Term
|
Definition
|
|
Term
| What are hormones physiological regulators of? |
|
Definition
| Growth, Metabolism, Homeostasis, Reproduction |
|
|
Term
| Where are hormones produced? |
|
Definition
|
|
Term
| What are 2 types of hormones? |
|
Definition
| Glandular hormones, Tissue hormones |
|
|
Term
| What are paracrine hormones? |
|
Definition
| Locally secreted hormones |
|
|
Term
| What are endocrine hormones? |
|
Definition
| Hormones secreted into circulation |
|
|
Term
|
Definition
|
|
Term
| What concentration are hormones present in? |
|
Definition
| Very low (pg - microg/ml) |
|
|
Term
| The _____ & _____ systems coordinate all body functions with hormones being ______ affecting virtually all tissues. |
|
Definition
| Nervous & Endocrine; Long-term regulators |
|
|
Term
| Where are ''classical hormones'' from? |
|
Definition
|
|
Term
| What tissues are the main producer of hormones? Second? |
|
Definition
|
|
Term
| What are the chemical classes of hormones? Are they hydrophilic or lipophilic? |
|
Definition
| Peptide/Protein (Hydrophilic); Steroid (Lipophilic); Amines/Tyrosine-derived (Both); Eikosanoid (Hydrophilic) |
|
|
Term
| Name some peptide/protein hormones. |
|
Definition
| Pancreatic hormones, many Hypothalamic hormones, many Pituitary gland hormones, PTH |
|
|
Term
| Name some steroid hormones. |
|
Definition
| Adrenal cortex hormone, Reproductive hormones, D hormone |
|
|
Term
| Name some amines/tyrosine-derived hormones. Are the hydrophilic or lipophilic? |
|
Definition
| Thyroid hormones (Lipophilic); Dopamine, Melatonin, Epinephrine (Hydrophilic) |
|
|
Term
| Name some eikosanoid hormones. |
|
Definition
| Prostaglandins, Leukotrienes |
|
|
Term
| Eikosanoid hormones are ______, derived from _____. |
|
Definition
| Tissue hormones; arachidonic acid |
|
|
Term
| Eikosanoid hormones are largely produced by _____. |
|
Definition
|
|
Term
| What initiates protein hormone synthesis? Give an example. |
|
Definition
| Respective stimulus to an endocrine gland cell; Blood Glc levels stimulate insulin |
|
|
Term
| In protein hormone synthesis, what is initially produced? |
|
Definition
|
|
Term
| What happens to pre-pro-hormones (protein hormones)? |
|
Definition
| Pre & Pro sequences are cleaved off leaving the actual hormone |
|
|
Term
| Are pre & pro hormones active? |
|
Definition
|
|
Term
| Where are protein hormones stored? |
|
Definition
| Secretory granules (vesicles) |
|
|
Term
| When are protein hormones secreted? How? |
|
Definition
| Upon respective stimulation via exocytosis. |
|
|
Term
| Protein hormones are _____ produced, & ______ released. (Speed) |
|
Definition
|
|
Term
| How do protein hormones behave in plasma? |
|
Definition
|
|
Term
| What is the minimum time it takes to produce protein hormones? |
|
Definition
|
|
Term
| How long does it take to release protein hormones? |
|
Definition
|
|
Term
| How long does insulin release take upon elevation of blood Glc? |
|
Definition
|
|
Term
| What is the half-life of protein hormones? Why? |
|
Definition
| Short (few min); Quickly destroyed by plasma & renal proteases |
|
|
Term
| What are steroid hormones derived from? How? |
|
Definition
| Cholesterol (from diet or de novo synthesis) |
|
|
Term
| Describe steroid hormone synthesis. |
|
Definition
| Respective stimulus activates enzymes --> conversion of cholesterol to steroid hormone |
|
|
Term
| Steroid hormones are _____ produced, & ______ released. (Speed) |
|
Definition
|
|
Term
| How are steroid hormones stored? |
|
Definition
|
|
Term
| What is the significance of the lipophilic nature of steroid hormones? |
|
Definition
| Require transport proteins in plasma |
|
|
Term
| What is the active form of steroid hormones? What % are in this form? |
|
Definition
|
|
Term
| What is the inactive form of steroid hormones? |
|
Definition
| Bound (acts as a hormone reserve in plasma) |
|
|
Term
| What is the significance of protein binding for steroid hormones? |
|
Definition
| Protects against quick destruction in the liver --> Longer half-lives |
|
|
Term
| What is the approximate half life of steroid hormones? |
|
Definition
|
|
Term
| What % of steroid hormones are protein-bound? |
|
Definition
|
|
Term
| What is the ultimate fate of steroid hormones? |
|
Definition
| Degraded by liver; Conjugated to glucuronic acid & excreted in bile |
|
|
Term
| How do hormones affect their target tissues? |
|
Definition
| By 1st forming a Hormone-Receptor Complex, which alters the activity of their target cells |
|
|
Term
| What is the receptor location for hydrophilic hormones? |
|
Definition
| Cell membrane (can not diffuse through lipid membrane) |
|
|
Term
| What is the receptor location for lipophilic hormones? |
|
Definition
|
|
Term
| What are hormone receptors? |
|
Definition
| Large protein molecules consisting of several subunits |
|
|
Term
| Hormone receptors are _____ & have _____ for their hormone. |
|
Definition
| Highly specific; High affinity |
|
|
Term
| When does hormone effect end? |
|
Definition
| After dissociation from receptor, after internalization of R-hormone complex, or degradation |
|
|
Term
| Receptor #s per target cell can _____ = ______ |
|
Definition
| change; up or down-regulation |
|
|
Term
| How many hormone Rs does each cell have? |
|
Definition
|
|
Term
| What do synthetic hormones do? |
|
Definition
| Bind to the same hormone Rs & either block the hormone's original action (antagonists) or mimic the hormone's action (agonists) |
|
|
Term
| Persistent stimulus leads to ______. |
|
Definition
|
|
Term
| ______ control whether p'way active or not. They may be influenced by _____. |
|
Definition
|
|
Term
| Do lipophilic hormones diffuse through cell membranes into cells? |
|
Definition
|
|
Term
| How do lipophilic hormones diffuse into cells? |
|
Definition
| Down concentration gradient |
|
|
Term
| What do lipophilic hormones do after diffusing through the cm of a target cell? |
|
Definition
| Find, bind to & activate R |
|
|
Term
| Where are the target Rs of steroid hormones? |
|
Definition
|
|
Term
| Where are the target Rs of thyroid hormones? |
|
Definition
|
|
Term
| What does the activated lipophilic hormone-R complex do? |
|
Definition
| Translocates to nucleus & binds to a DNA acceptor site & initiates gene transcription; new proteins are synthesized |
|
|
Term
| Lipophilic hormones induce _____, w/ the newly formed ______ being mostly _____, which now stimulate or inhibit certain ______ = _____ |
|
Definition
| Protein synthesis; Proteins; Enzymes; Metabolic p'ways; Metabolic Effect |
|
|
Term
| Give an example of the metabolic effect. |
|
Definition
| Aldosterone (steroid) initiates synthesis of ATPase in target cells --> stimulates Na/K pumps |
|
|
Term
| Initiation of protein synthesis & actual production ______ --> ______. |
|
Definition
| Require time; Characteristic time delay of steroid hormone effects (45min - several hrs) |
|
|
Term
| What does activated G protein do? |
|
Definition
|
|
Term
| What is the first step of protein hormone target cell response? |
|
Definition
| Protein hormone binds to its R site in its target cell membrane, inducing a conformational change |
|
|
Term
| What happens after a protein hormone binds its R? |
|
Definition
| R binds w/ another R subunit = G-protein, & activates it |
|
|
Term
| What does Adenyl Cyclase do? |
|
Definition
|
|
Term
