Endocrine Pt 1 Flashcards
where is the primary source of endogenous glucose production via glycogenolysis and gluconeogenesis
liver
a normal glucose level requires
a balance between glucose usage and endogenous production or dietary carb intake
what percent of glucose released by the liver is metabolized by insulin-insenstive tissues such as the brain, GI tract, and RBCs
70-80%
how long after meals is there a transition from exogenous glucose usage to endogenous production
2-4 hours - this is necessary to maintain a normal plasma glucose
which hormones can cause hyperglycemia (4)
glucagon, epinephrine, growth hormone, and cortisol
glucagon ______ glycogenolysis and gluconeogenesis; while _____ glycolysis
glucagon stimulates glycogenolysis and gluconeogenesis; while inhibiting glycolysis
Diabetes mellitus results from
an inadequate supply of insulin and or an inadeqaute tissue response to insulin
increased circulating glucose levels leads to eventual
microvascular and macrovascular complications
Type IA Diabetes is caused by
T-cell mediated autoimmune destruction of beta cells within pancreatic islets, resulting in minimal or absent circulating insulin levels
1a - autoimmune
Type 1B diabetes is a rare disease of
absolute insulin deficiency not immune mediated
Type 2 diabetes results from
defects in insulin receptors and post-receptor intracellular signaling pathways
also not immune-mediated
with type I diabetes, how long is the pre-clinical period of B-cell antigen production before onset of symptoms
9-13 years
what percent of Beta cell function is lost before hyperglycemia ensues in Type I diabetes
at least 80-90%
hyperglycemia over several days/weeks associated symptoms (7)
fatigue, weight loss, polyuria, polydipsia, blurry vision, hypvolemia, ketoacidosis
since type II diabetes is very underrecognized, how long do patients go before being diagnosed
4-7 years
in the inital stages of type II diabetes, insensitivity to insulin in peripheral tissues leads to
increased pancreatic insulin secretion
as DM progresses, pancreatic function decreases and insulin levels become
inadequate
what are the 3 abnormalities seen in DM2
increased hepatic glucose release (caused by reduction in insulin’s inhibitory effect on the liver)
impaired insulin secretion
insufficent glucose uptake in peripheral tissues
in DM2, where is insulin resistance characterized to
skeletal muscle, adipose, and liver
causes of insulin resistance (3)
abnormal insulin molecules
circulating insulin antagonists
insulin receptor defects
what are 2 contributing factors to DM2
obesity and sedentary lifestyle
diagnosis of DM
fasting blood glucose
HbA1C
diabetes diagnostic HbA1C criteria
normal?
Prediabetes?
Diabetes?
normal < 5.7%
prediabetes 5.7-6.4%
diabetes >6.5%
other criteria for diagnosis of diabetes
fasting blood glucose > 126 mg/dL
2-hour plasma glucose > 200 mg/dL during an oral glucose tolerance test (OB)
symptoms of hyperglycemia with a random plasma glucose > 200 mg/dL
DM2 treatment
diet
exercise/weight loss
PO antidiabetic drugs
metformin - biguanide
enhances glucose transport into tissues
decreases triglycerides and LDL levels
sulfonylureas
stimulate insulin secretion
enhances glucose transport into tissues
not effective long term due to progressive loss of B cell function
:( hypoglycemia, weight gain and cardiac effects
hypoglycemia with insulin can be exacerbated by what substances (6)
ETOH
metformin
sulfonyureas
ACE-Is
MAOIs
non-selective BB
repetitive hypoglycemic episodes can lead to what?
hypoglycemia unawareness - patient becomes desensitized to hypoglycemia and doesn’t show autonomic symptoms
what are signs of neuroglycopenia and treatment
fatigue, confusion, headache, seziures, coma
PO/IV/IM glucose
Kahoot Q
DKA is more common in which type of diabetes, what is its trigger
DM1, triggered by infection/illness
Kahoot Q
high glucose exceeding the threshold for renal reabsorption creates a
osmotic diuresis and hypovolemia
why does the liver start producing ketoacids in DKA
tight metabolic coupling of gluconeogenesis and ketogenesis
in DKA, excessive glucose - counterregulatory hormones with glucagon activate what?
lipolysis and free fatty acids which are substrates for ketogenesis
diagnostic features of DKA
serum glucose ?
pH ?
