Endocrine Flashcards
How is glucose made available to the body
Glycogenolysis: Glycogen breakdown— short term 6-12 hrs
Gluconeogensis: Production of glucose— Prolonged
Where is insulin released from
Beta cells in the pancreas when glucose is high
What are the counter regulatory methods for decreased glucose
glucagon, catecholamines, cortisol and growth hormone
Where is glucagon made and how does it work
alpha cells of pancrease.
Stimulates glycogenolysis via cAMP, phosphorylation of glycogen phosphorylase
How do catecholamines increase glucose
realsed via SNS stimulation from adrenal medulla
potienated glucagon’s activity of phosphorylase
How does gluconeogesis occur
pyruvate, lacatic acid, glycerol, and amino acids to form glucose
Cortisol mobilized protien and adipocytes for ammino acids and FFA; inhibits insulin and potientiates effects of glucagon/epi on the liver
How is the brain glucose levels compared to the rest of the body
Dependent on plasma glucose (don’t make own) 30 % less in brain cells than blood.
GLUT-1 glucose transporter for the brain
Neuronal damage, decreased cerebral ATP, cellular swelling, oxidative damage
Sympathoadrenal response
What are the broad categories of hypoglycemia
Excess secretion of insulin/ insulin like factors
Decrease glucose production
Excess glucose consumption (includes drugs)
Suprious (polycythemia, leukocytosis, error-handling)
What is an insulinoma and common signs
Functional beta cell tumor
Signs are seen after meals and exercise
Middle to large breed dogs
What are indicators on blood work of insulinoma
Hypokalemia due to insulin induced shift
low fructosamine levels
>30 insulin:glucose ratio supportive (can be seen with sepsis, non pancreatic neoplasia
What is the goal of medical management in insulinoma
Give enough dextrose for insulin there but no so much to increase insulin release.
glucacorticioids, glucagon CRI (short term)
How does stress hyperglycemia occur
200-400 mg/dl
Catecholamine excess
Increase lactate is also associated with increase hepatic glucose production
How does hyperglycemia with TBI occur
associated with catecholamine response
Degree of injury with degree of increase glucose
Generally don’t need insulin
Which ketones will react with the urine dipstick
acetone and acetoacetate
Beta-hydroxybuterate will not
What are the renal thresholds for glucose in a cat and dog
Dog 180 mg/dl
Cat 300 mg/dl
What does ketones mean with Diabetes mellitus
absolute or relative insulin deficiency promoting lipolysis
How does hyperglycemic hyperosmolar syndrome occur
sustained an insult leading to a marked reduction of GFR.
Ability to excrete glucose impaired leads to abnormal retention in the blood
What are laboratory findings of hyperosmolar hyperglycemic syndrome
Glu > 600 mg/dl
Osm/Kg > 350
Does not usually have ketones
What are the two types of diabetes
Type 1- insulin deficiency dogs; immune mediated destruction
Type 2- Insulin resistance Cats
How does insulin resistance occur
Through counter regulatory hormones (cortisol, epi, GH, progesterone elevated)
Exerts negative infulence on insulin sensitivity at the level of the insulin receptor or insulin signaling cascade
What are the negative effects of hyperglycemia
Reactive oxygen species
Pro-inflammatory cytokines (TNF alpha, IL-6, IL1 beta) - insulin resitant state
impair leukocyte function
limits neovascularization and collagen synthesis
How are ketones formed
increase glucose stimulates hormone sensitive lipase and FFAs released from adipocytes
FFAs metabolized to triglycerides, CO2/H20 or ketone bodies
Counter regulatory hormones released due to stress stimulate lipolysis leads to more FFAs
What are the mechanisms for decreased potassium in DKA/HHS
Osmotic diuresis- lytes lost along to maintain electroneutrality
Insulin defiency decrease amount of K co transported into the cell
Acidemia K shifts out of the cells in exchange for H+
Hyperosmolality
Hypervolemia induced and increased aldosterone – increase renal los
Decrease GI uptake
Why does potassium decrease when insulin is given
K+ will move into cell along with glucose (cotransport)
Acidemia improves K+ will shift into cells
What are the overarching treatment goals of DKA
Restore effective circulating volume
rehydration and maintenance fluids
supplement lytes to correct or prevent defficiencies
Initiate insulin therapy to reduce glucose levels and ketone production
Identify and treatment underlying disease
When would you consider bicarbonate treatment treatment in DKA
pH > 7.1 HCO3- < 8 mmol/L, with refractory hypotension, arrythmias, insulin resistance, stupor/coma despite adequate volume and lyte
What are the negative effects of bicarbonate treatment in DKA
Worsen Decrease K, Ca and hyper Osom
Induce paradoxical CNS acidosis
Poorer outcome when administered
What is the overarching treatment goal of HHS and when is insulin started
insulin should be started when patient adequately hydrated and fluids alone are decreasing gluc by < 50 mg/dl/hr
Insulin is generally dosed at 50% of DKA
What are the areas of the adrenal gland
GFR; Glomerulosa, fasiculata, reticularis
Salt, Steroid, Sex
What is pheochromocytoma
CAtecholamine producting tumors (medulla)
Intermittent supraphysiologic catecholemeins
Signs increase in sympathetic tone
What improves mortality with surgery of pheochromocytoma
Phenoxybenzamine: alpha adrenergic antagonist
3 weeks prior to sx
What is hyperaldosterism
Cats> dogs
autonamous secretion of aldosterone (adrenal cortical tumors, or hyperplasia)
What signs do you see with hyperaldosterism
Nephron retains both Na and H20 which increases blood volume and leads to BP
HypoK due to potassium wasting properties
What is the difference between primary and secondary hypoadrenocorticism
Primary- all three adrenal cortex regions affected with > 90% damage
Secondary: abnormal pituitary gland lack of ACTH or hypothalmus lack of CRH
What are the effects of glucocorticoid deficency
decreased intravascular volume, decreased blood pressure, hypogylcemia, GI ileus
Increase ADH, leads to more H2O reabsorption as cortisol inhibits ADH release
What does not interfere with ATCH stim test
Dexamethasone
What is a corisol result of < 2 mcg/dl indicate
only 1% of dogs with addisons will have > 2
but 21% of dogs with < 2 mcg/dl have another disease due to ACTH stim
How do you differentiate primary and secondary addison’s with plasma ACTH
Primary will have increased because no cortisol for negative feedback
Secondary will have less because will not be secreted
What hormone level of Thyroid is consitent with thyroid storm
There isn’t a level
Define myxedema
Protracted untreated Hypo T4 leads to hyaluronic acid accumulation within the dermis
extracellular fluid accumulates and skin thickening
What is the MOA of ADH on the kidney
V2 receptor activated G-protien coupled adenycylase which is stimulated to increase cAMP leads to protein kinase A activation and results in insertion of aquaporin 2 water channel in the collecting duct tubular membrane
JVIM 2019 When adjusted for age was DM associated with CKD in cats
yes
JVIM 2019 What was the recommended starting dose for DOCP
1.5 mg/kg
Dogs < 3 yrs needed higher doses
JVIM 2019 What has been shown with high doses of ketaconazole
Hypoadrenocorticism
Resoloves once discontinued
What is the MOA of metforman
Does not affect beta cell production in pancrease
Requires body have insulin
* Enhances muscle sensitivity to insulin and increases glucose metabolism
Decrease hepatic gluconeogensis and glycogenolysis
Why are dogs and Cats not able to get D3 from skin
Due to high activity of 7-dehydrocholesterol delta 7 reductase
2017 AJVR How effective was cortisol induced ALP at diagnosis HypoAC
Not good
in combo with other lab good
2017 Vet journal what was noted about cardiac function in cats with DM
Have diastolic dysfunction that progresses over a 6 month period
