Metabolism/Endocrine Lab Flashcards by Alyssa Sorum

What are the functions of the liver?

Production of cholesterol
- precursor to sex hormones, Vit D
Storage of Micronutrients:
- Minerals- Cu, Zn, Mg, Fe
- Vit- A, D, E, K, B12
Blood Sugar Balance:
- storage of glycogen
Production of Bile:
- Needed for digestion
- GI antimicrobial
Protein Synthesis:
- Blood clotting (prothrombin)
- Cholesterol transport (lipoproteins)
- Immune Function (globulins)
- Oncotic pressure (albumin)
- Copper Bioavailability (ceruloplasmin)
Immune System:
- Contains viruses and pathogens
- Maintenance of the hepatic and portal vein immune system
Metabolism:
- Conversion of T4 ⇢ T3
- Detoxification of Fat
Detoxification:
- Drugs/alcohol
- Fatty acids
- Steroid hormones
- Ammonia ⇢ urea
- Environmental toxins/allergens

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How is fat metabolized in hepatocytes?

3 outcomes for Free Fatty Acids (FFA) that are synthesized in the liver or taken up from the plasma
- Mitochondrial-oxidation to generate ATP
- Esterification and storage in the liver as triglycerides
- Secretions as very low-density lipoproteins (VLDL)
  - carry newly synthesized triglycerides from the liver to adipose tissue

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What are the Key Concepts of Hepatic Lipidosis?

Result of endogenous, intracellular accumulation of lipid within hepatocytes
- Cytoplasmic vacuoles which peripheralize the nucleus
Can be due to physiologic causes
- High fat diet
- Increased periparturient energy
- Anorexia
Can be due to pathologic caues
- Hepatotoxins
- Hypoxia
- Starvation

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Case #1 Sunny

OW left home for 2 months in neighbors care. Sunny was lethargic, very thin (down 11lbs) and jaundiced.

Summarize and interpret observations of these photos.

Sunny hasn’t had adequate access to food and has been stressed by the owners absence
Her liver is enlarged and pale
Has an abundance of abdominal Fat
Morphologic diagnosis: Liver, lipidosis
Most likely occurred due to excessive mobilization of peripheral fat to maintain energy production

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What is the Pathogenesis (story) of Hepatic Lipidosis?

Anorexia/Decreased caloric intake
Increased Mobilization of fat
Increased hepatic uptake of lipids
Lipid deposition in hepatocytes

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How does Hepatic Lipidosis affect cats?

Obesity is a common risk factor
Disease initiated by anorexia
Disruption of normal fat metabolism results in excessive deposition of lipid in hepatocytes
Hepatocyte alterations destabilize plasma membranes and cause cell enlargement
- Elevated liver enzymes (AST, ALT, ALP)
- Compression of bile canaliculi leading to cholestasis ⇢ Icterus
Without good, aggressive nutritional/fluid management this can be fatal
- feeding tube almost always needed

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What can cause anorexia in felines?

Other disease
Environmental changes
Poor ration
Stressful events

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How is lipid deposition in hepatocytes characterized?

By discrete vacuoles which peripheralize the nuclei

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How does fasting affect cat’s lipid metabolism?

Fasting promotes lipolysis in adipose tissue and transportation of FFA to the liver
The hepatic load of FA is also increased by hepatic synthesis of fatty acids
- Acetyl-CoA derived from carbohydrates (or FFA) enters the Krebs cycle to result in production of ketone bodies and additional FFA
An imbalance between these different aspects of the feline lipid metabolism leads to accumulation of lipids in the liver

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Case #2 Bob

7 YO intact CS. Hair Loss and thin haircoat in general. Gained 10Lbs. Lethargic, House-soiling, infertile

Summarize and interpret observations (several pictures missing)

Patchy hair loss and epidermis appears crusty and irregular
- Histologically the epidermis is thin, hyperkeratinized, hair follicles are dilated and filled with keratin, there is a deduction in sebaceous and sweat glands
Low RBC level and increased cholesterol
Thyroid gland is extremely small
- few recognizable follicles histologically
Liver is enlarged and tan-brown
Pale discolored regions in one of the hepatic vessels
Cardiac vessels are enlarged and have a whit/mottled appearance
- Histologically these vessels have thin walls thickened by white, foamy material along with excess number of cells.