HCO3?
serum osmol ?
serum and urine ketones?
serum glucose > 300 mg/dL
pH < 7.3
HCO3 < 18 mEq/L
serum osmol < 320 mOsm/L
serum and urine ketones mod to high
DKA treatment
IV volume replacement
insulin
correct acidosis - NaHCO3
lyte replacement (K+, Phos, Mg++, Na+)
kahoot Q
insulin dose for treating DKA
loading dose 0.1 units/kg Regular Insulin
infusion @ 0.1 unit/kg/hr
T/F correction of glucose without correcting Na+ may result in cerebral edema
True
characteristics of hyperglycemic hyperosmolar syndrome
severe hyperglycemia, hyperosmolarity, and dehdyration
who is most likely to experience hyperglycemic hyperosmolar syndrome
DM2 > 60 years old
hyperglycemic hyperosmolar syndrome evolves over days to weeks with persistent glucosuric diuresis… why
when glucose loads exceeds max renal glucose absorption, mass solute diuresis occurs
symptoms of HHS
hyperglycemic hyperosmolar syndrome
polyuria, hypovolemia, HypoTN, tachycardia, organ hypoperfusion
pts have some degree of acidosis but not DKA
treatment of HHS
fluid resuscitation, insulin bolus and infusion, electrolyte replacement
mortality 10-20%
DM complications
nephropathy occurs because the kidneys develop what 3 things
glomerulosclerosis, arteriosclerosis, and tubulointerstitial disease
symptoms of nephropathy
HTN, proteinuria, peripheral edema, decreased GFR
GFR < 15-20; no longer clearing K+ patient becomes hyperK and acidotic
what drug can slow the progression of proteinuria and the rate of GFR slowing
ACE inhibitors
transplantaion of what organ with the kidney can help prevent recurrent nephropathy
pancreas
peripheral neuropathy is distal symmetric diffuse sensory motor polyneuropathy.. where does it start and progress
starts in toes/feet and progresses proximally
loss of large sensory and motor fibers produces
decreased light touch and proprioception
loss of small nerve fibers leads to
decreased pain/temp perception leading to neuropathic pain
treatment for peripheral neuropathy
optimal glucose control, NSAIDs, antidepressants, anticonvulsants
retinopathy with DM is caused by (4)
microvascular changes including vessel occlusion, dilation, increased permeability and microaneursysms
what are the visual changes with retinopathy
color loss to blindness
glycemic control and BP management reduces the progression
autonomic neuropathy is caused by
damaged vasoconstrictor fibers, impaired baroreceptors, ineffective cardiovascular activity
CV symptoms of autonomic neuropathy
abnormal HR control and vascular dynamics, resting tachycardia, loss of HR variability, orthostatic hypotension and dysryhtmias
autonomic neuropathy in the GI tract cause decreased gastric secretion, and motility leading to what
what are symptoms and treatment
gastroparesis
symptoms: N/V, early satiety, bloating, epigastric pain
treatment: glucose control, small meals, prokinetics
in DM preop evaluation what is possible with autonomic neuropathy
silent ischemia
consider stress test
in DM preop evaluation how can you help the kidneys
attention to hydration status, avoid nephrotoxins, and preserve RBF
autonomic neuropathy predisposes patients to
dysthymias and hypotension
gastroparesis may increase ____ risk regardless of ______
aspiration, NPO status
which DM meds should be held day of surgey
hypoglycemics and noninsulin injectable drugs
insulinoma is diagnosed based on what triad
whipple triad
hypoglycemia with fasting
glucose < 50 with symptoms
symptom relief with glucose
kahoot Q
preop what med(s) can you give to inhibit insulin release from beta cells to help insulinoma patients undergoing surgery
diazoxide
other: verapamil, phenytoin, propanolol, glucorticoids, octeroide
with the rare, benign insulin secreting pancreatic islet tumor.. during what periods will patients have hyperglycemia and hypoglycemia
hypoglycemia can occur intra op, followed by hyperglycemia once the tumor is removed
tight glycemic control is paramount
thyroid gland weighs how much and is composed of two lobes joined by an
20g
isthmus
where is the thyroid gland located
closely affixed to the anterior and lateral trachea with upper boarder below the cricoid cartilage
parathyroid glands in relation to thryoid gland
located on posterior aspects of each lobe
a rich capillary permeates the entire thyroid gland and is innervated by which ANS
adrenergic and cholinergic nervous systems
which nerves are in initmate proximity to the thyroid gland
recurrent laryngeal nerve and external motor branch of superior laryngeal nerve
what is thyroglobulin
an iodinated glycoprotein that is a substrate for thryoid hormone synthesis
which portion of the thyroid gland produces calcitonin
parafollicular C cells
