Apex Endocrine Flashcards

1
Q

compare and contrast the architecture of the nervous system and endocrine system.

A

nervous system = wired

  • electrochemical
  • neurotransmitters
  • synapse
  • specific cell target
  • fast speed
  • short duration

endocrine system = wireless

  • travels in blood
  • hormones
  • endocrine, paracrine, autocrine
  • more widespread target
  • slow speed
  • long duration
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2
Q

compare and contrast positive and negative feedback loops in the endocrine system.

A

negative feedback: hormone reduces it’s own release via short or long loops

positive feedback: hormone increases it’s own release

pathway: 
hypothalamus
anterior pituitary
endocrine gland
hormone
target tissue
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3
Q

compare and contrast how the hypothalamus communicates w/ anterior and posterior pituitary glands.

A

posterior pituitary via neural connections

  • ADH produced by supraoptic nuclei
  • oxytocin produced in paraventricular nuclei
  • carried by axonal transport along the pituitary stalk

anterior pituitary via releasing and inhibiting hormones

  • released into the hypophyseal portal vessels
  • transported along the pituitary stalk to influence hormone secretion by anterior pituitary gland
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4
Q

name the 7 hypothalamic hormones, and identify their effects on the anterior pituitary gland

A

luteinizing hormone releasing hormone

  • increased FSH
  • icnreased LH

corticotropin releasing hormone
- increased ACTH

thyrotropin releasing hormone
- increased TSH

prolactin releasing factor and prolactin inhibiting factor
- prolactin

growth hormone releasing hormone and inhibiting hormone
- GH

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5
Q

where is the pituitary gland located? what is another name for the anterior and posterior pituitary glands?

A

in the sella turcica, and it is connected to the hypothalamus by the pituitary stalk.

anterior = adenohypophysis
posterior = neurohypophysis
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6
Q

what hormones are released from the anterior pituitary gland?

A
"FLAT PIG"
FSH
LH
ACTH
TSH
Prolactin
GH
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7
Q

what is the function of each anterior pituitary hormone?

A

FSH: germ cell maturation and ovarian follicle growth (females)

LH: testosterone production (males) and ovulation (females)

ACTH: adrenal hormone release

TSH: thyroid hormone release

prolactin: lactation

GH: cell growth

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8
Q

what hormones are released from the posterior pituitary gland? What are their functions?

A

ADH: water retention
oxytocin: uterine contraction and breast feeding

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9
Q

compare and contrast the presentation and treatment of SIADH and DI.

A

SIADH: too much ADH

  • d/t TBI, CA, lung dz, carbamazepine
  • presents as hyponatremia w/ hypotonic osm
  • can be euvolemic or hypervolemic
  • low UOP w/ high urine osm, Na+
  • tx: fluid restriction +/- hypertonic saline, demeclocycline

DI: too little ADH

  • d/t pit surgery, TBI, SAH
  • presents as polyuria w/ low urine osm, Na+
  • can be hypovolemic or euvolemic, w/ high serum osm and Na+
  • tx: DDAVP, supportive
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10
Q

what are the anesthetic implications of acromegaly?

A
  • distorted facial features = difficult mask
  • large tongue, teeth, epiglottis = difficult DL
  • subglottic narrowing + VC enlargement = use a smaller tube
  • turbinate enlargement = epistaxis risk, avoid nasal ETT
  • OSA is common
  • increased risk of HTN, CAD, dysrhythmias
  • glucose intolerance
  • skeletal m weakness
  • entrapment neuropathies are common
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11
Q

compare and contrast T4 and T3

A

T4

  • directly released from thyroid
  • highest concentration in the blood (think of it as a delivery vehicle)
  • high PB, low potency
  • t1/2 7 days

T3

  • some released from thyroid, but most is extrathyroid T4 conversion
  • highest concentration at the target cell (think of it as active form)
  • less PB, high potency
  • t1/2 1 day
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12
Q

how does iodine deficiency affect T3 and T4

A

TSH stimulates the iodide pump. Iodine is a substrate that the thyroid requires to synthesize T3 and T4. When iodine isn’t readily available, the thyroid is unable to produce a sufficient quantity

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13
Q

how does thyroid hormone affect cardiac function?

