Endo exam 4 Flashcards
Hormones baby!!!!
Name the organs of the Endocrine system?
Hypothalamus
pineal gland
pituitary
Thyroid
parathyroid
thymus
pancreas
ovaries
testes
adrenals
this organ is our primary source for glucose?
The liver
What is the percent range for the endogenous glucose metabolized ? by what cells/tissues?
70-80% Brain, Fat, muscles, RBCs
Roughly how long does it take to switch from exogenous to endogenous glucose production post eating?
2-4 hours
Formerly known as juvenile diabetes, an autoimmune destruction of Beta cells of the pancreas
Type 1a
Can occur up to 40 years of age, usually diagnosed in children, near their teens.
Type 1a vs Type 1b
Type 1a is an autoimmune destruction (causation undetermined)
Type 1b is an idiosyncratic lack of insulin production (rare).
Describe type 2 DM.
Tissues become resistant to insulin, nothing is technically wrong with the pancreas. This leads to a hyperglycemic state, and a global inflammatory response, which results in the multi organ dysfunction associated with the disease process.
What is the frequency in adults and is DM the most common endocrine disorder?
1 in 10 adults and yes.
Name a rapid, short, intermediate, and long acting insulin.
rapid= lispro
short= regular
intermediate= NPH
long= lantus
Phenomenon in which people are unaware their glucose levels are low?
hypoglycemia unawareness
How do you diagnose DM, what is your HgbA1C if your diabetic?
Fasting glucose or HgbA1C
>6.5%
This drug opposes the action of glucagon?
Metformin
These drugs stimulate the pancreas to release insulin?
Sulfonylureas
Why are Sulfonylureas not a good choice long term?
over time the pancreas either manufactures an abnormal insulin peptide or stops releasing all together.
What is DKA?
Usually precipitated by illness or stress. High levels of glucose cause an excessive release of glucagon. Fatty acid oxidation occurs, and we are left with an excess of ketones. Hyperglycemia leads to dehydration and electrolyte imbalance due to osmotic diuresis.
Prototypical DKA treatment?
IV volume replacement
Insulin: Loading dose 0.1u/kg Regular + low dose infusion @ 0.1u/kg/hr
Correct acidosis: sodium bicarb
Electrolyte supplement: k+, phos, mag, sodium
*Correction of glucose w/o simultaneous correction of sodium may result in cerebral edema
Pretty much isolated to type 1 for the most part.
DKA’s evil twin?
Hyperosmotic Hyperosmolar Nonketotic syndrome.
Presents very similar to DKA, just no ketones.
Tx: fluid resuscitation, insulin bolus + infusion, e-lytes
What are the long term consequences of DM?
Retinopathy, Nephropathy, microvascular, neuropathy, and ANS neuropathy.
This drug class prevents cardiac remodeling and can also attenuate the loss of GFR in DM?
ACE-Is
Treatment options for DM?
Diet, Lose weight, strength train, insulin, PO meds. Tight glycemic control in order to reduce HgBA1C and improve insulin resistance.
DM preop considerations?
Think multi system involvement. CNS, CV, Renal.
Hydration & Lytes
Gastroparesis
Holding or reduced medication dosing
Rare tumor found in the pancreas?
insulinoma
Insulinomas present with what features?
Hypoglycemia w/fasting
Glucose <50 w/sx
Sx relief w/glucose
aka Whipples triad
Preop- Diazoxide, which inhibits insulin release from B cells
Other tx: verapamil, phenytoin, propranolol, glucorticoids, octreotide
Surgery is curative
watchout for hypoglycemia
These two nerves run right next to the thyroid.
recurrent and superior laryngeal nerve (motor branch)
Why are thyroid procedures such a risk?
Highly vascular and nerve proximity.
What exogenous element do we need in low amounts to maintain our T3/T4 levels
iodine
Typical T3/T4 ratio?
10:1
Why is the thyroid so vital?
Thyroid hormones stimulate virtually all metabolic processes. They influence growth and maturation of tissues, enhance tissue function, and stimulate protein synthesis and carbohydrate and fatmetabolism
What are the major players anatomically when it comes to the thyroid?
hypothalamus, pituitary, and thyroid
The hormonal pathway for thyroxine synthesis?
TRH (Hypothalamus)
TSH (Anterior pituitary)
T3/T4 ( Thyroid)
T3/T4 turn off hypothalamus via negative feedback loop in the normal system
Common diagnostic testing for the thyroid?
TSH assay
TRH stimulation test assesses the functional state of the TSH-secreting mechanism
serum anti-microsomal antibodies, antithyroglobulin antibodies, and thyroid-stimulating immunoglobulins
Normal TSH level?
normal TSH level is 0.4-5.0 milliunits/L
Hyperthyroidism manifestations?
sweating, heat intolerance & fatigue w/inability to sleep
(Hypermetabolic state)
What hormone presentation of Grave’s disease is typical and whom does it typically effect?
low TSH + high T3 & T4
Women
What might occur in/around the airway with graves?
dysphagia, globus sensation, and inspiratory stridor from tracheal compression
Firstline treatment for graves?
