Endocrine Apex Flashcards
What describes a cell that releases a substance and travels through the bloodstream before it acts on different cells?
Endocrine
What describes a cell that releases a substance that works on adjacent cells?
Paracrine
What describes a cell that releases a substance that works on the surface of that exact same cell?
Autocrine
What 2 substances does the posterior pituitary release?
- Vasopressin (ADH)
2. Oxytocin
What 6 hormones does that anterior pituitary release? (mnemonic)
FLAT PiG
Follicle stimulating hormone
Luteinizing hormone
Adrenocorticotropin
Thyroid-stimulating hormone
Prolactin
ignore
Growth hormone
(Sex + growth hormones)
The other name for the anterior pituitary gland vs posterior pituitary gland
Adenohypophysis (Anterior) (A-Adeno)
Neurophypophysis (Posterior)
(Posterior releases ADH, causes of ADH can be NEUROlogic in nature)
What is follicle-stimulating responsible for?
Germ-cell maturation + ovarian follicle growth (females)
What is LH (luteinizing hormone) responsible for?
Testosterone production (males) Ovulation (females)
What is adrenocorticotropin responsible for?
Adrenal hormone release
What is TSH (thyroid stimulating hormone) responsible for?
Thyroid hormone release
What is prolactin responsible for?
Lactation
What is growth hormone responsible for?
Cell growth
What is antidiuretic hormone responsible for?
Water retention
What is oxytocin responsible for?
Uterine contraction & breast feeding
Does the hypothalamus reside inside or outside of the blood-brain barrier?
Outside - that’s how it’s able to secrete these substances into the bloodstream
Where is ADH formed?
In the supraoptic nuclei of the hypothalamus.
Where is oxytocin formed?
In the paraventricular nuclei of the hypothalamus
Which pituitary gland is always bigger?
Anterior
Which sits higher, the supraoptic or paraventricular nuclei of the hypothalamus?
The paraventricular
(Think the supraoptic sits closer to the eye and the paraventricular sits closer to the ventricles of the brain which are higher up)
What additional hormone does Luteinizing hormone-releasing hormone increase other than Luteinizing hormone?
Follicle-Stimulating hormone
T/F - Follicle-Stimulating releasing hormone increases the amount of follicle-stimulating hormone (FSH)
False! - Luteinizing releasing hormone increases FSH secretion.
What does corticotropin-releasing hormone cause?
increased adrenocorticotropin hormone (ACTH) from the anterior pituitary.
Which hormone released from the hypothalamus results in increased secretion of thyroid-stimulating hormone from the anterior pituitary?
Thyrotropin-releasing hormone
Where does that pituitary gland reside?
In the Sella Turcica
What connects the pituitary gland to the hypothalamus?
The pituitary stalk
What hormone stimulates germ cell maturation in males and females?
FSH
follicle-stimulating hormone
-Anterior Pituitary
What hormone stimulates ovarian follicle growth in females?
FSH
follicle-stimulating hormone
-Anterior Pitutiary
What hormone stimulates testosterone production in males?
LH
Luteinizing hormone
-Anterior pituitary
What hormone stimulates ovulation in females?
LH
Luteinizing hormone
-Anterior pituitary
What hormone stimulates adrenal hormone release?
ACTH
Adrenocorticotropic hormone
-from the anterior pituitary
What hormone stimulates the release of thyroid hormone?
Thyroid-stimulating hormone (TSH)
-from the anterior pituitary
What hormone stimulates lactation?
Prolactin
-from the anterior pituitary
What hormone stimulates cell growth?
Growth hormone
-from the anterior pitutary
Hypersecretion of what 2 hormones from the anterior pit can result in early puberty?
- FSH
- LH
(1. germ cell maturation and ovarian follicle growth
2. testosterone production and ovulation)
HYPOsecretio of what 2 hormones from the anterior pit can result in infertility?
- FSH
- LH
(1. germ cell maturation and ovarian follicle growth
2. testosterone production and ovulation)
(Hyper/Hypo)secretion of ATCH leads to (Cushings/Addisons) disease
Hypersecretion ACTH > cushings
Hyposecretion of ACTH > addisons
(adrenal hormone release)
(Hyper/Hypo)secretion of TSH leads to (hyper/hypo)thyroidism
Hypersecretion TSH > hyperthyroid
Hyposecretion of TSH > hypothyroid/cretinism
HYPERsecretion of which hormone from the anterior pit can result in infertility?
Prolactin
if your lactating all the time, ain’t no one gonna wanna get you pregnant there for you will be infertile
Hypersecretion of growth hormone results in what 2 conditions?
Acromegaly
Gigantism
Hyposecretion of growth hormone results in what condition?
Dwarfism
(Hyper/hypo) secretion of ADH results in (SIADH/DI)
hypersecretion of ADH = SIADH
hyposecretion of ADH = DI
Which endocrine hormone is a function of a positive feedback loop?
Oxytocin (birth/contractions)
What regulates the release of corticotropin-releasing hormone (CRH)?
cortisol >CRH > ACTH
What regulates the release of thyrotropin-releasing hormone (TRH)?
