6901 > Endocrine > Flashcards

Endocrine Flashcards

(77 cards)

Study These Flashcards
1
Q

Hormone function and types of hormones (3)

A

Function: Signals molecules or chemical messengers that transport information from one set of cells (endocrine) to another (target)
Types:
-Peptide/protein (insulin, GH, ADH, angiotensin, EPO)
-Amine/amino (catecholamines, thyroxine)
-Lipids (steroid, cortisone, aldosterone, estrogen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hormone receptors

A

Peptide/protein
-Receptor site on cell surface is activated and generates 2nd receptor (cAMP used by vaso, TSH, parathyroid hormone)
Lipid
-Attracts specific hormone, lipophilic, diffuse into the cell (thyroid and steroid hormones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hormone regulation (3 control mechanisms)

A
  • Neural controls (pain, smell, taste)
  • Biorhythms (circadian)
  • Feedback
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Endocrine system is involved in regulation of ____

A

Behavior, growth, metabolism, fluid status, development, reproduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Endocrine vs autocrine vs paracrine

A

Hormone enters…

  • Endocrine: blood, acts at distant site
  • Autocrine: at site of origin
  • Paracrine: adjacent to site of origin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Endocrine glands

A 
Pituitary
Thyroid
Parathyroid
Adrenal
Pancreas
Ovaries
Testes
Placenta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Body functions modified by the pituitary gland

A

Homeostatic
Developmental
Metabolic
Reproductive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pituitary glad located ___ connected to ___

A

Located at base of brain

Connected to hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Anterior vs posterior pituitary communication with hypothalamus

A

Anterior:
-Via vascular system
Posterior:
-Via neural pathways
Hypothalamus connection controls pituitary hormone secretion
-No BBB between the two so feedback/communication can occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

6 hormones secreted by anterior pituitary

A

Growth hormone (GH)
Adrenocorticotropic hormone (ACTH)
-Cortisol/androgenic hormone release from adrenal cortex
Thyroid-stimulating hormone (TSH)
Follicle-stimulating hormone (FSH)
-Ovarian follicle development, spermatogenesis
Luteinizing hormone (LH)
-Ovulation, corpus luteum development, testosterone production
Prolactin
-Mammary gland development, milk production
-Inhibits synthesis/secretions of LH, FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes of anterior pituitary hyposecretion

A
  • Large nonfunctional pituitary tumors - compress and destroy normal cells
  • Postpartum shock, irradiation, trauma, hypophysectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Panhypopituitarism

A

Lack of pituitary hormones

  • More common than a decrease in a single ant pit hormone
  • > decreased thyroid function d/t decreased TSH
  • > Decreased glucocorticoid production (by adrenal cortex) d/t decreased ACTH
  • > Depressed sexual development and function d/t decreased gonadotropic hormone secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment of pituitary tumor

A

Surgical removal

  • Transphenoidal (nasal)
  • Need thyroid hormone replacement and steroids peri-op
  • May get diabetes insipidus after removal (give vasopressin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Anterior pituitary hypersecretion

A

Most commonly tumors secrete prolactin, ACTH, or GH

  • Prolactin -> infertility, amenorrhea, decreased libido (treat with dopamine agonist-bromocriptine)
  • ACTH -> Cushings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Growth hormone

A

Hypothalamus regulates GH activity (negative feedback)

  • Increased secretion in childhood, more in adolescence, plateaus in adulthood and decreases in old age
  • Increased by stress, hypoglycemia, exercise, and deep sleep
  • Increases blood glucose levels (decreases sensitivity of cells to insulin by inhibiting glucose uptake into cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

GH hyposecretion vs hypersecretions

A

Hyposecretion
-Dwarfism, hypoglycemia
Hypersecretion
-Usually caused by GH secreting pituitary adenoma
-Acromegaly -> thick large bones, enlarged organs (cardiomyopathy, HTN, atherosclerosis, LVH), increased lung volumes (VQ mismatch, increased extrathoracic obstruction), coarse facial features
-Gigantism -> if GH is elevated before adolescence, grow to 8-9 feet
-Glucose intolerance, diabetes (GH antagonist to insulin)
-Treatment: Remove pituitary tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Anesthetic plan for GH hypersecretion pituiraty tumor removal

