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Health Assessment > Exam 2 Endocrine > Flashcards

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

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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3
Q

The hormone that increases BS by stimulating hepatic glucose production

A

Glucagon

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4
Q

The hormone that decreases BS

A

Insulin

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5
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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6
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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7
Q

PancreasInsulin/Glucagon Feedback Loop

A
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8
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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9
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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10
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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11
Q

DM Diagnosis

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

A
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12
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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13
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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14
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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15
Q

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

A
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16
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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17
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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18
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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19
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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20
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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21
Q

Macrovascular Complicationsof DM

A

Elevated triglyceride levels, low HDL, and high LDL

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22
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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23
Q

How many lobes and isthmus make up the thyroid?

A

2 lobes
1 isthmus

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24
Q

How many parathyroid glands are there?

A

4

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25
Q

Fucntion of Thyroglobulin and Parafollicular C cells

A

Thyroglobulin: T3 and T4 productions
Parafollicular C cells: calcitonin production, secreted d/t hypercalcemia

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26
Q

Thyroid HormoneSynthesis Process

A

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.

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27
Q

Hypothalamus Pituitary Thyroid (HPT) Feedback Loop

A

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

28
Q

ThyroidHormone Functions

A

Increases myocardial contractility decreases SVR, increases intravascular volume

Stimulates protein synthesis, carbohydrate metabolism, and lipid metabolism

Regulation of weight, temperature, energy levels

29
Q

Hyperthyroidism: TSH and T3/T4 levels

Hypothyroidism: TSH and T3/T4 levels

A

Hyperthyroidism = low TSH with elevated T3and T4

Hypothyroidism = high TSH with reduced levels of T3 and T4

30
Q

What is Hyperthyroidism?
Signs and symptoms.

A

Hyper-functioning thyroid gland, with excessive secretion of T3 and T4

31
Q

What is Graves disease?
Who does it occur more in?

A

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

32
Q

What is ThyroidThyroid Storm (Thyrotoxicosis)

Signs and Sx.

Treatment.

A

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

33
Q

Hyperthyroidism Treatment (Durgs/Procedures)

A

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

34
Q

HyperthyroidAnesthetic Considerations.
Meds:
Airway:
Drugs to Avoid:
Eyes:

A

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.

35
Q

Hypothyroidism characteristics and conditions.

What autoimmune disorder is associated with this?

What will TSH and T3/T4 labs look like?

Medication for Treatment.

A

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.

36
Q

Hypothyroidism S/S

A
37
Q

HypothyroidAnesthetic Considerations

A

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.

38
Q

Adrenal Gland is made of up what two components?
What does each component release?

A

Adrenal cortex (outer layer)
Glucocorticoids (Cortisol) - “Sugar”
Mineralocorticoids - “Salt”
Androgens - “Sex”

Adrenal medulla (inner layer)
Epinephrine (85%)
NE (15%)

39
Q

What is the hypothalamic-pituitary-adrenal (HPA) axis?

A

A neuroendocrine mechanism that mediates the effects of stressors by regulating numerous physiological processes, such as metabolism, immune responses, and the autonomic nervous system.

40
Q

What does cortisol regulate?

How is cortisol inactivated and how is it excreted?

A

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

41
Q

What isPheochromocytoma?

Where are chromaffin cells located?

What is the percentage of NE: EPI released d/t pheochromocytoma?

A

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.

42
Q

Pheochromocytoma S/S

A

Extreme HTN (>220/120)

Headache, sweating, pallor, and palpitations

ECG will show
ST-segment elevation or depression
Left Axis Deviation
Dysrhythmias

43
Q

PheochromocytomaAnesthetic Considerations

A

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

44
Q

What is Cushing Syndrome (Hypercortisolism)?

A

Chronic exposure to excess glucocorticoids.
Overproduction of ACTH leads to excess cortisol.
Can also develop from chronic exposure to exogenous corticoids.