| What does cAMP increase do? |
|
Definition
| Activates a protein kinase, which phosphorylates other enzymes |
|
|
Term
| What does enzyme phosphorylation lead to? |
|
Definition
| Stimulation (typically), or inhibition of enzymes |
|
|
Term
| The first messenger (_____) remains ______, & transmits its message via ______ (2nd messenger). |
|
Definition
| Hormone; outside target cell; cAMP |
|
|
Term
| _______ Rs --> Stimulation mechanisms |
|
Definition
|
|
Term
| Protein hormones lead to a ________, at the end of which ______ are either stimulated or inhibited. |
|
Definition
| Chain rxn; enzymes (=metabolic p'ways) |
|
|
Term
| Give an example of a protein hormone stimulating a metabolic p'way. |
|
Definition
| Glucagon --> cAMP --> Phosphorylation of Phosphorylase --> Glycogenolysis |
|
|
Term
| Name some other 2nd messenger systems. |
|
Definition
| Calmodulin sms, Cell membrane phospholipid sms |
|
|
Term
|
Definition
|
|
Term
| Hormone effects are proportional to _______ |
|
Definition
|
|
Term
| Hormone concentrations need to be _________ |
|
Definition
|
|
Term
| What are most hormones controlled by? |
|
Definition
|
|
Term
| Outline a negative feedback loop. (General Outline) |
|
Definition
| Stimulus --> Hormone production/secretion --> Target Cell response --> Metabolic change --> Reduction of original stimulus |
|
|
Term
| Give an example of a negative feedback loop. |
|
Definition
| Effect of plasma Glc levels on Glucagon secretion |
|
|
Term
| Negative Feedback Loops are an example of _______ of hormone action. |
|
Definition
|
|
Term
| The pancreas has _____ & _____ functions. |
|
Definition
|
|
Term
| What is the endocrine pancreas? |
|
Definition
|
|
Term
| What does the endocrine pancreas consist of? |
|
Definition
| Alpha, Beta, Delta, & F/PP Cells |
|
|
Term
| Alpha cells of the pancreas are _____ sensitive. |
|
Definition
|
|
Term
| What do Alpha cells of the pancreas produce? |
|
Definition
|
|
Term
| What do Beta cells of the pancreas produce? |
|
Definition
|
|
Term
| What do Delta cells of the pancreas produce? |
|
Definition
|
|
Term
| What do F/PP cells of the pancreas produce? |
|
Definition
|
|
Term
| What type of hormone is insulin? |
|
Definition
|
|
Term
| Where is insulin stored? What does this entail? |
|
Definition
| Vesicles --> Fast response |
|
|
Term
| What happens after insulin secretion? |
|
Definition
|
|
Term
| What is the half life of insulin? |
|
Definition
|
|
Term
|
Definition
| In liver & kidneys by hepatic & renal peptidases |
|
|
Term
| What controls secretion of insulin? |
|
Definition
|
|
Term
| What is insulin associated with? |
|
Definition
| Energy abundance & storage of excess energy (= Anabolic Hormone) |
|
|
Term
| What stimulates insulin release? What inhibits it? (Blood Glc levels) |
|
Definition
|
|
Term
| What else mildly stimulates insulin release? |
|
Definition
| Increased plasma levels of aa |
|
|
Term
|
Definition
| Gastric Inhibitory Peptide |
|
|
Term
| What, besides blood Glc & aa, stimulates insulin release? What is this referred to as? |
|
Definition
| GI hormones (ex: GIP); ''Warming up'' |
|
|
Term
| What % of body cells contain insulin Rs? |
|
Definition
|
|
Term
| What tissues contain insulin Rs? |
|
Definition
| Insulin-sensitive/Glc-independent tissues |
|
|
Term
| What cells have no insulin Rs? |
|
Definition
| neurons, retina, lens, blood cells, pancreatic beta cells, kidney, GI mucosa, placenta (insulin-independent/Glc-dependent tissues) |
|
|
Term
| What happens after insulin-R binding? |
|
Definition
| Beta parts of R become the activated tyrosine kinase (sm) |
|
|
Term
| What does tyrosine kinase do? |
|
Definition
| Phosphorylates many enzymes in target cell (inhibition/stimulation of certain metabolic p'ways) |
|
|
Term
| What happens after tyrosine kinase phosphorylates enzymes? (wrt Insulin) |
|
Definition
| GLUTs translocate from Golgi fraction to cm; GLUTs fuse w/ membrane & facilitate diffusion of Glc into cells --> Glc uptake occurs |
|
|
Term
| What type of metabolism does insulin affect? |
|
Definition
| Protein; Carbohydrate; Lipid |
|
|
Term
| What type of hormone is Glucagon? |
|
Definition
| Peptide hormone (short, 29 aa) |
|
|
Term
| Where is Glucagon secreted? |
|
Definition
| Pancreatic alpha cells & stomach (gut Glucagon) |
|
|
Term
| What is the half-life of Glucagon? |
|
Definition
|
|
Term
| Glucagon opposes ______ effects on _____ in the _____. |
|
Definition
| Insulin; Carbohydrate metabolism; Liver |
|
|
Term
| How does insulin affect protein metabolism? |
|
Definition
Increases: aa uptake; protein synthesis
Decreases: Proteolysis |
|
|
Term
| How does insulin affect carbohydrate metabolism? |
|
Definition
Increases: Glc uptake; Glycolysis (ATP stores); Glycogenesis
Decreases: Gluconeogenesis |
|
|
Term
| How does insulin affect lipid metabolism? |
|
Definition
Increases: Uptake/Storage; Lipogenesis
Decreases: Lipolysis (HSL inhibited) |
|
|
Term
| In the presence of insulin, what happens to Glc? |
|
Definition
| Made available & used by all tissues for energy (oxidation); Blood Glc levels decline; Excess Glc channeled into storage as glycogen & fat |
|
|
Term
| What happens to protein synthesis in the presence of insulin? |
|
Definition
| Protein synthesis (growth) is stimulated [insulin is essential for normal growth] |
|
|
Term
| What is actively inhibited by insulin? |
|
Definition
| Gluconeogenesis; Proteolysis; Lipolysis |
|
|
Term
| What does Glucagon stimulate? |
|
Definition
| Hepatic Glycogenolysis & Gluconeogenesis; Lipolysis in fat tissue in very high concentrations |
|
|
Term
| What happens when Glucagon stimulates hepatic glycogenolysis? |
|
Definition
| Blood Glc levels can double w/i mins |
|
|
Term
| How does Glucagon stimulate hepatic gluconeogenesis? |
|
Definition
|
|
Term
| What does Glucagon do to blood Glc levels? |
|
Definition
| Increases (Combats hypoglycemia) |
|
|
Term
| With a protein diet, Insulin & Glucagon work _______. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| With a carbohydrate diet, insulin & glucagon work _____. |
|
Definition
|
|
Term
| What is the main signal for glucagon release? What is an additional signal? |
|
Definition
| Hypoglycemia; High plasma aa levels, but only when blood Glc levels are low |
|
|
Term
| What happens when high plasma aa levels stimulate Glucagon? |
|
Definition
| aa are channeled into gluconeogenesis |
|
|
Term
| How do high plasma Glc levels affect glucagon secretion? |
|
Definition
|
|
Term
| What are pancreatic alpha cells sensitive to? |
|
Definition
|
|
Term
| How does insulin affect pancreatic alpha cells? |
|
Definition
| high plasma Glc --> high insulin --> Glc uptake into alpha cells --> Glucagon secretion inhibited |
|
|
Term
| What is the definition of Diabetes Mellitus? |
|
Definition
| Absolute or relative lack of insulin leading to impaired carbohydrate, lipid, & protein metabolism |
|
|
Term
| What type of DM is most common in dogs? |
|
Definition
|
|
Term
| What type of DM is most common in cats? |
|
Definition
|
|
Term
| What is another name for Type I DM? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| What is the Tx for Type I DM? |
|
Definition
| Give Insulin; Renal/Pancreatic Transplant |
|
|
Term
| What are the causes of Type I DM? |
|
Definition
| Islet cell destruction b/o pancreatitis, senile degeneration, or autoimmune dz |
|
|
Term
