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Emergency Medicine EOR > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is primary (Addison’s disease)?

A

autoimmune, infections, disease of the adrenal gland = decrease in cortisol secretion

  • adrenal gland destruction causing lack of cortisol and aldosterone secretion (usually autoimmune)
  • autoimmune (70%), infectious (tuberculosis), vascular (thrombosis/hemorrhage), metastatic, medications (rifampin, barbiturates, phenytoin, ketoconazole)
  • dx: increased ACTH, decreased cortisol, decreased aldosterone
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2
Q

What is secondary adrenal insufficiency?

A

pituitary adenoma or discontinuation of steroid - pituitary failure

  • exogenous steroid use (most common); hypopituitarism
  • dx: decreased ACTH, decreased cortisol, normal aldosterone
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3
Q

What is adrenal crisis?

A

acute adrenal insufficiency

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4
Q

How is adrenal insufficiency dx?

A
  • 8 am serum cortisol and plasma ACTH alone with ACTH stimulation test
  • high ACTH, low cortisol = primary
  • low SCTH, low cortisol = secondary
  • CRH stimulation test: differentiates between causes of adrenal insufficiency
  • primary/Addison’s (adrenal): high ACTH, low cortisol
  • secondary (pituitary): Low ACTH, low cortisol
  • adrenal autoantibodies can be assessed; CXR for TB (CT of adrenals)
  • autoimmune: atrophied adrenals
  • TB/granulomas: enlarged adrenals + calcification
  • bilateral adrenal hyperplasia = genetic enzyme defect
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5
Q

How is the tx for adrenal insufficiency?

A
  • addison’s: cortisol replacement therapy + androgen replacement
  • glucocorticoid + mineralocorticoid = hydrocortison = 1st line, fludrocortisone for primary Addison’s disease only
  • secondary: cause = focus of treatment (pituitary adenoma resection, wean steroid therapy slowly)
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6
Q

What is hyperthyroidism?

A

is the production of too much thyroxine hormone
-It can increase metabolism and accelerate the body’s metabolism, causing unintentional weight loss and a rapid or irregular heartbeat

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7
Q

What is the etiology of hyperthyroidism?

A

grave’s disease (autoimmune), toxic adenoma, thyroiditis, pregnancy, amiodarone

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8
Q

What are the features of hypertyroidism?

A

weight loss, anxiety, war, moist skin, onycholysis, insomnia, fine tremor, fatigue, muscle cramps, weakness, amenorrhea, tachycardia, palpitations, systolic HTN, PVCs, fib, brittle hair, heat intolerance, hyperreflexia

  • graves - diffuse goiter with a bruit, exophthalmos, pretrial myxedema
  • thyroid storm - fever, tachycardia, delirium
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9
Q

How is hyperthyroidism?

A
  • TSH (best test)
  • decreased in primary disease (decrease TSH and increase free T4)
  • elevated in secondary disease (increase TSH and increase free T4)
  • T4: elevated although may be normal
  • RAIU study shows increased uptake in graves disease and toxic multi nodular goiter
  • graves: diffusely high uptake
  • toxic multi nodular: discrete areas of high uptake
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10
Q

What are the antibodies with hyperthyroidism?

A

graves: anti-thyrotropin antibodies

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11
Q

What is the tx for hyperthyroidism?

A
  • beta-blockers (symptomatic), methimazole/propylthirouacil, radioactive iodine, thyroidectomy
  • thyroid storm - prompt beta-blockers, hydrocortisone, methimazole/propylthiouracil, iodine
  • thyroidectomy - most likely complication is recurrent laryngeal nerve damage (hoarseness)
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12
Q

What do you do about antithyroid drugs during pregnancy?

A

propylthiouracil used to be the drug of choice during pregnancy because it causes less severe birth defects than methimazole, but experts now recommend that propylthiouracil be given during the first trimester only, this is because there have been rare cases of liver damage in people taking propylthiouracil, after the first trimester, women should switch to methimazole for the rest of the pregnancy
-for women who are nursing, methimazole is probably a better choice than propylthiouracil (to avoid liver side effects)

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13
Q

What is Cushing’s syndrome?

