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S&H: Endocrine disorders

Terms in this set (41)

What is the basic pathogenesis of DKA?
Diabetes mellitus >> Glucose is not transported into cells >> Ketones synthesized from FAs as substitute form of energy >> Ketoacids cause acidosis + electrolyte abnormalities
In DM, the inability of glucose to enter cells means that there is dec activity of the citric acid cycle and therefore dec utilization (and therefore buildup) of acetyl-CoA, which is the precursor to the synthesis of what 3 ketone bodies in the liver?
-Acetoacetate
-β-hydroxybutyrate
-Acetone
What aspects of the pathogenesis of DKA leads to the development of severe metabolic acidosis in these patients? (2)
-Buildup of acetoacetate and β-hydroxybutyrate (anions of strong acids)
-Vomiting >> Dehydration >> Renal hypoperfusion
What are common clinical signs of patients in DKA? (6)
-PU/PD
-Lethargy, Hyporexia, Wt loss
-Vomiting
Approximately 50% of dogs (and many cats) with DKA have which CBC abnormality?
Nonregenerative anemia
What are common chemistry abnormalities in DKA patients? (10)
-Hyperglycemia
-Inc ALP +/- Inc AST, ALT
-Azotemia (cats >> dogs)
-Hyper or Hypo-K, Hypo or Hypo-P, HypoMg
-Hypo-Na, Cl, iCa
-Lactic acidosis (1/3 of dogs)
Why can DKA patients have either hypo- or hyper-kalemia?
-Initial presentation with hyperK d/t dehydration, dec renal excretion, acidemia (H moves into cells in exchange for K going out)
-HypoK once rehydrated, worsened by loss in vomiting / anorexia / osmotic diuresis / K binding to ketoacids
Why can DKA patients have either hypo- or hyper-phosphatemia?
-Hypo: Phos moves out of cells d/t acidosis, hypoinsulinemia, and hyperglycemia >> Once out of cell, phosphorus is lost via osmotic diuresis
-Hyper or normal: Dehydration + Dec excretion (resolves once rehydrated)
Why can DKA patients develop a pseudohyponatremia?
Hyperglycemia >> Shift of Na into cells (see total body Na is not necessarily decreased)
(NB: Osmotic diuresis in these patients can lead to PD
For a DKA patient, what would you expect venous pH to be?
pH less than 7.35 in all dogs and cats with DKA
Considering LRS, Plasmalyte, and 0.9% saline, which are better or worse for treatment of DKA? Why?
-LRS/ Plyte: Good options bc lactate or acetate/ gluconate are converted to bicarb >> help manage acidosis + both contain K
-0.9% saline NOT best choice in hyperosmolar syndrome and bc lacks a buffer and K
What are the 2 most important components of DKA therapy?
-Fluid therapy (Fluids alone w/o insulin can dec BG)
-Correction of electrolyte abnormalities (which can be life-threatening)
What is the max infusion rate of potassium that is generally considered safe?
Max 0.5 mEq/kg/h
Why is insulin therapy NOT immediately started for DKA patients?
Fluid therapy alone dec BG significantly in a few hrs, meaning that adding insulin can dec BG too rapidly >> Harmful osmotic shifts
(Wait 6 hrs after fluids begun to start regular insulin)
What clinical aspects defines Nonketotic Hyperglycemic Hyperosmolar syndrome (HHS)?
-Hyperglycemia (>600 mg/dL)
-Hyperosmolality (>350 mOsm/kg)
-No or minimal urine ketones
-Dec GFR
Pathogenesis of HHS is very similar to that of diabetic ketoacidosis, except that in HHS _________ is inhibited while __________ continues, thereby preventing ketosis and worsening hyperglycemia
Pathogenesis of HHS is very similar to that of DKA, except that in HHS lipolysis is inhibited while gluconeogenesis continues, thereby preventing ketosis and worsening hyperglycemia
Severe hyperglycemia (as is seen in cases of HHS) can occur only in the presence of _______________
Reduced GFR (bc there is no maximum rate of glucose loss via the kidney)
What are the 2 conditions that are commonly attributed to causing a diabetic patient to develop HHS?
Renal failure and CHF >> Dec GFR >> HHS
Glucose comes from what 3 sources?
-GI absorption of glucose via digestion of carbs
-Glycogenolysis
-Gluconeogenesis (from lactate, pyruvate, aa, glycerol)
What effects does insulin have? (6)
-Inhibit glycogenolysis and gluconeogenesis
-Promote glycogen storage
-Stim glucose uptake and utilization
-Dec glucagon secretion
-Stim production of triglycerides in fat tissue
-Syn of protein / glycogen in mm
Where does insulin come from vs glucagon?