| What is the state of Glc & I in Type I DM? |
|
Definition
| Constant Hyperglycemia w/ low circulating insulin levels |
|
|
Term
| What age group of dogs are most affected by Type I DM? |
|
Definition
|
|
Term
| What % of DM in cats is Type I? |
|
Definition
|
|
Term
| What is Type I DM in humans? What % of DM in humans is this type? |
|
Definition
| Juvenile form (autoimmune); 10-20% |
|
|
Term
| What is another name for Type II DM? |
|
Definition
|
|
Term
| What is the Tx for Type II DM? |
|
Definition
| Exercise, slow wt loss to prevent ketoacidosis, Overwhelm w/ daily insulin inj until situation reversed; Hypoglycemic drugs to increase insulin uptake |
|
|
Term
|
Definition
| Decreased sensitivity to insulin; Insulin Resistance; Relative lack of insulin |
|
|
Term
| What are some possible causes of Type II DM? |
|
Definition
| Decreased R #s; Changed Rs; Faulty Signal Transmission --> impaired binding or insulin action |
|
|
Term
| Beta cells respond to _____ & produce _____. |
|
Definition
|
|
Term
| In Type II DM, Hyperglycemia --> _____... |
|
Definition
| Constant insulin release --> Hyperinsulinemia --> eventually B cells become exhausted --> insulin levels can return to or fall below normal levels |
|
|
Term
| In end-stage Type II DM, what is the dz similar to? |
|
Definition
|
|
Term
| What is often a predisposing factor of Type II DM? |
|
Definition
| Obesity (via lipid metabolites?) |
|
|
Term
| Is Type II DM reversible? |
|
Definition
| Can be (via loss of body wt) if B cells are still producing insulin |
|
|
Term
| What % of DM in cats is Type II? |
|
Definition
|
|
Term
| What % of DM in humans is type II? |
|
Definition
|
|
Term
| What are some other names for Type III DM? |
|
Definition
|
|
Term
| What age group of cats are most affected by Type II DM? What sex? |
|
Definition
|
|
Term
| Is Type III DM common in vet med? Is it reversible? |
|
Definition
|
|
Term
| What is Type III DM secondary to? |
|
Definition
| excess cortisol, GH, Progesterone levels causing insulin-resistance a/o activated gluconeogenesis |
|
|
Term
| How is Type III DM treated? |
|
Definition
|
|
Term
| What syndrome is caused by excess Cortisol? |
|
Definition
|
|
Term
| What is the pathophysiology of DM? |
|
Definition
| Absolute/Relative lack of insulin --> Absolute/Relative excess of Glucagon (Glucagon cells are insulin-sensitive) --> Catabolic Situation |
|
|
Term
| What is the catabolic situation caused by DM? |
|
Definition
| Persistent hyperglycemia b/c of reduced cellular Glc uptake & increased gluconeogenesis; Reduced glycogenesis & protein synthesis; increased lipolysis & proteolysis |
|
|
Term
| What causes increased lipolysis in DM? |
|
Definition
| Lack of insulin/presence of glucagon activates HSL |
|
|
Term
| What age group of cats are most affected by Type I DM? |
|
Definition
|
|
Term
| What are some problems caused by DM? |
|
Definition
| Hyperosmolality of plasma; Lipolysis exceeds energy demands; Glc-dep tissues get too much Glc |
|
|
Term
| What causes polyuria in DM? |
|
Definition
| Hyperglycemia --> exceed renal threshold --> Glucosuria/osmotic diuresis = Polyuria |
|
|
Term
| What causes polydipsia in DM? |
|
Definition
| Hyperosmolality & polyuria --> IC & EC dehydration --> possibly hypovolemic shock/CNS damage/anuria/coma/death; compensation by drinking |
|
|
Term
| What causes proteolysis & lipolysis in DM? |
|
Definition
| Lack of insulin stimulates proteolytic & lipolytic (HSL) enzymes |
|
|
Term
| What are the effects of proteolysis in DM? |
|
Definition
| Weight loss, m. weakness, reduction of organ functions |
|
|
Term
| What are the effects of excessive lipolysis in DM? |
|
Definition
| Fatty Liver & Ketoacidosis --> Diabetic Coma |
|
|
Term
| What causes polyphagia in DM? |
|
Definition
| Initially only as hypothalamic satiety center is insulin-dependent; later anorexia & vomiting following tissue damages a/o acidosis |
|
|
Term
| What happens to Glc-dep cells with long-standing hyperglycemia? |
|
Definition
| Excess Glc enters Glc-dep cells --> Formation of glycated proteins (defective Hb A, defective myelin in n. sheaths, fructosamines in plasma) |
|
|
Term
| With longstanding hyperglycemia, what is excess Glc converted to? |
|
Definition
| Sorbitol --> Osmotically active --> Swelling --> Cataracts/Lens & n. damage |
|
|
Term
| With longstanding hyperglycemia, what is the importance of glycated proteins/acidosis/proteolysis/swelling? |
|
Definition
| structural changes in blood vessels & nn; microangiopathies & neuropathies (glomerula; tibial n. in cats; retina in humans) |
|
|
Term
| What are animals prone to after longstanding hyperglycemia? |
|
Definition
|
|
Term
| How long after hyperglycemia does HbA become glycated, leading to anemia? |
|
Definition
|
|
Term
| What are fructosamines? How long after hyperglycemia do they appear in blood? |
|
Definition
| PP (Albumin) + Glc; >2wks |
|
|
Term
| What is the reabsorption threshold of Glc in the kidneys? |
|
Definition
|
|
Term
| What is a major integrating link btw the nervous & endocrine systems? |
|
Definition
|
|
Term
| What does the hypothalamus receive input from? |
|
Definition
| various other CNS regions (thalamus, limbic system, cortex, RAS, sensory signals from viscera & eye) |
|
|
Term
| What does the hypothalamus largely control? |
|
Definition
| Homeostasis (Osmolality, Body Temperature) & ANS |
|
|
Term
| What else is the hypothalamus involved in? |
|
Definition
| Emotions, Stress, Fear, Control of hunger & satiety, Thirst, Sexual Behavior |
|
|
Term
| The hypothalamus is a ''_____'' |
|
Definition
|
|
Term
| The many _____ of the hypothalamus influence _____ as well as _____ via _____. |
|
Definition
| Neuroendocrines; other CNS areas; various peripheral endocrine glands; Pituitary gland |
|
|
Term
| What connects the hypothalamus to the pituitary gland? |
|
Definition
|
|
Term
| What does the pituitary gland consist of? |
|
Definition
| Anterior pituitary (Adenohypophysis), Posterior Pituitary (Neurohypophysis), & Pars intermedia |
|
|
Term
| In what animals is the pars intermedia of the pituitary important? What is its function? |
|
Definition
| Reptiles & Amphibians; MSH --> Body coloration/pigmentation |
|
|
Term
| Describe the Anterior Pituitary. |
|
Definition
| Formed by Rathke's Pouch; Glandular epithelium; produces & secretes hormones under hypothalamic control |
|
|
Term
| Describe the posterior pituitary. |
|
Definition
| Extension of the hypothalamus; Nervous tissue; Stores & releases the 2 hypothalamic hormones produced in the Nucleus Supraopticus & Nucleus Paraventricularis (ADH & Oxytocin) |
|
|
Term
| What does the Hypothalamic-Pituitary System involve? What is the term for these 3 structures together? |
|
Definition
| Hypothalamus, Anterior Pituitary Gland, Peripheral Endocrine Glands; Hypothalamic-Pituitary-Endocrine Axis |
|
|
Term
| What does the hypothalamus produce & secrete upon stimulation? |
|
Definition
| Releasing Hormones a/o Inhibiting Hormones into hypothalamic-hypophyseal portal system --> reach the anterior pituitary gland |
|
|
Term
| What does the anterior pituitary gland produce & secrete? |
|
Definition
| RHs/IHs stimulate/inhibit the production & release of hormones into circulation (mostly Tropic hormones) |
|
|
Term
| What do the peripheral endocrine glands produce & secrete? |
|
Definition