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What would the interpretation for Bob’s necropsy be?

Skin, epidermal atrophy and hyperkeratinization and adnexal atrophy
- “endocrine dermatopathy”
Anemia
Hypercholesterolemia
Thyroid gland, atrophy
Liver, lipidosis
Cardiac and hepatic vessels, atherosclerosis

Hypothyroidism

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Why was this clinical pathology seen in Bob?

Hematology:
- Mild non-responsive normochromic normocytic anemia will sometimes accompany decreased thyroid hormone levels due to decreased RBC formation
Cholesterol:
- Hypercholesterolemia reflects decreased utilization of cholesterol due to overall decreased metabolic rates

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What was the pathogenesis of Hypothyroidism and all other symptoms in Bob?

Thyroid atrophy⇢ loss of functional cells ⇢ decreased thyroid hormones
Hepatic lipidosis:
- Decreased thyroid hormone ⇢ reduced metabolic rate ⇢ (increased glycolysis, gluconeogenesis, glucose and protein absorption) increased lipid metabolism ⇢ Increased conversion of cholesterol into bile acids
Endocrine Dermatopathy:
- Decreased thyroid hormones ⇢ decreased stimulation of anagen phase of hair cycle ⇢ increased telogen (inactive) phase of hair cycle ⇢ Hair loss and increased keratin formation
Atherosclerosis
- Increased cholesterol ⇢decreased lipid metabolism ⇢increased deposition of cholesterol in vessels

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What are the potential causes of Thyroid atrophy?

Immune mediated:
- lymphocytic thyroiditis
- Autoantibodies produced against thyroglobulin/thyroid components
Idiopathic:
- unknown pathogenesis, possibly inherited
Physiologic loss of thyroid hormone:
- Decreased thyroid stimulation by thyrotropin or decreased Thyrotropin releasing hormone levels

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What are the Key features of Hypothyroidism?

Idiopathic/Autoimmune-induced atrophy of the thyroid gland leads to decreased thyroid hormones
Systemic lesions are due to loss of thyroid hormone stimulation of metabolism
Lipid accumulates in the liver due to altered mobilization from hepatocytes
High cholesterol levels and hyperlipidemia are present

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What is Atheromatous plaque formation?

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Atherogenic risk factors cause endothelial dysfunction
1. lipids deposit in the intima
2. Leukocyte adhesion molecules are expressed
3. Leukocytes migrate into vessel wall
Macrophages in the vessel internalize lipoproteins to become foam cells
Macrophages, T cells and other leukocytes release O₂ radicals pro-inflammatory cytokines, and growth factors
Vascular smooth muscle migrates into the intima and differentiates into a proliferating phenotype
1. produce extracellular matrix proteins, including collagen
Apoptosis of cells in the plaque leads to formation of a necrotic core
Neovascularization and MMP secretion by macrophages destabilizes the plaque, leading to plaque rupture
Exposure of plaque contents to blood initiates platelet activation, coagulation, and thrombus formation

Case #3 Sara

13 YO TS terrier

Hair loss, PU/PD, lethargy, polyphagia, weakness. High WBC and neutrophils. High AST and Glucose.

Summarize observations (some slides missing)

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Hair loss, and white, multifocal areas in cross sections of the skin
- Histologically, epidermis is thin, there are reduced numbers and size of adnexa, and large, irregular purple areas are present
Brain and pituitary look normal
White, nodular mass in the adrenal cortex comprised of large, round foamy cells
Multifocal groups of myofibers are small
Liver is enlarged and pale-tan
- hepatocytes are swollen nd have foamy cytoplasm
Urinary bladder mucosa isred and expanded (“puffy”)

What are the interpretations of the findings on Sara?

