Path 1 - Endocrine 6

drraythe's version from 2016-03-05 03:36

Endocrinology 6.6: Pancreas

Question Answer
Hypofxn of pancreatic islets results in what disorder? What is the characteristics of this disorder?Diabetes Mellitus. It is a metabolic disorder characterized by persistent hyperglycemia. (Results from diminished availability of insulin for normal fxn of many cells of the body)
Explain the pathogenesis of Diabetes Mellitus (from start to resulting coma)↓ insulin production → glucose unable to enter some tissues → hyperglycemia → mobilization of fat for energy → ketosis → acidosis → coma
Which age are you most likely to see Type 1 Diabetes in? What is happening to cz the hyperglycemia? What is this Type aka?Most often seen as a JUVENILE ONSET. There is a destruction of beta cells w/ progressive & eventual complete loss of insulin secretion. Bc there is NO insulin available, they require insulin from the time of diagnosis, i.e., insulin-dependent Diabetes Mellitus
*Which Type of Diabetes has ketosis & why?TYPE 1!!! Bc there is no insulin secretion, so glucose cannot be used at all, so body fat mobilized for energy → ketosis
What are some various possible czs of destruction of beta cells in Diabetes Type 1?Toxins, immune-mediated, viruses (chronic FMD in cattle), cytokines (IL-1), injury by free radicals, atrophy/hypoplasia/congenital aplasia of islets, neoplasia, acute pancreatic necrosis w/ necrosis of islets
Which age are you most likely to see Type 2 Diabetes in? What is happening to cz the hyperglycemia? What is this Type aka?MATURITY onset. In this case, there is insulin resistance &/or dysfxn of beta cells & then gradual loss of insulin secretion as beta cells are destroyed slowly. AKA non-insulin-dependent Diabetes Mellitus
What are insulin levels like in Type 1 Diabetes? Type 2?Type 1: There is no insulin being produced, so it is absent
Type 2: Insulin may be ↑, ↓ or normal but is unable to overcome insulin resistance in the peripheral tissues
What is the eventual fate of Type 2 Diabetes?In early stages of the disease → mild hyperglycemia & it's easily controlled w/ small doses of insulin, i.e., non-insulin-dependent Diabetes Mellitus. However, over time these develop into insulin-dependent Diabetes Mellitus
What is 2⁰ Diabetes Mellitus? What are 4 specific examples? What’s going on w/ the beta cells?Reflects antagonism in peripheral tissues btwn insulin & other hormones:
(1) Progesterone (e.g., diestrus/pseudo-pregnant bitch)
(2) Glucagon (with glucagonomas)
(3) Growth hormone (from pituitary tumors)
(4) Glucocorticoids (endogenous as in Cushing’s & exogenous as in iatrogenic). Although the problem is initially peripheral (insulin being antagonized), the hyperglycemia stimulates constant production of insulin which eventually exhausts the beta cells
**DM in DOGS → How common is this in dogs? Which Type is more common? Are females or males more common?Common endocrinopathy in dogs (1:200), w/ females being more prone than males. Dogs = TYPE 1
DM Type 1 in dogs → What is the pathogenesis of the destruction of the islets in dogs?Pancreatic necrosis/pancreatitis
Infiltrating tumor
Cytokines, etc
DM Type 1 in dogs → What happens to the islets of the pancreas? The pancreas, grossly? How are the beta cells destroyed?Atrophy/hypoplasia of pancreatic islets, which leads to generalized exocrine pancreatic hypoplasia. Immune destruction of beta cells can be from idiopathic czs , autoimmune, or 2º to isletitis
**DM in CATS → How common is this in cats? Which Type is more common?Common in CATS, it is mostly Type 2
**DM in cats → What is the pathogenesis of why the cat develops this? (2)(1) Amyloidosis of islets (accumulation of amyloid eventually interferes w/ insulin secretion & fxn)
(2) Severe vacuolation of islet beta cells (in response to long-term overstimulation (“exhaustion”) bc of peripheral insulin resistance)
**CS of DM (11)(1) Hyperglycemia & Glycosuria → ↓ insulin or insulin resistance
(2) PU/PD → glucosuria/osmotic diuresis
(3) ↑ food consumption → effect on satiety center
(4) Wt loss → glucosuria & catabolism
(5) *Bilateral cataracts → lens degeneration
(6) Weakness → hypoglycemia, protein catabolism, polyneuropathy
(7) *Hepatomegaly → hepatic lipidosis & cirrhosis
(8) *Recurrent infxns → emphysematouos cystitis, prostatis, bronchopneumonia, dermatitis
(9) Glycogen nephrosis → due to glucosuria
(10) Microangiopathy → glomerulosclerosis, retinopathy, gangrene
(11) Autonomic & *Peripheral NEUROPATHIES → sometimes in cats, less in other spp
CS of DM → How does DM affect the blood & the renal system?Czs hyperglycemia & glycosuria (due to ↓ insulin or insulin resistance), along w/ polyuria & polydipsia (glycosuria → osmotic diuresis → thirst)
CS of DM → How does DM affect appetite, weight?Appetite will INCREASE (↑ food consumption) bc of the effect of DM on the satiety center. However, they are eating more but are LOSING weight due to the glycosuria & catabolism (no sugar in cells, body utilized other sources for energy)
How does DM affect the eyes?It will result in bilateral cataracts, bc there will be an ↑ in glucose metabolized by sorbitol pathway, which leads to an ↑ in sugar alcohols, which czs lens degeneration
How does DM affect the energy of the animal? How does DM affect the liver?The animal will be weak (lack sugar in cells) bc of the hypoglycemia, protein catabolism & polyneuropathy. The liver will become enlarged (hepatomegaly) due to the hepatic lipidosis (mobilization of fat to liver due to lack of ability to utilize sugar) & there will also be cirrhosis (Chronic liver damage)
Explain how DM affects the immune system (& some of the resulting conditions- 4)DM will result in recurring infections, bc there is ↓ leukocyte kinetics leading to impaired chemotactic, phagocytic & microbicidal fxns & ↓ adherence of PMN leukocytes. These problems can result in emphysematous cystitis, prostatitis, bronchopneumonia & dermatitis
How does DM affect the kidneys, blood vessels & the nervous system?The kidney will be overloaded w/ glucose, which will result in glycogen nephrosis. There will be microangiopathes which means glomerulosclerosis, retinopathy & gangrene will occur. There might also be peripheral & autonomic neuropathies, which are less common in animals than they are in humans, but can occasionally be seen in cats
How common is Hyperfxn of pancreatic islets due to neoplasia? Which Type of neoplasia (malig or benign) is more likely to cz this? Is this a fxnal or non-fxnal neoplasm?This is an uncommon condition, w/ the malignant variety being more frequent. Only SOME ore fxnal, though.
Hyperfxn of pancreatic islets due to neoplasia → What kind of stuff are these tumors secreting? Which is more common?Most tumors appear to secrete multiple hormones. However, 1 hormone is usually dominant & most often, it is insulin, e.g., insulinomas
What are the 2 Types of neoplasms which result in hyperfxn of pancreatic islets?(1) Beta cell (insulin-secreting) neoplasms
(2) Non-beta (gastrin-secreting) islet cell neoplasms
(Hyperfxn of islets due to neoplasia) Beta cell (insulin-secreting) neoplasms → Who gets these most often? What do they do & what are they called?These are seen in seen in adult dogs, cattle & ferrets. They are often fxnal, producing excess insulin. Hence "insulinoma"
**(Hyperfxn of islets due to neoplasia) Beta cell (insulin-secreting) neoplasms → What are the 2 Types of tumor an insulinoma can be? Describe them grossly (how to differentiate)(1) Could be an Adenoma, which is encapsulated & is a single yellow to dark red, spherical, small (1 to 3 cm) nodule
(2) Could be a Carcinoma, which is larger multiple nodules
Which insulinoma (adenoma or carcinoma) will metastasize to extrapancreatic sites & where, usually? (2)CARCINOMAS which are insulinomas (remember they’re all multinodular, so easier to break off) will usually either metastasize to regional lymph nodes (duodenal, mesenteric, hepatic, splenic) OR viscera/tissues (liver, mesentery, omentum)
The clinical signs of Beta cell (insulin-secreting) neoplasms usually relates to the severe hypoglycemia by the overabundant insulin. What would these clinical signs be? What would the CNS signs be (explain them)?You'd have weakness, fatigue after vigorous exercise, ataxia, mental confusion & periodic convulsive seizures (due to hypoglycemia). As for CNS signs, uptake of glucose from the CNS is by hypoglycemia, the uptake is ↓. Also, the CNS depends primarily on metabolism of glucose for energy. This leaves the CNS very deprived of energy (hence the ataxia, mental confusion & periodic convulsive seizures)
Non-beta islet cell neoplasms → What are the 2 Types (based on what is secreted)Glucagonomas, Gastrinomas
Glucagonomas → How common are these? Who usually gets them? What problems stem from these tumors secreting glucagon?Rare but reported in dogs. The excess glucagon leads to 2⁰ Diabetes Mellitus & hepatocutaneous syndrome (superficial necrolytic dermatitis, necrolytic migratory erythema) ("red white & blue" liver)
Hepatocutaneous syndrome is czd by what problem?A GLUCOGONOMA! (Non-bet islet cell neoplasm) (anti insulin → no sugar → dead stuff)
Hepatocutaneous syndrome happens when & why does the epidermal necrolysis (responsible for the 'red white & blue' liver) occur w/ this problem? (2)Happens when there is a glucogonoma. The epidermal necrolysis occurs due to?