A

increases myocardial performance independent of the ANS:

  • increased chronotropy
  • increased inotropy
  • increased lusitropy
  • decreased SVR

effects on the ANS that impact cardiac function

  • increase # and sensitivity of cardiac B receptors
  • decrease # of cardiac muscarinic receptors
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14
Q

how does thyroid hormone affect the respiratory system?

A

increased BMR –> increased O2 consumption –> increased CO2 production –> increased MV (Vt and RR)

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15
Q

how does thyroid hormone affect MAC?

A

it doesn’t affect the brain, and by extension, hyper/hypothyroidism don’t affect MAC.

They do however, affect the speed of anesthetic induction when IA is used:

  • hyper = slower induction d/t higher CO
  • hypo = faster induction d/t lower CO
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16
Q

what is the most common etiology of hyperthyroidism? What are the other causes?

A

most common: graves (autoimmune)

others:
- myasthenia gravis
- multinodular goiter
- carcinoma
- pregnancy
- pituitary adenoma
- amiodarone

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17
Q

what is the most common etiology of hypothyroidism? What are the other causes?

A

most common: Hashimoto’s (autoimmune)

others:
- iodine deficiency
- hypothalamic-pituitary dysfunction
- neck radiation
- thyroidectomy

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18
Q

how are TSH, T3, and T4 levels affected by hyper and hypothyroidism?

A

hyperthyroidism: low TSH + high T3 and T4
hypothyroidism: high TSH + low T3 and T4

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19
Q

what is the difference b/n myxedema coma and cretisim?

A

myxedema coma occurs w/ end stage hypothyroidism. coma is a consequence (not a cause) of severely impared thyroid function

cretinism is caused by neonatal hypothyroidism that leads to physical and mental retardation

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20
Q

list 3 thionamides that can be used to treat hyperthyroidism. What is their mechanism of action?

A

thionamides: propylthiouracil (PTU), methimazole, carbimazole

inhibit thyroid synthesis by blocking iodine addition to the tyrosine residues on thyroglobulin. PTU also inhibits the peripheral conversion of T4 to T3

  • require 6-7 weeks to achieve a euthyroid state
  • only available PO, but can be crushed and given via OGT
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21
Q

why are beta blockers used to treat hyperthyroidism?

A

reduce SNS stimulation and inhibit peripheral conversion of T4 to T3

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22
Q

what are contraindications to radioactive iodine?

A

pregnancy

breast feeding

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23
Q

when is it ok for a patient w/ hyperthyroidism to undergo surgery? how about the hypothyroid patient?

A

hyper:
- do not proceed to elective surgery until pt is euthyroid.
- emergency surgery warrants administration of BB, potassium iodide, glucocorticoid, and PTU

hypo: ok to proceed if mild to moderate disease

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24
Q

what is the best way to secure the airway in a patient w/ a large goiter?

A

on boards, goiter = awake intubation

the next best response is a technique that maintains spontaneous ventilation

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25
Q

which anesthetic agents should be avoided in the hyperthyroid patient?

A

sympathomimetics
anticholinergics
ketamine
pancuronium

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26
Q

describe the presentation of thyroid storm

A

medical emergency that can occur in hyperthyroid and euthyroid patients

  • generally brought on by stressful events (infection, surgery, etc.)
  • most commonly occurs 6-18hrs after surgery

s/s

  • fever >38.5C
  • tachycardia/arrhythmias
  • HTN
  • CHF
  • shock
  • confusion and agitation
  • N/V

under anesthesia, thyroid storm can mimic:

  • MH
  • pheo
  • neuroleptic malignant syndrome
  • light anesthesia
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27
Q

how do you manage the patient w/ thyroid storm?

A
  • cardiopulmonary support
  • active cooling measures
  • PTU, methimazole
  • BB
  • tx fever w/ tylenol
  • avoid aspirin (it can dislodge T4 from plasma proteins and increase unbound fraction)
  • management is the same in pregnant and nonpregnant pts
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28
Q

discuss recurrent laryngeal nerve injury in the context of thyroidectomy.

A

RLN innervates all the intrinsic muscles except cricothyroid. Injury can cause upper airway obstruction

  • unilateral = hoarseness
  • bilateral = a/w obstruction
  • phonate “E” or “moon” to assess for nerve injury
  • NIMS tube provides ability to assess for nerve injury intraoperatively
  • at end of procedure DL can be used to assess VC function as well as glottic edema.
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29
Q

why is hypocalcemia a potential complication of thyroidectomy? How and when does it present?

