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70 Cards in this Set
- Front
- Back
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IRI
-define |
-immunoreactive insulin
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Methods to inc. [glucose]
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-increase gluconeogenesis in the liver
-increase glycogenolysis in the liver -increase dietary uptake by the intestine |
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Gluconeogenesis in ruminants and horses due to:
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-ruminant: rumen proprionate
-horse: colon proprionate |
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Methods to dec. [glucose]
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-glycolysis in muscle, WBCs, RBCs
-inc. glycogen synthesis in muscle, liver -inc. fat storage (glycerol --> triglycerides) -inc. urinary loss |
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Effect of insulin on blood [glucose]
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Lowers [glucose] by promoting storage in:
-liver (glycogen, pyruvate) -muscle (glycogen) -adipose tissue |
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Insulin release promoted by
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-inc. GH
-inc. glucose -inc. glucagon -inc. amino acids |
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Effect of glucagon on blood [glucose]
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Increases [glucose] by promoting mobilization from:
-liver -also releases fatty acids to blood |
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Glucagon release promoted by:
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-dec. glucose
-inc. Amino acids -Inc. cortisol |
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Effect of Cortisol on blood [glucose]
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Raises [glucose] by promoting gluconeogenesis and glycogen synthesis
-liver (pyruvate to glucose, glucose to glycogen) -pancrease (release glucagon) -reduce glucose into muscle cells |
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Cortisol is released from:
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-adrenal glands
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Epinephrine effect on blood [glucose]
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raises [glucose] by promoting glycogenolysis
-liver (glycogen to glucose) |
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Epinephrine released from:
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-adrenal glands
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Preferred sample for glucose concentrations
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-Serum
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What should you know when collecting blood for a glucose test in a red top tube?
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Clot tube
-harvest the serum within 1 hr because glucose is consumed at a rate of 5-10%/hr -rate of consumption is increased with inc. WBC or inc. RBC |
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What should you know when collecting blood for a glucose test in a red/black top tube?
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Gel separator between the serum and cells after centrifugation
-glucose concentration is fine for 48hrs @ 4C |
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What should you know when collecting blood for a glucose test in a grey top tube?
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Na/F tube
Many disadvantages -F inhibits glucose oxidase -hemolysis -H2O pulled out of the cells by hypertonic salts |
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Why does serum glucose not = blood glucose
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-Blood contains "other" solids which serum does not contain, therefore there is less glucose in a given volume of blood
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Types of hyperglycemia
-how do they result in hyperglycemia |
-Physiologic (no defect in control mechanisms)
-Pathologic (defect in control mechanisms) -Pharmacologic (drugs altering control mechanisms) |
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Reasons for Physiologic hyperglycemia
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-Postprandial (monogastrics, couple of hrs)
-Excitement & fright (epinephrine) -Steroids/Stress (cortisol) -Diestrus (progesterone) |
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What does it mean for hyperglycemia to be Transient?
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-no clinical signs of Diabetes Mellitus
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Classification of DM in people
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-Symptoms of diabetes plus casual plasma glucose conc. > 200 mg/dl
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Pathologic hyperglycemia due to:
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-diabetes mellitus
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Type 1 DM
-describe |
-beta-cell destruction
-insulin deficiency |
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Type 1 DM
-cause |
-idiopathic
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Type 2 DM
-describe |
-insulin resistance with inadequate compensatory insulin secretory response
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Type 2 DM
-cause |
-Pancreatic insular amyloidosis
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Type of DM more common in dogs
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-Type 1
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Type of DM more common in cats
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-Type 2
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Type 1 DM
-pathogenesis |
Beta-cell destruction
-dec. insulin production --insulin deficiency ---dec. glucose entry into muscle & adipose ----inc. gluconeogenesis ----inc. glycogenolysis -----hyperglycemia -Cells perceive starvation --inc. glucagon production ---inc. gluconeogenesis ---inc. glycogenolysis ----hyperglycemia |
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Type 2 DM
-pathogenesis |
Feline pancreatic amyloidosis
-dec. insulin production --insulin deficiency ---dec. glucose entry into muscle & adipose ----inc. gluconeogenesis ----inc. glycogenolysis -----hyperglycemia -defective target cell response --dec. glucose use by target cells ---hyperglycemia When cells perceive starvation -inc. glucagon production --hyperglycemia Glucose toxicosis -dec. insulin production |
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Amylin is produced by
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-Beta-cells
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Cushnoid DM
-pathogenesis |
Excess glucocorticoids (cortisol)