A

Examine airway

  • Difficult mask fit and DL due to tissue overgrowth and macroglossia
  • May need smaller ETT - vocal cord enlargement
  • Extubate alert
  • Pre-op glucose and lytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Posterior pituitary hormones (2)

A

Antidiuretic hormone (vasopressin, ADH)
-Controls water excretion/reabsorption in kidney
-Regulates serum osmolarity
Oxytocin
-Stimulates milk ejection during lactation
-Uterine smooth muscle contraction
-Derivatives used to induce labor/decrease postpartum bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ADH stimulation

A

When plasma osmolarity is 284mOsm/L
-Normal 285-290
10-20% decrease in plasma volume or BP
-Baroreceptors send signal via vagal/glossopharyngeal nerves to hypothalamus -> hypothalamus increases ADH synthesis and release
Pain, emotional stress, nausea, hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Diabetes insipidus

A

=Low ADH neurogenic (or inability of renal ducts to respond nephrogenic)

  • Polyuria, polydipsia
  • > Dehydration, hypernatremia
  • Hyperreflexia, weak, lethargic, seizures, coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Diabetes insipidus anesthetic considerations and treatment

A

Assess fluid status, electrolytes
-Surgery increases ADH release so pre-op vasopressin isn’t usually necessary with partial DI
-Monitor plasma osm, UOP, serum Na q1h
-Give isotonic fluids until serum osm=290, then hypotonic
Treatment (complete DI)
-Meds that increase ADH release or increase receptor response to ADH
-Short term=vasopressin
-Long term=desmopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Syndrome of inappropriate anti-diuretic hormone (SIADH) (characteristics, anesthetic consideration, treatment)

A

=High ADH levels
-Water reabsorbed in tubules even when hypoosmolar
-Low UOP -> water intoxication, hyponatremia -> brain edema
Slow emergence
Treatment
-Mild, without s/s of hyponatremia: fluid restriction (800mL/day)
-More severe: hypertonic saline with Lasix
-Correct Na levels slowly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Thyroid gland

A

Function
-Secrete thyroid hormones to regulate cellular metabolism and calcium balance
Nerves in proximity
-Recurrent laryngeal nerve and external motor branch of superior laryngeal nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