Triiodothyronine (T3) > TRH > TSH
What regulates the release of luteinizing hormone-releasing hormone (LHRH)?
Testosterone, Estrogen, Progesterone
> LHRH > FSH & LH
What regulates the release of growth hormone-releasing hormone (GHRH) and Growth hormone-inhibiting hormone (GHIH)? (2)
Growth hormone &
Insulin growth factor-1
Why do dopamine antagonists, such as metoclopramide cause hyperlactatinemia?
Prolactin is under neuronal control.
Normally Dopamine decreases prolactin.
So if it is inhibited, prolactin will accumulate
What is the most common cause of DI?
What about SIADH?
Pituitary surgery - DI
TBI - SIADH
Treatment for DI?
DDAVP (or vasopressin)
SC: 0.5-2mcg BID
Nasal: 5-40mcg QD
What syndrome does excess ADH in the blood create? what about too little?
SIADH - too much (si, ADH, too much, si)
DI - too little
What does the treatment of SIADH consist of? (3)
- Fluid restriction
- Demeclocycline
- Hypertonic saline (if severely hyponatremic)
What 4 airway challenges can present in a kid with acromegaly?
- difficult seal with BMV > distorted facial features
- difficult laryngoscopy > Large tongue, teeth, and epiglottis
- difficult ETT placement > subglottic narrowing and vocal cord enlargement
- Risk of epistaxis > enlarged turbinates
5 conditions associated with acromegaly
- OSA
- CAD (risk for rhythm disturbances and htn)
- Glucose intolerance
- skeletal muscle weakness
- entrapment neuropathies
5 causes of SIADH
- TBI (most common)
- small cell lung CA
- noncancerous lung disease
- Carbamazepine
- Hypothyroidism
4 Causes of DI
- Pituitary surgery (most common)
- Pituitary tumor
- TBI
- SAH
Presentation of SIADH
hyponatremia
presentation of DI
polyuria
SIADH vs DI plasma and urine osmolarity
Plasma Os:
SIADH: hypotonic <275mOsm/L
DI: hypertonic >290mOsm/L
Urine Os:
SIADH: higher than plasma os
DI: lower than plasma os
How does demeclocycline work?
It decreases the responsiveness to ADH
given to treat SIADH/excess ADH
When should you treat SIADH with hypertonic saline?
if they are symptomatic with their hyponatremia or if <120
How fast should you correct hyponatremia?
no more than 1meq/L/hr
What is another name for growth hormone?
Somatotropin
What condition results from oversecretion of growth hormone AFTER adolescence?
What is this most often caused by?
Acromegaly
-a pituitary adenoma
What condition results from oversecretion of growth hormone BEFORE puberty?
Gigantism
Why should you use a smaller ETT in a patient with acromegaly?
Bc of subglottic narrowing and vocal cord enlargement
What is thyroxine?
T4
What is triiodothyronine?
T3
The thyroid gland stores and secretes what 3 hormones?
thyroxine (T4)
triiodothyronine (T3)
Calcitonin (reduces serum CA)
What does calcitonin result in?
Reduced serum calcium/Hypocalcemia
What does the thyroid need to synthesize T3 & T4?
Iodine
What nerve is at risk during thyroid and parathyroid surgery and why?
Recurrent laryngeal nerve
> it runs along the lateral border of each thyroid lobe
What are the right and left thyroid glands attached by?
The thyroid isthmus
The thyroid gland lays:
Anterior to ___________
Inferior to______________
Superior to _____________
Anterior to the trachea
Inferior to the cricoid cartilage
Superior to the suprasternal notch
Which one is more potent : T3 or T4
T3 (active form)
Which one is more protein bound: T3 or T4
T4 (travels in blood)
Which one is directly released from thyroid: T3 or T4
T4
Where is T4 converted to T3 and what does this require?
In the target cell
-requires iodine
Which is the active form: T3 or T4?
T3
Half life of T3 vs T4
T3 = 1 day (short and potent) T4 = 7 days (long car drive, less potent)
Why does a hypothyroid patient have ELEVATED TSH?
Because the anterior pitutiary is releasing TSH to stimulate the thyroid to release T3/T4
> if the thyroid is hypoactive, it doesn’t secrete enough T3/T4 to tell the anterior pituitary to stop secreting TSH (negative feedback)
so anterior pituitary continues to sense these low levels of T3/T4 and keeps secreting TSH to try and boost them
Why does increased thyroid hormone result in vasodilation?
because increased BMR leads to increased O2 consumption. The vessels vasodilate in attempt to get more o2 supply to match the demand.
Why does excess thyroid hormone result in increased minute ventilation?
increased basal metabolic rate = increase end products of metabolism (CO2) - increased minute ventilation to blow off that CO2
What is the most common cause of hyperthyroidism?
Graves disease
What is the most common cause of hypothyroidism?
Hashimotos Thyroiditis
Why doesn’t hyper/hypothyroidism affect MAC?
because it alters o2 consumption in all tissues EXCEPT the CNS
How does hyperthyroidism affect MAC?
