Endocrinology - Exam 2 Flashcards
lipoprotein responsible for atherosclerotic plaques
LDL - taken up from vasculature and into subendothelial space where it is oxidized by foam cells and forms atherosclerotic plaques
when to use ACC/AHA CB risk calculator
no ASCVD
LDL cholesterol <190mg/dL
used to estimate a patients 10-year risk for developing CHD
life-habit risk factors for CHD
obesity (central) insulin resistance sedentary lifestyle high fat (triglyceride) diet stress
emerging risk factors for CDH
Apo B (on LDL)
lipoprotine a (side chain on LDL)
NMR spectroscopy: LDL particle size, number, etc.
Inflammatory markers (hsCRP)
measure “sub-clinical” atherosclerotic plaques using CT
only useful for moderate risk patients; only consider if will change your management
4 major statin benefit groups
- current guideline for statin tx
Individuals with known clinical ASCVD (atherosclerotic CVD)
Individuals with LDL ≥ 190 mg/dl
Individuals with diabetes (> 40 yo and LDL>70)
Individuals (>40 yo, LDL>70) w/o ASCVD or diabetes who have an estimated 10-year ASCVD risk ≥ 7.5%
using patient’s CHD risks to set goals for cholesterol (based on both lifestyle and medication therapy)
For individuals with 0 or 1 risk factor → LDL-C goal is <160 mg/dL.
For individuals with ≥2 risk factors (and a 10-year risk of 0%-20%) → LDL-C goal is <130 mg/dL
For individuals with established CAD or a CAD risk equivalent → LDL-C goal is <100 mg/dL.
not current guideline; no research has proven stratified approach
But, we know lower LDL = lower risk of CVD
therapeutic lifestyle change approach for dyslipidemia
heart healthy diet
exercise
maintain healthy weight
no smoking
medications for dyslipidemia
statins
nicotinic acid
fabric acid (fibrates)
statins
lower LDL
side effects: myopathy, inc. liver enzymes
contraindications: liver disease, DDI
nicotinic acid
elevated HDL
side effects: flushing
contraindications: uncontrolled DM, peptic ulcer, liver disease, gout
fibrates
inhibit VLDL production by liver
- use with hypertriglyceremia (obesity, DM)
side effects: raise LDL, GI side effects, cholelithiasis (gallstones)
contraindications: none
secondary causes of hypercholesterolemia
Diet: saturated or trans fats, weight gain, anorexia
Drugs: diuretics, cyclosporine, glucocorticoids, amiodarone
Hypothyroidism
Nephrotic syndrome
Biliary Obstruction
Pregnancy
goal of statin treatment
turn vulnerable lesions into stable lesions; reduce lesions (atherosclerosis) and therefore, reduce CVD-related events
findings on physical exam associated with hypertriglyceridemia
Lipemia retinalis (white instead of red vessels)
Eruptive xantomas: bumps on skin; papules (creamy center)
Lipemic serum: TGs likely over 1000
ADA criteria for diagnosis of DM
FBG:
- normal: <100
- inc. risk: 100-125
- DM: >125
2-hr PG:
- normal: <140
- inc. risk: 140-199
- DM: >200
Random BG:
- normal: n/a
- inc. risk: n/a
- DM: >200 + sxs
HbA1C:
- normal: <5.7
- inc. risk: 5.7-6.4
- DM: >6.5
Need 2 values to make dx (either same test repeated or 2 different tests)
Do not measure during acute illness
criteria for screening for DM
Age ≥ 45
Overweight (BMI ≥ 25) – regardless of age
Family history of diabetes
Sedentary behavior
Race/ethnicity: Hispanic, Indian, Pakistan
h/o IFG (impaired fasting glucose), IGT (impaired glucose tolerance), GDM (gestational diabetes mellitus)
HTN
Low HDL-C (good cholesterol) and/or elevated Triglycerides
PCOS: poly cystic ovarian syndrome
History of vascular disease
criteria for metabolic disease
Overweight: central obesity Sedentary HNT: > 130/85 High triglyceride level (>150mg/dl) Reduced HDL (<40 men, < 50 women) Elevated fasting blood sugar (glucose) (>100 mg/dL)
Note: must have 3 or more of following or taking meds to control these