production of normal thyroid hormone quantity is depending on exogenous
iodine
after ingesting iodine what happens to it in the body
iodine is reduced in GI tract to iodide and is absorbed into the blood, then transported from the plasma into the thryoid follicular cells
the binding of iodide to thyroglobulin is catalyzed by which enzyme
iodinase
T/F the thyroid contains a small store of horomones and has a fast turnover rate
FALSE! there is a large store with a low turnover rate, allowing protection against depletion if hormone synthesis is impaired
what is the normal T4/T3 ratio
10:1
3 major proteins that T3/T4 bind reversibly to
thyroxine binding globulin (80%)
prealbumin (10-15%)
albumin (5-10%)
thyroid hormone influences what metabolic processes in the body
growth and maturation of tissues, enhance tissue function, and stimulate protein syntesis and carbohydrate and lipid metabolism
thyroid function is controlled by
hypothalmus, pituitary and thryoid glands
____ is released from hypothalamus; _____ is released from the anterior pituitary
TRH- thyrotropin releasing hormone from hypothalmus;
TSH - thyroid stimulating hormone from the anterior pituitary
a decrease in TSH causes a decreased T3/T4 synetheisis which also decreases what
follicular cell size and vascularity
an increase in TSH yields an increase in hormone production, gland cellularity and
vascularity
how do thermal thyroid scans evaluate thyroid nodules
warm - normal function
hot - hyperfunctioning
cold- hypofunctioning
what are the 3 pathologies of hyperthryoidism
graves disease
toxic multinodular goiter
toxic adenoma
symptoms of hyperthryoidism
hypermetabolic state: sweating, heat intolerance, fatigue, inability to sleep
osteoporosis and weight loss
CV responses
more symptoms of hyperthryoidism
graves disease
autoimmune caused by thryoid stimulating antibodies that bind to TSH receptors stimulating growth, vascularity, and hypersecretion
females ages 20-40 y/o
presentations of graves disease
enlargement of goiter causing dysphagia, globus sensation, and possibly inspiratory stridor from tracheal compression
RX treatment for graves disease
methimazole or propylthiouracil (PTU)
high concentrations of iodine - short lived inhibition of release of thyroid hormone
beta blockers - may relieve symptoms
*propanolol impairs peripheral conversion of T4-T3
when is ablative therapy or surgery recommeneded for Graves disease
when medical therapy has failed
surgery - subtotal thryoidectomy is effective and low incidence of hypothyroidism than radioactive iodine
surgical complications of thyroidectomy
hypothyroidism, hemorrhage with tracheal compression, recurrent laryngeal nerve damage, damage to indavertent removal of parathyroid glands
emergent cases with a Graves disease patient preop consideratiosn
IV BBs, glucocorticoids, and PTU
evaluate upper airway for evidence of tracheal compression or deviation caused by a goiter
thyroid storm
exacerbation of hyperthryoidism precipitated by trauma, infection, medical illness, or surgery
when do thryoid storms most often occur
postop period in untreated or inadeqautely treated hyperthryoid patients after emergency surgery
Treatment - alleviation of thyrotoxicosis and supportive care
mortality is 20%
SIADH can occur in the presence of which pathologies
Intracranial tumors, hypothyroidism, porphyria, and lung carcinoma
kahoot Q
what signs are suggestive of SIADH
increased urine sodium and osmolarity in the presence of hyponatremia and decreased serum osmol
abrupt decrease in serum sodium can cause cerebral edema and seizures
treatment for SIADH
fluid restriction
salt tablets
loop diuretics
vasopressin antagonists
hyponatremia- hypertonic saline @ < 8 mEq/L within 24hrs
w hypertonic solution i though it <6mEq/L/24 hr from the renal lecture
kahoot Q
DI reflects
the absence of vasopressin (ADH)
causes of DI
destruction to posterior pituitary (neurogenic) or failure of renal tubules to respond to ADH (nephrogenic)
which form of DI (nephro/neuro) responds to desmopressin
neurogenic
symptoms of DI
polydipsia, and high output of poorly concentrated urine despite increased serum osmol
kahoot Q
treatment for DI
neuro vs nepro
intial - IV electrolytes to offset polyuria
neuro: DDAVP
nephro: low salt diet, low protein diet, diuretics, NSAIDs
anesthesia: monitor UOP/lytes
acromegaly and anesthesia implications
- distorted facial anatomy may interfere with placement of face mask
- enlarged tongue and epiglottis predisposes to upper airway obstruction and interferes with visualization of vocal cords on DL
- glottic opening narrowed due to vocal cord enlargement
- increased distance between lips and vocal cords
kahoot Q
considerations for acromegaly and intubation