It doesn’t
-it does increase cardiac output though which increases anesthetic uptake into the blood
>decreases the rate of rise FA/FI (slower induction)
7 causes of hyperthyroidism
- Graves disease (most common) : autoimmune
- Myasthenia gravis (autoimmune)
- Multinodal goiter
- Carcinoma
- Preganancy
- Pituitary adenoma
- Amiodarone (less common)
6 causes of hypothyroidism
- Hashimotos thyroiditis (most common): autoimmune
- Iodine deficiency
- Hypothalamic-pituitary dysfunction
- Neck radiation
- Thyroidectomy
- Amiodarone (more common)
Is amiodarone more likely to cause hyper or hypothyroidism?
hypothyroidsm
Diagnosis of hyperthyroidism
Low TSH
High T3, T4
Diagnosis of hypothyroidism
High TSH
Low T3, T4
What is thyroid storm?
Does it occur in patients with hyper or hypothyroidism?
What time frame is it seen?
When periods of increased stress (surgical), the thyroid gland increases thyroid hormone output.
Hyperthyroidism and can occur in euthyroid patients too.
6-18 hours AFTER surgery
What is myxedema coma?
A complication/consequence of severe hypothyroidism (not a cause of it!)
What does cretinism lead to?
Impaired physical and mental development
Which betablocker inhibits the conversion of T4 to T3?
Propanolol
4 classes of drugs to manage hyperthyroidism
- Thionamides (PTU, methimazole, carbimazole)
- Betablockers (Esmolol, Propanolol)
- Potassium Iodine
- Radioactive Iodine
What are the 3 thionamides and how do they work?
2 main side effects
Propylthiouracil (PTU), methimazole, carbimazole
-block thyroid synthesis by blocking further iodine on the tyrosine residues of thyroglobulin
- Hepatitis
- Agranulocytosis
What 2 drugs inhibit the peripheral conversion of T4 to T3?
Propylthiouracil (PTU) and propanolol
How does potassium iodine treat hyperthyroidism and how many days should it be administered before surgery?
It decreases thyroid hormone synthesis & release
*10 days prior to surgery
How does radioactive iodine treat hyperparathyroidism?
2 contraindications
It destroys thyroid tissue
No preggos or breastfeeding mamas
4 Complications that may occur secondary to subtotal or total thyroidectomy
- hypothyroidism
- hemorrhage > tracheal compression
- RLN injury
- Hypocalcemia
How do you manage a hyperthyroid patient presenting for an elective surgery?
cancel!
How should you manage a hyperthyroid patient presenting for emergency surgery?
-Betablockers, potassium iodine, glucocorticoids and start PTU.
What are your concerns with a goiter?
It can cause tracheal deviation or tracheomalacia
AWAKE INTUBATION (First choice)
2nd choice- a technique that maintains spontaneous ventilation
What 3 drugs should be avoided in patients with hyperthyroidism?
- Anticholinergics
- Ketamine
- Pancuronium (who even has that shit)
Why would the hyperthyroid patient be at risk for corneal abrasion?
If they have exophthalmos
When you have a patient presenting for an elective thyroidectomy d/t hyperthyroidism, what are your main concerns? (7)
1. Complications >hypothyroid >prolonged wakeup from decreased CO >hemorrhage > tracheal compression >RLN injury > bilateral = emergency >hypocalcemia> muscle weakness
- Ensure they are euthyroid
- Goiters
>tracheal deviation? tracheomalacia
>poss awake intubation (glide) or keep spontaneous resps - Are they exophthalmic?
>increased risk of corneal abrasion - Caution with NMB
>what’s the cause of the hyperthyroidism? it could be myasthenia gravis - Careful positioning
>increased bone turnover = increased risk of osteoporosis and risk of fractures - Consider DL prior to extubation to assess vocal cords and for any glottic edema
What does the RLN innervate?
All the intrinsic laryngeal muscles except the cricothyroid muscle which is innervated by the SLN.
What would you see on DL if there was unilateral RLN injury?
How would this patient present after extubation?
How would you best assess this?
The ipsilateral (same side) vocal cord would stay midline on inspiration
hoaRsNess (RNL)
Ask the patient to say “E” or “moon”
What would you see on DL if there was BILATERAL RLN injury?
How would this patient present after extubation?
Both cords would stay midline on inspiration
Complete airway obstruction!
Which is the emergency - B/L SLN or B/L RLN injury?
B/L RLN injury
- Complete airway obstruction
- RuNNNNNN!
T/F : hypocalcemia resulting from parathyroid resection can put your patient at increased risk for layngospasm in the immediate postop period
False - the hypocalcemia usually results in 24-48hrs after surgery.
8 s/s hypocalcemia
- Muscle spasm –> tetany
- Laryngospasm
- Chvostek’s sign
- Trousseau’s sign
- Mental status changes
- Parasthesias
- Hypotension
- Prolonged QT
What is chvosteks sign and what does it indicate?
tapping on the angle of the jaw (facial nerve/masseter muscle) causes ipsilateral facial contraction
-hypocalcemia
How to assess for Trousseau’s sign.