A

resection of parathyroid glands w/out reimplantation –> hypocalcemia at least 6-12hrs post-op.

s/s (d/t increased nerve and muscle irritability):

  • m spasm –> tetany
  • laryngospasm
  • MS changes
  • hypotension
  • prolonged QT
  • paresthesias
  • Chvosteks (jaw) and Trousseau’s (forearm)
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30
Q

how does hypothyroidism affect gastric emptying?

A

delays it

–> increased risk of aspiration

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31
Q

what are the 3 zones of the adrenal cortex? What substance does each synthesize?

A

outside to inside: “GFR releases salt, sugar, sex”

outermost: zona glomerulosa releases mineralocorticoids (aldosterone)
middle: zona fasciculata releases glucocorticoids (cortisol)
innermost: zona reticularis releases androgens (DHEA)

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32
Q

describe the steps involved in the RAAS.

A
  1. decreased renal perfusion, SNS activation (B1), and/or tubuloglomerular feedback
  2. increased renin released from juxtaglomerular cells

renin: angiotensinogen –> angI
ACE: ang1 –> ang2
- vasoconstriction

ang2 = increased aldosterone

  • increased Na+, H2O reabsorption
  • increased K+, H+ excretion
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33
Q

how much cortisol is produced per day? what is the normal cortisol level?

A

15-30mg/day
normal serum level 12mcg/dL

stress can increase cortisol production upwards of 100mg/day, w/ serum level 30-50mcg/dL during and after major surgery

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34
Q

how does cortisol affect cardiovascular function?

A

improves myocardial performance by increasing the number and sensitivity of B receptors on the myocardium

cortisol is also required for the vasculature to respond to the vasoconstrictive effects of catechols.

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35
Q

compare and contrast the glucocorticoid and mineralocorticoid potencies of the endogenous and synthetic steroids.

A
  • *no glucocorticoid effects = aldosterone
  • *no mineralocorticoid effects = dexamethasone, betamethasone, triamcinolone

glucocorticoid effect (anti-inflammatory)

  • cortisol > cortisone > aldosterone
  • dexamethasone = betamethasone > fludrocortisone
  • minimal: prednisone, prednisolone, methylprednisolone, triamcinolone

mineralocorticoid effect (sodium retaining potency)

  • aldosterone&raquo_space;» cortisol > cortisone
  • fludrocortisone by far the most
  • prednisone, prednisolone, and methylprednisolone = minimal
  • dexamethasone, betamethasone, triamcinolone = none

** study equivalent dosing + duration of action (all in the 8-54hr range)

36
Q

what are the unique side effects of epidural triamcinolone?

A

(treats lumbar disc disease)

unique b/c it’s associated w/ higher incidence of skeletal m weakness. It’s also more likely to cause sedation (not euphoria) and anorexia (not increased appetite)

37
Q

what is Conn’s syndrome? how does it present?

A

too much aldosterone

  • primary: increased release from adrenal gland
  • secondary: d/t increased renin release or aldosterone secreting tumor

presents w/ s/s of mineralocorticoid excess:

  • HTN (Na+, H2O retention)
  • hypokalemia (K+ wasting)
  • met alkalosis (H+ wasting)
38
Q

chronic consumption of what food can produce a syndrome that resemble hyperaldosteronism?

A

long term licorice ingestion (glycyrrhizic acid)

39
Q

what is the treatment for Conn’s syndrome?

A

aldosterone antagonists: spironolactone or eplerenoee

K+ supplementation
Na+ restriction
removal of aldosterone secreting tumor

40
Q

what is the difference b/n Cushing’s syndrome and Cushing’s disease?

A

although they present similarly, etiologies are a litle different.

Cushings syndrome = too much cortisol
Cushings disease = too much ACTH

41
Q

What are glucocorticoid effects?

A
  • hyperglycemia
  • weight gain (central obesity, buffalo hump, moon face)
  • increased risk of infx
  • osteoporosis
  • muscle weakness
  • mood disorder
42
Q

what are mineralocorticoid effects?

