Week 2 Flashcards
Cushing’s Disease. What is it?
overproduction of cortisol, pituary caused symptoms.
Cushing’s disease causes
long term use of glucocorticoid medications, steroids at high doses, Endogenous causes (excess adrenocorticotropic hormoneACTH from pituitary tumors or adrenal gland hyperproduction)
Cushing’s disease patho
hypothalamus regulates ACTH, which in turn regulates the production of glucocorticoids (cortisol).
cortisol responds to physical and psychological stressors.
clinical presentation of cushing’s disease
almost almost manifests with chronic changes ie rapid weight gain, loss of menses, decreased libido, weakness, bruising.
may have: HTN, glucose intolerance, insomnia.
memory disturbances, depression.
pediatric presentation for cushings
Most common causes are weight gain and depressed linear growth (height)
physical exam for cushings
pt will have central obesity, moon face, buffalo hump, htn, muscle weakness/wasting, hirsutism, red/purple abdominal straiae, acne, depression
diagnostics of cushings
24 hour urine (for urine cortisol level >100mcg would indicate cushings),
serum cortisol at midnight ( if level is above 7.5, it indicates cushing’s),
creatinine,
ACTH suppression test (endocrine specialist does)
management of cushings
consult with endocrine specialist.
depends on the source of hypercortisolism. the goal is to mitigate impact of cortisol
daily ketoconazole administration.
bone density measurement if on longterm corticosteroids due to risk for osteoporosis.
alternative therapies: to improve energy and increase physiological health: use licorice(suppressess fight of flight), st johns wort, ginseng, fish oils,sea salt
if there is a pituitary tumor- resection of tumor, chemo, radiation
complications of cushing’s disease
carefully monitor complications of longterm steroid use, osteoporosis is a common complication, along with infection, htn, diabetes.
referral/hospitalizations of cushing’s
if pt is in hypertensive crisis
surgical intervention of pheochromocytoma
consult to endocrine if diagnostic test suspects addison’s or cushing’s disease
pt education and health promotion of cushing’s
educate about complications chronic steroid use, doubling hydrocortisone dose is required with fever and common illnesses, alert medical personal if there is surgery, trauma, infection. Wear medical alert bracelet and have emergency med kit for extraparenteral steroids
type 2 diabetes diagnosis
fasting blood glucose > 126 on two separate occasions. do note need a1C to diagnose, however you can get it to establish baseline
DM diagnostic criteria
- random plasma glucose >200 and symptoms of diabetes (polyuria, polydipsia, DKA, unexplained weight loss)
OR - hgba1c >6.5
OR - fasting plasma glucose >126
- results of 2 hour 75 gram OGTT >200 @ 2 hrs
should be repeated on different day unless undeniably high
glycemic control algorithm
individualized goals of a1c < 6.5% for those without serious illness and at low hypoglycemic risk OR
hgb a1c >6.5% with concurrent serous illness and at risk for hypoglycemia
lifestyle therapy for all.
glycemic control therapy plan for hgb <7.5
Monotherapy.
metformin,
GLP1 (-tides, oxepmic, trilicity, vietna)
SGLT2: -flozin
Empagliflozin (jardiance), canagliflozin (invokana),
Dapagliflozin (faxiga).
DPP4: sitagliptin
TZD,
AGI,
Sulfoneureas,
If they dont reach goal in 3 months, go to dual therapy
glycemic control therapy plan for hgb > or equal to 7
dual therapy
metformin +basal insulin
if you dont reach goal in three months, go to triple therapy
glycemic control therapy plan for hgb >9
do they have symptoms? no: dual therapy or triple therapy.
if they have symptoms: insulin +- other agents
if you don’t reach in 3 months, go to insulin
initiation of basal insulin
stop sulfonyureas before starting insulin.
start insulin at dose of 0.1-0.2 units per kg for hgb a1c < 8
0.2-0.3 units per kg for hgb a1c > 8
increase by 2 units or 10 % every 2-3 days until glucose goal met
report all BG < 70
screening for renal nephropathy in type 2 diabetes
most appropriate time is at diagnosis.
done by random urine collection
normal urine albumin to creatinine ratio is <30mg/g
hirsutism
can be a result of cortisol excess
if cushing is suspected, perform salivary cortisol level and 24 hr urine for free cortisol or low dose overnight dexamethasone suppression test.
also perform fasting insulin, OGTT, and lipid profile
thyroid hormone excess
check TSH
causes of hirsutism
PCOS, adrenal hyperplasia, ovarian tumors, cushing syndrome, acromegaly,
hyperparathyroidism. What is it?