hemoglobin A1C
Detects amount of sugar attached to RBCs (hemoglobin)
Do not need to be fasting; give average glucose levels over 3 months (insurance covers q 3 mo)
- more accurate at higher levels
Note: some contraindications: iron deficiency anemia (A1C will be falsely elevated)
Normal: <5.7
Inc. risk: 5.7-6.4
Diabetes: >6.5
ADA recommendation for HbA1C treatment goal
<7 HbA1C
See most significant dec. in microvascular complications lowering to 8 or 9
approach to combination therapy for DM
1st choice: lifestyle modification (always should be in management plan)
2nd choice: oral mono-therapy (Metformin)
3rd: add another oral medication (“oral double therapy”): add SU, TZD, DPP-4, SGLT2
4th: add GPL-1 analog
5th: add or switch to insulin
Note: DM education –> person needs to understand disease and monitor
indications for insulin therapy in Type II DM
Poor control on oral agents Cannot take/tolerate oral agents Severe hyperglycemia (begin to consider insulin therapy with HbA1C >10) Hyperosmolar State and/or Ketoacidosis Pregnancy – insulin is only med approved
what is max dose of insulin
there is NO MAX DOSE for insulin
general approach to insulin therapy
basal insulin: begin w/ low doses and titrate slowely
bolus inulin: inc. insulin after meal (post prandial) - skip if you skip meal
Note: weight gain is common and expected (adipocytes now storing fat)
basal insulin therapy
Begin with intermediate or long-acting insulin (at bedtime, low dose – must avoid hypoglycemia)
Good for persistent fasting hyperglycemia
Added to current regime (medications)
Have patient self-titrate (inc. dose) until they reach FBG goal (they will monitor at home)
basal/bolus insulin therapy
Adding a fixed dose of a fast acting insulin before the largest meal of the day
• Dose that is 10-30% of the basal dose
Have patient monitor FBG and pre and post prandial BG
Either increase dose at the single meal, add same dose to a second meal, or add control factor (pm BP = am BG)
microvascular complications of DM
nephropathy (at least 1/yr)
retinopathy (every 1-2 yr)
neuropathy (at least 1/yr)
diabetic foot (at least 1/yr)
screening for nephropathy - microvascular complication of DM
Screen at diagnosis and 1/year:
- Urinary albumin
- Estimated GFR (if irregular, do 24 hour GFR)
Note: DM is most common cause of end stage renal disease
screening for retinopathy - microvascular complication of DM
Comprehensive Eye Exam by Ophthalmologist or Optometrist
• T1 DM within 5 years of Onset
• T2 DM at Diagnosis
• Before Pregnancy or in First Trimester then 1 year Post Partum
Then… every 1-2 years
screening for neuropathy - microvascular complication of DM
goal: prevent!!
Screening at least 1/year
• History, monofilament test, pinprick, temperature, vibration sensation
Assess for sxs of autonomic neuropathy
• Hypoglycemia unawareness: what it feels like to have low blood sugars
• Cardiac autonomic neuropathy: orthostatic HTN
• GI neuropathy: gastroperethes (stomach does not empty well – feel full or throw up)
• GU neuropathy: trouble emptying bladder
screening for diabetic foot - microvascular complication of DM
Screen at least 1/year (may need foot exam every visit)
• History: ulcer, amputation, smoking, signs of microvascular disease
• Comprehensive exam: neuro, inspection, and vascular exam, pulses, claudication (limping)
• Refer: podiatry for positive hx or PE
macrovascular complications of DM
controlling BP, cholesterol, triglycerides
Screening
• HTN: BP every visit (goal = <140/90)
• Lipid management: at diagnosis and every 5 years (or more)
- Statins often recommended
MOST people with Type II DM will die from CVD (MI or Stroke)
Note related to blood sugars!