3 hormones secreted by the thyroid gland

A 
T4
-Thyroxine
-93% of hormone
-less potent in blood
-prehormone: converted to T3 at tissue sites
T3
-Triiodothyonine
-7% of hormone
-more potent in blood
Calcitonin
-Regulates calcium short-term
Dependent on iodine for production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Actions of thyroid hormone
Increased metabolic rate, O2 consumption, heat production -Secondarily increased heart, lung, kidney function T3 plays a role in growth and development
26
Graves disease or thyrotoxicosis
Hyperthyroidism S/S: Goiter, ST, anxiety, tremor, heat intolerance, insomnia, weight loss, a fib, skeletal muscle weakness Dx: decreased TSH, increased T4 Tx: -Meds to inhibit hormone synthesis (methimazole, propylthiouracil, carbimazole) -Prevent hormone release (potassium, sodium iodine) -Mask adrenergic overactivity (propranolol, atenolol) -Destroy thyroid cell function (radioactive iodine) -Surgery: subtotal thyroidectomy
27
Anesthetic management for hyperthyroid
Untreated symptomatic patients should only go to OR if life threatening -Continue antithyroid meds and BB through morning of surgery to decrease SNS -Esmolol inhibits T4 to T3 Assess airway for tracheal deviation from thyroid enlargement *No ketamine, atropine, pancuronium (SNS stimulation) -Deep anesthesia before intubation -May need more inhalational agents (increased CO, blood volume) -Treat intraop hypotension with direct pressors (phenylephrine) *ETT with NIM (electrodes on VCs) to assess recurrent laryngeal nerve
28
Thyroid storm
Life-threatening Caused by acute stress in undiagnosed or untreated hyperthyroid patient -May occur anytime periop, more likely 6-18 hours posto -Different from MH: No muscle rigidity, elevated creatinine kinase, respiratory acidosis S/Sx: -Tachycardia, agitation, a fib, fever (>38.5) Tx: -IV hydration with glucose -Cooling/Tylenol -Beta blockers -Potassium iodide (block T4 and T3 release) -Correct electrolytes/acid base imbalance
29
Recurrent laryngeal nerve palsy
Postop thyroidectomy complication - Decreased occurance with NIM use - Unilateral-hoarseness - Bilateral-aphonia, stridor -> reintubate
30
Thyrotoxicosis vs MH
``` Thyrotoxicosis -Elevated HR/BP, A fib, CHF -Hyperprexia (fever), acidosis MH -Unexplained sudden increase in ETCO2 -Elevated HR, trismus (lockjaw), rapid temp rise, mottling, cyanosis ```
31
Hypothyroidism (etiology, s/sx, dx, tx)
``` Hashimoto thyroiditis Etiology -Autoimmune mediated inflammation -Iodine deficiency -Extreme=myxedema S/Sx -Lethargy, hypotension, bradycardia, CHF, gastroparesis, hypothermia, hypoventilation, hyponatremia, poor mentation Dx: Primary -Decreased T4 and/or T3 -Increased TSH Secondary -Decreased T4, T3, TSH Tx -Replace T4: synthroid ```
32
Preop anesthetic considerations for hypothyroid
Careful airway evaluation due to enlarged thyroid gland, enlarged tongue, myxedematous infiltration of VCs -Severe hypothyroid a/w multiple complications with anesthesia - myocardial and baroreceptor function may be depressed
33
Intraop management for hypothyroid
- No effect on MAC - Respiratory depression after opioids may be increased: assess for large tongue, goiter hypoxia and hypercarbia (ventilatory response to hypoxia/hypercarbia may be depressed) - Hypotension/myocardial depressed from inhalation agents may be increased, plasma volume reduced - Ketamine good for induction - Body temp closely for hypothermia - May be sensitive to NDMRs if experiencing muscle weakness - Slower GI emptying - aspiration risk (RSI?) - Potential adrenal insufficiency - periop cortisol
34
Myxedemia
End stage untreated severe hypothyroidism - Hypothermic, hypoventilation, hyponatremic - Only do surgery if lifesaving
35
Parathyroid hormone
Released in response to low serum ionized calcium - Or hyperphosphatemia or hypomagnesemia - Provides negative feedback control of calcium - Increases extracellular calcium, decreases extracellular phosphate - Increases renal calcium absorption and phosphate excretion
36
Calcitonin
Hormone secreted from thyroid in response to elevated ionized calcium, has weak effect (opposite of PTH)
37
Parathyroid dysfunction
Affects bone, intestinal tract (Ca absorption), kidney (VitD formation, Ca reabsorption, phosphate excretion) Hyperparathyroid -> hypercalcemia -HTN, ventricular dysrhythmias, shortened QT, impaired renal concentration, muscle weakness, osteoporosis, mental status changes -Calcifications in organs (pancreas, kidney, heart, stomach)
38
Treatment of severe hypercalcemia during surgery
>13-16 Isotonic saline and loop diuretic (Lasix) -Avoid hypoventilation - hyperventilation/alkalosis decreases active ionized calcium (decreases calcium and K)
