

What breeds are predisposed to equine metabolic syndrome? What are the clinical signs?

Back 39

Predisposed: Ponies, Mini horses, Donkeys, Warm Blood/Draft breeds, Arabians.
Clinical signs: Obesity, regional fat deposition (crest and rump), laminitis.

Front 40

What is the general pathophysiology of equine metabolic syndrome?

Back 40

Obesity leads to peripheral insulin resistance. Insulin resistance increases the risk of laminitis by decreasing glucose delivery to the hoof, altering blood flow, and producing a pro-inflammatory state (also caused by obesity).

Front 41

How is the diagnosis of equine metabolic syndrome made?

Back 41

1. Ruling out PPID-dex suppression or eACTH.
2. Confirming insulin resistance-Resting serum insulin concentrations, elevated insulin:glucose ratio, or combined glucose-insulin test

Front 42

What is the recommended management for horses with metabolic syndrome?

Back 42

Regular exercise if possible
Diet-limit calories, remove grain, decrease nonstructural carbs. If horse has regional adiposity but is not obese, may use fat (oil) to supplement calories instead of grain.
Thyroid supplementation may help weight loss, but should only be used for 3-6 months and then gradually weaned off.

Front 43

What are the proposed mechanisms of laminitis in PPID and EMS?

Back 43

Insulin resistance decreases glucose delivery to the hoof, decreases blood flow to the hoof, and produces a pro-inflammatory state.
Diets high in non-structural carbs can exacerbate insulin resistance, as well as altering gut microbial flora, potentially increasing the production of exotoxins, endotoxins, or vasoactive amines.

Front 44

What is the best described syndrome of actual hypothyroidism in horses?

Back 44

Congenital hypothyroidism and dysmaturity:
-prolonged gestation
-contracted tendons, limb contracture
-ruptured extensor tendons
-mandibular prognathism
-delayed ossification->degenerative joint disease.
Treated with supportive care-foal will become euthyroid and improper bone development will correct over time, but early compression/malformation of cartilage in the joints can lead to chronic musculoskeletal issues.

Front 45

How is the diagnosis of hypothyroidism made?

Back 45

Baseline thyroid hormone concentrations.
TSH concentrations
TSH or TRH stimulation tests
-None of these methods are very accurate or established in horses, making hypothyroidism very difficult to diagnose.

Front 46

Enlargement of the thyroid gland in older horses is most likely due to what condition?

Back 46

Benign, non-functional adenomas of the thyroid.

Front 47

What is the most common clinical sign of hyperthyroidism in horses?

Back 47

Weight loss.

Front 48

What are the 2 most common causes of hypercalcemia in horses?

Back 48

Hypercalcemia of malignancy and hypercalcemia associated with renal failure.
Primary hyperparathyroidism is RARE.

Front 49

What is the mechanism of hyperlipemia of horses?

Back 49

Negative energy balance->release of fatty acids from adipose tissue->FAs enter liver and cannot all be used->excess is exported as VLDL->VLDLs deposit into tissues (primarily liver, kidney, possibly brain)->failure of affected organs.
Elevated serum triglyceride levels will also further decrease appetite, perpetuating the disease.

Front 50

What is the most common signalment of horses with hyperlipemia/hepatic lipidosis?

Back 50

Ponies, miniature horses, donkeys, and obese pregnant mares. History of being off feed!

Front 51

What are the clinical signs of hyperlipemia in horses?

Back 51

Depression
Decrease in feed intake
Liver failure/icterus
Renal failure
Diarrhea
Edema
Steatorrhea
CNS-neurologic deficits

Front 52

What lab work abnormalities are expected with hyperlipemia/hepatic lipidosis?

Back 52

Elevated serum triglyceride concentrations
Gross lipemia

Front 53

How do you treat hyperlipemia in horses? What is the prognosis?

Back 53

Treat any concurrent diseases
Minimize stress
Get calories in!-Tube feed, IV dextrose, offer a variety of foods, etc.
Insulin-if BG remains above 200 for 2 hours.
Prognosis is guarded. Up to 80% mortality.