A
  • HTN
  • hypokalemia
  • met alkalosis
43
Q

What are androgenic effects?

A

women become masculinized (hirsutism, hair thinning, acne, amenorrhea)

men become feminized (gynecomastia, impotence)

44
Q

how does Cushing’s syndrome present? Why?

A

cortisol has glucocorticoid, mineralocorticoid, and androgenic effects, so it will present w/ excess of these 3 things:

glucocorticoid:
- hyperglycemia
- weight gain + abnormal fat pattern
- increased infx risk
- osteoporosis
- muscle weakness
- mood disorder

mineralocorticoid

  • HTN
  • hypokalemia
  • met alkalosis

androgenic: feminzation/masculanization

45
Q

what endocrine disorder can occur after transsphenoidal resection of the pituitary gland?

A

DI, usually transient

46
Q

describe the presentation of adrenal insufficiency

A

too little mineralocorticoid, glucocorticoid, and androgen

  • primary (Addisons): adrenal glands dont secrete enough hormone (usually autoimmune)
  • secondary: decreased CRH or ACTH (usually exogenous steroid use)

presentation:
- muscle weakness/fatigue
- hypotension
- hypoglycemia
- hyponatremia
- hyperkalemia
- met acidosis
- anorexia
- N/V
- hyperpigmentation of knees, elbows, knuckles, lips, and buccal mucosa

47
Q

what is the treatment for adrenal insufficiency?

A

steroid replacement therapy (15-30mg cortisol equivalent/day)

48
Q

what is acute adrenal crisis? How does it present?

A

adrenal insufficiency is a chronic state, but it can deteriorate into an acute crisis if the pt is faced w/ additional stress (infection, illness, sepsis, surgery). This is a medical emergency:

  • hemodynamic instability/collapse
  • fever
  • hypoglycemia
  • impaired MS
49
Q

what is the treatment for acute adrenal crisis?

A

steroid replacement therapy (hydrocortisone 100mg + 100-200mg Q24hrs)

ECF volume expansion (D5NS is best)

hemodynamic support

50
Q

describe the surgical stress response in patients on chronic steroid therapy

A

exogenous steroid supplementation suppresses ACTH release from the anterior pituitary gland. Some patients on chronic steroid therapy won’t be able to increase cortisol release in response to perioperative stress.

51
Q

How do you determine who should receive perioperative steroid supplementation?

A

yes if prednisone >5mg/day x3 weeks (or equivalent dosing)

higher risk for HPA suppression if dose >20mg/day

52
Q

what are the 4 endocrine hormones produced by the pancreas? which cell types produce each one?

A
alpha = glucagon
beta = insulin
delta = somatostatin
PP = pancreatic polypeptide
53
Q

what conditions increase insulin release?

A

glucose is the primary stimulator; thus anything that increases serum glucose will stimulate insulin release

  • PNS stim after meal
  • SNS stim
  • hormones: glucagon, catechols, cortisol, GH
  • beta agonists
54
Q

what conditions decrease insulin release?

A

anything that decreases serum glucose will also decrease insulin release

  • hormones: insulin, somatostatin
  • IA
  • B blockers
55
Q

describe the physiology of the insulin receptor.

A

made up of 2 alpha and 2 beta subunits that are jointed together by disulfide bonds.

when insulin binds the receptor, the beta subunits activate tyrosine kinase which then activates insulin-receptor substrates.

the insulin cascade turns on the GLUT4 transporter, which increases glucose uptake by skeletal m and fat

56
Q

what factors stimulate glucagon release?

A

secreted by alpha cells. It’s a catabolic hormone that promotes energy release from adipose and the liver (physiologic antagonist to insulin)

decreased glucose stimulates glucagon release (which increases glucose)

  • stress
  • trauma
  • sepsis
  • B agonists
57
Q

what factors inhibit glucagon release

A

increased glucose inhibits glucagon release (which decreases glucose)

  • insulin
  • somatostatin
58
Q

what are the other uses for glucagon?

A

1-5mg IV increases myocardial contractility, HR, AV conduction by raising the intracellular concentrations of cAMP.
since it’s independent of the ANS, it’s useful in:
- BB OD
- CHF
- low CO after MI or CPB
- improving MAP during anaphylaxis

also helpful during ERCP to relex SOO (side effect = N/V)

59
Q

what is somatostatin?

