Endocrine Flashcards
islets of langerhans
- make up 1-2% of pancreas weight
- hormones are produced and do not enter ducts but are secreted into the capillary blood vessel
- venous blood from islet drains into the hepatic portal vein and then into general circulation
four cells in the islets of langerhans
- delta
- pancreatic polypeptide (PP)
- alpha
- beta
beta cells
- compromise 60-70% of islet mass
- secrete insulin
alpha cells
- compromise 25% islet mass
- secrete glucagon
delta cells
secrete somatostatin
three major hormone classifications
- peptides/proteins –> insulin and glucagon
- amino acid –> dopa and epi
- steroids –> lipid soluble, derived from cholesterol (like estrogen or progesterone)
insulin
- synthesized in beta cells
- released via exocytosis to the capillary then enters portal circulation
- half life = 5-8 min
- major hormone degradation sites are liver and kidney
insulin function
- key hormone controlling glucose removal from the plasma
- facilitates transport of glucose by stimulating uptake into the liver, muscle, and adipose tissue
- brain = one of the few tissues that does not require insulin or glucose for transport into cells
- liver = insulin promotes efficient storage of excess glucose in the form of glycogen (glycogenesis)
pancreatitis
- inflammation of the pancreas which is commonly caused by gallstones and alcohol
- can also be caused by trauma such as ERCP, obstruction and certain medications
pancreatitis clinical presentation
- abdominal pain
- N/V
- febrile
pancreatitis anesthetic considerations
- early hydration
- pain meds
- electrolytes
- patient NPO until pain and inflammation has resolved
pancreatitis labs
- elevated WBC count
- possible ARF
- liver dysfunction
- electrolyte abnormalities
pancreatitis complications
- pancreatic necrosis = cell death secondary to inflammation
- pancreatic pseudocyst = contains only fluid and is the most common complication of chronic pancreatitis
pancreatic cancer
- fourth most common cause of cancer deaths in the US
- risk factors = obesity, smoking, chronic pancreatitis
pancreatic cancer s/s
- abdominal pain
- weight loss
- pain = retroperitoneal invasion
- jaundice = biliary obstruction
pancreatic cancer treatment
- surgical resection is the only effective treatment
- patient with tumor in head of pancreas develop painless jaundice and are usually candidates for surgical resection
- most common techniques = pancreatectomy or whipple
Cystic fibrosis
- autosomal recessive
- mutation of chromosome 7
- defective chloride ion transport in epithelial cells in lungs, pancreas, liver, GI and reproductive organs
- decreased chloride –> decreased transport of sodium and water –> viscous secretions that are luminal obstruction and scarring to exocrine glands
- primary M&M = chronic pulmonary infection
CF anesthetic implications
- elective surgery delayed until optimal pulmonary function obtained
- volatiles decrease airway pressure by decreasing bronchial smooth muscle and decreasing hyperactive airways
- AVOID anticholinergics to maintain secretions in less viscous state
- intubated –> need to suction
- DEEP - to minimize coughing
T1DM
- T cell mediated destruction of beta cells in pancreas
- 80-90% of beta cell function lost before hyperglycemia occurs
T1DM patient presentation
- hyperglycemia
- fatigue
- weight loss
- polyuria
- blurred vision
- intravascular volume depletion
T1DM diagnosis
BG >200
HgA1C > 7
what form of DM is DKA most associated with?
T1DM
T2DM
- insulin resistance and beta cell insufficiency
- insulin resistance leads to circulating free fatty acids, cytokines, insulin antagonist and target tissue defects at insulin receptors
- impaired glucose associated with increase in body weight, decrease in insulin secretion sand reduction in peripheral insulin action
- increased insulin levels = densitization of target tissue, causing decreased response to insulin
Symptoms of T2DM
- polyuria
- polydipsia
- weight loss
- fasting glucose >126
- 2 hour plasma glucose level >200 during oral glucose test
what are factors that can lead to insulin resistance?
- abd obesity
- excess calorie consumption
- lack of exercise
- genetic susceptibility
what are reasons preop hyperglycemia is undesirable?
- dehydration occurs due to osmotic diuretic effect of glucose
- accumulation of lactate
- impaired immune response which increases incidence of post-op infections
- exacerbation of brain, CV, and renal ischemic changes
systemic effects of hyperglycemia
- risk of heart disease
- fatigue and lack of energy
- pancreas malfunction
- risk of infection
- high blood pressure
- gastroparesis
- risk of cataracts and glaucoma
three life threatening complications of DM
- DKA
- HHS
- hypoglycemia
DKA
- most common cause is infection
- decreased insulin leads to catabolism of free fatty acids into ketones which results in DKA
DKA treatment
- correction of hypovolemia, hyperglycemia, and total body potassium deficit
- close anion gap!!
