Exam 2 Endocrine Flashcards
What are the functions of the Pancreas?
Digestion, metabolism, utilization, and storage of energy substrates.
Made up of Exocrine and Endocrine cells.
What are the functions of the Pancreas?
Digestion, metabolism, utilization, and storage of energy substrates.
Made up of Exocrine and Endocrine cells.
The endocrine cells (islets of Langerhans) of the Pancreas are composed of what kind of cells?
Exocrine cell function.
Alpha cells – 18-20% (Glucagon)
Beta cells – 75% (Insulin)
Delta cells – 5% (Somatostatin)
Exocrine secretes digestive enzymes into the small intestine to aid in digestion.
The hormone that increases BS by stimulating hepatic glucose production
Glucagon
The hormone that decreases BS
Insulin
Glucose physiology is a balance between_______
and _________.
Glucose physiology is a balance between glucose utilization
and endogenous production or dietary delivery.
What organ is the primary source of endogenous glucose production?
About 70 to 80% of the glucose that the ______ produces is metabolized by the _______, _________, and ________.
The Liver: Glycogenolysis (glycogen to glucose) and gluconeogenesis (synthesis of glucose from non-carb precursors)
About 70 to 80% of the glucose that the liver produces is metabolized by the Brain,GI tract,& RBCs.
PancreasInsulin/Glucagon Feedback Loop
What is Diabetes Mellitus?
Signs and Symptoms of Diabetes Mellitus
Inadequate supply of insulin
Inadequate tissue response to insulin
Hyperglycemia (several days to weeks), fatigue, weight loss
Polyuria, polydipsia, blurred vision,hypovolemia
DM can lead to Micro- and macrovascular complications
Type 1 DM Characteristics
T cell–mediated autoimmune destruction of beta cells
Absence or minimal circulating levels of insulin
80%–90% beta cell function lost
Always need insulin
Type 2 DM Characteristics
What are 3 things we see in DM 2?
Relative beta cell insufficiency and insulin resistance
Pancreatic cell function decreases⇨insulin levels are unable to compensate⇨hyperglycemia
- Increased rate of hepatic glucose release
- Impaired basal and stimulated insulin secretion
- Insulin resistance
DM Diagnosis
A1C:
Fasting Glucose (8 hours):
Glucose Tolerance Test:
Random Glucose:
DM Treatment (Initial Therapy)
Diet, weight loss, and increased activity
Biguanides – decreases hepatic gluconeogenesis and enhances the utilization of glucose by skeletal muscle and adipose tissue (metformin)- First-line treatment
Sulfonylureas – stimulating insulin secretion from beta cells (glyburide, glipizide, glimepiride)
Types of Insulin for DM Treatment.
Rapid Acting or Short Acting (Regular) -Provides glycemic control at mealtimes
Basal -Intermediate-acting and administered 2x daily
Long Acting -Administered once daily
What is DM DKA and Sign/Sx
Usually seen in DM-1 patients: Severe insulin deficiency and unrestrained lipolysis lead to hypovolemia and anion gap metabolic acidosis
Decreased sodium, potassium, and phosphorus
Signs and symptoms
Tachypnea (Kaussmal), N/V, altered LOC, dehydration
DM DKA
Serum Glucose Level
pH
HCO3-
Serum Osmolarity
Serum and urine ketone levels
DMDKA Treatment
IVF (NS or LR)
Regular insulin gtt (goal: pH > 7.3 and HCO3-> 18 mEq/L)
Replace electrolytes
NaHCO3- if pH < 7.0
Blood glucose levels Q1H or more
DMHyperglycemic hyperosmolar syndrome (HHS) description, labs, and symptoms.
Present in DM2 patients: Severe hyperglycemia, hyperosmolarity, and dehydration.
metabolic acidosis (only in severe dehydration or organ failure secondary to HHS)
DMHyperglycemic hyperosmolar syndrome (HHS) treatment.
Fluid resuscitation, insulin gtt ,and electrolyte replacement
Hypotonic saline if plasma osmolarity >320mOsm/L to bring osmolarity down.
What microvascular complications can be seen with DM?