| Tropic hormones stimulate peripheral endocrine glands to produce/release their own hormones |
|
|
Term
|
Definition
| Stimulating an endocrine gland to release a hormone; Stimulating growth |
|
|
Term
| How many levels of control/negative feedback are in the Hypothalamic-Pituitary systems? |
|
Definition
|
|
Term
|
Definition
| Thyrotropin Releasing Hormone |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| Growth Hormone IH (Somatostatin) |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| TRH is secreted by _____, causing release of ______ from the anterior pituitary, followed by _____ from the ______. |
|
Definition
| Hypothalamus; TSH; Thyroid Hormones; Thyroid Gland |
|
|
Term
| CRH is secreted by Hypothalamus, causing release of ______ from the anterior pituitary, followed by _____ from the ______. |
|
Definition
| ACTH; Glucocorticoids; Adrenal Cortex |
|
|
Term
| GnRH is secreted by Hypothalamus, causing release of ______ from the anterior pituitary, followed by _____ from the ______. |
|
Definition
| FSH & LH; Sex Hormones; Gonads |
|
|
Term
| GHRH is secreted by Hypothalamus, causing release of ______ from the anterior pituitary, followed by _____ from the ______. |
|
Definition
|
|
Term
| What tissues are targeted by Thyroid hormones? |
|
Definition
|
|
Term
| What tissues are targeted by Glucocorticoids? |
|
Definition
|
|
Term
| What tissues are targeted by Sex hormones? |
|
Definition
|
|
Term
| What tissues are targeted by Somatomedins? |
|
Definition
|
|
Term
| What tissues are targeted by Prolactin? |
|
Definition
|
|
Term
| What type of effects do thyroid hormones have on their target tissues? |
|
Definition
|
|
Term
|
Definition
| Thyroid Stimulating Hormone; Thyrotropin |
|
|
Term
|
Definition
| Adrenocorticotropic Hormone; Corticotropin |
|
|
Term
|
Definition
| Follicle Stimulating Hormone |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Somatotropic Hormone; Somatotropin; Growth Hormone |
|
|
Term
| What are the types of effects of GH? |
|
Definition
| Direct Effects & Release of Somatomedins from Liver |
|
|
Term
| What are the effects of prolactin? |
|
Definition
| Direct effects on Mammary Gland |
|
|
Term
| What does thyroid tissue consist of? |
|
Definition
|
|
Term
| What does a follicle consist of? |
|
Definition
| Thyroid cells in single layer = hormone producing cells; Colloid = hormone storage form |
|
|
Term
| What does the height of thyroid cell layer indicate? |
|
Definition
|
|
Term
| What is the final stage of thyroid hormone synthesis? |
|
Definition
|
|
Term
| What are thyroid hormones derived from? |
|
Definition
|
|
Term
| What is the 1st step of thyroid hormone synthesis? |
|
Definition
| Iodide uptake into thyroid cell via active pump |
|
|
Term
| (Thyroid Hormone Synthesis/Release) What happens after iodide uptake into thyroid cells? |
|
Definition
| Synthesis & Exocytosis of TGB |
|
|
Term
|
Definition
|
|
Term
| How many tyrosine aa does TGB contain? |
|
Definition
|
|
Term
| (Thyroid Hormone Synthesis/Release) What happens after exocytosis of TGB? |
|
Definition
| Oxidation of iodide to iodine via peroxidases & secretion into colloid |
|
|
Term
| (Thyroid Hormone Synthesis/Release) What happens after secretion of iodine into colloid? |
|
Definition
| Iodination of tyrosines w/i TGB via iodinase; Formation of T1 & T2 |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| (Thyroid Hormone Synthesis/Release) What happens after formation of T1/T2? |
|
Definition
| Condensation of T1 & T2 to T3 & T4 = storage form containing ~30 T4 & few T3 |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Tetraiodotyrosine (Thyroxine) |
|
|
Term
| (Thyroid Hormone Synthesis/Release) What happens after condensation to T3/T4? |
|
Definition
| Endocytosis of TGB & proteolytic cleaving via lysosomal enzymes |
|
|
Term
| (Thyroid Hormone Synthesis/Release) What happens after endocytosis of TGB & proteolytic cleaving? |
|
Definition
| Release of T4 & T3 into circulation |
|
|
Term
| What % of T3/4 released into circulation is each? |
|
Definition
|
|
Term
| (Thyroid Hormone Synthesis/Release) What happens after release of T3/T4 into circulation? |
|
Definition
| Binding of lipophilic T4 & T3 to PP (~99%) (eg. Thyroxine-binding protein [& albumin]) |
|
|
Term
| What is the half-life of T4 in dogs? Humans? |
|
Definition
|
|
Term
| What happens to T1, T2, & TGB? What happens to iodine & aa? |
|
Definition
| Remain w/i thyroid cell; Recycled |
|
|
Term
| In condensation to T3 & T4, how are T1 & T2 linked? |
|
Definition
| Via O2 (Coupling process) |
|
|
Term
| What are thyroid hormones controlled by? |
|
Definition
| Hypothalamic-Pituitary-Thyroid Axis |
|
|
Term
| What stimulates/inhibits Hypothalamic TRH release? |
|
Definition
|
|
Term
|
Definition
| Anterior pituitary to synthesize & secrete TSH |
|
|
Term
|
Definition
| Thyroid gland to synthesize & secrete thyroid hormones |
|
|
Term
| How does TSH stimulate the thyroid to synthesize & secrete TH? |
|
Definition
| Stimulation of: iodide pump, iodination of tyrosine, TGB proteolysis, Growth of thyroid cells (can lead to gland enlargement) |
|
|
Term
| What do increased levels of circulating TH do? |
|
Definition
| Inhibit further release of TSH by decreasing TRH receptor # |
|
|
Term
| How are thyroid hormones regulated? |
|
Definition
| Well-regulated; Nearly constant T3/4 levels; Influenced by ambient temperatures |
|
|
Term
|
Definition
| Low levels (looks like hypothyroid), but normal thyroid function |
|
|
Term
| What type of aa is tyrosine? |
|
Definition
|
|
Term
| Are T3/T4 hydrophilic or lipophilic? |
|
Definition
| Lipophilic (diffuse into target cells) |
|
|
Term
|
Definition
| Converted to T3 (active hormone) |
|
|
Term
| What does T3 bind to? What does it do? |
|
Definition
| Nuclear receptors (chromatin); activates transcription of many genes in virtually all tissues |
|
|
Term
| What does activation of transcription by T3 do? |
|
Definition
| Stimulation of synthesis of many enzymes, structural & transport proteins; Generalized increase of many metabolic activities in many tissues |
|
|
Term
| What is T3 deactivated by? |
|
Definition
| Peripheral tissue de-iodinases; Excreted via liver after conjugation w/ glucuronic acid --> diiodothyronine |
|
|
Term
| Is T3 or T4 more dominant in plasma? |
|
Definition
|
|
Term
| What do thyroid hormones regulate? |
|
Definition
| Basic metabolic activity of most tissues; ensure that energy is available |
|
|
Term
|
Definition
| Yes (In adults w/ excess TH) |
|
|
Term
| How does increased TH affect carbohydrate metabolism? |
|
Definition
| Increases: Glc absorption/uptake, Glc utilization for energy, Glc production; Geared toward supplying Glc for energy |
|
|
Term
| How does increased TH affect basal metabolism? |
|
Definition
| Increases: Metabolic rate, Nutrient utilization, ATP formation, Oxygen consumption, Heat production |
|
|
Term
| How does increased TH affect lipid metabolism? |
|
Definition
| Increases: Lipolysis, Beta oxidation, Bile secretion (Lowers blood cholesterol); Geared toward supplying fat for energy |
|
|
Term
| How does increased TH affect protein metabolism? |
|
Definition
| Normal growth depends on TH (Protein Anabolic) |
|
|
Term
| Does TH stimulate gluconeogenesis? |
|
Definition
|
|
Term
| How does TH exert its lipid metabolism effects? |
|
Definition
|
|
Term