A

a collection of signs and symptoms due to prolonged exposure to excess cortisol
-symptoms from increase cortisol secretion, it doesn’t specify cause or source of excess

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14
Q

What is cushing disease?

A

ACTH secreting pituitary micro adenoma usually very small on anterior pituitary; F 3x > M
-secondary - increase cortisol due to ACTH excess, typically caused by a pituitary adenoma - ACTH causes adrenals to secret cortisol

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15
Q

What are the features of Cushing disease?

A
  • hypercortisolism (increase cortisol) = obestiy (buffalo hump, moon facies, supraclavicular pads), HTN, thirst, polyuria, hypokalemia
  • proximal muscle weakness, pigmented striae, backache, headache, oligomenorrhea/amenorrhea/ED; emotional lability/psychosis
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16
Q

How is Cushing disease dx?

A

confirming high cortisol with a 24 hr urine free cortisol, late-night serum cortisol, and/or low-dose dexamethasone suppression test

  • 24-hour urinary free cortisol is the most reliable index of cortisol secretion
  • once confirmed, the source of the high cortisol needs to be determined with an ACTH level
  • a high ACTH level indicated an ACTH dependent cause, a low ACTH level indicates an ACTH independent cause (plasma or serum ACTH <20 pg/mL suggests adrenal tumor
  • if it is an ACTH dependent cause, an MRI of the brain should be done to look for pituitary adenoma (cushing disease), if it is an ACTH independent cause, a CT of adrenals should be done to look for an adrneal mass such as an adenoma
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17
Q

What is low dose dexamethasone suppression test?

A
  • give a steroid (dexamethasone) = failure of steroid to decrease cortisol levels is diagnostic = proceed next to high dose dexamethasone suppression test = no suppression = Cushing’s syndrome
  • suppression < 5 ugs/dL excludes Cushing with some certainty
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18
Q

What is the tx for Cushing disease?

A

transsphenoidal selective resection of pituitary tumor cures 75-90%

  • Irradiation provides remission in 50-60%
  • 95% 5-year survival
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19
Q

What is hypothyroidism?

A

95% are autoimmune; many associated with other autoimmune issues
-hashimoto’s (chronic lymphocytic/autoimmune), previous thyroidectomy/iodine, ablation, congenital

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20
Q

What are the features of hypothyroidism?

A

weakness, dry/coarse hair, lethargy, slow speech, cold intolerance, eyelid edema, forgetfulness, facial edema, constipation, coarse hair, weight gain, facial dullness, depression, anemia, bradycardia, hyperreflexia, enlarged thyroid

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21
Q

How is hypothyroidism dx?

A

the best test is TSH, hasimoto’s: antithyroid peroxidase, antithyroglobulin antiboides

  • normal/low normal free T4 and TSH = euthyroid
  • low free T4 and elevated TSH = primary hypothyroid
  • low free T4 and low/normal TSH = secondary hypothyroid
  • normal free T4 and elevated TSH = subclinical hypothyroid
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22
Q

What is the tx for hypothyroidism?

A

levothyroxine

-check levels of thyroid frequently

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23
Q

What is diabetes insipidus?

A

caused by a deficiency of or resistance to vasopressin (ADH), which decreases the kidneys’ ability to reabsorb water, resulting in massive polyuria

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24
Q

What is central diabetes insipidus?

A

deficiency of ADH from posterior pituitary/hypothalamus
-no ADH production most common type: idiopathic, autoimmune destruction of posterior pituitary from head trauma, brain tumor, infection, or sarcoidosis

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25
Q

What is nephrogenic diabetes insipidus?

A

lack of reaction to ADH
-partial or complete insensitivity to ADH: caused by drugs (lithium, amphoterrible), hypercalcemia and hypokalemia affect the kidney’s ability to concentrate urine, acute tubular necrosis

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26
Q

How is diabetes insipidus dx?