common symptoms of uncontrolled DM (hyperglycemia)
Polyuria: more glucose spills into urine, bringing water with it → inc. urination
Polydipsia: increased thirst since inc. urination
Severely over-weight
Generalized fatigue: body unable to use glucose for energy
Blurred vision: high glucose in vessels of eye draws water in, too, making vision blurry
Weight loss: increase adipocyte metabolisms (increase lipolysis and less fat storage) due to low insulin levels / insulin resistance
Acanthosis nigricans: dark velvety skin behind neck and under arms; caused by high insulin levels
o Insulin resistance: insulin does not work well so it takes more insulin to get sugar (glucose) into cell
treatment of type II diabetes - general
Lifestyle intervention is best at reducing rate at which people move from pre-diabetes to DM or progress in DM
o Loosing weight: diet and exercise (only 4-5% weight loss needed to see benefits)
Bariatric surgery – underutilized → this could be best tx
Drugs
o Don’t forget about weight loss drugs – this work and treat variety of symptoms
o Diabetic drugs: treat insulin issue
- Oral and injectable; non-insulin and insulin
management of type II diabetes - general
Acute: reverse acute symptoms of hyperglycemia
Chronic: glycemic control: prevent microvascular complications, prevent macrovascular complications
• Minimize hypoglycemia
o BP control
o Treatment of metabolic dyslipidemia
Treat other risk factors: smoking
endocrine causes of secondary HNT
Adrenal: Primary aldosteronisms: tumor - hold onto too much Na Cushing’s: excess cortisol - cause inc. production of aldosterone (hold onto to much Na) Pheochromocytoma
Non-adrenal: hypo- of hyperthyroidism hyperparathyroidism acromegaly - enlargement of hands, feet, facial features
screening for secondary HNT - who to screen?
HNT in young person: age < 30 (esp with no risk factors)
Severe/Resistant Hypertension (tried many meds and no improvement)
Family History of Endocrine Disease
“Spells”- Labile Hypertension (BP fluctuates high and low)
– Pheochromocytomas can do this
Worsening blood pressure after β-Blockers
Hypokalemia (on low dose diuretic)
- too much aldosterone can cause this
Premenopausal Osteoporosis (young women w/ fractures) – Cushing’s (excess cortisol) can cause osteoporosis
approach to incidental adrenal mass
conduct history and physical exam
screen for hyper secretion
- even if hx and PE are normal
screen for malignancy
- consider CT guided FNA
treatment:
- observation
- surgery: tumor >4-6cm, hormone secreting, concerning FNA (malignancy)
primary adrenal insufficiency - clinical features
Sxs: fatigue, weakness, anorexia, abdominal pain, nausea, weight loss
PE: hypotension (due to low aldosterone), tachycardia, fever, abdominal tenderness
- hyperpigmentation and vitilgo (high ACTH)
labs:
- low cortisol, low aldosterone, low testosterone
- High CRH and ACTH (since lack of negative feedback by low levels of adrenal hormones)
- Low Na (hypoatremia) and high K (hyperkalemia) → hint (occurs in primary mainly since aldosterone normal in secondary)
Main cause: addison’s disease (autoimmune disease)
secondary adrenal insufficiency - clinical features
hx: pt recently off steroid meds
Sxs: fatigue, weakness, anorexia, abdominal pain, nausea, weight loss
PE: hypotension (due to low aldosterone), tachycardia, fever, abdominal tenderness
labs:
- low cortisol (only stimulated by ACTH), normal levels of testosterone and aldosterone (since stimulated by other things)
- low levels of CRH and ACTH
- Na (hypoatremia)
Causes:
• Hypothalamic: glucocorticoid therapy (most common – steroid intake tells hypothalamus to stop making CRH), other drugs, tumors
• Pituitary: many things cause low ACTH secretion
Addison’s Disease
autoimmune disease causing primary adrenal insufficiency - body attacks adrenal gland
- see low levels of cortisol, low aldosterone, low testosterone
Sheehan’s disease
decrease functioning of pituitary gland post partum
- cause of secondary adrenal insufficiency
adrenal insufficiency - diagnostic methods
Random Cortisol < 3 μg/dl (hormones are released in pulsatile manner)
Cosyntropin Stimulaton Test (Gold Standard) – give ACTH and see how adrenal glands respond
• Baseline cortisol level
• Give 250 μg cortrosyn (ACTH) IV (or IM)
• Measure cortisol at 30, 60 minutes
• Adrenal Insufficiency = 30/60 min Cortisol < 20 μg/dl → know that adrenal glands are problem
• If cortisol rises, know adrenal glands are working and issue must be coming from above
Primary versus Secondary
• Serum ACTH > 100 pg/ml in Primary Adrenal Insufficiency (adrenal glands just cannot respond)
adrenal insufficiency - acute treatment
Give cortisol back to body (Addisionian crisis)
• Hydrocortisone 100 mg IV q 8 hrs
• Can also use dexamethasone if cannot wait for Cort Stim Test (urgent)
• Hydration and BP Support: saline, pressor agents
• Rule out and treat precipitating factors: trauma, infection, dehydration
• Taper as quickly as clinical condition allows
adrenal insufficiency - chronic treatment
Primary Adrenal Insufficiency
• Hydrocortisone ~30 mg/d (2-3 divided doses) - has glucocorticoid (cortisol) and mineralocorticoid (aldosterone) effect
- Consider DHEA (hormone) in women
Secondary Adrenal Insufficiency
• Prednisone ~5 mg once daily → cortisol - Pure glucocorticoid (since aldosterone levels will be normal since also stimulated by renin, etc.)