Renal failure
Proteinuria and decreased GFR
Peripheral neuropathy
Decreased perception of pain and temperature
Dysesthesia (abnormal sensation), paresthesia (pins/needle sensation), and neuropathic pain
Lower extremity ulcers, foot fractures, amputations
Retinopathy
Autonomic Neuropathy of DM
CV:
GI:
CV – systolic and diastolic dysfunction w/ reduced EF, dysrhythmias, orthostatic BP/HR changes (silent changes)
GI – gastroparesis (delayed gastric emptying), feel full early, N/V
Macrovascular Complicationsof DM
Elevated triglyceride levels, low HDL, and high LDL
DMAnesthetic Considerations
CV:
Renal:
GI:
MS:
Insulin and Meds:
CV: MI and myocardial ischemia, Pre-op EKG
Renal: Tight HTN control, maintain renal blood flow, Watch U/O if surgery is longer than hour, put in a foley.
GI: Gastroparesis Treat pt as full stomach
MS: limited joint mobility, position with care, and use pads, document. Prayer Hands, pictured
Insulin and Meds:
One-third to half of the usual NPH morning dose day of surgery- best to talk to patient
Hold regular or rapid-acting morning dose
Insulin pump – continue the basal rate or reduce up to 25%
D/C PO meds morning of sx
How many lobes and isthmus make up the thyroid?
2 lobes
1 isthmus
How many parathyroid glands are there?
4
Fucntion of Thyroglobulin and Parafollicular C cells
Thyroglobulin: T3 and T4 productions
Parafollicular C cells: calcitonin production, secreted d/t hypercalcemia
Thyroid HormoneSynthesis Process
Exogenous iodine comes from our diet (salt).
Iodine reduced to iodide
Iodide binds to thyroglobulin and gets catalyzed by peroxidase to form inactive monoiodotyrosine and diiodotyrosine which will undergo coupling to form T3 and T4.
Even though there is a 10:1 T4 to T3 ration, T3 is 3x-4x more active than T4.
Hypothalamus Pituitary Thyroid (HPT) Feedback Loop
Thyroid function controlled by hypothalamus, pituitary, and thyroid glands
Hypothalamus: Thyrotropin-releasing hormone (TRH) secreted to anterior pituitary
Anterior Pituitary: Thyrotropin-stimulating hormone (TSH) released to thyroid gland
Thyroid Gland: Synthesis and secretion of T4 and T3
Cell: T4 converted to T3 by iodinase enzyme
Homeostasis
ThyroidHormone Functions
Increases myocardial contractility decreases SVR, increases intravascular volume
Stimulates protein synthesis, carbohydrate metabolism, and lipid metabolism
Regulation of weight, temperature, energy levels
Hyperthyroidism: TSH and T3/T4 levels
Hypothyroidism: TSH and T3/T4 levels
Hyperthyroidism = low TSH with elevated T3and T4
Hypothyroidism = high TSH with reduced levels of T3 and T4
What is Hyperthyroidism?
Signs and symptoms.
Hyper-functioning thyroid gland, with excessive secretion of T3 and T4
What is Graves disease?
Who does it occur more in?
A systemic, autoimmune disease where thyroid-stimulating antibodies cause the thyroid gland to release large amounts of T3/T4 (you will see a low TSH level).
Occurs in females > males
What is ThyroidThyroid Storm (Thyrotoxicosis)
Signs and Sx.
Treatment.
Life-threatening exacerbation of hyperthyroidism
S/S: extreme anxiety, fever, tachycardia, CV instability, dehydration, and altered consciousness
TX: alleviate thyrotoxicosis and general supportive care
Crystalloids - should contain glucose
Dexamethasone - stop the peripheral conversion of T4 to T3
Propylthiouracil (PTU) - interferes with the peroxidase enzyme
Phenylephrine - if the patient goes into circulatory shock
Beta-blockers (propranolol) - control HR, and will also stop peripheral conversion from T4 to T3
Hyperthyroidism Treatment (Durgs/Procedures)
Propylthiouracil (PTU) - first-line treatment, overloads the peroxidase enzyme, 6-8 weeks before surgery to achieve a euthyroid state.
Iodide - large overdose will decrease T3 and T4 production (short-term fix).
Beta antagonists - Propranolol will decrease the peripheral conversion of T4 to T3.
Subtotal or total thyroidectomy- can inadvertently remove the parathyroid hormone
Ablation
HyperthyroidAnesthetic Considerations.
Meds:
Airway:
Drugs to Avoid:
Eyes:
Want to achieve euthyroidism (use PTU 6-8 weeks)
If it is an emergency case, use β-blockers (propranolol), ipodate (iodide), and glucocorticoids to achieve short-term euthyroid.
Upper airway evaluation (look for goiter)
Avoid drugs that cause SNS stimulation
Epinephrine, ephedrine, ketamine, pancuronium, atropine
Eye protection - Exophthalmos, use an ointment and tape their eyes.
Hypothyroidism characteristics and conditions.