A

serum osmolality (concentration) is high (unable to stop the secretion of water into the kidneys so blood becomes more concentrated) and urine osmolality is low because it is so dilute

  • water depression test - simplest/most reliable method - continues production of dilute urine despite water deprivation
  • desmopression stimulation test:
  • central: reduction in urine output indicating a response to ADH
  • nephrogenic: continued production of dilute urine (no response to ADH) because kidneys can’t respond
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27
Q

What is the tx for diabetes insipidus?

A
  • central = desmopressin/DDAVP

- nephrogenic = sodium and protein restriction, HCTZ, indomethacin

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28
Q

What are the causes of nonketotic hyperglycemia?

A
  • most commonly seen in type 2 DM in the setting of physiological stress
  • high blood sugar results in high osmolarity without significant keto acidosis
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29
Q

What is the presentation of nonkeotic hyperglycemia?

A
  • onset is typically over days to weeks
  • altered level of consciousness
  • signs of dehydration, weakness, leg cramps
  • vision problems
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30
Q

What are the precipitating factors of nonkeotic hyperglycemia?

A
  • acute infection and other medical conditions
  • drugs that impair glucose tolerance (glucocorticoids) or increase fluid loss (diuretics)
  • nonadherence to diabetes treatment
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31
Q

What are the complications of nonketotic hyperglycemia?

A
  • seizures
  • disseminated intravascular coagulopathy
  • acute renal failure
  • ARDS
  • rhabdomyolysis
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32
Q

How is nonketotic hyperglycemia dx?

A
  • blood sugar greater than 30 mol/L (600 mg/dL)
  • osmolatiry greater than 320 mOsm/kg
  • pH above 7.3
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33
Q

What is the tx for nonkeotic hyperglycemia?

A
  • intravenous normal saline 0.9%
  • IV insulin (as long as serum potassium is >3.3 mEq/L)
  • low molecular weight heparin to decrease the risk fo blood clotting
  • the goal is slow decline in blood sugar levels
  • potassium replacement is often required
  • hydration alone can sometimes precipitously decrease plasma glucose, so insulin dose may need to be reduced
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34
Q

What are the pearls of nonkeotic hyperglycemia?

A
  • quick reduction is osmolality can lead to cerebral edema
  • Infections, nonadherence and certain drugs can trigger marked glucose elevation, dehydration, and altered consciousness in patients with type 2 diabetes
  • patients have adequate insulin to prevent keto acidosis
  • target plasma glucose in acute treatment is between 250 and 300 mg/dL
  • give potassium replacement depending on serum potassium levels
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35
Q

What are type 1 diabetes mellitus?

A

MC in young people

  • little to no endogenous insulin secretion; elevated plasma glucagon pancreatic B cells don’t respond to stimuli
  • most are autoimmune (90%) with antibodies to insulin, islet cells, and glutamic acid decarboxylase
  • sx: polyuria, polydipsia, polyphagia, nocturia, rapid weight loss despite normal/increased appetite, blurred vision, glucosuria
  • random plasma glucose > 200 mg/dL, blurred vision, pruritus, weakness, paresthesias, vulvuovaginitis
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36
Q

How is type 1 diabetes mellitus dx?

A

random plasma glucose > 200 mg/dL with classic symptoms or fasting >126 or > on more than one occasion
-HbA1c > 6.5% or higher

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37
Q

How is type 1 diabetes mellitus tx?

A
  • diet (mediterranean)
  • insulin: regular insulin absorbed most rapidly in the abdomen
  • daily aspirin based on 10-year CVD risk; careful foot care, regular ophthalmology exams, moderate exercise, meticulous personal hygiene, prompt treatment of infection
  • adults show aim to get at least 150 minutes of moderate or 75 minutes of vigorous physical activity a week, which is consistent with prior guidance
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38
Q

What is type 2 diabetes mellitus?

A

younger persons who overweight/obese; central obesity

-features: polydipsia, polyuria, fatigue, candida vaginitis, skin infections, blurred vision, poor wound healing

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39
Q

How is type 2 diabetes mellitus dx?

A
  • random glucose > 200 with symptoms, fasting glucose >126 on more than one occasion, or A1c >6.5%
  • OGTT for pt. with fasting glucose levels between 100-125:
  • 2-hour plasma glucose of >200 on oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
40
Q

What is the diagnostic criteria for prediabetes?

A
  • A1C 5.7-6.4
  • fasting glucose 100-125
  • 2-hour oral glucose tolerance test 140-199
41
Q

How is type 2 diabetes mellitus tx?

A

weight loss, diet, exercise 150 min/week, monitor feet/eyes, control blood pressure, urine albumin/creatinine screenings

42
Q

What are the characteristics of metformin?

A

decreases hepatic glucose production and peripheral glucose utilization, decreases intestinal glucose absorption (these are reasons it leads to weight loss)

  • side effects: lactic acidosis, GI side effects, initiation is contraindicated with eGFR <30 mL/min and not recommended with eGFR 30 to 45 mL/min, discontinue 24 hours before contrast and resume 48 hours after with monitoring for creatinine, stop if creatinine is >1.5
  • benefits: weight loss, inexpensive
43
Q

What are the characteristics of sulfonylureas?

A

stimulates pancreatic beta-cell insulin release (insulin secretagogue)

  • glyburid (diabeta), glipizide (glucotrol), glimepiride(amarly)
  • side effects: hypoglycemia
  • benefits: cheap, rapidly effective
44
Q

What are the characteristics of thiazolidinediones?

A

increases insulin sensitivity in peripheral receptor site adipose and muscle has no effect on pancreatic beta cells

  • pioglitazone (actos), rosiglitazone (avandia)
  • contraindications: CHF, liver disease, fluid retention, weight gain, bladder cancer (pioglitazone), potential increase in MI (rosiglitazone)
45
Q

What are the characteristics of alpha-glucosidase inhibitors?

A

delays intestinal glucose absorption

  • acarboase (precose), miglitol (glyset)
  • GI side effects, three times a day dosing
46
Q

What are the characteristics of meglitinides?

A

stimulates pancreatic beta-cell insulin release

  • repaglinide (prandin) and nateglinide (starlix)
  • side effects: may cause hypoglycemia
47
Q

What are the characteristics of GLP-1 agonists?

A

lowers blood sugar by mimicking incretin - causes insulin secretion and decreased glucagon and delays gastric emptying

  • exenatide (bydureon, byetta), dulaglutide (trulicity), semaglutide (ozempic), liraglutide (victoza, saxenda)
  • side effects: requires injection, frequent GI side effects, caution if gastroparesis
  • benefits: weight loss, reduced CV mortality (semaglutide, liraglutide) in patients with CVD
48
Q

What are the characteristics of DPP-4 inhibitors?

A

dipetpidylpetase inhibition - inhibits degradation of GLP-1 so more circulating GLP-1

  • sitagliptin (januvia), saxagliptin (onglyza)
  • side effects: expensive, possible increased risk of heart failure with sazagliptin
49
Q

What are the characteristics of SGLT2 inhibitor?

A

SGLT2 inhibition lowers renal glucose threshold which results in increased urinary glucose excretion

  • canagliflozin (invokana or sulisent)
  • side effects: vulvovaginal candidiasis, urinary tract infections, bone fractures, lower limb amputations, acute kidney injury, DKA, long-term safety not established
  • benefits: weight loss, reduction in systolic blood pressure, reduced cardiovascular mortality in patients with established CVD
50
Q

What are the characteristics of insulin?

A

add if HbA1C > 9

51
Q

What is the follow up for a patient with type 2 diabetes mellitus?

A

annual - ophthalmologist visit, urine microalbumin

52
Q

What are the complications of type 2 diabetes mellitus?

A

neuropathy (most common), retinopathy (leading cause of blindness), nephropathy

53
Q

What are the ddx of palpitations?

A
  • anxiety
  • electrolyte abnormalities (hypokalemia, hypomagnesemia)
  • hyperthyroidism
  • ischemic heart disease
  • ingestion of stimulant drugs (cocaine, amphetamines, caffeine)
  • exercise, medications (digoxin, beta-blockers, calcium channel antagonists, hydralazines, diuretics, minoxidil)
  • pheochromocytoma
  • hypoglycemia in type 1 DM
  • mitral valve prolapse
  • atrial fibrillation
  • Wolff-Parkinson-White (WPW) syndrome
  • sick sinus syndrome
54
Q

How do you dx palpitations?

A

structural heart disease (CAD, cardiomyopathy, valve disease) = refer to electrophysiology EP study, possible ICD

  • history, ECG, echo, and exercise testing = identify and treat abnormal ECG
  • laboratories guided by differential = CMP, CBC, TSH, Urine Toxicology
55
Q

What is the tx of palpitations?

A

guided by diagnosis

56
Q

What is diabetic ketoacidosis?

A

a medical emergency and complications of diabetes

57
Q

What are the characteristics of diabetic ketoacidosis?

A
  • patients have increased insulin requirements, which leads to a shortage, as a response, the body begins burning excess fat (and fatty acids), causing ketone body accumulation
  • usually younger patients with type 1 DM
  • insulin deficiency = hyperglycemia = dehydration = ketonemia (anion gap metabolic acidosis) = potassium deficit
58
Q

What are the signs and symptoms of diabetic ketoacidosis?

A

thirst, polyuria, polydipsia, nocturia, weakness, fatigue, confusion, n/v, fatigue, chest pain, abdominal pain

59
Q

What is the PE of diabetic ketoacidosis?

A

tachycardia, tachypnea, hypotension, decreased skin turgor, fruity breath/Kussmaul’s respiration

60
Q

How is diabetic ketoacidosis dx?

A

lab values seen in DKA include blood sugars about 250 mg/dL and anion gap metabolic acidosis with pH below 7.3 and bicarbonate below 18

  • patients will also show present plasma ketones
  • due to an extracellular shift, patients may be hyperkalemic
61
Q

What are the lab values for mild diabetic ketoacidosis?

A 
plasma glucose >250
arterial pH >7.3
serum bicarb 15-18
ketones positive 
serum osm variable
62
Q

What are the lab values for moderate diabetic ketoacidosis?

A 
plasma glucose >250
arterial pH 7-7.24
serum bicarb 10-<15
ketones positive 
serum osm variable
63
Q

What are the lab values for severe diabetic ketoacidosis?

A 
plasma glucose >250
arterial pH <7
serum bicarb <10
ketones positive 
serum osm variable
64
Q

What is the tx for diabetic ketoacidosis?

A

IV fluids = critical 1st step, regular insulin (lowers serum glucose and switches the body from catabolic to anabolic state); potassium, bicarb in severe acidosis

65
Q

What is thyroiditis?

A

a general term that refers to inflammation of the thyroid gland and includes a group of individual disorders causing thyroidal inflammation but presenting in different ways

66
Q

What is hashimoto’s thyroiditis?

A

an autoimmune form of thyroiditis = autoantibodies directed against thyroid =thyroid tissue is destroyed over time = chronic hypothyroidism

67
Q

What are the characteristics of hashimoto’s thyroiditis?

A
  • the most common cause of hypothyroidism in the United States
  • Hashimoto’s thyroiditis may present similarly to subacute thyroiditis, but the presence of neck tenderness and a recent viral illness should make you think subacute thyroiditis
  • goiter on PE
  • high levels of anti-TPO antiboides
  • tx depends whether hypothyroidism is present
  • euthyroid: no treatment
  • chronic hypothyroidism: lifelong substitution with T4
68
Q

What is postpartum thyroiditis?

A
  • 2-12 months after giving birth
  • immune system diminished during pregnancy = after childbirth immune system is more active and might attack the thyroid
  • hyperthyroid phase 5-7 months after birth followed by normal thyroid function
69
Q

What is subacute thyroiditis (Quervain’s thyroiditis)?

A
  • the most common cause of thyroid pain and has a greater incidence in women
  • inflamed, painful thyroid, fever, and muscle aches
  • the etiology is often post-infectious and viral in origin
  • usually following symptoms such as fever, myalgia, and pharyngitis
  • early in course may be hyperthyroid followed by a period of hypothyroidism
  • increased ESR (60-100)
70
Q

What is drug-induced thyroiditis?

A

thyroiditis can also be seen in patients taking certain drugs

  • ant thyroid medications: methimazole and propylthiouracil
  • lithium - bipolar disorder
  • amiodarone - antiarrhythmic
  • interferon alpha
  • tyrosine kinase inhibitors (e.g sunitinib) - anti-cancer
  • checkpoint inhibitors (e.g nivolumab, pembrolizumab)
  • TSH should be checked every 6-12 months - T4 therapy given right away
71
Q

What is infectious bacterial thyroiditis?

A

(rare)
is often due to the hematogenous spread of staph or strep
-its signs are the classical ones of inflammation: fever, heat, pain, redness, and swelling
-increase WBC

72
Q

How is thyroiditis dx?

A

lab values depend on the cause of thyroiditis and may be euthyroid

  • with pain think: painful subacute (Quervain’s post-viral), infectious, radiation, trauma
  • no pain: postpartum (2-12 months after given birth), drug-induced (lithium/amiodarone), Hashimoto’s thyroiditis, fibrous
  • TFTs usually hyperthyroid at presentation, US/radioactive iodine scanning have little value
  • increase ESR (subacute)
  • increase WBC (infectious)
  • high levels of anti-TPO antibodies (Hashimoto’s)
73
Q

What is the tx for Hashimotos?

A

TX depends whether hypothyroidism is present

  • euthyroid: no treatment
  • chronic hypothyroidism: lifelong substitution with T4
74
Q

What is the tx for subacute and postpartum thyroiditis?

A

usually resolve on their own after 12-18 months, often only need pain management

  • beta-blockers during hyperthyroid state
  • T4 for several months during hypothyroid phase until TSH normalizes then can be stopped
  • occasionally permanent hypothyroidism
75
Q

What is the tx for drug-induced thyroiditis?

A

stop offending drugs lithium amiodarone will usually return to euthyroid state once the meds are stopped

76
Q

What is the tx for infectious bacterial thyroiditis?

A

the treatment is that for any febrile disease, including specific antibiotic drugs if the invading organism has been identified and its sensitivity to the drug established, surgical drainage if abscess present

77
Q

What is the presentation of heat intolerance?

A
  • uncomfortable in hot environments

- hot and sweats excessively

78
Q

What are the causes of heat intolerance?

A

heat intolerance can be seen in hyperthyroidism

  • other causes include:
  • amphetamines along with other types of stimulant medications
  • anticholinergics and other drugs that can impair sweating
  • caffeine
  • menopause
  • multiple sclerosis
  • fibromyalgia
  • diabetes
  • hypothalamic tumors
79
Q

What is the tx for heat intolerance?

A
  • resolve the underlying cause of the heat intolerance
  • symptoms can be reduced by staying in cool environment
  • drinking more fluids
  • cooling vests can be used as a preventative tool
80
Q

What are the pearls of heat intolerance?

A

heat intolerance symptoms can be endocrine disorders such as hyperthyroidism, drugs, or other medical conditions, rather than the result of too much exercise or ambient conditions

81
Q

What is the presentation of cold intolerance?

A

patient complains of intolerance to cold such as to the ambient conditions

82
Q

What is the cause of cold intolerance?

A

common symptoms of hypothyroidism include cold intolerance

  • some causes of cold intolerance are:
  • anemia
  • anorexia nervosa
  • raynaud phenomenon
  • chronic severe illness
  • general poor health
  • an underactive thyroid (hypothyroidism)
  • problems with the hypothalamus
  • fibromyalgia
83
Q

What is the treatment of cold intolerance?

A
  • resolve the underlying cause of the cold intolerance

- symptoms can be reduced by staying in a warm environment

84
Q

What are the pearls of cold intolerance?

A

cold intolerance symptoms can be endocrine disorders such as hypothyroidism, or other medical conditions, rather than the ambient conditions

85
Q

What are rest tremors?

A
  • parkinson’s disease
  • wilson’s disease
  • essential tremor only if severe: rest < postural and action
86
Q

What are postural and action (terminal) tremors?