hydrocortisone vs. prednisone
Hydrocortisone has glucocorticoid (cortisol) and mineralocorticoid (aldosterone) effect
- tx for primary adrenal insufficiency
Prednisone (cortisol) - pure glucocorticoid
- tx for secondary adrenal insufficiency
adrenal insufficiency - patient education
Stress/illness dosing of steroids (pts need to wear bracelet since they will need trauma dose of cortisol if in crises)
o Medical alert, family education
Lowest dose possible to avoid complications (Cushing’s syndrome, osteoporosis, DM)
major CDV risk factors
Cigarette smoking
Hypertension
Low HDL-C: <40 mg/dL*
Age
o male ≥45 years
o female ≥55 years
Family history of premature coronary heart disease (CHD) (1st-degree):
o male relative age <55 years
o female relative age <65 years
diseases considered to be CHD risk equivalents
clinical CHD
symptomatic CAD
peripheral arterial disease
abdominal aortic aneurysm
Cushing syndrome - clinical features
excess cortisol
central obesity (skinny legs) moon facies hirsutism purple straie low bone density (fractures) dorsal cervical fat pad low depression / HNT
hirsutism
male pattern hair growth
Cushing syndrome - screening tests
Low Dose Dexamethasone Suppression Test (suppresses ACTH release from pituitary)
• 1 mg at 10-11 pm and measure 8 AM cortisol
• cortisol should be suppressed
24-hr Urinary Free Cortisol → confirmatory test after failing Dex test
• Cushing’s Syndrome: > 4 x normal
Late night (midnight) salivary cortisol
Cushing syndrome - confirmatory test
two positive 24-hr urinary free cortisol tests
ACTH serum test: must determine if ACTH dependent or independent
determine if Cushing syndrome is ACTH dependent or independent
serum ACTH
ACTH low = ACTH independent
- coming from adrenal gland: CT or MRI of abdomen
ACTH high = ACTH dependent
- coming from pituitary or ectopic – extra ACTH coming from somewhere
- perform high dose Dex suppression test (suppress ACTH) and see what happens
- MRI or sella pituitary; inf petrosal sinus sampling (if think pituitary)
- PET scan if ectopic
Cushing Disease
excess cortisol as a result of excess ACTH secretion from pituitary
Cushing syndrome - treatment
Cushing’s Disease (cause is pituitary):
- transphenoidal surgery
Adrenal Tumor
- laproscopic surgery
- bilateral adrenalectomy: remove adrenal glands and supplement cortisol for rest of life
Ectopic ACTH:
- surgery (carcinoid)
- chemotherapy (small cell cancer)
hyperaldosteronism - clinical features
too much aldosterone results in high Na and low K
hypertension (high Na)
hypokalemia
metabolic acidosis
hyperaldosteronism - screening test
Morning Blood Sample (seated) for:
• Plasma Aldosterone (PA) - high
• Plasma Renin Activity (PRA) - low
Positive screen: PA/PRA ratio > 20 and PA > 15 ng/dl
hyperaldosteronism - confirmatory test
performed by endocrinologist
Sodium suppression testing: suppress aldosterone by loading diet w/ salt for 3 d
- High plasma aldosterone (>10ng/dl) = diagnostic result
hyperaldosteronism - treatment
Aldosterone antagonists (pre-operative) • ACE inhibitors:
Adrenalectomy:
pheochromocytoma
tumor in center of adrenal gland that releases catecholamines
pheochromocytoma - clinical features
HTN “spells” – labial highs and lows
Headaches, sweating, palpitations, pallor (like scared by something)
Do NOT get flushing
pheochromocytoma - screening tests
urine or plasma testing
24-hr Urine Metanephrines
• Positive: > 1,300 ug/24 hr
24-hr Urine Catecholamines
• Positive: > 2 fold elevated
Plasma Metanephrines
• Positive Metanephrine: > 0.5 nmol/L
• Positive Normetanephrine: > 2 fold
pheochromocytoma - diagnostic tests
Chromogranin A level → confirmatory test
Protein produced by cells of adrenal medulla (chromaffin cells)
