Exam 2 Flashcards
What are the initial lab tests that are ordered to evaluate thyroid function?
TSH, Free T4, T3 (add this for hyperthyroidism)
Name the two hormones produced by the thyroid gland
Triiodothyroine- T3 and thyroxine -T4
What primary hormones are produced by the pituitary gland?
Thyroid-stimulating hormone (TSH) and ACTH
What is the purpose of TSH?
TSH tells your thyroid how much thyroid hormone it needs to make; if thyroid hormone levels are too low, the pituitary produces more TSH
What is an expected TSH/T3/T4 levels for a patient with Grave’s disease?
-TSH: low
-T3/T4: high
What are expected TSH/T3/T4 levels for a patient with Hashimoto’s?
-TSH: high
-T3/T4: low
What are the expected TSH/T3/T4 levels for patients with central or secondary hypothyroidism?
-TSH: low
-T3/T4: low
What is the test that assesses the functional status of the thyroid to differentiate between Grave’s/subacute thyroidits, and toxic nodular goiters?
A 24-hour radioactive iodine uptake (RAIU) test which identifies areas of increased and decreased thyroid function (hot and cold spots)
What is the difference between anti-thyroid medication and an ablative dose of radioactive iodine to treat Graves’ disease?
Anti-thyroid medication work by inhibiting thyroid hormone synthesis ; often not used alone but in prep for surgery or at initiation of radioactive iodine; ablative radioactive iodine is curative whereas the anti-thyroid medication generally is not
What is the treatment of choice for hyperthyroidism in middle-aged and older adults?
Radioactive iodine
When is use of radioactive iodine contraindicated?
pregnancy and breastfeeding; women should not become pregnant until at least 4 months after therapy
How long will the patient require thyroid replacement therapy after ablative radioactive treatment for hyperthyroidism?
for the rest of their life
According to the American Association of Clinical Endocrinologists, what is the usual dose of levothyroxine per day for full replacement?
1.6 mcg/kg per day
How would you alter the dose for initiating synthetic thyroid replacement with an older patient with hx of cardiac issues?
These patients should begin with 1/2 the expected full replacement dose or 25-50 mcg per day
How would you increase synthetic thyroid replacement in those the older patient or those with cardiac issues?
Increase the dose gradually by 25 mcg/day once every 4 to 6 weeks
What would make you suspicious of thyroid cancer (clinical presentation)?
-Lump or nodule in the neck that is PAINLESS
-Tightness/full feeling in neck
-Difficulty breathing, swallowing, hoarse voice, hemoptysis, swollen lymph nodes
-Sudden hoarseness with hemoptysis
What is the difference between Cushing syndrome and Cushing disease?
Cushing’s syndrome is caused by cortisol hypersecretion from multiple different causes, whereas Cushing’s disease is the hypersecretion of ACTH caused by a pituitary adenoma
What is the clinical presentation of Cushing disease?
-S: Gradual development of weight gain, back pain, headaches, skin changes, muscle weakness, menstrual irregularities/hirsutism (women), decreased libido and impotence (men)
-O: central obesity, “moon face”, “buffalo hump”, atrophy of epidermis, easy bruising, fungal infections, acne, stretch marks
What is Addison’s disease?
-also known as primary adrenal insufficency; failure of adrenal glands to produce hormones because of a problem in the gland
What is the clinical presentation of Addison’s disease?
-S: fatigue, weakness, anorexia, weight loss, nausea, abdominal pain, diarrhea,
-O: hyperpigmentation, hypoglycemia, hypotension
Diagnostic tests for Addison’s
-Plasma cortisol level (0800 draw less than 3mcg/dL = + for Addison’s)
-ACTH level >200 pg/mL
What is the difference between DMI and DMII?
DMI is a metabolic disorder causing severe insulin deficiency, beta cell destruction, and is often caused by autoimmune destruction to beta cells of the pancreas; often triggered by an infection or toxic insult and must have insulin replacement
DMII results from abnormal secretion of insulin, resistance to the action of insulin in target tissues, and inadequate response at the insulin receptor; has a stronger genetic association than type I
Is there a difference in the clinical presentation of DMI and DMII?
Generally no, the symptoms are the same and result from hyperglycemia; however ketoacidosis primary only effects type I diabetics
What is the goal of treatment for DM1?
Initial goal: normalize the elevated blood glucose level
-Plasma glucose levels of 80-130
-Peak postprandial glucose level of less than 180
-A1C below 7%
What is the difference in S&S between Diabetic ketoacidosis (DKA) and Hyperosmolar Hyperglycemic Syndrome (HHS)?