A
  • physiologic tremor
  • exaggerated physiologic tremor (these factors can also aggravate other forms of tremor)
  • stress, fatigue, anxiety, emotion
  • endocrine: hypoglycemia, thyrotoxicosis, pheochromocytoma, adrenocorticosteroids
  • drugs and toxins: b-agonists, dopamine agonists, amphetamines, lithium, tricyclic antidepressants, neuroleptics, theophylline, caffeine, valproic acid, alcohol withdrawal, mercury (hatter’s shakes), lead, arsenic, others
  • essential tremor (familial or sporadic)
  • primary writing tremor
  • With other CNS disorders
  • parkinson’s disease
  • other akinetic-rigid syndromes
  • idiopathic dystonia, including focal dystonias
  • with peripheral neuropathy
  • Charcot-Marie-Tooth syndrome (controversial whether to call this the Roussy-Levy syndrome)
  • variety of other peripheral neuropathies (especially dysgammaglobuliemia)
  • cerebellar tremor
87
Q

What is kinetic (intention) tremor?

A

disease of cerebellar outflow = multiple sclerosis, trauma, tumor, vascular disease, Wilson’s acquired hepatocerebral degeneration, drugs, toxins (e.g mercury), others

88
Q

What are the miscellaneous tremor?

A

psychogenic, orthostatic, rhythmical movements in dystonia, oscillatory myoclonus, asterixis, clonus, nystagmus

89
Q

What is an essential tremor?

A
  • characteristics: usually presents with a postural tremor of the hands or head that is often worsened by psychic stress; can occur at any age
  • intention/action tremor - shaking occurs with simple tasks such as tying shoelaces, handwriting, shaving or simply holding hands against gravity
  • when laryngeal muscles are involved, the patient’s voice may shake as well
  • legs are usually spared in this condition
  • essential tremor usually becomes more prominent with age, though significant disability is rare
  • improved after drinking alcohol, exacerbated by action
  • MC caused by autosomal dominant - usually have family member with similar symptoms
90
Q

What is the tx of tremors?

A

beta-blockers (propranolol); symptomatic treatment is limited to patients with lifestyle-limiting tremors, in addition to propranolol, other therapies include primidone, alprazolam, topiramate, or gabapentin

91
Q

What is hyperparathyroidism?

A

a condition in which one or more of the parathyroid glands become overactive and secrete too much parathyroid hormone (PTH)

  • this causes the levels of calcium in the blood to rise
    1. increase PTH = bone breakdown = release Ca
    2. kidney holds onto Ca and increased Vitamin D3
  • the intestine absorbs more Ca
    3. the intestine absorbs more Ca = increased Ca in blood levels
92
Q

What are the two causes of hyperparathyroidism?

A

primary and secondary

  • primary: increased PTH usually caused by PTH secreting parathyroid ADENOMA
  • secondary: increase PTH by a physiologic response to hypocalcemia or vitamin D deficiency
  • chronic kidney disease is the most common cause of secondary hyperparathyroidism
93
Q

What is the presentation of hyperparathyroidism?

A

weakness, fatigue, constipation = stones, bones, abdominal groans, psych moans, and fatigue overtones

  • bone loss from increased PTH and Ca absorption from bones = pain in bones
  • renal loss of Ca and phosphorus = kidney stone
  • increase GI absorption of Ca and abdominal cramps = groans
  • irritability, psychosis, depression = maons
94
Q

What are the labs for hyperparathyroidism?

A
  • blood = increase Ca, increase PTH, and decrease phosphorus
  • urine = hyperphosphaturia, hypercalciuria (all Ca and phosphorus go out through kidneys to urine)
95
Q

What is the tx for hyperparathyroidism?

A
  • primary = surgical correction to remove the overactive parathyroid gland = if all 4, remove 3.5 glands
  • secondary = replace cause (vitamin D/Ca supplementation)
  • if Ca very high: IV fluids, lasix, calcitonin; treat osteoporosis with bisphosphonates

Emergency Medicine EOR (12 decks)

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