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Skin, epidermal and adnexal atrophy, with dermal mineralization
Pituitary gland, normal
Adrenal gland, cortex, adenoma
Skeletal muscle, atrophy, multifocal
Liver, lipidosis and glycogenosis
Urinary bladder, cystitis, emphysematous

What is Canine Hyperadrenocorticism?

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Commonly due to pituitary chromophobe adenoma
There is excessive and unregulated secretion of corticosteroids
- Corticosteroids are gluconeogenic, lipolytic, protein catabolic, anti-inflammatory and immunosuppressive
Common multisystemic effects:
- Liver (hepatic glycogenosis)
- Skin (Endocrine dermatopathy)
- Skeletal muscle (atrophy)

How does Excess glucocorticoids affect Hepatic lipidosis?

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Increase in appetite and high caloric intake
Increased blood glucose levels due to GC-induced gluconeogenesis
Stimulation of lipogenesis that is augmented by high glucose and insulin levels, and my GC itself
Increased release of FFA from adipose tissue and uptake of these by the liver

What is the Pathogenesis of Hyperadrenocorticism?

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Functional Adrenal neoplasia OR ACTH producing pituitary neoplasia OR iatrogenic steroid administration ⇢ Chronically increased cortisol ⇢ systemic effects
- Hepatic gluconeogenesis and hepatomegaly/pendulous abdomen
- Increased lipolysis and protein catabolism
- Pu/PD
- Polyphagia
- Alopecia
- Pyoderma
- Obesity
- Immune suppression and chronic infections
- Calcinosis cutis

Case #4 Nellie

33 YO mare

Polyphagia PD/PU, reluctant to work, Hyperglycemia, Increased Beta-endorphin, Increased Melanocyte stimulating hormone, increases ACTH

Summarize observations

some pictures missing

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Eats, drinks and urinates a lot
High glucose and ACTH
Hairy
Large pituitary
Adrenal gland looks okay
P3 and the hoof wall aren’t parallel
Hoof laminae are hypercellular

Interpret the findings on Nellie

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Polyphagia, polyuria, polydipsia
Hyperglycemia and high ACTH
Hypertrichosis
Pituitary adenoma (pars intermedia)
Normal adrenal gland
Hoof, laminitis

What is Equine Pituitary Pars Intermedia Dysfunction (PPID)?

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Equine par intermedia contains melanotropes
- Directly innervated by dopaminergic neurons of the periventricular nucleus
- Dopamine interacts with dopaminergic D2 type receptors on melanotropes to inhibit Proopiomelanocortin (POMC) expression
  - POMC is the pituitary precursor of circulating melanocyte stimulating hormone ( α MSH),
    ACTH, and β endorphin.
- Cortisol exerts negative feedback on ACTH secretion by the pars distalis but not the pars intermedia
PPID is due to oxidative injury to periventricular neurons
- Loss of inhibitory effect of dopamine results in melanotrope hyperplasia and unregulated production of POMC
- Predisposes to melanotrope neoplasia within pars intermedia.
- Hyperplasia/neoplasia compresses neurohypophysis, hypothalamus and optic chiasma

What are the Clinical Features of PPID?

* Increased age is the biggest risk factor * **Hirsutism/**hypertrichosis * delayed or absent seasonal molting resulting in long shaggy hair * PU/PD due to diabetes insipidus * NOT hyperglycemia * Hyperhidrosis * Myopathy with type 2 fiber atrophy * Weight loss and/or Obesity with excess fat in crest f the neck and supraorbital fossae * not specific to PPID - may be Equine Metabolic Syndrome * Laminitis * Obesity, insulin resistance, hyperinsulinemia and laminitis are correlated in horses * Rarely blindness * Clin path is variable * changes can include hyperglycemia, hyperinsulinemia, increased/decreased or normal cortisol

What is the Pathogenesis of PPID?

1. Adenoma of the pars intermedia 2. Physical disruption of the pars nervosa 3. Overproduction of pro-opiomelanocortin and ACTH 4. Chronic laminitis and insulin resistance, PU/PD, Hypertrichosis with wavy coat and failure to shed in the spring, Hyperhidrosis, narcolepsy, reoccurring infections, polyphagia, muscle wasting, pendulous abdomen

What is the morphologic diagnosis?