39
Bilateral RLN injury during parathyroidectomy
Requires immediate reintubation
40
Insulin effects on cells
Bind to receptor (peptide hormone) - Protein activation cascades start - Glut 4 transporter translocated to plasma membrane, influx of glucose - Glycolysis - Fatty acid synthesis
41
DM Type 1 (% of all DM, cause, characterized, risks)
5-10% of all DM cases - Autoimmune destruction of beta cells in the pancreas - Total deficiency in insulin production - At risk for DKA and rarely HHNC
42
DM 2 characteristic
Impaired insulin secretion, peripheral insulin resistance, excessive hepatic glucose production (environmental, genetic, lifestyle factors)
43
DM periop (impact on recovery, highest risk, concerns)
DM patients will spend 50% more time in the hospital recovering from surgery - Undiagnosed DM=higher risk - Concerns: End-organ complications, glucose-lower regimen
44
Autonomic neuropathy in DM patients
``` Impaired gastric emptying -Aspiration risk -Slow gastric emptying -Reflux esophagitis -H2 blocker or metoclopramide preop, RSI Dysfunction of cardiac vagus nerve -Orthostatic hypotension, tachycardia, dysrhythmias Higher morbidity/mortality ```
45
Oral hypoglycemic (biggest flag, risks, preop holding)
Metformin - Risk for hypotension and renal hypoperfusion -> lactic acidosis - Hold 48 hours prior to surgery (controversial) - New guidelines: Hold for 24 hours if renal compromise or giving contrast during surgery
46
DM medication instructions preop for Type I vs II vs insulin pump
DM I -Dependent on insulin, reduce dose -1/2 insulin PM before, no insulin or decreased dose AM DM II -1/2 insulin PM, none AM of surgery Insulin pump -Talk with patients, know settings, check site -Decrease rate in PM and basal rate intraop -Caution with radiation, electrocautery -Hold all oral hypoglycemics preop -Hold all non-insulin injectable medications DOS
47
Blood sugar goal during anesthesia
Mildly hyperglycemic (s/sx of hypoglycemia are masked) - 80-180 - Check q1h
48
Protamine and NPH
Protamine sulfate anaphylaxis can occur in patients taking NPH or protamine zinc insulin
49
Hypoglycemia treatment (& how much 15mL D50 raises glucose)
25-50mL D50 followed by D5 gtt - 70kg pt: 15mL D50 increase blood glucose by 30mg/dL - 1mL D50 increases BG by 2mg/dL
50
Mortality for DKA vs HHS
Higher for HHS, affects the elderly/DM II patients more after an acute illness
51
Goal plasma osmolarity for HHS treatment
Diagnosis=>330mOsm/L Give fluids -(1/2 NS) if >320mOsm/L until <320, then NS -Careful when giving fluids, patients typically elderly and can get cerebral edema or CHF
52
Adrenal cortex hormones
``` Mineralcorticoids -Aldosterone -Regulate extracellular volume and potassium (Na reabsorption, K secretion) Glucocorticoids -Cortisol -ACTH stimulates synthesis -Maintains/regulates immune/circulatory function Androgen hormones -Dehydroepiandrosterone ```
53
Adrenal medulla
Inner part of adrenal gland | -Secretes norepi, dopamine, and epi (80% catecholamine output)
54
Adrenal cortex dysfunction (types, effects, treatment)
Increased aldosterone production 2 types -Primary: from adrenal adenoma (Conn syndrome), no stimulus -Secondary: from increased renin production -> increased urinary sodium and potassium exchange -> hyperNa, hypoK (HTN, weakness) Tx: Remove tumor
55
Adrenal cortex dysfunction anesthetic plan
Correct fluid/lyte (K) balance preop Manage HTN: spironolactone (aldosterone antagonist) Peripheral nerve stimulator for muscle relaxants, hypoK may enhance MR -Avoid hyperventilation (decrease K more)
56
Cushings syndrome
``` Excess cortisol/glucocorticoid -Commonly caused by superphysiologic exogenous doses of glucocorticoids for arthritis, asthma, autoimmune d/o, allergies S/Sx: -Central obesity, thin extremities -HTN -Glucose intolerance -Increased intravascular fluid volume, hypokalemia -Moon face, buffalo hump ```
57
Anesthetic management for cushing syndrome
- Correct fluid/lyte imbalance preop - Spironolactone - Careful positioning (osteopenia) - Conservative with MR if skeletal muscle weakness - Thromboemboli more common
58
Addisons disease
Adrenocortical insufficiency, decreased cortisol -Adrenal androgen, glucocorticoid, mineralocorticoid all deficient S/Sx: Hyperpigmentation, s/s c/w cortisol deficiency, aldosterone deficiency Hemodynamic instability
59
Adrenal medulla dysfunction
Pheochromocytoma -Catecholamine secreting tumor S/Sx: -Paroxysmal headache, HTN, sweating, palpitations -Unexpected intraop HTN/tachycardia can be indication of this (during manipulation of abdominal cavity) Dx: -Clonidine will decrease neurogenic catecholamines but not ones from pheochromocytoma
