Exam 2 Endocrine Flashcards

1
Q

What are the functions of the Pancreas?

A

Digestion, metabolism, utilization, and storage of energy substrates.

Made up of Exocrine and Endocrine cells.

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2
Q

What are the functions of the Pancreas?

A

Digestion, metabolism, utilization, and storage of energy substrates.

Made up of Exocrine and Endocrine cells.

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3
Q
A
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4
Q

The endocrine cells (islets of Langerhans) of the Pancreas are composed of what kind of cells?

Exocrine cell function.

A

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.

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5
Q

The hormone that increases BS by stimulating hepatic glucose production

A

Glucagon

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6
Q

The hormone that decreases BS

A

Insulin

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7
Q

Glucose physiology is a balance between_______
and _________.

A

Glucose physiology is a balance between glucose utilization
and endogenous production or dietary delivery.

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8
Q

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 ________.

A

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.

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9
Q

PancreasInsulin/Glucagon Feedback Loop

A
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10
Q

What is Diabetes Mellitus?

Signs and Symptoms of Diabetes Mellitus

A

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

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11
Q

Type 1 DM Characteristics

A

T cell–mediated autoimmune destruction of beta cells
Absence or minimal circulating levels of insulin
80%–90% beta cell function lost
Always need insulin

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12
Q

Type 2 DM Characteristics

What are 3 things we see in DM 2?

A

Relative beta cell insufficiency and insulin resistance
Pancreatic cell function decreases⇨insulin levels are unable to compensate⇨hyperglycemia

  1. Increased rate of hepatic glucose release
  2. Impaired basal and stimulated insulin secretion
  3. Insulin resistance
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13
Q

DM Diagnosis

A1C:
Fasting Glucose (8 hours):
Glucose Tolerance Test:
Random Glucose:

A
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14
Q

DM Treatment (Initial Therapy)

A

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)

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15
Q

Types of Insulin for DM Treatment.

A

Rapid Acting or Short Acting (Regular) -Provides glycemic control at mealtimes

Basal -Intermediate-acting and administered 2x daily

Long Acting -Administered once daily

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16
Q

What is DM DKA and Sign/Sx

A

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

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17
Q

DM DKA
Serum Glucose Level
pH
HCO3-
Serum Osmolarity
Serum and urine ketone levels

A
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18
Q

DMDKA Treatment

A

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

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19
Q

DMHyperglycemic hyperosmolar syndrome (HHS) description, labs, and symptoms.

A

Present in DM2 patients: Severe hyperglycemia, hyperosmolarity, and dehydration.

metabolic acidosis (only in severe dehydration or organ failure secondary to HHS)

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20
Q

DMHyperglycemic hyperosmolar syndrome (HHS) treatment.

A

Fluid resuscitation, insulin gtt ,and electrolyte replacement

Hypotonic saline if plasma osmolarity >320mOsm/L to bring osmolarity down.

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21
Q

What microvascular complications can be seen with DM?

A

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

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22
Q

Autonomic Neuropathy of DM
CV:
GI:

A

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

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23
Q

Macrovascular Complicationsof DM

A

Elevated triglyceride levels, low HDL, and high LDL

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24
Q

DMAnesthetic Considerations
CV:
Renal:
GI:
MS:
Insulin and Meds:

A

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

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25
How many lobes and isthmus make up the thyroid?
2 lobes 1 isthmus
26
How many parathyroid glands are there?
4
27
Fucntion of Thyroglobulin and Parafollicular C cells
Thyroglobulin: T3 and T4 productions Parafollicular C cells: calcitonin production, secreted d/t hypercalcemia
28
Thyroid Hormone Synthesis 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.
29
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
30
Thyroid Hormone Functions
Increases myocardial contractility decreases SVR, increases intravascular volume Stimulates protein synthesis, carbohydrate metabolism, and lipid metabolism  Regulation of weight, temperature, energy levels
31
Hyperthyroidism: TSH and T3/T4 levels Hypothyroidism: TSH and T3/T4 levels
Hyperthyroidism = low TSH  with elevated T3 and T4 Hypothyroidism = high  TSH  with reduced levels of T3 and T4 
32
What is Hyperthyroidism? Signs and symptoms.
Hyper-functioning thyroid gland, with excessive secretion of T3 and T4
33
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
34
What is Thyroid Thyroid 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
35
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
36
Hyperthyroid Anesthetic 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.
37
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.**
38
Hypothyroidism S/S
39
Hypothyroid Anesthetic 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.
40
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%)**
41
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.
42
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**
43
What is Pheochromocytoma? 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.
44
Pheochromocytoma S/S
Extreme HTN (>220/120) Headache, sweating, pallor, and palpitations ECG will show ST-segment elevation or depression Left Axis Deviation Dysrhythmias
45
Pheochromocytoma Anesthetic 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**
46
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.
47
Cushing Syndrome (Hypercortisolism) S/Sx.
Truncal obesity Hyperglycemia HTN Skeletal muscle weakness Osteoporosis Hypokalemia
48
Cushing Syndrome Treatment
Transphenoidal microadenomectomy Anterior pituitary resection
49
Cushing Syndrome Anesthetic Considerations
Blood glucose and HTN control Assess skeletal muscle weakness Replace potassium 
50
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
51
Conn Syndrome Treatment and Anesthetic considerations.
HTN control Restricting sodium intake **Spironolactone** Potassium replacement Volume replacement 
52
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 
53
Addison’s Disease (Primary Adrenal Insufficiency) Anesthetic Considerations.
Anesthetic Considerations Preoperative glucocorticoid  coverage Electrolytes (Na+ replacement) Hydration Minimal doses of narcotics
54
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
55
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
56
PTH and Calcitonin reponse loop
57
What is Hyperparathyroidism, what is it caused by, and what age group does it most likely affect?
Excess production of PTH leads to hypercalcemia with 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.
58
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.
59
Hyperparathyroidism treatment and anesthetic considerations
Treatment: Parathyroidectomy Anesthetic Considerations Hydration **NMBDs unpredictable** - d/t hypercalcemia, use less **Positioning - osteoporosis** Confusion/weakness ECG
60
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
61
Hypoparathyroidism Treatment and Anesthetic Considerations
Treatment: Electrolyte replacement Anesthetic Considerations: Electrolytes cautious administration NMBDs and sedatives ECG  Avoid respiratory alkalosis (Lowers ionized Ca2+ levels).
62
Hormones of the Pituitary Gland
Anterior and posterior lobes Anterior pituitary GH, TSH, FSH, LH, ACTH, Prolactin Posterior pituitary Vasopressin (ADH) and oxytocin
63
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
64
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
65
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 
66
Diabetes Insipidus treatment and anesthetic considerations.
Treatment Neurogenic – DDAVP Nephrogenic – Diuretics Anesthetic considerations Monitoring urine output Monitor and replace electrolytes
67
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 
68
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
69
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)