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Adult Clinical Medicine > Endocrinology - Exam 2 > Flashcards

Endocrinology - Exam 2 Flashcards

1
Q

lipoprotein responsible for atherosclerotic plaques

A

LDL - taken up from vasculature and into subendothelial space where it is oxidized by foam cells and forms atherosclerotic plaques

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2
Q

when to use ACC/AHA CB risk calculator

A

no ASCVD
LDL cholesterol <190mg/dL

used to estimate a patients 10-year risk for developing CHD

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3
Q

life-habit risk factors for CHD

A 
obesity (central)
insulin resistance
sedentary lifestyle
high fat (triglyceride) diet
stress
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4
Q

emerging risk factors for CDH

A

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

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5
Q

4 major statin benefit groups

- current guideline for statin tx

A

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%

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6
Q

using patient’s CHD risks to set goals for cholesterol (based on both lifestyle and medication therapy)

A

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

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7
Q

therapeutic lifestyle change approach for dyslipidemia

A

heart healthy diet
exercise
maintain healthy weight
no smoking

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8
Q

medications for dyslipidemia

A

statins
nicotinic acid
fabric acid (fibrates)

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9
Q

statins

A

lower LDL
side effects: myopathy, inc. liver enzymes
contraindications: liver disease, DDI

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10
Q

nicotinic acid

A

elevated HDL
side effects: flushing
contraindications: uncontrolled DM, peptic ulcer, liver disease, gout

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11
Q

fibrates

A

inhibit VLDL production by liver
- use with hypertriglyceremia (obesity, DM)
side effects: raise LDL, GI side effects, cholelithiasis (gallstones)
contraindications: none

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12
Q

secondary causes of hypercholesterolemia

A

Diet: saturated or trans fats, weight gain, anorexia

Drugs: diuretics, cyclosporine, glucocorticoids, amiodarone

Hypothyroidism

Nephrotic syndrome

Biliary Obstruction

Pregnancy

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13
Q

goal of statin treatment

A

turn vulnerable lesions into stable lesions; reduce lesions (atherosclerosis) and therefore, reduce CVD-related events

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14
Q

findings on physical exam associated with hypertriglyceridemia

A

Lipemia retinalis (white instead of red vessels)

Eruptive xantomas: bumps on skin; papules (creamy center)

Lipemic serum: TGs likely over 1000

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15
Q

ADA criteria for diagnosis of DM

A

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

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16
Q

criteria for screening for DM

A

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

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17
Q

criteria for metabolic disease

A 
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

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18
Q

hemoglobin A1C

A

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

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19
Q

ADA recommendation for HbA1C treatment goal

A

<7 HbA1C

See most significant dec. in microvascular complications lowering to 8 or 9

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20
Q

approach to combination therapy for DM

A

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

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21
Q

indications for insulin therapy in Type II DM

A 
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
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22
Q

what is max dose of insulin

A

there is NO MAX DOSE for insulin

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23
Q

general approach to insulin therapy

A

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)

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24
Q

basal insulin therapy

A

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)

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25
Q

basal/bolus insulin therapy

A

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)

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26
Q

microvascular complications of DM

A

nephropathy (at least 1/yr)
retinopathy (every 1-2 yr)
neuropathy (at least 1/yr)
diabetic foot (at least 1/yr)

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27
Q

screening for nephropathy - microvascular complication of DM

A

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

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28
Q

screening for retinopathy - microvascular complication of DM

A

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

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29
Q

screening for neuropathy - microvascular complication of DM

A

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

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30
Q

screening for diabetic foot - microvascular complication of DM

A

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

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31
Q

macrovascular complications of DM

A

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!

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32
Q

common symptoms of uncontrolled DM (hyperglycemia)

A

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

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33
Q

treatment of type II diabetes - general

A

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

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34
Q

management of type II diabetes - general

A

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

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35
Q

endocrine causes of secondary HNT

A 
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
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36
Q

screening for secondary HNT - who to screen?