| How do TH levels relate to blood cholesterol levels? |
|
Definition
|
|
Term
| What is the main "accelerator" of the body? |
|
Definition
|
|
Term
| How does TH excess affect CNS? |
|
Definition
| Increases rapidity of cerebration; dissociation --> Nervousness, excitability, anxiety, insomnia |
|
|
Term
| How does TH deficit affect CNS? |
|
Definition
|
|
Term
| How does TH deficit affect Skin? |
|
Definition
| Follicle atrophy --> Bilateral alopecia, Myxedema, Pigmentation |
|
|
Term
| How does TH excess affect Circulatory & Respiratory system? |
|
Definition
| Tachycardia, Hypertension, Tachypnea (via increased metabolism & enhanced beta receptor excitability) |
|
|
Term
| TH Excess: _____; Deficiency: _____ |
|
Definition
| Everything is stimulated; Everything slows down |
|
|
Term
| How does TH excess affect Growth & body weight in young animals? |
|
Definition
| accelerates growth, but epiphyses close early --> stunted/heavy body |
|
|
Term
| How does TH deficiency affect Growth & body weight in young animals? |
|
Definition
| retards CNS & body growth --> cretinism |
|
|
Term
| How does TH excess affect Growth & body weight in adult animals? |
|
Definition
|
|
Term
| How does TH deficiency affect Growth & body weight in adult animals? |
|
Definition
|
|
Term
| What is the most common endocrinological disorder of cats? |
|
Definition
| Hyperthyroidism (37% have tumors) |
|
|
Term
| What is the definition of hyperthyroidism? |
|
Definition
| Excessive secretion of TH |
|
|
Term
| What species is affected by Hyperthyroidism? |
|
Definition
| common in middle-aged/old cats; rare in other spp. |
|
|
Term
| What are the causes of hyperthyroidism? |
|
Definition
| Mostly benign thyroid tumors secreting T4/T3 (Adenomas); Sometimes lung tumors |
|
|
Term
| What causes hyperthyroidism in humans? |
|
Definition
| Autoimmune dz; Ab's w/ TSH effect |
|
|
Term
| What is the definition of hypothyroidism? |
|
Definition
| Insufficient production/secretion of TH |
|
|
Term
| What species does hypothyroidism affect? |
|
Definition
| Common in middle-aged/old dogs; rare in other spp |
|
|
Term
| What causes hypothyroidism? |
|
Definition
| Mostly defects of the thyroid gland (autoimmune, lymphocytic infiltration or idiopathic atrophy) |
|
|
Term
| How do CS of hyperthyroidism progress? |
|
Definition
|
|
Term
| What happens to metabolism/functions in hyperthyroidism? |
|
Definition
| Accelerated in all organs |
|
|
Term
| What are some CS of hyperthyroidism? |
|
Definition
| Wt loss, m. weakness & wasting, mild fatty liver syndrome, normal/increased appetite, hyperactivity, nervousness, anxiety, 10% of cats are apathetic, heat intolerance, increased skin temp, tachycardia, hypertension --> retinal detachment, diarrhea, PU/PD (b/o medullary washout), skin changes (matted hair or alopecia b/o behavioral changes) |
|
|
Term
| Comment on CS of hypothyroidism |
|
Definition
| Variable d/o degree of reduction of metabolic rate |
|
|
Term
| What some CS of hypothyroidism? |
|
Definition
| Skin alterations: Dry skin, Alopecia, Flaking or Seborrhea, Pigmentation; Myxedema; Reproductive dysfunction; Rat Tail & Tragic Face |
|
|
Term
| What happens to metabolism/functions in hypothyroidism? |
|
Definition
|
|
Term
|
Definition
| Accumulation of hyaluronic acid in face & tail (sometimes in nn) |
|
|
Term
| What is another name for Goiter? |
|
Definition
|
|
Term
|
Definition
| Non-neoplastic hyperplasia of thyroid gland |
|
|
Term
|
Definition
| Dietary iodide deficiency; Goitrogenic substances --> conversion to goitrin in GI tract--> interferes w/ iodine pump |
|
|
Term
| What are some goitrogenic substances? |
|
Definition
| Progoitin in soybeans, cabbage, rapeseed |
|
|
Term
| Describe the pathogenesis of goiter. |
|
Definition
| Iodine deficiency --> TH decrease --> stimulates TRH & TSH release --> Stimulates thyroid cell growth --> Gland enlargement = compensatory gland hyperplasia |
|
|
Term
| What spp are affected by goiter? |
|
Definition
| Formerly a common disorder in all spp in iodine deficient areas; b/c of dietary supplementation, rare nowadays; seen in birds & occasionally lg animals; reptiles |
|
|
Term
|
Definition
| mild hypothyroidism or adequate compensation; offspring of affected animals can be stillborn or develop severe hypothyroidism (cretinism, retarded growth) |
|
|
Term
| What type of hormone is GH? |
|
Definition
| Anterior pituitary protein hormone produced by acidophils |
|
|
Term
| What tissues are affected by GH? |
|
Definition
| Nearly all tissues capable of growth (Hyperplastic & Hypertrophic) |
|
|
Term
|
Definition
| A tropic hormone: stimulates liver to produce somatomedins (or insulin-like growth factor) |
|
|
Term
| How are effects of GH achieved? |
|
Definition
|
|
Term
| Hyperplasia vs. Hypertrophia |
|
Definition
| Increased cell #; Increased cell size |
|
|
Term
| What are the metabolic effects of GH? |
|
Definition
| Promotion of growth via stimulation of protein synthesis (ip, during adolescent phase); Increases fat utilization/mobilization; Decreases Glc utilization |
|
|
Term
| What does GH force the body to do? |
|
Definition
| Use lipids for energy by reducing Glc availability |
|
|
Term
| What are the physical consequences of GH? |
|
Definition
| Increase in: lean body mass (protein); organ size/functions; linear body growth (before sexual maturity); bone thickness (after sexual maturity/closure of long bone epiphyses) |
|
|
Term
| What are the direct effects of GH? |
|
Definition
| Lipolytic; Glc sparing; Insulin-resistance (diabetogenic) |
|
|
Term
| What are the indirect effects of GH? |
|
Definition
| (Via Hepatic IGF) Protein anabolic (m., bone, liver); Increased aa uptake, DNA/RNA synthesis, protein synthesis, mitotic rates |
|
|
Term
| What is the relationship btw body size & amt of somatomedin? |
|
Definition
|
|
Term
| What is GH secretion controlled by? |
|
Definition
| Hypothalamic GHRH & GHIH (what stimulates this is unknown) |
|
|
Term
| What stimulates GH release in dogs & cats? (Clinically relevant) |
|
Definition
|
|
Term
| When in life is GH produced? |
|
Definition
| Life-long production of GH, decreases in old age --> mitotic tissues are not maintained --> tissue aging |
|
|
Term
| What is an additional effect of GH in ruminants? |
|
Definition
|
|
Term
| What are 2 results of GH deficiency? |
|
Definition
|
|
Term
|
Definition
| Inherited deficiency of GH a/o somatomedins |
|
|
Term
| Does GH deficiency affect the brain? Does TH deficiency? |
|
Definition
|
|
Term
|
Definition
| GH deficiency later in life, caused by damage to pituitary cells (tumor, hemorrhage, radiation) |
|
|
Term
| What results from GH excess before sexual maturity? |
|
Definition
| True Gigantism (very rare) |
|
|
Term
| What results from excess GH after sexual maturity? |
|
Definition
| Acromegaly cause by GH producing tumors in the pituitary gland (cats) or continuously high progesterone levels (dogs) |
|
|
Term
| What are signs of acromegaly? |
|
Definition
| Increased bone/cartilage growth (face, jts), Cardiac hypertrophy, Secondary DM |
|
|
Term
| What are the adrenal glands? |
|
Definition
| Paired glands at the Cr kidney poles |
|
|
Term
| What are the parts of the adrenal gland? |
|
Definition
|
|
Term
| What does the adrenal cortex produce? |
|
Definition
| >30 steroid hormones = adrenocortical hormones |
|
|
Term
