Endocrine Disease Flashcards
What Receptor types Bind to Endocrine Hormones?
Endocrine hormones act as a first messenger that binds to a receptor & tell a specific cell type to carry out a function.
Receptors can either directly influence gene expression and thus cell activity, or induce a secondary signaling cascade that will in turn influence cell activity.
Ion Channels
G-Proteins (cAMP 2nd messenger)
Enzymes
Gene Activation
Identify Pancreatic Cells function/secretion
Hint, Mnemonics for Pancreas
“P I G S” PANCREAS, INSULIN (Β CELL). GLUCAGON (Α CELL). SOMATOSTATIN (ẟ CELL).
Regulation of Hormone Secretion is through:
Neural Controls: ↑ or ↓ hormone secretion.
Pain, emotion, smell, touch, injury, stress, sight, and taste alter hormone release through CNS.
Biorhythms: Genetically encoded or acquired.
circadian (daily variability in sleep, glucocorticoid secretion), weekly/monthly (menstrual cycle), or seasonal (thyroxine production).
Feedback Mechanisms: Hormonal response is controlled (many endocrine disorders arise from the breakdown of feedback loops).
Negative Feedback Loop: Acts to limit or terminate the production & secretion of a hormone once the appropriate response has occurred. This prevents hormone excess & when hormone is low, feedback inhibition is ↓ and hormone secretion enhanced.
What is Metabolic Syndrome?
A Cluster of conditions which pose ↑ Risk of
CV Disease & Type II DM
Diagnostic Features:
At least three of the following:
Fasting plasma glucose level ≥ 110 mg/dL
Abdominal obesity (waist girth > 40 inches in men, >35 inches in women)
Serum triglyceride level ≥ 150 mg/dL
Serum high-density lipoprotein cholesterol level < 40 mg/dL in men, <50 mg/dL in women
Blood pressure ≥ 130/85 mm Hg
Identify Symptoms of Type I Diabetes.
Polyuria Polydispsia Polyphagia Weight Loss Fatigue Increase frequency of infections Rapid onset Insulin Dependent Familial Tendency Peak incidence from 10-15 years
Conditions associated with Diabetes Mellitis: Type II
Have peripheral insulin resistance
Not susceptible to ketoacidosis in the absence of insulin
Type II diabetics tend to be:
Overweight, resistant to ketoacidosis
Middle to older age group
Can develop hyperglycemic-hyperosmolar nonketotic state
Impaired glucose tolerance is associated with an increase in body weight, a decrease in insulin secretion, and a reduction in peripheral insulin action.
Elevated insulin can also hasten development of CV disease
Diabetes Treatment
Diet: ADA maintenance of optimal plasma glucose and lipid levels
Exercise
Weight Loss (improves hepatic & peripheral tissue insulin sensitivity, enhances postreceptor insulin action and may possibly ↑ insulin secretion.
Oral Agents: 4 types
Insulin
Describe 4 types of Glucose Lowering Oral Agents for Diabetes.
(1) the secretagogues (sulfonylureas, meglitinides), which increase insulin availability
(2) the biguanides (metformin), which suppress excessive hepatic glucose release
(3) the thiazolidinediones or glitazones (rosiglitazone, pioglitazone), which improve insulin sensitivity
(4) the α-glucosidase inhibitors (acarbose, miglitol), which delay GI glucose absorption
Describe Reasons for Potential Difficult Intubation for patients with Diabetes.
Stiff Joint Syndrome in Type I DM
This buildup in proteins is responsible for the stiff joint syndrome (and difficult intubation due to a fixed atlanto-occipital joint) as well as decrease wound healing.
Effects Atlantoociciptal, temporomandibular & other c-spine
↑(Hb)A1C & Morbid Obesity
Diabetic Ketoacidosis (DKA)
(DKA) is a complication of decompensated diabetes mellitus.
Signs & symptoms are primarily the result of abnormalities in carbohydrate and fat metabolism.
Episodes of DKA occur more commonly in patients with type 1 diabetes and are precipitated by infection or acute illness.
High glucose levels exceed the threshold for renal tubular absorption, which creates a significant osmotic diuresis with marked hypovolemia.
A tight metabolic coupling between hepatic gluconeogenesis and ketogenesis leads to overproduction of ketoacids by the liver.
An increase in production of ketoacids (β-hydroxybutyrate, acetoacetate, acetone) creates an anion-gap metabolic
Substantial deficits of water, potassium, and phosphorus exist, although laboratory values of these electrolytes may be normal or increased.
Hyponatremia results from the effect of hyperglycemia and hyperosmolarity on water distribution.
The deficit of potassium is usually substantial (3–5 mEq/kg), and the deficit of phosphorus can lead to diaphragmatic and skeletal muscle dysfunction and impaired myocardial contractility
What is the Treatment for DKA?
Treatment of DKA consists of administration of large amounts of normal saline, effective doses of insulin, and electrolyte supplementation.
An IV loading dose of 0.1 unit/kg of regular insulin plus a low-dose insulin infusion of 0.1 unit/kg/h is initiated.
Insulin administration must be continued until a normal acid-base status is achieved.
The insulin rate is reduced when hyperglycemia is controlled, blood pH is higher than 7.3, and bicarbonate level exceeds 18 mEq/L.
Potassium and phosphate are replaced with KCl and K2PO4.
Magnesium is replaced as needed.
Sodium bicarbonate is administered if blood pH is less than 7.1.