Oversecretion of PTH
Calcium absorption helps body decrease phosphorus levels
Causes of hyperparathyroidism
can be genetic endocrine disorders, familial hypocalciuric hypercalcemia, lithium related, radiation induced, carcinoma, thiazide related.
primary hyperparathyroidism PHPT
is caused by parathyroid adenoma
secondary hyperparathyroidism
is caused by renal failure (GFR < 50) or vitamin D deficiency (vit d level falls below 20).
In RF, decreased calcium causes PTH production.
Vitamin d deficiency causes decrease in calcium absorption.
tertiary hyperparathyroidism
prolonged secondary stage. hypercalcemia is a result
treatment for PHPT
close monitoring of calcium, creatinine, vitamin D, bisphosphonates, hormone replacement with estrogen, raloxifene (in patients with osteoporosis), cinicalet (cinimimetic agent that normalizes PTH and calcium ). ADEQUATE CALCIUM AND FLUID INTAKE.
treatment for secondary HPT
kidney transplantation, calcitriol, vitamin D, can also have parathyroidectomy
complications of HPT
Osteoporosis Nephrolithiasis Mortality Bone abnormalities Vascular complications Coronary valve disorders
diagnostic test for hyperparathyroidism
Intact PTH (Stop biotin 7 days before testing)
Serum calcium
Albumin
Vitamin d hydroxy
phosphorus
Bone mineral density assessment- of distal radius
24 hr urine
ECG - hypercalcemia can cause shortened QT interval
Renal ultrasound to rule out stones
Magnesium level- for hypothyroidism only
screening for diabetes
TheA1c, FPG, or the 2-hour 75-gram anhydrous OGTT are all equally appropriate diabetes screening testsby the ADA, according to the revised Standards of Care (no one test is preferred.) The ADA notes that the A1cmay have some advantages over the other tests (eg, convenience and less day-to-day variation, etc), but these must be balanced by the costs and availability of A1ctesting and by the lower sensitivity of this test.
testing for prediabetes in asymptomatic adults
Current recommendations are to test all adults beginning at age 45 years, regardless of their weight. Testing is also recommended for adults of any age who are overweight (BMI greater than or equal to 25 kg/m2[and greater than or equal to 23 kg/m2in Asian-Americans*]) and have additional risk factors2:
Members of a high-risk ethnic population (eg, African America, Hispanic/Latino, American Indian, Alaska Native, Asian American, and Pacific Islander), First-degree relative with diabetes, History of gestational diabetes or giving birth to a baby weighing > 9 lbs, Physical inactivity, Hypertension (BP ≥ 140/90 mm Hg) or on therapy for hypertension, HDL cholesterol < 35 mg/dL (0.90 mmol/L), Fasting triglycerides (TG) > 250 mg/dL (2.82 mmol/L), Women with polycystic ovarian syndrome (PCOS)
Previously noted A1cgreater than or equal to 5.7%, impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) on previous testing
Other clinical conditions associated withinsulinresistance (e.g., acanthosis nigricans, non-alcoholic steatohepatitis, polycystic ovary syndrome [PCOS], and small-for-gestational age birth weight1)
History of cardiovascular disease (CVD)
Treatment with atypical antipsychotics or glucocorticoids
Without the above criteria, testing for prediabetes and diabetes should begin at age 45 years.