| What is the adrenal medulla related to? What does it secrete? |
|
Definition
| SNS; Catecholamines (epi & nore) |
|
|
Term
| Which cortical zone of the adrenal gland releases mineralocorticoids? (%?) |
|
Definition
| Zona Glomerulosa (90%: Aldosterone) |
|
|
Term
| Which cortical zone of the adrenal gland releases Glucocorticoids? (%?) |
|
Definition
| Zona fasciculata (95%: Cortisol) |
|
|
Term
| Which cortical zone of the adrenal gland releases androgens? |
|
Definition
|
|
Term
| What is released by the medulla of the adrenal gland? |
|
Definition
|
|
Term
| Each cortical zone of the adrenal gland is controlled by ______. |
|
Definition
|
|
Term
| Which group of adrenal cortex members exhibit cross-activity? |
|
Definition
| Mineralocorticoids & Glucocorticoids |
|
|
Term
| What are mineralocorticoids & glucocorticoids derived from? |
|
Definition
|
|
Term
| How do exogenous glucocorticoids cross-react with mineralocorticoids compared to endogenous ones? |
|
Definition
| Less cross-activity and SEs |
|
|
Term
| Cortisol is a _____ hormone. |
|
Definition
|
|
Term
| In addition to stress, what stimulates cortisol? |
|
Definition
| Epi, Histamine, Pyrogens, Pain, Hypoglycemia (metabolic stress) |
|
|
Term
| What does stress stimulate? |
|
Definition
| Hypothalamus to release Corticotropin RH |
|
|
Term
|
Definition
| Release of ACTH from anterior pituitary |
|
|
Term
| What does ACTH stimulate? |
|
Definition
| Release of cortisol (& androgens) |
|
|
Term
| What does cortisol exert? |
|
Definition
| Neg fdbk on CRH & ACTH release |
|
|
Term
| Besides stress-related release, what do ACTH & Cortisol secretion follow? |
|
Definition
| Circadian rhythm: Highest conc seen during animal's activity phase (diurnal dog/nocturnal cat) |
|
|
Term
| When do dogs have highest cortisol levels? Cats? |
|
Definition
|
|
Term
| What type of hormones are glucocorticoids? |
|
Definition
| Stress hormones: provide fuel (Glc) in times of need to vital tissues |
|
|
Term
| What are the anabolic effects of glucocorticoids? |
|
Definition
| (Liver) Increased: Gluconeogenesis (from aa), Glycogenesis, Plasma Glc, aa uptake, protein synthesis, KBs & VLDLs |
|
|
Term
| Comment on glycogenesis from glucocorticoids. |
|
Definition
| Prereq for glucagon's glycogenolytic effects |
|
|
Term
| How much does gluconeogenesis exceed normal levels in long-standing stress? |
|
Definition
|
|
Term
| What are the catabolic effects of Glucocorticoids? |
|
Definition
(Extra-hepatic tissue) Decreased: Glc uptake/metabolism (in m. & fat tissue = anti-I effect); Proteolysis
Increased: Lipolysis (redistribution of fat to the abd) |
|
|
Term
| Which fat cells do not respond to cortisol? |
|
Definition
|
|
Term
| What are the effects of increased glucocorticoids on the liver? |
|
Definition
| Increased: size/wt (Glycogen & fat), KB & VLDL |
|
|
Term
| What are the effects of increased glucocorticoids on the mm? |
|
Definition
|
|
Term
| What are the effects of increased glucocorticoids on the CT? |
|
Definition
|
|
Term
| What are the effects of increased glucocorticoids on the fat tissue? |
|
Definition
| Decreased fat tissue/Redistribution |
|
|
Term
| What are the effects of increased glucocorticoids on the bone matrix? |
|
Definition
|
|
Term
| What are the effects of increased glucocorticoids on the GI? |
|
Definition
Increased: Appetite, Stomach HCl
Decreased: Mucus production |
|
|
Term
| What are the effects of increased glucocorticoids on the blood Glc? |
|
Definition
| Hyperglycemia; Steroid diabetes |
|
|
Term
| What are the effects of increased glucocorticoids on the CNS/Pituitary? |
|
Definition
| Decreased: ACTH, ADH, TSH, GH, FSH/LH |
|
|
Term
| What are the effects of increased glucocorticoids on inflammation? |
|
Definition
| Strong anti-inflammatory effects |
|
|
Term
| What are the effects of increased glucocorticoids on the hematology? |
|
Definition
Increased: RBCs, Neutrophils
Decreased: Lymphocytes, Eosinophils, Lymph Tissue |
|
|
Term
| What is a stress leukogram? When is it seen? |
|
Definition
| Neutrophilia + Lymphopenia; Increased Glucocorticoids |
|
|
Term
| What are among the most important (& misused) drugs in vet med? |
|
Definition
|
|
Term
| What is inflammation caused by? |
|
Definition
| Tissue damage & release of inflammatory mediators |
|
|
Term
| What are the 4 cardinal signs of inflammation? |
|
Definition
| Pain, Swelling, Redness, Pus |
|
|
Term
| Glucocorticoids prevent release of _________ |
|
Definition
| Inflammatory mediators (e.g., from lysosomes, macs, monocytes) |
|
|
Term
| What do glucocorticoids do to inflammation? How? |
|
Definition
| Reduce/Prevent it & resolve existing inflammations, probably by deactivating inflammatory mediators = physiological controller of inflammatory processes |
|
|
Term
| How does inflammation affect dairy cows? |
|
Definition
|
|
Term
| What are the long-term effects of glucocorticoids? |
|
Definition
| Depression of: Lymphocyte proliferation, Ab production/immunity, Collagen Synthesis/Wound healing; Atrophy of lymphatic tissue |
|
|
Term
| Which lymphocytes are most decreased by glucocorticoids? |
|
Definition
|
|
Term
| What is the pre-pro-hormone of ACTH? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| The cleaving of POMC gives rise to ______. |
|
Definition
| Several active polypeptides |
|
|
Term
| What polypeptides are formed by cleavage of POMC? |
|
Definition
| a-MSH; B-Endorphin; CLIP; ACTH |
|
|
Term
| What is MSH & what is its action? |
|
Definition
| Melanocyte Stimulating Hormone; Darkening of skin/mucosa |
|
|
Term
| What is the function of B-Endorphin? |
|
Definition
| Analgesic Opioid, Modulates pain perception & affective behavior |
|
|
Term
|
Definition
| Corticotropin-Like Intermediate Peptide |
|
|
Term
| What is the function of CLIP? |
|
Definition
| Probably little physiological function, but pathological effects in horses |
|
|
Term
|
Definition
| Controls release of Cortisol; Crucial to maintain viability of the entire adrenal cortex |
|
|
Term
| What hormone is crucial to maintain the viability of the entire adrenal cortex? |
|
Definition
|
|
Term
| Disorders of ACTH production can affect _______. |
|
Definition
|
|
Term
| What do longstanding exogenous/endogenous cortisol levels lead to? |
|
Definition
| Atrophy of the Adrenal Cortex through suppression of ACTH secretion --> may impair secretion of Gluco- & Mineralocorticoids |
|
|
Term
| What does Cortisol exert neg fdbk on? |
|
Definition
|
|
Term
| What is another name for Hyperadrenocorticism? |
|
Definition
|
|
Term
| What is the definition of Hyperadrenocorticism/Cushing's Syndrome? |
|
Definition
| Excess of Glucocorticoids |
|
|
Term
| What are the causes of Cushing's? |
|
Definition
| Adenomas of adrenal glands (rare); Adenomas of ant. pit. (common); Iatrogenic; Pit Pars Intermedia tumors in horses |
|
|
Term
| What do adenomas of the adrenal glands cause? |
|
Definition
| Excess Cortisol (Cushing's) |
|
|
Term
| What do Adenomas of the ant pit cause? |
|
Definition
| Excess ACTH --> Cortisol (Cushing's) |
|
|
Term
| What is the iatrogenic cause of Cushing's? |
|
Definition
| Prolonged glucocorticoid therapy |
|
|
Term
| What do tumors of the pit Pars Intermedia produce? |
|
Definition
| POMC (MSH, B-endorphin, CLIP, very little ACTH) |
|
|
Term
| What does CLIP do in horses w/ pit Pars Intermedia tumors? |
|
Definition