pheochromocytoma - treatment
Pre-operative:
• alpha blocker (1st – blood vessels) and beta blockers (2nd – heart) OR calcium channel blockers
Adrenalectomy
- with hormone supplementation
Addisionian crisis (acute adrenal insufficiency) - presentation
hx: recently went off exogenous steroid tx
Hypotension (low BP, orthostatic), tachycardia, fever, abdominal tenderness/guarding
Sxs: fatigue, weakness, anorexia, abdominal pain, nausea, weightless, myalgia, vomiting, postural dizziness, arthralgia, HA, salt cravings
Addisionian crisis (acute adrenal insufficiency) - management
give cortisol back to body
- Hydrocortisone 100 mg IV q 8 hrs
- Can also use dexamethasone if cannot wait for Cort Stim Test (urgent)
- Hydration and BP Support: saline, pressors
- taper as quickly as clinical condition allows
Cushing syndrome - causes
Overall: adrenal glands are making too much cortisol / too much cortisol in system
- Exogenous corticosteroids (Prednisone) – people taking external cortisol
• Main cause - Adrenal tumor: cortisol secreting tumor
- Pituitary tumor: ACTH secreting tumor → stimulates cortisol production
- Ectopic tumor (lungs): ACTH secreting tumor → stimulates cortisol production
hormones secreted by pituitary gland
Anterior Pituitary • Adrenocorticotropic Hormone (ACTH) • Growth Hormone • Prolactin • Thyroid Stimulating Hormone (TSH) • Luteinizing Hormone (LH) • Follicle Stimulating Hormone (FSH)
Posterior Pituitary
• Antidiuretic Hormone (ADH)
• Oxytoxicin
disorders of the pituitary
hormone over-secretion
- prolactinoma (most common)
hormon under-sectretion (pan hypopituitarism)
- mass effect
- Sheehan’s
mass effect: tumors can disrupt visual fields
incidental mass: observe and repeat imaging q 6-12 mo
prolactinoma - sxs
tumor of pituitary gland that produces excess prolactin
SXS: hypogonadsim, amenorrhea, impotence/ED, infertility, galactorrhea, HA, visual field defects
pan hypopituitarism - treatment
replace all hormones except prolactin
Hypogonadism:
• Testosterone (m)
• Estrogen ± progesterone (w)
Hypothyroidism:
• Levothyroxine (follow FT4 not TSH, aim for high-normal FT4)
Adrenal Insufficiency:
• Prednisone
Growth Hormone Deficiency:
• Daily injection
ADH intranasal as needed to control polyuria (diabetes insipidus)
overt thyroid disease
abnormal TSH with abnormal hormones (free T4, T4, T3)
→ sxs of hypo- or hyper-thyroidism
subclinical thyroid disease
abnormal TSH with normal hormones (free T4, T4, T3)
T4 and T3 (thyroxines) in plasma
most is bound to proteins (not biologically available)
- T3 is more potent and biologically active form of thyroxine
- 80% of T3 is produced outside thyroid by conversion from T4
thyroid disease - screening
Sensitive TSH assay is “gold standard” for screening
- TSH and T4 are highly correlated: small changes in T4 cause proportionally larger shifts in TSH levels
- As T4 decreases, TSH increases (linear, inverse relationship)
- TSH is a “magnification Marker” – small changes in T4 = large changes in TSH
TSH - normal range for diagnosis
Normal range is typically 0.5-5 microunits per milliliter (μU/ml)
TSH - range for meeting treatment goal
1-2 μU/ml
- different from screening goal
- monitor TSH 6 weeks after dose or brand change (Half-life = 7 days); monitor every 6-8 wks until stable
relationship b/t TSH and T4
- TSH and T4 are highly correlated: small changes in T4 cause proportionally larger shifts in TSH levels
- As T4 decreases, TSH increases (linear, inverse relationship)
- TSH is a “magnification Marker” (small changes in T4 = large changes in TSH)
suspected thyroid disease - how to order TSH
TSH with “reflex” T4 (will measure T4 if TSH is abnormal)