* Pituitary gland, pars distalis adenoma, chromophobe adenoma

What is this?

Secondary

Is this pheochromocytoma of the adrenal gland?

Case #5 Dolly 8 YO FS Dog Decreased appetite, PD, vomiting, breath smell worse, Painful urination - red and cloudy, High WBC, Neutrophils, Bands, and Monocytes. High Glucose and ALT What are the observations?

* WBC, Neutrophils, Band cells, monocytes are elevated * Glucose and ALT are elevated * There is opacity behind the iris * There are tan bands of tissue that separate and sometimes distort pancreatic lobules * Liver is slightly pale, has an accentuated lobular pattern * Histologically, the hepatocytes contain large vacuoles or have a foamy appearance * Urinary bladder is red and puffy * Histologically urinary submucosa is hypercellular an there are large open spaces multifocally i

What are the interpretations for Dolly's results?

* Leukocytosis, neutrophilia, monocytosis * Hyperglycemia and elevated liver enzymes * Lens, cataract * Pancreas, fibrosis, multifocal to coalescing * Liver, lipidosis and glycogenosis * Urinary bladder, cystitis, emphysematous

What is Canine Diabetes mellitus?

* Pancreas: Pancreatic fibrosis, diffuse, severe * Chronic damage to pancreas may have started as an acute injury/injuries (pancreatitis) * Damage to the Beta cells (insulin secreting cells) of the pancreas * Liver: Hepatic Lipidosis * Increased fat mobilization overloads ability of liver to metabolize lipids * Glucose is still able to enter hepatocytes (stored as glycogen) * Eye: Cataract * Excess glucose enters the lens nd is converted to sorbitol and fructose * These substances cannot diffuse out of the lens and osmotically attract water * Swelling and degeneration of lens fibers * Urinary bladder: Cystitis, emphysematous * High levels of glucose pass through the kidney ad enter the urinary bladder * Bacteria thrive in high glucose environments * Clinical Pathology: * Inflammatory leukogram (response to the bacterial cystitis) * Elevated glucose (lack of insulin) * Elevated ALT (hepatic lipidosis causes slight hepatocellular damage and leakage of intracellular hepatic enzymes)0 * In Advanced disease rapid breakdown of fats to release FA results in formation of ketoacids * Diabetic ketoacidosis suggests advanced, uncontrolled disease

Case #6 Franklin Observtations

* PB\< BUN and Phosphorus are all elevated, Ca low * Kidneys, pale, have irregularly contracted surface * Histologically fibrosis and increased cellularity in the interstitium, fibrosis in the glomeruli, and reduced numbers of tubules * Parathyroid glands are bilaterally enlarged * Maxilla is enlarged an lack of boney trabeculae on cut surface * Stomach contains multifocal red spots * Contains hemorrhage along with loss of mucosa, decreased gastric glands, or glands that are dilated and contain cellular debris. A gastric vessel contains acellular material in its lumen and appear hypercellular

What are the interpretations of Franklins observations

* Hypocalcemia and hyperphosphatemia * Markers for kidney disease are elevated * Kidney, glomerulonephritis and interstitial fibrosis * Parathyroid glands, hyperplasia, bilateral * Maxilla, fibrous osteodystrophy * Stomach, gastritis and hemorrhage, ulcerative, multifocal with vasculitis and thrombosis

What is Renal secondary hyprparathyroidism?

* Chronic renal failure leads to retention of phosphorus and loss of calcium * Hypocalcemia leads to parathormone (PTH) secretion to elevate serum calcium * Persistent hypocalcemia leads to parathyroid hyperplasia and continuous PTH secretion * Functions of PTH include to enhance renal retention of calcium, increase intestinal absorption of calcium and to mobilize calcium from bone * Mineralized bone is replaced by collagen (Fibrous osteodystrophy)

Metabolism/Endocrine Lab Flashcards

(35 cards)