- when glucose moves into the cell, so does potassium so you MUST monitor labs frequently
hypoglycemia
- brain depends on glucose as source of energy, which makes it very susceptible to hypoglycemia
- if not treated, mental status change, anxiety, lightheaded and coma may occur
systemic manifestations of hypoglycemia
- diaphoresis
- tachycardia
- nervousness
metabolic syndrome
- have clinical characteristics that are frequently seen in patients that are at risk for T2DM
- combo of insulin resistance with hypertension, hyperlipidemia, procoagulant state, and obesity
clinical manifestations associated with metabolic syndrome
- visceral obesity
- insulin resistance
- high triglycerides
- HTN
- low HDL cholesterol
in order to have metabolic syndrome you need to have at least three of the following…
- fasting glucose >110
- abdominal waist >40 inches (men) and > 35 in (women)
- triglyceride level > 150
- HDL < 40 (men) and < 50 (women)
- blood pressure > 130/85
hyperosmolar hyperglycemic state (HHS)
- hyperglycemia without the presence of ketone bodies
- more common in T2DM due to the fact that insulin is present enough to prevent breakdown of fats into ketone bodies
- osmotic diuresis as well which results in extreme dehydration and altered level of consciousness
DKA vs HHS s/s
- DKA = polyuria, dyspnea, N/V
- HHS = polyuria, polydipsia, confusion, lethargy
four major classes of oral antidiabetic meds
- sulfonylureas
- biguanides (metformin)
- glitazones
- glucosidase inhibitors
sulfonylureas
- long half life, so d/c 24-48 hours before surgery
- initial treatment for T2DM
- MOA = stimulate insulin secretion from pancreatic beta cells
- second generation = glyburide and glipizide, which are more potent and have hypoglycemia as side effect
sulfonylureas harmful cardiac side effects
-may potentially inhibit myocardial protection by decreasing ATP channels in myocardium which leads to a larger myocardial infarction
Biguanides (metformin)
- decrease hepatic gluconeogenesis and enhance glucose utilization across cell membranes
- most serious SE = lactic acidosis; this can occur if too much metformin accumulates due to acute or chronic dehydration
how much insulin does an adult secrete per day
50 units
insulin
- most important anabolic hormone
- facilitates glucose and potassium into the adipose and muscle cells, therefore increasing glycogen, protein and fatty acid synthesis
- decreases glycogenolysis and gluconeogenesis, lipolysis and catabolism
intermediate acting insulin
- NPH
- lente
- lispro protamine
short acting insulin
regular
rapid acting insulin
- lispro
- aspart
long acting insulin
- glargine (lantus)
- ultralente
anesthetic management goals for DM
- aggressive preop glucose control associated with less infection, improved wound healing and decrease in morbidity and mortality
- maintain glycemic control
- avoid further deterioration of pre-existing end organ damage
- optimize electrolyte abnormalities prior to surgery
- cervical spine mobility assessed preop
- difficult intubation in up to 30% of T1DM
insulinoma
- benign pancreatic tumors that occur in women twice as much as men
- tumor on pancreas that secretes LOTS of insulin
- diagnosis made by whipple’s triad
whipple’s triad
- hypoglycemia with fasting
- glucose of less than 50 with symptoms
- relief of symptoms with glucose administration
treatment insulinoma
- surgical removal is definitive treatment
- preoperatively patient is treated with diazoxide (inhibits insulin release from beta cells)
intraoperative management of insulinoma
- first hypoglycemia may occur then hyperglycemia after tumor removal
- important to monitor blood glucose levels because GA can mask s/s of hypoglycemia
S/S diabetic neuropathy
- HTN
- painless myocardial ischemia
- reduced HR to atropine or propranolol (diabetic autonomic neuropathy)
- resting tachycardia
- lack of sweating
- may limit ability of patient to compensate and predispose patient to CV instability (ex post induction hypotension and sudden cardiac death)
intraoperative blood glucose management
- goal = avoid hypoglycemia while keeping blood glucose below 180 mg/dL
- stress of surgery causes hyperglycemia through increase in counter regulatory hormones and inflammatory mediators
what is hyperglycemia in the perioperative period associated with?
- infection
- poor wound healing
- increased mortality
- worse neurologic outcomes