PTU or methimazole
Typical goal is to shrink the gland before operation is performed.
Complications of thyroidectomy?
Complications from surgery include hypothyroidism, hemorrhage with tracheal compression, RLN damage, and damage to or inadvertent removal of the parathyroid glands
Medication for symptom management in the context of Grave’s?
β-blockers
Propranolol (non selective) impairs the peripheral conversion of T4 to T3
Pre op concerns with graves?
Thyroid levelsshould be established preoperatively
Elective cases may need to wait 6-8 weeks for antithyroid drugs to take effect
In emergent cases, IV BBs, glucocorticoids, and PTU usually necessary
Evaluate upper airway for evidence of tracheal compression or deviation caused by a goiter
Condition is similar to MH, what is it and how do we manage?
Thyroid storm.
Get them through with symptom management. Try and shut down the thyrotoxicosis.
20% mortality rate.
Hormone presentation in hypothyroidism or hashimotos?
↓T3 & T4 production despite adequate TSH
Textbook presentation with hypothyroidism?
cold intolerance, weight gain, nonpitting edema.
Their body is in slow motion.
How to differentiate primary vs secondary hypothyroidism?
test to determine if its the pituitary or the thyroid.
TRH test is performed. If there is an appropiate TSH response, the pituitary is fine.
No TSH= Bad pituitary gland.
Patients can experience a psuedohypothyroidism ,
True or False?
True.
Low T3 & T4 w/normal TSH level
Likely a response to stress, and it can be induced by surgery
TSH >10 milliunits/L
puts you at risk for what?
CAD.
What is the DOC for hypothyroidism.
L-thyroxine
Hypothyroidism preop concerns?
Assess for airway compromise d/t swelling, edematous vocal cords, goitrous enlargement
Expect slower gastric emptying, aspiration rx
Cardiovascular system may be hypodynamic
Respiratory function may be compromised
More prone to hypothermia
Electrolyte imbalances possible
If elective case, Thyroid tx should be initiated at least 10 days prior
If emergent surgery: IV Thyroid replacement along with steroids ASAP
This is rare in hypothyroidism but can be deadly?
myxedema coma
50% mortality rate
Treatment for myxedema coma?
IV T4 & T3
IV hydration w/glucose-saline solutions, temp regulation, correction of e-lyte imbalances, and stabilization of cardiac & pulmonary systems are necessary
When is a surgery indicative for goiter?
Surgery indicated only if medical therapy is ineffective, and goiter is compromises AW or is cosmetically unacceptable
Most goiters go away if Iodine is adequate, and T4 is given.
Pre op airway concerns for goiter?
Evaluate airway, especially if dyspnea is present.
CT for tumor eval.
Limitations in the inspiratory limb of the loop indicate extra-thoracic obstruction
Delayed flow in the expiratory limb indicates an intra-thoracic obstruction
Why does thyroid surgery result in hoarseness?
RLN injury may be unilateral or bilateral and temporary or permanent
If there is bilateral involvement. We have paralyzed the vocal cords, person will most likely need a trach
A useful emergency measure to keep around for thyroid surgery?
A trach kit. Mark that membrane!!!!
Why would your patient be hypocalcemic post thyroidectomy?
Damage or removal of the parathyroids.
What function do the adrenals perform?
glucocorticoids, mineralocorticoids (aldosterone), and androgens
Catecholamine production
Hormonal pathway of the HPA
CRH –> ACTH –> Coritcoids
Why does cortisol raise our blood sugar, cause weight gain, and can lead to hypokalemia?
causes gluconeogenesis, reduces uptake into tissues.
Tells kidneys to hold onto to sodium. (water follows sodium, leading to retention)
Aldosterone and high enough levels of corticoids act on the eNAC. Absorbing Na+ in the collecting duct and secreting K+
This tumor reveals itself through impressive hypertension and thunderclap headaches?
Pheochromocytoma
How is Pheochromocytoma confirmed?
24h urine collection for metanephrines and catecholamines
CT & MRI, I-metaiodobenzylguanidine (MIBG) scintigraphy help localize the tumor
What paradoxical finding might you find with pheos?
orthostatic hypotension. Thier carotid receptors have been desensitized.
why do we worry about Calcium when it comes to pheos?
Calcium triggers catecholamine release from the tumor, and excess calcium entry into myocardial cells contributes to a catecholamine-mediated cardiomyopathy
How do we medically treat pheos?
Phenoxybenzamine
Prazosin & Doxazosin
why do we need to be careful when it comes to betablockers in the setting of pheos?
BB before α blocker b/c blocking vasodilatory β2 receptors results in unopposed α agonism, leading to vasoconstriction and hypertensive crises
What are the two forms of cushings?
ACTH dependent and ACTH independent
Clinical presentation of dependent cushings?
high plasma ACTH stimulates the adrenal cortex to produce excessive cortisol
Presentation of independent cushings?
excessive cortisol production by abnormal adrenocortical tissue that is not regulated by CRH and ACTH
Typically the result of a tumor.