DKA: The cardinal features of DKA include the following:
* Hyperglycemia—blood glucose level >359 mg/dL
* Ketonemia—plasma ketone level >5 mmol/L
* Acidosis—plasma bicarbonate level <9 mEq/L
HHS:Severe hyperglycemia—blood sugar >600 mg/dL
* No ketosis
* Hyperosmolality
* Dehydration
* Higher mortality rate
Which longer-acting insulins (lasting up to 24 hours) may be utilized to prevent early morning hyperglycemia?
Glargine (Lantus) or detemir (Levemir)
What are the diagnostic criteria for DM2?
- Hgb A1C level > or equal to 6.5% -or-
- Random plasma glucose level of 200 mg/dL with symptoms -or-
- Fasting plasma glucose level of 126 mg/dL or higher on 2 occasions -or-
- 2 hour postload plasma glucose level of 200 mg/dL or higher during an OGTT
What is the classification of the recommended first choice of oral antihyperglycemic medication in Type 2 DM?
Metformin: Biguanide
What is the contraindication to metformin?
renal impairment with eGFR <45
What periodic testing should you order if a patient has been on metformin long term and complains of neuropathy? Why?
Blood test for vitamin B12 becaue metformin can cause decreased absorption of B12
What is the goal of treatment for DM2?
To prevent or slow the development of diabetic complications such as peripheral neuropathy, retinopathy, organ damage
What subsequent laboratory tests are needed to evaluate the general health of patients with DM2 (consider co-morbidities)?
-Serial A1C- as often as 3 months, less often if controlled
Annually:
-Fasting lipid profile
-Serum creatinine
-eGFR
-LFTs
What is the treatment for acute hypoglycemia in an alert patient?
-6-12 oz of orange juice or other fruit juice without additional sugar or 1 cup of milk
Name some 2nd generation sulfonylureas
Glimepiride (amaryl), Glipizide, glyburide (Diabeta)
When is a sulfonylurea contraindicated?
in patients with impaired liver of kidney function
All oral anti-diabetics are indicated in adjunct with what?
Lifestyle modification: diet and exercise
Name some thiazolidinediones for PO treatment of DMII?
pioglitazone (actos) and rosiglitazone (avandia)
What are some side effects of pioglitazone?
weight gain, URI, edema, fluid retention, anemia, and hypoglycemia
How do GLP1 analogues work?
They enhance insulin secretion in a glucose-dependent manner in response to food intake; also improve insulin sensitivity
When is a GLP1 contraindicated?
Gastroparesis, use with caution in if renal impairment, anyone with personal or family history of thyroid cancer
Examples of GLP1s
Trulicity, Victoza, Ozempic
Exampls of SGT2-Is
Canagliflozin (Invokana), Dapagliflozin (Farxiga)
When is a SGT2-I contraindicated?
CHF, nephrotoxicity, or volume depletion
How does a Sodium-glucose transport-2 inhibitor (SGLT2-I: Invokana) work?
blocks the activity of the SGLT proteins in the renal proximal tubule, thereby reducing glucose reuptake and increasing the secretion of glucose in the urine.
When should you refer the DMII patient to a specialist?
Initially: dietician/diabetic educator, ophthalmology
-If the following is confirmed or suspected:
Retinopathy
HDL
Diabetic kidney disease
HTN
Macrovasular disease
Neuropathy
Pregnancy
What are the risk factors for gout?
-Men
-Elderly, especially on diuretics
-Family Hx
-African american
-Excessive intake of purine-rich foods
-Obesity
-Dehydration
-Alcohol abuse
-Hypothyroidism
What is the initial management for an acute attack of gout?
NSAIDs (most common- indomethacin), colchicine (if less than 36 hours from onset of sx), and corticosteroids (PO/IM)
What is the subsequent pharmacological management used to prevent further attacks of GOUT?
-Initiate after 2nd-3rd attack
-Colchicine (not for long-term use)
-probenecid 500 mg daily: first line for patients younger than 60 yrs
-allopurinol (zyloprim)- xanthine oxidase inhibitor that lowers plasma urate/uric acid levels
What educational information should you discuss with a patient diagnosed with gout?
-Avoid triggers (dehydration, alcohol)
-Adequate fluid intake
-Weight loss
-Avoid aspirin
-Wear good shoes
-Bedrest for 24 hours following an acute attack
-Avoid purine-rich foods: yeast, beans, mussels, meats and seafoods
How is obesity classified?
BMI
Overweight: 25-29.9 kg/m2
Obese: 30-34.9
Class 1: 35-39.9
Class 2: > 40
What are the consequences of obesity?
-Heart disease
-HTN
-HLD
-Type II DM
-OSA
-Metabolic syndrome
-Asthma
-Gout
-CA
-GERD
S&S of hyperthyroidism
difficulty focusing, mild exopthalmos, enlarged thyroid, elevated HR, palpitations, puffy eyelids, tremors
Differentials for hyperthyroidism
Panic attack, pheochromocytoma, weight loss= malignancy, mania, anemia, Addison’s disease
Normal TSH
0.5-5.0 MIU/dL
Labs to order when expecting hyperthyroid
CBC, CMP, TSH, Free T4, T3, hCG
Normal Total T4
6-12
What is the most common cause of hyperthyroidism?