If results are normal, the ADA notes that it is “reasonable” to test again at 3-year intervals, and consider more frequent testing depending on initial results and risk status.
reommended critria for testing for prediabetes or diabetes in asymptomatic children per ADA
The 2020 ADA guidelines recommend screening for type 2 diabetes or prediabetes in children and adolescents who meet the following criteria:
Overweight (BMI greater than the 85thpercentile for age and sex, weight for height greater than 85thpercentile, or weight greater than 120% of ideal for height)
AND who meet one or more of the following criteria
Maternal history of gestational diabetes mellitus (GDM) during the patient’s gestation.
Family history of type 2 diabetes in first- or second-degree relatives
High-risk race/ethnicity (same groups as for the adults, e.g., Native American, African America, Latino, American, Asian American, and Pacific Islander)
Signs ofinsulinresistance or conditions associated withinsulinresistance (eg, acanthosis nigricans, hypertension, dyslipidemia, PCOS, or small-for-gestational-age birth weight)
classifications of diabetes
- Type 1 diabetes (Note: The correct nomenclature is “type 1” not “type I” diabetes)
Immune-mediated diabetes with evidence of autoimmune β-cell destruction, typically leading to absoluteinsulindeficiency. N.B: There is some controversy over whether or not latent autoimmune diabetes of adults (LADA) warrants its own designation; in the current ADA, this condition is considered a slow-onset type 1 diabetes mellitus.7
Idiopathic type 1 diabetes – unclear etiology; these individuals are insulinopenic and prone to DKA, but lack evidence of β-cell autoimmunity. - Type 2 diabetes(Note: The correct nomenclature is “type 2” not “type II” diabetes)
Typically a multifactorial process, including relativeinsulininsufficiency (the pancreas does release enoughinsulin),insulinresistance, and often unregulated gluconeogenesis in the liver (producing glucose in the face of hyperglycemia) - Gestational diabetes mellitus (GDM)
Diabetes diagnosed during the second or third trimester of pregnancy that was not clearly present prior to gestation - Other specific types of diabetes
Monogenic diabetes syndromes (e.g., neonatal diabetes and maturity-onset diabetes of the young [MODY])
Diseases of the exocrine pancreas (e.g., cystic fibrosis)
Pancreatic insufficiency secondary to chronic/recurrent pancreatitis
Drug/chemical induced (e.g., as occurs in patients treated with glucocorticoids and those treated for HIV/AIDS or after organ transplantation)
Autoimmune disease to screen for when a pt diagnosed with typde 1 diabetes
The ADA recommends that physiciansconsiderscreening for thyroid disease and celiac disease soon after the type 1 diabetes diagnosis.
Specific autoimmune diseases that have been reported in patients with type 1 diabetes include: Hashimoto thyroiditis, Graves disease, Addison disease, autoimmune hepatitis, dermatomyositis, myasthenia gravis, vitiligo, and pernicious anemia.
ABCs for diabetes preventative care
A- a1c, aspirin or antioplatelet agents
a1c: Every 6 months in patients who are meeting treatment goals of stable glycemic control
Every 3 months in patients who are not at goal or whose therapies are changing
B- blood pressure, goal of < 140/90
C- cholesterol at diagnosis and q 5 years in pts < 40
s- screening for neuropathy, retinopathy and nephropathy, immunizations, tobacco cessation
children with type 1 diabetes screening:
celiac and hypothyroid disorders
diabetes meds weight neutral/weight loss
Biguanides– metformin (Glucophage and others)
Glucagon-like peptide-1 (GLP-1) receptor agonists–albiglutide(Tanzeum),dulaglutide(Trulicity), exenatide (Byetta, Bydureon), liraglutide (Victoza),lixisenatide(Lyxumia ), andsemaglutide(Ozempic)
Amylin agonist-pramlintide(Symlin)
Dipeptidyl peptidase-4 (DPP-4) inhibitors–alogliptin(Nesina),linagliptin(Tradjenta),sitagliptin(Januvia), andsaxagliptin(Onglyza)
Sodium/glucose cotransporter 2 (SGLT2) inhibitors (aka gliflozins)–canagliflozin(Invokana),dapagliflozin(Farxiga),empagliflozin(Jardiance), andertugliflozin(Steglatro)
Pramlintide(Symlin)
contraindication to metformin therapy
lactic acidosis,decompensated CHF, GFR < 30, liver failure patients, surgery, constrast dye (restart in 48 hours after dye).