What autoimmune disorder is associated with this?
What will TSH and T3/T4 labs look like?
Medication for Treatment.
Decreased production of thyroid hormones despite adequate or increased levels of TSH
Hashimoto thyroiditis - Autoimmune disorder where antibodies attack the thyroid gland. There will be a goiter present d/t inflammation and the TSH trying to stimulate the thyroid gland.
Labs: High TSH with reduced levels of T3 and T4
Treatment: Levothyroxine, Go ahead and take this medication before surgery.
Hypothyroidism S/S
HypothyroidAnesthetic Considerations
Continue Levothyroxine
Airway- look for goiter/obstruction
Decreased GI emptying- treat as full stomach if they are not compliant with levothyroxine.
Hypodynamic CV - give anesthesia with care
Decreased ventilatory responsiveness- may take longer
Hypothermia - warm them with blankets.
Elective surgeries can wait until the euthyroid state has been achieved.
Adrenal Gland is made of up what two components?
What does each component release?
Adrenal cortex (outer layer)
Glucocorticoids (Cortisol) - “Sugar”
Mineralocorticoids - “Salt”
Androgens - “Sex”
Adrenal medulla (inner layer)
Epinephrine (85%)
NE (15%)
What is the hypothalamic-pituitary-adrenal (HPA) axis?
A neuroendocrine mechanism that mediates the effects of stressors by regulating numerous physiological processes, such as metabolism, immune responses, and the autonomic nervous system.
What does cortisol regulate?
How is cortisol inactivated and how is it excreted?
Regulate:
Carbohydrate, protein, and fatty acid metabolism
Enhances gluconeogenesis
Anti-inflammatory effects
Maintenance of blood pressure
Promotion of appetite
Na/K maintenance
Cortisol is inactivated by the liver; excreted in urine
What isPheochromocytoma?
Where are chromaffin cells located?
What is the percentage of NE: EPI released d/t pheochromocytoma?
Catecholamine-secreting tumor from the Chromaffin cells. The cause is unknown.
Chromaffin cells are located in the adrenal medulla
85% Norepinephrine and 15% Epinephrine This percentage is switched in the normal adrenal medulla.
Pheochromocytoma S/S
Extreme HTN (>220/120)
Headache, sweating, pallor, and palpitations
ECG will show
ST-segment elevation or depression
Left Axis Deviation
Dysrhythmias
PheochromocytomaAnesthetic Considerations
Phenoxybenzamine
Non-competitive α-blocker
D/C 24-48 hours before surgery
Prazosin and doxazosin
α1-competitive blockers
Metyrosine - Catecholamine synthesis inhibitor
CCBs and ACE-I - use to control hypertension
Tachycardia > 120 bpm or other dysrhythmias after α-blockade, give β-adrenergic blocker
Avoid beta blockade before alpha blockade
What is Cushing Syndrome (Hypercortisolism)?
Chronic exposure to excess glucocorticoids.
Overproduction of ACTH leads to excess cortisol.
Can also develop from chronic exposure to exogenous corticoids.
Cushing Syndrome (Hypercortisolism) S/Sx.
Truncal obesity
Hyperglycemia
HTN
Skeletal muscle weakness
Osteoporosis
Hypokalemia
Cushing Syndrome Treatment
Transphenoidal microadenomectomy
Anterior pituitary resection
Cushing Syndrome Anesthetic Considerations
Blood glucose and HTN control
Assess skeletal muscle weakness
Replace potassium
Conn Syndrome(Primary Hyperaldosteronism) characteristics and S/S.
Mineralocorticoid (aldosterone) excess, usually a result of a tumor
S/S
Hypokalemic HTN (LOW K+ and High BP)
Skeletal muscle weakness and cramps
Headache
Polyuria
Nocturia
Conn Syndrome Treatment and Anesthetic considerations.
HTN control
Restricting sodium intake
Spironolactone
Potassium replacement
Volume replacement
Addison’s Disease (Primary Adrenal Insufficiency) Characteristics and S/S.
The underproduction of glucocorticoids, mineralocorticoids, and androgens d/t bilateral adrenal destruction
S/S
Fatigue, weakness,anorexia, N/V, hyperpigmentation (tan), hypovolemia, hyponatremia, and hyperkalemia
Addison’s Disease (Primary Adrenal Insufficiency) Anesthetic Considerations.