What does it indicate?
inflate upper extremity BP cuff x 3 mins
>decreased blood flow should accentuate neuromuscular irritability
>muscle spasms of hand and forearm
What contains more elemental calcium…. chloride or gluconate?
calcium chloride
gluconate usually used bc less risk of necrosis if infiltrate occurs
What is thyroid storm typically triggered by, who is affected, and when?
triggered by: stressful events: surgery, infection, ect.
who: hyperthyroid AND euthyroid patients
when: 6-18 hours AFTER surgery
7 s/s of thyroid storm
- Fever > 38.5
- Tachy
- HTN
- CHF
- Shock
- Confusion/Agitation
- N/V
What 4 things can thyroid storm mimic under GA?
- MH
- Pheo
- NMS
- Light anesthesia
What are the 4 B’s in treating thyroid storm?
Block synthesis (methimazole, PTU, carbimazole, potassium iodine)
Block release (potassium iodine, radioactive iodine)
Block T4-T3 conversion (PTU, propanolol, gluticocorticoids)
Block beta (propanolol and esmolol)
What drugs block the synthesis of thyroid hormone? (4)
- Methimazole
- PTU
- carbimazole
- potassium iodine
What drugs block the release of thyroid hormone (2)?
Potassium iodine and radioactive iodine
What drugs block the conversion of T4 to T3? (3)
PTU
Propanolol
glucocorticoids
Betablockers for hyperthyroidism or thyroid storm
propanolol
esmolol
Why shouldn’t you give aspirin to someone with hyperthyroidism or thyroid storm?
Because aspirin can dislodge T4 from plasma proteins
>increased free fraction of T4
>worsening situation
Those with hyperthyroidism have increased resistance to depolarizing or nondepolarizing NMB?
depolarizing
(hypocalcemia = more irritable muscles, will take more to relax them) - my thoughts at least idk
What sympathomimetic agent should you avoid when treating hypotension in a hypothyroid patient?
phenylephrine (want to enhance myocardial performance, not slow the rate)
In a hypothyroid patient whose BP is unresponsive to catecholamines, what would be the next agent to try?
-why?
Corticosteroids
-these patients often have decreased adrenal function
Your main thoughts when anesthetizing a patient with mild-moderate hypothyroidism (9)
- They’re probably going to obstruct on me
>big tongue, swollen VC, goiter - Risk of aspiration
>decreased gastric emptying - FASTER inhalation induction
- No change in MAC
- Avoid phenylephrine (don’t want to further depress cardiac rate)
- Refractory hypotension
>tx with corticosteroids (these pts often have decreased adrenal function) - If lethargic, they will prob be very sensitive to anesthetics
- Increased sensitivity to NDMRs
- Slowed hepatic metabolism and renal excretion can prolong drug effects
What two hormones act antagonistically to regulate the ionized calcium level?
Calcitonin & PTH
Where is calcitonin produced and what does it do?
It’s produced in C-Cells (Calcitonin) of the thyroid gland
> decreases ionized calcium
increases serum phos
Where is PTH produced and what does it do?
It’s produced in the chief cells of the Parathyroid
> it increases ionized calcium
decreases serum phos
What is the most common cause of hypercalcemia?
Primary hyperparathyroidism
What is the most common cause of primary hyperparathyroidism and how is it treated?
Parathyroid adenoma > primary hyperparathyroidism > hypercalcemia
*tx- surgical resection of the parathyroid glands
What is secondary hyperparathyroidism?
*most common cause?
Hyperparathyroidism that is caused by something that stimulates the parathyroid glands to increase PTH output
(the glands themselves are normal)
*CKD
T/F hypoparathyroidism causes hypocalcemia
True
What is the most common cause of primary hypoparathyroidism?
*treatment
iatrogenic gland removal during thyroidectomy
*Tx- Calcium, vitamin D, and Mag supplements
What are osteoblasts?
they are bone cells that add calcium to the bone
*this decreases CA+ concentration in the blood
(Blast calcium into the bone)
What are osteoclasts?
bone cells that remove calcium from bone and increase ionized ca++ levels in the blood
What bone cells promote bone deposition?
Osteoblasts (blast calcium into the bone)
What bone cells promote bone resorption?
Osteoclasts
Difference between calcitocin and calcitrol
Calcitonin decreases ionized CA and increases serum phos
Calcitrol is the active form of vitamin D
What functions as a resovior for calcium in our bodies?
*what is it stored as?
Bones
*Hydroxyapatite
What is ionized calcium?
The amount of free calcium not bound to plasma proteins
Calcitonin and PTH regulate calcium in what parts of the body (3)?
bones, kidneys, and intenstines
Normal Calcium level
8.5-10.5mg/dL
Normal ionized calcium level
4.5-5.5mg/l
(2.2-2.6meq/l)
What happens when an increased calcium level is detected?
Thyroid gland releases CALCITONIN which:
- Inhibits osteoclast activity
- decreases calcium resorption in the kidneys
What happens when a decreased calcium level is detected?