Are there any drug classes for the treatment of type 2 diabetes mellitus that have been shown to reduce cardiovascular disease?
SGLT2 (Empagliflozin,Canagliflozin andDapagliflozin), cardioprotective
GLP 1 Liraglutide
Based on the AACE/ACE Algorithm, are there any recommendations of how to start insulin?
Yes. The AACE/ACE algorithm (updated yearly) recommends starting with a basalinsulin. For persons whose A1cis less than 8%, the total daily dose (TDD) recommended is 0.1 to 0.2 U/kg. For persons whose A1cis greater than 8%, the recommended TDD is 0.2 to 0.3 U/kg. It is recommended that any sulfonylurea therapy be stopped or reduced when a basalinsulinis started.Please keep in mind that treatment regimens should be individualized to each particular patient.
Metformin :is it weight neutral or weight loss?
Metformin is a biguanide and is associated with weight loss.
What types ofinsulinare available and what are the differences in onset, peak, and duration?
Rapid Acting: Onset 5 to 15 minutes, Peak 30 to 90 minutes, Duration 4 to 6 hours:
Lispro (Humalog)
Aspart (Novolog, Fiasp)
Glulisine (Apidra)
Short Acting: Onset 30 to 60 minutes, Peak 2 to 3 hours, Duration 8 to 10 hours:
Regularinsulin(Humulin R, Novolin R).
Intermediate Acting: Onset 2 to 4 hours, Peak 4 to 10 hours, Duration 12 to 18 hours:
Isophaneinsulin(neutralprotamineHagedorn [NPH], Humulin N, Novolin N).
Long Acting:
Glargine (Lantus, Basaglar, Toujeo) – Onset 2 to 4 hours, no peak, Duration 20 to 24 hours
Detemir (Levemir) – Onset 2 to 4 hours, Peak 3 to 9 hours, Duration 6 to 24 hours
Degludec (Tresiba) – Onset 1 hour, Peak 9 hours, Duration greater than 42 hours.
Premixed: Onset 30 to 60 minutes, Dual Peak, Duration 10 to 16 hours
70% NPH / 30% regularinsulin(Humulin 70/30)
What are the screening recommendations for prevention of micro- and macrovascular complications of T1DM?
NEPHROPATHY:Annual screening for albuminuria with a random spot urine sample for albumin/creatinine ratio after child is 10 years old or olderandhas had diabetes for at least 5 years. Normal spot albumin/creatinine ratio is less than or equal to 30 mg/dg.
RETINOPATHY:Annual comprehensive and dilated eye exam after age 10 and when child has had T1DM for at least 3 to 5 years.
NEUROPATHY:Annual compressive foot exam starting at age 10 or after puberty has started (whichever is earlier) after diabetes duration of 5 years.
HYPERTENSION:Cuff blood pressure at time of diagnosis and every office visit thereafter. Elevated blood pressure should be confirmed on 3 separate days.
DYSLIPIDEMIA:Fasting lipid panel starting at age 10. If low-density lipoprotein (LDL) cholesterol is less than 100 mg/dL, then repeat every 3 to 5 years. If abnormal, monitor yearly. Initial therapy should consist of optimizing glucose control and medical nutrition therapy using a Step 2 American Heart Association (AHA) diet. Statin therapy is recommended after making lifestyle changes if LDL cholesterol is greater than 160 mg/dL, or greater than 130 mg/dL with 1 or more cardiovascular risk factors. Remember that statins are contraindicated in pregnancy, so consider birth control in adolescents who require statin therapy.
THYROID DISEASE
CELIAC DISEASE
For a child diagnosed with type 1 diabetes mellitus (T1DM) at age 7, when should screening for diabetic retinopathy begin?
10 years
Thyroid function is regulated by
TSH in the anterior pituitary gland. responds to TRH that is secreted by hypothalamus (negative feedback)
diagnosing thyroid disease
TSH, iodine uptake exam, ultrasound/fine needle aspiration, Fluorine 18 fluourodeoxyglucose PET.