A

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
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37
Q

approach to incidental adrenal mass

A

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)
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38
Q

primary adrenal insufficiency - clinical features

A

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)

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39
Q

secondary adrenal insufficiency - clinical features

A

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

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40
Q

Addison’s Disease

A

autoimmune disease causing primary adrenal insufficiency - body attacks adrenal gland
- see low levels of cortisol, low aldosterone, low testosterone

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41
Q

Sheehan’s disease

A

decrease functioning of pituitary gland post partum

- cause of secondary adrenal insufficiency

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42
Q

adrenal insufficiency - diagnostic methods

A

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)

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43
Q

adrenal insufficiency - acute treatment

A

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

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44
Q

adrenal insufficiency - chronic treatment

A

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.)

45
Q

hydrocortisone vs. prednisone

A

Hydrocortisone has glucocorticoid (cortisol) and mineralocorticoid (aldosterone) effect
- tx for primary adrenal insufficiency

Prednisone (cortisol) - pure glucocorticoid
- tx for secondary adrenal insufficiency

46
Q

adrenal insufficiency - patient education

A

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)

47
Q

major CDV risk factors

A

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

48
Q

diseases considered to be CHD risk equivalents

A

clinical CHD
symptomatic CAD
peripheral arterial disease
abdominal aortic aneurysm

49
Q

Cushing syndrome - clinical features

A

excess cortisol

central obesity (skinny legs)
moon facies
hirsutism
purple straie
low bone density (fractures)
dorsal cervical fat pad
low
depression / HNT
50
Q

hirsutism

A

male pattern hair growth

51
Q

Cushing syndrome - screening tests

A

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

52
Q

Cushing syndrome - confirmatory test

A

two positive 24-hr urinary free cortisol tests

ACTH serum test: must determine if ACTH dependent or independent

53
Q

determine if Cushing syndrome is ACTH dependent or independent

A

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
54
Q

Cushing Disease

A

excess cortisol as a result of excess ACTH secretion from pituitary

55
Q

Cushing syndrome - treatment

A

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)
56
Q

hyperaldosteronism - clinical features

A

too much aldosterone results in high Na and low K

hypertension (high Na)
hypokalemia
metabolic acidosis

57
Q

hyperaldosteronism - screening test

A

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

58
Q

hyperaldosteronism - confirmatory test

A

performed by endocrinologist

Sodium suppression testing: suppress aldosterone by loading diet w/ salt for 3 d
- High plasma aldosterone (>10ng/dl) = diagnostic result

59
Q

hyperaldosteronism - treatment

A 
Aldosterone antagonists (pre-operative)
•	ACE inhibitors:

Adrenalectomy:

60
Q

pheochromocytoma

A

tumor in center of adrenal gland that releases catecholamines

61
Q

pheochromocytoma - clinical features

A

HTN “spells” – labial highs and lows

Headaches, sweating, palpitations, pallor (like scared by something)

Do NOT get flushing

62
Q

pheochromocytoma - screening tests

A

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

63
Q

pheochromocytoma - diagnostic tests

A

Chromogranin A level → confirmatory test

Protein produced by cells of adrenal medulla (chromaffin cells)

64
Q

pheochromocytoma - treatment

A

Pre-operative:
• alpha blocker (1st – blood vessels) and beta blockers (2nd – heart) OR calcium channel blockers

Adrenalectomy
- with hormone supplementation

65
Q

Addisionian crisis (acute adrenal insufficiency) - presentation

A

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

66
Q

Addisionian crisis (acute adrenal insufficiency) - management

A

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
67
Q

Cushing syndrome - causes

A

Overall: adrenal glands are making too much cortisol / too much cortisol in system

  1. Exogenous corticosteroids (Prednisone) – people taking external cortisol
    • Main cause
  2. Adrenal tumor: cortisol secreting tumor
  3. Pituitary tumor: ACTH secreting tumor → stimulates cortisol production
  4. Ectopic tumor (lungs): ACTH secreting tumor → stimulates cortisol production
68
Q

hormones secreted by pituitary gland

A 
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

69
Q

disorders of the pituitary

A

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

70
Q

prolactinoma - sxs

A

tumor of pituitary gland that produces excess prolactin

SXS: hypogonadsim, amenorrhea, impotence/ED, infertility, galactorrhea, HA, visual field defects

71
Q

pan hypopituitarism - treatment

A

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)