Grave’s disease
Describe the negative feedback loop of the thyroid hormones
- Low levels of thyroid hormones trigger the release of TRH from the hypothalamus
- TRH stimulates the pituitary gland to release TSH
- TSH stimulates the thyroid gland to make and release T3, T4
- Increased levels of thyroid hormones
A high RAIU would indicate what disease?
Grave’s
Subsequent testing for hyperthyroidism
Assays for TSH receptor antibodies and RAIU, ultrasound of thyroid
Treatments for Grave’s disease
Pharmacological or surgical:
Pharm- Methimazole
Radioactive iodine, surgery
Other pharmacological interventions for hyperthyroid
Beta blocker (atenolol)
If concurrent asthma or intolerance to BB: diltiazem
-Propylthioruacil (PTU)
Patient education for Grave’s disease
Review diet to avoid weight gain
Referral to opthalmology
Assess for osteoporosis and anticipate- Vitamin D and calcium supplements
What is the most common cause of hirsutism?
PCOS
What is the emergency treatment for thyroid storm?
IV hydration, thyroid-blocking medications, beta blockers (or CCBs), corticosteroids, treat underlying infection
How long are pharmacological interventions continued after reaching a euthyroid state in hyperthyroidism?
6-24 months, tapered slowly; many patients can experience complete remission after 1-2 years of therapy with antithyroid medication
How long does it take anti-thyroid medications to work?
4-6 weeks
S&S of hypothyroidism
S: fatigue, myalgia, dry skin, hair loss, weight gain, cold intolerance, constipation
O: Coarse, thin hair, thick tongue, facial puffiness, brittle nails, bradycardia
What is the target TSH when treating hypothyroidism?
0.3-2.4
How often do you check TSH?
At first- every 4-8 weeks
Once stable- every 6 months to yearly
Patient education for administration of levothyroxine
-Take in AM at least 30 minutes before food
-If taking ferrous sulfate, carafate, or other antacids take synthroid 2 hours before
What symptoms are highly suggestive of thyroid cancer?
new onset of hoarseness with hemoptysis
DDX for thyroid cancer
Lymphocytic thyroiditis, multinodular goiter, benign nodule, cystic nodule
What is the treatment of choice for thyroid cancer?
Thyroidectomy followed by radioactive iodine
What is Cushing’s syndrome?
persistent, inappropriate hypercortisolemia; caused by cortisol hypersecretion by adrenal cortex or prolonged administration of exogenous glucocorticoid hormones
Diagnostics for Cushing’s
-Urine free cortisol
-1mg overnight dexamethasone suppression test (overnight DST)- give at 2300 and positive if 0800 cortisol level is over 1.8 mcg
-late night salivary cortisol level higher than 4.2 is positive
Tx for adrenal insufficiency (Addison’s)
-Hydrocortisone 15-30 mg or prednisone 2-4 mg AM, 1-2 mg PM
-Fludrocortisone acetate for mineralocorticoids
Pneumonic for S&S of addison’s
A: Added pigmentation, potassium
D: Decreased weight
D: Decreased BP, hair, sugar, energy
S: Sodium loss (less than 135)
S: Salt craving
Pneumonic for Cushing’s
C: Cushion (truncal obesity, moon hump)
U: Unusual hair growth
S: Skin- purple striae or butterfly mark
H: High sugar, BP, weight
What is diabetic retinopathy?
-dilation of retinal venules & capillary microaneurysms
-increased vascular permeability
-retinal ischemia due to vascular occlusion
-retinal hemorrhage
Examples of meglitinides (PO anti-diabetic class)
Ends in -linide Mitiglinide, Nateglinide, repaglinide
What is the difference between t4 and free t4?
T4 can be bound or free- bound T4 is attached to proteins and unable to enter body tissues; Free T4 is a measure of thyroxine that is available to be utilized by the tissues
Normal range of FT4
FT4 normal values are 0.7 to 1.9ng/dL
Why should cortisol levels be drawn at 0800?
Because cortisol levels fluctuate in a circadian pattern and peak from 6-8 AM
Primary symptoms of type I DM
polyuria, polydipsia, nocturnal enuresis, polyphagia with paradoxical weight loss (due to reduced glucose metabolism, despite increased consumption), visual changes (especially blurred vision), and eventual fatigue, weakness, and anorexia.
S&S of severe DKA
fatigue, cramping, abnormal respiratory pattern, fruity rotten breath or halitosis
Are diagnostics for DMI and DMII the same?
Yes, the initial diagnostic criteria are the same
What is the common dose range for levothyroxine?
common dosage is 75 to 150 mcg/day.
