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Bioscience II Josh > Endocrine System & Diseases > Flashcards

Endocrine System & Diseases Flashcards

1
Q

What is paracrine signaling?

A

Signaling between local cells

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2
Q

What is endocrine signaling?

A

Between remote cells

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3
Q

What are some general characteristics of hormonal function/regulation?

A
  • specific rates and rhythm of secretion
  • operate within feedback systems
  • only affects cells with appropriate receptors to initiate specific functions
  • either excreted by kidney or metabolized by liver
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4
Q

What are the 3 mechanisms involved in the regulation of hormone release?

A

Chemical factors (blood sugar, calcium levels), endocrine factors (hormone from one gland controlling another gland), neural control

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5
Q

Identify and explain the most common type of feedback system.

A

Negative feedback system: plasma levels of one hormone influence the plasma levels of another hormone

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6
Q

Explain the negative feedback system involved in the hypothalamic-pituitary-adrenal axis.

A

Normal hormone release is as follows… Hypothalamus secretes corticotropin releasing hormone (CRH)…. Triggers release of adrenocorticotropic hormone release by the anterior pituitary… Cortisol levels increase…

When they exceeds a certain plasma level the negative feedback system triggers the hypothalamus to stop releasing CRH

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7
Q

Are peptide and protein hormones water or lipid soluble? What effect does this have on a hormone?

A

Peptide/Protein hormones are water soluble…and circulate in free/unbound form (only unbound hormones can affect the target site)

Lipid soluble hormones are primarily circulated bound to a carrier or protein (only small % are unbound)

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8
Q

Where are hormone receptors located and how do water soluble and lipid soluble hormones bind?

A

They are located on plasma membrane or in intra cellular compartments of the target cell; water soluble hormones bind to receptors on the cell membrane, while lipid soluble hormones (such as steroid hormones) easily diffuse across the cell membrane and bind either cytosolic or nuclear receptors

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9
Q

Does the pancreas function as an endocrine system… Or as an exocrine system?

A

Both!: as an endocrine system it secretes insulin, glucagon, somatostatin, and pancreatic polypeptide

As an exocrine system it is composed of acinar cells that secretes enzymes and networks of ducts that secrete alkaline fluids with digestive functions (80-85% of the pancreas)
The alkaline juices neutralize acidic chyme that enters the duodenum from the stomach and facilitates absorption of fat in the intestine

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10
Q

What is secreted from the alpha and beta cells of the pancreas?

A

Alpha cells secrete glucagon, beta cells secrete insulin

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11
Q

What is the primary cause of acute pancreatitis?

A

Gallstones and heavy alcohol use are responsible for 60-80%; other causes include infection, trauma, surgery, metabolic disorders (hypercalcemia, hyperlipidemia), some meds (flagyl, tetracycline, ace inhibitors, corticosteroids)

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12
Q

What is the primary cause of damage during periods of inflammation of the pancreas?

A

Digestive enzymes become activated before entering the duodenum and begin attacking the pancreas

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13
Q

What is acute necrotizing pancreatitis?

A

A severe form of pancreatitis characterized by necrosis and subsequent infection

Inflammation leads to necrosis which will typically become infected by gram negative bacteria in the alimentary tract….. Tissues become infected (acinar, ductal, islets of L)…. Vascular injury can lead to massive hemorrhage within the pancreas

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14
Q

What is the primary signs, symptoms, and patho of acute pancreatitis?

A

Midepigastric pain radiating to the back, n/v, abdominal distention, tetany (from hypocalcemia), fever, paralytic ileus, hypoxemia

Injury or disruption of acinar cells permits leakage of pancreatic enzymes—- breaks down tissue and cell membranes— causes inflammation, edema, vascular damage, necrosis….

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15
Q

What is the hallmark sign used for diagnosis of acute pancreatitis?

A

Elevated serum amylase level; but serum lipase is more specific and sensitive for the diagnosis of AP

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16
Q

What are the normal values for serum amylase and serum lipase?

A

Amylase 60-180u/L
Lipase 10-140u/L
3 times normal with acute AP

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17
Q

What is the goal of treatment for acute pancreatitis?