-defective glucose transport --dec. glucose entry into muscle and adipose -inc. gluconeogenesis --hyperglycemia Cells perceive starvation -inc. glucagon production --hyperglycemia |
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"Other" reasons for DM
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-hyperadrenocorticism
-hyperpituitarism -megestrol acetate |
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Pharmacological hyperglycemia is what kind of hyperglycemia
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-transient (only occurs when drug is present)
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Pharmacological hyperglycemia
-causes |
-oral/IV glucose
-glucocorticoids -megestrol acetate (steroids, progesterone) -Ketamine (inc. epinephrine) -Glucagon -Thyroxine (dec. insulin secretion) -ethylene glycol (starved cells) |
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Pharmacologic drugs that decrease insulin production
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-xylazine
-detomidine -propranolol -insulin (somogeny) |
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Describe the somogeny effect of insulin administration
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Hyperglycemia from DM is present
-too much insulin given --marked hypoglycemia ---inc. glucagon release ----gluconeogenesis -----hyperglycemia |
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Types of hypoglycemia
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-Pathologic hypoglycemia (defect in control mechanisms)
-Pharmacologic hypoglycemia (drugs altering control mechanisms) -"Other" in vitro (sample handling) |
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In vitro hypoglycemia
-reasons |
-glucose consumption by cells over time
-excessive glycolysis because of leucocytosis or thrombocytosis -Br- interfering with i-STAT |
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Pathologic hypoglycemia
-causes |
-Pancreatic beta-cell neoplasm
-xylitol toxicosis -hypoadrenocorticism -hepatic insufficiency/failure -lactational hypoglycemia -sepsis w/ endotoxemia |
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Hypoglycemia due to pancreatic beta-cell neoplasm
-reason |
-inc. release of insulin
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Hypoglycemia due to xylitol toxicosis
-reason |
-xylitol is recognized as glucose and insulin is released
-the insulin cuases glucose consumption -only occurs in dogs |
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Xylitol
-found in |
-sugar-free gum
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Hypoglycemia due to Addison's disease
-reasons |
-decreased cortisol --> dec. insulin antagonists & dec. gluconeogenesis
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hypoglycemia due to Hepatic insufficiency/failure
-reasons |
-decreased gluconeogenesis
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Hypoglycemia due to lactational hypoglycemia
-reasons |
-inc. use
-dec. production |
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Lactational hypoglycemia
-aka |
-spontaneous bovine ketosis
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Hypoglycemia due to sepsis with endotoxemia
-reasons |
-stress
-not eating -tissue damage --> anaerobic glycolysis |
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Why is IRI preferred over insulin?
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-may include proinsulin molecules
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Hyperinsulinemia
-causes |
-Functional pancreatic beta-cell neoplasm (insulinoma)
-hyperglycemia not due to dec. insulin production (inc. cortisol, inc. GH) |
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IRI:Glucose ration from a Functional Beta-cell neoplasm
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-high
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IRI:Glucose ratio from a hyperglycemic disorder not due to dec. insulin production
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-WRI
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Hypoinsulinemia
-can be due to |
Dec. insulin production:
-Type 1 DM (Beta cell destruction) -Type 2 DM (advanced - Beta cell damage) -Physiologic (secondary to hypoglycemia) Rare documentation |
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IRG
-define |
-immunoreactive glucagone
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IRG
-physiologic processes |
-Polypeptide hormone produced by alpha cells
-maintains glucose concentration -stimulated by hypoglycemia -GLP-1 stimulates release of insulin to reduce hyperglycemia |
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Hyperglucagonemia
-cause |
-associated with pancreatic glucagonoma
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Clinical sign of pancreatic glucagonoma
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-concurrent superficial necrolytic dermatitis
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Ketoamine
-aka |
-glycated protein
-glucose + protein |
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Types of Ketoamines in blood
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-glycated hemoglobin
-glycated albumin and other proteins ---> fructosamine |
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Ketoamine
-use |
-monitor control of DM
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When is fructosamine formation increased?
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-hyperglycemia
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Fructosamine
-half-life |
-2-3 wks
-longer in horses (reliant on the half-life of albumin) |
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Why is there increased [fructosamine] with DM
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-persistent hyperglycemia --> inc. formation
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Why is there increased [fructosamine] with hypothyroidism?
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-dec. protein catabolism --> inc. albumin half-life --> inc. formation
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Reasons for increased [fructosamine]
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-DM
-hypothyroidism |
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Reasons for decreased [fructosamine]
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-insulinoma
-hypoproteinemia -cats with hyperthyroidism |
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Inc. formation of glycated hemoglobin
-due to |
-hyperglycemia
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Glycated hemoglobin half-life varies with:
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RBC life spans
-canine (100 days) -feline (70 days) -Equine/Bovine (150 days) |
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Inc. glycated hemoglobin %
-cause |
-DM (persistent hyperglycemia)
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Dec. glycated hemoglobin %
-cause |
-insulinoma (hypoglycemia)
-anemia |