Parathyroid glands release PTH, which:
- stimulates osteoclast activity (calcium release from bone into blood)
- Calcium is reabsorbed in the kidney (reabsorbs it into the blood)
- Vitamin D synthesizes absorption of calcium from the small intestines
T/F: only the ionized portion of calcium exerts physiologic effects
True
What is the term for bone disease caused by hyperparathyroidism secondary to CKD?
Renal osteodystrophy
The adrenal gland is composed of what 2 things?
Adrenal cortex (outer region) Adrenal medulla
Where are mineralocorticoids secreted from specifically?
Example of a mineralocorticoid
Zona-gloMerulosa of the adrenal cortex
- Aldosterone
- Salt
Where are corticosteroids produced specifically?
-Example of a corticosteroid
Zona- Fasiculata of the adrenal cortex
- Cortisol
- Sugar
(cortisol is Fascinating)
What is produced by the Zona Reticularis of the adrenal cortex?
- Androgens (Sex hormones)
(dehydro-epi-andosterone)
(Androgens are Ridiculous, zona Reticularis)
What 3 things cause the release of aldosterone?
- RAAS activation
- Hyperkalemia
- Hyponatremia
(holds onto sodium, releases K)
What stimulates the kidney to conserve sodium & water and to excrete potassium and hydrogen?
Aldosterone
T/F aldosterone regulates sodium concentration and osmolarity
False (ADH does this)
What increases cortisol production?
Stress
By what 3 methods does cortisol increases glucose?
- Gluconeogenesis
>liver converts aminoacids to glucose - Protein catabolism
>muscle breakdown to increase amount of aminoacids available for the liver to convert to glucose - Fatty acid mobilization
>increased fatty acid oxidation
>body able to use fat for energy instead of glucose
How does cortisol mitigate the inflammatory cascasde?
By stabilizing lysosomal membranes & decreasing cytokine release
3 catagories of steroids synthesized and released from the adrenal cortex
- Mineralocorticoids (aldosterone) (G) (salt)
- Corticosteroids (cortisol) (F) (sugar)
- Androgens (sex hormones) (R) (sex)
What steroid is required for the vasculature to respond to the vasoconstriction effects of catecholamines?
Cortisol
T/F- decreased levels of ACTH cause hypoaldosteronism
False- ACTH only has a minor influence on aldosterone release
What receptors on the cell membrane does cortisol bind to?
None- it diffuses through the lipid bilayer & binds with INTRACELLULAR steroid receptors
(process requires time, which is why there is a longer onset with steroids)
Normal cortisol production/day
15-30mg/day
Normal cortisol level
12mcg/dL
T/F - cortisol reduces histamine
false
Which endogenous steroid has equal glucocorticoid and mineralocorticoid effects?
Cortisol
T/F aldosterone has some glucocorticoid (anti-inflammatory) effects
False!
What should you think of when differentiating the effects of glucocorticoids and mineralocorticoids?
glucocortiocid = anti-inflammatory effects mineralcorticoid = sodium-retaining effects
Adrenocortical insufficiency is known as….
Addison’s disease
What is a good choice to treat adrenocortical insufficiency ( _________ disease) and why?
Addison’s disease
-Prednisone - bc it’s an analog of cortisol (meaning it most closely resembles cortisol of all the exogenous steroids)
Which exogenous steroids have no mineralocorticoid effects? (3)
- Dexamethasone
- Bexamethasone
- Triamcinolone
What is the name of the steroid commonly injected into the epidural space to treat lumbar disc disease?
Triamcinolone
3 things that make triamcinolone unique?
- Higher incidence of skeletal muscle weakness
- Can cause sedation rather than euphoria
- Anorexia rather than increased appetite
3 endogenous steroids
- Cortisol
- cortisone
- Aldosterone
Which disease states:
- insufficient cortisol
- excess cortisol
- excess aldosterone
- insufficient cortisol = Addison’s (need to ADD some cortisol)
- excess cortisol = Cushing’s (cush balls are so extra)
- excess aldosterone = Conn’s (aldosterone = the con man, cons off sodium for potassium) - extra conning going on
Another name for primary hyperaldosteronism
Conn’s Syndrome
3 Causes of Conn’s Syndrome
- Aldosteroma
- Pheo
- Primary Hyperthyroidism
Long-term licorice ingestion ( ________ acid) contributes to a syndrome that highly resembles what?
Hyperaldosteronism (Conn’s Syndrome)
-Glycyrrhizic Acid
3 Clinical features of hyperaldosteronism (Conn’s Syndrome)
- Hypertension (sodium and water retention)
- Hypokalemia (K+ excretion)
- Metabolic Alkalosis (H+ wasting)
Why would you want to avoid hyperventilating someone with Conn’s syndrome?
Bc hyperventilation activates the H+/K+ and will make hypokalemia and alkalosis worse
What results from when the anterior pituitary releases too much ACTH which then triggers the increased cortisol release from the zona fasciculata of the adrenal cortex?
Cushing’s syndrome
T/F - cortisol has glucocorticoid, mineralocorticoid, AND androgenic effects
True
*Cushing’s disease affects all these areas
What disease is caused by excess ACTH?