CRH and ACTH levels are actually suppressed
Clinical presentation of cushings?
sudden weight gain, usually central w/↑facial fat(moon face), ecchymoses, HTN, glucose intolerance,muscle wasting, depression, insomnia
Diagnosed via cortisol level
Cushing treatment options?
Surgery of pituitary, or removal of tumor present on the adrenal gland.
conn syndrome is also known as?
Primary hyperaldosteronism
Symptoms of Primary hyperaldosteronism?
HTN, hypokalemia, hypokalemic metabolic alkalosis
What should make you suspicious of conn’s or someone who likes licorice a bit too much?
Spontaneous hypokalemia in presence of systemic HTN is highly suggestive of hyper-aldosteronism
Why should one be careful with spirinolactone?
Hyperkalemia!!!
In which case of excessive aldosteronism is renin in excess?
secondary hyper-aldosteronism
hyper-aldosteronism in which renin is suppressed?
primary
Treatment for hypoaldosteronism?
liberal sodium intake and daily administration of fludrocortisone
What are you likely to see in hypoaldosteronism?
Hyperkalemia in the absence of renal insufficiency suggests hypoaldosteronism
Hyperkalemia may be enhanced by hyperglycemia
Hyperchloremic metabolic acidosis is common
Pts may experience heart block d/t hyperkalemia, orthostatic HoTN, and hyponatremia
Cause of hypoaldosteronism?
Lack of aldosterone may be c/b congenital deficiency of aldosterone synthetase or hyporeninemia d/t defects in the juxtaglomerular apparatus or ACE inhibitors
JFK was known to have this disease process?
Addison’s
Addison or primary is defined by what?
Adrenal glands unable to produce enough glucocorticoid, mineralocorticoid, and androgen hormones
The most common cause autoimmune adrenal destruction
Secondary adrenal insufficiency is a malfunction or lack of what?
CRH or ACTH, something is wrong upstairs either at the hypothalamus or pituitary.
Adrenal insufficiency is confirmed by what levels?
baseline cortisol < 20 μg/dL and remains <20 μg/dL after ACTH stimulation
How does one treat adrenal insufficiency?
steroids
What stimulates the release of PTH?
Hypocalcemia
PTH maintains normal plasma calcium levels by promoting the movement of calcium across GI tract, renal tubules, and the bone
Causes of hyperparathyroidism and what too watch out for?
Hypercalcemia
benign parathyroid adenoma (90%)
carcinoma (<5%)
parathyroid hyperplasia
Management of hyperparathyroidism?
Sx: sedation, n/v,↓strength,↓sensation, polyuria, renal stones, PUD, cardiac disturbances
Dx: Plasma calcium, 24 hr urinary calcium
Tx: surgical removal of abnormal portions of the gland
What is secondary hyperparathyroidism a function of ?
Another disease process, think chronic renal failure.
What is almost always iatrogenic?
Hypoparathyroidism
Levels to confirm the diagnosis of hypoparathyroidism?
hypocalcemia < 4.5 mEq/L and iCa² < 2.0 mg/dL, along w/↓PTH & ↑phosphate
How do we treat low calcium levels
with calcium and vitamin D
duh
congenital disorder in which the kidneys dont respond to PTH?
Pseudohypoparathyroidism
chronic Hypocalcemia symptoms?
assoc w/fatigue, cramps, prolonged QT interval, lethargy,cataracts, SQcalcifications, thickening of theskull, neurologic deficits
What to watch out for with acute hypocalcemia post parathyroid removal?
stridor, reflects irritation of the laryngeal nerves.
Most common cause of hypocalcemia?
chronic renal failure
Name the six hormones released by the anterior pituitary gland, the two released by the posterior?
anterior= GH, ACTH, TSH, FSH, LH, prolactin
posterior= oxytocin, ADH
Why is acromegaly a concern for anesthesia?
Overgrowth of soft tissues make pts susceptible to upper AW obstruction
Hoarseness & abnormal mvmt of vocal cords or RLN paralysis may result from overgrowth of the surrounding cartilaginous structures
Peripheral neuropathy is common d/t nerve trapping by connective tissues
Treatment for acromegaly?
surgical excision of pituitary adenoma
or long acting somatostatin
Airway management for acromegaly?
smaller ETT, VL, awake fiberoptic intubation
Hallmarks of DI, nephro and neuro?
Nephro- no longer responding to ADH, causing water wasting.
neuro- damage to pituitary causing lack of available ADH.
How to treat neuro DI?
ADH or DDVAP
How to manage neprho DI?
low salt, low protein, thiazide diuretics, NSAIDs
Anesthesia concerns for DI?
: monitor UOP & serum electrolyte concentrations
What should you look for if you suspect SIADH?
High urine sodium
low serum sodium.
treatment- fluid restriction, salt tablets, loop diuretics & ADHantagonists-Demeclocycline
Hyponatremia may be treated w/hypertonic saline @ <8 mEq/L over 24-hrs
