Endocrine Flashcards
What cells are pheochromocytoma derived from?
Chromaffin cells of the adrenal medulla.
Chromaffin cells also called APUD cells → responsible for amine precursor uptake and decarboxylation
What are the clinical signs of pheochromocytoma?
Systemic hypertension, weakness, collapse, lethargy, v/d, PUPD, tachypnea, abdominal distention, syncope, tachyarrhythmias, bradyarrhythmias, abdominal pain
* sustained or paroxysmal
True or False: High concentration of urinary normetanephrine was highly suggestive of pheochromocytoma.
True
* Urinary normetanephrine-to- creatinine ratio proved to be superior to epinephrine-, norepinephrine-, or metanephrine-to-creatinine ratios
In human, what drug can be given to reverse the catecholamine-induced vasoconstriction from pheochromocytoma?
Phentolamine, an reversible non-selective α-adrenergic antagonist
What drugs should be avoided in pheochromocytoma patients due to possible acute hypertensive crisis?
Metoclopramide***, histamine, tyramine, glucagon
What are the pre-, peri-, and post- anesthetic management for pheochromocytoma?
Pre:
1) start non-competitive α-adrenergic blockade with phenoxybenzamine (0.5 to 2.5 mg/kg PO q12h) 1 week before sx
2) blood type
Peri:
1) opioid + bzd + propofol for premed and induction
2) avoid halothane → sensitizes the myocardium to catecholamine- induced arrhythmias
3) monitor ECG and blood pressure
4) prepare esmolol (0.05 to 0.5 mg/kg IV followed by 10 to 200 mcg/kg/min IV), vasodilators such as nitroprusside (0.5 to 5 mcg/kg/min IV) or magnesium sulfate
5) prepare phenylephrine (0.5 to 5 mcg/kg/min IV) or norepinephrine (0.1 to 2 mcg/kg/ min IV) because patient may become hypotensive after tumor removal
What is the medical management for pheochromocytoma?
Phenoxybenzamine, β-blockers, and/or other anti-arrhythmic agents
* β-Blockers should not be given without concurrent α-blockade → loss of β2 receptor–mediated vasodilation may exacerbate hypertension
What is Budd-Chiari-like syndrome?
Mechanical obstruction of the hepatic venous outflow → liver congestion, right upper quadrant pain, ascites
For pheochromocytoma, what is the negative prognostic indicators for surgical outcome?
Vena cava invasion, older age, intra-op arrhythmias, prolonged surgical time
How are NE and Epi synthesized?
Tyrosine enters the nerve → DOPA → Dopamine → enters the vesicles → NE → exits the vesicle and receives a methyl group → Epi → re-enters the vesicles
Resources: https://cvpharmacology.com/norepinephrine
How are NE and Epi metabolized?
1) Neuronal re-uptake
2) Catechol-o-methyltransferase (COMT) and monoamine oxidase(MAO)
How is the ketone body synthesized?
Fatty acids went through 𝜷-oxidation and form Acetyl-CoA.
Normal situation: Glucose degraded into pyruvate → both Acetyl-CoA and pyruvate enter TCA cycles
Diabetic: No pyruvate; two Acetyl-CoA → form ketone bodies
What are three types of ketone bodies?
Acetoacetate (strong acid)
𝜷-hydroxybutyrate (strong acid)
acetone
Which ketone body cannot be detected by the urine strip test (nitroprusside reaction)?
𝜷-hydroxybutyrate
Why occasionally there will be negative urine ketone on day 1 but became positive on day 2 or 3 after the treatment is started?
After starting the insulin treatment, the urine 𝜷-hydroxybutyrate : Acetoacetate ratio may decrease because more 𝜷-hydroxybutyrate is metabolized back to acetoacetate and therefore can be detected with nitroprusside test
What are the most common concurrent diseases in dogs with DKA?
Acute pancreatitis
Bacterial UTI
Hyperadrenocorticism
What are the most common concurrent diseases in cats with DKA?
Hepatic lipidosis
CKD
Acute pancreatitis
Bacterial/viral infection
Neoplasia
What is the concentrations of K and Phos in Kphos?
K: 4.4 mEq/ml
Phos: 3 mM/ml
What is the rate to supply phos in patient with DKA and hypophoshpatemia?
0.03 - 0.12 mM/kg/hr
Describe the CRI regular insulin protocol for DKA.
What is the recommendation from The American Diabetes Association for bicarb supplementation for pediatric DKA patients?