smaller ETT
video laryngoscopy
awake fiberoptic intubation
what is acromegaly
excessive secretion of growth hormone in adults caused by adenoma in the pituitary gland
abnormal labs in the acromegaly pt
elevated serum insulin- like growth factor (IGF-1)
OGTT
which hormones are synthesized in the hypothalmus and then transported and stored in the posterior puitary
ADH (vasopressin) and oxytocin
stimulus for release from the posterior pituitary arises from osmoreceptors in the hypothalamus that sense plasma osmolarity
Overproduction of anterior pituitary hormones is often assoc w/
hypersecretion of ACTH (Cushing syndrome) by anterior pituitary adenomas
T/F thyroid hormone levels in thryoid storm are 5 fold than basic hyperthryoidism
false - they may not be much higher than basic hyperthyroidism
primary hypothyroidism
decreased T3 & T4 despite adequate TSH
2 most common causes of hypothyroidism
- abation of the gland by radioactive iodine or surgery
- iodiopathic and prolly autoimmune (antibodies blocking TSH)
hashimoto thyroiditis
autoimmune disorder characterized by goitrous enlargement and hypothyroidism that usually effects middle age women
symptoms of hypothyroidism
cold intolerance, weight gain, nonpitting edema
what is also common with hypothyroidism
SIADH, along with fluid overload, plueral effusions, and dyspnea
GI function is slow, and an adynamic ileus may occur
additional symptoms of hypothryoidism
secondary hypothryoidism diagnosis
reduced T3, T4, & TSH
TRH stimulation tests can confirm if the pituitary is the cause of hypothyroidism
T/F in primary hypothryoidsim, TRH elevates TSH
T/F with pituitary dysfunction, there is no repsonse to TRH
true
true
what is euthryoid sick syndrome
abnormal thyroid function tests in critically ill patients
low T3/T4/ normal TSH
likely a response to stress, can be induced by surgery
drug of choice for hypothryoidism
L-thyroxine (synthroid)
airway considerations for hypothyroidism
airway compromise due to swelling, edematous vocal cords, goitrous enlargement
additional preop considerations in hypothyroidism
decreased gastric emptying (aspiration risk)
CV system may be hypodynamic
resp function may be compromised
prone to hypothermia
lyte imbalances
hypothryoidism in an elective procedure vs emergent surgery
elective - thryoid therapy should be initiated 10 days prior
emergent- IV thryoid replacement with steroids ASAP
myxedema coma
severe form of hypothryoidism - delirium, hypoventilation, hypothermia, bradycardia, hypotension, and dilutional hyponatremia
triggers for myxedema coma
infection, trauma, cold, and CNS depressants
commonly occurs in elderly women with a long history of hypothyroidism
what is a cardinal feature due to impaired thermoregulation with myxedema coma/hypothryoidism
hypothermia
treatment for myxedema coma
IV Levothyroxine or L-triiodothryonine
IV hydration with glucose- saline solutions, temp regulation, correction of lyte imbalances, and stabilization of cardiac and pulmonary systems
how do goiters form
swelling of thryoid due to hypertrophy and hyperplasia of follicular epithelium
causes of a goiter (patho)
lack of iodine, ingestion of goitrogen (cassava, phenylbutazone, lithium) or defect in hormonal biosynthetic pathway
T/F a goiter is associated with a decompensated euthyroid state
false - its associated with a compensated euthyroid state
when is surgery for goiter indicated
medical therapy ineffective and goiter compromises the airway or cosmetically unacceptable
what is a predictor of airway obstuction during GA with a goiter
history of dyspnea in upright or supine position
flow-volume loops in upright & supine will demonstrate the site degree
limits in the inspiratory limb of the flow volume loop indicate
extra thoracic obstruction
delayed flow in the expiratory limb of the flow volume loop indicates
intrathoracic obstruction
complications of thryoid surgery
Recurrent Laryngeal Nerve injury be unilater or bilatreral; temperoray or permenant
if a patient experiences unilteral trauma to the recurrent laryngeal nerve how long will they experience hoarsness without airway obstruction
3-6 months
_____ or _____ of the recurrent laryngeal nerve results in permenant hoarsesness
ligation or transection
bilateral recurrent laryngeal nerve injury may cause
airway obstruction and problems with coughing/pulmonary toilet
may warrant tracheostomy
hypoparathyroidism may resuly from inadvertant parathyroid damage - symptoms of what electrolyte imbalance may occur in the first 24-48hours postop
hypocalcemia
immediate postop thryoid surgery needs what at the bed side due to what complication
hematoma - trach set
adrenal gland consists of
cortex and a medulla