The infrequent but devastating development of cerebral edema can result from correction of hyperglycemia without simultaneous correction of serum sodium level.
What is Hyperglycemic Hyperosmolar Syndrome (HHS)?
Characterized by severe hyperglycemia, hyperosmolarity, and dehydration.
Usually occurs w acute illness in patients with type 2 diabetes who are older than 60 y.o.
Lasting days to weeks, with a persistent glycosuric diuresis.
The patient experiences polyuria, polydipsia, hypovolemia, hypotension, tachycardia, and organ hypoperfusion.
Hyperosmolarity (>340 mOsm/L) is responsible for mental obtundation or coma.
Patients may have some degree of metabolic acidosis but do not demonstrate ketoacidosis.
Describe Hyperglycemic Hyperosmolar Syndrome (HHS) Treatment.
Treatment includes significant fluid resuscitation, insulin administration, and electrolyte supplementation.
If plasma osmolarity is greater than 320 mOsm/L, large volumes of hypotonic saline (1000–1500 mL/h) should be administered until the osmolarity is less than 320 mOsm/L, at which time large volumes of isotonic saline (1000–1500 mL/h) can be given.
Insulin therapy is initiated with an IV bolus of 15 units of regular insulin followed by a 0.1-unit/kg/h infusion. The insulin infusion is decreased to 2–3 units/h when the glucose level decreases to approximately 250–300 mg/dL. Electrolyte deficits are significant but usually less severe than in DKA.
Describe the Diabetes Complication of Microvascular Dysfunction.
Microvascular Complications Microvascular dysfunction is unique to diabetes and characterized by nonocclusive microcirculatory disease and impaired autoregulation of blood flow and vascular tone. Chronic hyperglycemia is essential for development of these changes, and intensive glycemic control delays the onset and slows the progression of microvascular effects.
Diabetes and Peripheral Neuopathy
> 50% of patients who have had diabetes for longer than 25 years develop a peripheral neuropathy.
Sensory deficits usually overshadow motor abnormalities and appear in the toes or feet and progress proximally toward the chest in a “stocking-glove” distribution.
Loss of large sensory and motor fibers produces loss of light touch and proprioception as well as muscle weakness.
Loss of small fibers decreases the perception of pain and temperature and produces dysesthesia, paresthesia, and neuropathic pain.
Foot ulcers develop from mechanical and traumatic injury as a result of loss of cutaneous sensitivity to pain and temperature and impaired perfusion.
Significant morbidity results from recurrent infection, foot fractures (Charcot joint), and subsequent amputations. Treatment of peripheral neuropathy includes optimal glucose control as well as use of nonsteroidal antiinflammatory drugs, antidepressants, and anticonvulsants for pain control.
What is Diabetic Retinopathy?
Diabetic retinopathy results from a variety of microvascular changes.
Visual impairment can range from minor changes in color vision to total blindness.
Strict glycemic control and blood pressure control can reduce the risk of development and progression of retinopathy.
Identify Major Risk Factors For Diabetic Patients Undergoing Surgery
Cardiovascular dysfunction
Renal insufficiency
Joint collagen tissue abnormalities (limited neck ROM)
Poor wound healing
Inadequate granulocyte production
Neuropathies
Elevate A1c is an independent predictor of poor perio-perative outcomes
Intra-operative Management for Patients with Diabetes
Intraoperative serum glucose 120-180mg/dL (Range Varies Slightly)
When levels go beyond 200mg/dL you might want to think of beginning a regular insulin infusion
BS should be checked every hour when an insulin infusion is running
We need to be on top of electrolyte abnormalities every 1-2 hours depending on lab values
Potassium loss needs to be aggressively treated.
Infusions 20meq/hour- run through a peripheral line
Describe Pheochromocytoma
catecholamine-secreting tumors that arise from chromaffin cells of the sympathoadrenal system
Pheo < 0.1% of all HTN cases, detection is imperitive since it’s highly lethal & curable
Pheochromocytomas are usually an isolated finding (90% of cases); 10% are inherited
Both sexes are equally affected, & peak incidence is in the third to fifth decades of life
Eighty percent of pheochromocytomas are located in the adrenal medulla
Following resection of benign tumors, 5%–10% of patients have a benign recurrence.
Most pheochromocytomas secrete norepinephrine, either alone or, more commonly, in combination with a smaller amount of epinephrine in a ratio of 85:15—the inverse of the secretion ratio in the normal adrenal gland. Approximately 15% of tumors secrete predominantly epinephrine.
What is the Pre-Operative Patient preparation for Pheochromocytoma Patients?
α-blockade to lower blood pressure, increase intravascular volume, prevent paroxysmal hypertensive episodes, allow resensitization of adrenergic receptors, and decrease myocardial dysfunction.
Phenoxybenzamine is the most frequently prescribed α-blocker for preoperative use. It is a noncompetitive α1-antagonist with some α2-blocking properties.
The goal of therapy is normotension, resolution of symptoms, elimination of ST-segment and T-wave changes on the ECG, and elimination of dysrhythmias.
optimal duration of α-blockade therapy is undetermined and may range from 3 days to 2 weeks or longer
discontinue its use 24–48 hours before surgery to avoid vascular unresponsiveness immediately following removal of the tumor
Prazosin and doxazosin, pure α1-competitive blockers, are alternatives to phenoxybenzamine. They are shorter acting, cause less tachycardia, and are easier to titrate to a desired end point than phenoxybenzamine.