A

aka growth hormone-inhibiting hormone

regulates endocrine hormone output from the islet cells

  • it’s released by delta cells
  • inhibits insulin AND glucagon
  • also inhibits splanchnic blood flow, gastric motility, and gall bladder contraction
60
Q

what is pancreatic polypeptide?

A

inhibits pancreatic exocrine hormone secretion, gallbladder contraction, gastric acid secretion, and gastric motility

61
Q

what are the diagnostic criteria for diabetes mellitus?

A

fasting glucose >126

random glucose >200 + classic symptoms

2hr glucose >200 during oral glucose tolerance test

HgbA1C >6.5%

62
Q

what is the classic triad of DM? Why does it occur?

A

polyuria
dehydration
polydipsia

  • hyperglycemia –> glycosuria (acts as osmotic diuretic) –> hypovolemia
63
Q

what’s the difference b/n type I and type II diabetes mellitus?

A
T1DM = lack of insulin production
T2DM = relative lack of insulin + insulin resistance
64
Q

what are the most common causes of T1DM and T2DM?

A
T1DM = autoimmune (early in life)
T2DM = obesity (later in life, but prevalence is increasing in obese children)
65
Q

discuss diabetic ketoacidosis

A
  • more common w/ T1DM
  • usually d/t infection
  • not enough insulin –> ketoacidosis, hyperosmolarity (from increased glucose) + dehydration
  • BS >250, but cells are starved for fuel
  • met acidosis = Kussmaul respirations
  • acetone = fruity breath
  • tx: volume resus, insulin, K+ after acidosis subsides
66
Q

discuss hyperglycemic hyperosmolar state.

A
  • more common w/ T2DM
  • usually d/t insulin resistance or inadequate production
  • enough insulin is produced to prevent ketosis but not hyperglycemia
  • BS >600 = sign increase in osm
  • glycosuria –> dehydration and hypovolemia
  • mild met acidosis may occur (no anion gap)
  • tx: volume resus, insulin, correct e-lytes

c/w DKA, HHS = higher BS and osm

67
Q

describe the long term complications associated w/ DM.

A

microvascular:
- neuropathy
- retinopathy
- nephropathy

macrovascular:
- CAD
- PVD
- CVD

other:
- stiff joint syndrome
- poor wound healing –> infection
- cataracts
- glaucoma

68
Q

how does DM affect the ANS?

A
  • painless myocardial ischemia (referred pain pathways are dysfunctional)
  • reduced vagal tone = ST
  • risk of dysrhythmias
  • orthostatic hypotension
  • impaired resp comp to hypoxia and hypercarbia
  • delayed gastric emptying
  • impaired thermoregulation
  • RA may worsen neuro defects
  • diarrhea and constipation
69
Q

what is the prayer sign?

A

DM can cause glycosylation of the joints –> stiff joint syndrome w/ reduced ROM of AO joint

prayer sign suggests joint glycosylation and an increased risk of difficult intubaiton

70
Q

what is the mechanism of action of the biguanides? list an example from this drug class.

A

MOA: inhibit gluconeogenesis and glycogenolysis in the liver and decrease peripheral insulin resistance

ex: metformin

key facts:

  • does NOT cause hypoglycemia
  • risk: met acidosis
  • often used for polycystic ovarian disease
71
Q

what is the mechanism of action of the sulfonylureas? List examples from this drug class.

A

MOA: stimulate insulin secretion from pancreatic beta cells

ex: glyburide, glipizide, glimepiride

key facts:

  • risk of hypoglycemia
  • avoid if sulfa allergy
72
Q

what is the mechanism of action of the meglitinides? List examples of this drug class.

A

MOA: stimulate insulin secretion from the pancreatic beta cells

ex: repaglinide, nateglinide

key facts:
- risk of hypoglycemia

73
Q

what is the mechanism of action of the thiazolidinediones? List examples from this drug class.

A

MOA: decrease peripheral insulin resistance and increase hepatic glucose utilization

ex: rosiglitazone, pioglitazone

key facts:

  • does NOT cause hypoglycemia
  • black box warning d/t risk of CHF
74
Q

what is the mechanism of action of the alpha-glucosidase inhibitors? List examples from this drug class.