Cushing’s syndrome
Causes of Cushing’s syndrome
- Pituitary tumor > “Cushing’s disease”
- Adrenal tumor
- Other
Difference between Cushing’s syndrome and Cushing’s disease
Cushing’s disease causes Cushing’s syndrome
Cushing’s disease = oversecretion of ACTH from pituitary tumor > increased cortisol release from adrenal cortex
What does the destruction of all 3 zones of the adrenal cortex result in?
Adrenal insufficiency
What are your concerns with someone who has adrenal insufficiency?
That it can turn into an adrenal crisis which is triggered by additional stress on the body (surgery, pain, infection, sepsis
How does Etomidate cause dose-dependent adrenocortical suppression?
By inhibiting 11-Beta hydroxylase
What happens with primary adrenal insufficiency (Addison’s disease)
ADrenal glands don’t secrete enough steroid hormone (cortisol)
Anterior pituitary will increase ACTH secretion in attempt to stimulate the failing gland
Most common caue of primary adrenal insufficiency (Addison’s disease) in the US vs worldwide
US- autoimmune destruction of both glands
WW- TB
(HIV also a cuase)
What happens with secondary adrenal insufficency?
There is decreased cortisol-releasing hormone or decreased ACTH release which results in decrease stimulation of the adrenal gland and decreased cortisol release
Most common cause of secondary adrenal insufficency?
Exogenous steroid administration
or HPA disease from tumor, infection, surgery, or radiation
Clinical features of adrenal insufficiency (8)
Muscle weakness/fatigue
Hypotension
Hypoglycemia
Hyponatremia, Hyperkalemia, Metabolic Acidosis
N/V
Hyperpigmentation of knees, elbows, knuckles, lips, and buccal mucosa (Primary adrenal insufficiency)
Treatment for adrenal insufficiency
Steroid replacement therapy
15-30mg cortisol equivilent/day
4 S/S of adrenal crisis
- Hemodynamic instability (collapse)
- Fever
- Hypoglycemia
- . Change in MS
Treatment for Adrenal Crisis (3)
- Hydrocortisone 100mg + 100-200mg/day
- ECF volume expansion with D5NS
- Support hemodynamics
How does exogenous steroid supplementation work?
It decreases ACTH release from the anterior pituitary
> decreased ACTH = decreased cortisol (pt’s wont be able to increase cortisol in response to surgical stress)
What dose/duration of prednisone poses the following risks of HPA suppression?
- Yes:
- Maybe:
- No:
Which require stress- dose steroids?
Yes: >20mg/day for > 3 weeks *Stress dose
Maybe: 5-20mg/day for >3 weeks *Stress dose
No: <5mg/day for any period of time
or any dose for < 3 weeks !
Pre-op hydrocortisone dose for superficial procedures such as dental work and biopsies? Taper?
None
Pre-op hydrocortisone dose for minor surgical procedures such as inguinal hernia repairs and colonoscopy. Taper?
25mg IV
-no taper
Pre-op hydrocortisone dose for moderate surgical procedures such as: Colon resection, TJR, total abdominal hysterectomy? Taper?
50-75mg IV
-taper over 1-2days
Pre-op hydrocortisone dose for major surgical procedures such as CV, whipple, thoracic, liver? Taper?
100mg-150mg IV
-taper over 1-2 days
How long does the adrenocortical supression effects of etomidate last after a single induction dose?
5-8 hours (some sources say up to 24)
In addition to etomidate, what other drug can inhibit cortisol synthesis?
Ketoconazole (an antifungal)
What are the 2 broad groups of hormones secreted by the pancreas, where are they secreted, and what are they produced by?
- Endocrine > released into the duodenum for digestion > Acini tissue
- Exocrine > released into circulation for metabolism > islets of Langerhans
What cells are glucagon secreted from and what does it do?
Alpha cells > increase blood glucose
What cells are insulin secreted from and what does it do?
Beta cells > reduce blood glucose
What cells are somatostatin secreted from and what does it do?
Delta cells > inhibits insulin and glucagon; inhibits splanchnic blood flow, gastric acid secretion, and gastric motility, and GB contraction
What inhibits pancreatic exocrine secretion, GB contraction, gastric acid secretion, and gastric motility?
Pancreatic Polypeptide
What is the primary stimulator of insulin release from the pancreatic beta cells?
Glucose
therefore anything that increases serum glucose will increase insulin release
Cerebral function steadily declines with glucose levels are less than what?
< 50mg/dL
How does glucagon increase cardiac contractility, HR and AV conduction?
By increasing intracellular cAMP (occurs independently of the ANS)
1-5mg
How does insulin lower potassium levels?
Because it stimulates the NA/K ATPase pump
>3 sodium out of cell, 2 potassium into cell
-D50 is given to prevent hypoglycemia
What is the physiologic antagonist to insulin?
Glucagon
What are key side effects of glucagon?
N/V!