(1) Hypoaminoacidemia → protein depletion in the epidermis
(2) Hyperglucagonemia → ↑ arachidonic acid synthesis in keratinocytes → dermatitis & necrosis (esp. over pressure points)
GASTRINOMAS → Who usually gets these? What cells does this neoplasm originate in & what do these cells usually secrete?This Type of neoplasm is rare but reported in dogs & cats. This neoplasm originates from ectopic amine precursor uptake decarboxylase cells (APUD cells) in the pancreas. (NOTE: (normally secreted by cells of the antral & duodenal mucosa) which secrete secretin, cholecystokinin, etc ) (a PU bc PU from stomach)
What does excess gastrin secretion by a gastrinoma do to the body? What are the clinical signs you'll see?Excess gastrin czs ulceration of the gastrointestinal mucosa (Zollinger-Ellison syndrome), which czs clinical signs of anorexia, hematemesis, intermittent diarrhea, progressive weight loss & dehydration
Chemoreceptor organs are? Fxn?NON-Chromaffin paraganglia (be able to compare the different ones)
Fxn = senses changes in the blood CO2/O2 content, pH → changes in RR, BP, HR, etc
Chemoreceptor organ Neoplasms are called?Chemodectomas
**Chemoreceptor organ Neoplasm (Chemodectoma) types(1) Aortic body adenomas/carcinomas
(2) Carotid body adenomas/carcinomas
(3) Ectopic thyroid tissue czing heart-base neoplasms
**What do you need to know about Aortic body adenomas/carcinomas? DDx?More common than carotid body tumors
Cz Heart failure due to space-occupying nature in the pericardium
Are NON-fxnl (usually)
Common cz of heart-base tumors
DDx = Ectopic Thyroid
**What do you need to know about Carotid body adenomas/carcinomas?Located near the bifurcation of the common carotid artery in the cranial cervical area
Usually unilateral (rarely bilateral)
Slow growing
1-4cm in diameter, well encapsulated w/ smooth external surface
Adenomas: Larger, multinodular, invade the capsule, penetrate walls of adjacent blood/lymph vessels
May interfere w/ swallowing & blood flow
**What do you need to know about Ectopic Tyroid Tumor? DDx?5-10% of "heart-base" neoplasms in dogs
Compress or invade structure in the cranial mediastinum near the BASE of heart
Cells are smaller w/ hyperchromatic nuclei & eosinophilic cytoplasm
NOT subdivided into small packets by fine strands of CT
Infrequent giant cells
Stroma is NOT prominent
Primitive follicular structures or colloid-containing follicles can be seen
DDx = Hemangiosarcoma (if in Rt Atrium in dogs, bloody)


Question Answer
Manifestations of hypothyroidism in the dog could include each of the following EXCEPT:
   A. epidermal atrophy
   B. dermal myxedema
   C. atherosclerosis
   D. abnormal estrus cycles
   E. elevated basal metabolic rate
E. elevated basal metabolic rate
Which of the following lesions would NOT result in diabetes insipidus?:
   A. tumor metastasis into the pituitary gland
   B. destruction of hypothalamic neurosecretory cells
   C. pituitary gland abscess causing destruction of the pars nervosa
   D. adrenocortical atrophy w/ destruction of the zona glomerulosa
   E. traumatic severance of the infundibular stalk of the pituitary gland
D. adrenocortical atrophy w/ destruction of the zona glomerulosa
Which one of the following features would NOT be expected with a very large functional tumor arising from the pars intermedia in the horse?:
   A. hirsutism from interference w/ cyclic shedding
   B. abnormal ACTH plasma levels
   C. diabetes insipidus
   D. hyperglycemia
   E. decreased susceptibility to bacterial infxns
E. decreased susceptibility to bacterial infxns
A horse with Hirsutism from interference with cyclic shedding is due to:
   A. pars intermedia tumor
   B. widespread tumor metastasis
   C. a functional adrenocortical adenoma
   D. epidermal atrophy
   E. abnormal estrus cycle
A. pars intermedia tumor