45
Q

Cushing Syndrome (Hypercortisolism) S/Sx.

A

Truncal obesity
Hyperglycemia
HTN
Skeletal muscle weakness
Osteoporosis
Hypokalemia

46
Q

Cushing Syndrome Treatment

A

Transphenoidal microadenomectomy
Anterior pituitary resection

47
Q

Cushing Syndrome Anesthetic Considerations

A

Blood glucose and HTN control
Assess skeletal muscle weakness
Replace potassium

48
Q

Conn Syndrome(Primary Hyperaldosteronism) characteristics and S/S.

A

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

49
Q

Conn Syndrome Treatment and Anesthetic considerations.

A

HTN control
Restricting sodium intake
Spironolactone
Potassium replacement
Volume replacement

50
Q

Addison’s Disease (Primary Adrenal Insufficiency) Characteristics and S/S.

A

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

51
Q

Addison’s Disease (Primary Adrenal Insufficiency) Anesthetic Considerations.

A

Anesthetic Considerations
Preoperative glucocorticoid coverage
Electrolytes (Na+ replacement)
Hydration
Minimal doses of narcotics

52
Q

HPA Suppression and Stress Dose

A

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

53
Q

What hormone does the parathyroid gland release? What is its function?

A

PTH
Calcium levels and bone remodeling

Low Serum calcium and Low vitamin D will increase PTH

54
Q

PTH and Calcitonin reponse loop

A
55
Q

What isHyperparathyroidism, what is it caused by, and what age group does it most likely affect?

A

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.

56
Q

Hyperparathyroidism S/S
CNS:
NM:
GI:
Renal:
Early S/S:

A

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.

57
Q

Hyperparathyroidism treatment and anesthetic considerations

A

Treatment: Parathyroidectomy

Anesthetic Considerations
Hydration
NMBDs unpredictable - d/t hypercalcemia, use less
Positioning - osteoporosis
Confusion/weakness
ECG

58
Q

Hypoparathyroidism characteristics and S/S.
CNS:
MS:
Respiratory:
CV:

A

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

59
Q

Hypoparathyroidism Treatment and Anesthetic Considerations

A

Treatment: Electrolyte replacement

Anesthetic Considerations:
Electrolytes
cautious administration NMBDs and sedatives
ECG
Avoid respiratory alkalosis (Lowers ionized Ca2+ levels).

60
Q

Hormones of the Pituitary Gland

A

Anterior and posterior lobes

Anterior pituitary
GH, TSH, FSH, LH, ACTH, Prolactin

Posterior pituitary
Vasopressin (ADH) and oxytocin

61
Q

What is the cause of Acromegaly?

S/S.
Airway:
MS:
Glucose:
CV:

A

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

62
Q

Acromegaly treatment.

Anesthetic considerations.

A

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

63
Q

Diabetes Insipidus Characteristics

What is used to differentiate neuro DI vs nephro DI?

S/S of DI.

A

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

64
Q

Diabetes Insipidus treatment and anesthetic considerations.

A

Treatment
Neurogenic – DDAVP
Nephrogenic – Diuretics

Anesthetic considerations
Monitoring urine output
Monitor and replace electrolytes

65
Q

Syndrome of Inappropriate ADH (SIADH) Characteristics and S/S.

A

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

66
Q

Syndrome of Inappropriate ADH (SIADH) treatment.

A

Treatment of the malignancy
Restrict free water
Demeclocycline - inhibits ADH in renal tubules
Severe hyponatremia - give NS or 3% saline

67
Q

Syndrome of Inappropriate ADH (SIADH) anesthetic considerations.

Frequent measurements of:
IVF:
What drugs to avoid:

A

Frequent measurement of urine osmolality, plasma osmolality, and serum Na

Careful administration of IVF

Avoid drugs that increase confusion (BZD, ketamine)

Health Assessment (26 decks)

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