-Insulin: Pancreatic β cells
-Glucagon: Pancreatic α cells
What effects does glucagon have? (4)
-Stim hepatic glycogenolysis
-Stim hep gluconeogenesis (to a lesser extent)
-Mobilizes gluconeogenic precursors
-Dec peripheral glucose utilization
What effects does epinephrine have on glucose regulation? (2)
-Limits insulin secretion
-Inc glucagon secretion
What effects does cortisol have on glucose regulation? (2)
-Stim lipolysis
-Stim release of aa from muscle
(Both for gluconeogenesis in the liver)
Why is the brain so susceptible to hypoglycemia?
-Limited ability to use other substrates
-Limited store of glycogen
-Can't make glucose
What are clinical signs of neuroglycopenia? (4)
-Altered mentation, dullness, sleepiness
-Weakness, ataxia
-Blindness or altered vision
-Seizures, Shaking, Trembling
Define hypoglycemia in SA
60 mg/dL or less
What is Whipple's triad?
Guidelines for identifying hypoglycemia
1) Clin signs consistent w/ hypoglycemia
2) Low BG level
3) Resolution of clin signs w/ correction of BG
What are the 4 general categories of causes hypoglycemia?
-Excess insulin/ Insulin analogs
-Inc glucose utilization
-Dec glucose production
-Artifact
What lab artifacts can lead to falsely low BG readings? (2)
-Waiting longer than 30 mins to test the BG or to separate the plasma from the RBCs
(Bc RBCs continue to consume glucose in the tube)
-Polycythemia/ Leukocytosis (high [ ] of blood cells consume glucose in vitro and sometimes in vivo)
What are examples of causes of hypoglycemia due to excess insulin or insulin analogs? (4)
-Exogenous insulin overdose
-Insulinoma
-Paraneoplastic syndrome (many!)
-Toxins (xylitol)
What are examples of causes of hypoglycemia due to excess glucose utilization? (4)
-Sepsis
-Polycythemia/ Leukocytosis
-Pregnancy
-Paraneoplastic
What are examples of causes of hypoglycemia due to decreased glucose production? (4)
-Neonatal/ toy breed hypoglycemia
-Hepatic dysfx (PSS, hepatitis, neoplasia)
-Addison's (hypocortisolism)
-β-Blockers (atenolol may interfere w/ adrenergic regulatory mechs)
How do you treat a hypoglycemic crisis?
-50% dextrose 0.5-1 ml/kg diluted 1:2 or 1:4, given IV over 5 mins (hypertonic so can cause phlebitis)
-CRI 2.5-5% dextrose (diluted in LRS or 0.9% saline)
Why should care be taken using IV dextrose in animals with suspected insulinoma or other tumors secreting insulin-like analogs? What are possibly better options for treatment?
-A bolus of dextrose can stim release of more insulin from the tumor >> Rebound hypoglycemia
-Better: Glucagon CRI or pred/ dexamethasone
Diabetes insipidus results from a lack of secretion of or a lack of an appropriate renal response to a hormone known as ___________.
Vasopressin, aka antidiuretic hormone (ADH)
Primary diabetes insipidus is most commonly acquired and central in origin. Common causes include __________ and _____________. What is the pathpgenesis?
-Trauma and Intracranial masses
(Caused by a complete or partial lack of secretion of vasopressin from the axon termini in the anterior lobe of the pituitary gland)
Secondary diabetes insipidus is usually renal in origin (aka nephrogenic DI). Common causes include what 9 things? (Hint - they are not all directly related to the kidney)
-Hypercalcemia, Hypokalemia
-Sepsis, Pyometra
-Pyelonephritis
-PSS, Liver insufficiency
-Addison's, Hyperthyroidism
1. What are major concerns when preparing to anesthetize a dog with DI?
Severe hyperNa + Dehydration (d/t urinary free water losses w/o appropriate water intake)
-May need desmopressin
Where does vasopressin bind its receptor in the kidney?
Distal tubule and CD
What happens when vasopressin binds and activates its receptors in the kidney?
Activation >> Inc water permeability of luminal mem by insertion of aquaporin-2 water channels in renal epithelial cells >> More rapid passive flow of water from lumen and into solute-rich, concentrated interstitium >> Inc osmolality w/i tubular lumen
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