| Increases ACTH efficiency sixfold |
|
|
Term
| What is the predilection of Cushing's/Hyperadrenocorticism? |
|
Definition
| Common in middle-aged to old dogs (boxer, poodle, terrier, dachshund); 90% PDH; Middle-aged/old horses (ponies>horses); Very rare in cats |
|
|
Term
|
Definition
| Pituitary-Dependent Hyperadrenocorticism |
|
|
Term
| How do the CS of Cushing's differ b/o whether the cause is central or peripheral? |
|
Definition
|
|
Term
| What are the 3 metabolic components of the pathophysiology of Cushing's? |
|
Definition
| Increased Proteolysis & Lipolysis; Increased Gluconeogenesis --> Hyperglycemia |
|
|
Term
| What is the effect of increased proteolysis in Cushing's? |
|
Definition
| m. atrophy, weakness, lethargy, osteoporosis, reduced collagen (thin skin), bilateral hair loss/dogs, slow hair shedding/horses (Hirsutism), discoloration/bleaching of hair/dogs |
|
|
Term
| What is the strongest stimulator of gluconeogenesis? |
|
Definition
|
|
Term
| What are the effects of increased lipolysis in Cushing's? |
|
Definition
| Fat redistribution; Hepatomegaly, enlarged abdomen + weakened abd mm. --> Potbelly |
|
|
Term
| What are the effects of hyperglycemia in Cushing's? |
|
Definition
| Hyperglycemia + insulin release --> Steroid Diabetes --> PU/PD (often ''prediabetic'') |
|
|
Term
| In Cushing's, what can Cortisol also be caused by? |
|
Definition
| Compression of post pit --> lack of ADH, or inhibition of ADH Rs |
|
|
Term
| What are some other CS of Cushing's? |
|
Definition
| Immunodepression, Polyphagia, Pit Gland Depression (TSH, FSH, LH, GH) --> Panhypopituitarism, Behavioral changes (docility in horses caused by endorphins), Gastric Ulcers, Hyperpigmentation of mucus membranes if ACTH is increased |
|
|
Term
| What is different about Cushing's compared to DM? |
|
Definition
| Skin effects; No wt loss despite lipolysis b/c polyphagia & redist. of fat |
|
|
Term
|
Definition
| Surgical removal of tumors (difficult); Suppression of adrenocortex w/ mitotane (=DDD insecticide) |
|
|
Term
|
Definition
| Poisons adrenal cortex, Decreases hormone prod, Destroys GC producing cells 1st, then MC producing cells |
|
|
Term
| Is Hyperadrenocorticism/Cushing's reversible? |
|
Definition
|
|
Term
| What are some additional CS of Cushing's in humans? |
|
Definition
|
|
Term
| In which type of Cushing's will ACTH not respond to the neg fdbk of Cortisol? |
|
Definition
|
|
Term
| What is the main stimulus of Aldosterone? What are other stimuli? |
|
Definition
| Hypovolemia --> Renin-Angiotensin-Aldosterone; Hyperkalemia, Hyponatremia (moderately) |
|
|
Term
| What is the function of renin? |
|
Definition
| Converts angiotensinogen to Angiotensin I |
|
|
Term
|
Definition
|
|
Term
| Where does angiotensinogen come from? |
|
Definition
|
|
Term
|
Definition
| Converts Angiotensin I to Angiotensin II in lung |
|
|
Term
|
Definition
| Angiotensin Converting Enzyme |
|
|
Term
| What is Angiotensin II converted into? Where? |
|
Definition
| Aldosterone; Adrenal Cortex |
|
|
Term
| Aldosterone is a _____ saver & _____ loser. |
|
Definition
|
|
Term
| How is Aldosterone a ''sodium saver?'' |
|
Definition
| (in kidney) hypovolemia --> Aldosterone release; Increases Na absorption (via Na/K pump) & increases osmotic absorption of water; Na & water are retained; Plasma Na concentration unchanged, but ECF increases --> Normovolemia |
|
|
Term
| How is Aldosterone a K/H Loser? |
|
Definition
| Stimulates renal K excretion via Na/K pump; Stimulates renal H excretion via Na/H exchanger |
|
|
Term
| What other systems is Aldosterone involved in? |
|
Definition
| Increased Na absorption/K secretion in sweat glands, salivary glands, intestines |
|
|
Term
| What is another name for Hypoadrenocorticism? |
|
Definition
|
|
Term
| What is Hypoadrenocorticism/Addison's Dz? |
|
Definition
| Deficiency in adrenal cortex hormones --> GCs (1st) & MCs (later) are reduced |
|
|
Term
| What is excessive/uncontrolled aldosterone secretion? |
|
Definition
|
|
Term
| What causes hyperaldosteronism? |
|
Definition
| Any condition that leads to chronic hypovolemia; Most often seen w/ renal dz/PU --> cont'd stim of renin-angiotensin sys |
|
|
Term
| What is the pathogenesis of Hyperaldosteronism wrt excessive aldosterone release? |
|
Definition
| Excessive Aldosterone release --> continuously increased Na & water retention --> Hypervolemia (inc ECF) --> inc arterial P --> P diuresis --> Na & H2O excretion inc --> intravascular fluid V remains slightly above normal & animal develops permanent hypertension (''renal hypertension'') |
|
|
Term
| In what spp is ''renal hypertension'' very common? |
|
Definition
|
|
Term
| What is the pathogenesis of hyperaldosteronism wrt uncontrolled loss of K & H? |
|
Definition
| Uncontrolled loss of K/H--> Hypokalemia & metabolic alkalosis leads to hyperpolarization of membranes (mild alkalosis stimulates Na/K pumps) --> retards AP transmission in nn & mm --> neuromuscular excitability dec --> m. weakness, hyporeflexia, lethargy |
|
|
Term
| What is caused by decreased aldosterone? |
|
Definition
| PU/PD, Dehydration, Hypovolemia, Dec Na/K Pump |
|
|
Term
|
Definition
|
|
Term
| What causes Hypoadrenocorticism/Addison's dz? |
|
Definition
| immune-mediated destruction of cortex (young bitches; incidence is increasing); Mitotane induced adrenocortical necrosis (mitotane therapy); long-standing cortisol therapy |
|
|
Term
| How does longstanding cortisol therapy cause Addison's? |
|
Definition
| --> depression of ACTH --> Atrophy of AC |
|
|
Term
| GC deficiency usually shows _______ signs. |
|
Definition
|
|
Term
| What are CS of GC deficiency? |
|
Definition
| Pt's are unable to cope w/ stressful situations or to maintain blood Glc levels btw meals (gluconeogenesis) --> hypoglycemia, lethargy |
|
|
Term
| What happens in MC deficiency? |
|
Definition
| Na/H2O loss; K/H retention --> Na/K plasma ratio less than 20 |
|
|
Term
| What is the normal Na/K plasma ratio? |
|
Definition
|
|
Term
| What is acute MC deficiency? |
|
Definition
| Addison's Crisis: Hypovolemia --> Shock/Collapse/Death |
|
|
Term
| Describe retention of K/H in MC Deficiency. |
|
Definition
| --> Hyperkalemia, metabolic acidosis, m. shivering, paradoxically increases K conductivity of heart pm cells --> cardiotoxic --> bradycardia, arrhythmia, cardiac arrest |
|
|
Term
| What is used for euthanasia? (wrt MC deficiency) |
|
Definition
|
|
Term
| What is the relative distribution of Ca in the body (3 areas)? |
|
Definition
|
|
Term
| How much of the body's Ca is in plasma? |
|
Definition
|
|
Term
| What portion of Ca in the body is critically regulated? |
|
Definition
|
|
Term
| How much of plasma Ca is protein bound? Complexed to anions? Ionized? |
|
Definition
|
|
Term
| What are the physiological functions of Ca? |
|
Definition
| Electromechanical coupling, m. contraction, release of hormones & enzymes, stabilizes Na channels in membranes, reduces basement membrane permeability, co-factor in blood clotting, component of bone & teeth |
|
|
Term
| What effect does small disturbance in Ca homeostasis have? P? |
|
Definition
Ca: Small disturbances can have major effects;
P: even large fluctuations are well-tolerated |
|
|
Term
| What % of phosphate is in bone/IC/ECF? |
|
Definition
|
|
Term
| What are physiological functions of P? |
|
Definition