72
Q

overt thyroid disease

A

abnormal TSH with abnormal hormones (free T4, T4, T3)

→ sxs of hypo- or hyper-thyroidism

73
Q

subclinical thyroid disease

A

abnormal TSH with normal hormones (free T4, T4, T3)

74
Q

T4 and T3 (thyroxines) in plasma

A

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
75
Q

thyroid disease - screening

A

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
76
Q

TSH - normal range for diagnosis

A

Normal range is typically 0.5-5 microunits per milliliter (μU/ml)

77
Q

TSH - range for meeting treatment goal

A

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
78
Q

relationship b/t TSH and T4

A
  • 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)
79
Q

suspected thyroid disease - how to order TSH

A

TSH with “reflex” T4 (will measure T4 if TSH is abnormal)

80
Q

acute monitoring following treatment for hyper- or hypothyroid

A

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

81
Q

nuclear medicine - role in thyroid disease

A

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)

82
Q

nuclear scans for hyperthyroidism - helps to differentiate

A

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)

83
Q

ultrasound - role in thyroid disease

A

help characterize nodules, monitor change in size, distinguish solid from cystic lesions

84
Q

fine-needle aspiration - role in thyroid disease

A

evaluating solitary nodules in euthyroid (normal TSH/FT4 levels) patients

85
Q

hyperthyroidism presentation - young v. old

A

young: sxs of inc. metabolic rate (tachycardia, heat intolerance, hyperactive reflexes, and hyperhidrosis (increased sweating)
elderly: blunted response; inc. atrial fibrillation and anorexia

86
Q

Grave’s disease - etiology and treatment

A

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

87
Q

thionamides (antithyroid drugs)

A

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

88
Q

hashitoxicosis - etiology and treatment

A

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

89
Q

toxic adenoma - etiology and treatment

A

cause of hyperthyroidism

Cause: nodule that secretes excessive thyroxine; typically occurs in younger patients

Tx: radioactive or surgical ablation

90
Q

multinodular goiter - etiology and treatment

A

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)

91
Q

thyroiditis

A

causes initial hyperthyroidism (due to inflammation of thyroid follicular cells) followed by hypothyroidism (as cellular function recovers)

two types

92
Q

three types of thyroiditis

A

Subacute granulomatous thyroiditis

Subacute lymphocytic thyroiditis

Hashimoto thyroiditis

93
Q

Subacute granulomatous thyroiditis - etiology and treatment

A

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

94
Q

Subacute lymphocytic thyroiditis - etiology and treatment

A

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)

95
Q

what do you think if you see high TSH ADN high FT4 (usually inverse)

A

TSH producing pituitary tumor (rare)

96
Q

hyperthyroidism - general

A

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

97
Q

hypothyroidism - general

A

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

98
Q

Hashimoto thyroiditis

A

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

99
Q

thyroiditis - evaluation

A

hyperthyroidism followed by hypothyroidism

Pain/tenderness?

  • Yes:
    1. history of radiation or trauma: radiation or traumatic thyroiditis,
  1. 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)
  1. Not 1 or 2: Hashimoto’s versus Subacute Lymphocytic Thyroiditis
    - likely subacute lymphocytic thyroiditis
100
Q

hypothyroidism v. depression

A

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

101
Q

hypothyroidism and depression - link

A

always keep each on differential

Remember: can have BOTH

102
Q

hypothyroidism - medication and starting dose

A

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

103
Q

recommendation for dyslipidemia screening

A

Fasting lipid panel at least every 5 yrs (adults 20 and older)

104
Q

what does fasting lipid panel measure

A

total cholesterol, HDL, triglycerides

105
Q

Fridewald formula

A

In fasted state (TG <400): LDL = Total-C – HDL – TG/5 (mg/dL)
• Note: LDL is only calculable if TG<400 mg/dL

106
Q

how often should you re-calculate ASCVD risk - to determine if use of statins is recommended

A

Recalculate every 4-6 years in individuals 40-75 y/o without criteria 1-3 above

107
Q

severe hypertriglyceremia treatment

A

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

108
Q

moderate hypertriglyceremia treatment

A

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

109
Q

hypertriglyceridemia - approach to treatment

A 
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

Adult Clinical Medicine (5 decks)

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