When might glucagon be used? (5)
- Betablocker overdose
- CHF
- Low cardiac output after MI or CPB
- Improving map during anaphylaxis
- Relax the biliary sphincter during ERCP
Somatostatin vs Somatotropin
Somatotropin = Growth hormone (Your TROPS grow after cardiac ischemia)
Somatostatin = Growth hormone-inhibiting hormone (Statins inhibit cholesterol)
Which type of diabetes is due to beta cell destruction?
Type 1 (lack of insulin production)
Which type of diabetes is characterized by insulin resistance and a relative lack of insulin
Type 2
What describes a group of characteristics that are common do diabetics or those at risk for developing diabetes?
Metabolic syndrome
What are the 5 criteria for metabolic syndrome and how many of them do you need?
Fasting glucose > 110mg/dL
Abdominal obesity (waist > 40” in men, >35 in females)
Triglycerides > 150mg/dL
Serum HDL <40mg/dL in men and <50 in females
BP 130/85mmHg
Type 1 and 2 diabetes, which one for DKA and which one for Hyperglycemic Hyperosmolar state
1- DKA
2- HH
The usual cause of DKA and treatment
- infection
tx: volume resuscitation, insulin, and potassium once acidosis subsides
is metabolic acidosis worse in DKA or HH?
DKA
may not even be acidotic in HH
Diagnostic criteria for diabetes mellitus (4)
- Fasting glucose > 126mg/dL
- Random glucose > 200mg/dL + classic sx
- 2Hr plasma glucose >200mg/dL during an oral glucose tolerance test
- Hgb A1C > 6.5%
What causes fruity-smelling breath in diabetics?
Acetone
What causes kussmauls respirations?
Metabolic Acidosis
Which type of diuretics increase serum glucose?
List 3 examples
Thiazide diuretics
HCTZ, metalozone [zaroxolyn], indapamide
Why should LR be avoided in diabetics?
Because the lactate can be converted to glucose and contribute to hyperglycemia
Which oral diabetic agent carries a risk of lactic acidosis? How long is it recommended to be held before surgery?
Metformin
-Hold 24hr before surgery
How does metformin work?
It disrupts mitochondrial function
>decreases intracellular levels of ATP
Pyruvate is the final product of glycolysis
>if mitochondrial are dysfunctional, the cell shits to anaerobic metabolism and produces lactate
Which class of oral hypoglycemic agents shouldn’t be used in someone with a sulfa allergy?
Sulfonylureas (Glyburide)
-dont know why I have to know this shit, I’m not going to be prescribing oral hypoglycemic agents
Which class of oral hypoglycemic agents is contraindicated in pts with liver failure?
Thiazolidinediones (Rostiglitazone)
MOA of Biguanides
Example (1)
- Inhibits gluconeogenesis and glycogenolysis in the liver
- Decreases peripheral insulin resistance
(inhibits body from making more glucose and allows insulin to act on cells in order to get glucose into them)
Metformin
MOA of Sulfonylureas
Example (6)
Stimulate insulin secretion from pancreatic beta cells
Glyburide (-ride) Gliimepiride (-ride) Glipizide (-zide) Gliclazide (-zide) Chlorpropamide (-mide) Acetohexamide (-mide)
Tolbutamine (-mine)
MOA of Megalitinides
Examples (2)
Stimulate insulin secretion from the pancreatic beta cells
Repa-glinide
Nate-glinide
Nate and Repa are so mega
MOA of Thiazolidinediones
Examples (2)
Decrease peripheral insulin resistance and increase hepatic glucose utilization
Rosi-glitazone
Pio-glitazone
-glitazone
Drug class ending in “-glitazone”
Thiazolidinediones
Drug class ending in “-glinide”
Megalitinides
Which class of oral hypoglycemic agents may cause vitamin B12 deficiency?
Biguanides (Metformin)
How should you treat lactic acidosis from metformin? (3)
Hemodialysis, sodium bicarb, CV support
Which class of oral hypoglycemic agents is often used for polycystic ovarian disease?
Biguanides (Metofrmin)
In what patient populations should metformin be avoided in due to accumulation of drug increasing the risk of lactic acidosis? (5)
Liver disease, Renal disease, Acute MI, CHF, Iodinated Contrast Media
Which oral hypoglycemic drug class expands ECF and can lead to edema?
Thiazolidinediones
> Rosi-glitazone & Pio-glitazone
MOA of alpha-Glucosidase inhibitors
2 examples
slow digestion and absorption of carbs from the GI tract
-Acarbose and miglitol
MOA of Glucagon-Like Peptide-1 Receptor Agonists
2 examples
- Increase insulin release from pancreatic beta cells
- decrease glucagon release from alpha cells
- prolong gastric emptying
ExenaTIDE, LiragluTIDE
MOA of Dipeptidyl-Peptidase-4 Inhibitors
Suffix of these drugs
Increase insulin release from pancreatic beta cells
-decrease glucagon release from alpha cells
“-leptin”
MOA of Amylin Agonists
1 example
Inhibit glucagon release from the pancreatic alpha cells
-decrease gastric emptying
Pramlintide
Out of the oral hypoglycemic drug classes, which ones do NOT cause hypoglycemia? (3)
Biguanides (Metformin)
Thiazolidinediones (-“glitazone)
Alpha-Glucosidase inhibitors (Acarbose/Miglitol)
Which oral hypoglycemic drug class poses a risk of hypoglycemia when used with insulin?