A

Stop auto digestion and prevent systemic complications

Aggressive fluid administration, Demerol over morphine (< sphincter of oddi spasm), bowel rest (NGT and TPN), h2 blocker, stone removal, antibiotics if necrotizing, surgery (ERCP, surgical debridement)

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18
Q

What is the patho and primary causes of chronic pancreatitis?

A

Chronic alcohol, smoking, obstruction from gallstones, autoimmune, obesity, genetic mutations

Toxic metabolites and chronic release of cytokines contribute to destruction of acinar cells and islets of langerhans—-> fibrosis structures, calcification, ductal obstruction, pancreatic cysts

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19
Q

What are the signs and symptoms of chronic pancreatitis? Preventative measures?

A

Abdominal pain (continuous or intermittent), weight loss, DM, steatorrhea (pooping excess fat d/t decreased absorption)

Lifestyle modification, fat free diet, enzyme replacement, surgical drainage or resection

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20
Q

What are some anesthetic considerations for patient with pancreatitis?

A

Consider RSI (aspiration), fluid and electrolyte disturbance, monitor glucose, check Coags, pulmonary assessment, monitor renal function (UOP > 0.5 ml/kg/hr

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21
Q

What 3 physiologic processes do thyroid hormones have the most profound effects?

A

Growth, development, metabolism

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22
Q

Explain the primary characteristics of T3 and T4. Compare and contrast.

A

T3 is primary made during the conversion of T4 at the target tissues. It only comprises 10% of the circulating thyroid hormone but is responsible for 80% of the metabolic activity due to its high potency.

T4 is secreted by the thyroid and makes up 90% of the circulating thyroid hormone.

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23
Q

Explain the regulation of thyroid hormone.

A

Stimulus such as hypothermia causes the hypothalamus to secrete thyrotropin releasing hormone (TRH) which signals the thyrotropic cells of the anterior pituitary to secrete thyroid stimulating hormone (TSH)….. TSH causes follicular cells of the thyroid to release thyroid hormone….TH stimulates target cells to increase metabolic activity, resulting in an increase in body temperature….. Increased temperature is detected by the hypothalamus which discontinues release of (TRH)…. TH also blocks the ability of TRH to interact with the anterior pituitary gland to prevent TSH formation….. This is a type of negative feedback system

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24
Q

The ability of the thyroid to have normal quantities of thyroid hormones depends on what source?

A

Exogenous iodine

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25
Q

What are normal serum TSH levels?

A

0.5-5 mu/L; small changes in thyroid function causes significant changes in TSH; single best test of thyroid hormone action at the cellular level

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26
Q

What are some signs and symptoms of hypothyroidism?

A

Weight gain, cold intolerance, muscle fatigue/weakness, constipation, depression, decreased CO, SV, HR, contractility

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27
Q

What is the concern with severe hypothyroidism?

A

Myxedema coma… From extreme hypothyroidism…. Impaired mentation, hypo ventilation, CHF, hypothermia

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28
Q

What is autocrine signaling?

A

Signaling within the cell

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29
Q

When is it appropriate to place a PA catheter for resection of a pheochromocytoma?

A

In presence of CHF or decreased cardiac reserve; monitor pulmonary capillary wedge pressure

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30
Q

What is the purpose of the alpha adrenergic blockade in a pheochromocytoma case?

A

BP reduction/control and to assist with vascular relaxation to allow volume expansion

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31
Q

Why is a high sodium diet recommended after the second or third day of alpha blockade, and when is it contraindicated?

A

To assist in volume expansion with adequate alpha blockade; contraindicated in presence of CHF and renal insufficiency

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32
Q

Why should beta blockade never be initiated before alpha blockade?

A

Because blockade of vasodilatory peripheral beta receptors with unopposed alpha adrenergic receptor stimulation can lead to further elevation in BP

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33
Q

What would be the primary differential diagnosis if your patient experiences acute pulmonary edema after initiation of beta blockade?

A

Underlying catecholamine excess cardiomyopathy

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34
Q

If a patient experiences intolerable side effects with alpha blockade, what drug class can be used in its place or as a supplement?

A

CCB’s

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35
Q

What is the role of metyrosine in preparation for pheochromocytoma surgery?

A

Inhibits catecholamine synthesis; a study showed patients given metyrosine had smoother intra op course than those receiving phenoxybenzamine alone; most reports state to use it with caution only when other preop methods are not tolerated or ineffective; according to short term therapy used by Mayo, the main side effect is hyper somnolence

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36
Q

What curative treatment options are available for malignant pheochromocytoma?

A

No curative treatment unless sites of the disease are surgically resectable

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37
Q

What is an appropriate medication to give preop if your patient is planned to have a bilateral adrenalectomy?

A

Glucocorticoid stress coverage

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38
Q

According to one article, what risk factors are associated with increased incidence of intra op hypertensive events?

A

Higher preop norepinephrine plasma concentration, larger tumor size >4cm, more pronounced postural BP fall after alpha blockade (>10mmhg)

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39
Q

What drugs can be used intraoperatively with the occurrence of a hypertensive crisis associated with a pheochromocytoma?

A

IV sodium nitroprusside (ideal vasodilator….rapid onset and short duration…0.5-5mcg/kg/min…prolonged infusion no more than 3mcg/kg/min), phenolamine (short acting non-selective alpha adrenergic blocker…initial test dose of 1mg followed by repeat 5mg bolts or infusion…bolus lasts about 10-15 min), or nicardipine (CCB… Can start at 5mg/hour…titration to max of 15mg/hr)

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40
Q

Why can hypoglycemia occur after a thyroidectomy or removal of a pheochromocytoma?

A

Catecholamines suppress insulin secretion…. So removal of surplus Catecholamines will stop suppression of insulin… Thus causing potential for hypoglycemia?

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41
Q

What is the classic triad of pheochromocytoma?

A

Episodic headache, sweating, and tachycardia in association with hypertension

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42
Q

In the case of pheochromocytoma, a patient with MEN2 and evidence of bilateral disease on imaging should receive what type of surgical intervention?

A

Bilateral adrenalectomy d/t risk of recurrent pheochromocytoma

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43
Q

In the case of pheochromocytoma, a patient with VHL and evidence of bilateral disease on imaging should receive what type of surgical intervention?

A

VHL is a less diffuse medullary disease…. Suggest cortical sparing bilateral adrenalectomy… D/t risk of recurrence, long term biochemical monitoring is suggested

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44
Q

What is the suggested surgical intervention for patient with MEN2 or VHL with unilateral pheochromocytoma?

A

Unilateral adrenalectomy…. Then annual biochemical testing for contralateral pheochromocytoma

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45
Q

Just some information on complications that are associated with diabetic patients:

A

Heart disease 68%, hypertension 67%, nervous system 60-70%, amputations 60% of all non-traumatic cases, stroke 16%, kidney disease

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46
Q

What is the general definition of diabetes?

A

A disease process that results in either an inadequate production of insulin, or inadequate tissue response to insulin

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47
Q

Describe the process of blood glucose homeostasis that is maintained by the pancreas and liver upon consuming food.

A

Blood sugar rises…. Beta cells of pancreas secrete insulin into the blood…muscle and other cells use this glucose as energy or converts it to glycogen…liver converts glucose into glycogen, fats, and protein… Homeostasis is achieved when blood glucose is < 110mg/DL

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48
Q

Describe the process of blood glucose homeostasis that occurs between meals when glucose levels may fall.

A

Cells use or store glucose between meals….this creates a low blood sugar…alpha cells of pancreas release glucagon…glucagon converts glycogen stored in the liver into glucose… As blood sugar rises, less glucagon is produced

49
Q

In regards to insulin, where is it synthesized, what 3 things regulate it, what is its purpose, and where is it metabolized?

A

It is synthesized in the beta cells of the pancreas…. Regulated by chemical, hormonal, and neural control…it facilitates glucose uptake into cells to use for energy…and is metabolized by liver and kidneys

50
Q

What is the cause and prevalence of type 1 diabetes?

A

Represents approximately 5-10% of all cases… Caused by T cell mediated autoimmune destruction of beta cells, resulting in 80-90% destruction and minimal to no circulating insulin…. Exact cause is unknown

51
Q

What are some characteristics of type 2 diabetes?

A

Represents approximately 90% of cases….most people have it for 4-6 years before diagnosis…slow insensitivity and resistance to insulin…slow exhaustion of beta cells and inhibition of signaling

52
Q

Compare and contrast type 1 & 2 diabetes.

A

Type 1: sudden onset, occurs at any age but mostly young, thin or normal weight, ketoacidosis is common, autoantibodies are usually present, endogenous insulin is low or absent, 5-10% of cases

Type 2: gradual onset, occurs mostly in adults (genetic or obesity), often obese, ketoacidosis is rare, autoantibodies are absent, normal-increased-or decreased endogenous insulin, 90-95% of diabetes

53
Q

What are some clinical characteristics of diabetes?

A

Polydipsia, polyuria, polyphagia, tiredness, fungal infection, poor wound healing, deterioration of vision

54
Q

What are some characteristics of DKA?

A

It occurs when glucose levels exceed renal tubular excretion…more common in type 1 (d/t absent or minimal insulin production)….diuresis and hypovolemia…increased ketoacidosis…substantial deficits of water, Na, K, and phosphorus

55
Q

What are some characteristics of HHS?

A

More common in type 2…onset is days to weeks…persistent glycosuric diuresis…leads to: polydipsia, polyuria, hypovolemia, hypotension, tachycardia, organ hypo perfusion, mental obtundation…vascular occlusions

56
Q

What effect does an increase in stress hormones, such as glucagon, Catecholamines, cortisol, and growth hormone have on insulin?

A

Hyperglycemia d/t decreased insulin use and increase glucose production

57
Q

What are some of the causes of hypothyroidism?

A

Autoimmune (hashimoto), decreased iodine intake, anti thyroid meds, thyroidectomy, radioactive iodine

58
Q

A euthyroid state is required for any patient with hypothyroidism. (T/F?)

A

False: while euthyroid state is ideal, a mild to moderate hypothyroidism is not a contraindication to surgery

59
Q

What are some pre-operative anesthetic considerations for patients with hypothyroidism?

A

typically do not require much sedation; prone to respiratory depression; d\t delayed gastric emptying, may consider H2 blocker or Reglan; Regional is a good alternative if not contraindicated

60
Q

Why are patients with hypothyroidism more susceptible to hypotensive effects of anesthetic agents?

A

d\t decreased CO and intravascular volume, and blunted baroreceptor reflexes; Ketamine is recommended

61
Q

What are some potential problems an anesthetist can experience intraop with a hypothyroid patient?

A

d\t large tongue, may have difficult intubation; hypoglycemia, anemia, hyponatremia, hypothermia

62
Q

With hypothyroidism, why would you consider reducing the dose of opioids and muscle relaxant?

A

b\c drug metabolism may be slower; also use twitch monitor

63
Q

What effect may hypothermia have on emergence?

A

delayed recovery (also d\t resp depression and slower drug biotransformation)

64
Q

What are the 3 primary causes of hyperthyroidism that account for 99% of all cases?

A

Grave’s disease, toxic multinodular goiter, toxic adenoma

65
Q

What is hyperthyroidism?

A

excessive secretion of thyroid hormones

66
Q

What are the s\s of hyperthyroidism?

A

“hyper metabolic state”: anxious, restless, weight loss, fine tremor, heat intolerance, exopthalmos, goiter

67
Q

Drugs such as propylthiouracil, methimozole, propanolol, and radioactive iodine are typically involved in the treatment of ___________.

A

Hyperthyroidism

68
Q

What are some preoperative anesthetic considerations for hyperthyroidism?

A

must be euthyroid–> HR can take 6-8 weeks of medical treatment

continue thyroid meds and beta blockers, if there is a goiter ask about duration d\t possible tracheomalacia, examine neck and trachea for possible deviation/compression (especially if stridor or dyspnea are present— CT), SVC obstruction— distended neck veins that do not change with respirations, consider awake/asleep FOI

69
Q

What are some intraoperative anesthetic considerations for hyperthyroidism?

A

pad eyes (exop.), monitor temp and CV function, avoid meds that stimulate SNS, chronic hypovolemia=exaggerated hypotension, ensure adequate depth before DL or incision, cautious NMB use d\t increased myopathies and Myasthenia Gravis

70
Q

During surgery of a patient with hyperthyroidism he exhibits the following signs: altered LOC, hyperpyrexia, tachycardia, and HTN. The room nurse runs for the malignant hyperthermia cart. What are your thoughts?

A

thyroid storm: onset usually 6-24 hours postop, but can occur intra-op; mimics MH (no acidosis, muscle rigidity, elevated CK)

treat with hydration and cooling, esmolol infusion (HR), propylthiouracil 250-500mg Q6h, and correct precipitating cause

71
Q

What are postoperative concerns for a patient following a thyroidectomy?

A

postop stridor is indicative of bilateral RLN injury; hematoma (airway compromise…. remove sutures and call surgeon); hypoparathyroidism d\t accidental removal of parathyroid glands…. check calcium 24hrs postop

72
Q

Accidental removal of the parathyroid glands during a thyroidectomy is a possible risk. What are signs in the post-operative period that this may have occurred?

A

hypocalcemia: neuromuscular excitability, circumoral tingling, tetany, ventricular arrythmias, laryngospasm

73
Q

The adrenal glands consist of 2 portions called what?

A

inner medulla & outer cortex; they have different embryonic origins, different structures, and different hormonal functions

74
Q

What hormones are secreted by the inner medulla of the adrenal glands?

A

catecholamines: epinephrine, norepinephrine, dopamine

75
Q

What are the 3 structures of the outer cortex of the adrenal glands?

A

zona glomerulosa, zona fasiculata, zona reticularis

76
Q

Where is the zona glomerulosa, zona fasiculata, and zona reticularis located… and what hormones do they secrete?

A

within the outer cortex of the adrenal glands

zona glomerulosa: produces aldosterone
zona fasiculata & zona reticularis: other mineralcorticoids, androgens, estrogens, glucocorticoids (cortisol)

77
Q

Where are Chromaffin cells located?

A

in the adrenal medulla

78
Q

What is the name of a tumor that is located in Chromaffin cells?

A

pheochromocytoma

79
Q

What physiological alterations are associated with hypofunction of the adrenal medulla?

A

there are NO KNOWN alterations from hypofunction

80
Q

What is a pheochromocytoma?

A

a tumor in the Chromaffin cells of the adrenal medulla causing adrenomedullary hyperfunction–> secreting norepinephrine, epinephrine, or dopamine; solid, highly vascular

81
Q

Pheochromocytoma’s are the cause of approximately 0.1% of hypertension. (T/F?)

A

True

82
Q

How much norepinephrine is typically contained within an adult size pheochromocytoma?

A

100-800mg NE

83
Q

All pheochromocytomas are malignant. (T/F?)

A

false; < 10% are malignant

84
Q

What is the MOST frequent s\s of a pheochromocytoma?

A

HTN!!!!; other signs include headache, sweating, pallor, palpitations

85
Q

Acute presentations of a pheochromocytoma include: ???

A

CHF, MI, CVA

86
Q

Why is orthostatic hypotension common in patients with pheochromocytoma’s?

A

secondary to hypovolemia and impaired venous and arterial vasoconstrictor reflex response

87
Q

What are common diagnostic tests for a pheochromocytoma, and which is the MOST sensitive?

A

most sensitive for high risk individuals is plasma free metanephrines

other tests: adrenal CT/MRI, elevated urinary free catecholamine levels and their metabolites (24hr)

Can also do echo (catecholamine cardiomyopathy) & blood glucose level

88
Q

Describe the typical pre-operative preparation for a patient that will be undergoing surgery for removal of a pheochromocytoma?

A

initiate alpha blockade (phenoxybenzamine) approx 10-14 days before, but exact length is unknown….. start CCB if needed…… add beta blocker for tachycardia (cardioselective) prior to surgery…. monitor patient in house for 1-2 days prior to surgery and provide fluid replacement during the night before surgery

89
Q

When should alpha blockade be initiated for surgery involving a pheochromocytoma?

A

BEFORE BETA….. optimal duration is unknown…. 3 days to 2 weeks or >

90
Q

When should alpha blockade be stopped?

A

recommended to stop 24-48 hrs before surgery to avoid vascular unresponsiveness immediately following removal of tumor

91
Q

What are some recommended guidelines for a patient receiving surgery for a pheochromocytoma?

A

no inpatient BP > 160/90 24 hrs prior to surgery, no orthostatic BP < 80/45, no ST segment or T wave abnormality on ECG, no marked s\s of catecholamine excess or more than 1 PVC q5min

92
Q

What are some intraoperative anesthetic considerations?

A

avoid drugs/maneuvers that promote catecholamine release; ensure adequate depth prior to DL or incision; decrease stress, fear, anxiety, shivering, hypoxia, hypercarbia; avoid histamine release (morphine, atracurium); avoid vagolytic or sympathomimetic drugs (sux, atropine, pancuronium); arterial line, CVC + CVP; check BG, may be hypoglycemic after tumor is resected

common meds: nipride, magnesium, nicardipine, phentolamine, esmolol

93
Q

What should the anesthetist be prepared for following the ligation of the blood supply for a pheochromocytoma?

A

sudden HYPOTENSION; treat with volume support & direct acting vasopressor (phenylephrine)

94
Q

What is the most frequent cause of death in the post-op period following removal of a pheochromocytoma?

A

hypotension (vasopressors & fluids)

also consider hypoglycemia in post-op period (dextrose IV fluids, monitor BG for 24hrs)

95
Q

What is the difference in Cushing’s and Addison’s?

A

Cushing’s is a glucocorticoid excess and Addison’s is a glucocorticoid or mineralcorticoid deficiency

96
Q

What are the two types (locations) of Cushing’s disease? Why?

A

adrenal cortex (excess cortisol produced by adrenal gland tumors… hyperplasia, or nodular adrenal hyperplasia) or anterior pituitary (a benign pituitary adenoma secretes ACTH…. accounts for 70% of endogenous Cushing’s syndrome)

97
Q

What are the s\s of Cushing’s disease?

A

MOON FACE (volume OVERLOAD), obese, sleep apnea, muscle weakness, HTN, glucose intolerance, LVH, osteoporosis

98
Q

What are common anesthetic considerations for Cushing’s disease?

A

volume OVERLOAD, hypokalemic metabolic acidosis, risk for fractures with positioning, sensitive to NMB, GERD

99
Q

What is primary and secondary Addison’s disease?

A

both result in glucocorticoid/mineralcorticoid deficiency

primary: destruction or adrenal cortex by autoimmune, infection, septicemia, AIDs, hemorrhage, metastases, surgery
secondary: insufficient ACTH to stimulate the cortex d\t pituitary suppression by exogenous steroids or generalized hypopituitarism

100
Q

What are the s\s of Addison’s disease?

A

weakness, fatigue, skin hyperpigmentation, n/v/d, myalgias, postural hypotension (volume DEPLETION), decreased response to catecholamines, chronic hypotension/hypovolemia

101
Q

What are some anesthetic considerations for Addison’s disease?

A

continue steroids, sensitive to sedation, avoid ETOMIDATE (ADRENAL SUPPRESSION)

102
Q

What is the s\s, cause, and treatment of Addisonian crisis?

A

precipitated by stress, trauma, or infection;
s\s: tachycardia, n/v, hypotension, hypotension unresponsive to IV fluids, abdominal pain, AMS;
Tx: fluids with dextrose, steroid replacement, inotropes, electrolyte correction

103
Q

What cells do NOT require insulin for the transport of glucose?

A

brain and blood

104
Q

What percent of beta cells are typically destroyed before hyperglycemia ensues?

A

80-90%

105
Q

What is the typical treatment for nephropathy in diabetic patients?

A

treatment of HTN to retard the process… ACE inhibitors are beneficial because they decrease proteinuria and GFR; many diabetics are prophylactically treated with ACE in the absent of HTN to prevent nephropathy

106
Q

Explain the clinical course of nephropathy.

A

Glomerulosclerosis is a scarring and hardening of the glomeruli, tiny blood vessels that are involved in filtering urine. Along with this, glomerular basement membrane thickening and arteriosclerosis and tubulointerstitial disease.

Clinical course is recognized with symptoms of hypertension, albuminuria, peripheral edema, progressive decrease in GFR. When the GFR decreases below 15-20ml/min the body cannot excrete potassium and acids leading to hyperkalemia and metabolic acidosis.

107
Q

What are some drugs commonly used for treatment of type 2 diabetes?

A

Biguanides (also used as anti malarial; does not effect output of insulin, so it can be used for type 2 and in type 1 in conjunction with insulin therapy—metformin—increase sensitivity of insulin, thus decreasing circulating glucose), sulfonylureas (increase insulin release from beta cells of the pancreas…but d/t this MOA it can induce hypoglycemia, especially in periods of fasting….teratogenic…induces weight gain by increasing levels of insulin and thus the use of glucose and other metabolic fuels), thiazolidinediones (aka glitazones…increase synthesis of certain proteins involved in fat and glucose metabolism, reducing levels of lipids and circulating free fatty acids…main side effect is water retention), incretin mimetics (glucagon like peptide 1 agonist…lower risk of hypoglycemia than with sulfonylureas), alpha-glucosidase inhibitors (prevents digestion of carbohydrates which are normally converted into simple sugars and absorbed by the intestine…flatulence and diarrhea may result since carbs don’t get absorbed in the intestine and instead are broken down in the colon), insulin

108
Q

When a patient is hypoglycemic they will most likely present with a (sympathetic/parasympathetic??) response, which is characterized by what symptoms?

A

sympathetic response: HTN, tachycardia, diaphoresis, lacrimation

109
Q

What is the difference in MOA for sulfonylureas, thiazolinediones, biguanides, and alpha-glucosidase inhibitors?

A

sulfonylureas increase insulin secretion by beta cells, thiazolinediones and metformin (biguanides) enhance tissue sensitivity to insulin, and alpha-glucosidase inhibitors decrease postprandial glucose absorption

110
Q

Patients with ________ disease have increased serum cortisol levels resulting in hypokalemia, hyperglycemia, and skeletal muscle relaxation.

A

Cushings

111
Q

Why would you consider avoiding high doses of non-depolarizing muscle relaxants in patients with Cushings?

A

because they already experience skeletal muscle relaxation that may be potentiated by the use of NDMB.

112
Q

T/F? Patients undergoing a bilateral adrenalectomy should avoid supplemental steroid administration prior to induction and the use of Etomidate.

A

Etomidate may decrease adrenal funciton temporarily…. and although it doesn’t need to be avoided… it doesn’t produce any therapeutic effect in these patients; patients undergoing bilateral adrenalectomy exhibit rapid decrease of serum cortisol levels, so steroid therapy should be initiated prior to or during surgery

113
Q

In which area of the adrenal gland is cortisol produced?

A

zona fasiculata; 3 zones from outer to inner are the zona glomerulosa (produces mineralcorticoids such as aldosterone), the zona fasiculata (produces glucocorticoids such as cortisol), and zona reticularis (produces sex steroids such as androgens)

114
Q

Adrenal insufficiency d\t autoimmune destruction of the adrenal gland that results in combined glucocorticoid and mineralcorticoid deficiency is __________.

A

Addisons disease: an idiopathic autoimmune destruction of the adrenal gland that results in combined gluco and mineral corticoid deficiency; symptoms include hypotension, hyperpigmentation, hyperkalemia, and a decreased response to catecholamines.

115
Q

What is an advanced glycation end product and its role in diabetes mellitus?

A

they are substances that can be a causative factor in the development or worsening of many degenerative diseases; can effect nearly every cell type and are thought to be one factor in aging and many age related chronic disorders; they are also believed to play a CAUSATIVE role in BLOOD VESSEL COMPLICATIONS OF DM; they speed up oxidative damage of cells and alter their normal behavior; in diabetes, hyperglycemia results in higher intracellular glucose levels which inhibits parts of the electron transport chain…. causing multiple disturbances…. but ultimately results in increased production of AGEs (basically: increased sugar causes increased AGEs that break down endothelial cells

116
Q

What is a dietary method of reducing AGE’s?

A

eating brown rice instead of white rice

117
Q

What are some of the pathology effects of AGEs?

A

AGEs have a range of pathological effects, such as:
Increased vascular permeability.
Inhibition of vascular dilation by interfering with nitric oxide.
Oxidizing LDL.
Binding cells—including macrophage, endothelial, and mesangial—to induce the secretion of a variety of cytokines.
Enhanced oxidative stress.

118
Q

In what form are AGEs excreted?

A

in the urine as AGE free adducts (AGE peptides to a lesser extent, but can accumulate in the plasma of patients with renal failure)

Bioscience II Josh (18 decks)

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