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
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
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
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
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
6
Q
what hormones are released from the anterior pituitary gland?
A
"FLAT PIG" FSH LH ACTH TSH Prolactin GH
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
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
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
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
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
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
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
14
Q
how does thyroid hormone affect the respiratory system?
A
increased BMR –> increased O2 consumption –> increased CO2 production –> increased MV (Vt and RR)
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
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
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
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
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
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
21
Q
why are beta blockers used to treat hyperthyroidism?
A
reduce SNS stimulation and inhibit peripheral conversion of T4 to T3
22
Q
what are contraindications to radioactive iodine?
A
pregnancy
breast feeding
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
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
25
which anesthetic agents should be avoided in the hyperthyroid patient?
sympathomimetics
anticholinergics
ketamine
pancuronium
26
describe the presentation of thyroid storm
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
27
how do you manage the patient w/ thyroid storm?
- 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
28
discuss recurrent laryngeal nerve injury in the context of thyroidectomy.
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.
29
why is hypocalcemia a potential complication of thyroidectomy? How and when does it present?
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)
30
how does hypothyroidism affect gastric emptying?
delays it
| --> increased risk of aspiration
31
what are the 3 zones of the adrenal cortex? What substance does each synthesize?
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)
32
describe the steps involved in the RAAS.
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
33
how much cortisol is produced per day? what is the normal cortisol level?
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
34
how does cortisol affect cardiovascular function?
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.
35
compare and contrast the glucocorticoid and mineralocorticoid potencies of the endogenous and synthetic steroids.
* *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 >>>> 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
what are the unique side effects of epidural triamcinolone?
(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
what is Conn's syndrome? how does it present?
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
chronic consumption of what food can produce a syndrome that resemble hyperaldosteronism?
long term licorice ingestion (glycyrrhizic acid)
39
what is the treatment for Conn's syndrome?
aldosterone antagonists: spironolactone or eplerenoee
K+ supplementation
Na+ restriction
removal of aldosterone secreting tumor
40
what is the difference b/n Cushing's syndrome and Cushing's disease?
although they present similarly, etiologies are a litle different.
Cushings syndrome = too much cortisol
Cushings disease = too much ACTH
41
What are glucocorticoid effects?
- hyperglycemia
- weight gain (central obesity, buffalo hump, moon face)
- increased risk of infx
- osteoporosis
- muscle weakness
- mood disorder
42
what are mineralocorticoid effects?
- HTN
- hypokalemia
- met alkalosis
43
What are androgenic effects?
women become masculinized (hirsutism, hair thinning, acne, amenorrhea)
men become feminized (gynecomastia, impotence)
44
how does Cushing's syndrome present? Why?
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
what endocrine disorder can occur after transsphenoidal resection of the pituitary gland?
DI, usually transient
46
describe the presentation of adrenal insufficiency
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
what is the treatment for adrenal insufficiency?
steroid replacement therapy (15-30mg cortisol equivalent/day)
48
what is acute adrenal crisis? How does it present?
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
what is the treatment for acute adrenal crisis?
steroid replacement therapy (hydrocortisone 100mg + 100-200mg Q24hrs)
ECF volume expansion (D5NS is best)
hemodynamic support
50
describe the surgical stress response in patients on chronic steroid therapy
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
How do you determine who should receive perioperative steroid supplementation?
yes if prednisone >5mg/day x3 weeks (or equivalent dosing)
higher risk for HPA suppression if dose >20mg/day
52
what are the 4 endocrine hormones produced by the pancreas? which cell types produce each one?
```
alpha = glucagon
beta = insulin
delta = somatostatin
PP = pancreatic polypeptide
```
53
what conditions increase insulin release?
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
what conditions decrease insulin release?
anything that decreases serum glucose will also decrease insulin release
- hormones: insulin, somatostatin
- IA
- B blockers
55
describe the physiology of the insulin receptor.
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
what factors stimulate glucagon release?
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
what factors inhibit glucagon release
increased glucose inhibits glucagon release (which decreases glucose)
- insulin
- somatostatin
58
what are the other uses for glucagon?
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
what is somatostatin?
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
what is pancreatic polypeptide?
inhibits pancreatic exocrine hormone secretion, gallbladder contraction, gastric acid secretion, and gastric motility
61
what are the diagnostic criteria for diabetes mellitus?
fasting glucose >126
random glucose >200 + classic symptoms
2hr glucose >200 during oral glucose tolerance test
HgbA1C >6.5%
62
what is the classic triad of DM? Why does it occur?
polyuria
dehydration
polydipsia
- hyperglycemia --> glycosuria (acts as osmotic diuretic) --> hypovolemia
63
what's the difference b/n type I and type II diabetes mellitus?
```
T1DM = lack of insulin production
T2DM = relative lack of insulin + insulin resistance
```
64
what are the most common causes of T1DM and T2DM?
```
T1DM = autoimmune (early in life)
T2DM = obesity (later in life, but prevalence is increasing in obese children)
```
65
discuss diabetic ketoacidosis
- 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
discuss hyperglycemic hyperosmolar state.
- 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
describe the long term complications associated w/ DM.
microvascular:
- neuropathy
- retinopathy
- nephropathy
macrovascular:
- CAD
- PVD
- CVD
other:
- stiff joint syndrome
- poor wound healing --> infection
- cataracts
- glaucoma
68
how does DM affect the ANS?
- 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
what is the prayer sign?
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
what is the mechanism of action of the biguanides? list an example from this drug class.
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
what is the mechanism of action of the sulfonylureas? List examples from this drug class.
MOA: stimulate insulin secretion from pancreatic beta cells
ex: glyburide, glipizide, glimepiride
key facts:
- risk of hypoglycemia
- avoid if sulfa allergy
72
what is the mechanism of action of the meglitinides? List examples of this drug class.
MOA: stimulate insulin secretion from the pancreatic beta cells
ex: repaglinide, nateglinide
key facts:
- risk of hypoglycemia
73
what is the mechanism of action of the thiazolidinediones? List examples from this drug class.
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
what is the mechanism of action of the alpha-glucosidase inhibitors? List examples from this drug class.
MOA: slows digestion and absorption of carbs from GI tract.
ex: acarbose, miglitol
key facts: does NOT cause hypoglycemia
75
what is the mechanism of action of the glucagon-like peptide1 receptor agonists? List examples from this drug class.
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
what is the mechanism of action of the dipeptidyl-peptidase-4 inhibitors? List examples from this drug class.
MOA: increase insulin release from pancreatic beta cells and decrease glucagon release from alpha cells
ex: suffix -liptin
key facts: risk of hypoglycemia
77
what is the mechanism of action of the amylin agonists? List examples from this drug class.
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
compare and contrast the onset, peak, and duration of exogenous insulin preparations.
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
discuss the presentation, risks, and treatment of hypoglycemia in the perioperative period.
- 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
discuss the association b/n insulin and allergic reactions.
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
what drugs counter the hypoglycemic effect of insulin?
epi
glucagon
cortisol
82
what drugs extend or enhance the hypoglycemic effect of insulin?
MAOI
salicylates
tetracycline
83
discuss the patho of carcinoid syndrome.
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
what are the systemic effects of the hormones released by a carcinoid tumor?
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
what are the s/s of carcinoid crisis?
life threatening
tachycardia
HTN or hypotension
intense flushing
abdominal pain, diarrhea
86
what drugs are used in the treatment of carcinoid crisis?
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
what drugs should be avoided in the patient w/ carcinoid syndrome?
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