60
Preop plan for pheochromocytoma
1: Alpha blocker, volume replacement -1-2 weeks preop 2: Beta blocker if necessary for reflex tachycardia -Added after several days of a-blockade -Don't add first because can cause vasodilation which can worsen HTN Goals -BP<160/90 for >24hrs -Orthostatic hypotension (not <80/45 standing) -<1 PVC every 5 mins -No ST segment changes/T wave inversions on ECG for 1 week -Hct decrease 5%: suggests adequate intravascular volume expansion, satisfactory alpha-blockade
61
Intraop pheochromocytoma (equipment/monitoring, meds, what to avoid)
``` A line Large bore PIVs Deep intubation (LTA kit helpful) Foley CVP/Swan Anticipate labile CV Meds -1 Alpha blockers -2 Beta blockers -Nicardipine -Magnesium sulfate -Nitroprusside, nitroglycerine Avoid -Ephedrine -Ketamine -Hypoventilation (stimulate SNS) -Atracurium (histamine release) -Morphine (histamine release) ```
62
Pheochromocytoma after tumor removal
``` Hypotension -d/t hypovolemia, a-blockade, tolerance to endogenous catecholamines which are now gone Tx: -Fluids -Phenylephrine -Norepi ```
63
Multiple endocrine neoplasia (MEN)
Overactivity of 1 + endocrine glands -Inherited genetic effect MEN 1: -Parathyroid tumors*, pancreatic tumors, pituitary tumors MEN 2a: -Medullary thyroid cancers*, pheochromocytoma, parathyroid tumors MEN 2b: -Medullary thyroid cancers, pheochromocytoma, mucosal neuromas* *=most commonly occuring
64
Carcinoid syndrome S/Sx
``` Results from slow growing tumors -Vasoactice substances are secreted from enterochromaffin cells S/Sx depend on vasoactive substance involved) (serotonin -> vasoconstriction, kallikrein and histamine -> vasodilation) -Right-sided heart failure (serotonin) -Labile BP (kallikrein, histamine) -Cutaneous flushing (kallikrein) -Bronchospasm (kallikrein, histamine) -Diarrhea, abdominal pain (serotonin) ```
65
Carcinoid syndrome (Dx, Tx, preop)
Dx: Serotonin metabolites in urine, elevated plasma chromogranin A Tx: Surgical removal or management or symptoms Preop: -H1 and H2 blockers -Evaluate extraintestinal manifestations (AXR) -Octreotide 2 weeks before surgery
66
Octreotide and somatostatin for carcinoid syndrome
Octreotide -Serotonin antagonist -Inhibits all bioactive substances Somatostatin -Antagonize and suppress release of tumor products -Binds to tumor cell receptors -> decreased secretion
67
Carcinoid syndrome intraop
A line, large PIV, CVP - Avoid causing release of vasoactive substances from the tumor - Treat refractory hypotension with vasopressin - Octreotide available - Steroids, H2 blockers - Avoid histamine releasing substances (morphine, atracurium, succs) * Deep anesthesia (eliminate cardiac fluctuations from light anesthetic
68
Hypoparathyroidism anesthetic implications
-Hypocalcemia -Risk of laryngospasm -Respiratory distress due to edema, bleeding, or bilateral RLN injury (requires immediate reintubation) -Avoid hyperventilation Tx: IV CaCl
69
Islets of Langerhans cell types
Cells in pancreas Alpha: secrete glucagon Beta: secrete insulin
70
Islet of Langerhans alpha, beta, delta cells
Alpha: Produce glucagon Beta: Produce insulin Delta: Produce somatostatin -Inhibits GI motility and secretion of stomach acid
71
Insulins anabolic action
Anabolic=simpler molecules->complex, builds up tissues Glucose -> glycogen and triglycerides And has anticatabolic effect (prevents tissue breakdown to glucose)
72
6 endocrine organs that provide the endocrine component of the stress response
Anterior and posterior pituitary Hypothalamus Adrenal cortex and medulla Pancreas
73
Hormonal response to surgical stress
``` Increased -Cortisol, glucagon, GH, catecholamines Decreased -Insulin Both ->Decreased glucose clearance and increased gluconeogenesis ```
74
Dawn phenomenon vs somogyi effect
Dawn phenomenon -GH, cortisol, glucagon secreted overnight, increased blood glucose -Need insulin overnight to counteract this Somogyi effect -When too much insulin is given at HS and pt gets hypoglycemic overnight
75
Insulin transport to systemic circulation
Produced by pancreas ~60 units/day -First goes to liver where 20-50% is metabolized/deactivated -When passing through liver, hepatic glucose production is suppressed
76
Metformin MOA
Decreases hepatic glucose production -Prevents conversion of lactate to glucose Increases insulin sensitivity (GLUT 4 transport to cell membranes)
77
IV insulin half life
7.5 minutes Will be gone in 35 mins Best to do drip
6901
flashcards
Decks in class (9)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions