Endocrine Flashcards
Diabetes Mellitus (DM)
A metabolic disease resulting from the breakdown in the ability of the body to either produce and/or utilize insulin, resulting in inappropriate hyperglycemia.
DM type 1 and DM type 2
Diabetes type 1
Previously known as insulin dependent or juvenile diabetes.
Most commonly seen in caucasians and diagnosed before age 20.
Genetic predisposition.
Virtual absence of circulating insulin.
Positive autoimmune antibodies with the presence of Human Leukocyte Antigen (HLA-DR3 or HLA-DR4) and having antibodies against Glutamic Acid Decarboxylase (GAD-65) and Islet cell antibodies (ICA)
Ketone development usually occurs, tyoically seen with type 1 and not type 2.
Believed to be the restul of an infectious or toxic environment insult to pancreatic B cells o genetically predisopsed persons.
S/S of type 1 DM
Polyuria
Polydipsia
Polyphagia
Nocturnal ensuresis
Weight loss
Weakness/fatigue
Labs/diagnostics for type 1 and type 2
Serum fasting (at least 8 hours) blood glucose of >= 126 on more than one occasion OR
Random plasma glucose >=200 with signs of hyperglycemia (polyuria, polydipsia and weightloss) OR
Plasma glucose >=200 measured 2 hours after a glucose tolerance test OR
A1C >=6.5
Type 2 DM will not have ktones in blood/urine.
Management of type 1 DM and type 2
Treatment plans for all diabetics must be highly individualized.
Analyze baseline studies: Onset of age, obesity, cardiac risk factors, presence of ketones, diagnostic markers, cholesterol/triglycerides/EKG, renal studies, baseline physical exam.
- Type 1:
Optimal insulin regimens is a basal insulin + mealtime boluses of a rapid acting or sort acting insulin.
-Basal insulin: delievered daily or twice daily of an intermediate acting (NPH) or long acting (detemir) or continuous subq insulin infusion via a pump using a rapid acting insulin preparation (lispro).
-Mealtime boluses + additional insulin used to correct additional hyperglycemia. - Type 2: Therapy should begin with weight control for obses pts, Dietary treatment with guidelines, Exercise.
-After third failure of fasting blood glucose, pt has diagnosed DM type 2.
-Starter drug is Metformin, if dose >1G then can add a GLP-1 agonist due to increased side effects (dulaglutide, semaglutide).
Somogyi Effect
Nocturnal hypoglycemia develops stimulating a surge of counter regulatory hormones (somogyi means opposite) which raises blood sugar.
Note that the pt is hypoglycemia at 0300 but rebounds with an elevated blood glucose at 0700.
Treatment: Reduce or omit the bedtime dose of insulin.
Dawn Phenomenon
Results when tissues become desensitized to insulin nocturnally.
Note that the blood glucose becomes progressively elevated throughout the night, resulting in elevated glucose levels at 0700.
“The dawn is rising”
Treatment: Add or increase the bedtime dose of insulin
Diabetes Type 2
Previously known as non-IDDM or adult onset DM.
Most common DM in U.S.
Usually seen in adults >45
* Circulating insulin exists enough to prevent ketoacidosis but is inadequate to meet the pts insulin needs.
* Caused by either tissue insensitivity to insulin or an insulin secretory defect resulting in resistance and/or impaired insulin production.
Not linked to antigen/antibodies.
Associated with metabolic syndrome, previously known as Syndrome X.
Metabolic syndrome
These are characteristics that set someone up for sudden cardioembolic death namely stroke and MI.
Also sets someone up for having DM.
1.) Waist circumference: >= 40 inches in men and >=35 inches in woman.
2.) BP>=130/85
3.) Triglycerides >=150
4.) FBG >=100
5.) HDL <40 in men and <50 in women
Needs 3 to diagnose metabolic syndrome.
1.) Liklely to be diabetic if you have 3 of these
2.) Risk of sudden cardioembolic death is increased.
S/S of DM type 2
Insidious onset of hyperglycemia, pt may be asymptomatic.
Polyuria
Polydipsia
Overweight
Reccurent vaginitis is often the first symptom in women
Peripheral neuopathies
Blurred vision
Chronic skin infections, including pruritis.
Types of insulin
- Rapid acting:
-Lispro, aspart
-Onset ~15 minutes
-Peaks ~90 minutes
-Duration ~3 hrs - Short acting:
-Regular, humulin
-Onset ~ 30 minutes
-Peaks ~ 2 hours
-Duration ~ 8 hours - Intermediate acting:
-NPH
-Onset ~ 2 hrs
-Peaks ~ 6 hrs
-Duration ~ 24 hrs - Long acting:
-Detemir, glargine
-Onset ~ 1 hr
-Peaks ~ no peak
-Duration ~ 24 hrs
Metformin
Biguanide
The drug of choice as a starter dug for most pts with DM type 2.
Lowers basal and postprandial glucose levels by affecting glucose absorption and hepatic gluconeogenesis.
May cause some weight loss and reduces LDLs, may cause lactic acisosis (caution against excessive alcohol ingestion).
D/C 1-2 days before recieving contrast.
Black box warning of lactic acidosis.
GLP-1 agonist
Dulaglutide, semaglutide (dosed once weekly, most popular)
Mimics endogenous incretin glucagon like peptide (GLP-1); stimulates glucose dependent insulin release, reduce glucoagon, and slow gastric emptying.
Used with metformin or sulfonylurea may cause modest weight loss.
Black box warning of thyroid cancer
RIsk evaluation and mitigation strateies program (REMS): pancreatitis.
Diabetic Ketoacidosis (DKA)
A state of intracellular dehydration as a result of elevated blood glucose levels.
Often is an acute complication of type 1 DM, although type 2 DM pts can get this if they’ve lost >90% of B cell function.
Hyperglycemia increases serum osmolality causing a shift of intracellular water into the intravascular space.
Characterized by hyperglycemia, hyperkalemia and low pH.
S/S of DKA
Polyuria including nocturia, polydipsia, weakness/fatigue, N/V, Kussmauls breathing, altered LOC, fruity breath, orthostatic hypotension with tachycardia, poor skin turgor, hypothermia unless infection is present.
Lab/diagnostics of DKA
Hyperglycemia (>250)
Ketonemia/ketouria
Markered glycosuria
Acidosis
Low HCO3 (22-32)
Low serum CO2 (40-50)
Elevated hct/BUN/Cr
Hyperkalemia
Leukocytosis
Hyperosmolality (275-295, or 2x sodium)
Increased anion gap (7-17)
Serum osmolality equation
2[Na+K]+glucose/18
Management of DKA
Protect the airway, administer O2
Isotonic fluids at least 1L in first hour then 500ml/hr after.
If glucose >500 then use 1/2NS after first hour for intracellular hydration.
When glucose falls >250 change to D51/2NS to prevent hypoglycemia.
Insulin bolus of 0.1u/kg then drip of 0.1u/kg/hr (IV). If glucose does not fall by 10% after first hour then repeat bolus.
If pH<7.1 then correct severe acidosis with bicarb drip.
Do not treat hyperkalemia
Hyperosmolar Hyperglycemic State (HHS)
State of greatly elevated serum glucose, hyperosmolality and severe intracellular dehydration without ketone production.
Usually occurs as a complication of DM type 2
Patients cannot produce enough insulin to prevent severe hyperglycemia, osmotic diuresis and extracellular fluid depletion.
S/S of HHS
Polyuria
Weakness
Changes in LOC (may be most obvious presenting sign)
Hypotension
Tachycardia
Poor skin turgor
Labs/diagnostics of HHS
Greatly elevated serum glucose >600-1000)
Hyperosmolality (275-295 or 2x sodium)
Elevated BUN and Cr
Elevated A1C
Releatively normal pH and HCO2 (22-32)
Normal Anion gap (7-17)
Management of HHS
Almost identical to DKA
Manage airway
Administer O2
Isotonic fluids, atleast 1L in the first hour then 500mL after.
If glucose >500 use 1/2NS after first hour for intracellular hydration.
When glucose <250 switch to D51/2NS
Insulin bolus of 0.1u/kg then drip of 0.1u/kg/hr and reapeat bolus if glucose does not fall by 10% after first hour.
These pts will come off the insulin drip faster due to being able to make insulin.
Hyperthyroidism
A condition of excess secretion of T4 and T3 resulting from a variety of clinical disorders.
Most common in women
Graves disease is the most common presentation.
Other causes include toxic adenoma, subacute thyroiditis, TSH secreting tumor of the pituitary, and high dose amiodarone.
S/S of hyperthyroidism
The thyroid gland is the bodys major metabolic gland.
Overdrive, everything is hyper:
Nervousness, anxiety, increased sweating, fine tremors, hyperreflexia of DTRs, increased appetite but weightloss, exophthalmos, increased incidence of afib.
Lab/diagnostics of hyperthyroidism
TSH is the most sensitive test and is low in most cases.
Increase T3 (80-230), T4 and thyroid resin uptake.
Serum ANA is usually elevated without evidence of lupus or other collagen diseases.
Thyroid radioactive iodine uptake and scan usually performed to establish etiology of hyperthyroidism.
-A high iodine uptake=graves disease
-A low iodine uptake=subacute thyroiditis.
MRI of the orbits is the preffered choice for visualized graves ophthalmopathy.
Management of hyperthyroidism
Specialist referral.
Propanolol gives symptomatic relief of hypermetabolism such as palpitations/shakes. 10mg PO, up to 80mg QID.
Thiourea drugs (antithyroid meds) are used for milk cases, small goiters or fear of isotopes.
-Methimazole- 30-60mg daily
-Propylthiouracil (PTU)- 300-600mg daily
Radioactive iodine used to destroy goiters.
Thyroid surgery (pt must be euthyroid)
Lugol solution is used to reduce vasculatiry of the gland.
Pts with subacute thyroiditis are best treated syptomatically with propanolol.
Hypothyroidism
Primary disease of the thyroid gland
Pituitary deficiency of TSH
Hypothalamic deficiency of TRH
Iodine deficiency
Hashimotos disease is #1 cause
Damage to the gland
S/S of hypothyroidism
Everything is sluggish
Extreme weakness, fatigue, constipation, weight gain, dry skin, hair loss, bradycardia, slow DTRs
Lab/diagnostics
TSH elevated
T3 and T4 low
Hyponatremia
Hypoglycemia
Management of hypothyroidism
Levothyroxine
For pts youngr than 60 with no CAD:
50-100mcg daily, increased by 25mcg every 1-2 weeks until symptoms stabilize
If pt is >60 with CAD then lower the dose to 25-50mcg and increase by 25mcg ever 1-2 weeks until symptoms stabilize
TSH rechecked every 8 weeks after dose adjustment
Take medication 30-60 minutes before breakfast or at bedtime 4 hours after last meal.
Thyroid crisis
A deadly, hypermetobolic state casued by inadequatly controlled hyperthyroidism.
Can be caused by undiagnosed hyperthyroidism, trauma, stress, infection, thyroid drug OD, uncontrolled DM
4 drug classes:
- Meds that inhibit synthesis of thyroid hormone:
Methimazole and propylthiouracil - Meds that inhibit the release of thyroid hormone:
-Lugols solution and iodide - Meds that block the effect of thyroid hormone:
Propanolol - Meds that prevent the conversion T4 and T3
Hydrocortisone
Avoid ASA, can exacerbate thyroid storm.
Myxedema coma
A rare condition of greatly decreased metablism resulting from a deficiency of circulating thyroid hormone.
Protect airway, as oxygenation and mechanical ventilation is almost always needed.
IV thyroid replacement 400mcg IV once then 100mcg qday.
Support hypotension
Slow rewarming with blankets, not hyperthermia blankets due to rapid vasodilation may lead to circulatory collapse.
Cushings syndrome
Too much steroid
Elevated cortisol levels inhibit the protein synthesis and uptake of glucose into cells.
Adrenocorticotropic hormone hypersecretion by the pituitary
Caused by adreanal tumors, pituitary tumors, and/or chronic administration of glucocorticoids.
S/S of cushings syndrome
- Central obesity (due to increased steroids causing fat mobilization to abdomen)
- Moonface with buffalo hump
- Ane
- Poor wound healing
- Purple striae
- Hirsutism (increased hody hair)
- Hypertension (increased steroids can cause vasoconstriction)
- Weakness
- Amenorrhea
- Impotence
- HA
- Polyuria and polydipsia (mimicks DM due to increased steroids inhibit glucose uptake into cells)
- Labile mood
- Prequent infections (due to increased glucose)
Lab/diagnostics of cushings syndrome
Triad to help differentiate between addisons (opposite for addisons)
* Hyperglycemia
* Hypernatremia
* Hypokalemia
Glycosuria
Leukocytosis
Increased ACTH
Dexamethasone suppresion test to differentiate cause
Elevated plasma cortisol in AM
Management of Cushings
Depends on the cause
-D/C meds inducing symptoms
-Transsphenoidal resection of a pituitary tumor
-Surgical removal of adrenal tumors
-Resection of ACTH secreting tumors
Manage electrolyte imbalances.
At risk for PE d/t hypercoagulable state.
Addisons disease
Not enough steroids
A condition characterize by a deficiency of cortisol, androgens, and aldosterone as a result of of destruction of the adrenal cortices.
Can be caused by:
* Autoimmune destruction of adrenal gland
* Bilateral adrenal hemorrhage (due to anticoagulation therapy, trauma, surgery)
* Metastatic cancer
* Pituitary failure resulting in decreased ACTH
* Infection of adrenal gland
S/S of Addisons disease
- Hyperpigmentation in buccal mucosa and skin creases especially knuckles, nail beds, nipples, palmar creases and posterior neck (signs of deresed cortisol).
- Diffuse tanning and freckles
- Orthostasis and hypotension
- Scan axillary and pubic hair
Acute changes: - Rapid worsening of chronic S/S
- Changes in LOC
- Fever
Lab/diagnostics of Addisons
Triad to help differentiate between Cushings (opposite)
* Hypoglycemia
* Hyponatremia
* Hyperkalemia
Elevated ESR
Lymphocytosis
Plasma cortisol <5 @ 0800
Metabolic acidosis
Cosyntropin stimulation test to r/o Addisons disease
Management of Addisons disease
Consult with specialist
- Outpatient management:
-Glucocorticoid and mineralcorticoid reaplcement with hydrocortisone (replaces glucocorticoids) and aludrocortisone acetate (replaces mineralcorticoids) - Inpatient management:
-Obtain cortisol level and initiate IV hydrocortisone 100-300mg with NS
-Replace volume with D5NS at 500ml/hr x4 hrs and then taper per condition
-Vaso pressors are usually ineffective.
-Treat underlying cause which is usually sepsis.
Syndrome of Innappropriate Antiduiretic hormone (SIADH)
A grouping of symptoms caused by increased antidiuretic hormone (ADH).
Causes inappropriate water retention despite low serum osmolality.
Occurs independently of osmolality or volume dependent stimulation.
ADH is made in hypothalamus and released by posterior pituitary gland or malignant tumors.
Can also be caused by skull fractures/head trauma, CNS disorders, and chronic lung disease.
S/S of SIADH
Neurologic changes from hypnatremia such as mild HA, seizures, coma.
Decreased DTR
Hypothermia-cold intolerance
Weight gain/edema
N/V
Concentrated urine
Decrease UO
Lab/diagnostics of SIADH
Hyponatremia (<135) yet euvolemic
Decreased urine osmolality <280
Increased urine osmolality >100
Urine sodium >20
Increase urine specific gravity >1.030
Management of SIADH
Treat underlying cause and manage hyponatremia.
If Na+ >120, restrict total fluid to 1000ml/24 hours
If Na+ 110-120 w/o neuro symptoms, restrict fluids to 500ml/24hours
If Na+ <110 or neuro symtpoms present, replace with isotonic or hypertonic fluids and lasix to have Na+ increase by 1-2meq/hr
Diabetes insipidus
Excessive urination and extreme thirst from an inadequate output of the pituitary hormone ADH or the lack of the normal response by the kidney to ADH.
Three types:
* Central: caused by a deficiency of ADH production or release. Affects the synthesis or secretion of vasopessin.
-Idiopathic, damage to hypothalamus or pituitary, surgical damage, trauma, infections, metastatic cacinoma.
* Nephrogenic-Renal insensitivity to ADH, thereby interfering with water reabsorption. Unresponsive to vasopressin.
-Familiar x-linked trait
-Acquired due to pyelonephritis, K+ depletion, sickle cell anemia, chronic hypercalcemia, medications (lithium, methacillin)
* Psychogenic-refer out.
S/S of DI
Anything consistent with being dry or losing fluids.
Thirst/craving for water and drinking up to 20L/day
Polyuria and nocturia up to 20L/day
Weight loss/fatigue
Changes in LOC
Dizziness
Elevated temp
Tachycardia
Hypotension
Poor turgor and dry mucus membranes
Labs/diagnostics of DI
Hypernatremia
Elevated BUN/creatinine (due to being dry) (BUN 10-20) (Cr .5-1.5)
Serum osmo <290
Urine osmo <100
Urine SG <1.005
Hypokalemia
Hyercalcemia
Test for DI is the vasopressin (or desmopressin) challenge test. If the test is positive it’s central DI if it’s negative its Nephrogenic DI.
If no apparent case then do MRI to look for mass/lesions.
Management of DI
If Na>150, give D5W IV to replace 1/2 volume deficit in 12-24 hours.
More rapid lowering of Na+ can cause cerebral edema, do not exceed 10-15meq/day of lowering)
When Na<150, switch to 1/2 NS or NS
Can use DDAVP 1-4mcg IV or SQ for acute situation
Can go home on intranasal DDAVP
Pheochromocytoma
A rare but serious disease resulting from excess catecholamines (epi and norepi) release, characterized by paroxysmal (sudden start and sudden stop) or sustained HTN; almost always due to a tumor of the adrenal medulla.
S/S of pheochromocytoma
Looks alot like hyperthyroid, but labile BP and postural hypotension tells you its not.
Labile HTN
Diaphoresis
Hyperglycemia
Severe HA
Palpitations
Profuse sweating
Tremor
Tachycardia
Weight loss
Postural hypotension
Labs/diagnostics of pheochromocytoma
1- TSH
#2- Plasma free-metanephrines
#2- 24hours urine (if you have the time) of (1) urine catecholamines (total and fractionated), (2) Metanephrines, (3) vanillylmandelic acid (VMA) and (4) creatitine.
Confirmatory, not inital test, is a CT to confirm and localize tumor.
Management of pheochromocytoma
Surgical removal of tumor is treatment of choice
Although, treat BP prior to surgery with alpha adrenergic medications:
-Phentolamine IV then switch to Oehnoxybenzamine PO ASAP
Post operatively watch for hypotension, adrenal insufficiency and hemorrhage.