Amylin agonists (Pramlintide)
Which oral hypoglycemic drug class may cause N/V
Amylin agonist (Pramlintide)
What kind of insulin is the only kind that can be administered IV?
Regular insulin (Rapid-Acting)
Which receptors stimulate and inhibit insulin secretion?
Beta-2 –> Stimulate insulin secretion
Alpha 2 –> inhibit insulin secretions
What organ secretes insulin?
The pancreas
Onsets for Insulins:
- Ultra-Rapid-Acting:
- Rapid-acting:
- Intermediate acting:
- Long-Acting
- Ultra-long-acting:
- Ultra-Rapid-Acting: 5-15 mins
- Rapid-acting: 30 mins
- Intermediate acting: 2 hours
- Long-Acting: 2 hours
- Ultra-long-acting: 2 hours
Peaks for insulins:
- Ultra-Rapid-Acting:
- Rapid-acting:
- Intermediate acting:
- Long-Acting
- Ultra-long-acting:
- Ultra-Rapid-Acting: 1 hour (45-75 minutes)
- Rapid-acting: 2-4 hours
- Intermediate acting: 4-12 hours
- Long-Acting: 3-9 hours (glargine no peak)
- Ultra-long-acting: none
Durations for insulins:
- Ultra-Rapid-Acting:
- Rapid-acting:
- Intermediate acting:
- Long-Acting
- Ultra-long-acting:
- Ultra-Rapid-Acting: 2-4 hours
- Rapid-acting: 6-8 hours
- Intermediate acting: 24 hours (18-28hrs)
- Long-Acting: 6-24 hrs detrimir; 24hrs gargline
- Ultra-long-acting: 48 hours (40+hrs)
What are the 3 ultra-rapid-acting insulins?
Lispro
Insulin Aspart (Novolog)
Glulisine
Goals of insulin therapy:
AIC < ____%
Blood glucose before a meal: ______-_______
Blood glucose after a meal:
AIC < 7%
Blood glucose before a meal: 70-130
Blood glucose after a meal: <180
S/E of hypoglycemia (3) under anesthesia
SNS stimulation: increased HR, BP, and diaphoresis
>difficult to detect if beta blocked!
(the brain needs glucose: confusion, seizures, coma, death)
3 drugs that counter the hypoglycemic effect of insulin
- Epi
- Glucagon
- ACTH
3 drugs that extend or enhance the hypoglycemic effects of insulin
- MAOis
- Salicylates
- Tetracycline
What syndrome is associated with secretion of vasoactive substances from the enterochromaffin cells?
Carcinoid syndrome
> usally associated with tumors found in the GI tract but can arise outside GI tract as well
Two categories of drugs to avoid in pts with carcinoid syndrome
- Histamine releasing drugs:
Morphine, meperidine, atracurium, sux, thiopental
*fasciculations from sux can also stimulate secretions from tumors
(meperidine, atracurium, thiopental)
- Sympathomimetics
Ketamine, ephedrine, NE
what drugs to tx hypotension in a patient with carcinoid syndrome?
Neo & Vasopressin
Treatment for carcinoid syndrome (4)
- Somatostatin
>Octreotide or Lanreotide
>inhibit the release of vasoactive substance from carcinoid tumors, improving hemodynamic stability - Antihistamines (H1 + H2 blocker):
>diphenhydramine +
>ranitidine or cimetidine - Steroids
- 5-HT3 antagonists (Zofran)
2 most common signs of carcinoid syndome
Hypotension & Flushing
bronchoconstriction, h/a, abdominal pain
3 groups of hormones released with carcinoid syndrome
- Histamine
- Kinins & Killikrean
- Serotonin
What two cardiac conditions are often co-exisiting in someone with carcinoid syndrome
Pulmonic stenoisis and TR
5 s/s of carcionid crisis
- Tachycardia
- Hyper or hypotension
- Abdominal Pain
- Diarrhea
- Intense Flushing
Exogenous somatostatin (2)
Octreotide & Lanreotide
5 Drugs at your disposal that cause histamine release (Acronym)
MMAST (mast cells release histamine)
Morphine Meperidine Atracurium Sux Thiopental
Normal Phosphate level
2.5-4.5mg/dL
Suffix “-tropin”
a substance that is going to travel to another part of the body to tell it to release another hormone
What is the cortex? What does it secrete?
The outer portion of the adrenal gland
>aldosterone (mineralocorticoid/salt/Glomerulosa)
>cortisol (glucocorticoid/sugar/Fasiculata)
>androgens (sex/Reticularis)
What is the medulla?
The inner portion of the adrenal gland
What is erythropoietin, where is it produced, and why?
It increases RBC production
>produced in the kidneys
>to maintain it’s own o2 rich blood supply
(kidneys will increase RBC production in response to hypoxia, or venous congestion)