acute monitoring following treatment for hyper- or hypothyroid
TSH changes slowly after T4 is normalized, in both hypo- and hyperthyroid conditions
- Up to a month may be required for TSH to come into the normal range
During this time, monitor free T4 or FTI (free thyroxine index)
Once TSH normalizes, it is the analyte of choice for following patients
nuclear medicine - role in thyroid disease
thyroid scan and uptake
Uptake of radioactive compound is measured at 6 and 24 hours and compared with normal values
The “scan” is an image of the distribution of the radio-labeled compound in the thyroid
Normal range: 15-20% uptake
• High uptake is referred to as a “hot” scan (Graves’ Disease)
• Low uptake is a “cold” scan (thyroiditis)
nuclear scans for hyperthyroidism - helps to differentiate
Hyperthyroidism: low TSH, high FT4
High, diffuse: Graves
High, nodular (single): Toxic Adenoma
High, nodular (multiple): Toxic Multinodular Goiter
Low: Thyroiditis v. exogenous T4 (over treatment with levothyroxine)
Elevated TSH and high FT4: TSH secreting pituitary tumor (rare)
ultrasound - role in thyroid disease
help characterize nodules, monitor change in size, distinguish solid from cystic lesions
fine-needle aspiration - role in thyroid disease
evaluating solitary nodules in euthyroid (normal TSH/FT4 levels) patients
hyperthyroidism presentation - young v. old
young: sxs of inc. metabolic rate (tachycardia, heat intolerance, hyperactive reflexes, and hyperhidrosis (increased sweating)
elderly: blunted response; inc. atrial fibrillation and anorexia
Grave’s disease - etiology and treatment
cause of hyperthyroidism
Cause: autoimmune disease, antibodies bind to the TSH receptor and cause a TSH-like response
Tx:
• Radioactive ablation with I-131: most common (need lifelong levothyroxine supplementation)
• Surgical ablation of thyroid: higher risk
• Antithyroid drugs (LT or ST use)
• Symptomatic managment
thionamides (antithyroid drugs)
work by blocking thyroid peroxidase (inhibiting incorporation of iodide into tyrosine residues)
Propylthiouracil (PTU): preferred in pregnancy and nursing and for severe thyrotoxicosis
Methimazole (MMI): generally considered safer in non-pregnant patients
hashitoxicosis - etiology and treatment
cause of transient hyperthyroidism followed by hyperthyroidism
Cause: early phase of Hashimoto Thyroiditis (thyroid is being destroyed by an autoimmune process, spilling thyroxine into the circulation)
Tx:
hypo: symptomatic management with beta-blockers and steroid
hyper: Levothyroxine
toxic adenoma - etiology and treatment
cause of hyperthyroidism
Cause: nodule that secretes excessive thyroxine; typically occurs in younger patients
Tx: radioactive or surgical ablation
multinodular goiter - etiology and treatment
cause of hyperthyroidism
Cause: disease of elderly patients; manifests as diffuse nodular enlargement of the gland
Tx:
Radioactive or surgical ablation
Symptomatic management with beta-blockers and steroids
Antithyroid drugs (not good for long-term tx)
thyroiditis
causes initial hyperthyroidism (due to inflammation of thyroid follicular cells) followed by hypothyroidism (as cellular function recovers)
two types
three types of thyroiditis
Subacute granulomatous thyroiditis
Subacute lymphocytic thyroiditis
Hashimoto thyroiditis
Subacute granulomatous thyroiditis - etiology and treatment
Cause: follows acute viral illness; painful, tender gland
- uptake is low on nuclear scan
Tx:
• NSAIDS or steroids for pain and inflammation
• Beta-blockers for symptom management
• Thionamides (anti-thyroid drugs) in some cases
Subacute lymphocytic thyroiditis - etiology and treatment
Cause: post-partum, painless thyroid gland
- drugs can induce