Hypothyroidism
TSH > 4
hyperthyroidism
TSH < 0.3
Perform T3 if abnormal
how to diagnose hashimoto’s (hypo) or graves (hyper)
Autoantibodies, thyroid globulin, thyroid peroxidase TPO
clinical presentation of Graves can have:
toxic nodules, or thyroiditis (hyperthyroidism)
Fluorine 18 fluourodeoxyglucose PET scan
for metastatic thyroid lesions
hyperthyroidism. what is it
excess production of thyroid
hyperthyroidism diagnosis
THS <0.3.
TSH, TRAb level in graves (antibody), liver function tests, alkaline phosphatase, total bilirubins, radioidoine uptake (to distinguish between graves and thyroiditis), ESR( will be elevated in subacute thyroiditis), free t4,
hyperthyroidism clinical presentation
dry eyes, goiter (graves), tachycardia, HTN, hyperdefecation, weight loss, anorexia, amenorrhea, infertility, heat intolerance, anxiety, irritability, sleeplessness.
pharmacologic management of hyperthyroidism
thioamides. in graves, treat with Beta blockers to relieve symptoms of tachycardia, tremor (avoid in pregnancy)
Thioamide therapy in pregnancy
In pregnancy, start with PTU, only in first trimester. Methimazole for second trimester.
nonpharmacologic therapy for hyperthyroidism
thyroidectomy. can also be done for pregnant women
causes of secondary HTN
hyperthyroidism, pheochromocytoma, neuroblastoma & cushings syndrome
when the serum free t4 concentration falls, what happens with TSH
it rises
When does someone with hypothyroidism require immediate ED referral
myxedema coma (resp depression, hypotermia) requires pressors (levo), warming, vent support, glucocorticoid therapy
Amiodarone
concentrates in thyroid. before starting patients on amiodarone, check thyroid function
what do you hold before TFT levels
biotin for 3 days
hypothyroidism. what is it
TSH >4
causes of hypothyroidism
lithium, iodine, amiodarone, interpheron alpha, contrast, tyrosine kinase inhibitors
clinical manifestiations of hypothyroidism
increased sensitivity to cold, fatigue, heavy irregular menses, dry skin, dry hair,depression, parasthesias, constipation, goiter, slow deep tendon reflexes(most prominent in achilles), weight gain, impaired energy, bradycardia, dim bowel sounds, increased diastolic BP, hypercholesterolemia, macrocytic anemia
in subclinical hypothyroidism, what would TSH and t4 look like
elevated TSH, normal free t4.
diagnostics for hypothyroidism
TSH, free t4, Anti TPO antibody (elevated in thyroiditis)
management of hypothyroidism
levothyroxine daily
referral to endo if nodule requiring biopsy
monitor at 4-6 weeks once medications start
daily dosing is monitored once per year
hashimoto’s thyroiditis is characterized by
rubbery, firm, symmetric goiter (when the antibodies are elevated).
anti TPO will be elevated
Thyroid nodule/ cancer diagnosis
TSH,t3 and t4 if TSH is suppressed, ultrasound, radionuclide scan, fine needle aspiration, molecular markers,
if a nodule is benign, when do you follow up?
a follow up ultrasound should be performed in 6-12 months
american thyroid association recommends WHAT in thyroid cancer?
recommends against doing radioactive iodine ablation in patients with low grade thyroid cancer.
precautions for post radioiodine therapy
No kissing, exchanging saliva, dishes should be washed in dishwasher, no close contact with infants, avoid pregnant women for 5 days,No breast feeding, flush toilets twice, take acetaminophen or aspirin for pain, notify MD if nervous, tremulous, or palpitations.
complications of surgery in thyroid cancer include
hypoparathyroidism and hoarseness
what diabetes medication can cause parasthesias
metformin
what causes increase in blood sugar for patients on insulin?
stress, illness, surgery
what medication will not slow the progression of diabetic nephropathy
use of calcium channel blockers
beta blocker is contraindicated for which patient
asthmatic patient