| Constituent of many compounds (nucleic acid, ATP, cAMP, creatine P, membranes); Phosphorylation processes; Buffer; Component of bone & teeth |
|
|
Term
| What is the relationship btw Ca levels & Na conductivity? |
|
Definition
|
|
Term
| What are the plasma forms of P? |
|
Definition
|
|
Term
| What is adult bone composed of? %? |
|
Definition
| 30% organic matrix/70% Salts |
|
|
Term
| What is the organic matrix of adult bone? |
|
Definition
| Collagen fibers = ground substance |
|
|
Term
| What are the salts of adult bone? |
|
Definition
| Crystalline Hydroxyapatite (Ca10[PO4]6[OH]2) |
|
|
Term
| Describe calcification of bone. |
|
Definition
| Osteoblasts secrete collagen mol's --> polymerization --> collagen fibers (osteoid); Ppt of amorphous (non-crystalline) Ca salts (CaHPO4); Conversion into hydroxyapatite crystals |
|
|
Term
| Ca/P conc's are close to _______ |
|
Definition
| saturation pt (Ppt in other tissues is avoided via inhibitors like Pyrophosphate) |
|
|
Term
| Describe remodeling of bone. |
|
Definition
| Continual process of bone deposition (osteoblasts) & absorption (osteoclasts) --> bone can adjust to altered stress |
|
|
Term
| Some _____ are usually present & can be mobilized rapidly = ________ |
|
Definition
| Amorphous Salts; Exchangeable Ca Pool (Ca Buffer Sys) |
|
|
Term
| How many systems control Ca (& P) homeostasis? What are they? |
|
Definition
| 3; Ca inc: PTH, Vit D/D Hormone; Ca dec: Calcitonin |
|
|
Term
| What does Calcitonin do to Ca? P? |
|
Definition
|
|
Term
| What does PTH do to Ca? P? |
|
Definition
|
|
Term
| Plasma Ca conc is maintained w/i +/- _____% of normal. |
|
Definition
|
|
Term
| What is the most powerful hormone controlling plasma Ca & P levels? |
|
Definition
|
|
Term
| How does PTH control Ca & P levels? |
|
Definition
Stimulates: Bone mobilization (resorption); Renal Ca absorption; Activation of Vit D
Inhibits: Renal P absorption |
|
|
Term
| What does bone mobilization do to plasma Ca? P? |
|
Definition
|
|
Term
| What does renal Ca absorption do to plasma Ca? |
|
Definition
|
|
Term
| What does activation of Vit D to do plasma Ca? How? |
|
Definition
|
|
Term
| What does inhibition of renal P absorption do to plasma P? |
|
Definition
|
|
Term
| What is the net effect of PTH? |
|
Definition
| Plasma Ca inc; Plasma P dec |
|
|
Term
| What are the 2 main factors of control of PTH release? |
|
Definition
| Hypocalcemia; Hyperphosphatemia |
|
|
Term
| How does hypocalcemia affect PTH? |
|
Definition
| Sm changes lead to immediate PTH response (chronic hypocalcemia --> compensatory hypertrophy of parathyroid glands) |
|
|
Term
| What can cause chronic hypocalcemia? |
|
Definition
| Malnutrition, Lactation, Pregnancy |
|
|
Term
| What does Hyperphosphatemia do to PTH? |
|
Definition
| Indirect effect b/c high P levels --> binding of Ca ions to form CaHPO4 --> Hypocalcemia |
|
|
Term
| What is Vit D3 derived from? D2? |
|
Definition
| Diet or de novo synthesis in liver followed by UV activation in skin; plant tissue (less effective) |
|
|
Term
| Where does activation of Vit D3 to DH occur? |
|
Definition
|
|
Term
| What is the active form of DH? |
|
Definition
| 1.25-Dihydrocholecalciferol |
|
|
Term
| What does conversion to 1.25-Dihydrocholecalciferol require? Where does it occur? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| What are the actions of DH? |
|
Definition
| Increases intestinal & renal Ca & P absorption; Increases mobilization of bone (in high conc) |
|
|
Term
| What is another name for D Hormone? |
|
Definition
|
|
Term
| What stimulates Calcitonin? |
|
Definition
|
|
Term
|
Definition
| Decreases activity & proliferation of osteoclasts (indirectly favors osteoblasts); Favors bone formation; Decreases Ca & P levels |
|
|
Term
| Where is Calcitonin produced? |
|
Definition
|
|
Term
| In what animals is calcitonin more important? |
|
Definition
| Young animals; Removal of thyroid gland/C cells in adults has little effect on Ca balance |
|
|
Term
| Where are calcitonin secreting C cells? |
|
Definition
| Btw thyroid follicle cells |
|
|
Term
| Chronic Hypocalcemia leads to compensatory ______ |
|
Definition
|
|
Term
| What can cause chronic hypocalcemia? |
|
Definition
| Lack of dietary Vit D or lack of UV exposure; Dietary Ca/P imbalances; Renal dz w/ insufficient P excretion |
|
|
Term
| Lack of dietary Vit D or lack of UV exposure --> |
|
Definition
| Reduced Ca absorption --> Hypocalcemia (Rickets/young or Osteomalacia/adult) |
|
|
Term
| Dietary Ca/P imbalances (cereals & innards) --> |
|
Definition
| Hyperphosphatemia/Hypocalcemia |
|
|
Term
| What is the normal Ca/P ratio? |
|
Definition
|
|
Term
| What is the Ca:P ratio in cereals & innards? |
|
Definition
|
|
Term
| What can occur from lack of dietary Vit D or lack of UVB exposure in reptiles & birds? |
|
Definition
|
|
Term
| Renal dz w/ insufficient P excretion --> |
|
Definition
| P deposits as CaHPO4 --> Hypocalcemia |
|
|
Term
| What happens in all cases of chronic hypocalcemia? |
|
Definition
| Body releases PTH --> Mobilizes Ca from bone tissue --> plasma Ca returns to low/normal --> if long-term, leads to softening of bone = Demineralization; Compensatory Hyperparathyroidism |
|
|
Term
| What can occur in dogs with renal hyperparathyroidism? |
|
Definition
|
|
Term
| What is an example of acute hypocalcemia? |
|
Definition
| Parturient Paresis/Milk Fever in cows |
|
|
Term
| In what spp is parturient paresis seen most often? |
|
Definition
|
|
Term
| Give an example of acute hypocalcemia in dogs & horses |
|
Definition
| Eclampsia/Puerperal Tetany |
|
|
Term
| What is Eclampsia/Puerperal Tetany? |
|
Definition
| Acute hypocalcemia during 1st wks of lactation (peak lactation) |
|
|
Term
| What are the symptoms of Eclampsia/Puerperal Tetany? |
|
Definition
| Relate to increased nerval/muscular excitability = spasms, tetany, panting, tachycardia, seizures, coma, death |
|
|
Term
| Why do cows with milk fever have decreased body temp? |
|
Definition
| Decreased m. contractions |
|
|
Term
| What is the Tx for milk fever? |
|
Definition
| Infuse Ca; Pre-birth: Lower dietary Ca; Give PTH 2 days pre-birth to activate osteoclasts |
|
|
Term
| What is parturient paresis/milk fever? |
|
Definition
| Acute hypocalcemia w/i 72h pp due to rapid loss of Ca via milk |
|
|
Term
| What happens from rapid loss of Ca via milk? (Milk Fever) |
|
Definition
| PTH is released, but osteoclasts are reduced in # or inactive due to: insufficient stimulation during dry period (low Ca demand, low PTH); inhibition by calcitonin (high dietary Ca); Bone can't respond fast enough --> acute hypocalcemia |
|
|
Term
| What is the pathophysiology of milk fever? |
|
Definition
| Interference btw Ca & Na channels; Increased conductivity of Na channels --> excitability, tremors, seizures, tachycardia |
|
|
Term
| What pathophysiology is in cows mostly? |
|
Definition
| Uncoupling of neuromuscular transmission --> flaccid paresis (no exocytosis of ACh); may be caused/exacerbated by concomitant Mg increase) |
|
|
Term
| What are the symptoms of milk fever? (Stages 1-3) |
|
Definition
1. Nervousness, excitability, tremor (mild, short phase)
2. Sternal recumbency, flaccid paresis, GI stasis, low temp
3. Lateral recumbency, complete flaccid paresis, coma, death |
|
|
Term
| What causes GI stasis in milk fever? |
|
Definition
|
|
Term
| What does GI stasis lead to in milk fever? |
|
Definition
|
|