Tx: for hypo- or hyperthyroidism → typically use anti-thyroid meds short-term since body will re-regulate (work on getting her asymptomatic)
what do you think if you see high TSH ADN high FT4 (usually inverse)
TSH producing pituitary tumor (rare)
hyperthyroidism - general
less common, more likely in older puts
low TSH, high FT4
most common cause = Grave’s disease
younger pts: sxs of inc. metabolic rate: tachycardia, heat intolerance, hyperactive reflexes, and hyperhidrosis (increased sweating), baby soft skin
older pts: atrial fibrillation, anorexia
hypothyroidism - general
more common, women>60
high TSH, low FT4
most common cause = Hashimoto thyroiditis
sxs of dec. metabolic rate: weakness, dry or course skin, lethargy, cold sensation, dec. sweating, coarse hair, forgetfulness, constipation
Hashimoto thyroiditis
most common cause of hypothyroidism
thyroid is being destroyed by an autoimmune process
• Initially → spilling thyroxine into the circulation (transient hyperthyroidism)
• Thyroid cells destroyed → hypothyroidism
Classic clinical sxs: low metabolic rate, puffy face w/ eyebrow thinning and truncation laterally
thyroiditis - evaluation
hyperthyroidism followed by hypothyroidism
Pain/tenderness?
- Yes:
1. history of radiation or trauma: radiation or traumatic thyroiditis,
- no history of rad/trauma: Subacute Granulomatous Thyroiditis
- No:
1. Meds associated with thyroiditis: Drug-induced
2. Post-partum - check TSH:
o High or normal: Post-partum or Hashimoto’s
o Low: Post-partum vs Graves (RAI uptake to distinguish – Graves has hot scan)
- Not 1 or 2: Hashimoto’s versus Subacute Lymphocytic Thyroiditis
- likely subacute lymphocytic thyroiditis
hypothyroidism v. depression
Hypothyroidism: related to decreased metabolic rate → weakness, dry or course skin, lethargy, cold sensation, dec. sweating, coarse hair, forgetfulness, constipation
Specific hypo sxs: bradycardia, lipid disorder, cold intolerance, hair/skin changes, goiter, delayed DTRs
Shared Symptoms: mood, concentration, libido, appetite, fatigue, sleep disorder, weight gain
Specific depression sxs: delusions, suicidal ideation, insomnia, inc. appetite
hypothyroidism and depression - link
always keep each on differential
Remember: can have BOTH
hypothyroidism - medication and starting dose
Levothyroxine (T4): 1.6 mg/kg/day (based on pt weight)
Goal: 1-2 mIU/L (different from screening range of 0.5-5 mIU/L)
- monitor every 6-8 weeks after dose or brand change and until stable
recommendation for dyslipidemia screening
Fasting lipid panel at least every 5 yrs (adults 20 and older)
what does fasting lipid panel measure
total cholesterol, HDL, triglycerides
Fridewald formula
In fasted state (TG <400): LDL = Total-C – HDL – TG/5 (mg/dL)
• Note: LDL is only calculable if TG<400 mg/dL
how often should you re-calculate ASCVD risk - to determine if use of statins is recommended
Recalculate every 4-6 years in individuals 40-75 y/o without criteria 1-3 above
severe hypertriglyceremia treatment
TG>500 g/dL
associated with acute pancreatitis (not stroke or MI)
Reduce chylomicronemia: very low fat diet
No alcohol, weight management, physical activity
Meds: Fibrates or fish oils
moderate hypertriglyceremia treatment
TG 200-499 g/
Use elevated TG as a risk marker and treat LDL with statin therapy if indicated per guidelines
Treat/Eliminate secondary causes of dyslipidemia
Intensify weight management, physical activity, higher mono-, poly-unsaturated fat diet
hypertriglyceridemia - approach to treatment
rule out secondary cases look for PE findings treat based on TG # - >500: fibrates, very low fat diet - 200-499: statins (lower LDL), high poly and mom-unsaturated fat diet