Anesthetic Considerations
Preoperative glucocorticoid coverage
Electrolytes (Na+ replacement)
Hydration
Minimal doses of narcotics
HPA Suppression and Stress Dose
Exogenous glucocorticoids suppress cortisol secretion
Adrenal insufficiency and adrenal atrophy
May blunt the normal cortisol hypersecretion
Stress dose with HPA Suppression if patient has taken
>20 mg prednisone/day, >3 weeks
No suppression with short-duration, low-dose steroids
What hormone does the parathyroid gland release? What is its function?
PTH
Calcium levels and bone remodeling
Low Serum calcium and Low vitamin D will increase PTH
PTH and Calcitonin reponse loop
What isHyperparathyroidism, what is it caused by, and what age group does it most likely affect?
Excess production of PTH leads to hypercalcemiawith calcium levels exceeding 5.5 mEq/L (normal 4.4-5.2 mEq/L).
Usually caused by parathyroid hyperplasia or a parathyroid adenoma (90%).
Age group affected: the 30s-50s.
Hyperparathyroidism S/S
CNS:
NM:
GI:
Renal:
Early S/S:
CNS: confusion, depression
NM: weakness, fatigue
GI: anorexia, N/V, constipation, PUD
Renal: kidney stones
Early S/S: sedation and vomiting. Loss of skeletal muscle strength and mass noted.
Hyperparathyroidism treatment and anesthetic considerations
Treatment: Parathyroidectomy
Anesthetic Considerations
Hydration
NMBDs unpredictable - d/t hypercalcemia, use less
Positioning - osteoporosis
Confusion/weakness
ECG
Hypoparathyroidism characteristics and S/S.
CNS:
MS:
Respiratory:
CV:
Absence/ deficiency of PTH secretion or resistance of PTH to peripheral tissues which will lead to Hypocalcemia (Ca < 4.5 mEq/L).
CNS: fatigue and seizures
MS: skeletal muscle spasms, tetany
Respiratory: stridor and apnea
CV: Prolonged QT
Hypoparathyroidism Treatment and Anesthetic Considerations
Treatment: Electrolyte replacement
Anesthetic Considerations:
Electrolytes
cautious administration NMBDs and sedatives
ECG
Avoid respiratory alkalosis (Lowers ionized Ca2+ levels).
Hormones of the Pituitary Gland
Anterior and posterior lobes
Anterior pituitary
GH, TSH, FSH, LH, ACTH, Prolactin
Posterior pituitary
Vasopressin (ADH) and oxytocin
What is the cause of Acromegaly?
S/S.
Airway:
MS:
Glucose:
CV:
Excessive secretion of GH
S/S:
Airway: tongue and epiglottis enlargement, hoarseness
MS: OA, osteoporosis, skeletal muscle weakness, fatigue
Glucose intolerance
CV: systemic HTN, ischemic heart disease
Acromegaly treatment.
Anesthetic considerations.
TX: transsphenoidal surgery
Anesthetic Considerations
Distorted facial anatomy - difficult to bag mask
Airway obstruction and poor visualization of vocal cords
History of dyspnea on exertion, hoarseness, stridor
Monitor blood glucose
Muscle weakness
Diabetes Insipidus Characteristics
What is used to differentiate neuro DI vs nephro DI?
S/S of DI.
Decrease of synthesis and release of ADH (neurogenic)
Resistance or insensitivity of renal tubules to ADH (nephrogenic)
Response to DDAVP differentiates neurogenic from nephrogenic. Neurogenic DI will respond to the DDAVP challenge.
S/S:
Polydipsia, eleavated serum osmolality, and large volume diluted urine. AMS/seizures,fatigue, weakness, and hemodynamic instability
Diabetes Insipidus treatment and anesthetic considerations.
Treatment
Neurogenic – DDAVP
Nephrogenic – Diuretics
Anesthetic considerations
Monitoring urine output
Monitor and replace electrolytes
Syndrome of Inappropriate ADH (SIADH) Characteristics and S/S.
Excessive secretion of ADH is usually from lung carcinoma.
S/S: nausea, weakness, lethargy, confusion, depressed mental status, and seizures
Hyponatremia, decreased serum osmolality, and increased urine osmolality
Syndrome of Inappropriate ADH (SIADH) treatment.
Treatment of the malignancy
Restrict free water
Demeclocycline - inhibits ADH in renal tubules
Severe hyponatremia - give NS or 3% saline
Syndrome of Inappropriate ADH (SIADH) anesthetic considerations.
Frequent measurements of:
IVF:
What drugs to avoid:
Frequent measurement of urine osmolality, plasma osmolality, and serum Na
Careful administration of IVF
Avoid drugs that increase confusion (BZD, ketamine)