A

MOA: slows digestion and absorption of carbs from GI tract.

ex: acarbose, miglitol

key facts: does NOT cause hypoglycemia

75
Q

what is the mechanism of action of the glucagon-like peptide1 receptor agonists? List examples from this drug class.

A

MOA: increases insulin release from beta cells, decrease glucagon release from alpha cells, and prolongs gastric emptying

ex: exenatide, liraglutide

key facts: risk of hypoglycemia

76
Q

what is the mechanism of action of the dipeptidyl-peptidase-4 inhibitors? List examples from this drug class.

A

MOA: increase insulin release from pancreatic beta cells and decrease glucagon release from alpha cells

ex: suffix -liptin

key facts: risk of hypoglycemia

77
Q

what is the mechanism of action of the amylin agonists? List examples from this drug class.

A

MOA: decrease glucagon release from pancreatic alpha cells and reduce gastric emptying

ex: pramlintide

key factors: risk of hypoglycemia if co-administered w/ insulin

78
Q

compare and contrast the onset, peak, and duration of exogenous insulin preparations.

A

very rapid acting (lispro, aspart, glulisine)

  • onset 5-15min
  • peak 45-75min
  • DOA 2-4hrs

rapid acting (regular)

  • onset 30min
  • peak 2-4hrs
  • DOA 6-8hrs

intermediate acting (NPH)

  • onset 2hrs
  • peak 4-12hrs
  • DOA 18-28hrs

long acting (detemir, glargine)

  • onset 1.5-2hrs
  • peak: detemir 3-9hrs, glargine has no peak
  • DOA up to 24hrs

ultra long acting (degludec)

  • onset 2hrs
  • no peak
  • DOA 40+hrs
79
Q

discuss the presentation, risks, and treatment of hypoglycemia in the perioperative period.

A
  • highest risk = insulin admin during fasting
  • s/s: SNS stim (tachy, HTN, diaphoresis)
  • difficult to diagnose under GA (esp w/ BB)
  • possible cause of delayed emergence
  • rebound hyperglycemia (Somogyi) effect may cloud diagnosis
  • tx: D50 (50-100mL) or glucagon (0.5-1mg IV or SQ)
80
Q

discuss the association b/n insulin and allergic reactions.

A

insulin allergy was more common when animal derived insulin was used

chronic NPH use (or fish allergy) may sensitize the pt to protamine (may not manifest until a large dose is administered - cardiac surgery)

81
Q

what drugs counter the hypoglycemic effect of insulin?

A

epi
glucagon
cortisol

82
Q

what drugs extend or enhance the hypoglycemic effect of insulin?

A

MAOI
salicylates
tetracycline

83
Q

discuss the patho of carcinoid syndrome.

A

associated w/ secretion of vasoactive substances from enterochromaffin cells.
usually associated w/ tumors of the GI tract, but can also arise from locations outside of the GI tract as well (lungs)

release histamine, serotonin, kinins, kallikrein

84
Q

what are the systemic effects of the hormones released by a carcinoid tumor?

A

most common: flushing, diarrhea

histamine:
- bronchoconstriction
- vasodilation, hypotension, flushing (head and neck)

kinins, kallikrein

  • bronchoconstriction
  • vasodilation, hypotension, flushing
  • increases histamine release from mast cells

serotonin

  • bronchoconstriction
  • vasoconstriction, HTN, SVTs
  • increased GI motility (diarrhea, abdominal pain)
85
Q

what are the s/s of carcinoid crisis?

A

life threatening

tachycardia
HTN or hypotension
intense flushing
abdominal pain, diarrhea

86
Q

what drugs are used in the treatment of carcinoid crisis?

A

somatostatin (octreotide or lanreotide): inhibits release of vasoactive substances from carcinoid tumors

antihistamines (H1 and H2: benadryl + ranitidine or cimetidine)

5-HT3 antagonists

steroids

phenylephrine/vasopressin for hypotension (no ephedrine)

87
Q

what drugs should be avoided in the patient w/ carcinoid syndrome?

A

histamine releasing drugs (morphine, meperidine, atra, thiopental, sux)

sux-induced fasciculations can cause hormone release from the tumor

exogenous catechols can potentiate hormone release

sympathomimetic agents: ephedrine and ketamine