1) Who should be treated?
who maintain a pH < 7.0 after 1 hour of fluid therapy
2) How to treat it?
Sodium bicarb 2 mEq/kg added to 0.9% NaCl, in a solution that does not exceed 155 mEq/L of sodium, over 1 hour.
3) How to monitor?
The pH is monitored q1h and treatment is repeated until pH ≥ 7.0
What is the hallmarks for HHS?
- BG > 600 mg/dL
- Minimal or negative urine ketone
- Serum osmolarity > 350 mOsm/kg (cat) or 325 mOsm/kg (dog)
- Ketotic vs non-ketotic
Describe the pathogenesis of HHS.
1) Hormone alteration
Insulin deficiency + increased countercurrent hormone (e.g. epinephrine, glucagon, cortisol, growth hormone)
- Epinephrine & glucagon inhibit insulin-mediated glucose uptake in muscle and stimulate hepatic glycogenolysis and gluconeogenesis
- Cortisol & growth hormone inhibit insulin activity and potentiate the effects of glucagon and epinephrine
2) Decrease GFR
3) Presence of concurrent disease
- CKD, CHF, pancreatitis (dog), neoplasia, other endocrinopathies
What is the main difference between HHS and DKA?
HHS usually has higher BG level and higher osmolarity. Patients with HHS also have higher circulating insulin level and lower glucagon level → this inhibits the liver to perform lipolysis due to presence of insulin.
What is the equation of serum osmolality?
Serum osmolality (mOsm) = 2 x Na + BUN/2.8 + BG/18
- Unit for Na = mEq/L
- Unit for BUN & BG = mg/dL
What is the equation of effective osmolality
Effective osmolality (mOsm) = 2 x Na + BG/18
What are the main contributors for metabolic acidosis in DKA and HHS, respectively?
DKA: ketones
HHS: uremic acids, lactic acids
What is the equation to correct Na in HHS patient?
Corrected Na = Patient’s Na + 1.6 x [(Measured BG - Normal BG)/100]
- Unit for Na = mEq/L
- Unit for BG = mg/dL
True of False: For HHS management, using IM or IV protocols of regular insulin at dosages 50% of those used for DKA should reduce the risk of a too rapid decline of serum glucose.
True
What is the target rate to reduce BG in HHS patients?
No more than 50-75 mg/dL/hr
True or False: Many dogs with HHS has recent steroid administration
True (18%)
- In the same study, poor outcome was associated with abnormal mentation and low venous pH
Reference: Trotman TK, Drobatz KJ, Hess RS. Retrospective evaluation of hyperosmolar hyperglycemia in 66 dogs (1993-2008). J Vet Emerg Crit Care (San Antonio). 2013;23(5):557-564.
How is potassium affected in patients with DKA/HHS?
1) Acidosis → K+ is shifted out of the cell in exchange with H+
2) Decreased dietary intake → K ↓
3) Hypovolemia induced hyperaldosteronism → increased renal loss
4) Insulin deficiency → decreases the amount of K co-transported into cells
5) Decreased GFR → K accumulates in the blood
True or False: The BG level in the brain is the same as plasma.
False
Glucose concentrations in the brain are up to 30% lower compared to plasma
What is the cutoff to diagnose insulinoma with insulin:glucose ratio?
> 30 is supportive of insulinoma
- Equation: AIGR = (insulin × 100) ÷ (plasma glucose − 30)
- Need to collect the blood when BG < 60
What is the formula to correct point-of-care BG based on PCV?
Corrected POC BG = Measured POC BG + [(1.6 x PCV) - 81.3]
Reference: Lane SL, Koenig A, Brainard BM. Formulation and validation of a predictive model to correct blood glucose concentrations obtained with a veterinary point-of-care glucometer in hemodiluted and hemoconcentrated canine blood samples. J Am Vet Med Assoc. 2015;246(3):307-312.
Where is the glucagon from? Where does it work?
1) 𝜶 cells in the pancreas
2) liver, promote glycogenolysis and gluconeogenesis
How does 𝜷-blocker cause hypoglycemia?
interference with adrenergic counterregulatory mechanisms
**bad question - it usually cause hyperglycemia
When should you raise a concern for insulin resistance?
when insulin dose > 1.5U/kg q12h
What are the four factors contributing to thyroid storm in cats?
1) Higher concentration of circulating thyroid hormone
2) Acute, rapid increase of circulating thyroid hormone
3) Hyperactivity of the sympathetic nerve system
4) Increased cellular response to thyroid hormone